LIBRARY OF CONGRESS. 
 Chap. J>_r Copyright No 
 
 Shelf. 
 
 J3&& 
 
 UNITED STATES OF AMERICA. 
 
A 
 
 TEXT=BOOK 
 
 PAT H O LOGY 
 
 BY 
 
 ALFRED STENGEL, M. D. 
 
 Instructor in Clinical Medicine in the University of Pennsylvania ; Professor of Clinical 
 Medicine in the Woman's Medical College ; Physician to the Philadelphia Hos- 
 pital ; Physician to the Children's Hospital, Philadelphia, etc. 
 
 WITH 372 ILLUSTRATIONS 
 
 PHILADELPHIA 
 
 W. B. SAUNDERS 
 
 925 Walnut Street 
 
 1898 
 
16843 
 
 Copyright, 1898, 
 By W. B. SAUNDKRS. 
 
 
 
 
PREFACE 
 
 In writing this book the author has tried to present the sub- 
 ject of Pathology in as practical a form as possible, and always 
 from the point of view of the clinical pathologist. Considerable 
 parts of the book were first prepared and used as the basis of 
 demonstrations upon clinical pathology for students of medicine ; 
 prominence is therefore given to pathologic physiology, and dis- 
 cursiveness and citation of authorities are avoided. 
 
 Except in a few instances, discussion of methods of examina- 
 tion has been omitted, because it seemed unwise to increase the 
 size of the book with matter that is appropriately presented in 
 special works on technique. For similar reasons the author has 
 decided to exclude the pathology of the skin and of the organs 
 of special sense. 
 
 Controversial matter has been avoided as much as possible, 
 excepting in certain parts of the sections on General Bacteriology 
 and on Neuropathology, in which it seemed proper to discuss 
 conflicting theories. 
 
 Full use has been made of works on pathology and of special 
 monographs in English as well as in French and German. 
 
 The author is greatly indebted to Dr. Samuel S. Kneass and 
 Dr. Alonzo E. Taylor for assistance in the sections on General 
 Bacteriology and the Degenerations in Part I., and especially 
 to Dr. Joseph Sailer, who prepared almost wholly the sections 
 on Neuropathology. Acknowledgment is also due Mr. Thos. 
 F. Dagney, of Mr. Saunders' editorial office, for his uniform 
 courtesy and assistance in many ways, and Mr. R. W. Greene 
 for the preparation of the Index. 
 
CONTENTS. 
 
 PART I.— GENERAL PATHOLOGY. 
 
 CHAPTER I. 
 
 The Etiology of Disease 18 
 
 Traumatism, 19. — Physical Conditions, 20. — Poisons, 23.— Bacteria 
 and Parasites, 29. 
 
 CHAPTER II. 
 
 Disorders op Nutrition and Metabolism 31 
 
 Food, 31. — Diminished Supply of Food, 31. — Increased Supply of 
 Food, 32. — Excessive Tissue-destruction, 33. — Acid-intoxication, 33. — 
 Formation of Albumoses, 35. — Alloxin Bases and Uric Acid, 36. — 
 Gout, 36.— Glycosuria, 37.— Diabetes, 38.— Fever, 41. 
 
 CHAPTER III. 
 
 Disturbances of the Circulation of the Blood 43 
 
 General Disturbances, 43. — Local Hyperemia, 46. — Local Anemia, 
 47. — Hemorrhage, 48. — Embolism, 51. — Infarction, 53. — Thrombosis, 
 55. — Edema, 59. 
 
 CHAPTER IV. 
 
 Retrogressive Processes 62 
 
 Atrophy, 62. — The Degenerations, 64. — Cloudy Swelling, 64. — Fatty 
 Infiltration, 66. — Fatty Degeneration, 68. — Amyloid Degeneration, 71. 
 — Hyaline Degeneration, 74. — Mucoid Degeneration, 76. — Colloid De- 
 generation, 78. — Glycogenic Infiltration, 79. — Dropsical Infiltration, 80. 
 — Cellular Necrosis, 97. — Abnormal Cell-division, 97. 
 
 CHAPTER V. 
 
 Inflammation and Regeneration 98 
 
 Inflammation, 98. — Regeneration, 109. — Metaplasia, 113. 
 
 CHAPTER VI. 
 
 Progressive Tissue-changes 113 
 
 Hypertrophy, 113. — Tumors, 115. — Fibroma, 120. — Myxoma, 124. — 
 Lipoma, 125. — Xanthoma, 126. — Chondroma, 127. — Osteoma, 130. — 
 Lymphangioma, 132. — Hemangioma, 132. — Lymphadenoma, 135. — 
 
 9 
 
10 CONTESTS. 
 
 PAGE 
 
 Sarcoma, 145. — Spindle-celled Sarcoma, 141. — Round-celled Sarcoma. 
 142. — Angiosarcoma, 144. — Cylindroma, 145. — Melanosarcoma, 146. — 
 Giant-celled Sarcoma, 147. — Mixed Tumors, 149. — Chloroma. 149. — 
 Psammoma, 149.— Mycosis Fungoides, 149. — Endothelioma, 150.— 
 Glioma, 151.- Neuroma, 154. — Leiomyoma, 154. — Rhabdomyoma, 157. 
 — Papilloma, 157. — Adenoma, 159. — Carcinoma, 163. — Epithelioma, 
 171. — Glandular Carcinoma, 172. — Colloid Cancer, 174. — Syncytioma 
 Malignum, 175. — Cysts, 176. — Teratoma, 179. 
 
 CHAPTER VII. 
 Bacteria and Diseases due to Bacteria 181 
 
 Classification, 182. — Morphology, 183. — Demonstration, 186. — Biol- 
 ogy, 188. — Functions and Products of Bacteria, 192. — Effects of Toxic 
 Products of Bacteria, 196. — Immunity, 197. 
 
 Diseases due to Bacteria, 201.— Suppurative Diseases, 202.— 
 Gonorrhea, 206.— Croupous Pneumonia, 207. — Other Forms of Pneu- 
 monia, 209. — Rhinoscleroma, 210. — Diphtheria, 211. -Typhoid fever, 
 214.— Bacillus Coli Communis, 218.— Cholera, 219.— Tuberculosis, 223. 
 — Fowl-tuberculosis, 235. — Leprosy, 235. — Glanders, 239. — Malignant 
 Edema, 240.— Anthrax, 242. — Infectious Emphysema, 244. — Tetanus, 
 246.— Actinomycosis, 247. — Mycetoma, 250. — Relapsing Fever, 251. — 
 Influenza, 252. — Bubonic Plague, 253.— Syphilis, 254. — Soft Chancre, 
 259.— Yellow Fever, 260.— Measles, 261.— Scarlet Fever, 261.— 
 Mumps, 261. — Whooping-cough, 261. — Typhus Fever, 262.— Rabies, 
 262. — Hemorrhagic Diseases, 262. — Rheumatism, 263. — Malta Fever, 
 264.— Beri-Beri, 265. 
 
 CHAPTER VIII. 
 
 Animal Parasites and Diseases Caused by Them 265 
 
 Protozoa, 265.— Amoeba Coli, 265.— Other Amoebae, 266— Hemato- 
 zoon Malaria?, 267. — Coccidium Oviforme, 269. — Animal Parasites and 
 Carcinoma, 270. — Animal Parasites and Molluscum Contagiosum, 272. 
 — Variola and Vaccinia, 273. — Varicella, 274. — Measles, Scarlet Fever, 
 and other Diseases, 274. — Cercomonas Intestinalis, 274. — Trichomonas 
 Intestinalis, 275. — Trichomonas Vaginalis, 275. — Other Forms of 
 Trichomonas, 275. — Balantidium Coli, 276. — Megastoma Entericum, 
 276. 
 
 Cestodes, oi Tape=worms,277.— Ta>nia Solium, 279.— Taenia Sagi- 
 nata, 280.— Taenia Nana, 281.— Taenia Elliptica, 282.— Taenia Flavo- 
 punctata, 282.— Taenia Madagascariensis, 282.— Other Forms of Taenia, 
 282.— Bothriocephalic Latus, 285.— Bothriocephalus Cordatus, 286.— 
 Bothriocephalic Cristatus, 286. — Bothriocephalus Liguloides, 286. 
 
 Nematodes, or Round=worms, 286. — Ascaris Lumbricoides, 286. 
 — Ascaris Mystax, 287. — Ascaris Maritima, 287, — Oxyuris Vermicu- 
 laris, 287.— Trichina Spiralis, 288.— Ankylostoma Duodenale, 289.— 
 Anguillula Intestinalis and Rhabditis Stercoralis, 290. — Trichncephalus 
 Dispar, 290. — Filaria Medinensis, 291. — Filaria Sanguinis Hominis, 
 291.— Other Forms of Filaria, 293.— Echinoooccus Gigas, 293.— 
 Eustrongylus Gigas, 293. — Strongylus Longevaginatus, 293. 
 
 Trematodes, or Fluke=worms, 293.— Distoma Hepaticum, 294. — 
 
CONTENTS. 11 
 
 PAGE 
 
 Distoma Lanceolatum, 294. — Distoma Hematobium, 294. — Distoma Pul- 
 monale, 296. — Other Fluke-worms, 296. 
 
 Annelids, 296. 
 
 Arthropodia, 296. — Pentastomum Denticulatum, 297. — Myiasis, 297. 
 
 PAET II.— SPECIAL PATHOLOGY. 
 
 CHAPTER I. 
 
 Diseases op the Blood 298 
 
 Anatomy, 298. — Blood-formation, 303. — Pathologic Changes in Red 
 Corpuscles, 303. — Pathologic Changes in Leukocytes, 305. — Pathologic 
 Changes in Plasma, 306.— Plethora, 306.— Oligemia, 307.— Hydremia 
 and Anhydremia, 307. — Lipemia, 308. — Melanemia, 309. — Hemocytol- 
 ysis and Hemoglobinemia, 309. — Polycythemia, 310. — Leukocytosis, 
 310.— Hypoleukocytosis, 312.— Anemia, 313.— Chlorosis, 315.— Pro- 
 gressive Pernicious Anemia, 317. — Leukemia, 319. — Hodgkin's Disease, 
 323. — Pseudoleukemia Infantum, 323.— Foreign Bodies and Parasites, 
 324.— Methods of Examining the Blood, 324. 
 
 CHAPTER II. 
 Diseases of the Lymphatic Tissues 326 
 
 Spleen, 326. — Abnormal Development and Situation, 327. — Circu- 
 latory Disturbances, 328. — Inflammation, 329. — Atrophy and Degenera- 
 tion, 331. — Tumors and Parasites, 332. — Infectious Diseases, 333. 
 
 Lymphatic Glands, 334.— Atrophy, 334.— Hypertrophy, 334.— 
 Degenerations, 334. — Inflammation, 336. — Infectious Diseases, 338. — 
 Tumors, 341. 
 
 Bone=marrow, 343.— Degenerations, 343.— Atrophy, 344.— Hyper- 
 trophy, 344. — Inflammation, 344. — Infectious Diseases and Tumors, 
 345. 
 
 Thymus Gland, 345. 
 
 CHAPTER III. 
 
 Diseases of the Circulatory System 346 
 
 Heart, 346. — Congenital Diseases and Deformities, 346. — Circulatory 
 Disturbances, 350. — Endocardium, 352. — Endocarditis, 352. — Circulatory 
 Disturbances, 359. — Degenerations, 359.— Inflammation, 364. — Hypo- 
 plasia and Atrophy, 370. — Hypertrophy and Dilatation, 371. — Aneurysm, 
 374. — Wounds and Rupture, 374. — Infectious Diseases, 375. — New 
 Growths and Parasites, 375. — Pericardium, 375. — Circulatory Disturb- 
 ances, 376. — Inflammation, 376. — Infectious Diseases, 380. — Tumors and 
 Parasites, 380. — Pneumopericardium, 380. 
 
 Arteries, 381.— Congenital Defects, 381.— Hypertrophy, 381.— 
 
12 CONTENTS. 
 
 PAGE 
 
 Atrophy, 381. — Degenerations, 382. — Inflammation, 383. — Infectious 
 Diseases, 388. — Aneurysm, 388. 
 
 Veins, 395. — Circulatory Disturbances, 395. — Degenerations, 396. — 
 Inflammation, 396. — Dilatation, 397. — Tumors, 398. — Infectious Dis- 
 eases, 399. 
 
 Lymphatic Channels, 399.— Inflammation, 399.— Dilatation, 399. 
 —Infectious Diseases, 400.— Tumors, 401.— Parasites, 401. 
 
 Thoracic Duct, 401. 
 
 CHAPTER IV. 
 
 Diseases of the Respiratory System 402 
 
 Nasal Cavities, 402. — Congenital Abnormalities, 402. — Circulatory 
 Disturbances, 402. — Inflammation, 402. — Infectious Diseases, 403. — 
 Tumors, 403.— Parasites and Foreign Bodies, 404. 
 
 Larynx, 404. — Congenital Abnormalities, 404. — Circulatory Dis- 
 turbances, 404. — Inflammations, 404. — Infectious Diseases, 406. — 
 Tumors, 407. — Parasites and Foreign Bodies, 408. 
 
 Trachea, 408. — Malformations, 408. — Circulatory Disturbances, 408. 
 — Inflammation, 408. — Infectious Diseases, 409. — Tumors, 409. 
 
 Bronchi, 409. — Congenital Malformations, 409. — Circulatory Dis- 
 turbances, 409. — Inflammations, 409. — Stenosis and Obstruction, 412. — 
 Dilatation, 412. — Infectious Diseases, 413. — Tumors, 413. — Parasites 
 and Foreign Bodies, 413. 
 
 Lungs, 415. — Congenital Defects, 415. — Circulatory Disturbances, 
 415. — Hypertrophy and Atrophy, 419. — Emphysema, 419. — Atelectasis, 
 423. — Inflammation or Pneumonia, 425. — Gangrene, 442. — Tubercu- 
 losis, 443. — Syphilis, 454.— Glanders, 456. — Actinomycosis, 456. — 
 Tumors, 457. — Parasites, 459. 
 
 Pleura, 460. — Circulatory Disturbances, 460. — Inflammation, 461. — 
 Infectious Diseases, 465. — Tumors and Parasites, 465. 
 
 CHAPTER V. 
 Diseases of the Gastro-intestinal Tract 467 
 
 Mouth, 467. — Congenital Abnormalities, 467. — Circulatory Disturb- 
 ances, 467. — Inflammation, 468. — Atrophy and Degeneration, 471. — 
 Infectious Diseases, 471. — Tumors, 473. 
 
 Teeth, 474. 
 
 Pharynx and Toncils, 475. — Circulatory Disturbances, 475. — In- 
 flammations, 475. — Pressure-necrosis, 478. — Infectious Diseases, 479. — 
 Tumors, 480. 
 
 Salivary Glands, 481. 
 
 Esophagus, 482. — Congenital Defects, 482. — Circulatory Disturb- 
 ances, 482.— Inflammations, 482.— Stenosis, 483.— Dilatation, 483.— 
 Perforation and Rupture, 484. — Infectious Diseases, 484. — Tumors, 484. 
 
 Stomach, 485. — Congenital Defects, 485. — Circulatory Disturbances, 
 485. — Inflammations, 486. — Peptic Ulcer, 489. — Atrophy and Degener- 
 ations, 491. — Alterations in Position and Size, 492. — Infectious Dis- 
 eases, 493.— Tumors, 493. 
 
 Intestines, 497. — Abnormalities, 497. — Intestinal Obstruction, 500. 
 —Prolapse of Rectum, 502.— Atrophy and Degeneration, 502.— Circu- 
 
CONTENTS. 13 
 
 PAGE 
 
 latory Disturbances, 503. — Inflammation, 504. — Inflammation of Special 
 Parts, 506. — Infectious Diseases, 510. — Tumors, 516. — Parasites, 519. — 
 Intestinal Rupture and Foreign Bodies, 520. 
 
 Liver, 521. — Malformations and Changes of Position, 521. — Circu- 
 latory Disturbances, 522. — Atrophy and Degenerations, 524. — Inflam- 
 mations, 529. — Hypertrophy, 534. — Rupture, 534. — Infectious Diseases, 
 543. — Tumors, 536. — Parasites, 539. 
 
 Biliary Ducts and Gallbladder, 541. — Inflammations, 541. — 
 Stenosis and Dilatation, 542. — Gall-stones, Cholelithiasis, 543. — Tumors, 
 544.— Jaundice, 544. 
 
 Pancreas, 546. — Congenital Abnormalities, 546 — Circulatory Dis- 
 turbances, 546. — Atrophy and Degenerations, 546. — Inflammations, 548. 
 — Infectious Diseases, 549. — Tumors, 549. — Pancreatic Duct, 550. 
 
 Peritoneum, 551. — Congenital Abnormalities, 551. — Circulatory 
 Disturbances, 551. — Inflammations, 553. — Tumors, 557. — Parasites, 558. 
 
 CHAPTER VI. 
 
 Diseases of the Ductless Glands 558 
 
 Thyroid Gland, 558. — Congenital Defects, 559.— Disturbances of 
 Circulation, 559. — Inflammations, 559. — Struma or Goiter, 559. — Infec- 
 tious Diseases, 562. — Tumors and Parasites, 562. — General Results of 
 Thyroid Disease, 562. 
 
 Suprarenal Bodies, 564. — Congenital Anomalies, 564. — Degenera- 
 tions, 565. — Infectious Diseases, 565. — Circulatory Disturbances, 566. — 
 Inflammation, 566. — Tumors, 566. — General Effects of Suprarenal Dis- 
 eases, 566. 
 
 CHAPTER VII. 
 
 Diseases of the Urinary Organs 567 
 
 Kidneys, 567. — Congenital Anomalies, 567. — Changes of Position, 
 568. — Circulatory Disturbances, 568. — Inflammations, 570. — Atrophy 
 and Hypertrophy, 585. — Degenerations, 586. — Concretions in the Urin- 
 iferous Tubules, 589. — Infectious Diseases, 590. — Tumors, 590. — Para- 
 sites, 594. 
 
 Pelvis of Kidney and Ureter, 595.— Congenital and Acquired 
 Malformations, 595. — Calculus, 596. — Inflammation, 596. — Infectious 
 Diseases, 597. — Tumors, 598.— Parasites, 598. 
 
 Urinary Bladder, 599. — Malformations, 599.— Changes of Position, 
 599. — Rupture, 600. — Circulatory Disturbances, 600. — Inflammation, 
 600. — Infectious Diseases, 602. — Calculi and Foreign Bodies, 603. — 
 Tumors, 604. — Abnormal Conditions of the Urine, 606. — Chemical 
 Changes and Sediments of Urine, 611. 
 
 Urethra, 614. — Congenital Abnormalities, 614. — Inflammations, 614. 
 — Injuries, 617. — Infectious Diseases, 617. — Tumors, 618. 
 
 CHAPTER VIII. 
 
 Diseases of the Reproductive Organs 618 
 
 Uterus, 618. — Development and Anatomy, 618. — Congenital Abnor- 
 malities, 619. — Alterations of Position, 620. — Stenosis, Dilatation, and 
 
14 CONTENTS. 
 
 PAGE 
 
 Rupture, 622. — Circulatory Disturbances, 623. — Inflammations, 624. — 
 Infectious Diseases, 628. — Atrophy and Degenerations, 631.— Hyper- 
 trophy and Hyperplasia, 631. — Tumors, 632. — Parasites, 637. 
 
 Ovaries, 637. — Development and Anatomy, 637. — Congenital Ab- 
 normalities, 638. — Changes in Position, 638. — Circulatory Disturbances, 
 638. — Inflammation, 63 l J. — Infectious Diseases, 639. — Tumors, 640. — 
 Cysts of the Parovarium, 643.— Cysts of Kobelt, 644. 
 
 Fallopian Tubes, 644. — Congenital Abnormalities, 644. — Changes 
 of Position, 644. — Stenosis, 645. — Dilatation, 645. — Circulatory Disturb- 
 ances, 645. — Inflammations, 646. — Infectious Diseases. 648. — Tumors, 
 649. — Extra-uterine Pregnancy, 650. 
 
 Vagina, 652.— Prolapse of Vaginal Wall, 652. — Stenosis, 652. — 
 "Wounds and Fistulse, 052. — Circulatory Disturbances, 653. — Inflamma- 
 tions, 653. — Infectious Diseases, 654. — Tumors, 654. 
 
 Decidua, Placenta, and Fetal Membranes, 654. — Anatomic 
 Considerations, 654. — Abnormalities of Development, 655. — Circulatory 
 Disturbances, 655. — Inflammation, 656. — Infectious Diseases, 657. — 
 Hyperplasia, 657. 
 
 Vulva, 659. — Circulatory Disturbances, 659. — Inflammation, 659. — 
 Infectious Diseases, 660. — Tumors, 660. 
 
 Penis and Scrotum, 661.— Congenital Abnormalities, 661. — In- 
 flammation, 661. — Infectious Diseases. 662. — Tumors, 662. — Injuries, 
 663. 
 
 Testicles, 663. — Congenital Abnormalities, 663. — Atrophy and 
 Hypertrophy, 663. — Degenerations, 664. — ( irculatory Disturbances, 
 664. — Inflammation, 664.— Infectious Diseases, 667. — Tumors, 669. — 
 Parasites, 671. 
 
 Prostate Gland, 671.— Inflammation, 671. — Atrophy and Degener- 
 ation. 672. — Concretions, 672. — Infectious Diseases, 672. — Hypertrophy 
 and Tumors, 672. 
 
 Cowper's Glands, 675. 
 
 Seminal Vesicles, 675. 
 
 Mammary Glands, 676. — Congenital Abnormalities, 676. — Circu- 
 latory Disturbances, 676. — Inflammations, 677.— Atrophy and Hyper- 
 trophv, ti78. — Degenerations, 678. — Infectious Diseases, 678. — Tumors, 
 679. ' 
 
 CHAPTER IX. 
 
 Diseases of the Bones 682 
 
 Anatomy and Development, 682. — Rickets, 683.— Regeneration of 
 Bone, 685.— Circulatory Disturbances, 688.— Inflammations, 688.— 
 Hypoplasia and Atrophy, 692.— Degenerative Conditions, 692. — Infec- 
 tious Diseases, 694. — Tumors, 698. 
 
 CHAPTER X. 
 
 Diseases of the Joists 700 
 
 Luxation and Ankylosis, 700.— Distortion, 700.— Circulatory Disturb- 
 ances, 700. — Inflammations, 701. — Infectious Diseases, 704. — Tendon- 
 sheaths and Bursae, 706. 
 
CONTENTS. 15 
 
 CHAPTER XI. 
 
 PAGE 
 
 Diseases of the Voluntary Muscles 706 
 
 Hypertrophy, 706. — Circulatory Disturbances, 707. — Inflammations, 
 707. — Atrophy and Degenerations, 709. — Infectious Diseases, 712. — 
 Tumors and Parasites, 712. 
 
 CHAPTER XII. 
 
 Diseases of the Brain and its Membranes 713 
 
 Dura Mater, 713. — Circulatory Disturbances, 713. — Inflammations, 
 713. — Infectious Diseases, 714.— Tumors, 715. 
 
 The Pia and Arachnoid, 715.— Circulatory Disturbances, 715 — 
 Inflammation, 716. — Infectious Diseases, 719. — Tumors, 721. 
 
 Brain, 723. — Development and Anatomy, 723. — Congenital Abnor- 
 malities, 727. — Post-mortem Degenerative Conditions, 732.— General 
 Pathologic Anatomy of the Nervous System, 732. — The Blood-vessels, 
 743. — Circulatory Disturbances, 745. — Inflammation, 753. — Injuries of 
 Central Nervous System, 760.— Choroid Plexus and Ventricles, 761. — 
 Tumors, 768. — Pituitary Body or Hypophysis Cerebri, 771. 
 
 CHAPTER XIII. 
 
 Diseases of the Spinal Cord and its Membranes 775 
 
 Dura Mater, 775.— Fatty Infiltration, 775.— Hemorrhage, 775.— 
 Tuberculosis, 775.— Syphilis, 776. 
 
 Pia and Arachnoid, 777. — Circulatory Disturbances, 777. — Degener- 
 ations, 777. — Inflammations, 777. — Infectious Diseases, 778. 
 
 Cord, 778. — Anatomy of the Cord, 778. — Congenital Abnormalities, 
 780. — Hydromyelia and Syringomyelia, 781. — Circulatory Disturbances, 
 785. — Inflammations, 787. — Primary Degenerations, 793. — Secondary 
 rations, 800.— Tumors, 802. 
 
 CHAPTER XIV. 
 
 Diseases of the Peripheral Nervous System 802 
 
 Ganglia of the Cranial Nerves, 802. 
 
 The Nerves, 803. — Circulatory Disturbances, 803.— Atrophy and 
 Degeneration, 803. — Inflammation, 806. — Infectious Diseases, 808. — 
 Tumors, 809. 
 
A TEXT-BOOK OF PATHOLOGY. 
 
 PART I. 
 GENERAL PATHOLOGY. 
 
 Pathology is the science that deals with disease in all its 
 aspects. It includes the study of the causes, the manifestations, 
 and the results of disease. 
 
 Three important subdivisions of the study of pathology are 
 recognized, viz., etiology, or the study of the causes of disease ; 
 morbid or pathologic anatomy, the study of the structural changes 
 in disease ; and morbid or pathologic physiology, the study of 
 disturbances of function. In the latter group is included patho- 
 logic chemistry, as morbid chemical action and its results are the 
 outcome of disturbed function. 
 
 Pathology, or more especially pathologic anatomy, may be di- 
 vided into general and special pathology. The former treats of 
 pathologic processes irrespective of any individual part ; the latter 
 deals with the processes or changes in individual organs or parts. 
 
 Disease itself may be denned as abnormality in structure, in 
 function, or in both combined. It is doubtful whether alteration 
 of function can occur without some alteration in structure, but it 
 frequently happens that functional disturbances are present though 
 no structural alterations are discoverable even by the most precise 
 methods of investigation. 
 
 The symptoms of disease are the expressions of abnormal func- 
 tional activity, and are therefore properly discussed under the 
 head of pathologic physiology ; but they are so important from a 
 practical standpoint, and form such an extensive subject of inves- 
 tigation, that they are usually considered apart from pathology, 
 in special treatises dealing with diagnosis and the practice of 
 medicine. 
 
18 TEXT-BOOK OF PATHOLOGY. 
 
 CHAPTER I 
 
 THE ETIOLOGY OF DISEASE. 
 
 The causes of disease may be classified as 'predisposing and 
 determining. The former prepare the system or part by rendering 
 it weaker and less resistant ; the latter are the immediate or spe- 
 cific causes of disease. 
 
 Predisposing Causes. — The normal system is able to cope 
 with the determining causes of disease to a certain point by its 
 general vitality and regulative functions. Thus heat and cold 
 may prove harmless if not too intense or prolonged. In the case 
 of exposure to heat, the superficial capillaries become dilated, 
 sweating increases, and there is increased heat dissipation from 
 the surface at the same time that increased respiratory function 
 occasions evaporation and loss of heat through the lungs. In 
 the case of exposure to cold, increased muscular exercise leads to 
 greater heat production, while contraction of the superficial blood- 
 vessels restricts the elimination of heat. When, however, a cer- 
 tain point of intensity is reached in the case of heat, cold, or other 
 causes of disease, the normal organism is unable to oppose suffi- 
 cient resistance, and disease or injury results. The degree of 
 resistance differs in different individuals, in different races, or 
 people living under varying climatic conditions, etc. In some 
 the degree of resistance may be so great that certain diseases are 
 never contracted. The term immunity (q. v.) is applied to this state. 
 In other persons there is a recognizable weakness of resistance in 
 one direction or another which constitutes a definite predisposition. 
 The latter may be either hereditary or acquired. Acquired pre- 
 disposition results from previous disease, vices of living, and like 
 causes. 
 
 Heredity as a predisposing factor in disease is probably less 
 important than was formerly believed, but undoubtedly plays a 
 part in many conditions. By hereditary predisposition is desig- 
 nated abnormal weakness of resistance transmitted from the mother 
 or father to the offspring. There may be congenital weakness 
 that is not definitely hereditary, as it is more or less accidental — 
 that is, not the outcome of tendencies of the same kind (latent or 
 active) in the parent. Heredity may be direct or immediati — 
 that is, from the parent (himself or herself presenting the condi- 
 tion) to the offspring — or remote, as in eases in which the hereditary 
 trait is latent in the parent. One or several generations may thus 
 be free from certain diseases or tendencies which reappear in 
 later generations. This return to conditions present in remote 
 ancestors has been likened to atavism in the Darwinian sense. In 
 some cases hereditary traits are conveyed from the male parent to 
 the male children, or from the female parent to the female off- 
 
THE ETIOLOGY OF DISEASE. 19 
 
 spring ; in other cases there is crossed transmission. A peculiar 
 form of heredity is seen in hemophilia and some other diseases, 
 which are transmitted through the female members of a family, 
 who generally remain unaffected, to the male offspring. Heredi- 
 tary traits sometimes predispose to a number of allied affections. 
 This is particularly striking in the case of the neuropathic heredity, 
 in which various forms of nervous disease may appear in members 
 of an affected family. 
 
 Determining Causes. — Among the immediate or deter- 
 mining causes of disease are those which originate outside the 
 body and those which are generated within the body. Among 
 the former are included traumatism, heat, cold, and other physical 
 agents, poisons, and living organisms, including bacteria and va- 
 rious animal parasites. The causes of disease originating within 
 the body itself are less definitely known, but it has been found in 
 chemical studies that various products of normal metabolism when 
 accumulated in abnormal quantity, or products of disturbed metab- 
 olism, may occasion local or widespread disease of various sorts. 
 This self-poisoning is designated auto-intoxication. 
 
 TRAUMATISM. 
 
 Traumatism, or mechanical injury, may be of various sorts, 
 gradual or sudden, small or large ; and the effects are dependent 
 upon the form and severity of the injury. Pressure brought to 
 bear upon a part leads to disturbances of the circulation and more 
 or less direct injury of the cellular elements. When the pressure 
 is gradual true atrophy of the part may occur, as in the case of the 
 atrophic liver resulting from lacing. When the pressure is greater 
 and the circulation is completely arrested more destructive change 
 may result, such as necrosis or gangrene. This is seen in the 
 necrotic atrophy of bone resulting from the pressure of aneurysms, 
 or the gangrene of extremities resulting from ligation. Fre- 
 quently, inflammatory reaction occurs in the surrounding tissues 
 when traumatic injuries have been sustained. This is strikingly 
 illustrated in all forms of wounds, and it is through the inflam- 
 mation and subsequent regeneration of tissue that the areas of 
 destruction are restored. In cases of injury by fine particles, as 
 in powder-marks of the skin, or the surface injuries sustained by 
 miners and metal-workers, or in individuals inhaling sharp par- 
 ticles like coal-dust, marble-dust, or steel-filings, small injuries of 
 the tissues result. The foreign bodies may be subsequently dis- 
 charged, leaving a focus of inflammation, or the inflammation may 
 surround the particle imbedded in the tissue, and encapsulation by 
 fibrous -tissue formation may occur. Large injuries in which the 
 tissues are contused or broken may lead to extensive inflamma- 
 
20 TEXT-BOOK OF PATHOLOGY. 
 
 tion, in part the result of the direct injury to the tissues and in 
 part the result of injury of the blood-vessels. 
 
 PHYSICAL CONDITIONS. 
 
 Heat. — High temperatures produce local or general results 
 according to the mode of application and degree of heat. 
 
 Local excess of heat produces various lesions. Moderate excess 
 leads to relaxation of the walls of the blood-vessels; with increas- 
 ing grades of temperature there is in addition necrotic change in 
 the cells of the part, and exudation of serum causes vesicle for- 
 mation. Still higher grades of temperature produce immediate 
 destruction, perhaps with charring, of large or small areas, while 
 the surrounding tissues suffer from reactive inflammation and 
 hyperemia. Extensive burns involving one-third or more of the 
 surface of the body frequently cause death. In these cases it is 
 likely that poisonous products are formed, either directly through 
 tissue- and blood-destruction, or indirectly through disturbances 
 of the functions of the skin or internal organs. The immediate 
 manner of death is often in the form of shock ; when the termi- 
 nation is more delayed various vascular, hemic, and tissue-disturb- 
 ances may occur. Intravascular coagulation is not unusual, and 
 is not improbably the result of the liberation into the blood of 
 tissue-elements set free in the areas of local destruction, or to sub- 
 stances produced by direct destruction of the blood. The same 
 substances may account for the existence of fever (ferment intoxi- 
 cation). The intravascular coagulation caused in this or other 
 ways may induce venous stasis and localized hemorrhages. Focal 
 necrosis or degeneration of the tissues of various organs, such as 
 the liver, kidneys, or the mucous membranes, may be due to 
 thrombotic occlusion of vessels, or to the direct influence of cir- 
 culating poisons without thrombosis, or to both. Duodenal ulcer 
 is a lesion often referred to as an occasional result of extensive 
 burns. The blood itself may present evidence of disease in the 
 form of degenerations of the corpuscles, in the reduction of their 
 number and of the amount of coloring matter; while regenerative 
 changes frequently present themselves some time later (nucleated 
 red corpuscles). Changes in the urine may occur in eases of ex- 
 tensive burns in consequence of the tissue-destruction (hemo- 
 globinuria, albumosuria). 
 
 Exposure to general high temperature varies in its effects accord- 
 ing to the manner of exposure (as with dry air, steam, etc.). An 
 animal exposed to a constant temperature somewhat above the 
 usual surrounding temperature presents a slight increase of its 
 body-heat, which is compensated for by increase in the respi- 
 rations and pulse-rate. Much higher temperatures may cause 
 death by coagulation of the tissues ; notably, the muscular struct- 
 
THE ETIOLOGY OF DISEASE. 21 
 
 ure of the heart, or the respiratory muscles. Before this extreme 
 is reached, however, it may be found that the consumption of the 
 tissues of the body is greatly in excess, though the respiratory 
 quotient is altered in favor of the amount of air inhaled. Con- 
 tinuous exposure to excessive heat frequently causes peculiar dis- 
 turbances in man, known as heatstroke, sunstroke, or insolation 
 and heat-exhaustion. In these conditions hyperemia and edema, 
 or even inflammation of the meninges, may occur. These lesions 
 are sometimes supposed to be the result of the direct effect of 
 the heat ; but there is reason to believe that they may be occa- 
 sioned by poisonous substances produced within the body by dis- 
 turbed metabolism, as a result of the heat. 
 
 Cold. — Exposure to extreme degrees of cold may cause results 
 quite similar to those produced by heat. Exposure of the skin to 
 liquefied air, solidified mercury, or other substances at excessively 
 low temperatures produces vesiculation and necrosis of the tissues 
 like those produced in burns. 
 
 Exposure of the body to greatly reduced but bearable tempera- 
 tures of the surrounding atmosphere causes vascular disturbances 
 followed by necrosis of the tissues and inflammatory changes. 
 The parts so affected are the extremities or projections of the 
 body, like the toes and fingers, nose and ears. The primary 
 result of cold is vascular constriction and local anemia. These 
 serve the purpose of preserving the body heat by preventing heat 
 radiation ; later the blood-vessels are paralyzed and extreme hyper- 
 emia results. Then cellular exudation and necrosis may occur. 
 These changes are well seen in the condition termed chilblain. 
 In prolonged exposure to cold there are a gradual reduction in 
 the activity of the various organs and a gradual obtunding of 
 the sensibility till the patient becomes comatose. The retention 
 of excrementitious products of metabolism, or the formation of 
 products of abnormal metabolism, may be important in causing 
 this condition. 
 
 Exposure to cold plays an important part as a clinical cause of 
 disease. Various forms of pharyngitis and coryza or bronchitis 
 so frequently follow such exposure that the term " cold " is gener- 
 ally used. Other conditions, like rheumatism, pleurisy, pneumonia, 
 and the like, bear a similar relation. It is now recognized that in 
 most of these cases cold is merely a predisposing cause, the imme- 
 diate cause being in many, if not all, cases specific micro-organ- 
 isms. The mode of action of the exposure is uncertain ; probably 
 it causes a reduction in the resisting powers of the organism and 
 thus favors the activity of bacteria. In some cases it may be that 
 the cold alters the fluids of the body in such a Avay as to permit 
 increased virulence of micro-organisms already present, or to pro- 
 mote their entrance into the system. 
 
 Increased Atmospheric Pressure. — Exposure to extreme 
 
22 TEXT-BOOK OF PATHOLOGY. 
 
 pressure of several atmospheres may occur among deep-sea divers, 
 or in men working in caissons used in bridge building. But little 
 disturbance may be caused at first, or for a long time ; but on 
 return of the workmen to the usual atmospheric conditions symp- 
 toms make their appearance (caisson disease). Among these symp- 
 toms are bleeding from the nasal or other mucous membranes, 
 great depression, delirium, and paralytic conditions. Degenera- 
 tions and vacuolations in the spinal cord have been discovered in 
 some cases. 
 
 Decreased Atmospheric Pressure. — Effects of decreased 
 pressure are seen in inhabitants of high altitudes and in persons 
 ascending in balloons. Marked excitement of the vascular system, 
 hemorrhages, vomiting, and similar symptoms are observed ; in 
 less marked cases a general excitement of the nervous system, 
 sleeplessness, etc., occur. These symptoms have been attributed 
 to lack of oxygen ; to a certain extent they are probably mechani- 
 cal and due directly to the reduced pressure on the exterior. 
 Recent studies show that the blood contains greatly increased 
 numbers of red corpuscles in a given volume, and the percentage 
 of hemoglobin is correspondingly increased. This is probably due, 
 to a large extent, to disturbance in the distribution of the cor- 
 puscles with stagnation in the peripheral vessels (see Diseases of 
 the Blood). 
 
 Insufficiency of Respiratory Air. — A certain amount of 
 air is necessary for the continuance of health or life. Insufficiency 
 may be due to diseases which obstruct the air-passages or affect 
 the pulmonary tissue itself, and to foreign bodies (solid bodies, water 
 in drowning) within the air-passages. Changes in the atmosphere 
 or gases taken into the lung may cause insufficiency in the supply 
 of oxygen, notably in CO-poisoning, in which the foreign gas enters 
 into firm combination with the hemoglobin of the blood and thus 
 excludes oxygen. 
 
 Moderate decrease of the supply of air causes labored and rapid 
 breathing, more or less cyanosis, depression, and stupor. This 
 condition is termed asphyxia. Complete lack of air causes increase 
 of these symptoms and deatli by suffocation. In these cases the 
 blood is exceedingly dark and fluid, and hemorrhages may be 
 found in various situations. The latter result from excessive blood- 
 pressure during the death agony. Long-continued insufficiency 
 of oxygen may directly or indirectly occasion degenerative dis- 
 eases of the tissues. 
 
 It has often been asserted that anemia causes many of its symptoms and 
 results because the blood is incapable of carrying sufficient oxygen in its 
 reduced state. As a matter of fact, however, physiologic experiments 
 have demonstrated that the respiratory exchange (inhalation of oxygen and 
 exhalation of carbonic acid gas) is but little affected and is as frequently 
 increased as decreased. 
 
THE ETIOLOGY OF DISEASE. 23 
 
 Electrical Influences. — Electrical discharges may cause 
 burns or similar lesions of the surface, and frequently cause intense 
 shock. Disturbances of the central nervous system of various sorts 
 may occur immediately or some time after the exposure. Doubt- 
 less there are distinct organic changes in the nervous tissues, but 
 these have not been determined. Gross injuries of organs, such 
 as rupture and degenerative changes, may be occasioned. 
 
 POISONS. 
 
 Definition. — The term poison may be applied to substances 
 which when introduced into the living organism disturb the struct- 
 ure or functional activity. 
 
 The Action of Poisons in General. — Gaseous poisons act 
 mainly upon the respiratory mucous membranes with which they 
 come in contact, or after absorption into the blood disorganize this 
 fluid or lead to disturbances of the nervous system. Liquid poi- 
 sons are generally absorbed through the gastro-intestinal mucous 
 membrane, but may be received directly into the tissues by injec- 
 tion under the skin. They are rarely absorbed through the skin. 
 Solid poisons must in all cases first be dissolved, and are then ab- 
 sorbed like the liquid poisons. They may by their strong attrac- 
 tion for water absorb the latter directly from the tissues, and by 
 this process alone may bring about important changes. 
 
 The lesions due to a poison may be entirely local, as in the 
 case of certain corrosives or caustics ; in other cases the point of 
 entrance is unaffected, the pathologic manifestations being en- 
 tirely due to the changes in different parts of the body, or to ner- 
 vous disturbances resulting from the circulation of the poison in 
 the blood. 
 
 The fate of poisons after ingestion is very different in dif- 
 ferent cases. Some poisons circulate with the blood and are 
 eliminated unchanged. Others may suffer chemical change within 
 the stomach or other cavities of the body before absorption, and 
 may be either completely neutralized, or may be converted into 
 forms which are subsequently slowly absorbed. After absorption 
 into the blood other chemical reactions may occur, and the poison 
 may be more or less neutralized, the system then suffering either 
 from the resulting compounds or from the changed conditions of 
 the blood. Active destruction of the poison may occur in the 
 blood or in the various organs. In these processes, however, the 
 glandular organs may suffer seriously, various forms of degenera- 
 tion or necrosis resulting. 
 
 The effect of poisons depends upon the dose as well as upon 
 the nature of the substance, and also upon the individual. The 
 repeated ingestion of certain poisons, such as arsenic or opium, 
 may generate a considerable degree of immunity or tolerance. 
 
24 TEXT-BOOK OF PATHOLOGY. 
 
 Similar immunity may be characteristic of a given individual or 
 of classes or species. Susceptibility to the action of poisons is 
 further influenced by age and constitutional vigor. Children bear 
 certain poisons better, comparatively speaking, than adults, while 
 the reverse is true of other substances. Sometimes there are idio- 
 syncrasies which lead to peculiar results not observed in the aver- 
 age individual. In consequence of this, substances ordinarily not 
 toxic may be extremely injurious to certain persons. 
 
 Elimination. — The excretion of poisons may take place 
 through the kidneys, lungs, the mucous membrane of the gastro- 
 intestinal tract, or through the skin. In some instances a poison 
 is almost completely eliminated in the excreta. In other cases it 
 suffers complete change, and is not present at all in the excretions. 
 The rate of elimination varies greatly, and is more or less depend- 
 ent upon conditions of the system. Some poisons, as phosphorus 
 and mercury, may be stored up within the body for a considerable 
 period, subsequently suffering slow elimination. 
 
 Classification. — The number of substances which may act as 
 poisons is very great, and the manifestations are of very different 
 sorts. Classification of poisons is therefore difficult and not en- 
 tirely satisfactory. We may crudely distinguish between gaseous, 
 liquid, and solid poisons ; between animal and vegetable, organic 
 and inorganic, and the like ; but these classifications have no 
 scientific value. 
 
 From the point of view of the action of the poisons we may 
 distinguish corrosive poisons, or those which have a local action ; 
 orga nic or parenchyma-poisons, or those which act less strongly at 
 the point of application than upon the various organs to which 
 they are conveyed through the blood ; blood -poisons, or those 
 which exercise their effects primarily upon the blood ; and the 
 herve-poisotts, or those which disturb the functional activity of the 
 nervous system without producing definitely discoverable lesions. 
 
 Corrosive Poisons ; Escharotics ; Caustics. — Under this heading 
 are included various acids, alkalies, and mineral poisons, such as 
 sulphuric, nitric, oxalic, carbolic, and hydrofluoric acids, caustic 
 potash or soda and ammonium, and gases like chlorin and bromin. 
 Nitrate of silver, bichlorid of mercury, sulphate of copper, and 
 other inorganic compounds have a similar action, and certain 
 organic bodies, such as cantharidin and croton oil, belong to the 
 same class. 
 
 All these poisons exercise a destructive effect upon the cells 
 with which they come in contact, partly by abstraction of water 
 and partly as a result of a coagulating power or similar action. 
 The degree of injury depends upon the poison and the amount in 
 contact with the tissues. There may be only a superficial injury 
 of the outer layer of epithelial cells or extensive destruction. 
 Reactive inflammation is almost always present. The affected 
 
THE ETIOLOGY OF DISEASE. 25 
 
 part may present slight areas of necrosis with reactive hyperemia 
 and inflammation beneath and around them, or deep eschars, 
 vesicles, or large bullae. In the process of healing extensive scars 
 may form, and these may be serious in their effects, as in the case 
 of strictures of the esophagus. 
 
 Organic Poisons; Parenchyma-poisons. — This large group in- 
 cludes many metallic compounds that have a local corrosive or 
 escharotic effect, but which may gain entrance to the blood and 
 cause extensive organic lesions. It also includes poisons of vege- 
 table origin and products of bacterial growth. In general these 
 poisons have a similar action. The kidneys and the mucous mem- 
 brane of the intestines are especially active in their elimination 
 and suffer most seriously. Degenerations of the epithelial cells 
 of various sorts are met with, such as nuclear degenerations, 
 coagulation necrosis, fatty degeneration, and even calcification. 
 The changes may be diffuse or may be scattered in small foci. In 
 the latter case small areas of granular appearance, having a lighter 
 color than the surrounding tissues, are seen ; and on staining the 
 cells are found to color poorly or not at all, the nuclei often show- 
 ing this change first. Nuclear degenerations (fragmentation, hyper- 
 chromatosis, etc.) are observed, and in some instances marked fatty 
 degeneration of the cells occurs. Around the foci of degeneration 
 there is more or less round-cell infiltration (polymorphonuclear 
 cells), and to a less degree the degenerated area itself is infiltrated. 
 In cases in which diffuse change occurs there is equally diffuse 
 round-cell infiltration. After the acute process has subsided 
 hyperplasia of the connective tissues may occur and the affected 
 part becomes more or less sclerotic or indurated. Regeneration 
 of the parenchyma-cells is less apt to occur. 
 
 Some of the more important of the poisons of the group may 
 now be separately considered. 
 
 Phosphorus is a poison of considerable activity in the yellow 
 form ; the red variety is inert. Workmen in match factories are 
 the most frequent victims of this form of intoxication, but occa- 
 sionally accidental poisoning by swallowing occurs. In the latter 
 the manifestations are acute. The pathologic changes are catarrhal 
 inflammation of the gastro-intestinal mucous membrane and more 
 or less widespread fatty degeneration of various tissues and organs. 
 The liver suffers most severely, being enlarged, light yellow or 
 reddish in color, and friable or doughy. Microscopically the liver- 
 cells are found extensively degenerated (fatty). Similar but less 
 marked fatty degeneration is found in the renal tubules, gastro- 
 intestinal epithelia, and heart-muscle, and in the intima of the 
 blood-vessels. Extensive jaundice is frequent and numerous 
 hemorrhages may occur. In the more chronic poisoning of match- 
 makers the poison enters through the mouth and respiratory pas- 
 sages, being inspired as dust. Chronic catarrhal inflammation of 
 
26 TEXT-BOOK OF PATHOLOGY. 
 
 the respiratory tract may occur and a peculiar form of necrosis of 
 the bones (see Bones) is met with. 
 
 Arsenic is poisonous in certain forms (white arsenic, arsenous 
 acid) and inert in other forms (the sulphids). Acute poisoning 
 occurs when toxic forms are swallowed in large doses ; the chronic 
 forms of poisoning result from gradual ingestion or the inhalation 
 of dust containing arsenic. Cases of the latter sort occur when 
 wall-paper, hangings, and the like, colored with arsenic-pigments, 
 are used. The lesions in acute arsenic-poisoning resemble those 
 produced by phosphorus. The gastro-intestinal inflammation is, 
 however, more severe ; while the fatty degeneration of the organs 
 is less marked. In chronic arsenic-poisoning changes in the 
 peripheral nerves (degeneration and inflammation) are most im- 
 portant. It is likely that focal or diffuse myelitis may likewise be 
 caused by this poison. Chronic inflammations of the gastro- 
 intestinal or respiratory mucous membranes are met with in some 
 cases. Inflammatory lesions of the skin are frequent. 
 
 Lead. — Among the compounds leading to acute or subacute 
 poisoning the chromate, the acetates, the carbonate, and oxid are 
 most important. Chronic poisoning occurs in workmen in paint 
 manufactories and among painters, and in persons drinking certain 
 waters that have been conducted through lead pipes. Less rarely 
 the use of cosmetics, dyestuffs, etc., containing lead causes chronic 
 poisoning. In the acute forms of lead-poisoning moderate gastro- 
 enteritis occurs. In the chronic form changes in the nervous sys- 
 tem are most important. Peripheral neuritis is the most frequent 
 lesion, but changes in the large ganglionic cells of the gray matter 
 of the cord have sometimes been found. Diffuse sclerosis of the 
 blood-vessels, interstitial nephritis, and the lesions of gout may be 
 present. Atrophy and fatty degeneration of the muscle-fibers are 
 less important lesions. A blue line on the gums at the junction 
 with the teeth (due to deposit of sulphid of lead) is a lesion of 
 clinical importance. 
 
 Mercury. — Poisoning with mercury may be acute, subacute, or 
 chronic. The first is due especially to the corrosive chlorid and 
 other mercuric salts ; the second to calomel or small doses of those 
 of the former group. Chronic poisoning occurs as a result of inhala- 
 tion of fumes or dust containing mercury, and is seen in workmen 
 in mirror manufactories. In the acute cases violent inflammatory 
 and necrotic lesions of the gastro-intestinal tract are seen. Paren- 
 chymatous degeneration, fatty change, and even calcification of the 
 renal epithelium may occur; and fatty degeneration in other 
 organs may sometimes be met with. In subacute cases marked by 
 ptyalism sonic change is doubtless present in the salivary glands, 
 but the nature of this has not been determined. 
 
 Ergot. — Ergot is a poison capable of producing intense toxic 
 results. It contains two important toxic principles, sphacelinic 
 
THE ETIOLOGY OF DISEASE. 27 
 
 acid and an alkaloid, cornutin. Acute poisoning sometimes re- 
 sults from overdosage ; while chronic intoxication occurs from 
 the use of affected grain, particularly in famine years. Wide- 
 spread poisoning of communities has sometimes resulted. The 
 lesions produced are not definite or uniform. Gastro-intestinal 
 inflammation and erosion of the mucous membrane have been ob- 
 served, but are not habitual ; sclerotic change in the spinal cord 
 has been found in a few cases. Gangrene is a frequent lesion, 
 probably resulting from vascular obstruction due to contraction 
 of the blood-vessels. Enlargement of the spleen has sometimes 
 been noted. 
 
 Toxalbumins from Plants. — Certain vegetable bodies, like 
 ricin derived from the castor bean and abrin derived from 
 jequirity bean, are exceedingly toxic, acting in part as blood- 
 poisons but also as parenchyma-poisons. Injected into animals 
 these substances cause violent intoxication, and focal areas of 
 necrosis in various situations, notably in the liver. In part these 
 lesions result from vascular thrombosis ; in part from direct ac- 
 tion. The study of the action of these poisons is of particular 
 interest from the resemblance of the lesions to those caused by 
 certain bacteria and bacterial poisons. 
 
 Toxic Products of Bacteria. — In the growth and multiplica- 
 tion of various bacteria definite toxic substances are produced, 
 and through the latter the lesions of infection are to a large ex- 
 tent produced. Such poisonous bodies may be generated in the 
 growth of the bacteria outside of the body, as well as within the 
 body. In the latter case the pathologic lesions at the point of 
 infection may be the focus of origin of toxic substances which 
 are then distributed throughout the body in the blood. This is 
 eminently true of tetanus, and to a large degree of diphtheria. 
 In other cases the bacteria themselves are transported to various 
 parts of the body, and finding lodgement in the tissues set 
 up changes by which their toxic products are evolved. The 
 latter increase the local foci of pathologic change and then 
 spread in the circulation and cause general intoxication. Fur- 
 ther discussion of these poisons will be included under the 
 individual bacteria. 
 
 The venom of serpents and of various insects contains 
 toxic bodies, some of which are albuminous in nature. These vary 
 in their action, being to some extent blood-poisons, but more par- 
 ticularly parenchyma-poisons. The lesions produced are local and 
 general. Locally there are intense inflammatory reaction and 
 edema around an area of cellular necrosis or destruction where the 
 poison has come in immediate contact with the tissues. The blood 
 seems to suffer great disorganization and corpuscular change. 
 Petechial hemorrhage and foci of cellular necrosis occur in various 
 organs ; and edema of the lungs is frequently present. The action 
 
28 TEXT- BOOK OF PATHOLOGY. 
 
 of the venom of different animals varies in kind and intensity to 
 a certain extent, but is in general of a similar type. 
 
 Blood-poisons. — Various liquid or gaseous substances are termed 
 blood-poisons because of their especial action upon this liquid. 
 The blood-poisons may be classified as (a) those which combine 
 with the hemoglobin without changing the corpuscles ; (6) those 
 which alter the red corpuscles and the coloring matter ; (c) those 
 which affect the blood as well as the tissues generally ; and (d) 
 those which cause changes in the blood-plasma, increasing or de- 
 creasing the tendency to clotting. 
 
 (a) Among the poisons which act by entering into combination 
 with the hemoglobin without changing the corpuscles, carbon 
 monoxid, cyanogen, and hydrogen sulphid are important. In 
 carbon-monoxid poisoning, which often results from inhalation of 
 the fumes of charcoal burning with insufficient air, the blood has 
 a light color and light petechial discolorations may be seen in 
 various parts of the body. In cyanogen-poisoning the blood is 
 similarly light in color ; while in H 2 S-poisoning the blood is often 
 dark, sometimes quite black. 
 
 (6) Among the poisons which disorganize the blood-corpuscles 
 and later the hemoglobin are a large number of chemical agents 
 used in medical practice or in the arts, including potassium chlo- 
 rate, nitroglycerin, anilin, nitrobenzol, various coal-tar derivatives, 
 and arseniuretted hydrogen. Certain poisonous plants (toadstools) 
 act similarly. These poisons lead to a reduction of the hemoglobin 
 with generation of methemoglobin and at the same time destruc- 
 tion of the corpuscles themselves, with release of the hemoglobin 
 into the serum. The altered condition of the blood often induces 
 secondary changes, such as fatty degeneration and hemorrhages in 
 various organs. The blood-corpuscles are found in variously de- 
 generated conditions, showing microcytosis and poikiloevtosis in 
 particular. Nucleated red corpuscles may be present as in other 
 conditions of blood-destruction with attempted regeneration. 
 
 (c) Among the poisons which disorganize the blood and at the 
 same time cause changes in the parenchyma of organs, reference 
 has been made to abrin and ricin. In addition to the organic 
 changes, these substances cause certain alterations in the blood 
 itself, increasing the coagulability and thus inducing thrombosis. 
 
 (d) Various substances introduced in sufficient quantity are 
 capable of affecting the plasma of the blood or the corpuscles in 
 such a way as to affect its coagulability. Calcium salts, carbonic 
 acid gas, and fibrin-ferment are active in this way, but the last 
 alone produces toxic results through this function. Ferment-in- 
 toxication may occur in consequence of various other intoxications, 
 when corpuscular or tissue-destruction has liberated the ferment. 
 Among the poisons which decrease coagulability peptone (albu- 
 mose) is important. 
 
THE ETIOLOGY OF DISEASE. 29 
 
 Nerve-poisons. — This group contains a large number of sub- 
 stances capable of producing violent symptoms and even death 
 without definite change in the tissues of the body. Recent inves- 
 tigations showing certain alterations in the finer structure of the 
 nervous system in disease and in cases of intoxication suggest that 
 histologic changes in the central neurons may be found to result 
 from poisoning by these substances. Changes of this kind (thick- 
 ening, contraction, or disappearance of dendrites, etc.) have been 
 described in the gray matter of animals poisoned with alcohol and 
 certain toxins of bacterial origin. It is not unlikely that similar 
 changes will be found in other cases. 
 
 Among the nerve-poisons are alcohol, chloroform, ether, and 
 various alkaloids like morphin, atropin, etc. In this same group 
 might be included some of the poisons contained in the venom of 
 serpents and other animals, but these frequently cause definite 
 lesions in the blood or tissues of the body. Another group of 
 poisons of similar action are those produced within the body by 
 putrefactive action or in various foodstuffs before ingestion. Fre- 
 quently cases have been observed in which all the members of a 
 family or even large numbers of people have been poisoned by 
 eating certain meats, sausages, ice-cream, and other foods. In 
 some of these cases it has been found that the toxic element was 
 a basic compound resembling the alkaloids in chemical structure. 
 To these putrefactive compounds the name ptomain is given. 
 One of these compounds, which occurs in cheese, and occasion- 
 ally in milk, has been termed tyrotoxicon. Intoxications of 
 this class must be distinguished from infections resulting from 
 the use of food contaminated with micro-organisms. The symp- 
 toms may be so rapidly developed (absence of incubation period) 
 and so immediately generalized that the distinction can be 
 arrived at clinically, but the absolute diagnosis is made bac- 
 teriologically. 
 
 A considerable number of ptomains have been separated, in- 
 cluding neurin, obtained from putrid flesh ; muscarin and ethy- 
 lendiamin, derived from decayed fish ; mydalein, and mydatoxin. 
 Some of these substances produce toxic results indistinguishable 
 clinically from those produced by certain alkaloids. This fact has 
 become one of great importance in medicolegal investigations. 
 
 BACTERIA AND PARASITES. 
 
 Bacteria are by far the most important causes of disease. 
 The belief in a living cause or contagium vivum is by no means a 
 recent acquisition, but the actual demonstration that diseases may 
 be caused by minute living organisms has only recently been 
 reached. The micro-organisms in question belong for the most 
 part to the vegetable kingdom and constitute the lowest orders of 
 
30 TEXT-BOOK OF PATHOLOGY. 
 
 fungi. Their biologic characters and their relations to special 
 diseases will be described in a subsequent chapter. 
 
 Etiologic Relationship of Bacteria to Disease. — It is difficult to 
 prove the specific relation of bacteria to disease. Koch has laid 
 down four important laws which must be conformed with before 
 the etiologic importance of a bacterium is admitted. These are : 
 (1) the bacterium must be found in the diseased person ; (2) it 
 must be cultivatable upon media outside the body ; (3) pure 
 cultures introduced into a healthy animal must produce the dis- 
 ease in the animal ; and (4) the bacterium must be recoverable 
 from the body of the animal. In a number of diseases micro- 
 organisms have been proved to be the specific causes according to 
 the requirements of Koch's rules. In other diseases it has not 
 been possible to furnish absolute proof, though the presump- 
 tive evidence, furnished by constant occurrence of the bacteria, 
 suggestive association with the lesions of the disease, absence of 
 the bacteria in other diseases, etc., is sufficient to satisfy all but the 
 most sceptical. 
 
 Classification of Diseases due to Bacteria. — The general term 
 infections disease is applied to all such as are caused by bacteria. 
 In some cases the diseases are readily communicated from person 
 to person, even though contact has not been immediate. These 
 are termed contagious diseases, while the term noncontagious is 
 given to those in which such ready transference is not observed. 
 As a matter of fact, the distinction is artificial. Any infectious 
 disease may be communicated from the diseased to the healthy if 
 the germs or bacteria are transferred. In some diseases this trans- 
 ference readily occurs, even through the air and at considerable 
 distances ; in others actual contact is necessary ; while in still 
 others secretions or excretions of the diseased must be conveyed 
 to the healthy. Contagiousness is therefore a matter of degree 
 only. 
 
 Infectious diseases may at times spread in communities, affect- 
 ing large numbers of people. Such a dissemination is termed 
 epidemic, and the disease an epidemic disease. Other infections are 
 constantly present in a locality; for such the terms endemic and 
 endemic disease are used. Some endemic diseases are restricted to 
 certain localities and seem in some measure dependent upon local 
 conditions (of atmosphere, soil, etc.) for their continuance. These 
 are called miasmatic diseases. 
 
 Infectious diseases are frequently described as local or general. 
 Local infections are those that present specific pathologic change 
 in a restricted area ; the general organism suffers more or less in con- 
 sequence. Examples of this are erysipelas and diphtheria. Gen- 
 eral infections are marked by an immediately generalized disease, 
 as in typhoid fever. These terms, like others, are much less appli- 
 cable at the present time than formerly. Among purely local 
 
DISORDERS OF NUTRITION AND METABOLISM. 31 
 
 infections might be named the diseases of the skin due to vege- 
 table micro-organisms. 
 
 Entrance of Micro-organisms into the Body. — Bacteria may be 
 inhaled or swallowed, may enter through abrasions in the mucous 
 membranes or skin, and may be transferred in utero from the 
 maternal to the fetal blood. The mode of entrance in individual 
 diseases depends upon the nature of the bacterium, its habitat, and 
 surrounding conditions. Some may enter in but one way ; others 
 gain access in any of the different ways. Details regarding this 
 subject will be given in the discussion of special infections. 
 
 Animal parasites of various kinds act as causes of disease. 
 This group of diseases is termed the parasitic diseases or invasion 
 diseases. In some instances the clinical course is similar to that 
 of infectious diseases (malaria, dysentery, trichinosis) ; in other 
 cases the manifestations bear little resemblance to infections. 
 
 CHAPTER II. 
 
 DISORDERS OF NUTRITION AND METABOLISM. 
 
 Food. — In the life of the organism certain substances are 
 needed for the repair of tissues consumed in the wear and tear of 
 life and to supply heat and other energy. Among these foods are 
 proteids, carbohydrates, fats, inorganic salts, and water. A con- 
 tinuance of normal existence requires more or less definite propor- 
 tions of the first three and at least a sufficiency of salts and water. 
 The amount of food and the exact proportions vary somewhat in 
 individual cases and under varying circumstances. Voit found 
 that a laboring man under ordinary conditions requires 118 g. of 
 proteid, 56 g. of fats, and 500 g. of carbohydrates. The proteids 
 of the diet are necessary to restore tissue-waste, since the organ- 
 ism cannot build up proteids from simpler compounds. This con- 
 sumes part of the nitrogenous foodstuffs. The rest, with the fats 
 and carbohydrates, is mainly useful in contributing energy. 
 
 Diminished Supply of Food ; Inanition ; Starvation.— 
 Either the want of food or disorder of the gastro-intestinal tract 
 may lead to insufficient nourishment. This causes a loss of body 
 weight, as the necessary heat-producing and energy-giving sub- 
 stances must be supplied to maintain life, and the tissues are con- 
 sumed for this purpose. The carbohydrates (glycogen of liver and 
 muscles) and fats suffer first and most profoundly, and unimportant 
 parts are reduced before the vital structures are attacked. The 
 subcutaneous and other adipose tissues and the muscles first waste, 
 then the liver, bones, heart, etc. 
 
32 TEXT-BOOK OF PATHOLOGY. 
 
 The functions of various organs suffer greatly : the respirations 
 and heart-action are weak, muscular exertions are reduced to a 
 minimum, the endurance and nervous force decline, and finally 
 death may occur from exhaustion or secondary affections conse- 
 quent upon the disturbed nutrition (see Acid-intoxication). The 
 blood in starvation preserves its corpuscular richness surprisingly, 
 even after prolonged abstinence. This is doubtless due to loss or 
 evaporation of liquid ; the actual number of corpuscles probably 
 suffers reduction. 
 
 Increased Supply of Food; Overfeeding. — The effect 
 of this depends upon individual conditions, such as the amount of 
 exercise, the surrounding temperature, and less easily demonstrable 
 peculiarities of the individual. An excess of proteid food leads to 
 increased excretion of the end-product of its metabolism — urea. 
 A very small proportion may contribute to building up a reserve 
 amount of albuminous tissue. Great excess of proteid eventually 
 disturbs digestion and leads to its discharge with the feces. 
 
 The carbohydrates and fats are broken up in the body and ex- 
 creted mainly as carbonic acid and water. An excess of these 
 foods tends to cause increased deposition of reserve fat and gly- 
 cogen, which may be called upon at subsequent times of need. 
 This deposition is a normal or physiologic process and has the 
 distinct purpose just indicated. Exceptionally in the condition 
 called obesity the storing up of fat is inordinate and probably 
 pathologic. 
 
 Obesity. — The origin of fat is still a subject of controversy 
 among physiologists. According to the oldest view, the fat of the 
 body is derived from that of the food, and the possibility of this 
 has actually been demonstrated. Under ordinary circumstances, 
 however, but little if any of the fat is so produced. Another 
 school of physiologists maintained that the proteids of the food 
 break up into a nitrogenous and a non-nitrogenous part, the former 
 being finally excreted as urea and other substances or repairing 
 the tissue-waste, the latter part contributing energy or forming fat. 
 At the present time it must be admitted that though proteids may 
 possibly form fat in this manner, the actual demonstration is still 
 wanting. The main source of fat is certainly the carbohydrates 
 of the food. 
 
 Causes of Obesity. — Excessive ingestion of food by persons 
 •having active digestion and leading sedentary lives may occasion 
 unusual deposition of fat. It is difficult, however, to determine 
 the limits between physiologic and pathologic fatness. In some 
 cases patients assert that the amount of food has not been exces- 
 sive, and this may be actually true. Obesity in such individuals 
 is undoubtedly pathologic and due to some inherent abnormality 
 of metabolism. A further proof of the existence of such a ten- 
 dency is seen in certain families, in which excessive fatness is 
 
DISORDERS OF NUTRITION AND METABOLISM. 33 
 
 common, even in childhood. The nature of this metabolic dis- 
 order is obscure. It has often been held that the power of oxida- 
 tion is lacking, and, as u matter of course, the amount of oxygen 
 consumed is deficient in comparison with the amount of food in- 
 gested. This must be true, or the fat could not accumulate ; but 
 it remains to be shown whether the diminished oxygen-consump- 
 tion is the primary cause or only an incident in the disease. 
 
 Pathologic Anatomy. — The excessive adipose tissue in this 
 disease is found in the skin and subcutaneous tissues, in the omen- 
 tum and peritoneum, around the kidneys, heart, and mediastinal 
 tissues, in the liver, and less commonly elsewhere. The amount 
 varies from slight excess to monstrous deposits. Secondary changes 
 in the organs (notably the heart-muscle) may be due to pressure 
 or functional inactivity. 
 
 Associated Conditions. — Fatness is more or less closely re- 
 lated to certain other diseases of metabolism, such as diabetes and 
 gout. Anemia is frequently present and has sometimes been re- 
 garded as a cause, operating by reducing oxidation. (Further 
 discussion of this subject is included under Fatty Infiltration.) 
 
 Excessive Tissue-destruction. — This has been referred to 
 in connection with inanition ; but it may occur as a condition in- 
 dependent of the amount of food ingested. Among the conditions 
 in which this is observed may be mentioned fever, infectious or of 
 other forms ; chronic infectious diseases, with or without fever ; 
 tumors, especially carcinoma ; intoxications of various sorts ; some 
 cases of Graves' disease, etc. In all of these conditions the fats 
 of the body may waste as in simple inanition ; but there is an early 
 and marked tendency to consumption of the more important pro- 
 teid substances. This latter consumption may proceed along 
 physiologic lines, or there may be distinctly pathologic modifica- 
 tions sometimes leading to serious results (see Acid-intoxication). 
 
 The nature of the metabolic disturbances in these cases is ob- 
 scure, though it is likely that toxic substances of various sorts are 
 the direct causes. This is most probable in the case of direct in- 
 toxications (phosphorus), but is also supported by other facts. In 
 Graves' disease and carcinoma, as well as in fevers, there are 
 doubtless poisonous substances in the blood, but whether these are 
 the causes of the metabolic changes or not requires further study. 
 The fact that thyroid extract is capable of causing excessive de- 
 struction of tissue in normal or obese persons is significant in this 
 connection. 
 
 Acid-intoxication.— In the final metabolic transformation 
 of proteids there are produced ammonium, urea, uric acid, kreat- 
 inin, and other nitrogenous substances. The formation of urea is 
 still obscure in some particulars. It is certain that a large part is 
 produced in the liver, and it is probable that some is formed in 
 the muscles. The intermediate steps in the manufacture of urea 
 
34 TEXT-BOOK OF PATHOLOGY. 
 
 have not been definitely determined, but it is known that the liver 
 is capable of converting ammonium salts directly into urea, and it 
 is probable that ammonium is an important intermediate product 
 of proteid transformation. An excess of acids in the body (either 
 from introduction from without or production in the body) is in 
 part neutralized by ammonium, and in consequence the urea of 
 the urine decreases and the ammonium salts are increased. The 
 quantity of such salts is therefore in a measure an indication of the 
 condition which has been termed acid-intoxication. In part the 
 neutralization of acids is effected by the fixed alkalies of the body, 
 and thus occurs the reduced alkalinity of the blood and juices of 
 the body. 
 
 Experimental acid-intoxication is easily produced in animals by 
 feeding them with foods deprived of alkaline bases, or by direct 
 administration of acid. In the former case the acids resulting 
 from transformation of food and tissues must be neutralized by 
 the alkalies of the body ; in the latter case there is direct excess 
 of acid. Such acid-intoxication is readily produced in herbivorous 
 animals, as the amount of proteid food is small and in consequence 
 but little ammonium is produced. Various nervous symptoms are 
 ol (served. The animal breathes quickly, the pulse grows rapid, 
 muscular weakness, ataxia, and tremor develop, and finally coma 
 or collapse terminates the disease. The administration of alkalies 
 may completely arrest the progress of the condition and full 
 restoration may occur. 
 
 Acid-intoxication in Man. — Somewhat similar symptoms are 
 seen in man in certain diseases in which increased elimination of 
 ammonium with decrease of urea, decreased alkalinity of the 
 blood, and the excretion in the urine of certain organic acids have 
 been discovered. The assumption is warranted that these are 
 cases of acid-intoxication. 
 
 Etiology. — Among the diseases in which this occurs are fever, 
 diabetes, carcinoma, acute yellow atrophy of the liver, severe 
 anemia, phosphorus-poisoning, advanced gastro-intestinal disease, 
 and inanition. Sometimes no discoverable cause can be detected 
 (cryptogenetic acid-intoxication). 
 
 In these conditions abnormal metabolism leads to excess of 
 various acids, such as lactic, sarcolactic, sulphuric, phosphoric, 
 diacetic, and /9-oxybutyric acid. These in part combine with the 
 fixed alkalies and with ammonium, and in part are excreted as 
 such. Some, as sarcolactic acid, usually suffer decomposition in 
 the body, and are therefore rarely met with in the urine. 
 
 The origin of the acids of the fatty acid series has been the 
 subject of much controversy. Undoubtedly they may be derived 
 from the non-nitrogenous part of proteids, and in most of the 
 diseases above enumerated this is probably the case ; but they may 
 be formed from carbohydrates as well. The increase of diacetic 
 
DISORDERS OF NUTRITION AND METABOLISM. 35 
 
 and /3-oxybutyric acids in cases of diabetes when small amounts 
 of carbohydrates are supplied, and their decrease when the carbo- 
 hydrates are increased, point to the fact that destructive consump- 
 tion of proteids is the important source, though it may not be the 
 only or invariable source. 
 
 There is always reduction of oxidation in cases of acid-intoxi- 
 cation, but it is not known whether this is the primary disturb- 
 ance, or whether it is but an accompaniment. Experimentally it 
 has been shown by several observers that diminution in the supply 
 of oxygen will lead to increase of these acids. They probably owe 
 their presence to the failure of the normal oxidation which would 
 reduce such bodies to simple excretory products. Other substances 
 may result from the same tissue-destruction with insufficient oxi- 
 dation. Among these are the amido-bodies, leucin and tyrosin, 
 found in the urine in phosphorus-poisoning and acute yellow 
 atrophy of the liver as well as in other conditions. 
 
 Symptoms. — The symptoms of acid-intoxication in man may 
 be quite similar to those seen in experiments upon animals. De- 
 pression, stupor, and deep coma (coma carcinomatosum, diabeti- 
 cum) are some of the more pronounced manifestations. The pro- 
 duction of these may be direct or indirect. In diabetes it is 
 generally held that the diacetic and oxybutyric acids are harmless, 
 but that the acetone derived from them causes the violent symp- 
 toms. Aside from such direct action acid-intoxication may effect 
 its results by lessening the alkalinity of the blood and abstracting 
 fixed alkalies from the fluids of the body. 
 
 Formation of Albumoses. — In disturbed conditions of 
 metabolism albumoses, or probably very rarely peptone, are formed. 
 
 The causes which lead to the presence of these substances in 
 the blood and their excretion in the urine are numerous. Fever 
 of all kinds may be attended by this condition, and it may occur 
 in the course of suppurations, or other forms of tissue-destruction 
 (acute yellow atrophy, phosphorus-poisoning). It is found in 
 ulceration of the gastro-intestinal tract, and in some cases of new 
 growths. The presence of albumoses in osteomalacia has long 
 been recognized. 
 
 In all cases there is rapid tissue-destruction in which the albu- 
 mins become hydrated, forming some variety or varieties of albu- 
 moses, and possibly in rare cases peptone. Formerly the term 
 peptonuria was generally used to designate what is now called albu- 
 mosuria. The presence of albumoses in the blood causes no well 
 recognized results. It is known that they retard coagulability, 
 and their ingestion often causes leukocytosis. It is very likely 
 that they have other effects, but these are obscure. 
 
 The term peptone is now quite generally limited to the final hydration 
 product according to the definition of Kiihne. The peptone of Briicke 
 includes certain bodies now recognized as albumoses. 
 
36 TEXT-BOOK OF PATHOLOGY. 
 
 Alloxin Bases and Uric Acid. — The investigations of 
 recent years have shown that these substances are derived from 
 the nuclein of cellular nuclei. The alloxin bases, xanthin, guanin, 
 adenin, and hypoxanthin, are intermediary products which partially 
 or largely become oxidized to uric acid. Normally the amount of 
 uric acid is far in excess of that of the bases. Some of the uric 
 acid may become further oxidized, with formation of urea. The 
 great source of these products is cellular destruction, and especially 
 that of the leukocytes. Abnormally large quantities are found in 
 the urine in leukemia and in some cases of leukocytosis ; and in a 
 measure the substances furnish an indication of leukocytic destruc- 
 tion. The kind of diet may influence the amount of these bodies, 
 according as it is rich or poor in cellular tissue. The attempt to 
 establish a relationship between certain disorders (headaches, mi- 
 graine, etc.) and increased production of alloxin bases has not as 
 yet proved satisfactory. 
 
 A disease in some way dependent upon or associated with ab- 
 normal formation of uric acid and alloxin bases is gout. 
 
 Gout. — In its typical form gout is a paroxysmal disease 
 marked by deposits of urates in the joints and other structures, 
 and by coincident or consequent inflammatory disturbances. There 
 are many varieties, however, of irregular gout in which the par- 
 oxysms may be partly or wholly wanting and in which the disease 
 takes the form of a general systemic disorder, or of organic mala- 
 dies of various sorts. 
 
 Etiology.— Gout is essentially a hereditary affection, the heredity 
 not rarely being polymorphous. By this is meant that in certain 
 families gout and other diseases, such as obesity, diabetes, and 
 arterial sclerosis, may occur interchangeably. Gout usually de- 
 velops in the later years of life, and among the contributing causes 
 are the use of alcohol, overeating, sedentary life, and chronic lead- 
 poisoning. 
 
 Pathologic Anatomy. — The conspicuous anatomic lesions are 
 those of the joints, and consist of the deposit of urate of sodium 
 in the cartilages and connective tissue, and secondary inflammatory 
 changes. The latter may cause great distortion and fibrous over- 
 growth. Similar urate deposits may occur in the cartilages of the 
 ear, eye, and nose, and in the subcutaneous connective tissue or 
 elsewhere. These deposits, called the gouty tophi, may subse- 
 quently disappear by absorption or by discharging through the 
 skin. Cirrhosis in various organs and tissues of the body fre- 
 quently occurs in the course of gout. Among these the cirrhotic 
 or gouty kidney is most important. Atheroma, cirrhosis of the 
 liver, hypertrophy and fibroid change in the heart, and chronic 
 valvular disease are also frequent. 
 
 Pathogenesis. — According to the older theory of gout, the dis- 
 ease is due to increased quantities of uric acid in the blood. Re- 
 
DISORDERS OF NUTRITION AND METABOLISM. 37 
 
 cent investigations warrant a return to this view. The uric-acid 
 excretion of the urine has been found to decrease markedly during 
 a few days before an attack, and the assumption is warranted that 
 the acid accumulates in the blood, and is then deposited in the 
 tissues. Prior to the deposits local cellular necroses are believed 
 by many to be necessary for the deposit, and these necroses have 
 been attributed to the excessive amount of acid. Proof is wanting, 
 however, to show that excessive quantities of uric acid are capable 
 of causing such degenerations or necrosis. In some cases trauma- 
 tism may play a part in localizing the gouty precipitations ; in 
 most cases, however, the cause is obscure. 
 
 The causes of the increased production of uric acid and the 
 exact mechanism of this abnormal formation are still obscure. 
 An old theory that diminished oxidation in the tissues is the 
 immediate cause is no longer tenable ; and a newer view which 
 asserts that the accumulation is the result of failure of the renal 
 function has not been established. 
 
 Glycosuria and Diabetes. — A certain amount of grape 
 sugar occurs in the blood and urine of normal persons. The 
 quantity in the blood varies from 0.1 to 0.2 per cent. Notable 
 increase above these figures constitutes a pathologic condition, 
 glyeemia. Sometimes other forms of sugar, as levulose, occur in 
 the blood and urine. When there is sufficient sugar in the urine 
 to be discoverable by the ordinary tests the condition is pathologic, 
 and is termed glycosuria. This may be transient and trivial in 
 character, or a manifestation of a definite diseased condition called 
 diabetes. 
 
 The disposition made of carbohydrates by the animal body is 
 not definitely known in all particulars. It is certain, however, 
 that these substances are deposited in the liver and in the muscles 
 in the form of glycogen, that they form fats, and are in part con- 
 sumed by oxidation. The deposit of glycogen is of the nature of 
 a reserve store, the system thus being prepared for intervals of 
 abstinence. The glycogen is gradually discharged from these 
 tissues, and thus the quantity of sugar in the blood is maintained 
 at a more or less constant level. 
 
 Alimentary glycosuria is a term applied to glycosuria occurring 
 in healthy or diseased persons as a result of excess of carbohydrate 
 food. It is easily produced by the administration of considerable 
 quantities of milk-sugar, levulose, cane-sugar, or glucose. The 
 drinking of beer seems to aid particularly in its development. 
 The explanation of this condition seems a simple one. The 
 organism is unable to store up or consume the amount of carbo- 
 hydrates administered, and the excess is therefore discharged 
 through the kidneys. The ease with which such glycosuria is 
 developed differs in different individuals, and researches have been 
 made to determine the conditions that favor its development. The 
 
38 TEXT-BOOK OF PATHOLOGY. 
 
 liver in particular has been suspected as the organ most likely 
 inefficient in these cases, but thus far no definite facts have 
 been learned ; and the role of this organ has probably been exag- 
 gerated. 
 
 Experimental glycosuria, produced by administration of phlorid- 
 zin, offers several puzzling facts for consideration. It shows that 
 excess of glucose in the blood (hyperglycemia) is not a necessary 
 condition for the occurrence of glycosuria. After administration 
 of phloridzin, a glucoside which contains about 40 per cent, of 
 sugar, there is no excess of sugar in the blood, but glucose appears 
 in the urine, and indeed more than could have been produced by 
 the entire quantity of phloridzin administered. This shows that 
 there is abstraction of sugar from the reserve stores in the body. 
 It is not unlikely that the renal cells play a part in the occurrence 
 of this unusual excretion ; and this fact, together with the dis- 
 appearance of sugar from the urine in the late stages of some eases 
 of diabetes, when renal disease has occurred, has suggested to some 
 the possibility of renal forms of glycosuria and diabetes. This 
 view, however, has not yet been established. 
 
 Clinical Causes of Glycosuria. — Glucose appears in the urine in 
 many conditions, including various infectious diseases, various 
 intoxications, and concussion, injury, or disease of the central 
 nervous system, especially the Moor of the fourth ventricle. 
 
 Diabetes is a disease in which polyuria and glycosuria are 
 marked symptoms. It is not improbable that the term includes 
 disorders of quite different sorts, but no differentiation of such is 
 possible at the present time. A mild and a severe form are dis- 
 tinguished, and these present some striking differences, to which 
 reference will be made below. 
 
 Etiology. — Diabetes is frequently a hereditary disease, occurring 
 in families in which the same disease or obesity and gout have 
 occurred. The Jews seem particularly liable to it. Overeating 
 and sedentary life are causes of some importance, especially of the 
 milder form. Sometimes abnormal conditions of the nervous 
 system may be the underlying cause. Among these are functional 
 depressions, as in cases of excessive grief; traumatic injuries with 
 concussion of the brain ; and local diseases at the base of the brain 
 in the vicinity of the medulla. In some cases disease of the pan- 
 creas is the probable cause. Diabetes may occur in the young or 
 after middle life, the milder cases more frequently occurring at the 
 latter period. 
 
 Pathogenesis. — In the milder cases of diabetes the same ex- 
 planation may be applicable as that given for glycosuria, viz., the 
 liver and muscles do not store up the carbohydrates carried to 
 them, and the excess of sugar is not burned up in the tissues. 
 Hyperglycemia with consequent glycosuria results. In these cases 
 the withdrawal of carbohydrate food or temporary abstinence from 
 
DISORDERS OF NUTRITION AND METABOLISM. 39 
 
 all food causes the disappearance of the glycosuria. In severe 
 cases this explanation is not entirely applicable, since the amount 
 of glucose in the urine is often but little affected by abstinence 
 from carbohydrate food or even by starvation. It is quite certain 
 that in these severe cases the carbohydrate moiety of the proteids 
 of the food or tissues furnishes the sugar excreted in the urine. 
 In normal individuals and even in those suffering with mild dia- 
 betes the carbohydrates thus liberated by proteid decomposition 
 are stored up as glycogen or fat, or burned up in the tissues. 
 Glycosuria does not therefore occur, according to this view, which 
 is held by many. Severe and mild diabetes differ only in degree — 
 in one case the power to consume sugars is greatly deficient ; in 
 the other, only moderately so. 
 
 The nature of the metabolic disturbances that lead to this 
 inability to dispose of carbohydrates is still very obscure. The 
 old theory, that there is a lack of oxidating power, is disposed of 
 by the experimental demonstration that oxidation may be nor- 
 mally active. The influence of the nervous system is undoubted. 
 Reference may here be made to the occurrence of diabetes after 
 puncture of certain parts of the brain (medulla). At one time 
 this was thought to act through the vasomotor mechanism, con- 
 gestion and disturbance of function of the liver being regarded 
 as the important consequence of vasomotor derangement. At the 
 present time the part played by the liver is considered less im- 
 portant. No plausible explanation of the rdle of the nervous 
 system in the etiology of diabetes has been presented. 
 
 Older pathologic studies showed that diseases of the pancreas 
 are frequently associated with diabetes ; and recent experimental 
 investigations emphasize this relationship. Removal of the pan- 
 creas in the lower animals causes diabetes. It has not, however, 
 been shown in what way pancreatic disease or ablation acts, though 
 Lepine and others believe that the pancreas elaborates a glucose- 
 destroying (glycolytic) ferment, whose absence under the conditions 
 named causes accumulation of sugars in the blood and consequent 
 glycosuria. Unfortunately, this view is not confirmed by the ex- 
 periments of others ; and the theory is certainly not generally 
 applicable, since diabetes may occur without discoverable disease 
 of the pancreas. 
 
 Metabolism in Diabetes. — The essential facts are the inability 
 of the body to consume carbohydrates for the production of energy. 
 This leads, sooner or later, to destruction of the proteids of the body 
 with increased excretion of urea. Emaciation may be prevented 
 for a time by increased consumption of proteid food, but eventually 
 occurs. , In the destruction of the proteids of the food and tissues 
 acids are formed in excess (phosphoric from the phosphorus, sul- 
 phuric from the sulphur, /3- oxybutyria and diacetic from the non- 
 nitrogenous part of the albumins), and the condition termed acid- 
 
40 TEXT-BOOK OF PATHOLOGY. 
 
 intoxication (see above) results. A consequence, and to some 
 extent a measure, of this is the increased excretion of ammonium 
 salts in the urine. The uric acid of the urine is hut little increased 
 in diabetes. Acetone, a derivative of j0-oxybutyric and diacetic 
 acid-, and possibly (though not probably) these acids themselves, 
 may occasion still further proteid destruction by direct toxic ac- 
 tion. Acetone is certainly the important element in the production 
 of diabetic coma. 
 
 Pathologic Anatomy. — Aside from the lesions already referred 
 to as in some way related to the causation of the disease, there are 
 found pathologic changes of various kinds that result from it. 
 The lesions of gout (arteriosclerosis and cirrhotic kidneys) may be 
 of the nature of mere concomitants, or may be direct results of 
 diabetes. Renal diseases are of peculiar interest. Late in diabetes 
 albuminuria frequently develops and interstitial nephritis may fol- 
 low. When this occurs the glycosuria and other symptoms of 
 diabetes sometimes subside. The explanation of this is obscure 
 (see under Glycosuria). Changes in the liver (cirrhosis) have 
 often been found, and have been regarded as causative in some 
 cases. A peculiar form of diabetes with hepatic disease and 
 general icteroid staining of the skin and other tissues lias 
 been described under the title diabete bronze. Skin eruptions 
 (eczema, furuncles, carbuncles) are frequent in certain forms 
 of diabetes ; and gangrene of the extremities is common. Pneu- 
 monia and pulmonary tuberculosis are among the frequent devel- 
 opments of late stages of the disease. Chronic endocarditis, neu- 
 ritis, and cataract are comparatively rare lesions. The blood in 
 diabetes is less alkaline than normal and contains an excess of 
 solid matter, particularly when great polyuria has led to inspis- 
 sation. 
 
 Oxalliria. — This term is, strictly speaking, applicable only to increase of 
 oxalic acid in the urine, but is usually employed for cases in wbich crystals 
 of oxalate of lime are found abundant in the urine. The normal maximum 
 of oxalic acid is 20 mgr. for twenty-four hours. It has been sometimes held 
 that oxaluria is a result of deficient oxidation of the carbohydrates or of 
 the albumins of the body, but this theory has not been established. True 
 oxaluria determined by chemical estimation of the total excretion of oxalic 
 acid bas been found in jaundice and in some cases of diabetes. The authors 
 who have argued in favor of a specific disease marked by nervous symptoms 
 and oxaluria based their observations on the presence of an excess of oxa- 
 late sediment, rather than on chemical examinations. Increased sediment 
 occurs in certain instances of gout in which the oxalates alternate with uric 
 acid or coexist with this. 
 
 Phosphaturia. — This term should be restricted to increased excretion 
 of phosphoric acid, rather than to the presence of increased phosphate sedi- 
 ment in the urine. The latter may be due simply to want of acidity of the 
 urine. The daily maximum of phosphoric acid with ordinary diet is from 
 3.5 to 4 g. The "term phosphaturia might also he applied to cases in which 
 no absolute excess of phosphoric acid is found, but in which this substance 
 is relatively in excess when compared with the excretion of nitrogen. The 
 
DISORDERS OF NUTRITION AND METABOLISM. 41 
 
 normal proportions are from 17 to 20 parts of phosphoric acid for 100 parts 
 of nitrogen. Phosphaturia in the sense just described has been found in 
 some cases of inanition. Decided increase in the phosphatic excretion, ab- 
 solute as well as relative, occurs in some cases of diabetes ; also in cases of 
 tuberculosis and disease of the bones, such as ostitis and osteomyelitis. The 
 term diabetes phosphaticus has been used by Teissier for phosphaturia in the 
 sense of increased total excretion, and four varieties have been described : 
 (a) cases with polyuria and marked nervous symptoms ; {b) cases preceding 
 or accompanying pulmonary diseases, especially tuberculosis ; (c) cases in 
 which phosphaturia alternates with or coexists with glycosuria ; and (d) 
 cases in which oxaluria, polyuria, and slight albuminuria are present and 
 in which there is some relationship with gout. 
 
 The nature of the metabolic disturbances in phosphaturia are obscure. 
 Sometimes the disorder of metabolism seems to be merely quantitative, in 
 other cases doubtless qualitative. 
 
 FEVER. 
 
 Definition. — It is not easy to define this term accurately, 
 though we may regard as fever a condition in which the tempera- 
 ture of the body is elevated above the normal (98.6° F. ; 37° C.) 
 and in which the tissue-metabolism is altered in the direction of 
 increased consumption. There are cases in which the latter is in- 
 significant or wanting, and there are other instances in which the 
 temperature remains normal or subnormal under influences that 
 ordinarily provoke fever. At the present time, however, elevation 
 of temperature seems a necessary condition to the existence of 
 fever. 
 
 Nature. — It is important, first, to consider the regulation of 
 the temperature in health. In the normal individual heat is pro- 
 duced in the body by constant oxidation and other metabolic 
 activities, and the excess is dissipated by radiation from the sur- 
 face and the heating or evaporation of excreta. These processes 
 of heat-production and heat-dissipation are regulated in an orderly 
 manner under the influence of the nervous system. Special centers 
 for the production, dissipation, and regulation of heat have been 
 described by the physiologists, though their location and method 
 of operation still remain in doubt. "Whatever the exact mechanism 
 may be found to be, it is quite certain that in some way the ner- 
 vous system exercises a control over production and discharge of 
 heat. 
 
 The excessive heat of fever may conceivably be due to excess 
 of heat-prod action, diminution of the dissipation, to both of these 
 conditions, or to increase of both with greater excess of production. 
 In most instances of fever in man it appears that production and 
 dissipation are both increased, though the latter is insufficient. The 
 increased production results from increased oxidation and other 
 metabolic processes. A study of the respiratory exchange of gases 
 shows that oxygen is consumed in greater quantity than normally, 
 and the quantity of C0 2 is correspondingly increased. The excess 
 
42 TEXT-BOOK OF PATHOLOGY. 
 
 may amount to as much as 20 per cent. Investigation of the ex- 
 creta shows at the same time evidences of more or less rapid and 
 extensive tissue- waste. The quantity of nitrogen eliminated is in 
 excess of that consumed in the food ; and wasting of the tissues 
 results. The albuminous elements suffer particularly in the meta- 
 bolic wasting, the decrease of fat being especially dependent on 
 insufficiency of food. 
 
 Etiology. — The causes of fever doubtless vary greatly. Di- 
 rect exposure to heat does not aifect the temperature more than a 
 fraction of a degree in healthy persons, unless the surrounding 
 temperature is very great. Ordinarily the heat-regulating mech- 
 anism maintains a proper adjustment. Excessive heat may, how- 
 ever, bring on fever, as in the case of sunstroke. Here, it has 
 been held that the heat leads to direct disturbances of the nervous- 
 regulating apparatus ; but recent investigations seem to show that 
 there arc first produced toxic substances which secondarily influ- 
 ence the heat-centers of the brain. In another class of cases still 
 more direct disturbance of heat-regulation seems to occasion fever. 
 Among these cases are the instances of fever in hysteria and other 
 nervous diseases. 
 
 In the great majority of cases of fever it is quite certain that 
 toxic substances are the cause of the febrile disturbances. These 
 sul (stances may be of quite different sorts. In the case of infections 
 it is known that certain substances contained within the bacteria 
 themselves may cause fever, and that products of the growth of the 
 micro-organisms may have the same effect. The latter are prob- 
 ably bodies of albuminous nature. Other albuminous bodies re- 
 sulting from normal or disturbed metabolism, independent of the 
 action of bacteria, such as albumoses, peptone, tissue-fibrinogen, 
 etc., may be equally potent ; and various ferments, such as pepsin, 
 fibrin-ferment, diastase, etc., are known to have the same power. 
 These facts explain the multiplicity of causes capable of producing 
 fever, as any chemical, mechanical, or bacterial injury of the tis- 
 sues may liberate toxic substances, which in turn act upon the 
 nervous system and occasion the phenomena of fever. 
 
 Pathologic Results. — Fever is accompanied by or leads to 
 a variety of disorders. The appetite is lost, there is excessive 
 thirst, emaciation is habitual, and the functions of the various 
 organs arc more or less disturbed. To a large extent these results 
 are doubtless due to the presence of toxic substances in the blood 
 and to other changes in this fluid. There is always a tendency to 
 inspissation of the blood, the number of corpuscles being augmented 
 (relatively) and the specific gravity increasing. This is not, how- 
 ever, invariably the case, as destruction of the solid matters of the 
 blood may exceed the loss of liquid. The alkalinity of the blood 
 is more or less reduced by the production of lactic acid or other 
 acids in the tissue-destruction. There is little accurate knowledge 
 
DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 43 
 
 of the toxic substances in the blood. The original poisons that 
 caused the fever may be toxic for the entire organism, and other 
 poisons may be produced by the elevation of temperature and 
 disturbed metabolism. 
 
 Definite morbid changes may occur in the various tissues of 
 the body, notably the muscles, heart, liver, and kidneys. Among 
 these changes are cloudy swelling, fatty degeneration, and coagu- 
 lation-necrosis. It is unlikely that these changes are the direct 
 result of the increased temperature. More probably they result 
 from the action of toxic substances generated in the course of the 
 fever. 
 
 Conservative Bffects of Fever. — While fever occasions 
 many disturbances and leads to various pathologic consequences, it 
 is not improbable that there is a certain measure of usefulness in 
 it. Some authors have called attention to the fact that rapid 
 reduction of the temperature under the influence of antipyretics 
 is often followed by harmful consequences. This does not neces- 
 sarily prove the usefulness of the fever, as the antipyretics are all 
 capable of harm in themselves. A more definite proof of the uses 
 of fever is that obtained by subjecting infected animals to high 
 temperatures or to febrile conditions, and studying the progress 
 of the infection. Under these circumstances it has been found 
 that the course of various infections, such as with the Diplococcus 
 pneumoniae, the bacillus of typhoid fever, and other organisms, is 
 much milder and the consequences less serious than in animals not 
 placed uuder the same conditions. These results agree very well 
 with experiments with bacteria outside the animal body. For 
 example, it is known that many of the bacteria are influenced 
 unfavorably in their growth and virulence by excessive tempera- 
 tures (104° to 107.6° F. ; 40° to 42° C). Whether in the body 
 the temperature affects the micro-organisms directly or indirectly 
 through the production of antitoxic substances, or in other ways, 
 remains unsettled. 
 
 CHAPTER III. 
 DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 
 
 GENERAL DISTURBANCES. 
 
 The circulation of the blood is maintained by the rhythmic 
 contractions of the auricles and ventricles of the heart, aided by 
 the elasticity of the arteries ; by the compression of the veins by 
 
44 TEXT-BOOK OF PATHOLOGY. 
 
 the muscles ; and by the suction of* the inspiratory movements of 
 the chest. 
 
 General disturbances of the circulation result from lessened or 
 excessive heart-power, from arterial disturbances, or from changes 
 in the quantity or character of the blood. Muscular and respira- 
 tory weakness may be contributing causes. 
 
 Weak Heart. — There are a variety of heart-diseases that may 
 lead to disordered circulation. The muscle itself may be weakened 
 from overstrain, the fevers or other diseases, the action of poisons, 
 or insufficient nourishment as in the anemias, or in narrowing of 
 the coronary artery. The muscle may be soft and cloudy, fatty, 
 or hardened by sclerotic changes. There may be no evident mus- 
 cular disease, but functional weakness of the intracardiac ganglia. 
 The valves or orifices of the heart may be diseased, and regur- 
 gitation or obstruction of the blood-flow results. Sometimes 
 blood-clots form within the heart and similarly cause obstruc- 
 tion of the current. Finally, pericardial effusions or adhesions 
 or tumors pressing upon the heart may seriously disturb its 
 action. 
 
 The result of the weakened state of the heart must be the 
 accumulation of blood in the venous system. The place of 
 engorgement depends upon the part of the heart specially weak- 
 ened. If the left ventricle fails, the blood backs into the left 
 auricle and the lungs. As long as the right heart maintains its 
 poAver the venous congestion goes no further ; but when this fails 
 repletion of the right auricle and of the systemic veins ensues. 
 When the right heart is first at fault general venous congestion 
 is an earlier manifestation. In all cases the arterial pressure falls 
 and the blood-current is slowed, whereas the venous pressure is 
 increased. 
 
 Hypostatic Congestion. — In cases of serious weakness of the 
 heart, in which it is quite unable to maintain an active circulation, 
 the blood tends by the force of gravity to sink to dependent parts. 
 This condition is known as hypostatic congestion. It occurs very 
 frequently in low fevers and quite commonly just before slow death 
 resulting from any cause. Dilatation of the vessels from vaso- 
 motor paresis, general muscular weakness, and the failure of 
 vigorous inspiratory efforts are secondary causes. 
 
 The blood accumulates in the skin of the back, especially about 
 the buttocks. The skin is of a livid color, but is bloodless over 
 the bony points; the tissues tend to become sodden from transu- 
 dation of liquid from the blood-vessels. Sloughing and gan- 
 grene (bedsores) may result. Internally, hypostatic congestion 
 affects the lungs particularly, and a form of pneumonia may 
 follow. 
 
 Post-mortem lividity is allied to hypostatic congestion. After 
 death the blood gravitates to the dependent parts and accumulates 
 
DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 45 
 
 especially in the veins, as the arteries contract as soon as the heart- 
 action ceases. Sudden and complete failure of the heart leads to 
 anemia of the brain and syncope, which may prove fatal if not 
 instantly relieved. 
 
 Overaction of the heart is less frequent. Temporary over- 
 action occasions increased activity of the circulation and eleva- 
 tion of blood-pressure, sometimes sufficient to cause hemorrhage. 
 More prolonged overaction due to overwork, to excessive feeding, 
 or to nervous stimulation, as in Graves's disease, causes hyper- 
 trophy of the left ventricle, and later of the whole organ. In 
 consequence the circulation may be more or less permanently over- 
 active. 
 
 Arterial Disorders. — Both organic and nervous disturbances 
 are important. Of the organic disturbances the most frequent is 
 sclerosis of the arteries, which offers a constant impediment to the 
 arterial circulation. Hypertrophy of the heart overcomes the ob- 
 stacle, but when the heart fails venous congestions and dropsy en- 
 sue. Sclerosis may also affect the veins, but much less commonly. 
 Local diseases of the aorta, as congenital narrowing, compression 
 by enlarged glands or tumors, aneurysms, and blood-clots may 
 obstruct the flow of blood to the arteries, and thereby cause 
 stagnation of the blood in the heart, lungs, and venous 
 system. 
 
 Vasomotor disturbances are dependent upon the nervous system. 
 Under the influence of certain diseases of the nervous system or 
 of poisons (as carbonic acid gas in asphyxia) acting locally on the 
 vessels or upon the vasomotor center in the brain, contraction of 
 the smaller arterioles occurs ; and in consequence the blood-press- 
 ure is greatly elevated, the heart is impeded, and venous conges- 
 tion results. On the other hand, the arterioles may distend from 
 vasomotor paresis, the blood-pressure falls, and unless the heart is 
 active there is a tendency to hypostatic congestion. 
 
 Changes in the Blood. — Increase and decrease of the 
 quantity of the blood are generally merely passing conditions to 
 which the circulation readily adapts itself by dilatation or con- 
 traction of the vessels. Sudden losses of blood, if large, may be 
 fatal by syncope. Smaller losses are soon repaired by absorption 
 of water from the tissues and by regeneration of blood. Increases 
 in the quantity of the blood by ingestion of liquids never disturb 
 the circulation greatly. Rapid excretion soon reduces the quantity 
 to the normal. 
 
 Changes in the character of the blood affect the circulation 
 greatly. The accumulation of carbonic acid and probably other 
 effete products of tissue-change impede the flow by exciting vaso- 
 motor contraction. This is probably brought about by the action 
 of the poisons on the terminal nerve-filaments in the blood-vessels 
 or directly on the walls of the vessels. This is the best explana- 
 
46 TEXT-BOOK OF PATHOLOGY. 
 
 tion of the increase of pressure in cases of Bright's disease without 
 arteriosclerosis. The poisons in this ease are the retained renal 
 excreta, 
 
 LOCAL HYPEREMIA. 
 
 Local hyperemia is increase in the quantity of blood in a part 
 of the body. This may be due to increase of the flow to that part, 
 or to obstruction of the outflow. The former is called active or 
 arterial hyperemia or congestion; the latter, passive or venous 
 
 lii/jii rem id. 
 
 Active hyperemia occurs in organs during periods of func- 
 tional activity, the increased blood-supply here being due to 
 increased demand for nutrition. Pathologically, active hyperemia 
 is due to causes which lead to dilatation of the arteries of a certain 
 part. This dilatation may be due to influences acting through the 
 vasomotor nervous system or to local affections of the vessel-walls. 
 The vasomotor nervous system may be affected at its center in the 
 medulla or peripherally. The latter is seen when the sympathetic 
 perves, which contain vasoconstrictor fibers, are severed or com- 
 pressed by tumors, the vessel-walls thereby becoming paralyzed 
 [neuroparalytic hyperemia). On the other hand, the vasodilator 
 fibers in the spinal nerves may be stimulated, as in certain cases 
 of neuritis, with a similar result {neurotonic hyperemia). Direct 
 injury to the vessel-walls by heat, traumatism, inflammation, 
 drugs, or by the vascular fatigue following temporary stoppage 
 of circulation, is a frequent cause. 
 
 Active hyperemia is spoken of as collateral when anemia in one 
 part leads to overfilling of the vessels of an adjoining or even 
 distant part. 
 
 The hyperemic area is bright red in color, the temperature is 
 elevated, and there is slight swelling. After death the distended 
 arteries and capillaries may contract and the part grows paler. 
 Arterial hyperemia Is one of the phenomena of beginning inflam- 
 mation, and in any case if prolonged may terminate in inflam- 
 mation. Functional activity is increased by moderate conges- 
 tions. 
 
 Passive hyperemia is due to impediments to the outflow of 
 the blood through the veins. This may be brought about by 
 compression of veins by tumors, by thickening of their walls, or 
 by thrombi within. Little disturbance results from obstruction 
 01 a small vein, because of the freedom of collateral circulation, 
 provided the heart is active. In cases of weak heart-power, how- 
 ever, slight obstructions may determine local venous hyperemia, 
 or by gravity alone the blood may sink to dependent parts. The 
 latter constitutes hypostatic congestion (see page 44). 
 
 Areas the seat of passive hyperemia are dark red (cyanosis) and 
 lowered in temperature. The veins are distended, and very soon 
 
DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 47 
 
 the watery elements of the blood transude and the part becomes 
 edematous and swollen. In severe cases red blood-corpuscles 
 escape by diapedesis. Later fatty de- 
 generation results from the imperfect ___. _- '^~i?"^--^- .-? 
 
 nutrition of the tissues ; or even ne- :^ ^ -'; ~ : ^^^^: ; 
 crosis and gangrene may occur. In ; . gS 
 
 long-continued moderate passive hy- 
 peremia overgrowth of connective tis- 
 sue and pigmentation of the tissue by 
 broken-down blood-corpuscles is ob- 
 served (brown induration). 
 
 Complete stoppage of the circula- 
 tion in a localized area is called stasis 
 (Fig. 1). This may be an extreme 
 grade of passive hyperemia. The blood- 
 corpuscles accumulate in the small ves- 
 sels (arteries, capillaries, and veins) and 
 the plasma is slowly pressed out of the 
 vessels or onward. There results a 
 filling of the vessel with a homogene- 
 ous red material, which is composed 
 of the red corpuscles so closely packed 
 as to be indistinguishable. On relief 
 of the stasis the corpuscles become free 
 again. Stasis may also be produced by chemical agents which 
 rapidly withdraw the plasma from the vessels, leaving the corpus- 
 cles unable to circulate ; or similarly by rapid evaporation of the 
 liquor sanguinis from internal structures (as the peritoneum) ex- 
 posed to the air. 
 
 Passive congestion of any grade and stasis interfere with func- 
 tional activity in two ways : by the reduction of nutrition of the 
 cells and by the pressure exercised upon them by the accumulating 
 blood and serum. 
 
 Fig. 1.— Stasis of blood in the 
 superficial vessels in a case of val- 
 vular disease and heart-failure 
 (modified from Ziegler). 
 
 LOCAL ANEMIA. 
 
 Local anemia or ischemia is the condition in which a tissue 
 contains less than its proper quantity of blood. This may be 
 direct when it results from causes obstructing the flow into the 
 arteries, or collateral when it is due to withdrawal of blood into 
 hyperemic areas in other parts. of the body. Of the causes acting 
 directly, pressure is the most frequent. There may be general 
 pressure upon an organ or localized area of the body, as in the 
 application of elastic bandages ; or pressure upon the vessels 
 within the tissue itself, as in amyloid disease, the amyloid sub- 
 stance compressing the arteries and capillaries, or there may be 
 direct compression of an artery by tumors. The circulation in an 
 
JS 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 artery may be impeded by sclerosis of the vessel-walls and by 
 emboli or thrombi within the vessel. Local anemia of moderate 
 or even severe grade may be due to nervous influences acting 
 through the vasomotor system, as in the 
 earlier manifestations of Raynaud's disease. 
 Collateral anemia is well illustrated by the 
 anemia of the brain occurring in animals 
 in which the splanchnic nerves have been 
 cut, with the consequent production of ab- 
 dominal hyperemia. When ischemia is 
 due to obstruction of a single vessel the 
 circulation is generally soon restored by 
 collateral anastomosis; the collateral ves- 
 sels sometimes reach considerable dimen- 
 sions (Fig. 2). When an artery which has 
 few anastomoses and which soon splits up 
 into capillaries is obstructed the phenom- 
 ena of infarction (see page 53) ensue. 
 
 An anemic area is pale, reduced in size 
 and temperature, and functionally less ac- 
 tive than normal. If the condition per- 
 sists, fatty degeneration and necrosis 
 result. When a severe local anemia is 
 relieved it is apt to be followed by hyperemia of the same area, 
 due to exhaustion or degenerative weakness of the vessel-walls. 
 
 Fig. 2.— Anastomoses three 
 months after ligation of the 
 femoral artery ofa dogi Porta (. 
 
 HEMORRHAGE. 
 
 By hemorrhage is meant the escape of the several con- 
 stituents of the blood from the blood-vessels. It is said to be 
 arterial) venous, or capillary according to the vessel from which 
 the flow of blood takes place, and parenchymatous when it comes 
 from all of the vessels. Hemorrhage may occur either by dia- 
 pedesis and extravasation through intact vessels (hemorrhage per 
 diapedesim) or by actual rupture of a vessel {hemorrhage per rhexin). 
 The former process is seen only in the capillaries and smaller veins j 
 the latter occurs mainly in the arteries and veins. 
 
 Diapedesis and Emigration. — ruder normal conditions 
 a certain number of white corpuscles by virtue of their ameboid 
 movements escape from the capillaries, and become wandering 
 cells which move about in the tissues or are carried by the lymph- 
 stream. This process is called emigration. There is at the same 
 time some transudation of plasma, which, with the leukocytes, 
 enters the lymphatic circulation, ruder certain abnormal condi- 
 tions the red corpuscles also pass through the vessel-wall and col- 
 lect in the tissues. This is known as diapedesis (Fig. 3). It may 
 be studied very readily under the microscope in the mesentery of a 
 
DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 49 
 
 living frog. It is noticed that the red corpuscles approach certain 
 parts of the wall of the capillary or vein and become fixed ; then 
 a small projection appears outside the vessel, opposite the corpus- 
 cle, and as this increases the corpuscle within grows smaller, until 
 the whole body has gradually passed through. Not rarely several 
 
 -Diapedesis of the red blood-corpuscles through 
 (after Thoma). 
 
 capillary of a frog's tongue 
 
 corpuscles pass through in one mass ; as has been particularly 
 noted by Thoma. Outside the vessel the corpuscle at once as- 
 sumes its ordinary shape. 
 
 Diapedesis was first studied by Strieker and Cohnheim. Arnold, whose 
 investigations are most important, first believed that the emergence of the 
 red corpuscles takes place through orifices or stomata ; but later recognized, 
 as is now generally believed, that the supposed stomata are merely accumu- 
 lations of intercellular substance in certain places between adjoining endo- 
 thelial cells or at the junction of several cells. The active cause of the 
 extrusion of the red corpuscles is the pressure of the blood. 
 
 The leukocytes emigrate from the vessel in exactly the same 
 way as the red corpuscles, but mainly by their own ameboid move- 
 ments. At the same time there is a more or less copious outflow 
 of plasma. 
 
 Diapedesis is readily induced by mechanical compression of a 
 vein, which elevates the blood-pressure ; or it may follow elevation 
 of blood-pressure from any other cause. On the other hand, with 
 normal pressure increased permeability of the vessel-walls may 
 occasion diapedesis. Such degenerative conditions of the vessels 
 may be due to the action of poisons, to various infectious diseases, 
 to moderate traumatism, or to temporary obstruction to the flow 
 of blood into a certain area. Perhaps also altered states of the 
 blood may play a part when both the vessels and pressure are 
 normal. Hemorrhages by diapedesis are generally small and 
 punctate (petechia), but may be quite large, as sometimes in the 
 conjunctiva. 
 
 Causes of Hemorrhage. — The ordinary form of hemor- 
 rhage per rhexin may be due to traumatism, to diseases of the 
 
50 TEXT-BOOK OF rATHOLOGY. 
 
 vessels, to increase of the blood-pressure, and to certain vague 
 nervous influences. 
 
 1. Traumatic hemorrhage may be due to direct laceration of a 
 vessel <>r t<> contusions which merely weaken the vessel-wall and 
 lead to subsequent rupture. 
 
 2. Diseases of the blood-vessels causing hemorrhage generally 
 originate from causes within the vessel, and are due to such con- 
 dition- as poisoning, infectious fevers, cachexias, or the anemias. 
 Among the diseases of the vessels are fatty degeneration of the 
 ultima or media, atheroma, and miliary aneurysm. On the other 
 hand, the outer coat may be eroded by surrounding disease and 
 hemorrhage ensue (hemorrhage per rfiabrosin). This is seen in 
 phthisical cavities in the lungs. 
 
 3. Increase of blood-pressure may be absolute or relative. The 
 former occurs from emotional excitement, from hypertrophy of the 
 heart, during paroxysms of whooping-cough, croup, and various 
 convulsive disorders. In asphyxia there is decided increase of 
 blood-pressure both from vasomotor contraction and from the 
 violent muscular efforts. Relative increase of pressure occurs 
 when the pressure external to the vessel is reduced, as in balloon 
 ascension, or in the pleura in cases where during violent inspiratory 
 efforts the air cannot enter the lungs, as in the fetus attempting to 
 breathe during labor. 
 
 1. Neuropathic Hemorrhage. — The nervous system exercises a 
 peculiar influence upon the vessels. In cases of apoplexy and 
 epilepsy, of section of the spinal cord, and in other nervous con- 
 dition-, spontaneous hemorrhages from the nose or stomach, or into 
 the lungs, suprarenal bodies, and other organs, are not infrequent. 
 In the same group also are to be reckoned the instances of 
 vicarious hemorrhage due to suppression of the menses, and the 
 remarkable cases of stigmatization. The lust named is a condition 
 in which under nervous exaltation or hysteria spontaneous hemor- 
 rhages occur from various parts of the body, especially from the 
 part- wounded in the crucifixion. 
 
 6, The Hemorrhagic Diathesis. — Certain persons present an in- 
 herited tendency to bleed spontaneously or after very trivial injuries. 
 Such persons are known as "bleeders," and the condition as hemo- 
 philia. The exact pathologic condition which occasions the 
 hemorrhages is still uncertain. A hemorrhagic diathesis may also 
 be developed as a result of various diseases, as typhus fever, 
 anthrax, septicemia, or phosphorus-poisoning. The same is ob- 
 served in the Bcvere forms of anemia, like progressive pernicious 
 anemia and leukemia. In these cases altered blood states and 
 disease of the vessel-walls are doubtless the causes at work. 
 
 Classification of Hemorrhages. — Hemorrhage may occur 
 on free surfaces <>r into the tissues. In the former ease various 
 Mines are applied to designate the locality, such as epUtaxis, nose- 
 
DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 51 
 
 bleed ; hemoptysis, hemorrhage from the lungs ; hematemesis, from 
 the stomach ; enter or rhagia, from the bowel ; metrorrhagia, uterine 
 hemorrhage between, and menorrhagia at, the menses. 
 
 Hemorrhages into the tissues take their names from the size 
 and nature of the lesion. A hemorrhagic infiltration beneath a 
 surface, as of the skin or mucous membrane, is called an ecchymosis, 
 which if small and well defined is a 'petechia, but if large and 
 diffuse, a suggillation or suffusion. A distinct accumulation of 
 blood, constituting a veritable blood-tumor, is known as a hema- 
 toma. Infiltrations of a peculiar sort, involving localized portions 
 of a tissue or organ, are known as hemorrhagic infarcts (q. v.). 
 
 Results of Hemorrhage. — A very large hemorrhage may 
 lead to sudden death by cerebral anemia. More frequently the 
 patient remains unconscious for a time and then slowly recovers. 
 The hemorrhage ceases spontaneously by the diminution in heart- 
 action, by clotting of the blood at the point of rupture, by retrac- 
 tion of the elastic vessels, and by pressure of the surrounding 
 tissues. Blood extravasated in the tissues soon coagulates and 
 subsequently undergoes disorganization, the red corpuscles break- 
 ing down into pigment-matter, which may be carried away or 
 deposited at the seat of hemorrhage. The fluid elements may be 
 completely absorbed, or, stained with coloring-matter, may remain 
 as a cyst. A focus of hemorrhage may set up reactive inflam- 
 mation and lead to encapsulation by new connective tissue. Some- 
 times hemorrhagic accumulations become inspissated and undergo 
 calcification. Blood in the serous sacs does not readily coagulate, 
 but mingles with the normal liquid secretion. It may be grad- 
 ually absorbed or may undergo degenerative changes, especially 
 when infected by micro-organisms. Large hemorrhages cause acute 
 anemia ; repeated small extravasations may lead to profound sec- 
 ondary anemia. (These conditions will be more fully discussed 
 under Diseases of the Blood.) 
 
 EMBOLISM. 
 
 Embolism is the process in which foreign bodies of various 
 kinds are carried in the blood and deposited in the smaller arteries 
 or capillaries through which their size does not permit them to 
 pass. The bodies deposited are called emboli. 
 
 Sources and Nature of Emboli. — The most common form 
 of embolism is that in which portions of thrombi situated in 
 the heart, the large veins of the extremities or pelvis, or on ather- 
 omatous patches in the aorta, are swept into the circulation and 
 lodge in the smaller vessels. Softening of the original thrombus 
 is generally the immediate cause. More rarely portions of a dis- 
 eased heart- valve or of the intima of the heart or arteries, liver 
 or placental cells, or parts of tumors, are carried in the circulation 
 
52 TEXT-BOOK OF PATHOLOGY. 
 
 and deposited as emboli. Disorganization of the blood may cause 
 embolism of pigment-particles, as in malaria, or of small hyaline 
 masses, as in burns and certain forms of poisoning. In cases of 
 fracture of bones particles of fat may be dislodged from the mar- 
 row and enter the circulation, while in wounds of the large veins 
 of the neck or elsewhere air-embolism is observed. Finally, 
 masses of bacteria, scoliccs of echinococcus, and other parasites 
 are a serious form of emboli. 
 
 Seats of Embolism. — The final place of lodgement of an 
 embolus depends mainly on its source. Those derived from the 
 general venous circulation are usually carried through the right 
 heart to the lungs, where they occlude branches of the pulmonary 
 artery. Emboli in the portal circulation may lodge in the liver, or 
 pass through the liver to the heart and lungs. In cases of whooping- 
 cough or other conditions attended with increased intrathoracic 
 pressure emboli in the inferior vena cava may be carried in the 
 direction opposite to the usual blood-current, and may be con- 
 veyed into the liver through the hepatic veins. This is known 
 as retrograde embolism. 
 
 Emboli coming from the left heart or from the aorta are dis- 
 tributed in the general arterial circulation. They are most fre- 
 quently found in the spleen, kidneys, and brain. Other organs or 
 the peripheral vessels may likewise be affected, but the results of 
 embolism are less marked in them and are frequently overlooked. 
 Emboli from the veins may reach the general circulation in cases 
 in which the foramen ovale or septum ventriculorum is perforated 
 (paradoxic embolism), or by being broken up into smaller emboli 
 in the lungs and thus passing through the pulmonary capillaries. 
 The latter is not infrequent in cases of fat-embolism of the lungs. 
 
 Results of Embolism. — A large embolus may cause sudden 
 death by occluding one of the main branches of the pulmonary 
 artery, one of the coronary arteries, or a large cerebral vessel. If 
 the vessel is not wholly occluded, secondary thrombosis may com- 
 plete the obstruction and death maybe slow; or in the case of less 
 important vessels merely local anemia results. This may be re- 
 lieved by establishment of collateral circulation or may cause more 
 Or less extensive necrosis if not relieved. The original embolus 
 and the secondary thrombus may undergo softening or organization 
 in the same manner as ordinary thrombi (7. v.). 
 
 The results of occlusion of smaller vessels by emboli depend on 
 the nature of the embolus. They are either purely mechanical 
 when the embolus is aseptic, or septic when the embolus is infec- 
 tious. The important mechanical result of small emboli is the 
 pathologic condition called infarction. 
 
DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 53 
 
 INFARCTION. 
 
 Infarcts occur in situations in which there are small arteries 
 having only capillary or at most very slight arterial anastomosis 
 with neighboring arteries. Such arteries were called endarteries 
 by Cohnheim. They are found especially in the kidney, spleen, 
 lungs, retina, base of the brain, and 
 parts of the heart. When one of 
 these is occluded by an embolus in- 
 farction occurs. 
 
 Infarcts may be hemorrhagic or 
 anemic. The former are dark red in 
 color, situated in the peripheral part 
 of the organ, and harder than the sur- 
 rounding tissue. They are wedge- 
 shaped, the base being outward toward 
 the periphery of the organ. Infarcts 
 may result sometimes from occlusion Fig. 4.— Anemic infarct of the 
 
 r> i r> v • • . ■ l kidney: the embolus, occluding a 
 
 Ot a number Ot adjoining arterioles 01' branch of the renal artery, is shown 
 
 capillaries, and in this case are irregu- J^. lower part of the picture 
 lar in outline. Anemic or white in- 
 farcts present the same general features, but are less elevated and 
 are yellowish or grayish in color. They are frequently surrounded 
 by a zone of congestion or hemorrhage (Fig. 4). 
 
 Formation of Infarcts. — The first effect of occlusion of an 
 endartery by an embolus is stoppage of the circulation beyond the 
 embolus. A wedge-shaped anemic area results. This may remain 
 anemic and undergo coagulation-necrosis, with the formation of 
 an anemic or white infarct. In other cases, however, the vessels 
 of the occluded area, after a temporary period of anemia, become 
 overfilled with blood, extravasation occurs, and an hemorrhagic in- 
 farct results. Various theories are offered to explain the persist- 
 ence of anemia in the first case and the overfilling with blood in 
 the second. In anemic infarcts the persistent anemia in some 
 cases is due to thrombosis in the venules which receive the blood 
 from the occluded endartery and in the anastomotic capillaries. 
 At times rapid swelling of the parenchymatous cells of the organ 
 compresses the capillaries and maintains the anemia. Some con- 
 tend that white infarcts are frequently formed by rapid absorption 
 and removal of the coloring-matter of the blood from hemorrhagic 
 infarcts. In the latter the overfilling of the vessels results either 
 from a backflow of blood from the veins (Cohnheim) or from free 
 capillary-anastomosis. The latter would be especially apt to occur 
 when the general or local blood-pressure was previously elevated, 
 or when the lodgement of the embolus caused reflex contraction 
 of the surrounding vessels, and thus overflow of blood into the 
 occluded area through the capillary-anastomosis. The hyperemia 
 
54 TEXT-BOOK OF PATHOLOGY. 
 
 thus produced soon leads to extravasation of blood, because the 
 vessels of the occluded areas rapidly undergo degenerative changes. 
 Infarcts in the lungs are nearly always hemorrhagic; those in the 
 kidneys and especially the spleen are frequently anemic. 
 
 Subsequent Changes. — In anemic infarcts coagulation-necro- 
 sis and caseati< m are the marked degenerative changes. The broken- 
 down tissue is gradually absorbed and reactive inflammation and 
 organization cause cicatrization. Not infrequently a small amount 
 of calcareous matter is deposited, especially in infarcts of the lungs. 
 In hemorrhagic infarcts the extravasated blood breaks up into 
 pigment-matter and the tissues suffer degenerations similar to those 
 seen in anemic infarcts. The final result in either case is generally 
 a scar, which is pigmented in cases of hemorrhagic infarcts. More 
 rarely infarcts undergo liquefaction and cyst-formation, especially 
 in the brain. The infarct may become infected by micro-organisms 
 after its formation and abscess may result, as in cases in which the 
 embolus itself was an infectious one. 
 
 Infectious embolism occurs in cases of purulent softening 
 of thrombi, in cases of local suppuration or necrosis, in ulcerative 
 endocarditis, and the like. The first effect may be the formation 
 of a hemorrhagic or anemic infarct ; but the micro-organisms soon 
 multiply and invade the tissues, causing suppurative or gangrenous 
 processes. Metastatic abscesses are produced in this manner. 
 Similar results follow when an infarct is secondarily infected. 
 This is not infrequent in the lungs, where the air-passages furnish 
 a ready path for the entrance of micro-organisms. 
 
 Dust-embolism. — Small particles of coal, iron, marble, or clay entering 
 tbe lungs in respiration may penetrate the tissues, are largely taken up by 
 phagocytic cells, and for the most part are carried to the bronchial lym- 
 phatic glands. If the latter are surcharged and soften, the dust-particles may 
 gain access to the circulation through the efferent lymph-channels of the 
 gland or by rupture of the gland into neighboring veins. More rarely dust- 
 particles may enter the blood-vessels in the lungs, directly, by penetration. 
 After their entrance into the blood they are deposited in the capillaries 
 and substance of the liver, spleen, and bone-marrow, where they may re- 
 main permanently, either free or enclosed in fixed cells, or whence they 
 may be removed by wandering cells. The final discharge occurs especially 
 from the lungs, the tonsils, the lymphatic structures of the intestines, and 
 from the liver in the bile. 
 
 Air-embolism. — Small quantities of air may occasion no serious dis- 
 turbances ; but when large quantities enter the veins the right heart is 
 found full of frothy blood and the pulmonary arterioles are occluded by 
 small bubbles. Sudden death in these cases is not unusual. Some recent 
 experiments in dogs seem to cast doubt on the seriousness of air-embolism, 
 but the matter is not yet settled. 
 
 Fat-embolism. — Sudden death may occur when a large number of the 
 pulmonary vessels ;l re obstructed by embolic oil-drops. When the process 
 is less extensive little disturbance arises, as the oil is soon broken up into 
 droplets and passes through the pulmonary capillaries, or it may be ab- 
 sorbed in the lungs. 
 
 Pulmonary infarcts may be due to embolic occlusion of the blood-vessels, 
 
DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 55 
 
 but also to obstruction of a bronchiole. Any kind of hemorrhagic extrava- 
 sation in the lungs may assume a wedge-shape, because the area infiltrated 
 is the wedge-shaped area included in the divisions of a terminal bronchiole. 
 (For details, see the chapter on the Lungs.) 
 
 THROMBOSIS. 
 
 Thrombosis is the coagulation of blood within the blood-ves- 
 sels or heart during life. At the very beginning of the process 
 the formation is not a coagulum in the ordinary sense, but subse- 
 quently coagulation is the essential feature. After death clots form 
 within the heart and vessels, as in blood removed from the body. 
 
 Causes. — The conditions favorable to thrombosis are alter- 
 ations in the blood-current, changes in the vessel-walls, and alter- 
 ations in the blood itself. For the most part two or all of these 
 conditions are present in cases of thrombosis. 
 
 Alterations in the Blood-current. — Anything which slows the 
 current, such as narrowing of the blood-vessels, weakness of the 
 heart, or pressure upon the vessels, favors thrombosis. Complete 
 arrest of the current in a part may lead to ordinary clotting, such 
 as occurs post-mortem ; but with careful precautions a vessel may 
 be ligated at two points without the occurrence of clotting in the 
 occluded portion — at least for a long time. Some change in the 
 blood-vessel wall is generally necessary in addition. Thrombi due 
 to slowing of the current are frequently seen in the heart, the ves- 
 sels of the lower extremities, and in the sinuses of the brain in 
 the course of exhausting fevers or other asthenic conditions. They 
 are called marantic thrombi. 
 
 Changes in the vessel- walls play an important part. Atheroma, 
 inflammatory or degenerative changes in the vessels of areas of 
 inflammation or necrosis, ligation and other traumatic injuries, and 
 diseases of the endocardium are all examples of conditions leading 
 to thrombosis. Dilatation of the arteries (aneurysm) or veins 
 (phlebectasia) or of the cavities of the heart act largely by slowing 
 the current of blood or by producing irregular currents. 
 
 Alterations in the Blood. — Experimentally, thrombosis may be 
 induced by injection into the circulation of extracts of the thymus 
 gland, the suprarenal bodies, the testicles, and other organs. 
 These extracts contain large quantities of the fibrin-ferment re- 
 garded by Schmidt as an essential factor in coagulation. Patho- 
 logically, it is probable that the tendency to thrombosis in typhoid 
 fever, sepsis, and other diseases is due to increase of similar fibrin- 
 forming factors in the blood. The name fermentation-thrombosis 
 is applied in these cases. 
 
 According to Schmidt, coagulation is due to the reaction of fibrinogen 
 (derived from the plasma) with fibrinoplastin under the influence of a fibrin- 
 ferment (the two latter derived from the leukocytes). Fibrinoplastin is 
 probably not essential (Hammarsten), while calcium salts are (Arthus and 
 Pages). 
 
56 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 Pathologic Anatomy. — The appearance and construction 
 of thrombi depend upon the manner of formation. 
 
 When formed in consequence of almost complete stoppage of 
 the circulation they are dark-colored, soft, red clots, similar in every 
 way to post-mortem coagula ; and under the microscope show fib- 
 rillar fibrin enclosing mainly red corpuscles. 
 
 Yellowish or white thrombi are formed slowly from actively 
 circulating blood and are more consistent. Their composition will 
 be understood from the mode of formation. In the normal circu- 
 lation the red corpuscles and blood-plaques move in a column in 
 the center of the stream, separated from the wall of the vessel by 
 a plasmatic zone in which the leukocytes may be seen. When the 
 circulation is slowed the plaques approach the vessel-wall and tend 
 to adhere in small masses to any point of disease in the endothe- 
 lium and also to each other. This has been termed conglutina- 
 tion of the blood-plaques. Gradually the mass grows and subse- 
 quently leukocytes are added. These set on foot true fibrin- 
 formation or coagulation. White thrombi therefore consist of 
 conglutinated plaques, leukocytes, and fibrin. They first appear as 
 hyaline, viscid masses; but subsequently become granular from 
 partial disintegration. If the circulation is alternately slow and 
 more rapid, distinct layers are seen in the thrombus, first dark 
 colored from admixture of red corpuscles, then lighter in hue. 
 Such thrombi are called stratified. If the circulation is irregular 
 from dilatation of the vessels or other causes, the light and dark 
 areas of the thrombus may be more irregularly disposed. 
 
 The thrombus first formed is the primary thrombus. Subse- 
 quently it extends by additions (secondary thrombus) in the direction 
 of the current of blood as far as the next collateral branch of the 
 vein or artery, into which the thrombus frequently extends as a 
 rounded prominence. In the case of the veins a new thrombus 
 may start from such projection (Fig. 5), and eventually the clot 
 
 Fig. 5.— Thrombus in the femoral vein in a rase of phlebitis (from a specimen in the 
 Museum of the Philadelphia Hospital). 
 
 may extend as far as the heart. The thrombus may be lateral — 
 that is, when it lies against the vessel-wall — or obstructive, when 
 the lumen is completely obliterated. In the veins small thrombi 
 are frequently formed in the valvular pouches in marantic subjects. 
 
DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 57 
 
 In the heart thrombi are especially common on diseased valves, in 
 the auricular appendages, and in the intertrabecular spaces. They 
 frequently appear as polypoid masses, and may be attached by 
 slender pedicles. A curious form, called ball thrombi, is seen in 
 the auricles. These are rounded clots wholly or almost wholly 
 separated from the wall, and may occasion serious obstruction at 
 the orifices of the heart. 
 
 Effects. — Frequently the collateral circulation is so quickly 
 established that no untoward results are seen. When a large vein 
 is obstructed venous congestion and dropsy may follow ; obstruc- 
 tion of an artery causes local anemia, and subsequently, if the col- 
 lateral circulation is not established, degenerations or necrosis. 
 Thrombotic obstruction of small arteries may cause hemorrhagic 
 infarction. Embolism and general pyemia result from softening 
 of the thrombus. 
 
 Subsequent Changes. — After their formation all thrombi 
 contract. In this way the red forms may become light colored 
 by extrusion of the red corpuscles. In small vessels red thrombi 
 often become light colored by removal of hemoglobin and a 
 species of hyalin-transformation. These may have the appear- 
 ances of white thrombi and are only distinguished by careful 
 examination. 
 
 After the thrombus has contracted it may undergo various 
 degenerative changes. Frequently the white corpuscles, plaques, 
 
 Fig. 6.— Thrombosis in cardiac 
 chambers, showing cyst-like struct- 
 ure (Orth). 
 
 Fig. 7.— Branch of the brachial artery after 
 amputation, showing vascularization of the 
 thrombus, Th (Weber). 
 
 and fibrin are broken down into an emulsion by liquefaction- 
 necrosis and fatty degeneration, and the red corpuscles converted 
 into granular pigmented masses. These softened portions are 
 swept into the circulation and occasion embolism. Frequently 
 
58 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 this form of simple softening occurs in the center of large thrombi 
 and gives rise to cyst-like formations (Fig. 6). 
 
 A more serious form of softening occurs when the thrombus is 
 infected by micro-organisms. In this case true purulent softening 
 takes place, and the Avail of the blood-vessel shares largely in 
 the suppurative processes. This form occurs especially in the 
 thrombi blocking blood-vessels of suppurating or necrotic tissues. 
 General pyemia and infections embolism result. 
 
 Fig. 8.— Canalization of a thrombus (Karg and Schmorl). 
 
 A more favorable termination of a thrombus is calcification. 
 This is most frequent in the clots in dilated veins, the calcareous 
 thrombi being known as phlcbolitlis. Arterioliths and cardioliths 
 are rarely met with. 
 
 Organization of the thrombus may result from the irritation 
 it occasions. New blood-vessels and proliferating connective-tis- 
 sue cells spring from the vasa vasornm and lining membrane of 
 the blood-vessel as well as from endothelial cells covering the throm- 
 bus, and penetrate the thrombus (Fig. 7). From these organi- 
 zation proceeds as elsewhere, and as it advances the thrombus 
 itself is absorbed. Finally, the clot is fully replaced by connec- 
 tive tissue enclosing a small amount of blood-pigment or calcified 
 remains of the thrombus. The blood-vessel may be converted into 
 a solid fibrous cord, or may be distorted and narrowed by bands of 
 connective tissue in the interior. Sometimes after partial vascu- 
 larization of a thrombus small vessels running parallel with the 
 lumen of the obstructed vessel become dilated and thus partly re- 
 establish the channel. This is termed canalization of the throm- 
 bus (Fig. 8). In other cases canalization may begin as a process 
 of simple softening. 
 
DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 59 
 
 EDEMA. 
 
 Definition. — The term edema is applied to a condition in 
 which the liquid within the tissues is increased in quantity. 
 
 Etiology. — It is primarily necessary to understand the methods 
 by which the liquids normally present in the tissues escape from 
 the blood-vessels, their original source. 
 
 Several processes are concerned in this escape of fluid. In the first 
 place, the pressure of the blood serves to cause a certain amount of direct 
 filtration, just as liquid enclosed in tubes of permeable animal-membrane 
 escapes when the pressure oiitside is less than within. In this process of 
 direct filtration the state of the tissues themselves plays a part. If the 
 normal elasticity of the tissues and degree of pressure of the liquid in the 
 interstitial spaces are lowered, liquid escapes through the capillary-walls 
 to equalize the pressure. A second process at work is that known as 
 diffusion or osmosis. In this there is an exchange between the blood and 
 the tissue-liquids, certain substances being taken into the blood in ex- 
 change for water and other constituents of the blood-plasma. The liquid 
 thus discharged from the blood-vessels enters into the metabolic activity 
 of the tissues to a greater or less degree, is somewhat altered in character, 
 and the surplus is carried off in the lymphatic capillaries as lymph. Cer- 
 tain physiologists (Heidenhain et al.) believe that there is a farther and 
 very important factor of a vital sort. This is described as an active secre- 
 tory function of the endothelial cells of the capillaries and lymphatic 
 spaces ; so that, according to this view, lymph-formation is in a measure 
 at least a direct secretion. This view is not generally accepted. 
 
 Briefly, then, lymph-formation may be described as the escape of water 
 and other substances through a more or less permeable membrane, the 
 capillary-walls, in consequence of direct filtration and osmosis. The 
 quantity present in the tissues depends upon the quantity escaping from 
 the blood-vessels and the amount carried away by the lymphatic circu- 
 lation. 
 
 The causes of increased accumulation of liquid in the tissues 
 may then be readily determined. Among these are («) increase 
 of blood-pressure, or (6) decrease of tissue-elasticity and pressure ; 
 (c) alterations of the blood rendering it more diffusible, or (d) of 
 the liquids in the tissues increasing the osmotic power of these ; 
 (e) increased permeability of the walls of the blood-vessels; (/) 
 obstruction to the flow in the lymphatic vessels. These causes 
 will be considered separately with reference to certain well-known 
 clinical types of edema. 
 
 (a) Increased blood-pressure always occasions increased escape 
 of liquid from the vessels (transudation) and thus increased forma- 
 tion of lymph. In active hyperemia with excess of pressure the 
 amount of liquid rarely becomes so great that the lymphatic ves- 
 sels cannot carry it off, and edema does not therefore occur. In 
 passive congestions, however, as in heart-disease, pressure upon 
 veins, etc., the escape of liquid becomes more rapid and copious, 
 and the lymphatic circulation is insufficient. Edema or dropsy 
 results. In this process of direct nitration the transudate consists 
 
60 TEXT-BOOK OF PATHOLOGY. 
 
 mainly of the Mater and saline constituents of the plasma and to a 
 relatively small degree of the albuminous constituents. 
 
 (6) Decreased tissue-elasticity and pressure is rarely a factor of 
 prime importance, though it may be a contributing cause in many 
 cases. In one class of cases termed oedema ex vacuo it is the 
 principal cause. In these cases liquid escapes from the blood- 
 vessels to fill a space left vacant by disease or atrophy of tissue- 
 elements. This is frequently seen in the subarachnoid spaces of 
 the brain and in other parts of the central nervous system. 
 
 (c) Alterations of the blood, though theoretically very impor- 
 tant as direct causes, probably act indirectly. It has been found 
 by experiment that artificial hydremia, even though combined 
 with considerable increase of the bulk of blood, does not cause 
 edema unless by some means the walls of the blood-vessels have 
 been injured. It is probable, therefore, that the edema of anemic 
 and marantic persons is similarly due to increased permeability of 
 the vessels. This in itself might occasion edema, though the 
 degree is probably greater as a consequence of the anemic state of 
 the blood. The vascular disease itself is probably in some way 
 (perhaps by the action of circulating toxic substances) brought 
 about by the condition of the blood. 
 
 (d) Alterations of the liquids of the tissues may, conceivably, 
 occasion increased diffusion of liquid, but practically little is 
 known of the operation of this element. There are, however, 
 certain eases in which disturbed metabolic activity of the tissues 
 seems to alter the tissue liquids in such manner as to favor the 
 development of dropsy. 
 
 (e) Increased permeability of the capillary -walls is of great 
 importance and probably plays a part in every case of edema. Ex- 
 perimentally it is easy to prove that this factor alone may cause 
 pathologic transudation. Applications of heat to a part or the 
 introduction of poisons capable of causing disease of the walls of 
 the blood-vessels may thus occasion edema. Clinically this factor 
 is of importance in the edema of Bright's disease. Formerly the 
 dropsies of renal disease were attributed to hydremia, but the 
 experiments cited above show this factor to be insufficient. On 
 the other hand, changes of the vascular system are known to occur 
 in Bright's disease, and particularly in cases usually attended with 
 marked edema (glomerulonephritis). Changes in the blood may, 
 of course, contribute, as may also stasis due to cardiac weak- 
 ness. 
 
 Disease of the capillary-walls is also an important cause of 
 edema in and about areas of inflammation (inflammatory edema). 
 In these cases the toxic products of inflammation doubtless attack 
 tin' walls of the vessels and render them more porous. Such 
 edema may occur only in the vicinity of an inflamed area, or may 
 be quite widespread. Thus in some cases edema of the lungs and 
 
DISTURBANCES OF THE CIRCULATION OF THE BLOOD. 61 
 
 other internal organs may be occasioned by bacterial toxins derived 
 from a distant focus of infection. 
 
 Cases of hereditary edema have been described. These may 
 owe their origin to a congenital excess of vascular permeability. 
 
 Finally, there are cases of edema in which the nervous system 
 seems to exercise an influence. Among these are the dropsies 
 attending cases of neuritis, neuralgia, or organic diseases of the 
 cord. In these instances changes in the blood-vessels and per- 
 haps in the tissue-elasticity may be important causes. An inter- 
 esting form of this sort is that known as angioneurotic edema, in 
 which local edema of various forms (often as giant-urticaria) makes 
 its appearance under the influence of nervous irritations. 
 
 (/) Obstruction of the lymphatic circulation does not ordinarily 
 occasion edema, because the collateral circulation is sufficient to 
 carry away the lymph. When, however, larger trunks, especially 
 the thoracic duct, or numerous smaller lymphatics are obstructed 
 edema may result. This is observed in the chylous ascites due to 
 obstructions of the thoracic duct and in the edema of elephan- 
 tiasis. 
 
 Pathologic Anatomy. — Edema may take various forms 
 according to its situation. In some cases it is localized, affecting 
 a limited part of the body, as a single organ or member. In other 
 cases it is widespread in the subcutaneous tissues and skin, when 
 the term anasarca is applied. It may occur in the serous cavities 
 in the form of serous transudates (hydrothorax, pleural effusion, 
 hydropericardium, etc.). 
 
 The liquid itself varies in character according to the cause. In 
 the pure transudates due to increased nitration the liquid is watery, 
 low in specific gravity (below 1016), and comparatively poor in 
 blood-corpuscles and albuminous constituents. In cases in which 
 disease of the vessel-walls has played a large part in the causation, 
 especially in the inflammatory edemas, the liquid is more dense 
 and contains more corpuscles and albuminous bodies. 
 
 The transudate first occupies the lymph-spaces or interstices of 
 the tissues, causing a more or less uniform swelling and bogginess. 
 The tissue pits on pressure, and on section more or less abundant 
 liquid exudes. The solid organs (kidneys, liver) are lighter in 
 color, less dense, and more moist on section than normal ; but the 
 appearances of edema are here less characteristic than in the sub- 
 cutaneous or submucous tissues, or in the softer organs like the 
 lungs and brain. 
 
 Microscopically the tissue-elements are seen to be pushed apart 
 by the transudate, and in some cases the cells themselves may be 
 diseased (see Dropsical Infiltration). 
 
 Results of Bdetna. — The function of edematous parts is 
 necessarily impaired. Sometimes serious consequences ensue, as 
 in the case of edema of the epiglottis, the lungs, or the brain. 
 
62 TEXT-BOOK OF PATHOLOGY. 
 
 Secondary changes may occur in parts the seat of continued edema. 
 Among these are various degenerations of the cells and a productive 
 change in the connective tissues. The latter is well illustrated in 
 the sclerotic change in the subcutaneous tissues of long-standing 
 dropsy, elephantiasis, etc. 
 
 .CHAPTER IV. 
 RETROGRESSIVE PROCESSES. 
 
 ATROPHY. 
 
 Definition. — Atrophy is a condition in which a tissue or organ 
 undergoes a more or less uniform diminution, without definite 
 disease of its constituent parts. A condition allied to atrophy is 
 that termed hypoplasia., in which certain parts tail of their normal 
 development. There may be entire absence of a part, and to this 
 the term aplasia may be given. Hypoplasia is frequently seen in 
 the vascular system, affecting the heart and great vessels conspicu- 
 ously, but probably also all parts of the system. This occurs in 
 some cases of chlorosis and in other conditions characterized by 
 constitutional weakness or want of development, such as in those 
 predisposed to tuberculosis. 
 
 Ktiology. — The causes of atrophy may be varied. It occurs 
 as a result of want of functional demand, as in the atrophies 
 affecting palsied limbs; and sometimes as a result of disturbances 
 of the trophic- nervous system, as in diseases of the anterior horns 
 of the spinal gray matter. In the latter instances lack of use is a 
 contributing cause. In the involution processes of old age there 
 is more or less general atrophy, which might be designated as 
 physiologic. Similar normal or physiologic atrophy occurs in 
 certain organs before the general manifestations of old age. Thus 
 the atrophy of the thymus-gland in early childhood and of the 
 genital organs at the menopause are instances of cessation of func- 
 tion, and consequent or concomitant atrophy of physiologic char- 
 acter. Atrophy may be more definitely pathologic, and the 
 result of distinct causes, such as want of local or general nourish- 
 ment by occlusion of the vessels, pressure, etc. In these cases the 
 process may be purely atrophic, or there may be distinct degenera- 
 tive disease of the cells with diminution of bulk. 
 
 Pathologic Anatomy. — Atrophy may be si tuple or numerical. 
 In the former kind, to which the term true atrophy might also be 
 applied, the individual cells decrease in size without manifest dis- 
 
RETROGRESSIVE PROCESSES. 63 
 
 ease ; in the latter the cells are reduced in number, and are usually 
 first altered by some form of degenerative disease, so that the proc- 
 ess is not, strictly speaking, true atrophy. r , —--, 
 The parenchyma of organs suffers first and g % > *, 
 most characteristically, the connective tissues "~f •. \ | | 
 remaining unaffected or even undergoing hy- i^':'l' 'frn t,3 %■' 
 perplasia. In true atrophy the cells may ! .\"1 '3)'ii\ i. •'..■. |j 
 present no definite alteration, excepting per- .' • ' | : v ; "■' 
 haps slightly increased pigmentation. This #. „ ■• -■ , : f 
 is sometimes due to the fact that the normal '■.'.:.;£■' , ; . \ « .. |^ 
 pigment of the cell does not suffer reduction ff ^ J | 
 
 as do the other constituents of the cell, but "'' '' '' u3=i - '— j 
 in other eases there is actual deposition of FlG - t 9 h7hean n m a uscri! y ot 
 pigment (hematogenous). Cases of the latter 
 
 kind are designated as brown atrophy (Fig. 9). This is seen most 
 strikingly in the heart-muscle in advanced old age or in persons 
 dead of some chronic cachectic disease. In some of the conditions 
 generally described as atrophy the cells show degenerations of 
 various forms, such as cloudy swelling, coagulation-necrosis, fatty 
 degeneration with vacuolization, and other gross alterations of 
 structure. 
 
 Secondary degenerative changes may occur in the connective 
 tissues after the parenchyma-cells have become atrophic. Tims, 
 after the physiologic atrophy of the thymus-gland has occurred 
 the connective tissues of the gland and of the surrounding parts 
 become converted into fatty tissue. In other cases myxomatous 
 change may be observed. 
 
 Organs Avhich have undergone atrophy are often quite irregular 
 on the surface from unequal involvement of the different con- 
 stituents. The consistency may be little changed or- may be 
 greatly reduced, particularly when some form of cellular degenera- 
 tion is present. On the other hand, the organ may be hard and 
 tough from secondary hyperplasia of the connective tissue. The 
 capsule is generally wrinkled from the shrinkage of its contents, 
 and secondary thickening is not unusual, especially in the heart 
 and spleen. The color of the organ, like that of the individual 
 cells, often becomes darker than normal and may be decidedly 
 changed in brown atrophy. 
 
 In cases of pressure-atrophy various distortions of the affected 
 organ may be observed. These are particularly marked in the 
 livers of women who have laced excessively. The right lobe of 
 the organ often presents a deep groove or furrow corresponding 
 with the loAver border of the ribs, and each of the ribs with which 
 the organ comes in contact may cause a depression. 
 
 Pathologic Physiology. — The function of an atrophic 
 organ is necessarily impaired. In the atrophies of old age this 
 may be of little consequence, as the functional demand grows less 
 
64 TEXT-BOOK OF PATHOLOGY. 
 
 and less. In premature atropines general as well as local disturb- 
 ances may occur. These disturbances vary with the varying 
 functions of the organs, and will be separately discussed. 
 
 THE DEGENERATIONS. 
 
 The general term degeneration is applied to changes in the 
 tissues by which their integrity is altered in the direction of 
 lowered vitality. There may be a conversion of the protoplasm 
 of the cell into substances abnormal to it either in kind or quantity. 
 This is termed degeneration in a narrower sense. In a second 
 class there are deposited in the cell, from the blood or other fluids 
 of the body, substances abnormal to the cell in kind or quantity. 
 The name infiltration is applied to these processes. In individual 
 cases it is often difficult to distinguish between the two varieties. 
 
 CLOUDY SWELLING. 
 
 Definition. — Cloudy swelling, also termed albuminous infil- 
 tration and parenchymatous degeneration, may be defined as an 
 edema of the cellular protoplasm, with alterations in the proto- 
 plasmic proteid and the production of opacity. 
 
 Ktiology. — Cloudy swelling is an almost universal accom- 
 paniment of inflammations. Circulatory disturbances (anemia) 
 were formerly supposed to be important, but are now considered 
 to be of little significance. Fever per se can produce cloudy swell- 
 ing, probably not so much the result of the simple degree of heat 
 as of metabolic disturbances induced thereby. The most frequent 
 cause of cloudy swelling is intoxication, either by bacterial toxins, 
 as in the infectious and septic conditions, or by innumerable organic 
 and inorganic substances. Cloudy swelling is also caused by nu- 
 tritional disturbances ; starvation of an organ will produce it as the 
 first stage of atrophy ; and, on the contrary, the cells may in other 
 cases be so overloaded with nutritional substances as to become 
 temporarily transformed into this condition, as in the glandular epi- 
 thelium of the liver during active digestion. It is further known 
 that excessive cellular activity may result in a cloudiness of the 
 protoplasm, as in the kidney and in glands excited by nervous 
 stimulation. These latter processes should be viewed as normal 
 phenomena, analogous to the physiologic fatty degenerations. 
 
 Pathologic Anatomy. — The swollen cells present a fine 
 opacity which under high powers is seen to be due to the presence 
 of diffused refractile granules (Fig. 10). The normal protoplasmic 
 granulations have disappeared ; in muscle-fibers the striatums are ob- 
 scured or obliterated. Vacuolation may be seen in the late stages. 
 The cell-wall becomes indistinct, so that the cells appear to have 
 coalesced. The nuclei may be little altered. Generally the 
 chromatin becomes diffusely stained ; it may elect the acid-stains 
 
RETROGRESSIVE PROCESSES. 
 
 65 
 
 or may refuse all staining. Marked nuclear degenerations are 
 not seen in simple cloudy swelling, or at least very rarely. In late 
 stages the entire cell may have lost its normal reactions to stain- 
 
 -fv- 
 
 ♦■..*"' 4 * % * -• ■ 
 
 
 
 
 Fig. 10.— Cloudy swelling and necrosis of the epithelial cells of the renal tubules, due to 
 sublimate-poisoning (Karg and Schmorl). 
 
 ing-reagents. The distinctive granules are not soluble, in alcohol 
 or ether, but are dissolved by acetic acid and alkalies. 
 
 The large glandular organs, the liver and kidneys, illustrate 
 the condition exquisitely. The entire organ is symmetrically 
 swollen ; the general consistency perhaps a little decreased. On 
 section the surface may be found a little moist and the paren- 
 chyma protrudes. The color is an opaque pallor, quite like the 
 appearance of boiled flesh. 
 
 Seats. — The glandular epithelise (liver and kidney) and the 
 muscle-fibers are the striking seats of this degeneration. 
 
 Pathologic Physiology. — The opacity seems to be due to 
 a coagulation or precipitation of a part or all of the protoplasmic 
 proteid. Some systematic writers have attempted to divide it into 
 two groups : albuminous infiltration, in which the material has 
 been deposited in the cell and then been precipitated ; and albu- 
 minous degeneration, in which the inherent cellular proteid has 
 been precipitated. It is doubtful whether this division is justified. 
 The chemic relations are entirely obscure. It is as yet incompre- 
 hensible how bacterial toxins, themselves apparently proteids, can 
 precipitate other and higher proteids. In the case of inorganic 
 poisoning (metallic salts, acids) the process is more readily under- 
 stood. The swelling is probably a simple edema, due, it may be 
 inferred, to disturbed osmotic relations. 
 
 The function of organs is more or less profoundly disturbed by 
 
06 TEXT-BOOK OF PATHOLOGY. 
 
 this form of degeneration. Complete recovery is easy and fre- 
 quent. If the causes persist, the cells pass into other degenera- 
 tions, usually fatty metamorphosis. 
 
 FATTY INFILTRATION. 
 
 Definition. — Fatty infiltration is the deposition of fats derived 
 from the circulation in cells and tissues which normally contain 
 none, or the deposition of an excess of fats in cells and tissues 
 which normally contain such. 
 
 Etiology. — Fatty infiltration may be physiologic or patho- 
 logic in its origin. In conditions of general obesity the regular 
 consumption of excessive quantities of nourishment may lead 
 to the most marked degrees of fatty infiltration ; an inherited 
 predisposition and lack of exercise acting as contributing causes. 
 In rare instances it seems possible that with the normal physio- 
 logic diet persons of exceptional digestive power and living 
 under conditions which restrict combustion may become affected 
 with pathologic fatty infiltration. The condition may occur 
 during pregnancy, and is frequent at the menopause. In a 
 large class of cases an abnormal diet, or the presence in the 
 diet of substances which tend to the formation of fats, such as 
 alcohol, are responsible for the condition. It is doubtful whether 
 poisons produce general fatty infiltration ; they frequently, how- 
 ever, indirectly produce local or visceral infiltrations. In cachexias 
 certain organs may become loaded with fats, as is sometimes seen 
 in the liver in phthisis. In carcinoma the cells of the neoplasm 
 may become infiltrated with fats. In organic diseases of the ner- 
 vous system accompanied by extensive disintegration of myelin, in 
 bone-diseases, and even following fractures of or operations on 
 bones, the liberated fats are taken up by the circulation and 
 deposited in susceptible localities. There is probably a rare fatty 
 infiltration of senile origin, and also a type which appears at 
 puberty. Of general diseases which may cause an undoubted 
 general fatty infiltration chlorosis and diabetes may be mentioned. 
 Fats may be deposited locally as substitution-tissue, as in the 
 capsule about sclerosed kidneys, in the place of atrophied muscu- 
 lar fibers, in the bones, and about areas of local disease. The 
 protective areas of fibrous tissue which wall off pathologic pro- 
 eesses of various kinds may become extensively infiltrated. 
 
 Pathologic Anatomy. — Normal tissue plus fat describee 
 the appearance-. The fat may be diffuse, in localized areas, or in 
 streaks along the planes of fibrous tissue. The appearances natu- 
 rally vary with the tissue affected. Only rarely does the essential 
 tissue of the part display disease. Microscopically the fat-drops 
 are seen both within and without the cells. Without the cells 
 they are most prominent along the fibrous strands, under the 
 
RETROGRESSIVE PROCESSES. 
 
 67 
 
 endothelial membranes, about the lymph-channels, between the 
 muscular fibrillse, and to a marked extent just beneath the true 
 skin, and indeed about all fasciae. In the kidney the collections 
 are between the tubules ; in the liver, in the fibrous trabecule, 
 
 Fig. 11.— Fatty infiltration of the liver. 
 
 but especially in the hepatic cells ; in the heart, underneath the 
 serosa and between the bundles of fibers. Within the cells, and 
 this is most marked in glandular epithelial cells, the fat is seen 
 as distinct drops within the cell-wall. The fat-drops are always 
 of considerable size, and soon run together, forming one drop, 
 which pushes the protoplasm and nucleus against the cell-wall. 
 The nuclei are usually normally distinct and well stained ; the 
 cell-protoplasm is clear and presents its normal granules ; the cell- 
 wall is intact, though often bulging to accommodate the excess of 
 contents. In rare, prolonged, and extreme instances the bulk of 
 the fat may be such as to interfere with the functions and nutrition 
 of the cells, whose nuclei and protoplasm will then show patho- 
 logic alterations. Crystalline formations, as of margarin and 
 cholesterin, and tiny balls of lecithin may be present, but are 
 more often seen in fatty degenerations. The fat may be stained 
 with osmic acid or suelan III. 
 
 Seats. — The favorite seats of fatty infiltration are the subcu- 
 taneous and subserous tissues, the mesenteries and omentum, 
 along the fascia?, between the muscles, about the kidneys, and in 
 the liver and heart. The lungs and central nervous organs are 
 rarely and only slightly affected. 
 
 Pathologic Physiology. — I have attempted to define this 
 condition rigidly as an infiltration of fat into cells or tissues, dis- 
 tinct from formation of fat in them. Confessedly in individual 
 cases the separation may be impossible ; all doubtful cases are 
 
68 TEXT-BOOK OF PATHOLOGY. 
 
 probably degenerative. Infiltration arises whenever there is an 
 abnormal quantity of fat in the circulation; the causes of this 
 were pointed out in the etiology. Infiltration into imperfect or 
 diseased cells may, however, occur with only normal quantities of 
 circulating fats ; this is probably the explanation of many of the 
 local varieties. All cells and tissues are not of the same degree 
 of susceptibility ; when, therefore, isolated areas occur in unusual 
 localities a pre-existing disease should be suspected. The mech- 
 anism of deposition is not well understood ; it is perhaps effected 
 by circulating cellular carriers. 
 
 Unless very extreme, fatty infiltration does not seriously em- 
 barrass the functions nor threaten the existence of tissues, and 
 complete recovery and restitution are the rule. It may, however, 
 lead to secondary degenerations, which, particularly in the heart, 
 may be of serious consequence to the organ. 
 
 FATTY DEGENERATION. 
 
 Definition. — This is defined as a metamorphosis, the conver- 
 sion of the cellular protoplasm into fat. The classic physiologic 
 illustration is the fat-production in the secretion of milk. The 
 nature of this process has not, however, been certainly determined. 
 The majority of secreting cells do not die or show pathologic alter- 
 ations ; while for such cells as are cast off, as the colostrum-cells, 
 it has not been shown that their fat was not an infiltration. 
 
 Etiology. — Fatty degenerations frequently follow upon cloudy 
 swelling, and the causes detailed for the one apply also to the other. 
 Of all agents, poisons are the most important. These may be me- 
 tallic, as mercury, arsenic, lead, phosphorus — indeed most of the 
 metals. Compounds which directly bind the hemoglobin or reduce 
 it, or break up the red corpuscles, likewise produce it. Such are 
 carbonic oxid, chlorates, pyrogallic acid, some coal-tar compounds, 
 etc. Certain poisons, like chloroform, ether, iodoform, and the 
 acids, seem to act directly on the cell-nutrition. In the case of 
 most of these substances it seems to have been shown in more or 
 less accurate chemical studies that the poison acts by disturbance 
 of the gaseous cellular metabolism. More important as causative 
 agents are the toxins of bacteria ; these cause the majority of fatty 
 metamorphoses. Their mode of action is not clear, and the anal- 
 ogy with the metallic poisons which naturally suggests itself has 
 not been made out. In all anemias and cachexias fatty degenera- 
 tion is common ; it is rare in uncomplicated chlorosis. The de- 
 generation in these eases was formerly regarded as due to suboxi- 
 dation. Since, however, it has been shown that no suboxidation 
 occurs in such chronic anemias, the degeneration may best be 
 classed also as toxic. It seems possible, however, that extreme 
 hemorrhage can produce fatty degeneration in this way. Metab- 
 
RETROGRESSIVE PROCESSES. 69 
 
 olic diseases can also produce it, as is sometimes seen in diabetes. 
 Fever can produce it, but the temperature must be high and 
 prolonged. 
 
 Local fatty degenerations may be produced by local disturb- 
 ances in nutrition, if not too sudden. This is seen in cases of con- 
 gestion, thrombosis, embolism, atheroma, in tumors, and in tuber- 
 cular and syphilitic deposits. The fatty changes of senility are 
 probably of like origin. In the involution of tissues, as in the 
 thymus, corpus luteum, uterus, etc., fatty degenerations are com- 
 mon. Trophic disturbances produce the degeneration, as is seen 
 in the voluntary muscles. In many pathologic processes, as in 
 caseation, liquefaction-necrosis, and the resolution of pneumonia, 
 this metamorphosis plays an important r6le. In rare instances, as 
 mentioned, fatty infiltration may pass into fatty degeneration. 
 The transformation en masse of tissue into fat, as in fat-necrosis, 
 should not be termed fatty degeneration. 
 
 Pathologic Anatomy. — Organs the subject of marked fatty 
 degeneration are often somewhat increased in size : to this, how- 
 ever, there are many exceptions ; a notable one is acute yellow 
 atrophy of the liver. The consistency is usually lessened, though 
 associated fibrosis may render the affected part abnormally dense. 
 The specific gravity of the tissue is notably reduced. In the ner- 
 vous system and in caseation and allied conditions liquefaction 
 
 
 •7 .♦ 
 
 a r 
 
 Fig. 12.— Fatty degeneration of the epithelium of the renal tubules ; stained with osmic 
 acid (Simmonds). 
 
 may occur. The color in typical instances is a pale yellow ; the 
 existence and degree of congestion, pigmentation, or jaundice, will 
 obviously alter the color. The areas of degeneration may be uni- 
 
* 
 
 I 
 
 70 TEXT-BOOK OF PATHOLOGY. 
 
 form or isolated. In the heart and liver particularly streaks or 
 irregular areas may produce a mottled appearance. On section 
 free fat may drip from the knife and cut surface ; in other cases 
 no fat-droplets can he seen macroscopically. In rare instances 
 fat-crystals may he visihle to the naked eye. 
 
 Jlicfoscojjir Appearances. — The parenchyma-cells are first and 
 most extensively affected, though the connective tissue may be- 
 come involved. The cells are usually somewhat enlarged. The 
 I ^ m natural granules of the protoplasm disappear, and 
 in their stead are fine dark granules, which usually 
 stain black with osmic acid (Figs. 12, 13), and 
 ;.">.', which are dissolved by alcohol, ether, etc., but 
 ■ lr. not by acetic acid. A peculiar reaction of the 
 ••> ;v; granules is their staining Avith fuchsin (fuch- 
 4 ".*?? sinophile granules). Usually the granules are 
 very fine and only slightly retractile ; they may, 
 however, be large, and considerable droplets may 
 appear or the entire cell become one large fat- 
 fig. i?,.-Fatty de- drop, as in fatty infiltration. The nuclei in many 
 HarSmiBcle! the cases of moderate degree show no changes ; later 
 in the process, however, the chromatin becomes 
 diffused and refuses to stain and the nucleus may entirely disap- 
 pear. Large hyalin balls may form inside the cells ; these stain 
 with acid-stains. The cell-membrane sooner or later breaks down, 
 and the fatty contents and detritus fill the space. Cholesterin, 
 lecithin, and fatty crystalline formations are often seen. 
 
 Seats. — Fatty degeneration occurs in nearly all tissues. The 
 epithelial structures, especially the liver and kidneys, the heart- 
 muscle, and the central nervous organs are the tissues most fre- 
 quently affected. As before stated, interstitial as well as paren- 
 chymatous tissues may be involved. The cellular constituents of 
 exudates and transudates are also liable to the change, and may 
 present more or less the appearance of an emulsion. 
 
 Pathologic Physiology. — The manner of occurrence of 
 fatty metamorphosis is as yet entirely obscure. If it were proved 
 that fats can be formed out of proteids, this fact would warrant 
 the simple explanation that in fatty degeneration the protoplasmic 
 protcid is directly converted into fat. Certain evidence of this has, 
 however, never been presented, and our reactions for fat are too un- 
 reliable to warrant deductions from simple microscopic studies. It 
 has become apparent that the old and still largely accepted phys- 
 iologic theory has never been demonstrated, even though it be 
 true. No one has as yet produced fat in an animal fed on proteids 
 entirely freed from fats and carbohydrates, and in the experi- 
 ments with meats which contain both it has not been shown that 
 any carbon-retention was unaccompanied by nitrogen-retention 
 and that the carbon was retained in the form of fats or glycogen. 
 
RETROGRESSIVE PROCESSES. 71 
 
 It is, of course, quite possible that the proteids may be directly 
 converted into fat, and in recent experiments upon starving frogs 
 poisoned with phosphorus this was apparently demonstrated ; but 
 even in these experiments it is likely that the glycogen of the 
 liver was the source of the fat produced. 
 
 Unlike fatty infiltration, fatty degeneration tends to cell-death, 
 as must in the nature of things be obvious, for it is an expression 
 of cell-disease. Mild grades with the preservation of the nuclei 
 undoubtedly admit of recovery ; severe grades go on to necro- 
 biosis. The function of the cells is, of course, disturbed. This 
 may be in the direction of simple reduction of function or it 
 may cause distinctly abnormal activity with pathologic metabolic 
 products. 
 
 THE ALBUMINOID DEGENERATIONS. 
 
 The amyloid, hyaline, mucoid, and colloid degenerations rep- 
 resent proteid metamorphoses which are closely related. In 
 typical instances they can be quite clearly differentiated from each 
 other, and for the sake of clearness and convenience they will be 
 separately described. It must be understood, however, that the 
 products are closely related substances whose chemical character- 
 istics and relations are not clear, and which cannot in many cases 
 be distinguished. 
 
 AMYLOID DEGENERATION. 
 
 Definition. — This consists in the appearance in tissues of 
 amyloid material ; whether formed in loco or deposited is not quite 
 clear. Amyloid seems to be a combination of chondratin-sulphuric 
 acid with a proteid. 
 
 Etiology. — The common conditions under which amyloid 
 degeneration arises are suppuration and ulceration. In tubercu- 
 losis, especially of the lungs and skeleton, and particularly in cases 
 of mixed infection, and in syphilitic ulceration are found the con- 
 ditions most favorable to its production. It occurs, however, in 
 ulcerations of various sorts, in cutaneous ulcerations, in gastro- 
 enteritis, in connection with neoplasmic necrosis, in actinomycosis. 
 Rarely it occurs under conditions of cachexia without suppuration, 
 as in cancer, malaria, leukemia. In a few instances it occurs 
 without any apparent cause. 
 
 Local amyloid formations are probably in no wise connected 
 with the general condition and undoubtedly are often entirely 
 physiologic. 
 
 Pathologic Anatomy. — In marked instances the organs are 
 enlarged, and their specific gravity increased. On section the 
 tissue is firm : the cut surface is smooth and neither contracts nor 
 
72 TEXT-BOOK OF PATHOLOGY. 
 
 extrudes. The consistency varies with the coexistence and degree 
 of fibrosis, fatty degeneration, etc. The color of the organ is 
 usually pale, but may obviously be altered by congestion, pigmen- 
 tation, or fatty degeneration. The amyloid substance itself has a 
 glistening, waxy, translucent appearance which is almost pathog- 
 nomonic. This waxy appearance is not always uniform. Amyloid 
 substance is more inelastic than any other degenerative material. 
 Mild or even moderate degeneration may not present macroscopic 
 appearances ; in fact, apparently quite normal tissues may be 
 highly amyloid microscopically. The special appearances in 
 various organs will be described in the appropriate chapters. 
 
 Microscopic Appearance*. — The favorite seats are the intima and 
 media of the blood-vessels, the adventitia being rarely affected, the 
 endothelium apparently never. The fixed connective tissues of the 
 organs are the parts affected, the wandering cells and leukocytes 
 being rarely involved. Muscle-cells are undoubtedly susceptible ; 
 but recent studies seem to show that glandular and lining epithe- 
 
 Fio. 14.— Amyloid degeneration of the kidney, showing amyloid substance in the walls 
 of the blood-vessels of the glomerulus at b, and hyaline tube-casts in the renal tubules 
 at g (Ziegler). 
 
 Hum is never involved. Such cells may, and often do, show fatty 
 or other degenerations or necrosis, but the presence of amyloid 
 substance within their protoplasm has not been shown. The sub- 
 stance appears as irregular elumps or streaks in the interstitial 
 tissues, often compressing the cells and blood-vessels. It presents 
 
RETROGRESSIVE PROCESSES. 73 
 
 a glistening homogeneous appearance. The cells usually present 
 evidences of atrophy and other degenerations. In the renal glome- 
 ruli and in the Malpighian corpuscles of the spleen the appear- 
 ances are perhaps most distinctive. Without staining amyloid 
 degeneration cannot always be distinguished from other degenera- 
 tions ; indeed, not always with staining reactions. The substance 
 is highly resistant to bacterial decomposition and to digestion. 
 
 Reactions (see also below). — The gentian-violet reaction seems 
 to be the most invariable. In sections of tissue fixed for micro- 
 scopic study gentian-violet colors the normal tissues blue ; the 
 amyloid substance is a light pink or red. A mahogany-red reac- 
 tion with Lngol's solution of iodin is quite constant, but fails in 
 the isolated amyloid bodies. It is easily obtained in fresh speci- 
 mens. The red color is changed to a blue by treating with sul- 
 phuric acid or chlorid of zinc. 
 
 Seats. — In the order of frequency amyloid degeneration affects 
 the kidney, liver, and spleen, then the larger blood-vessels, the 
 intestinal mucosa, the lymph-glands, the skeleton, the adrenal 
 bodies, and the heart. It rarely affects the pulmonary mucosa, the 
 bladder and genitalia, the thyroid body, the voluntary muscles, 
 and, apart from the local amyloid bodies, the nervous system or 
 the integument. 
 
 Local Amyloid Formations. — These occur in the nervous system, 
 especially in advanced years and in scleroses, grouped about the 
 blood-vessels, most marked in the posterior cord and in the brain ; 
 in the prostate gland ; about inflammatory areas ; in infarcts ; in 
 granulomata, especially syphilis ; and in neoplasms. They present 
 themselves as small round bodies which usually have a concentric 
 arrangement resembling starch-granules. These do not usually 
 present the typical amyloid reactions ; often they react more like 
 hyaline substance, and indeed the blood-vessels in their situation 
 seem especially affected with hyaline change. The special appear- 
 ances and reactions of the amyloid bodies of the nervous system 
 will be described in connection with neuropathology. 
 
 Pathologic Physiology. — As stated, amyloid substance 
 seems to be a combination of chondratin-sulphuric acid with a 
 proteid. It is composed of hydrogen, nitrogen, carbon, and sul- 
 phur, and is insoluble in weak alkalies. Chondratinic acid is 
 normally present in bones, cartilages, and elastic tissue. It seems 
 to have been shown that an amyloid-like substance exists in the 
 elastic coat of the blood-vessels — perhaps a different combination 
 of chondratinic acid. Our present knowledge suggests that amy- 
 loid substance is not entirely abnormal, but rather an abnormal 
 combination of normal substances. It seems to result from pro- 
 teid alterations in connection with the pathologic processes already 
 detailed. That bacterial influences are not necessary is suggested, 
 though not proved, by the fact that amyloid change has been pro- 
 
74 TEXT- BO OK OF PATHOLOGY. 
 
 duced by long-continued aseptic suppuration induced by turpentine 
 injections. 
 
 Amyloid substance cannot be removed, but does not of itself 
 compromise life. It may become transformed into typical hyaline 
 substance. Amyloid degeneration interferes with functional activ- 
 ity by pressure upon the parenchyma and by vascular disturb- 
 ances. By its situation in the blood-vessels it may occasion 
 thrombosis. 
 
 HYALINE DEGENERATION. 
 
 Definition. — This is a retrogressive process consisting in the 
 appearance of a homogeneous proteid substance of obscure nature. 
 It is closely allied to amyloid, mucoid, and colloid degeneration, 
 and can certainly pass into each of them. The hyaline change of 
 epithelium of older authors is now by general consent classed as 
 a mucoid transformation. 
 
 Etiology. — Hyaline degeneration occurs under the following 
 pathologic circumstances : in the muscles during infections and 
 septic processes and following traumatism ; in intoxications, as by 
 lead ; in interstitial hemorrhages and hematoma ; in struma ; in 
 cicatrices ; in the blood-vessels in old age, arteriosclerosis, or aneu- 
 rysm ; in all forms of arteritis, especially of the nervous system ; 
 in the endocardium and cardiac valves in all diseases affecting 
 them ; in the granulomata ; in neoplasms, especially cylindromata 
 and keloids ; in the lungs in pneumonia ; in the kidneys in nephri- 
 tis ; and in all conditions of coagulation-necrosis and fibrinous 
 exudation, for in these processes hyaline degeneration seems to be 
 a factor. 
 
 Pathologic Anatomy. — Hyaline change is not usually mas- 
 sive enough to be macroscopieally appreciable. When so, the organ 
 or tissue is enlarged, dense, and presents a pale, homogeneous, 
 opaque appearance. Upon the mucous and serous membranes small 
 collections may be readily seen, and may present either a pseudo- 
 membranous appearance or may appear as opaque plates upon or 
 beneath the surface. Microscopically there are three chief sites : 
 («) In the blood-vessels, where the degeneration may appear 
 in the endothelium, beneath it, between the coats and fibers of 
 the vessel, or surrounding the vessel. The wall is thickened, the 
 lumen is narrowed or obliterated ; the endothelium may be in a 
 state of proliferation. Perivascular hyaline change is well seen in 
 certain tumors — cylindromata (Fig. 15). (b) In the interstitial 
 tissues, as between the muscle-fibers, the hepatic cells, the renal 
 tubules, in the reticulum of lymph-glands, in the retina, and in 
 neoplasms and cicatrices. It may be uniform in distribution, but 
 is more often irregularly clumped or maybe in concentric whorls, 
 (c) Within the cells. This condition is probably limited to meso- 
 
RETROGRESSIVE PROCESSES. 
 
 75 
 
 dermic cells. It may be seen in muscle- and giant-cells, and in 
 endothelium, leukocytes, or wandering cells to a less degree. 
 "Whether the epithelial cells take part in this transformation in the 
 
 |iiP 
 
 
 Fig. 15.— Cylindroma, showing a number of blood-vessels whose walls have become 
 converted into hyaline material. 
 
 coagulation-necrosis of mucous membranes and in the production 
 of casts in nephritis has not been decided. It has not been pos- 
 sible in the intercellular or interstitial varieties to decide whether 
 the substance was formed there or deposited there ; in the vascular 
 form, and especially in coagulation-necrosis and fibrinous exuda- 
 tions, it is more probable that it is formed in loco. 
 
 Unstained, the substance has a glistening, waxy appearance ; 
 it is less translucent than amyloid. Typically it evinces an affin- 
 ity for the acid anilin-stains. It may or may not take the fibrin- 
 stains ; it often takes basic stains in a modified manner. In truth, 
 the reactions of hyaline material are very uncertain and shifting, in 
 many instances it can scarcely be distinguished from amyloid, and 
 is then called a hyalo-amyloid change ; in other instances it closely 
 resembles mucin and the colloid substance. The cells of affected 
 parts often show fatty degeneration or other alterations. 
 
 Seats. — The locations most often affected are the muscles, espe- 
 cially the recti, the mucous membranes, the liver, kidneys, and 
 adrenal bodies, the cardiovascular system, the nervous system, the 
 serous membranes, and the retina and choroid coats of the eye. 
 The other locations are suggested in the discussion of the etiology. 
 
 Pathologic Physiology. — Von Recklinghausen believed it to 
 
76 TEXT-BOOK OF PATHOLOGY. 
 
 be a coagulation of normal proteid upon the death of the cells ; 
 this explanation is, however, insufficient. It appears more likely 
 either that it consists of proteid modified in loco by disturbed 
 actiou of cells, or that it is a deposition by cellular carriers of 
 insoluble material formed elsewhere. The exact nature of the 
 transformation is entirely obscure ; it cannot be held analogous 
 to the coagulation of proteids by heat; nor to the precipitation by 
 metals or salts, since in these events the proteids are not usually 
 rendered permanently insoluble in water and are in other ways 
 clearly different. Hyaline material can undoubtedly be recon- 
 verted, absorbed, and removed. Its presence rarely compromises 
 the parenchymatous structures to an extreme degree. It may be 
 converted into the other albuminoid degenerations, and may un- 
 dergo caseation and also calcareous infiltration. 
 
 MUCOID DEGENERATION. 
 
 Definition. — Theoretically this is the conversion of cellular 
 protoplasm into mucin. Mucin is a glycoproteid, which contains 
 no phosphorus, and which by virtue of its carbohydrate moiety 
 reduces cupric sulphate in alkaline solution. It is quite insoluble 
 in water, but has itself a marked capacity for taking up water. It 
 is very soluble in alkaline solutions, but is precipitated by satura- 
 tion with most neutral salts. It is precipitated by acetic acid in 
 solutions poor in salts ; also by heat, alcohol, and many of the 
 metals. It does not dialyze. The secretions from different classes 
 of epithelium differ notably among themselves, and the pathologic 
 mucins differ still more. 
 
 Etiology. — Mucoid transformation should be distinguished 
 from hypersecretion of mucin. Hypersecretion is a common re- 
 sult of inflammation or irritation of all sorts ; it is seen in the 
 pulmonary, gastro-intestinal and urinary mucous membranes, in 
 the glands of Cowper, the gall-bladder, the salivary glands, in the 
 antrum of Highmore, in the lachrymal glands, and in the testicles. 
 The product of the epithelium of the urinary tract and gall-blad- 
 der, usually called mucin, is more often nucleo-albumin. Mucoid 
 degeneration in the strict sense occurs most frequently in meso- 
 blastic tissues, the abnormal substance lying between the cells. 
 It is in some way connected with inflammatory processes, as, apart 
 from its occurrence in tumors, it is found only in tissues the seat of 
 inflammation. Any of the connective tissues of the body may be 
 affected. Widespread myxomatous degeneration of the subcuta- 
 neous tissues may be seen in myxedema. In some cases of myx- 
 edema, scleroderma, and the other pachydermia affections, mucin 
 has been extracted from the skin ; other attempts in similar cases 
 have failed. Neoplasms comprise the third group of mucoid phe- 
 nomena. The transformation occurs in sarcomata, carcinomata, fibro- 
 
RETROGRESSIVE PROCESSES. 77 
 
 mata, lipomata, chondromata, and especially in the myxomata, where 
 mucin is the essential element, while in the other growths it is an 
 accidental and occasional transformation. In the epithelial tumors 
 the epithelial cells themselves may be affected. 
 
 Pathologic Anatomy. — The gross appearances may consist 
 in nothing but the appearance of the mucin. Upon catarrhal 
 mucous membranes is a coat of thick, tenacious mucus, with or 
 without congestion or other changes. In localities where the 
 mucin becomes pent up it swells markedly, dilates the chambers, 
 flattens the epithelium (which may then atrophy), and later 
 becomes converted into a simple albuminous fluid. Such a pro- 
 cess is seen in the antrum of Highmore, in Cowper's glands, in 
 the salivary glands, etc. ; in these cases the appearances are those 
 of a cyst. In mucoid degenerations in the connective tissues the 
 appearances are often not characteristic of mucin ; the tissues are 
 soft and elastic and tear easily. In tumors cysts are usually 
 formed along with general mucoid infiltration. In cystic ovarian 
 neoplasms the production is often massive, and the substance is 
 often peculiar in refusing precipitation by acetic acid, and has 
 therefore been termed pseudomucin. In myxomata the substance 
 is usually much more dense. 
 
 Mieroscopie Appearances. — In catarrhal mucous membranes 
 the goblet-cells are seen in excessive quantity. Only in extreme 
 instances is the process accompanied 
 by the death of the cell. The cells 
 are much swollen, and the distal 
 end is especially bulged out with 
 its drop of mucin. There is usually 
 a submucous inflammatory reaction, 
 and pus-cells containing mucoid ma- C| * - v.\ 
 terial may be seen (Fig. 16). In , *-f ^s. .<*** * 1%v .»^\ -J 
 the connective tissues it is seen that 
 the mucin lies between the cells and 
 that the ground-substance has disap- 
 peared — i. e., been converted into 
 mucus. The cells very rarely pre- 
 sent mucous change, but are often "~~~ 
 
 i , -. . ,i t FlG - 16.— Myxomatous degeneration 
 
 degenerated m other ways. In tu- of a sarcoma, showing stellate ceils 
 mors the change occurs everywhere, ^SS^S^uSSS^^ ma ' 
 in and between the cells and in the 
 
 form of cysts, whose walls may or may not present a cellular 
 lining. The blood-vessels are rarely affected. In all situations 
 mast-cells may be seen, often abundantly. 
 
 Mucin is best fixed with corrosive sublimate. As a rule, it 
 elects basic stains. It stains only moderately with hematoxylin, 
 but very well with methyl ene-blue and indeed with most of the 
 basic anilin-stains. Thionin and tuloidin-blue are the best stains, 
 
 .'< ^ 
 
 . .'St- 
 
78 TEXT-BOOK OF PATHOLOGY. 
 
 giving it a purple-red color. These staining reactions arc not en- 
 tirely distinctive, and it is often impossible to differentiate mucoid 
 from colloid material, and even from hyaline and amyloid material. 
 
 Seats. — Of normal epithelial tissues the mucosa of the respi- 
 ratory and gastro-intestinal tracts, the salivary glands, and the 
 uterus are most often affected ; any epithelium may, however, be 
 involved. The connective tissues have been sufficiently consid- 
 ered. Of neoplasms, ovarian cysts, abdominal carcinomata, and 
 mesoblastic tumors anywhere are most liable. 
 
 Pathologic Physiology. — Since the deposition of mucin 
 seems to he excluded, the only explanation is to assume the con- 
 version of other proteids into mucin. The causes and modus 
 operandi are not clear ; the fact, however, that in the cysts the 
 mucin may be reduced to simple albumin, shows the possibility 
 of such transformations. 
 
 Unless the disease is very prolonged, the affected mucous mem- 
 branes may recover. The connective-tissue forms do not of them- 
 selves threaten the life of the tissue ; and the deposit is often 
 removed by reabsorption. In neoplasms the degeneration seems 
 an evidence of cell-death. 
 
 COLLOID DEGENERATION. 
 
 Definition. — This consists in the abnormal appearance of a 
 substance whose prototype is the colloid material of the thyroid 
 gland. It is not precipitated by acetic acid nor alcohol, does not 
 take up water avidly, and is therefore quite like the pseudomucin 
 already noted. 
 
 Htiology. — It occurs in goiters and in thyroid neoplasms, in 
 the hypophysis cerebri, in the kidneys (some cases of congenital 
 cysts), and the adrenal bodies, in the prostate and seminal vesicles, 
 in the atrophic gastric mucosa, in cysts of the lips and larynx, and 
 in the cervix uteri. Colloid transformation in neoplasms apart 
 from the thyroid body is very rare. Colloid may arise from or 
 become converted into mucoid material, and stands very close to 
 the hyaline substance. 
 
 Pathologic Anatomy. — Affected organs maybe enlarged, and 
 may be hard or quite soft. On section the colloid areas appear as 
 yellowish-brown translucent bodies ; rarely they are arranged in 
 large clumps. They may be macroscopically invisible, or, on the 
 contrary, may form large cystic collections with thin, flattened 
 walls. Colloid degeneration may be accompanied by serous trans- 
 udation, due probably to vascular disturbances. The serous trans- 
 udation seems to dissolve the colloid material, so that finally the 
 cysts are converted into compartments filled with a chocolate- 
 colored fluid containing pus, blood, and crystals of cholesterin, 
 sodium chlorid, and calcium oxalate (Fig. 17). 
 
RETROGRESSIVE PROCESSES. 
 
 79 
 
 Microscopically the material is found in the glandular acini, in 
 the cells, and in the connective tissues. There are often signs of 
 pressure, and, probably from the same cause, the areas are anemic 
 and have a poor vascular distribution. The arrangement is 
 
 Fig. 17.— Colloid degeneration of the thyroid gland, showing masses of colloid matter in 
 the gland acini (Karg and Schmorl). 
 
 usually in balls or scrolls, homogeneous as a rule, but often with 
 concentric or radiating lines. The areas often intercommunicate, 
 and extensions may be traced into the adjacent tissues. The cells 
 usually show degenerative changes, and inflammatory reactions 
 are often present. Crystals of calcium oxalate are common. Acid 
 stains are usually elected, as in hyaline degeneration. The indefi- 
 niteness of the reactions may make it impossible to exclude hya- 
 line and mucoid changes. 
 
 Pathologic Physiology. — This is obscure, but seems to be 
 analogous to that of mucoid change. The substance is undoubt- 
 edly produced in loco. 
 
 Colloid is a grave degeneration, usually connected with marked 
 cellular disturbances. The substance may become hyaline or mu- 
 coid, or may be reduced to a simple or purulent transudation. 
 
 GLYCOGENIC INFILTRATION. 
 
 Definition. — This condition consists in the presence of gly- 
 cogen in cells which normally contain none, or the presence of an 
 excess in cells which normally contain it, as in the liver, cartilage, 
 muscles, leukocytes, in the embryo in all tissues, and in the uterus. 
 The attempt has been made to separate glycogenic infiltration 
 from a glycogenic degeneration, but the conversion of protoplasmic 
 proteid into glycogen has never been demonstrated. 
 
80 TEXT-BOOK OF PATHOLOGY. 
 
 Etiology. — The condition is not infrequent. It is seen in the 
 tissues in diabetes, especially in the kidneys, muscles, liver, and 
 circulating leukocytes. Jt occurs in neoplasms, especially in 
 malignant growths of mesoblastic origin, being rare in most carci- 
 nomata. In leukocytosis of different varieties the cells may con- 
 tain an excess, and granules of the glycogen may float free in the 
 plasma. In purulent collections and in inflammatory areas the 
 cells may be markedly infiltrated. The infectious granulomata, 
 however, seem exempt. The amylaceous bodies of the prostate 
 are closely allied to glycogen. 
 
 Pathologic Anatomy. — Tissues rich in glycogen may pre- 
 sent a hyaline appearance ; usually there are no macroscopic alter- 
 ations. Microscopically the material is generally found within 
 the cells ; it may, however, be in the intercellular substance, and 
 may be free in the plasma of blood or the fluid of exudates. It 
 is commonly deposited as round balls, which may be concentri- 
 cally striated. In fresh tissues it is soluble in water, but loses its 
 solubility after fixation by alcohol, etc. 
 
 Glycogen is stained brown by iodin, but the brown is not 
 turned blue on the application of sulphuric acid. Ptyalin or amyl- 
 opsin converts it into sugar, with the loss of the color-reaction. 
 
 The pathologic physiology is obscure. In diabetes it is 
 simply an expression of the general hyperglycemia. In neoplasms 
 and suppurations the collections are probably depositions. 
 
 DROPSICAL INFILTRATION. 
 
 By dropsical infiltration is meant edema of the cells, the pres- 
 ence in cells of an excess of plasma. This does not always occur 
 
 Fig. 18.— Dropsical Infiltration of the epithelial cells of a carcinoma of the breast: a. 
 ordinary epithelial cells; b, dropsical ceils; r, dropsical nuclei; </, enlarged nucleoli 
 (Ziegler). 
 
 in general dropsy, the fluid being between the cells and often 
 compressing them to a marked degree. In other instances the 
 
RETROGRESSIVE PROCESSES. 81 
 
 cells take up the fluid. In burns and pemphigus and in other 
 skin-lesions connected with vesiculation, and in various inflamma- 
 tions of organs, edema of the cells occurs. It is also a part of the 
 degeneration termed cloudy swelling. 
 
 The cells are enlarged, often to an extreme degree, and they 
 may even burst. The protoplasm sooner or later becomes cloudy 
 and often presents degenerative changes — fatty metamorphosis in 
 particular. Vacuolation is frequently observed (Fig. 18). 
 
 The condition is probably a purely physical phenomenon in the 
 dropsies. In the cutaneous lesions other factors are operative. 
 
 CALCIFICATION. 
 
 Definition. — Calcification consists in the abnormal deposition 
 in tissues of earthy salts. The phosphates and carbonates of cal- 
 cium are the chief salts concerned ; the oxalates, however, are 
 usually present, and the corresponding magnesium salts may be 
 mixed with them. The best physiologic examples are the senile 
 change in the vascular apparatus and the formation of the brain- 
 sand (acervulus cerebri). Impregnation of the skeletal tissues is 
 usually accomplished as a physiologic condition through the activ- 
 ities of special cells ; this is an essential element in ossification. 
 
 Ktiology. — The deposition generally occurs in diseased tis- 
 sues, especially in those the seat of vascular disorders. Local 
 necrosis or fibrosis antedates intercellular calcification, and the 
 process may be accompanied by atrophy and absorption of certain 
 cellular elements. In neoplasms the abnormal cellular conditions 
 obviously predispose ; but here, too, the vascular relations are of 
 notable importance. Hyaline and fatty degenerations often pre- 
 cede or accompany it. In rare instances no local predispositions 
 can be determined. Cases of this kind occur in old age, and for 
 these it is inferred that owing to increased lime-resorption from 
 the skeleton the system is saturated to the point of precipitation. 
 Similar supersaturation of the blood with calcareous matter may 
 occur in cases of extensive disease of bones, and may lead to wide- 
 spread deposition. 
 
 Pathologic Anatomy. — Early in the process no macroscopic 
 signs are apparent. On microscopic examination the salts are seen 
 as fine granules scattered through the intercellular substance. Cel- 
 lular infiltration, however, is not uncommon, and in such instances 
 the cells show more or less extensive nuclear and protoplasmic 
 degenerations. By the coalescence of the granules larger, irregular 
 spherical bodies may be formed. These usually have a concen- 
 tric arrangement (psammoma bodies). Definite crystals are rare, 
 but may be seen. The next adjacent tissue may present an opaque 
 appearance. In certain localities, especially the blood-vessels and 
 serous membranes, calcareous plates are formed. The depositions 
 
82 TEXT-BOOK OF PATHOLOGY. 
 
 may attain a surprising size, especially in the vessels and in 
 neoplasms. The macroscopic color is usually white, grayish, or 
 yellow; accidental pigments may, however, produce discolorations. 
 
 On staining the deposition takes up both carmine and hematoxy- 
 lin, but exhibits no elective attraction for the anilin dyes. The 
 salts arc dissolved by acids, best by hydrochloric acid; in the case 
 of carbonates, with evolution of carbonic acid gas. Many organic 
 and inorganic acids arc employed in the decalcification of tissues 
 for purposes of microscopic study. Fibrosis, cellular necroses, 
 and degenerations can be demonstrated in the tissues by suitable 
 methods. 
 
 Seats. — It is in the cardiovascular system that the condition is 
 of the most importance. It occurs often as a simple senile change, 
 usually connected with an atrophy of the elastic tissues of the 
 vessel-walls, hyaline degeneration of the connective tissue, and 
 general fibrosis. It is almost invariably an accompaniment of 
 sclerotic endocarditis and arteriosclerosis. In the endocardium the 
 valves are most frequently affected ; of the vessels, the aorta, the 
 coronary arteries, and the cerebral vessels. The process is, how- 
 ever, often universal, and the splanchnic vessels and radial arteries 
 seem very susceptible. It affects chiefly the intima and media. In 
 the pericardium the deposition is uncommon without the previous 
 occurrence of pericarditis ; in adherent pericardium the heart may 
 be literally enclosed in a calcified sac. In the myocardium calci- 
 fication is usually interfibrillar, but may involve the fibers. Large 
 collections may occur in the pituitary body, the meninges, and in 
 the ventricular plexuses. It is common in the joints, uncommon 
 in the pleura, rare in the peritoneum. In the muscles local for- 
 mations are not rare, and usually occur at the seat of previous in- 
 jury or irritation. In the lungs and liver it is not unusual in and 
 around foci of necrosis due to various causes (tuberculosis, parasites, 
 etc). Cicatricial tissue often becomes calcified. In the Avails of 
 cysts, in the biliary and urinary bladders, in the limiting Mall of 
 old abscesses and heinatomata, in thromboses, and even in cutaneous 
 scars calcification is a common incident. In the kidneys infarcts 
 of these salts may be formed. The neoplasms most subject are 
 the avascular tumors ; uterine fibromata, fibromata in general, der- 
 moid cysts, goiters, scirrhous carcinomata, and tumors of the pit- 
 uitary bodies. The special term psammoma (7. v.) is applied to 
 certain calcified neoplasms. It may, however, occur in the most 
 vascular sarcomata. Lithopedia arc the calcified fetuses of extra- 
 uterine pregnancy. Apart from neoplasms, the most striking in- 
 tracellular depositions are seen in the ganglion-cells in areas of 
 softening and in the renal cells following certain metallic poison- 
 ings (mercury ). It is interesting to note that the intestinal epi- 
 thelium, which normally secretes the larger part of the lime-salts 
 discharged from the bod)-, is rarely infiltrated by them. 
 
RETROGRESSIVE PROCESSES. 83 
 
 Pathologic Physiology. — Various views are held to ex- 
 plain the depositions. An excess of the salts in the blood or tissue- 
 liquids must be rare. On the one hand, it has been assumed that 
 the soluble are converted into insoluble salts, and, on the other 
 hand, that the tissues have become less solvent for the salts. 
 Probably the best established view is that the salts are precipi- 
 tated as insoluble combinations with proteids. 
 
 Calcareous deposits are probably never removed, but once 
 formed remain permanently. There is no doubt that they in- 
 fluence the adjacent tissues to degenerations. 
 
 OSSIFICATION. 
 
 Ossification implies the deposition of lime-salts and other changes 
 through the agency of osteoblastic cells. It occurs in cartilages, and in 
 tumors connected with the bones, cartilages, and periosteum. The salts are 
 more regularly deposited and are usually in masses between the cells. An 
 accurate differentiation from calcification can in some instances be made 
 only by the detection of osteoblasts after decalcification of the material. 
 
 URATIC INFILTRATION. 
 
 Deposits of urate of sodium in the cartilages and fibrous tissues of joints 
 and in various other situations occur in the course of gout (see Disturbances 
 of Metabolism and Diseases of Joints). 
 
 PIGMENTATION. 
 
 According to the origin and variety of the pigments, pigmenta- 
 tions may be divided into four groups : 1, those in which the pig- 
 ments are derived from external sources ; 2, those derived from 
 the hemoglobin ; 3, those derived from the bile ; 4, those derived 
 from cellular activity within the organism. 
 
 Pigmentation from the Exterior. 
 
 Of the first group, those caused by entrance of foreign bodies 
 through the air-passages are the most important. The condition 
 now generally termed pneumonokoniosis is commonly a disease 
 of occupation. Coal, iron, and stone are the most frequent foreign 
 substances inhaled. Vegetable particles, as grain-dust and textile 
 fibers, and animal hairs and furs are not uncommonly the cause of 
 such pigmentations. Corresponding to the agent, there are such 
 terms as anthracosis (coal-dust pigmentation), siderosis (iron), cal- 
 cicosis (stone), etc. (Fig. 19). Inhaled substances probably do not 
 reach the alveoli, but are caught by the bronchial cellular cilia. 
 In part they are coughed up or otherwise cast off with the bron- 
 chial secretions ; in part they penetrate the bronchial walls or are 
 
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 Fig. 19.— Tuberculosis of the lung, showing anthracotic pigmentations in the lower part. 
 
 carried by phagocytic cells into the submucosa (Fig. 20). They 
 may become deposited in the latter situation, or may be carried in 
 
 Fio. 20.— Phagocytic cells of the bronchial secretion (sputum) containing black particles 
 of dust ana carbon ; the cells on the right are stained with methylene-blue (Jakob). 
 
 the lymphatic circulation to the peribronchial and mediastinal 
 gland's, the fibrous tissue of the lung, or the subpleural tissues. In 
 rare instances the pigment finally reaches the general circulation, 
 
RETROGRESSIVE PROCESSES. 85 
 
 following which it is deposited largely in the spleen, liver, intes- 
 tinal mucosa, and kidneys. In these cases the mucous membranes 
 from the lips downward may be more or less pigmented. 
 
 Pigmentation through the alimentary tract is best illustrated by 
 argyria following the excessive ingestion of soluble salts of 
 silver. The depositions seem to consist of a reduced form of a 
 silver albuminate. In the skin the pigment lies directly under the 
 epithelial layer, between the cells, and in the intercellular tissue 
 and lymph-spaces. The gastric and intestinal walls are deeply 
 affected. The liver and kidneys are usually involved ; in the 
 former the deposition is periportal, in the latter the glomeruli and 
 the corticomedullary boundary contain the pigment ; in both the 
 cells are free. Among the rarer sites are the choroid plexus, the 
 various glands of the body, and the Avails of the blood-vessels. 
 
 Pigmentation by cutaneous absorption apart from tattooing is 
 problematical ; it has been alleged to occur in workers in copper. 
 
 Hematogenous Pigmentation. 
 
 This concerns the deposition of pigments derived from the 
 hemoglobin, of which there are two groups, the siderous and the 
 non-siderous. The chief siderous pigment is hemosiderin, which 
 has, however, many modifications ; the non-siderous pigments are 
 derivatives of hematin — hematoidin, hemofuscin, melanin, etc. 
 In the course of time the siderous pigments may lose their iron. 
 Probably all formation and further elaboration of these pigments 
 are the result of specific cellular activities. Two groups of hema- 
 togenous pigmentations may be distinguished, (1) those in which 
 the hemolytic agents act in the circulating blood or the associated 
 organs, and (2) those in which the reductions occur in local tissues. 
 
 (1) To the first group belong the general hemolyses. In per- 
 nicious anemia and leukemia, in malaria, in severe cachexias, in 
 occasional infectious and septic processes, in poisonings (as by pyro- 
 gallic acid, chlorates, arseniuretted hydrogen, by some mollusks, 
 by pyridin and tuluylendiamin, etc.), the hemoglobin is set free in 
 the circulation. It is promptly excreted by the kidneys, and to a 
 limited extent by the intestines ; much is converted into bile in 
 the liver, some little passing into the bile unchanged. A certain 
 amount is reduced by the tissues (apparently by the liver) to the 
 two before-mentioned series of pigments, which are then carried in 
 the lymphatic and vascular circulation and by means of cellular 
 carriers and deposited in various places. As time passes, these 
 pigments seem to become reduced, the iron being excreted by the 
 intestine and the remainder by the kidneys as urobilin. In the 
 liver the depositions are largely in the periphery of the lobule ; in 
 the spleen, in the regions of the follicles ; in the kidney the most 
 marked collections are in and about the glomeruli and the tubules. 
 
86 TEXT-BOOK OF PATHOLOGY. 
 
 In all tissues the (((positions arc both intercellular and intracellu- 
 lar ; the cells may either take up pigment or have it deposited in 
 them. 
 
 A peculiar form of hematogenous pigmentation is that seen in 
 the gastro-intestinal tract and other abdominal organs of drunk- 
 ards. In other instances the presence of siderous pigments in the 
 intestine is to he viewed as a process of excretion, since the greater 
 mass of iron is eliminated through the bowels. 
 
 The appearance of organs with marked pigmentation varies 
 with the variety and stage. A rusty-red color is the usual early 
 appearance ; later a brown, then a greenish color may be produced, 
 and finally a dark blackish-brown. The association of jaundice, 
 which is common, alters appearances very much. 
 
 (2) The two chief causes of heal pigmentation are thrombosis and 
 interstitial hemorrhage and coagulation. The pigmentations seen 
 in the indurations resulting from prolonged venous stagnations and 
 congestions are probably of analogous origin. Under these cir- 
 cumstances the hemoglobin is diffused from the blood-cells, and a 
 portion passes directly into the plasmatic circulation and is carried 
 away to be eliminated ; soon, however, the area becomes walled 
 off and the two sets of pigments are then formed within. The 
 siderous pigments are most frequently seen in small lesions and at 
 the periphery of large ecch ymoses ; the hematoidin series is most 
 prevalent within the cystic contents. The pigments change in 
 color (the color-changes in a bruise are due to this), and finally 
 become a brownish amorphous powder, which in turn disappears. 
 Phagocytic cells take up all forms of the pigments (Fig. 21), and 
 
 Fk;. 21.— Phagocytic cells of the sputum containing blood-pigment, from a case of cardiac 
 congestion of the lungs (Jakob). 
 
 carry them to various parts of the body, especially to the liver, 
 hematopoietic organs, intestines, and glands; the depositions in 
 them are known as pigment-metastases. 
 
RETROGRESSIVE PROCESSES. 87 
 
 The distinctive reactions of the various pigments are not well 
 known. Of hematin and hemin it is known that they are insolu- 
 ble in water, alcohol, and ether ; slightly soluble in weak acetic 
 and mineral acids ; easily soluble in chloroform and in weak alka- 
 lies, from which solution they are precipitated on the addition of 
 lime- or baryta-water. Hematoidin differs from these in being 
 somewhat soluble in ether, but insoluble in weak acetic acid, and 
 gives with strong nitric acid the spectral play of colors. Apart 
 from the iron reactions little is known of hemosiderin. The iron 
 is best demonstrated by its conversion into the sulphid by means 
 of ammonium sulphid, or by the Prussian-blue reaction with weak 
 hydrochloric acid and potassium ferrocyanid. 
 
 Microscopically hematogenous pigment presents three chief 
 appearances : small needles, rhombic crystals, and amorphous 
 masses or fine balls clumped together (Fig. 22). The first two 
 
 Fig. 22.— Hematoidin-crystals from an old hemorrhagic focus (Jakob). 
 
 forms are very rarely seen within cells, the last form commonly. 
 The colors vary from a pink-red to a deep rubin, from pale yellow- 
 green to a deep brown or absolute black. 
 
 Hepatogenous Pigmentation. 
 
 Pigmentations derived from the bile are due to bilirubin (iso- 
 meric with hematoidin) and its oxidation-product, biliverdin. As 
 will be elsewhere explained in detail, all jaundice is now held to 
 be of hepatic origin ; so far as known, only the hepatic and renal 
 cells can produce bilirubin from hematin. 
 
 The deposition of these pigments may be either in solution in 
 the tissues, in granular precipitations, or in crystals (needles and 
 rhombic plates). The cerebral substance alone seems never, ex- 
 cept in the new-born, to be pigmented. The liver, skin, mucous 
 membranes, the endarterium and other serous membranes, and the 
 
88 TEXT-BOOK OF PATHOLOGY. 
 
 glandular and tatty tissues arc especially susceptible. The color 
 is first yellow and gradually deepens to a deep olive, the urine 
 presenting similar transitions. The lachrymal and salivary glands, 
 the manuine, and the intestinal mucosa seem to be able to keep the 
 pigment from passing out with their secretions. The ocular fluids 
 are colored. 
 
 The pigment in solution saturates the tissues. The granular 
 pigments, yellow, brown, or greenish in color, may be seen in the 
 cells or in the interstitial tissues; the crystals, yellow or red in 
 color, are usually extracellular. The pigment displays the spec- 
 tral play of colors on contact with strong nitric acid, and is turned 
 green by weak tincture of iodin. 
 
 A special form of deposition is the bilirubin-infarcts in the uri- 
 nary tubules. These arc seen in severe jaundice of the new-born, 
 but may occur in deep icterus of adults, as in acute yellow atrophy. 
 
 Metabolic Pigmentation. 
 
 The pigmentation derived from cellukr activity may be prop- 
 erly termed metabolic. We know isolated facts about the differ- 
 ent forms, but there is little systematic fundamental knowledge. 
 Two tacts, however, seem clear : that these pigments are formed 
 by migratory and resident pigment-building cells, which with 
 leukocytes and plasma-cells accomplish their transportation and 
 deposition ; and that hemoglobin is in some way or other the raw 
 material for their manufacture, with, perhaps, the exception of 
 some pigments in melanosarcoma, which seem derived from 
 proteids. 
 
 The manifestations may be local or general. Among the former 
 are the pigmentations of nevi and moles, of pregnancy, of the 
 corpus lutcuni, freckles, some scars, certain skin-diseases, as chlo- 
 asma and xanthelasma, of the lesions secondary to some cutaneous 
 parasites, etc. A special local type is that seen in tumors, notably 
 in melanosarcomata. Lipomata and sarcomata (chloromata) may 
 be analogously affected. 
 
 Among the general pigmentations are those of Addison's disease, 
 of certain severe anemias and cachexias; of some cases of diabetes 
 {diabUe bronzg) ; tuberculosis of the peritoneum, intestines, and re- 
 troperitoneal glands; of abdominal neoplasms, and of senility. The 
 cases associated with abdominal lesions are held to be connected 
 with disturbances of the adrenal bodies or of the splanchnic sym- 
 pathetic system, which has been considered to have control of 
 pigment-formations. 
 
 The metabolic pigments are very varied, and a detailed discus- 
 sion of them here would be unprofitable. They may have a high 
 percentage of sulphur, and may or may not contain iron. They 
 are commonly deposited in and between the cells as granules, but 
 
RETROGRESSIVE PROCESSES. 89 
 
 may be crystalline. They do not give a play of colors with nitric 
 acid, and have varying solubility. 
 
 NECROSIS. 
 
 Definition. — Necrosis may be defined as the death of tissues. 
 The death of individual cells is termed neerobiosk ; death of tissue 
 en masse, usually accompanied by putrefactive changes, constitutes 
 gangrene. 
 
 j^tiology. — All classes of cellular death may be brought un- 
 der four etiologic groups : 1, those due to nutritional and circula- 
 tory disturbances ; 2, those due to trophic disturbances ; 3, those 
 due to poisons — animal, vegetable, bacterial, and inorganic ; and, 
 4, those due to traumatism, employing the term in its broadest 
 sense. It has been attempted, without success in our opinion, to 
 class the trophic necroses as identical with those due to circulatory 
 and nutritional disturbances ; similarly the poisons and traumatism 
 have been considered as acting only through the circulatory and 
 nutritional paths, but it seems evident that in the light of our 
 present knowledge the four groups are to a greater or less degree 
 distinct. 
 
 The various causes do not produce constant types of necrosis, 
 but occasion one form in some cases, another in other cases. Prom- 
 inent among these varying circumstances are the native health of 
 the tissues and their vital resistance, the circulatory relations of the 
 part involved, the activity and duration of the causal agents, the 
 age of the subject, the presence of other diseases, the temperature 
 of the tissues, etc. It will therefore be better first to consider col- 
 lectively the causes of necrosis, and subsequently detail the varieties 
 of it. There can be no doubt, however, that in the direct forms 
 of necrosis the results are to a marked extent individual to the 
 agent ; for example, cells killed by the action of acids, alkalies, 
 and metallic salts present appearances quite characteristic of 
 each. 
 
 Circulatory Derangements. — The circulatory disturbances in- 
 clude many conditions. Acute and chronic ischemia, however 
 produced — by embolism, thrombosis, arteriosclerosis and atheroma, 
 by extra-arterial pressure, cardiac weakness, or by arterial spasm, 
 as in Raynaud's disease, and perhaps in ergotism — are important 
 conditions. Venous stagnations are responsible for many instances. 
 Actual stasis is a rare cause, being mechanical obstructions and such 
 poisonings as produce coagulations. Heat and cold act partly by 
 circulatory disturbances. Among the general disorders of circu- 
 lation and nutrition may be mentioned the anemias, the cachexias, 
 senility, and certain metabolic diseases, such as diabetes. In these 
 conditions there is much probability that poisoning by metabolic 
 products plays an important part. 
 
90 TEXT-BOOK OF PATHOLOGY. 
 
 Trophic Derangements. — Forms of necrosis due to trophic dis- 
 turbances are well illustrated by bedsores (decubitus), myelitic 
 cystitis, the ulcerations seen in trigeminal neuritis, and the 
 arthropathies. These forms of cell-death cannot be brought under 
 the circulatory, toxic, or traumatic classification. They can be 
 explained only by the assumption that the biologic mechanism of 
 the cell is disturbed, and that in consequence death occurs. 
 
 Intoxications. — The group due to poisons is very extensive 
 and the particular subdivisions numerous. The toxins of bacteria 
 furnish many direct examples ; and indirectly many forms which 
 seem circulatory or traumatic are not really so, since these factors 
 only lower the resistance of tissues, which then become susceptible 
 to bacterial infection. Experimentally the most exquisite forms 
 of cell-degenerations and necrosis can be produced by the injec- 
 tion of toxins or analogous substances like ricin and abrin. The 
 alkaloids possess marked power in the production of necrosis. 
 Acids, alkalies, metallic salts, and innumerable other chemical sub- 
 stances may produce direct necrosis by immediate action, or indi- 
 rect necrosis by the preliminary production of degenerations. The 
 same substances often cause both circulatory and mechanical dis- 
 turbances, which augment their direct effects. Heat and cold act 
 like chemicals ; heat alters the properties of proteids ; cold affects 
 the fluids rather than the protoplasmic substances ; both also 
 induce marked circulatory disturbances. 
 
 Mechanical Agents. — The mechanical causes of necrosis are 
 many and varied. Pressure per se may cause the death of cells, 
 but is often aided by the circulatory disturbances which it occa- 
 sions. That tension causes necrosis is an old surgical truth, well 
 illustrated by the results of collections of exudates below the peri- 
 osteum and by the results of strangulations. The pressure of cal- 
 culi, concretions, enteroliths, and exostoses may cause important 
 necrotic processes. Circulatory disturbances often are a very ac- 
 tive factor — indeed, many forms of traumatism act solely through 
 them. 
 
 Inflammation, whatever its original inception, may become so 
 extreme as to lead to necrosis. Necrosis, on the other hand, often 
 leads to inflammation, the dead cells constituting veritable irri- 
 tants. 
 
 All forms of necrosis are accompanied to a greater or less 
 extent by the various degenerations. In particular the cellular 
 alterations are constantly present, and constitute the evidences of 
 morbific action. (Reference will be made below to the cellular 
 changes.) 
 
 There are several general forms of necrosis which, however 
 produced, have a sufficiently distinct character to warrant separate 
 descriptions. They are coagulation-necrosis, liquefaction-necrosis, 
 caseation, fat-necrosis, hemolysis, and gangrene. 
 
RETROGRESSIVE PROCESSES. 
 
 9.1 
 
 COAGULATION=NECROSIS. 
 
 Definition. — This is defined as that form of death of tissue 
 in which the proteid suffers a change similar to or identical with 
 coagulation. It is seen only in those tissues which are rich in 
 proteids. The process is partly at least a species of fibrin-forma- 
 tion, and is allied to hyaline degeneration. 
 
 Etiology. — The causes of this condition are those above de- 
 tailed for necrosis in general. Circulatory disturbances, except 
 thrombosis or infarctions, play a minor role here. Chemical irri- 
 tants and high temperatures frequently produce it. Bacterial 
 poisons are very prone to produce it, especially those elaborated 
 by the pyogenic bacteria, the tubercle bacillus, and the Bacillus 
 diphtherias. About every abscess is found more or less coagula- 
 tion-necrosis ; it is one of the early changes in tubercles, and the 
 fundamental element in the production of pseudomembranes. All 
 exudates and transudates are liable to coagulation. 
 
 The serous and mucous membranes are most susceptible ; next 
 the muscular tissues (often the myocardium). 
 
 Pathologic Anatomy. — The tissue has a glazed, opaque, 
 waxy appearance, and is firmer and paler than normal. In later 
 stages the color becomes gray and the tissue inclines to soften. 
 Microscopically it is seen that there is an exudate which has been 
 
 Fig. 23.— Obstruction of a branch of the renal artery with micro-organisms : necrosis 
 of the tissue around the artery, and round-cell infiltration of the neighboring tissue 
 (Thoma). 
 
 fixed in the tissues ; the fibrin is seen (with suitable stains) in 
 granules and fibrils with the homogeneous exudate closely packed 
 about it. The cells soon lose their election for stains (Fig. 23). 
 Early in the process the nuclei may stain faintly and present a 
 
92 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 homogeneous appearance ; later the cell disintegrates completely. 
 In muscles the striations disappear ; and iu the cardiac muscle the 
 intercellular cement-substance seems to be dissolved, for the cells 
 often lie separated and present vacuolation and fragmentation. 
 Pus, leukocytes, and red blood-cells in the affected areas all suffer 
 the fate of the fixed tissue. The blood-vessels at the margin of 
 the area are seen to be thrombosed. In the kidneys the tubules 
 may contain firm casts. 
 
 Morbid Physiology. — Many chemicals cause coagulation by 
 direct action. In the larger number of instances, however, it 
 must be assumed that the fibrinogenetic substances which bring 
 about the coagulation of the proteids are derived from the necro- 
 biotic cells in the area or are carried thither by the lymphatic 
 
 ■ 
 
 ♦ l .■* * 9 
 
 ' if 
 
 Fig. 24.— Coagulation-necrosis of the hepatic cells in a case of puerperal eclampsia 
 (Karg and Schraorl). 
 
 cells. There is considerable evidence that bacterial products 
 may act fibrinogenetically (Fig. 24). 
 
 An area of coagulation may be cast off by the process of ulcer- 
 ation, may undergo liquefaction, caseation, or suppuration, may be 
 encysted, and apparently may be dissolved and reabsorbed. The 
 area of disease may finally be converted into scar-tissue by 
 secondary regeneration. More or less complete loss of function 
 results from this form of necrosis. 
 
 LIQUEFACT10N=NECROSIS. 
 
 Definition. — This change consists in the death of tissue with 
 colliquation. It may be divided into primary and secondary 
 forms. Secondary liquefaction-necrosis is the form in which other 
 varieties of necrosis or degeneration are followed by liquefaction. 
 Thus, areas of coagulation-necrosis, cheesy necrosis, and of inflam- 
 mation, gangrenous tissue, and tumors may become liquefied. 
 
 Among the special forms may be mentioned vesicle-formation 
 
RETROGRESSIVE PROCESSES. 
 
 93 
 
 and the softening of caseous tuberculous lesions. A very frequent 
 seat of liquefaction-necrosis is the central nervous system, where 
 the conditions are unfavorable to coagulation, so that liquefaction 
 here follows pathologic conditions which would elsewhere produce 
 coagulation. Circulatory disturbances, traumatism, and intoxica- 
 tions all cause softening in the central nervous system ; the 
 peripheral nerves are much less susceptible. 
 
 Pathologic Anatomy. — In the early stages the tissue is 
 softer than normal and very rich in juices. Later, when the solu- 
 tion of the fibrillar tissues is advanced, the area becomes filled 
 with a liquid of greater or less consistency, depending upon the 
 tissue involved. The cells in the area are seen in all stages of 
 degeneration ; later, nothing but detritus is visible. In some 
 instances, instead of becoming more and more fluid, the exudate 
 undergoes coagulation. The color may be white, from the presence 
 of an emulsion of fats ; yellow, from fats and pigments ; red and 
 brown, from the presence of blood-pigment ; and deeply colored 
 Avhen jaundice is associated. 
 
 The process consists in the infiltration of fluid into tissues and 
 the more or less complete solution of the tissue-elements in it. 
 It has been compared to the alterations of proteids by digestion — 
 a reasonable deduction, since enzymes are 
 often elaborated in the processes which give 
 rise to liquefaction. In other respects the 
 process resembles the solution in distilled 
 water of proteids precipitated by salt so- 
 lutions. 
 
 Areas of liquefaction may discharge 
 their contents, may coagulate, may be re- 
 absorbed, encysted, or in uncommon in- 
 stances organized. 
 
 CASEATION. 
 
 Caseation is the crude name applied to 
 a complex process whose product has a 
 cheese-like appearance (Fig. 25). 
 
 The condition is most frequently seen 
 in connection with tuberculosis, although 
 it is found in the other granulomata, and 
 also in other pathologic processes. The 
 preliminary conditio sine qua non of casea- 
 tion is coagulation-necrosis. 
 
 The early tubercle, before the occur- 
 rence of softening, has an appearance like 
 that of cheese, but is less homogeneous and more granular (Fig. 
 26). A form of caseation quite similar in appearance occurs in 
 
 Fig. 25.— Tuberculosis of the 
 suprarenal capsule, showing 
 caseation of the tuberculous 
 areas (modified from Kast and 
 Rumpel). 
 
94 TEXT-BOOK OF PATHOLOGY. 
 
 pneumonia, in tumors, and especially in syphilis. Soft caseation 
 is usually coagulation-necrosis advanced to liquefaction, together 
 with tatty metamorphosis, so that the appearances are those of 
 soft, creamy cheese. The liquefaction-necrosis of the central ner- 
 vous system may present similar appearances. 
 
 Microscopically, the tissues in caseation show no cells preserv- 
 ing their staining-reactions ; everything is converted into debris. 
 Around the affected area is usually found a zone of coagulation, of 
 inflammation, or both. 
 
 
 
 
 Fig. 26.— Large tubercle of the lung, showing cheesy necrosis in the center. 
 
 Tissues that have undergone caseation may be cast off, reab- 
 sorbed, or encysted ; resolution is not possible. Calcification is a 
 frequent termination. 
 
 FAT=NECROSIS. 
 
 This term is now used to designate a peculiar type of necrosis 
 to which the fatty tissues are subject, and is distinct from ordinary 
 fatty metamorphosis. In human beings it is seen almost exclu- 
 sively in the abdomen, abdominal walls, and subperitoneal fat. 
 Tn nearly all instances it appears in connection with pancreatic 
 disease — cysts, tumors, obstruction to the duct, and the various 
 forms of acute pancreatitis. In rare instances the pancreas has 
 not seemed especially diseased. In one case I have seen of hyper- 
 trophic cirrhosis of the liver the omentum was affected, while the 
 pancreas showed nothing but a moderate degree of fibrosis.. 
 
 The affected areas are white in color, usually not larger than a 
 pea ; they may be soft or quite gritty. Inflammatory reaction 
 may or may not surround them. On microscopic examination 
 crystals of the fatty acids may be seen together with more abun- 
 dant crystals of a combination of lime with the fatty acids. This 
 
RETROGRESSIVE PROCESSES. 95 
 
 combination, it appears, is not a primary feature in the necrosis, 
 suggesting that the fatty acids are first set free and then unite 
 with lime-salts. In experimental work by Hildebrand and Flex- 
 ner it seems to have been shown that the typical condition may 
 be the result of direct action of the fat-splitting ferment of 
 the pancreatic secretion. It is certain, however, that in some 
 cases of pancreatic cysts containing steapsin no fat-necrosis has 
 occurred. Bacteria have been supposed by some to be the essen- 
 tial agents causing the change, but this has not been demonstrated. 
 
 HEMOLYSIS. 
 
 Hemolysis, or blood-destruction, is a term limited to the red 
 cells, and indicates destruction of the cell with dispersion of its 
 hemoglobin. (The causes and other features are described under 
 Pigmentations and Diseases of the Blood.) 
 
 GANGRENE. 
 
 Definition. — Gangrene, formerly defined as the death of tis- 
 sue en masse, is perhaps best defined as the putrefaction of areas 
 of necrosis. It may be primary, when a particular bacterium 
 produces a gangrenous inflammation as its direct result, as in 
 malignant edema ; or secondary, when saprophytic bacteria decom- 
 pose an area already necrosed from other causes. It may be dry 
 or moist, according to the location and supply of fluids. It may 
 furthermore be circumscribed, progressive, or metastatic. 
 
 Primary gangrene constitutes a specific affection, or rather a 
 number of specific affections. Malignant edema, infectious em- 
 physema,- and some forms of anthrax may be included in this 
 group. In these conditions there is violent infective inflammation 
 with practically immediate gangrene of the affected parts. 
 
 Secondary gangrene is more common, and the appearances are very 
 varied. The essential condition is putrefaction of a necrosed area. 
 
 Dry gangrene is usually due to vascular disturbances. As a 
 result of arterial obstruction it is seen in the extremities in senility, 
 and following arterial embolism or thrombosis of whatsoever nature 
 if the collateral circulation be insufficient to nourish the part. 
 Freezing may produce a dry form of gangrene, the vessels being 
 blocked by thrombosis. Ergotism causes dry gangrene as a rule ; 
 the same may be said of Raynaud's disease. Finally, dry gan- 
 grene may result from the moist form when putrefaction is slow 
 and evaporation of the fluids occurs. The putrefactive processes 
 in the dry type are not marked, and may cease entirely. Dry gan- 
 grene is generally circumscribed, and the end-result of a typical 
 case is mummification. The color is usually dark, finally black ; 
 early it may be yellow or brown ; rarely, the tissues are very pale. 
 There is little toxic absorption in these cases. 
 
96 TEXT-BOOK OF PATHOLOGY. 
 
 Moist gangrene presents numerous varieties. It is rarely pro- 
 duced by arterial occlusion, but is the usual result of extensive 
 venous occlusion. Internal emboli, as in the pulmonary arteries 
 or veins or mesenteric arteries, not infrequently cause gangrene of 
 this form. It also occurs in the lungs as a result of inspirational 
 or other pneumonias, abscess, neoplasms, bronchiectasis, and in 
 diabetes. It is seen as a result of traumatism and pressure in 
 severe contusions (especially with vascular injuries), in intussus- 
 ception and strangulation of the bowel ; as a result of torsion in 
 movable kidneys, spleens, or tumors. It is frequent in the ob- 
 structed or strangulated vermiform appendix. Extensive moist 
 gangrene of the extremities or other parts is not rare in connec- 
 tion with diabetes. The mucous membranes may become gan- 
 grenous as a result of various infections. A particular form is 
 noma of the mouth and genitalia. It is seen as a rare condition 
 in certain skin-diseases ; and is not unusual in severe trophic 
 lesions, as decubitus, cystitis, mal perforant, etc. 
 
 In moist gangrene the consistency of the part becomes progres- 
 sively softer. There may be local or widespread emphysema. 
 The color is usually dark brown, due' to disorganized blood-pig- 
 ment; the skin commonly becomes black, and is covered with 
 blebs. About the area there may be a zone of coagulation-necro- 
 sis with vascular thrombosis ; or a zone of inflammatory reaction 
 which will produce a line of demarcation. In some cases, espe- 
 cially the diabetic, neither of these zones is formed. 
 
 The cells first succumb. The protoplasm and nuclei exhibit 
 various evidences of degeneration, the nuclei disappearing and 
 the cells becoming converted into granular detritus. Fat and the 
 my el in-sheaths of nerve-fibers are reduced to free fat and fatty 
 crystals. The muscle-cells lose their striations and become frag- 
 mented ; the axis-cylinders of nerves fibrillate. Hemorrhages into 
 the area are common, due either to erosion of vessels and expulsion 
 of their thrombi by the pressure of the blood-current, or to a genu- 
 ine hemorrhagic condition the result of toxemia. Connective tissue 
 and elastic fibers resist longer than the cells, but finally become 
 liquefied. The affected area contains crystals of pigment, fatty 
 acids, cholesterin, leucin, ty rosin, phosphates, and carbonates. 
 Ammonia, the fatty acids, indol and skatol, amins, sulphuretted 
 hydrogen, carbonic acid, and other gases, usually of pronounced 
 odor, are formed. There is more or less toxic absorption from 
 these areas. 
 
 But two things can happen to an area of gangrene; it may 
 progress and cause the death of the individual, or may become cir- 
 cumscribed. In dry gangrene and in the vascular forms of moist 
 gangrene limitation is the rule ; the other moist forms tend to be 
 progressive. In the circumscribed form a line of demarcation is 
 formed by inflammatory reaction, and the mass is finally cast off 
 
RETROGRESSIVE PROCESSES. 97 
 
 as a sphacelus or slough if the area be superficial, or encysted if 
 the area be internal. The latter cases may be followed by reab- 
 sorption of the contents and calcification of the sac. 
 
 GENERAL PATHOLOGY OF CELLULAR NECROSIS. 
 
 The cell as an individual element is liable to pathologic processes of 
 various kinds that merit brief consideration, apart from definite forms of 
 tissue-degeneration and necrosis. 
 
 Etiology. — The causes of cellular degeneration and necrosis are numer- 
 ous, including mechanical, thermal, electrical, chemical, and vital (trophic) 
 influences of various kinds. It is easy to demonstrate the influence of 
 some of these causes in the unicellular organisms such as amebse, and the 
 changes thus produced may also be seen under proper conditions in the 
 cells of the animal body. 
 
 Pathologic Anatomy. — The cell as a whole may show various forms of 
 distortion, or internal change. Increased irritability and mobility of the 
 protoplasm cause the projection of pseudopodia, and these may be separated 
 from the body of the cell as rounded particles more or less resembling the 
 original cell. This is easily demonstrable in red blood-corpuscles sub- 
 jected to heat. Sometimes particles of the substances are discharged from 
 the cell and vacuolations (expulsion-vacuoles) result. Certain influences, 
 like cold, and metallic salts or other poisons, cause a reduced mobility and 
 general contraction of the cell. Granular precipitation may at the same 
 time occur within the protoplasm. In other cases solution of parts of the 
 cellular protoplasm occurs, and vacuoles of varying size are thus produced. 
 
 Similar changes have been discovered in the nuclei of the cells, but 
 certain special forms of nuclear change require special mention. 
 
 Nuclear solution or hypochromatosis may occur as a process of gradual 
 fading or disappearance. The nucleus becomes more and more pallid, and 
 finally is indistinguishable. 
 
 Karyorrhexis is a form of nuclear fragmentation in which the chromatin 
 of the nucleus becomes broken up into small particles. 
 
 Hyperchromatosis is a degenerated condition of the nucleus, involving 
 the nuclear membrane in particular. The body of the nucleus becomes 
 pale and finally quite colorless, while the periphery is much more apparent 
 and thickened. With the further destruction of the nucleus and cell the 
 pigment-particles arranged around the periphery of the nucleus may become 
 scattered through the cell. 
 
 Pyknosis is the name used to designate degeneration of the cell and 
 nucleus in which the protoplasmic substance of these structures becomes 
 more dense and their size correspondingly decreased. The cells become 
 darker and frequently densely granular. When the nucleus is affected this 
 contraction may leave a vacant zone about it, so that the nucleus apparently 
 lies within a vacuole. 
 
 ABNORMAL CELL=DIVISION. 
 
 In addition to these diseases of the cell and its nucleus there are certain 
 disorders of cell-multiplication that may be here described. Karyokinesis, 
 instead of being a regular process of division of the nucleus into two 
 daughter-nuclei, may proceed irregularly. Sometimes the process is asym- 
 metric — i. e., does not lead to equal division ; in other cases it is multipolar, 
 several instead of two daughter-nuclei resulting. Other less definite irregu- 
 larities are sometimes observed, and some have held that cell-division may 
 occur by a process of mixed karyokinesis and amitosis. It is important to 
 recognize that some of the forms of nuclear degeneration (karyorrhexis; 
 hyperchromatosis) may be mistaken for normal or abnormal karyokinesis. 
 7 
 
98 TEXT-BOOK OF PATHOLOGY. 
 
 CHAPTER V. 
 INFLAMMATION AND REGENERATION. 
 
 INFLAMMATION. 
 
 Definition. — By this name are designated the vascular exuda- 
 tive, degenerative, and regenerative changes which occur in the 
 living tissues as a result of irritation by chemical, mechanical, or 
 thermal agents. No short definition contains the essence, for in- 
 flammation is by no means a simple process. It varies with the 
 varying anatomical conditions or the vitality of the tissue involved, 
 and with the intensity or nature of the irritant. Galen and his 
 followers defined it by giving the cardinal symptoms : heat (calor), 
 redness {rubor), pain (dolor), and swelling (tumor). To these may 
 be added altered function (functio kesa). 
 
 Historical. — The earliest conceptions of inflammation were those of a 
 specific entity. Subsequently various theories were offered in explanation 
 of the several phenomena or symptoms. First, the blood-vessels were sup- 
 posed to be influenced through the nervous system [vascular theories). 
 Next, it was taught that the inflammatory irritant excites proliferative 
 changes in the tissues (thus giving rise to round cells), and that this stimu- 
 lation of the cellular activity invites more blood to the part (hence the 
 hyperemia). This was the cellular and attraction theory of Yirchow. 
 Others, notably Cohnheim, described the emigration of leukocytes from the 
 blood-vessels, and held this to be the essential feature of inflammation. 
 This emigration was first described by Dutrochet (1824), Waller (1842), and 
 Strieker ; but Cohnheim was the first to systematize the emigration theory. 
 According to Virchow, the first step is a formative stimulation of the cells ; 
 according to Cohnheim, degeneration of the vessels leading to emigration ; 
 according to Weigert, at least in many cases, the first step is necrosis of the 
 parenchymatous cells. At the present day inflammation is generally re- 
 garded as purely reactive in nature, the irritation causing sometimes one 
 and sometimes another primary lesion. 
 
 Phenomena in Inflammation. — These may be well studied 
 in the mesentery or tongue of a frog. When the mesentery is ex- 
 posed and spread under a microscope the first visible effect is a very 
 temporary contraction of the arteries, which may disappear before 
 the examination can be made. It is followed by dilatation of the 
 arteries, and then of the capillaries and veins. The blood-current is 
 first more rapid than normal, then slower, and may finally stop 
 entirely (stasis), especially in the capillaries in the center of the 
 inflamed area. Notable changes are seen in the circulating cor- 
 puscles. As the current becomes slower the leukocytes in the 
 plasmatic zone increase in number and stick to the vessel-walls in 
 a continuous row. In the capillaries clumps of leukocytes fre- 
 quently alternate with masses of red corpuscles, or of red and 
 white corpuscles in their customary proportion. Next, it may be 
 observed that the leukocytes are passing through the walls of the 
 
INFLAMMATION AND REGENERATION. 99 
 
 capillaries and veins and spreading in the outside tissues. At the 
 same time a certain number of red corpuscles are passed through 
 the capillary walls, and altered plasma escapes and infiltrates the 
 tissues. In the connective tissues outside the vessels proliferative 
 changes take place, leading to karyokinesis and formation of round 
 cells resembling the emigrated leukocytes (Fig. 27). In struct- 
 
 FiG. 27.— Inflammation of the mesentery, showing overfilling of the blood-vessels, with 
 emigration of leukocytes and diapedesis of red corpuscles (Ziegler). 
 
 ures in which there are parenchymatous (archiblastic) cells the 
 latter undergo various degenerative changes, such as cloudy swell- 
 ing, mucous degeneration, fatty degeneration, or even necrosis. 
 Less frequently proliferation of the parenchymatous cells takes 
 place. Every case of inflammation does not present all of these 
 phenomena, nor is the subsequent fate of the exudate and altered 
 cells always the same. 
 
 The phenomena must now be separately considered. 
 
 1. Changes in the Vessels. — The first effect of irritation may be 
 momentary contraction of the arteries ; but this is rarely observed. 
 Usually the arteries dilate at once, and dilatation of the capillaries 
 and veins promptly follows. The cause of this dilatation was for- 
 merly looked for in the nervous system, but it is more probably 
 to be found in some degeneration of the vessel-walls. The micro- 
 scope does not reveal this, but some of the phenomena connected 
 with exudation and the circulation of the blood show that the 
 cause must be in the vessel-walls. 
 
 2. Exudation. — The blood-current is at first more rapid, then 
 slower, than normal. The former is due to dilatation of the 
 arteries ; the latter doubtless to some change in the walls of the 
 blood-vessel increasing the friction. Mere dilatation of the vessels 
 could not affect the current in this way. As the current grows 
 slower the leukocytes in the plasmatic zone of the blood-stream 
 increase in number and cling to the wall of the vessel. This is 
 
100 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 W 
 
 purely a mechanical result of the slower rate of the blood-current. 
 Finally, the leukocytes pass through the vessel-walls between the 
 endothelial cells and collect on the outside of the blood-vessel, 
 whence they more slowly migrate through the tissues (Fig. 27). 
 This emigration of leukocytes occurs to a moderate degree normally, 
 but is abnormal in degree in inflammation. Cohnheim ascribed it 
 
 to disease of the vessels — in- 
 creased permeability — the leu- 
 kocytes being purely passive. 
 Later observation indicates that 
 the chief role in this excessive 
 emigration must be assigned to 
 the stimulated ameboid move- 
 ments of the leukocytes. Degen- 
 eration of the vessel-walls, espe- 
 cially swelling and softening of 
 the cement-substance between the 
 endothelial cells, and the press- 
 ure of the blood, aid ; but only to 
 a minor extent. The cause of 
 this active ameboid motion and 
 tendency to emigration has re- 
 cently been found to be an attrac- 
 tive force peculiar to the causes 
 of inflammation. Pfeffer found 
 that certain substances manifest 
 strong attractive power for mo- 
 tile bacteria and various spores 
 of plants. This has been termed 
 ■positive chemotaxis. A repellant 
 influence is peculiar to other sub- 
 stances, such as the toxins of bac- 
 teria, and to this the term nega- 
 tive chemotaxis has been applied. 
 The irritant substances which 
 cause inflammation are probably 
 positively chemotactic in action ; 
 and in eases where mechanical 
 injury causes inflammation such 
 substances first result from me- 
 chanical destruction of cells and 
 then occasion the subsequent phenomena of inflammation. In 
 other inflammations the irritant causing the disorder may itself 
 contain the positively chemotactic substance (see under Suppurative 
 Inflammation). The microscopic appearance of the tissues after 
 emigration of the leukocytes is characteristic. The capillaries are 
 dilated and obscured by a mantel of exuded white corpuscles, and 
 
 
 
 : v . f '-"■-' ■ ■ 
 
 Fir;. 28.— Acute appendicitis, with exten- 
 sive round-cell inliltration of ull of the coats 
 of the appendix. 
 
INFLAMMATION AND REGENERATION 101 
 
 the tissue around is infiltrated with migratory leukocytes. This 
 appearance is called round-cell infiltration or inflammatory infiltra- 
 tion (Fig. 28). The round cells are mostly leukocytes, but some 
 are new-formed connective-tissue cells, as will be subsequently 
 described. 
 
 Coincidently with leukocytic emigration there is exudation of 
 more or less altered blood-plasma. This is richer in albumin and 
 more coagulable than dropsical fluid, which is a further indication 
 that the blood-vessels are more permeable in inflammation than in 
 health or mere congestion. 
 
 Finally, a certain number of red corpuscles escape from the 
 capillaries by diapedesis. This is a purely passive process as far 
 as the red corpuscles are concerned, being due to pressure of the 
 blood. It is particularly marked when stasis has occurred. Ac- 
 cidental hemorrhage by rhexis may add to the blood in an exudate, 
 but is not truly exudative. 
 
 3. Degenerative Changes in the Tissues. — The action of the irri- 
 tants which excite inflammation sooner or later affects the tissues 
 and causes degeneration or death. The first effect may fall upon 
 the blood-vessel walls or upon the tissues. Weigert, Neumann, 
 and others hold that the " primary effect " in inflammation is 
 generally or always this tissue-degeneration, which excites second- 
 ary proliferation. This is certainly the case at times ; and the 
 discovery that tissue-degeneration leads to the formation of sub- 
 stances positively chemotactic in action would indicate the manner 
 in which inflammation is brought about in these cases. The degen- 
 erative changes may be merely physiologic (some form of altered 
 functional activity), or there may be structural alterations, such as 
 cloudy swelling, liquefaction, fatty change, coagulation- or other 
 forms of necrosis. The nature of the degeneration depends largely 
 upon the severity of the irritation. Very powerful irritants cause 
 necrosis at once, and not inflammation. It is the irritants which 
 disorder, but do not entirely destroy, cells that are especially apt to 
 excite inflammation. 
 
 4. Proliferative Changes. — Sooner or later in an inflamed area 
 there are evidences of cellular proliferation, which occasions the 
 appearance in the tissue of round cells closely resembling the out- 
 wandered leukocytes. They differ, however, in being somewhat 
 larger, in having a larger and paler nucleus which is rounded or 
 oval, and in their exhibiting evidences of karyokinesis. These 
 cells are derived from pre-existing connective-tissue cells. Re- 
 cently it has been claimed that they are in part redevelopments 
 of cellular remnants which had almost or quite lost their cellular 
 character, such as fibrillar protoplasmic prolongations of connec- 
 tive tissue. These are the " slumbering cells " of Grawitz. 
 Virchow held the proliferative changes to be the essential 
 feature in inflammation, and believed that all round cells have 
 
102 TEXT-BOOK OF PATHOLOGY. 
 
 this origin ; Cohnheim denied the occurrence of proliferation, and 
 ascribed to emigration the essential role. Later, it was held that 
 the proliferative changes are not in reality a part of inflammation, 
 but rather regenerative and for the purpose of repairing the tissue- 
 injuries after inflammation (Fig. 29). At the present time we 
 
 rV-V f& ill ^tftf* 
 
 Fig. 29.— New blood-vessels and fibroblastic cells in a beginning adhesion of the peri- 
 cardial layers. 
 
 must regard as factors in inflammation both emigration and pro- 
 liferation, whether the latter in any individual case is due to direct 
 stimulation of the cells, or is secondary to destructive changes, or 
 is merely the result of increase of nutrition from the inflammatory 
 congestion. It is conjectured by some that under chemotactic 
 influences the cell-contents of fixed cells are incited to movements 
 terminating in karyokinesis, just as the whole cell is influenced in 
 the case of movable cells. Proliferative changes also occur in the 
 parenchymatous cells, but in that case they are more strictly regen- 
 erative in nature. 
 
 Btiology. — Irritation by mechanical, chemical, thermal, or in- 
 fectious agents causes inflammation when it is severe enough to dis- 
 turb the vitality of the tissue and not sufficient to cause necrosis at 
 once. When the irritant is brought to bear upon the tissues 
 directly there is probably, first, cell-degeneration, followed by 
 vascular disturbances and emigration. When the irritant acts 
 through the blood, vascular disorders probably, as a rule, precede 
 the tissue-changes. Micro-organisms may act by first destroying 
 the cells, or may by their own death liberate from their substance 
 some poison (protein) which is chemotactic. Disturbances of 
 circulation, innervation, or metabolism may so alter cellular pro- 
 cesses as to occasion the production of irritating and chemotactic 
 products. 
 
 Special Forms of Inflammation. — The nature of the exu- 
 
INFLAMMATION AND REGENERATION. 
 
 103 
 
 date and its subsequent changes lead to a variety of forms of 
 inflammation. Other varieties depend on the activity and dura- 
 tion of the process. 
 
 (a) Edematous or serous inflammation is characterized by a 
 copious exudation of fluid with comparatively little cellular mat- 
 ter, as in edema of the larynx, serous effusions in the serous sacs, 
 etc. The fluid differs from dropsical fluid in containing more 
 albumin and fibrin-factors. 
 
 (b) Fibrinous Inflammation. — The plasmatic exudate may clot 
 at once and form a fibrinous membrane on free surfaces or a net- 
 work within the tissues ; this is termed fibrinous inflammation. 
 Inflammations of the serous membranes are nearly always more or 
 less fibrinous. Croupous pneumonia furnishes another example. 
 
 (c) Diphtheritic inflammation differs from the last in having 
 associated with the coagulation of the exudate coagulation-necrosis 
 of the cells of the part inflamed. Diphtheritic inflammation 
 occurs especially in the pharynx and larynx, where it occasions 
 pseudomembranes (Fig. 30). This is most frequently due to the 
 
 -Pseudomembranous inflammation of the uvula: a, masses of micrococci; b, 
 necrotic cells ; c, round-cell infiltration ; d, fibrin-network (Ziegler). 
 
 specific cause of the disease called diphtheria ; but diphtheritic in- 
 flammation may result from a variety of severe irritations, such as 
 bacteria, superheated steam, and chemical irritants. The diphthe- 
 ritic membrane consists of a network of fibrin or of homogeneous or 
 granular fibrin-masses enclosing degenerated epithelial cells and 
 emigrated leukocytes. Sometimes it is quite superficial, involving 
 only the surface-layer of epithelium ; at other times the whole 
 depth of the mucous membrane is implicated. The former are 
 sometimes called croupous and the latter diphtheritic false mem- 
 branes. These terms, however, are ill-defined and objectionable. 
 
104 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 (J) Suppurative inflammation is characterized by unusual abun- 
 dance of emigrated leukocytes and by the tendency to li qui 
 factmn Bacteria are most frequently the cause; but i has 
 been shown experimentally that croton oil, calomel, tu pontine 
 
 the bactena, the commonest are the so-called pyogenic staphylo- 
 cocci and streptococci; but numerous forms, not La tiall vo 
 geme may occasionally prove so. Such 'arc the bacdhis' V 
 typhoid fever, the gonococcus, the Bacillus coli, and others 
 Recent studies ascribe to chemotaxi.s the important r6le in the 
 act,™ of baetern in inflammation and suppuration. Either he 
 products of the bacteria or substances derived from their own 
 Protoplasm (bacterioprotein-Buclmer) exercise a powerful duT 
 
 i Xytef IS' £? TIT ° CCaSi ° n ^ "^ ot ™« 
 leukocytes (i,g. 31 j. Ihe same or similar substances further 
 
 prevent fibrin-formation or cause a solution of fibrin already 
 fomed, and thus the exudate liquefies and forms pu This con' 
 
 with ' Iflf ■'', '"'',""' ''''',""■ ' <*>* »'«lifi«l Uooi-plasma 
 
 which diiferefrom ordinary plasma in being less coaeulaole Zl\ 
 contauung notable qnantities of albumose J^JS a corn^ 
 cular part, consisting chiefly of multinucle^r leukocytes iZTn^ 
 h- derated, lome proliferated connective-Se "ells or 
 
 rib^dforifS " n V r " "V '" ration into th * °ody mv take 
 
 plaoe directly through wounds, or somewhat indirectly through 
 small abras.ons m t he various mucous membranes. Some fel 
 
INFLAMMATION AND REGENERATION. 105 
 
 Abscess. — When this occurs in the substance of a tissue or 
 organ the lesion is called an abscess. This consists of a collection 
 of pus, which usually presents a creamy yellow color, but may be 
 variously altered in odor or color by subsequent changes. Around 
 the abscess the tissues present the proliferative changes described 
 as part of inflammation. There are numerous round cells, differ- 
 ing from emigrated leukocytes and showing karyokinetic figures 
 in the nuclei, and there are new blood-vessels and beginning organ- 
 ization. This restraining-wall of granulation-tissue was formerly 
 regarded as a pus-producing membrane, and therefore called the 
 pyogenic membrane. Abscesses, especially such as are due to bac- 
 teria, tend to soften the surrounding tissues in the direction of 
 least resistance, and thus to break on the surface, discharging their 
 contents by sinuous tracts or sinuses. Sometimes the pus of an 
 abscess becomes inspissated by absorption of the liquid part and 
 the residue undergoes various degenerative changes, such as mu- 
 cous, fatty, or calcareous. At* the same time the surrounding 
 membrane advances to complete organization, and thus encapsu- 
 lates the abscess. 
 
 Ulcer. — Suppurative inflammation with erosion of areas of the 
 skin or mucous surfaces occasions ulcers. These have the same 
 histologic construction as the wall of an abscess, the base of the 
 ulcer being the same as the pyogenic membrane. In it may be 
 seen small red points or granulations, which consist of loops of 
 capillary blood-vessels surrounded by round cells. (The his- 
 tology of granulation-tissue is more minutely described under 
 Regeneration.) 
 
 The appearance and pathologic course of ulcers vary widely. Some- 
 times rapid destruction of the tissues causes large and spreading ulcers, 
 called phagedenic. Others extend in one direction while healing in other 
 parts, and are called serpiginous. The granulations may be too rapid in 
 growth, forming red fungous masses which fill up the ulcer. In other cases 
 the ulcer remains dry and indolent, showing little tendency to heal. 
 
 In suppurative inflammation of mucous membranes without 
 ulceration the emigrated leukocytes reach the surface between the 
 epithelial cells, some of which are loosened and cast off together 
 with an excessive excretion of mucus (Fig. 32). The result of 
 these processes is a mucopurulent catarrh. 
 
 Suppurative inflammation of serous membranes leads to col- 
 lections of pus in the serous sacs. Unlike other tissues, there is 
 usually considerable fibrin -formation combined with the purulent 
 exudation in these situations. 
 
 (e) Productive Inflammation ; Chronic Inflammation. — In this 
 form the proliferative changes predominate over exudation and 
 degeneration. This may be due to the extent of the primary 
 tissue-injury or to the nature of the cause. Whether the regen- 
 erative processes are always reactive and consequent upon primary 
 
106 
 
 TEXT-BOOK OF PATHOLOGY 
 
 destruction, or may be stimulated directly by the irritant, is un- 
 settled. This form of inflammation is often called interstitial when 
 occurring in the substance of organs, and is distinguished from 
 parenchymatous inflammation, in which the parenchymatous or 
 proper cells of the organ are said to be involved. Strictly speak- 
 
 | 
 
 ft|f 
 
 (3. 
 
 . « ! i ; I i 
 
 
 PlG. 32.— Acute bronchial catarrh, showing the escape of leukocytes from the submucous 
 tissue between the epithelial lining cells (Thoma). 
 
 ing, this distinction is ill-founded, but the terms are convenient to 
 distinguish cases in which parenchymatous degeneration is promi- 
 nent from those in which proliferation and new formation of con- 
 nective tissue are the more striking features. 
 
 Repair of "Wounds. — Productive inflammation is well illus- 
 trated in the healing of wounds. If the lips of a clean, incised 
 wound are drawn together at once and kept closely apposed, rapid 
 healing occurs, which is called healing by immediate union. In 
 these cases a microscopic examination shows slight exudation from 
 the surfaces of the wound and proliferated connective-tissue cells. 
 The epithelial continuity is restored by proliferation of the old 
 epithelial cells. Should apposition be less immediate or less accu- 
 rate, the amount of exudation is greater. If the wounded surfaces 
 are examined twenty-four hours after the injury, they are found 
 red and swollen and soon they become glazed in appearance. The 
 
INFLAMMATION AND REGENERATION. 
 
 107 
 
 microscopic features here are the same as in the case of healing by 
 immediate union, excepting the amount of exudation is greater. 
 Healing proceeds in the same way but more slowly, and is called 
 healing by first intention. In neither case is there great congestion. 
 If the wound be irritated by foreign bodies or kept exposed, there 
 will be seen on the surfaces, after two or three days, small red 
 elevations, known as granulations, which 
 consist of loops of new-formed capillaries 
 covered by emigrated and new-formed 
 round cells, and sometimes (after longer 
 intervals of time) giant-cells (Fig. 33). 
 The surface may be covered with pus. 
 The proliferated round cells gradually 
 elongate and form new fibrous tissue (see 
 Eegeneration), which afterward contracts, 
 forming cicatrices or scars. The epithelial 
 continuity is re-established by multipli- 
 cation of the old epithelial cells at the 
 edges of the wound. This form of heal- 
 ing is called healing by second intention 
 or healing by granulations. 
 
 The formation of adhesions follow- 
 ing inflammation of the serous surfaces occurs in much the same 
 
 -Loops of blood- 
 vessels in granulation-tissue 
 (Thiersch). 
 
 Fig. 34.— Adhesive pericarditis, showing fibrin-deposit, with new blood-vessels extending 
 upward into it (Perls). 
 
 way as wounds heal. The primary exudation is largely fibrinous 
 and causes agglutination of neighboring surfaces. Subsequently 
 
108 TEXT-BOOK OF PATHOLOGY. 
 
 the proliferated connective-tissue cells penetrate this fibrinous ex- 
 udate, as do newly-formed blood-vessels (Fig. 34). Thus a union 
 of vascular channels is effected between the adjacent inflamed 
 surfaces and organization follows. 
 
 Precisely similar changes occur in the tissues surrounding a foreign body, 
 as a piece of sponge, or around a portion of dead tissue. In these cases the 
 exudative and proliferated cells tend to penetrate into the foreign mass, as 
 occurs also in the organization of thrombi. There is also in these cases a 
 greater tendency to the formation of giant-cells (by division of nuclei with- 
 out division of the cell-body) than in ordinary granulations. If the foreign 
 mass can be softened and absorbed, this gradually occurs, and later merely 
 a scar will indicate the location ; if it cannot be absorbed, connective tissue 
 encloses or encapsulates it. * 
 
 General Fibrosis. — A tendency to widespread productive in- 
 flammation is noted in certain individuals. This affects the blood- 
 vessels especially (general arteriocapillary fibrosis, general angio- 
 sclerosis), and also the liver (cirrhosis of the liver), the kidneys 
 (interstitial nephritis), and other organs (Fig. 35). The cause of 
 these changes is supposed to be some general intoxication — 
 alcoholic, gouty, syphilitic, or the like. 
 
 
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 Pie. 86. — Chronic interstitial nephritis: great increase of connective tissue around the 
 glomeruli, renal tubules, and blood-vessels ; from a case of arteriocapillary fibrosis. 
 
 Productive inflammation may affect other tissues than the fibrous 
 connective tissues. Reference has already been made to epi- 
 thelial proliferation in the healing of wounds. Similar epithelial 
 processes of greater activity or duration may lead to warty growths 
 of the skin or polypoid outgrowths on the mucous membranes. In 
 pharyngeal catarrhs considerable proliferation of the adenoid tis- 
 
INFLAMMATION AND REGENERATION. 109 
 
 sues is not unusual. So also thickening of cartilages, bones, or the 
 periosteum is not an unusual result of inflammation of these 
 structures. 
 
 (/) Hemorrhagic Inflammation. — More or less diapedesis of red 
 corpuscles generally occurs in inflammation ; but sometimes the 
 irritating cause falls with such peculiar force on the blood-vessels, 
 or the general condition of the patient (cancer, tuberculosis, hemo- 
 philia, scurvy) is so unsatisfactory that the exudate is unusually 
 rich in red corpuscles. These are always serious inflammations, 
 and are to be distinguished from ordinary inflammations in which 
 accidental hemorrhage occurs. 
 
 (g) Necrotic or gangrenous inflammations likewise depend for 
 their occurrence upon the severity of the irritation or the state of 
 the general system. 
 
 Resolution after Inflammation. — In cases of trivial 
 exudation the emigrated leukocytes may re-enter the blood-cur- 
 rent or may escape through the lymphatics. The liquid exudate 
 is similarly disposed of; while the proliferated connective-tissue 
 cells (if there be any proliferation) remain in loco or become 
 wandering cells. When the exudate is more abundant the liquid 
 elements may be removed in the same way, but the cells first 
 undergo degenerative softening and are reduced to the form of an 
 emulsion, which is gradually absorbed. The degenerated paren- 
 chyma in inflammation may recover if the degeneration is not 
 severe, or may be softened and removed. Phagocytic cells often 
 play a prominent part in the removal of broken-down cellular 
 remains, pigment-masses, and the like. 
 
 The reparative changes in inflammation may be so slight as to 
 lead to no discoverable lesion for some time after the process is 
 completed ; but where large damage has been done there is apt 
 to be a permanent scar or some other productive lesion. 
 
 REGENERATION. 
 
 Definition. — The term regeneration is applied to the forma- 
 tion of new cells or tissues to take the place of those destroyed. 
 Regeneration may be physiologic or pathologic. The former is 
 that which occurs in the normal life of the organism and by which 
 the cellular wear and tear is counterbalanced. Pathologic regen- 
 eration is the more massive and often atypical reconstruction that 
 follows disease or injuries. 
 
 Etiology. — The cause or mechanism by which normal regen- 
 eration is brought about is more or less obscure. The cells have 
 an inherent tendency to multiply, and this goes on to a certain 
 point at which the normal development is complete. This limit is 
 probably maintained by some restraining influence, but the nature 
 of this is unknown. In the skin and mucous membranes, where 
 
110 TEXT-BOOK OF PATHOLOGY. 
 
 physiologic regeneration is most active, new cells are constantly 
 produced and the older cast off. In what manner the balance is 
 so maintained that production and destruction keep their equal 
 pace is as yet matter only for speculation. The idea of action and 
 reaction occurs naturally to the mind, and it seems probable that 
 the reproductive processes are dependent in some May upon the 
 loss of substance. In some cases the normal restraining influence 
 seems to be deficient and giant-growth results. In all forms of 
 aormal or physiologic regeneration the reconstructed cells are 
 exactly like the pre-existing cells, and the status of the tissue is 
 unaffected. In highly-specialized cells, such as those of the 
 nervous system, regeneration seems to be intracellular — that is, 
 the cells are constantly rejuvenated by supplies of nutriment 
 rather than reproduced in toto. 
 
 In pathologic regeneration there seems to be abnormal stimu- 
 lation of the reproduction of cells as well as a reduced restraint. 
 It is not improbable that various toxic substances have the power 
 of stimulating the formative process, though this has not been 
 actually demonstrated. In all cases in which regeneration follows 
 mechanical, thermal, or toxic causes there is, first, destruction of 
 cells, and following this regeneration. In such cases the relief 
 from the accustomed pressure may serve as a withdrawal of re- 
 straint, but at the same time there is doubtless augmented form- 
 ative energy. The latter may result from the same agency as 
 that which caused the primary cell-destruction, or it may be due 
 to the influence of formative irritants derived from the dying and 
 dead cells. The demonstration that micro-organisms are able to 
 produce substances having a strong attractive or repellant influence 
 upon leukocytes gives some warrant to the belief that similar sub- 
 stances are at work in the regenerative changes that accompany 
 bacterial diseases. In the case of tissue-destruction due to other 
 causes similar products possibly play a part. 
 
 Pathologic Anatomy. — In the normal regeneration of cells 
 the process is one of gradual cell-multiplication without marked 
 changes of any sort. Pathologic regeneration may be equally 
 simple, but more often there are complicated changes in the pre- 
 existing tissues and new formation of blood-vessels preceding or 
 accompanying the regeneration. The vascular regeneration is a 
 necessary preliminary, having the purpose of supplying abundant 
 nutriment to the tissues undergoing proliferation. 
 
 Cell-multiplication occurs in two ways, the direct and the in- 
 direct. The former method is one of simple cleavage, by which 
 the cell is divided into two or more parts. This mode of division 
 is unusual. The common method is called indirect segmentation, 
 karyokmesis, or karyomitosis. In this method complicated changes 
 begin in the nucleus and finally lead to division of the cell into 
 two or rarely into several parts. It is unnecessary to refer to the 
 
INFLAMMATION AND REGENERATION. Ill 
 
 histologic stages in detail, but in a general way we may describe 
 the process as follows : (1) the nucleus of the cell enlarges and the 
 chromation-fibers become thicker and less closely woven than 
 normally ; (2) U-shaped loops of chromatin-fibers arrange them- 
 selves around a central clear space or polar field to form a mother- 
 wreath; (3) these loops then undergo longitudinal cleavage and 
 the separated parts move one to one pole and the other to the 
 opposite pole of the cell, forming daughter-stars, which eventually 
 become coarse and then fine skeins of new nuclei ; (4) the proto- 
 plasm of the cell finally divides and the process becomes complete. 
 
 Pathologic Regeneration. — In the reconstruction of areas of 
 destruction of surface-epithelium (mucous membranes, skin) the 
 process of cell-multiplication, as above described, occurs in the 
 epithelial cells under and around the area of destruction, and 
 eventually the surface is fully restored. The same form of regen- 
 eration may occur in other surface-cells, as those of serous mem- 
 branes, and also in the substance of organs or solid tissues when 
 the cellular damage is slight. In cases of more extensive destruc- 
 tion the connective tissues play an active part and the restoration 
 is atypical, the new-formed tissue containing a greater amount of 
 connective tissue than the pre-existing tissue. In the case of 
 highly specialized tissues, such as the gray matter of the brain or 
 cord, the regeneration is confined to the connective tissues. In 
 massive regeneration or regeneration of specialized tissues, then, 
 the principal changes are those affecting the connective tissues. 
 
 Regeneration of Fibrous Connective Tissues. — It is difficult to 
 draw a line between the process of inflammation and regeneration. 
 In the latter process there is always some congestion and cellular 
 infiltration (emigration of leukocytes) ; later, multiplication of the 
 fixed connective-tissue cells and new formation of blood-vessels 
 occur. 
 
 The multiplication of connective- tissue cells may be more or less 
 abundant. The old connective-tissue cells swell and the nuclei 
 divide by karyokinesis, new cells of rounded outline and with rather 
 pale nuclei resulting. At the same time the cells of the capillary 
 blood-vessels become swollen and here and there budding pro- 
 cesses are sent outward (Fig. 36). These may unite with similar 
 processes from an adjacent or the same capillary and then undergo 
 central vacuolization, which proceeds along the loop, converting it 
 into a channel with here and there new-formed nuclei within the 
 protoplasmic wall. The latter finally becomes differentiated into 
 definite endothelial plates and the new capillary is completed. 
 Around these capillary loops lie the emigrated leukocytes, and 
 especially the new-formed connective-tissue cells. The latter are 
 the formative cells of the regenerating tissue. In the case of 
 fibrillar connective tissues they are called fibroblasts (Fig. 37) ; 
 in the case of cartilage, chondroblasts ; in the case of bone, osteo- 
 
112 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 blasts. The process is practically the same in the different con- 
 nective tissues, the differentiation occurring secondarily. The for- 
 mative cells become larger and more or less elongated, and the 
 formation of intercellular substance then follows. In the case of 
 fibrillar connective tissue the cells 
 elongate considerably, and by seg- 
 mentation of their extremities in 
 part contribute to the formation 
 of the intercellular fibrils. The 
 rest of the fibrils are formed by 
 cleavage of the homogeneous in- 
 
 Fig. 36.— Formation of new blood- 
 vessels, as seen in the tail of a tadpole 
 (Arnold). 
 
 Fig. 37.— Fibroblasts forming fibrous tissue 
 (Ziegler). 
 
 tercellular substance in which the cells are at first embedded. 
 This intercellular substance, in part at least, is doubtless a product 
 of cellular activity. 
 
 When the processes of regeneration have reached this stage 
 the new-formed tissue consists of an abundance of round and 
 elongated cells, with a small amount of fibrillar intercellular 
 substance. Subsequently the latter increases in amount and by 
 contraction further adds to its density. During this late stage the 
 number of cells becomes less considerable, and eventually there 
 may be only here and there a cell embedded in dense bands of 
 fibrils. Nearly always, however, there is greater cellular richness 
 in new-formed connective tissues than in the normal tissues of the 
 same kind. 
 
 Regeneration <>/ other Connective Tissues. — The reconstruction 
 of cartilage and bone may occur by primary formation of ordi- 
 nary connective tissue and subsequent transformation. This 
 is especially the case when the regeneration springs from the 
 periosteum or from membranous connective tissues. In other 
 cases, however, the regenerative processes produce cartilage and 
 bone directly. In the regeneration of fatty tissue there is first 
 formed an ordinary connective tissue, and subsequently the fatty 
 deposit occurs within the cells. 
 
 Regeneration of Parenchymatous Tissue. — When connective- 
 
PROGRESSIVE TISSUE-CHANGES. 113 
 
 tissue regeneration follows lesions of the parenchymatous organs 
 the cellular elements of the latter are reproduced in some measure 
 at the same time that connective-tissue hyperplasia is taking place. 
 The degree of restoration of the normal structure on the one hand 
 or of formation of connective tissue on the other hand depends 
 upon the intensity of the original cause of destruction and the 
 extent of the injury. In glandular organs reproduction of acini 
 may occur to a considerable extent, but these are usually atypical 
 in character. In some cases this atypical glandular formation 
 may become pronounced, and an adenomatous structure may 
 result. (For further details regarding this, see Adenoma.) 
 
 Regeneration may occur in practically all of the tissues of 
 the body, though in a varying degree. It has not been shown, 
 however, that the large nerve-cells are capable of proliferation, 
 though the occurrence of such cells in certain tumors suggests 
 the possibility. 
 
 METAPLASIA. 
 
 Metaplasia is the term applied to the transformation of one 
 form of tissue into another without the intervention of a stage of 
 regeneration by cellular multiplication. In many instances the 
 change consists of a transformation of the intercellular substance, 
 as, for example, when ordinary connective tissue is converted into 
 myxomatous tissue, or fibrillar connective tissues are altered to car- 
 tilaginous or even bony tissue. The cells themselves suffer second- 
 ary changes. In other cases of metaplasia the cells may be 
 primarily altered, as when ordinary connective tissue is changed 
 to fatty tissue. 
 
 CHAPTER VI. 
 
 PROGRESSIVE TISSUE=CHANGES. 
 
 This term may be used to designate pathologic conditions in 
 which there is a decided tendency to formation of new tissue. 
 
 HYPERTROPHY. 
 
 Definition. — The term hypertrophy is applied to a pathologic 
 condition in which a certain part increases beyond the normal 
 size, without marked alterations from the normal structure. The 
 term hypertrophy is frequently used loosely to designate enlarge- 
 ments of various kinds in which but one tissue of an organ is 
 increased, or in which there is deposit of abnormal exudate. Such 
 instances are not, strictly speaking, cases of hypertrophy. 
 
114 TEXT-BOOK OF PATHOLOGY. 
 
 Ktiology. — The causes of hypertrophy are quite numerous. 
 In some cases there is a distinct increase of functional demand 
 brought about in some way or other, as in the hypertrophy of the 
 muscles of athletes ; in the hypertrophy of a kidney after disease 
 or removal of its fellow ; or in the hypertrophy of a limb after 
 injury to the opposite limb. The direct increased demand for 
 work occasions the hypertrophy. Sometimes there appears to be 
 a special tendency to hypertrophy, as is evidenced by the occur- 
 rence of congenital or hereditary giant growth. Most of these, 
 however, are instances of peculiar and abnormal development, 
 rather than of hypertrophy, the latter being a condition developed 
 pathologically in parts previously well formed. Disturbances of 
 the nervous system may play a part in the development of some 
 hypertrophies, but these influences are obscure. Continued con- 
 gestion undoubtedly stimulates tissue-growth, but this element is 
 the means whereby hypertrophy is effected rather than the original 
 cause. 
 
 Pathologic Anatomy. — Parts the seat of genuine hyper- 
 trophy are uniformly increased in size. This is well seen in the 
 condition termed giant growth, or gigantism, in which the bony 
 framework and other tissues may be uniformly affected, the indi- 
 vidual being of excessive size. Sometimes local giant growth of 
 the skeleton and external tissue is observed ; as in the case of one 
 member or a single finger. This has often been found in corre- 
 sponding members on the two sides of the body. In certain cases 
 termed hypertrophy, in which this designation is more or less 
 justified, lack of uniformity in the increase of the organ or part 
 affected causes irregular increase in size. 
 
 Histologically, hypertrophy may be simple or true hypertrophy, 
 and numerical (hyperplasia). In the former there is increase in 
 the size of the individual cells ; in the latter the cells increase in 
 number, though the individuals are not excessive in size, and 
 indeed often smaller than the normal cells. In the hypertrophy 
 of the uterus during pregnancy and of the heart-muscle in com- 
 pensatory enlargement, simple hypertrophy predominates. Hyper- 
 plasia is very commonly a factor in hypertrophy of any kind, but 
 may be so strictly limited to one tissue of an organ, notably the 
 connective tissue, that the term hypertrophy is in no way appli- 
 cable. Between these extremes there are all grades of cases, in 
 many of which it is difficult to determine whether the designation 
 hypertrophy is applicable or not. In some cases the clinical desig- 
 nation hypertrophic enlargement is used, though the condition is 
 strictly one of hyperplasia of the connective tissue, with a ten- 
 dency rather to atrophy than hypertrophy of the proper substance 
 of the organ. Instances of this are hypertrophic cirrhosis of the 
 liver, some cases of hypertrophy of the heart-muscle, etc. 
 
 Pathologic Physiology.' — Hypertrophy results from an 
 
PROGRESSIVE TISSUE-CHANGES. 115 
 
 increased demand upon an organ or member, and leads to increased 
 functional capacity. Thus in the case of a diseased kidney the 
 opposite kidney may be capable of compensating for the defi- 
 ciency ; in the case of laborers the enlarged muscles may meet 
 every demand made upon them. There are occasional instances 
 of more or less genuine hypertrophy, resulting from diseased con- 
 ditions, in which the excessive functional capacity causes marked 
 disturbances, as, for example, in case of enlargement of the thy- 
 roid gland. 
 
 TUMORS. 
 
 Synonyms. — New-growth, Neoplasm, Pseudoplasm. 
 
 Definition. — In its broadest etymologic significance the term 
 tumor designates an abnormal swelling in any part of the body. 
 This definition, however, is not applicable to tumors in the ordi- 
 nary sense. Inflammatory growths and collections, such as ab- 
 scesses, hyperplastic deposits, and the like, are excluded. Path- 
 ologists, however, have always found it difficult to construct an 
 accurate definition for tumors or to draw sharp lines of separation 
 between them and the inflammatory or infectious swellings that 
 occur in various diseased conditions. An attempt to establish an 
 ultimate boundary-line is evidenced by the term autonomous new- 
 growths applied by Thoma. This name is used to designate the 
 supposed spontaneous origin of new-growths and their independence 
 of ordinary causes, such as are recognized in the production of 
 inflammatory outgrowths and the like. It cannot be said, how- 
 ever, that tumors are causeless, and in the discussion of the eti- 
 ology we shall have occasion to refer to certain definite factors 
 known to aid in their production. It is true, however, that the 
 growth of tumors is practically always out of proportion to the 
 amount of local irritation or to the severity of other factors that 
 may be conceived as playing some part in the etiology ; and in the 
 great majority of cases the causes, whatever they may be, are 
 obscure or unknown. A negative definition perhaps best suits for 
 the delimitation of this term tumor. Thus we may exclude from 
 the category of tumors all swellings in which some sufficient cause 
 is discoverable, and include the apparently causeless growths 
 among the true tumors. 
 
 Etiology. — A great number of theories have been entertained 
 to explain the causation of tumors. 
 
 Among the older writers there was a disposition to attribute 
 the occurrence of tumors to a constitutional dyscrasia, or a diseased 
 state of the fluids of the body. This explanation, however, is 
 based entirely upon speculation, and is most unsatisfactory in that 
 the original dyscrasia is as difficult to explain as the tumor sup- 
 posed to result from it. 
 
116 TEXT-BOOK OF PATHOLOGY. 
 
 Recently a Dumber of more elaborate theories have been con- 
 Structed that resemble thi> older one, in ascribing the growths to 
 some form of disturbance of vital activity and of cell-proliferation, 
 without explaining the cause of such disturbance. For example, 
 we may refer to the theory that tumors result from a retrograde 
 change in vital properties of certain cells, so that they tend toward 
 the original properties of the sperm-cells and multiply in a pur- 
 poseless and indeterminate manner. Another theory would ex- 
 plain the occurrence of new growths somewhat upon the basis of 
 infection, assuming instead of an exogenous infection with micro- 
 organisms an endogenous infection. The author of this theory 
 explains that in consequence of some thermic, chemical, or other 
 irritation certain cells may become, so to speak, infectious, assum- 
 ing the role of a sperm-cell and stimulating the adjacent cells to 
 abnormal multiplication. Such theories, however, are entirely 
 speculative, and leave the etiology as little settled as before. 
 
 Virchow strongly advocated the theory of external irritation, 
 and was able to cite numerous examples of tumors that had arisen 
 in consequence of more or less definite causes. Thus in cases of 
 carcinoma of the breast, in the epithelioma occurring on the lips 
 in pipe-smokers, and in the epithelioma of chimney-sweeps, there is 
 at times a definite history of unusual irritation, and the relation of 
 cause and effect seems easily traceable. It must be admitted, 
 however, that there is some further underlying cause which 
 renders one individual liable to tumor-growth, while another is 
 not thus predisposed, and though it is probable that some tumors 
 owe their origin to irritation as the exciting-cause, all cases can- 
 not be thus explained. 
 
 Cohnheim advanced the interesting theory that defective devel- 
 opment lies at the basis of tumor-formation. According to his 
 theory, there are frequently small errors of development leading 
 to the inclusion or misplacement of portions of the original blasto- 
 derm in the midst of tissues derived from a different layer of the 
 embryo. These inclusions or embryonic rests are independent of 
 the function of the part in which they lie, and are assumed to be 
 liable to subsequent sprouting with the consequent formation of 
 tumor-. There is evidence that this theory contains a certain 
 measure of truth, and some tumors, as, for example, certain 
 Ovarian growths, tumors of the parotid region, and others, seem to 
 originate in this way. The theory, however, is not by any means 
 universally applicable. 
 
 Recently an infectious character has been ascribed to malignant 
 or benign growths, and there is no doubt that in certain respects 
 tumors resemble infectious processes of definitely ascertained 
 kinds. Their effect upon the general health and their tendency 
 to metastasis are very significant facts. Notwithstanding this, 
 however, the proof of the infectious nature of tumors remains to 
 
PBOGEESSIVE TISSUE-CHANGES. 117 
 
 be furnished. In the case of certain sarcomata (lymphosarcoma) 
 it seems possible that bacteria are the immediate factors. In 
 carcinomata and other epithelial new-growths, as well as in sar- 
 coma, certain forms of intracellular animal parasites have been 
 described, though the nature of these bodies remains still in 
 doubt ; and recently the theory is gaining ground that blastomy- 
 cetes are active in the production of tumors. Upon the whole, 
 though it must be admitted that the infectious nature of tumors 
 is probable, the actual proof still remains wanting. In experi- 
 ments upon animals it has been possible in a few cases to demon- 
 strate inoculability. The significance of this fact, however, must 
 not be overestimated, and it certainly cannot be assumed with- 
 out further proof that this evidences the infectious nature of the 
 growths. 
 
 Predisposing Conditions. — Whatever may eventually prove to 
 be the immediate cause of tumors, it is certain that predisposing 
 causes are often of great importance. The occurrence of certain 
 forms of tumors in persons of advanced age and the occurrence 
 of tumors in other persons whose vitality has been reduced by 
 disease give evidence that a constitutional predisposition is some- 
 times requisite for the formation of the new growth. The nature 
 of this vital defect has sometimes been speculated upon, and retro- 
 grade vital metamorphosis of the cells or other like changes have 
 been assumed to occur. These theories, however, are purely specu- 
 lative. In some cases there is evidence of a family predisposition, 
 and heredity was formerly regarded as of great importance. While 
 this element cannot be entirely denied, it has certainly been over- 
 estimated. 
 
 The Structure of Tumors. — In their histologic structure 
 tumors do not differ absolutely from healthy tissues. In all cases 
 they conform more or less with the structure of some one or more 
 tissues. The cells composing tumors invariably represent some 
 one or several types of normal cells, though they may differ in 
 being larger or smaller than the normal cells, or in being of 
 embryonal or undeveloped character. In the arrangement of the 
 cells, however, there is a notable difference, and tumors may be 
 described as being atypical proliferations as far as their organic or 
 tissue arrangement is concerned. The orderly disposition of cells 
 and stroma or intercellular substance seen in the normal tissues 
 and organs is wanting, particularly in the tumors in which organic 
 arrangement is simulated. There may be in some cases entirely 
 typical glandular acini, but the relation of these to each other 
 and the absence of regularly disposed excretory ducts render the 
 tissue as a whole atypical. 
 
 The structure of tumors is always closely related to that of 
 the tissue from which it springs, a primary tumor invariably grow- 
 ing in a part in which there is some tissue at least of the type 
 
118 TEXT-BOOK OF PATHOLOGY. 
 
 simulated by the tumor, and it is from this tissue doubtless that 
 the tumor takes its origin. A connective-tissue growth invariably 
 springs from a part in which connective tissue of some form has 
 pre-existed, and epithelial growths from a part in which there has 
 been epithelium. Metaplasia, or the transformation of one variety 
 of tissue into another variety, with the production of a tumor, does 
 not occur. This statement, though applicable also to secondary 
 tumors, is sometimes difficult of demonstration from the fact that 
 the secondary growths may take origin from cells transported to 
 the scat of growth from a primary tumor, though not normally 
 found in the part in which the secondary tumor has arisen. The 
 occasional discovery of a primary tumor in a locality in which the 
 form of tissue composing the tumor does not occur may be ex- 
 plained upon the assumption (based on some actual demonstrations) 
 that embryonic rests had been deposited in the seat of tumor by 
 faulty development. 
 
 The Shape of Tumors. — This depends to a large extent 
 upon their manner of growth, their situation, and the influence of 
 surrounding parts. AVe may distinguish, first of all, between 
 circumscribed and infiltrating growths. The former may be of 
 various shapes, but are distinguished by their sharp delimitation 
 and often by the existence of a distinct capsule ; the latter are 
 indeterminate, and the extent to which they involve the healthy 
 tissues cannot be accurately determined. Circumscribed tumors 
 usually grow centrally or in an expansive manner, the new cells 
 being produced in the interior and gradually pushing the older 
 parts outward toward the surrounding tissues. The infiltrating 
 growths are eccentric in development, and may result from a 
 gradual extension of parts of the periphery of the original growth 
 or by the development of secondary nodules in the neighborhood 
 which become confluent with the original mass. Of the circum- 
 scribed growths we may distinguish small nodules of spherical or 
 ovoidal form buried in the substance of the tissue or projecting 
 from some surface as more or less hemispherical elevations. These 
 may be large or small, and the terms miliar}/, tubercular, nodular, 
 and the like are employed to designate the individual grades. 
 When a tumor projects from the surface in such a manner that the 
 projecting part i-; larger than the part between the projection and 
 the surface of the body or the organ involved, the term fun r/i [form 
 or fungoid tumor may be applied, while in the cases in which the 
 new growth is attached by a more or less narrow pedicle the name 
 polyp or polypoid tumor is applicable. Wart-like growths are 
 known as vt rruco.se or papillary tumors, and those in which a dis- 
 tinct cauliflower-form is developed are called dendritic. 
 
 The Number of Tumors. — Primary tumors are usually 
 solitary at their onset, though examples of multiple primary 
 growths, such as carcinoma involving both breasts simultaneously, 
 
PROGRESSIVE TISSUE-CHANGES. 119 
 
 or simultaneous appearance of carcinomata or sarcomata in differ- 
 ent parts of the mucous membrane or elsewhere, may be observed. 
 In these cases it is often likely that there was a single tumor at 
 the very onset, with secondary growths originating before the 
 primary growth had reached any considerable magnitude. Primary 
 benign tumors are usually solitary, but sometimes may be found 
 in considerable number, and there may be enormous numbers 
 scattered in various parts of the body. Thus in cases of multiple 
 enchondromata or multiple fibromata the number may from the 
 first be very great. 
 
 Secondary tumors are usually multiple. In most cases the 
 number of nodules found post-mortem or during life is considerable, 
 and sometimes they are so numerous that large portions of the 
 body may be literally studded with new-growths. This is seen 
 very well in the secondary sarcomatous or carcinomatous nodules 
 involving the peritoneum and the other serous surfaces, in which 
 cases the degree of involvement is simulated only by that seen in 
 miliary tuberculosis. 
 
 Pathologic Physiology. — In most cases tumors take no 
 part in the functional life of the part or of the individual. What 
 influence they may bear to the general metabolism is as yet prac- 
 tically unknown. Cases, however, are recorded in which large 
 lipomatous or other tumors have been found to suffer practically 
 no change, while the individual in whom they occurred was un- 
 dergoing progressive emaciation from lack of nutrition. That 
 there is a certain amount of function, however, in some cases is 
 shown by the fact that biliary pigment is detected in the cells in 
 certain carcinomatous tumors of the liver or abortive milk-forma- 
 tion in cancers of the breast. It may be that the want of proper 
 organic arrangement and particularly the lack of excretory ducts 
 account for the lack of function ; but whatever the cause, it is 
 certain that as a rule the functional activity is practically nil, or 
 at all events perverted. With very few exceptions it may be said 
 that tumors are entirely parasitic, living at the expense of the 
 organism and contributing nothing to its development or nutri- 
 tion. 
 
 Certain tumors disturb the general health. This result may be 
 due to secondary degenerative or inflammatory changes dependent 
 upon lack of nutrition or upon irritation and bacterial infection ; 
 or to obscure causes connected with the tumor-growth itself. The 
 progressive cachexia of carcinoma is still unexplained, though in 
 some cases hemorrhage and interference with organic function 
 play a part. 
 
 Tumors may be classified as benign or malignant. The former 
 do not affect the general health of the patient in any notable de- 
 gree, and are dangerous mainly by reason of the pressure they may 
 exert on vital structures or the secondary changes (hemorrhages, 
 
120 TEXT-BOOK OF PATHOLOGY. 
 
 softening, suppuration) to which they are liable. Malignant 
 tumors generally disturb the general health from the first, and, in 
 addition, tend to recur alter removal and spread to other parts of 
 the body (l>v direct invasion or by metastasis through the circu- 
 lation or Lymphatic channels). The terms primary and secondary 
 tumors refer to the original and the metastatic growths respectively. 
 Classification of Tumors. — No very satisfactory classifica- 
 tion is possible at the present time, and it is unlikely that any will 
 be constructed until more definite knowledge regarding the etiology 
 is obtained. The older classifications were based upon the shape, 
 the physicar properties, or the nature (whether destructive or 
 harmless) of various forms. Virchow offered a classification 
 based on the histology (histogenetic classification); others have 
 grouped tumors according to the embryologic derivation of the tis- 
 sues from which the new-growths originate or of the tissue com- 
 posing the tumor. It is perhaps wisest to attempt no classification 
 of any kind, and in the following sections I have arranged the 
 various tumors according to their histologic characters without 
 attempting to establish groups. 
 
 FIBROMA. 
 
 Definition. — A fibroma is a tumor composed of connective- 
 tissue cells and fibers resembling those seen in fibrillar tissue. 
 
 Htiology. — The causes of fibroma are as obscure as are those 
 of tumors in general. There are many facts, however, which 
 point to the importance of irritation or injury as exciting causes. 
 Among these may be mentioned the development of a peculiar 
 form (keloids) in scar-tissue and the resemblance of these tumors 
 to spontaneous fibromata, and the appearance of fibrous nodules in 
 the skin at points of friction or definite pressure or in places irri- 
 tated by discharges. 
 
 It is impossible to draw sharp lines between fibromata and 
 hyperplasias of connective tissue following irritation. In the 
 skin and superficial tissues there occur hyperplastic connective- 
 tissue processes, constituting elephantiasis, which in some cases 
 are distinctly the result of irritation and in other cases seem 
 purely spontaneous. The elephantiasis of tropical countries, often 
 due to occlusion of the lymphatic channels by filaria?, and the 
 thickening of the skin and adjacent connective tissue of the legs 
 around old ulcerations or eczematous areas, are instances where 
 distinct irritation is the cause. On the other hand, congenital 
 elephantoid conditions of the skin are seemingly spontaneous or 
 causeless, and sonic of the cases in later life have the same char- 
 acteristic. The dimise hyperplasias of the viscera, though often 
 distinctly inflammatory, may appear without adequate discover- 
 able cause, and, according to the view of some authorities, are 
 to be looked upon as diffuse fibrosis or fibromatosis, rather than 
 
PROGRESSIVE TISSUE-CHANGES. 
 
 121 
 
 as inflammatory conditions. In ordinary cases of cirrhosis of 
 the organs the connective-tissue growth is entirely diffuse, but 
 thickenings may occur in certain situations and the resemblance 
 to tumor-formation is much more striking. This is sometimes 
 the case in the liver, but particularly in the kidneys. In the 
 breast there are cases in which no dividing-line can be drawn 
 between chronic interstitial mastitis and fibroma. The micro- 
 scopic appearances are practically identical. A distinction, if any 
 can be made, is based upon the nodular character and spontaneous 
 origin in the one and the opposite conditions in the other. 
 
 Appearance. — The naked-eye appearance of fibromata is 
 usually quite characteristic. The tumor may be hard (Fig. 38) 
 
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 Fig. 38.— Hard fibroma (Warren). 
 
 or soft (Fig. 39), according as it resembles loose or dense con- 
 nective tissue in structure and according to the amount of 
 
 Fig. 39.— Soft fibroma of the subcutaneous tissue. 
 
 edematous liquid or associated myxomatous degeneration of the 
 intercellular substance. The growth is more or less rounded and 
 
122 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 usually enclosed in a distinct capsule. In the substance of organs 
 it is spherical or tuberous, and when near the surface projects more 
 or less. When it springs from a mucous or serous membrane or 
 from the skin the weight of the tumor may gradually lead to a 
 polypoid formation. Some of the fibromata of the skin are arbo- 
 rescent or dendritic in form, and keloids are frequently irregular 
 or star-like in outline. The rounded and encapsulated tumors 
 may be lobulated, though more frequently they occur in a uniform 
 mass. 
 
 Seats. — The points of origin from which fibroid tumors arise 
 are very numerous, though they always spring from pre-existing 
 connective tissue. Among some of the more common localities 
 may be mentioned the subcutaneous connective tissue, the sub- 
 mucous tissue, the periosteum of bones, tendons and tendon- 
 sheaths, and the fibrous covering of nerves. Of the internal 
 organs, the uterus, the ovaries, the kidneys, and heart-muscle are 
 the most important. Less frequently fibromata are found in the 
 serous membranes of the chest and abdomen or of the central ner- 
 vous system. The fibroids of the skin, the uterus, the nerves, 
 and the mucous membrane of the nose are the most important. 
 
 The mammary gland presents several interesting forms of in- 
 flammatory or fibromatous new-growth. First, there is a diffuse 
 form of interstitial mastitis in which the entire breast becomes 
 indurated ; this is distinctly inflammatory. In other cases nodular 
 or Lobular areas of thickening occur, and in these the evidences of 
 
 Fig. 40.— Intractmali 
 
 Perls). 
 
 inflammatory action are sometimes obscure or wholly wanting. 
 Some of these are certainly instances of true fibroma (fibroma 
 mammas nodulv/m). In still another group of cases the fibromatous 
 proliferation of the connective tissue projects into the tubules and 
 acini of the gland, pushing the epithelium before it and sometimes 
 sprouting or proliferating in polypoid form within the tubules. 
 
PROGRESSIVE TISSUE-CHANGES. 123 
 
 The gland in such cases may present a striking macroscopic appear- 
 ance on section. Numerous cystic formations may be visible with 
 projecting dendritic formations within, causing an appearance 
 somewhat like that of a section through a cauliflower (Fig. 40). 
 Microscopically the proliferations of the connective tissue between 
 the tubules and projecting within the tubules constitute the 
 characteristic features. The term intracanalicular fibroma has 
 been given to such cases. Obstruction of the tubules in certain 
 areas may lead to very marked cystic distention. Combinations 
 with sarcoma are frequent. 
 
 Structure. — The definition explains the structure of fibro- 
 mata. On section through the body of the tumor the fibrous 
 nature may be revealed by a distinct concentric or radiating 
 striation, particularly in the case of hard fibromata. The softer 
 varieties are much less likely to present this feature. The color 
 is usually gray or whitish, and may be glistening when there is 
 mucous degeneration, or yellow in the case of associated lipoma. 
 Microscopically a striking feature is the connective-tissue cell, 
 which is star-like and branching in the softer tumors, and com- 
 pressed, spindle-shaped, or elongated in the case of the hard 
 varieties. The intercellular substance is composed of a fibrillar 
 network and homogeneous or granular material traversed by thin- 
 walled blood-vessels, ofttimes having merely an endothelial coat. 
 Cavernous dilatation and rupture of the vessels may cause a dis- 
 tinct hemorrhagic appearance of the section ; but such conditions 
 are rare. 
 
 In some cases embryonal round cells may be abundant and a 
 distinct sarcomatous transformation of the tumor may occur. 
 This, however, is rare. In other instances, as has already been 
 remarked, myxomatous tissue may be conspicuous, and all grades 
 of transformation from a pure fibroma to a pure myxoma may be 
 met with, especially in the case of soft fibroma. Fatty degenera- 
 tion of the cells and lipomatous infiltration or associated lipoma 
 are also frequent. These forms, the myxomatous and lipomatous, 
 are particularly frequent in the submucous and subcutaneous con- 
 nective tissues. Calcareous degeneration occurs in large fibrom- 
 atous tumors, particularly in those of the uterus, and very rarely 
 true ossification has been reported. Less commonly association 
 of fibroma with other forms of tumor-growth is found. Among 
 these the combination of fibroma with leiomyoma is usual in the 
 uterus. 
 
 Nature. — Fibroma is essentially a benign tumor, though 
 recurrence occasionally takes place after removal, this being par- 
 ticularly the case with keloids and some of the polypoid growths 
 of mucous membranes. In some of these instances there is 
 undoubtedly a resemblance to sarcoma, if not actual sarcomatous 
 transformation. As a rule, fibroid tumors are destructive only in 
 
124 
 
 TEXT-BOOK OF PATHOLOGY 
 
 so far as they are capable of producing mechanical injury by press- 
 ure. The growth of the tumors is usually exceedingly slow. 
 
 MYXOMA. 
 
 Definition. — Myxoma is a tumor composed of connective- 
 tissue cells and an intercellular substance containing mucoid 
 material in more or less abundance. The gelatinous substance of 
 Wharton in the umbilical cord and the vitreous humor of the eye 
 are normal types which myxomata resemble in their structure. 
 
 Etiology. — The causes and the nature of myxomata are 
 practically the same as those of fibroma, and intermediate forms 
 make it difficult to draw a sharp line between the two. 
 
 Appearance. — A typical myxoma is a soft, more or less 
 flabby growth enclosed by a capsule, and having a rounded out- 
 line. It may project from the surface of the body or of an organ 
 as a hemispherical elevation, or may hang by a narrowed pedicle 
 in the form of a distinct polyp. The latter is frequent in the 
 mucous membranes, but may occur in the skin as well. Some- 
 times the tumor is lobulated, and the lobules may be visible or 
 may be easily felt. Occasionally lipomatous growths are diffuse, 
 having no capsule and marked by no definite limits. 
 
 Seats. — Among the common situations are the subcutaneous 
 and submucous tissues and the connective tissues of certain organs, 
 notably the mammary glands. They may occur along the course 
 of nerves, in the brain or the spinal cord. The tumor may be 
 
 V : . 
 
 ^^ 
 
 .. ^^ 
 
 ■ 1 K 
 
 • w 
 
 
 
 Fig. 41.— Myxoma, showing stellate cells separated by a gelatinous (mucoid) 
 intercellular material. 
 
 solitary, or, like fibroma, maybe met with in numbers. Congeni- 
 tal myxoma has frequently been found. 
 
 Structure. — Microscopically the characteristic features are 
 stellate or spindle-shaped connective-tissue cells which lie within 
 
PROGRESSIVE TISSUE-CHANGES. 125 
 
 a matrix of myxomatous material (Fig. 41). The latter is homo- 
 geneous or slightly granular, and somewhat refractive to the light, 
 giving the surface a glistening quality. The cells themselves may 
 be entirely normal young connective-tissue cells, or they may present 
 evidences of fatty degeneration. Round granulation-tissue cells 
 are met with in some instances, either scattered through the tumor 
 or in certain areas, and may be so abundant as to justify the term 
 myxosarcoma. The vascular supply is usually poor, and the 
 blood-vessels resemble those of fibroma in being only partially 
 developed. Association with fibroma and lipoma is frequent. 
 Cartilaginous tissue may be found in myxomatous tumors of the 
 parotid gland or testicle, and in these cases the myxomatous 
 portion is rather an association than a degeneration of the original 
 chondroma. Myxomatous degeneration of chondromata, osteo- 
 mata, fibromata, and sarcomata is, however, a frequent occurrence. 
 Nature. — Myxoma is benign like fibroma, but recurrence is 
 not infrequently observed, and in a few instances metastasis has 
 been reported. It is difficult, however, to assert the absence of 
 sarcomatous change in these instances. The growth of myxomata 
 is slow. 
 
 LIPOMA. 
 
 Definition. — A lipoma is a tumor composed of fatty tissue 
 like that of the normal subcutaneous tissue. The epiploic -ap- 
 pendages of the intestines are the normal type which lipomata 
 resemble. 
 
 Etiology. — There seems to be a tendency, consisting perhaps 
 in some derangement of the trophic nervous system, to the growth 
 of these tumors. It is difficult at times to draw a sharp line be- 
 tween circumscribed lipomata and diffuse fatty growth. Localized 
 fatty or myxolipomatous accumulations in myxedema and a curious 
 and apparently causeless deposit of fatty tissue sometimes observed 
 in the subcutaneous tissue of the neck in men, represent the bor- 
 der-line between lipomata and ordinary obesity. Some individuals 
 have a marked liability to constant overgrowth of fat in different 
 parts of the body, and the term " lipomatosis " is not inapplicable. 
 This fatty growth does not apparently depend upon the character 
 or quantity of food, nor even upon sedentary life in some cases, 
 but rather on an obscure tendency to adipose accumulation. 
 Traumatism seems to play no part, though fatty infiltrations are 
 prone to occur around areas of injury or disease, and in degenerated 
 organs. 
 
 Appearance. — Lipomata are usually circumscribed and en- 
 capsulated tumors having a lobulated character, the latter being 
 due to septa of connective tissue. On the surface of the body 
 they appear as somewhat hemispherical elevations which may 
 reach enormous proportions. Earely they become polypoid. In 
 
126 TEXT-BOOK OF PATHOLOGY. 
 
 the interior of the body, a>, for example, when they arise in 
 the submucous or subserous connective tissue, they are very 
 frequently, though not always, polypoid. Sometimes they be- 
 come detached and may be retained in one of the cavities of 
 the body as free bodies. On section the appearance is that of 
 fatty tissue, though in some cases it is more firm from the associa- 
 tion of fibrous tissue, and in other cases less firm from the nature 
 of the fatty tissue itself or from associated myxomatous change. 
 Lipomata may be solitary tumors, or there may be many. As a 
 rule, they appear in adult years or middle life, but congenital 
 lipomata arc not very rare ; and occasionally they are found to 
 begin in childhood. 
 
 Seats. — Among the situations in which lipomata occur the most 
 common are the subcutaneous fatty tissue of the back, shoulders, 
 buttocks, or limbs, the submucous, and the subserous tissues. 
 They may arise either in the normal fatty tissue or in connective 
 tissues in which fat is not normally present. Some authors, how- 
 ever, deny the possibility of lipomata arising excepting from pre- 
 existing fatty tissue. Of the organs, the mammary gland and the 
 kidney are most frequently involved. 
 
 Structure. — Microscopically lipomatous tumors resemble the 
 normal fat. It is notable that the cells are larger — that is, con- 
 tain more oil — than the normal fat-cells, and this is strikingly the 
 case in some instances, but is not always demonstrable. The 
 vascular supply is about the same as in normal fat, though occa- 
 sionally large vessels with thin walls are seen. Associated myx- 
 omatous or fibrous change may cause a variation of the microscopic 
 appearance. 
 
 Lipomata may undergo softening from necrosis, but more fre- 
 quently become calcareous in part or completely. 
 
 Nature. — This is the most benign form of- tumors. Recur- 
 rence after more or less complete removal does, however, at times 
 occur. A lipoma is dangerous only from its weight or position. 
 It docs not contribute to the support of the system in case of 
 starvation. 
 
 XANTHOMA. 
 
 Definition. — This term is applied to two possibly distinct though similar 
 forms of new growth. The xanthoma vuigare occurs most frequently in 
 the eyelids and may be confined to that situation. The growth appears in 
 the form of flat elevations of a yellow color. Generalized xanthoma begin- 
 ning about the eyes is loss frequent. Xanthoma diabeticorum is a similar 
 affection of diabetic patients. It occurs at a more advanced age, is more 
 distinctly inflammatory, the masses are more rounded, and the eyelids and 
 face are rarely affected. 
 
 Structure. — The histology of xanthoma is that of modified fatty tissue. 
 It resembles embryonal adipose tissue, and there is usually more or less 
 round-cell infiltration as well. Some authors regard the latter as a tendency 
 to sarcomatous change; others look upon it as inflammatory. 
 
 Nature. — Xanthoma is eminently benign. The diabetic form is subject 
 
PROGRESSIVE TISSUE-CHANGES. 127 
 
 to sudden and apparently causeless involution. The ordinary form may 
 similarly subside, though much less commonly. 
 
 CHONDROMA. 
 
 Definition. — A chondroma is a tumor composed largely or 
 entirely of cartilage. It is difficult to draw a sharp line between 
 outgrowths of cartilage from existing cartilage or bone due to irri- 
 tation from definite and independent tumor-like growths. A 
 group of cases of intermediary character is that including carti- 
 laginous nodules formed in tendons of muscles subjected to fre- 
 quent irritations, as in the deltoid muscles in soldiers carrying 
 heavy arms, and in the adductor muscles of the thigh in horse- 
 back riders. In these cases normal connective tissue seems to be 
 directly transformed into cartilage, though the influence of irrita- 
 tion is undoubted. 
 
 Etiology. — A congenital disposition, sometimes hereditary, is 
 unquestionably present in certain cases. Virchow maintained that 
 chondromata often spring from remnants or islands of cartilage 
 left in abnormal situations, as in the midst of bone, as the result 
 of imperfect fetal development. The same explanation woiild 
 account for parotid chondromata on the assumption that parts of 
 the branchial arches are misplaced and remain in the substance of 
 the parotid gland. 
 
 Irritation has been referred to. Direct traumatism is some- 
 times the cause of cartilaginous outgrowths from bone, particularly 
 when fractures have occurred. 
 
 Appearance. — Two distinct forms may be considered, and 
 these are somewhat different in appearance. They are (1) carti- 
 laginous outgrowths, ecchondroses or ecchondromata, and (2) 
 independent cartilaginous tumors, or chondromata proper. 
 
 Ecchondromata present themselves as rounded or somewhat 
 'irregular outgrowths from bones or cartilages. Sometimes they 
 are wart-like in form and may occur in rows or groups. They 
 may be firmly attached, or may be loosely united to the bone. 
 The most frequent and the most characteristic are the outgrowths 
 in the articular cartilage occurring in chronic arthritis, particularly 
 in rheumatoid arthritis. Occasionally they become detached after 
 their formation, and in the joints may thus become free bodies. 
 The large chondromata are generally distinctly lobular or irregular 
 in outline. 
 
 Chondromata springing from the inner surface of bones (pos- 
 'sibly originating from the marrow itself) may grow uniformly by 
 repeated or constant proliferation and lead to a globular swelling 
 of the affected bone (Fig. 42). The true bony covering becomes 
 more and more thin until it may actually perforate. 
 
 The true chondromata are usually rounded bodies ; they pre- 
 
128 TEXT-BOOK OF PATHOLOGY. 
 
 sent Lobular irregularity when they reach considerable size, the 
 Lobules being separated by connective tissue. 
 
 All forms arc hard, though secondary softening may occur. 
 
 Fig. 42.— Chondroma of the thumb (Warren). 
 
 In cases in which association of mucous, sarcomatous, or other 
 soft tissue is present the consistency is correspondingly less. In 
 some cases central softening leads to cystic formation. The 
 liquid in the cyst is more or less turbid and occasionally san- 
 guinolent. 
 
 Seats. — Ecchondroses and chondromata, for the most part, 
 take their origin from bone, cartilage, or periosteum. In some 
 cases, however, they originate in connective tissue, as that of the 
 tendons, by a process of cartilaginous metaplasia. Cartilage- 
 tumors are nut with in some of the glandular organs, notably the 
 parotid gland, testicle, and ovary; and rarely they occur in the 
 Lungs, especially at the root and springing from the peribronchial 
 cartilages. 
 
 Ecchondroses are most frequent about the long bones, as those 
 of the extremities, and particularly at the epiphyseal attachments. 
 They are not at all infrequent, and may reach considerable propor- 
 tions in these situations. Situations of great clinical importance 
 are the interpubic and occipitosphenoidal junctions. In the former 
 situation ecchondroses projecting inward may interfere seriously 
 with labor, and in the latter place cartilaginous outgrowths may 
 penetrate the dura and exercise injurious compression on the brain. 
 Allusion has been made to the ecchondroses of the joints in 
 arthritis. 
 
 Chondromata proper may occur in the neighborhood of bones, 
 in the muscles and tendons near their bony attachments, and in 
 the organs mentioned, but in the last situation are rarely pure, 
 myxoma being the most frequent associate. 
 
 Structure. — Chondromata resemble hyaline, fibrous, or elastic 
 
PROGRESSIVE TISSUE-CHANGES. 129 
 
 cartilage, the first-named being much the most frequent. The 
 tissue differs from normal cartilage in the fact that the cells are 
 frequently without capsules and are much less regularly arranged 
 (Fig. 43). The intercellular substance is more abundant and is 
 
 * §y> ^&< v - 
 
 : K ^W - .-.■•--- .. (-. 
 
 Fig. 43.— Chondroma of the hyaline type. 
 
 frequently gelatinous, mucoid, or fibrous, and not rarely the differ- 
 ent types of cartilage occur within narrow limits. Association 
 with myxoma and sarcoma, or both, is common, especially in the 
 parotid and testicles, the proportion of the several ingredients 
 varying greatly. Tumors of this kind are spoken of as mixed 
 tumors. Calcification and true ossification are not infrequent, par- 
 ticularly in cartilage-tumors intimately connected with bone. The 
 term osteochondroma is applied in such cases. The name osteoid- 
 chondroma is applied to chondromata in which the intercellular 
 substance is trabecular in arrangement, suggesting bone-structure, 
 but in which actual ossification has not occurred. Such growths 
 are met with about the bones and, as a rule, spring from the 
 periosteum. 
 
 Degenerative changes are frequent. Myxomatous degenera- 
 tion may occur, though myxoma is more frequent as an association 
 than as a degeneration. Softening may occur in the center of the 
 mass, and may lead to cyst-formation, this being particularly com- 
 mon in the myxochondromata. Growths of this kind are fre- 
 quently quite vascular and hemorrhages into the cysts may occur. 
 Eventually such cases may show scarcely any cartilage-cells, a few 
 being perhaps detected in some part of the cyst-wall. A single 
 hard lump may be left at one side of the cyst, the rest of the 
 tumor having softened. 
 
 Nature. — Chondromata are essentially benign, and are danger- 
 
130 TEXT-BOOK OF PATHOLOGY. 
 
 ous only through the pressure they exert. Removal of a part may 
 have :i beneficial influence in causing calcification of the remainder. 
 Metastasis may undoubtedly occur in pure chondromata through 
 transportation of particles in the circulation. Such cartilaginous 
 emboli have often been demonstrated. The secondary growths are 
 most frequent in the lungs. Metastatic chondromata are, however, 
 more frequently chondrosarcomata than pure chondromata. 
 
 OSTEOMA. 
 
 Definition. — An osteoma is a tumor composed of osseous 
 tissue. Osteomata are closely allied to cartilaginous tumors, and 
 frequently transformations occur. 
 
 Etiology. — The same difficulty is experienced in distin- 
 guishing inflammatory outgrowths or exostoses from true bony 
 tumors, as in the case of cartilaginous growths. Enlargement 
 
 Fig. 44.— Exostoses of the elbow-joint. 
 
 of the facial hones in leontiasis ossea, of the bones of the extrem- 
 ities in acromegaly and hypertrophic pulmonary osteoarthrop- 
 athy, and ossifications of the muscles in myositis ossificans, are 
 instances of border-line conditions separating true tumors from 
 inflammatory hyperostoses. Irritation and traumatism undoubt- 
 edly play a part in the etiology, even in neoplasms unattached to 
 the hone, ;md in the case of bony outgrowths injury is generally 
 the immediate cause. An underlying predisposition undoubtedly 
 exists, and explains the occurrence of congenital multiple bony 
 tumors. 
 
 Appearance. — Two forms may be distinguished, as in the case 
 of chondromata : (1) outgrowths or exostoses and osteophytes, and 
 (2) the osteomata proper, or heteroplastic osteomata. Exostoses 
 and osteophytes are distinguished one from the other by their 
 shape and appearance rather than by any essential difference. The 
 former are direct outgrowths of more or less wart-like character: the 
 
PROGRESSIVE TISSUE-CHANGES. 
 
 131 
 
 Fig. 45.— Osteoma of the lower jaw 
 (Warren). 
 
 latter are more extensive and present the appearance of bony deposits 
 upon bones, and are less closely attached (Fig. 44). In both forms 
 the surface of the growth is irregular, nodulated, or wart-like 
 (Fig. 45). The consistency is that of bone, and the size varies 
 from that of small outgrowths to 
 masses as large as a fist. On 
 section two forms may be dis- 
 tinguished ; the hard or osteoma 
 durum, and the soft or osteoma 
 spongiosum. Sometimes the sub- 
 stance of the tumor is exceedingly 
 dense, and the term osteoma ebur- 
 neum is applied. 
 
 The heteroplastic osteomata, or 
 those separated from the bone, are 
 more rounded and, when of con- 
 siderable size, usually nodulated 
 and lobulated. In the serous 
 membranes they occur as flat 
 bony plates. 
 
 Seats. — Osteomata spring from the bone or cartilage, or from 
 connective tissue near the bones. More rarely they arise in other 
 connective tissues, in the serous membranes, or in certain organs, 
 notably the testicle and parotid gland. 
 
 Osteomata connected with bones are most frequent about the 
 epiphyses, at the attachments of muscles, or at the seat of old 
 fractures from which abundant callous has been deposited. The 
 skull-bones may be aifected on the outer or inner surface, and 
 often an elevation is noted without and within at the same spot. 
 A form of clinical importance is that in which exostoses occur on 
 the inner aspect of the metatarsal bone of the great toe from com- 
 pression of tight shoes. In the maxillary bones osteomata may 
 originate about the roots of malformed teeth. In cases of accumu- 
 lation of cement-substance beginning at the neck of the tooth the 
 term dental osteoma is applied, and these are strictly comparable 
 to osteomata. In cases in which proliferation of the dental pulp 
 has occurred the term odontoma is applicable, and the tumor is not 
 of osseous character. The bony growths sometimes seen in the 
 serous surfaces nearly always arise in areas in which there has 
 been thickening from chronic inflammation. They are most fre- 
 quent in the dura mater of the brain, particularly the falx cerebri ; 
 though the membranes of the cord, the pleura, or pericardium may 
 be involved. 
 
 Structure. — Microscopically osteomata resemble more or less 
 accurately bone-tissue. They vary, however, in different areas, 
 and mixtures of cartilage with bony tissue are frequent. Second- 
 ary degenerative changes (softening) may occur and association 
 
132 TEXT-BOOK OF PATHOLOGY. 
 
 ■with tumors of other character are not infrequent (chondroma, 
 myxoma, fibroma, sarcoma). 
 
 Nature. — These growths are eminently benign, do not recur, 
 and do not give metastasis. Their situation sometimes makes 
 them troublesome or dangerous. 
 
 LYMPHANGIOMA. 
 
 A lymphangioma is a tumor composed of dilated lymph-vessels 
 or lymph-spaces; more frequently the latter. It is difficult to 
 separate dilatations of lymphatic channels due to obstruction from 
 hyperplastic processes. Congenital enlargements of certain parts 
 arc met with which seem entirely dependent upon the abnormal 
 development of the lymph-spaces. These constitute the condition 
 called elephantiasis congenita mollis, in which the subcutaneous 
 tissues arc boggy or edematous, and even distinct cystic formations 
 occur. Congenital cystic hygroma is an instance of dilatation of 
 the lymph-spaces. Congenital enlargement of the tongue, termed 
 macroglossia ; of the lips, maerocheilia ; and of the skin, rwetous 
 lymphaticus ; are other instances of the same process. In all of 
 these, in addition to the dilatation of the lymphatic spaces, a 
 marked proliferation of the connective tissues as well as the 
 muscle (in the case of the tongue) is striking ; but the process in 
 all probability originates as a dilatation of the lymph-spaces. 
 The terms lymphangioma cavernosum and eavemoma lymphaticum 
 have been suggested for these cases of dilatation of the lymph- 
 spaces. On staining with silver-salts the endothelial lining of the 
 spaces may be readily demonstrated. Actual enlargement and 
 varicosity of existing lymphatic vessels may occur, but is ex- 
 tremely rare in the form of circumscribed growths ; it is met with 
 more frequently in association with general processes, such as ele- 
 phantiasis. The bursting of dilated lymphatics may lead to 
 lymphorrhea or external discharge of lymph when the process 
 involves the skin, or to effusions of lymphatic character when the 
 serous cavities are involved. Chylous pericarditis, pleuritis, and 
 ascites are thus produced. Rupture of dilated lymphatics along 
 the urinary tract (kidney or bladder) occasions chyluria. Lymph- 
 angioma is a benign process in the pathologic sense. 
 
 HEMANGIOMA. 
 
 Definition. — An hemangioma, or angioma as it is more fre- 
 quently called, is a tumor-like formation composed principally of 
 blood-vessels. Strictly speaking, many of these are not tumors, 
 being merely localized dilatations and elongations of pre-existing 
 blood-vessels. Some, however, represent actual prolife rations. 
 Two varieties may be described, that in which the blood-vessels 
 are merely distended [angioma tdeangiectaticum), and that in which 
 
PROGRESSIVE TISSUE-CHANGES. 133 
 
 there are enlarged spaces lined with endothelium (angioma cavern- 
 osum or cavernoma). In many tumors the blood-vessels are some- 
 what enlarged ; these are spoken of as telangiectatic. 
 
 Etiology. — Congenital malformation certainly plays some 
 part in certain cases, as the frequency of hemangiomata in the 
 new-born and particularly at the junction of the branchial arches 
 would indicate. Injury, however, and mechanical causes gener- 
 ally also play a part, and pre-existing disease, particularly fibroid 
 inflammatory processes, may contribute to the subsequent dilata- 
 tion and proliferation of the vessels (see below). 
 
 Appearance and Seats. — The angioma teleangiectaticum 
 may involve only the arterioles and capillaries, and in this case a 
 bright-red color is observed. The tumor appears as a spot on the 
 surface of the skin, more or less sharply outlined from the sur- 
 rounding tissue. It is not elevated and has the same consistency 
 as the healthy parts. Usually it occurs as a multiple condition, 
 and the larger are often surrounded by smaller spots. The skin 
 is the favorite seat ; but the subcutaneous tissue and sometimes 
 the mucous membranes are involved. Less commonly the veins 
 are implicated, when a dark-red color is observed (port-wine- 
 stains). 
 
 If a circumscribed portion of the circulation is uniformly in- 
 volved, the vessels thicken and elongate, and a peculiar form of 
 hemangioma results. In these cases the arteries are greatly thick- 
 ened and tortuous, and form bunches under the skin, suggesting to 
 palpation a bundle of earth-worms ; while the surface of the skin 
 presents peculiar irregular elevations without of necessity any 
 change of color (aneurysma racemosum seu cirsoideum). This is 
 not infrequent in the scalp. A similar condition of the vessels is 
 observed in the varicosity of the legs, labia, or other parts. It is 
 most frequent in the hemorrhoidal veins, constituting the ordinary 
 hemorrhoids. (These conditions will be more fully described in 
 discussing the diseases of the vessels.) 
 
 Cavernous angiomata present themselves as more distinctly 
 tumor-like formations of dark venous color, involving the skin or 
 subcutaneous tissues, the retrobulbar tissue of the eye, the mucous 
 membranes of the nose or pharynx, and certain organs, as the 
 mammse, the kidney, the spleen, but particularly the liver. Like 
 the other variety, they may be congenital, but more frequently 
 arise in later life, especially that of the liver, which is most com- 
 mon in old persons. The appearance is that of a more circum- 
 scribed tumor, sometimes showing a distinct capsule and varying 
 in consistency with the degree of distention of the blood-spaces. 
 In the skin it projects slightly from the surface (naevus promi- 
 nens) ; in the liver the tumor does not project. 
 
 Structure. — The definition explains the structure in general. 
 The blood-vessels of teleangiectatic angiomata may be simply di- 
 
134 TEXT-BOOK OF PATHOLOGY. 
 
 lated capillaries with a lining of endothelium and a fibrous outer 
 coating. More commonly the vessels are considerably thickened 
 and held together by a reticular connective tissue. In rare in- 
 stances the vessels arc so closely packed and the walls so thickened 
 that when the blood is removed the appearance is not unlike that of 
 the tubules of a sweat-gland. The cavernous angiomata present 
 large spaces lined with endothelial cells (Fig. 46). Between these 
 
 Fig. 1G.— Cavernous angioma (Warren). 
 
 spaces arc parallel fibers of connective tissue which form the frame- 
 work of the tumor. In cases involving the liver the proper sub- 
 stance of this organ disappears completely, leaving only anastomos- 
 ing spaces with a fibrous framework. Virchow taught that the 
 fibrous process was primary, and by traction and pressure gradually 
 induced dilatation of the vessels and atrophy of the liver-substance. 
 Some of the more recent writers believe that the dilatation of the 
 vessels is the primary condition. The capsule sometimes found 
 surrounding the cavernous angioma is certainly a secondary 
 formation. 
 
 Angiomata of the skin may enclose the hair-follicles and 
 sweat-glands; those of the subcutaneous tissue frequently show 
 areas rich in fatty tissue (angiolipoma) j secondary angiomatous 
 change of tumors is probably the result of dilatation of the pre- 
 existing or new-formed vessels. Sometimes secondary change 
 may occur in the connective tissue of the vessels of an angioma, 
 
PROGRESSIVE TISSUE-CHANGES. 135 
 
 as in the plexiform angiosarcornata, in which the blood-vessels are 
 surrounded by ensheathing sarcoma-cells (see Fig. 46). Certain 
 cylindromata have the same origin. 
 
 Nature. — Angioma is essentially benign, and may continue 
 through life without enlarging. Hemorrhage and inflammatory 
 or necrotic changes are its dangerous consequences. 
 
 LYMPHADENOMA. 
 
 Definition. — This term is here used to designate a more or 
 less malignant form of new-growth affecting the lymphatic glands 
 or other lymphadenoid tissues, and having the structure of lym- 
 phatic tissue. The lymphadenomata may be considered as forms 
 of sarcoma. The term lymphosarcoma is sometimes applied, but 
 is more appropriately given to growths of more definite sarcom- 
 atous nature, but having the reticulated structure of lymphad- 
 enoid tissue. Other names applied to lymphadenoma are malig- 
 nant lymphoma and lymphoma. 
 
 Etiology. — It is exceedingly difficult to establish the limita- 
 tions of the term, and especially to decide whether or not certain 
 cases in which definite etiologic factors have been discovered 
 belong to the group under consideration or should be separated. 
 There are cases of infectious enlargement of the glands and trau- 
 matic swellings that cannot be distinguished histologically. In 
 some cases even the clinical course is the same and a separation 
 seems impossible. For example, the glands in a number of 
 instances of Hodgkin's disease (as far as the clinician can es- 
 tablish this diagnosis) have been found to contain tubercle-bacilli. 
 We must conclude that general lymphatic tuberculosis may occur 
 in the clinical form of Hodgkin's disease, but cannot assert that 
 all cases of the latter are tuberculous. In other cases various 
 micrococci and bacilli have been found, but none of these organ- 
 isms have been shown to be specific. In a few instances bodies re- 
 sembling protozoa have been discovered. 
 
 Appearance and Seats. — Lymphadenomata present them- 
 selves as more or less considerable enlargements of the lymphatic 
 glands of a single group or more commonly of a number of groups 
 in different parts of the body. Ail of the glands of the group 
 may be involved, or only a few. The individual glands retain 
 their shape, as there is usually no tendency to extension beyond 
 the capsule of the gland. In exceptional cases, however, the proc- 
 ess is of a more infiltrating kind and the capsule is penetrated or 
 destroyed. These instances furnish a connecting link between the 
 lymphadenomata confined within the capsule of the glands and the 
 true lymphosarcomata, tumors of lymphadenoid structure occur- 
 ring in tissue normally devoid of lymphoid elements. 
 
 Lymphadenomata may be soft or hard, according to the amount 
 
136 
 
 TEXT-BOOK OF PATHOLOGY 
 
 of connective tissue and the denseness of the cellular infiltration 
 and proliferation. On section the tumors are found to be grayish 
 or whitish in appearance, and exceptionally may show slight areas 
 of necrosis or softening. Extensive softening is exceedingly rare. 
 The individual glands of the group may he clearly distinct, or may 
 be fused together by interglandular connective-tissue overgrowth 
 or by the penetration of the lymphadenomatous process through 
 the capsule. 
 
 When superficial lymphatic groups are involved tumors of 
 various sizes are produced, and project as knobby or rounded en- 
 largements beneath the skin. The latter is freely movable over the 
 tumor unless the growth has penetrated the capsule or secondary 
 inflammatory changes have occurred. In the case of internal 
 
 Fi<;. 47— Lymphadenoma (lymphosarcoma) probably originating in remnant of thymus 
 gland: the tumor covered the upper part of the heart like a hood. The illustration 
 shows the tumor turned upward and exposing the pericardium on its under surface. 
 
 glands large intrathoracic or abdominal growths may be formed, 
 and may exercise destructive compression of vital parts. 
 
 Similar lymphadenomatous growths may spring from the lym- 
 phatic tissues of the gastro-intestinal tract — tonsils, lymphatic 
 follicles of gastric and intestinal mucosa. 
 
 Sometimes the primary growth seems to begin in the thymus 
 gland or its remnant ( Fig. 47). Tumors of considerable size are 
 produced in these eases, and their origin is recognized by their shape 
 [two lateral parts united l>v a sort of isthmus) and by the absence 
 
PROGRESSIVE TISSUE-CHANGES. 137 
 
 of the appearance of a conglomeration of glands. In these cases 
 the adjacent glands, and later more distant groups, are involved. 
 Lymphadenoma may be confined to the glands, but frequently 
 extends to the solid organs by metastasis. The spleen, liver, and 
 kidneys are the organs most frequently affected. They become 
 enlarged and indurated, and on section show light-colored areas of 
 lymphadenoid tissue. Similar " lymphoid infiltration " may be 
 seen in the heart, lungs, or other parts. 
 
 Lymphadenoma may affect the bone-marrow secondarily and 
 perhaps primarily. (Reference will be made to this under the title 
 Myeloma.) Sometimes the tumors have a yellow or green color and 
 are called chloromata (q. v.). 
 
 Structure. — The finer structure of lymphadenomata is pre- 
 cisely that of lymphadenoid tissues. There is a reticulum, more 
 or less pronounced, formed by branching cells which are united by 
 their prolonged extremities. In the meshes of this lie round cells 
 containing large rounded nuclei. The cells are perhaps less 
 uniform in size than those of normal lymphatic glands and large 
 cells are more abundant. The secondary lymphomatous infiltra- 
 tions of the spleen, liver, etc., have similar structure, but the 
 reticulum is less distinct. Sometimes this may not be apparent in 
 the primary growths ; in such instances the tumor is likely to be 
 considered a simple round-celled sarcoma. 
 
 Nature. — Lymphadenoma is variably malignant. In a small 
 proportion of the cases this malignancy is of local character — that 
 is, the growth tends to invade the neighboring parts. In most 
 instances there is rather a tendency to general involvement of the 
 lymphatic system, Math metastatic deposits in various organs. To 
 cases of this kind the terms Hodgkin's disease, pseudoleukemia, 
 and adenia have been given. These cases present themselves in 
 the form of a progressive anemia (lymphatic anemia — Wilks), often 
 with irregularly relapsing fever (chronic relapsing fever — Epstein), 
 and especially with lymphadenomatous tumors in the superficial or 
 deep lymphatic groups (axillary, cervical, inguinal, mediastinal, or 
 abdominal). The disease progresses more or less rapidly, and 
 terminates in death from cachexia and exhaustion in from one to 
 three years. Occasionally the course is rapid, repeated hemor- 
 rhages or purpura may occur, and a fatal termination is reached in 
 a few weeks or months. The whole course of the disease is sug- 
 gestive of an infectious process. 
 
 The relation of cases like the above and leukemia is certainly 
 very close. The glandular tumors and the secondary changes in 
 the organs are the same, excepting that the lymphatic glands are 
 more prominently involved in ordinary lymphadenoma. The only 
 striking difference is found in the blood. In leukemia there is 
 marked and characteristic leukocytosis ; in the other condition this 
 is absent. Many cases have, however, been observed in which 
 
138 TEXT-BOOK OF PATHOLOGY. 
 
 Hodgkin's disease has become leukemia ; and some authors do not 
 hesitate to speak of the two diseases as identical and representing 
 merely two stages of a common affection. According to this view, 
 we might classify cases as leukemic or aleukemic lymphadenoma. 
 This view seems to me well grounded. 
 
 The blood in aleukemic cases shows more or less pronounced 
 reduction in the number of red cells, and a normal, reduced, occa- 
 sionally a moderately increased, proportion of leukocytes. The 
 mononuclear leukocytes are sometimes in relative excess. In 
 acute eases nucleated red cells may be found. 
 
 The causes and nature of the irregular fever are uncertain. It 
 may be due to an infectious cause, or may be the result of breaking 
 up of leukocytes and liberation of ferments. 
 
 SARCOMA. 
 
 Definition. — The term sarcoma is applied to tumors composed 
 of connective-tissue cells with very little intercellular substance. 
 It is often said that sarcoma-cells resemble those of embryonal 
 connective tissue ; more properly speaking, they may be likened 
 to the ordinary connective-tissue cell falling short of complete 
 development. There is little tendency in sarcoma to the forma- 
 tion of fibrous intercellular substance, but a great tendency to 
 continuous cell-proliferation. 
 
 Etiology. — Of all the tumors sarcoma furnishes the best 
 ground for Cohnheim's theory. Its frequent occurrence in young 
 persons, the relation of melanosarcomata to congenital pigment- 
 spots of the skin, and the sarcomatous mixed tumors of the parotid 
 and testis were cited by Cohnheim among the evidences pointing 
 to a congenital origin. Traumatism and inflammation certainly 
 play sonic part, either in stimulating sudden growth of a latent 
 sarcoma or in developing a lesion from which sarcoma springs. 
 The parasitic theory has gained many adherents in recent years. 
 The resemblance to tubercle is very striking in certain cases and 
 the peculiar dissemination is most suggestive. No specific form of 
 bacteria, however, has been demonstrated, and experiments at im- 
 plantation of the disease in animals have been unsatisfactory (von 
 Eiselberg, Duplay and Cazin). Recently intracellular protozoan 
 organisms have been described, but whether these are really organ- 
 isms or cellular degenerations is doubtful. In some cases the 
 structures described arc certainly nuclear degenerations. It is 
 do1 improbable that lymphosarcomata are due to the action of 
 bacteria. 
 
 In connection with the supposed infectious nature of sarcoma it is of 
 interest to note that a relationship has been observed between syphilis and 
 sarcoma. This is based on the fact that some cases disappear under anti- 
 syphilitic treatment. 
 
PROGRESSIVE TISSUE-CHANGES. 139 
 
 Appearances. — Sarcomata are generally more or less rounded 
 tumors often enclosed by capsule ; they may, however, be irregu- 
 lar, infiltrating, and therefore unencapsulated. Some forms appear 
 on surfaces, spreading as flat elevations more or less irregular in out- 
 line. The consistency is soft or hard according to the number of 
 cells and the amount of intercellular substance, or according to 
 the kind and amount of associated tissue (myxomatous, chondrom- 
 atous). Typical sarcoma, as the name implies (<xa/?£, flesh), is flesh- 
 like in consistency, and frequently on section the color is pink or 
 of a flesh tint. Many of the sarcomata, however, are quite white 
 or gray, and a whitish liquid exudes from the surface on section. 
 
 Dilatation of the blood-vessels may cause a decidedly hemor- 
 rhagic appearance, and actual hemorrhages may take place, causing 
 
 Fig. 48.— Secondarx sarcomata of the lung: the primary growth was attached to the 
 pleura. 
 
 blood-cysts or, subsequently, serous cysts. Other degenerative 
 changes, such as necrosis, mucoid change, and simple liquefaction- 
 necrosis, may render sarcomata soft and often cystic. Sarcomata of 
 glandular organs like the breast may present a cystic appearance 
 in consequence of compression of the glandular ducts and acini 
 and consequent dilatation. 
 
 Angiosarcomata (the variety in which sarcoma-cells spring 
 
140 TEXT-BOOK OF PATHOLOGY, 
 
 from the adventitia of blood-vessels) present themselves as more 
 or less irregular growths, frequently flattened and branching when 
 the surfaces of organs are involved. 
 
 Secondary sarcomata are nodular in character and nearly al- 
 ways present a capsule if the size is at all 'considerable (Fig. 48). 
 They arc usually white or pinkish ; on section rather firm, but 
 with a tendency to central necrosis or softening. In some cases 
 almost every part of the body may be studded with minute white 
 spots scarcely distinguishable from miliary tubercles. This con- 
 dition is called sarcomatous. 
 
 Seats. — Sarcomata spring from pre-existing connective tis- 
 sues, such as the subcutaneous, intermuscular, periosteal, or tendi- 
 dous tissues ; bone, cartilage, fat, lymphatic glands, the submucous 
 and serous surfaces. They may arise in the internal organs : kid- 
 ney, liver, spleen, thyroid gland, testis. The individual seats will 
 be further considered under the different forms. 
 
 Structure. — The sarcoma-cell is rounded, cylindrical, spindle- 
 shaped, or of polymorphous forms, the latter usually being larger 
 than the round or spindle-forms. The large number of cells in 
 comparison with the amount of intercellular substance is always 
 conspicuous. The cells themselves contain rather large nuclei of 
 a some what vesicular appearance, though sometimes quite granular. 
 In rapidly growing tumors karyokinetic figures may be very 
 abundant ; less frequently the cells show evidence of direct divis- 
 ion of the nuclei. Nuclear degenerations (karyorhexis, karyo- 
 lysis, and hyperchromatosis) are frequent, and doubtless cause 
 sonic of the appearances supposed to be protozoa. The arrange- 
 ment of the cells in sarcomata is usually very irregular ; in some 
 cases, however, particularly in spindle-celled sarcomata, the cells 
 lie in fasciculi or parallel columns. The intercellular substance 
 consists of a homogeneous matrix with a few fibers in the case 
 of the spindle-celled variety, but with none at all in most other 
 cases. The cells may be all of one type, but more frequently 
 different forms or shapes occur in the same tumor. Among the 
 polymorphous forms of cells may be noted large flattened cells 
 resembling endothelial plates and giant-cells resembling myelo- 
 plaques. (These forms will be discussed under the headings 
 Endothelioma and Giant-celled Sarcoma.) 
 
 The blood-vessels of sarcoma, are usually channels lined with a 
 single endothelial coat (see Fig. 50), or there may be more fully 
 developed vessels. In some cases the vascular network is very 
 conspicuous and forms the skeleton of the tumor, the sarcoma- 
 cells being ranged round the vessels in the form of mantles and 
 probably springing from the adventitia. Secondary changes may 
 occur in the cellular masses surrounding the vessels, and peculiar 
 forms of tumors thus result (see Cylindroma). 
 
 Combinations of sarcoma with other forms of tumor are not 
 
PROGRESSIVE TISSUE-CHANGES. 141 
 
 rare. All grades between the true sarcoma and the fibroma may- 
 be met with, and it is difficult to draw a line of distinction. 
 Wherever a tendency to cellular proliferation is conspicuous and 
 the formation of fibroblastic cells with elongated fibrous projec- 
 tions is not conspicuous it is warranted to record the tumor as 
 sarcomatous. Primary fibromata may become sarcomatous, and 
 sarcomatous tumors perhaps at times become more benign by 
 fibromatous transformation. Combinations with chondroma, os- 
 teoma, myxoma, and other connective-tissue tumors ; with adenoma, 
 rhabdomyoma, and fibromyoma are not infrequent. More rarely 
 the fibrous tissue of the benign tumors may undergo sarcomatous 
 change. 
 
 The structure of individual forms of sarcoma will be separately 
 considered. 
 
 Nature. — Sarcoma is essentially malignant. It tends to recur 
 after removal ; it affects the general health of the patient ; and 
 metastasis is frequent. Metastasis occurs through the circulation. 
 The degree of malignancy varies greatly. The small round- 
 celled and melanotic varieties are the most dangerous. Some 
 forms, as the giant-celled and the fibrosarcomata, are compara- 
 tively benign. The relatively benign form of tumor called recur- 
 rent fibroid tumor by Paget is in reality a fibrosarcoma. The 
 growth of sarcomata is usually rather rapid, and may become very 
 rapid in consequence of irritation. 
 
 Sarcomata are injurious to the general health in some obscure 
 way. The evidence of this is the anemia and leukocytosis and the 
 irregular fever observed in various cases. The anemia may be 
 trivial or severe, and may become extreme. Leukocytosis is fre- 
 quent, but rarely marked. The polymorphous elements may be 
 specially increased, but I have found the lymphocytes excessive in 
 a number of cases. Irregular fever is often noted in lymphosar- 
 coma and general sarcomatosis. Necrotic change may increase 
 the tendency to fever. The exact influence of sarcoma on metab- 
 olism is unknown. 
 
 Spindle-celled Sarcoma. 
 
 This form may consist of either large or small spindle-shaped 
 cells with attenuated and sometimes branching extremities (Fig. 
 49). Angular or stellate cells are not infrequent. The cells 
 may be ranged in parallel columns, so that the tissue becomes 
 quite compact ; and fasciculi of such cell-masses may run in differ- 
 ent directions, interlacing, and thus giving the section a fibrous 
 appearance. In other cases the cells present no definite arrange- 
 ment. Spindle-celled sarcomata are harder than the round-celled 
 varieties and usually more grayish or flesh-colored. They may be 
 quite soft and white or degenerated and cystic. 
 
142 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 The amount of intercellular substance in some cases is quite con- 
 siderable, and the term fibrosarcoma may be justified. It is very 
 
 Fig. 49.— Cells from a large spindle-celled sarcoma (Ziegler). 
 
 difficult sometimes to decide whether the tumor is sarcomatous or 
 purely fibromatous. 
 
 Spindle-celled sarcomata occur in the dense connective tissue 
 of the periosteum, tendons, and fascia? ; less frequently in the 
 softer tissues. Relatively they are benign, seme cases showing no 
 tendency to metastasis, though recurring after removal. 
 
 Round=celled Sarcoma. 
 
 Sarcomata may be composed almost entirely of spherical or 
 round cells, small or large in size. The designations small and 
 large round-celled sarcomata are used, but do not really define 
 separate varieties. The round cells when small resemble those of 
 
 Fig. 50.— Small round-celled Barcoma : in the center is seen a blood-vessel with its wall 
 of endothelium. 
 
 lymphatic organs. There is little intercellular substance. The 
 blood-vessels may be quite large and hemorrhages with secondary 
 changes may occur (Fig. 50). The larger cells contain relatively 
 more protoplasm, frequently several nuclei, and not rarely different 
 forms of cells (spindle-shaped and polymorphous) are associated. 
 
 The naked-eye appearances of round-celled sarcomata are usu- 
 ally quite characteristic. They are milky-white, gray, or pink in 
 
PROGRESSIVE TISSUE-CHANGES. 143 
 
 color ; sometimes quite soft or cheesy in the center, and a milky 
 liquid exudes. Cystic changes and even calcification may occur 
 in the center. The small-celled variety is, as a rule, softer than 
 the larger, though both are soft. 
 
 Round-celled sarcomata are always malignant, the small-celled 
 form being perhaps the most malignant of all varieties. 
 
 I/ymphosarcoma is a variety of round-celled sarcoma. The 
 appearance is the same as that of the other forms, but micro- 
 scopically a close resemblance of structure with that seen in lym- 
 phatic glands is discovered. The principal characteristic is the 
 reticulum or stroma formed by branching stellate cells united by 
 their prolongations. In the meshes of this reticulum lie lymphoid 
 round cells (Fig. 51). The stroma may not be plainly visible 
 
 Fig. 51.— Lymphosarcoma of nasal mucous membrane : a, on left side a blood-vessel, on 
 right side reticulum ; b, cells of reticulum ; c, sarcoma-cells (Ziegler). 
 
 unless sections are shaken to dislodge the cells from the reticulum. 
 Lymphosarcomata occur in the lymphatic glands and lymphad- 
 cnoid tissues of the mucous membranes. Occasionally the thymus 
 gland and other organs may be the seat. The distinctions from 
 lymphadenoma have been discussed under that heading. 
 
 Alveolar sarcoma is a sub-variety of round-celled sarcoma, 
 though there are always spindle-cells as well. It is distinguished 
 by the occurrence of acini filled with large round cells having a 
 more or less decided epithelioid appearance. The stroma forming 
 the acini is composed largely of spindle-shaped cells with a certain 
 amount of fibrous tissue (Fig. 52). The blood-vessels supplying 
 the tumors traverse these trabecule. The round cells within the 
 alveoli may vary greatly in size, though they are usually large. 
 The macroscopic appearance is not specially distinctive ; many 
 of the cases, 4 however, are pigmented (see below). Alveolar 
 sarcoma is most frequent in the skin, where it springs from moles 
 and warts. It may also occur in the lymphatic glands, the serous 
 membranes, and other parts. 
 
 In some cases the alveolar appearance of the sarcoma is due to 
 
144 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 the fact that the sarcomatous proliferation has occurred in the 
 adventitia of blood-vessels forming a plexus. In this way the 
 
 Fig. 52.— Alveolar sarcoma (Warren). 
 
 meshes of the vascular plexus become filled with round cells 
 and the alveolar appearance results. In other cases the alveolar 
 character is due to the occurrence of sarcomatous foci of circum- 
 scribed character in a connective tissue. These in their growth 
 push the connective-tissue elements aside and thus form alveolar 
 structures. 
 
 Angiosarcoma. 
 
 In this variety the sarcomatous proliferation begins in the 
 adventitious coat of blood-vessels. Certain authors have at- 
 tempted to show that all forms of sarcoma originate in the blood- 
 vessels; this view, however, cannot be supported. Angiosarcomata 
 are met with in the serous membranes, in the skin, and especially 
 in the salivary glands. Very rarely they occur in other parts of 
 the body. The tumor is, as a rule, quite vascular, but may not be 
 strikingly so. Sometimes telangiectatic change in the blood- 
 vessels has been noted. Histologically these growths are charac- 
 terized by round-celled masses surrounding the blood-vessels. 
 The origin of the cells from the adventitia may be evident or ob- 
 scure. In cases in which a vascular network is involved and 
 each vessel has a coating of sarcoma-cells a plexiform appear- 
 ance or arrangement results {Plexiform A)i</iosareoma). In other 
 instances in which a network of vessels is involved the sar- 
 coma-cells accumulate in the vascular meshes in the form of cell- 
 nests, and thus give rise to an alveolar form (Alveolar Angiosar- 
 coma). Such form- occur in sarcomata springing from moles or 
 warts. They are prone to melanotic change. The endothelium 
 
PROGRESSIVE TISSUE-CHANGES. 
 
 145 
 
 of the vessels is occasionally the point of origin of vascular sarco- 
 mata ; this form is a rare variety of endothelioma. The angiosar- 
 comata are liable to degenerations, chiefly myxomatous (Fig. 53) 
 
 v 4 
 
 
 
 ;■?, 
 
 
 
 Fig. 53.— Angiosarcoma with myxomatous degeneration. (cylindroma) : the figure rep- 
 resents one of the blood-vessels with the sarcomatous cells springing from its walls, and 
 outside of these myxomatous tissue. 
 
 and hyaline, and thus a certain proportion of the cases of cylin- 
 droma (see below) have their origin. The blood-vessels may give 
 way and hemorrhagic infiltration results. 
 
 Angiosarcomata are in a measure benign, metastasis being very 
 rare in the ordinary forms. The alveolar and melanotic varieties 
 are highly malignant. 
 
 Cylindroma. 
 
 This term was originally applied by Billroth to tumors show- 
 ing gelatinous masses or trabecular traversing their substance. 
 Histologically different forms of growths may be distinguished. 
 We deal here only with Sarcomatous Cylindromata. 
 
 The latter may be simply sarcomata in which hyaline or 
 myxomatous degeneration has occurred in more or less insular 
 fashion, or in which sarcoma and myxoma are peculiarly com- 
 bined. Nearly always there is some hyaline change with the myx- 
 omatous. In most cases it is the angiosarcomata that present this 
 peculiar condition. The sarcoma-cells surrounding the blood- 
 vessels become converted into hyalomyxomatous tissue or cause 
 the formation of this. There result branching columns of hyalo- 
 
146 TEXT-BOOK OF PATHOLOGY. 
 
 myxomatous character traversing the sarcoma. In some cases the 
 walls of the blood-vessels themselves may be the seat of hyaline 
 change (Fig. 54), the proliferated sarcoma-cells surrounding the 
 
 e f 
 
 Fig. 54.— Cylindroma showiDg pronounced hyaline degeneration of the walls of the 
 blood-vessels. 
 
 vessel being merely pushed aside. The term Angiosarcoma 3Iyx- 
 omatodes is given to these vascular forms. Cylindromata occur in 
 the salivary glands, the brain, the lachrymal glands, and rarely in 
 the subcutaneous tissues. In nature they are more or less benign. 
 
 Melanosarcoma. 
 
 Melanosarcoma, or pigmented sarcoma, is a form in which the 
 tumor is dark colored from the presence of black or brown pig- 
 ment. The latter, according to the careful chemical studies of 
 Berdez and Nencki, contains no iron, and is therefore not simply 
 blood-pigment. Ferruginous pigment has been found by certain 
 authors, but is always outside the cells, and very probably is 
 accidental, resulting from hemorrhagic extravasations. True mel- 
 anotic pigment occurs in the cells or intercellular substance as 
 a brownish-black granular matter, or in the cells as a diffuse stain. 
 The tumor itself lias not any definite characteristics aside from the 
 pigment ; it may be round-celled (Fig. 55) or spindle-celled; very 
 Frequently it Is angiosarcomatous and alveolar in type. Melanotic 
 sarcomatata most frequently arise in the skin, particularly in pig- 
 mented moles or warts, in the eye or in the pia mater. They are 
 
PROGRESSIVE TISSUE-CHANGES. 
 
 147 
 
 exceedingly malignant, often grow with great rapidity, and give 
 rise to widespread metastasis, the liver being peculiarly liable to 
 
 .. 
 
 : *a. 
 
 . . m*. . .<M&k 
 
 - ■ ' ; «■ 
 
 Fig. 55.— Melanosarcoma, mainly round-celled : from a nodule in the skin. 
 
 involvement. The secondary growths have the same structure as 
 the primary, and frequently are even more pigmented than the 
 original tumor. 
 
 Giant=celled Sarcoma. 
 
 This variety is characterized by the presence of large multi- 
 nuclear cells resembling exactly the myeloplaques of bone. The 
 remaining portions of the tumor may be spindle-celled or round- 
 celled ; perhaps more frequently round and spindle-cells are asso- 
 ciated. The giant-cells are often exceedingly large and contain 
 several or many nuclei in the center of the cell (Fig. 56). The 
 formation of these cells is most likely due to rapid nuclear multi- 
 plication. In some cases they would seem to be caused by obliter- 
 ation and transformation of capillary blood-vessels ; but the theory 
 that they result from a fusion of cells seems unwarranted. Ziegler 
 maintains that the presence of giant-cells does not form an essen- 
 tial characteristic of a peculiar type of tumor, but that it is acci- 
 dental, resulting from continued irritation. The occurrence of 
 giant-cells in sarcomata of bones would then be explained by the 
 constant irritation of the bony particles, as in some cases the 
 presence of masses of blood-pigment in the sarcoma accounts for 
 the development of giant-cells in the vicinity. This view is sup- 
 ported by considerable authority and seems reasonable. 
 
 Giant-celled sarcomata occur most frequently about bone, and 
 the terms osteosarcoma and myeloid sarcoma have been given in 
 consequence. They may, however, occur in other situations. 
 Their nature is usually benign, metastasis being rare. 
 
148 
 
 TEXT-BOOK OF PATHOLOGY 
 
 
 
 The giant-celled sarcoma of bone is usually rather slow in 
 growth, and gives rise to hard and irregular tumors, firmly attached 
 
 Fig. 67.— Myelogenous osteosarcoma of the tibia (modified from Kast and Rumpel). 
 
 to the bone-structures. It may begin within the hone as a myefogr- 
 enousform (Fig. 57)or from the periosteum. Secondary myxoma- 
 
PROGRESSIVE TISSUE-CHANGES. 149 
 
 tous or other change may cause more or less softening. The bone 
 most frequently involved is the maxilla, the tumor known as epulis 
 (sarcoma springing from the gums or alveolar processes) being 
 generally a giant-celled sarcoma. 
 
 MIXED TUMORS. 
 
 All forms of connective-tissue tumors may be associated one with another; 
 association of several forms are known as mixed tumors. Very frequently 
 there is more or less sarcomatous tissue in such growths. With this will be 
 found myxomatous, fibromatous, chondromatous, or osteomatous elements. 
 The various constituents of the tumor are arranged with no special order, but 
 simply present themselves as masses of cells or intercellular substance of 
 different forms combined to make a heterogeneous tissue. Among the fre- 
 quent seats of such mixed tumors the parotid gland and the testicle are 
 most important. 
 
 Chloroma. 
 
 This tumor is no special form of new growth, but rather a variety of 
 lymphosarcoma or round-celled sarcoma occurring with special frequency 
 in the periosteum or the bones of the head and secondarily in other parts 
 of the body. The name is applied because of the peculiar greenish pig- 
 mentation of the cells. The nature of this pigment is not certainly deter- 
 mined. Clinically cases of chloroma may present symptoms of leukemia 
 or pseudoleukemia. 
 
 Psammoma. 
 
 This represents no distinct species of tumor-growth, but rather a pecu- 
 liarity of different kinds. The ( name refers to the presence of calcareous 
 matter like that of the brain-sand (acervulus cerebri), and psammoma has 
 sometimes been called acervuloma. The calcareous matter occurs in the 
 form of rounded masses or concentrically arranged whorls. The tumor- 
 elements themselves may be fibromatous, gliomatous, sarcomatous, or even 
 adenomatous or carcinomatous. In most instances it is angiofibromata or 
 angiosarcomata that present these appearances. Psammomata are met 
 with in the membranes of the brain, the choroid plexus, and the pineal 
 gland. 
 
 MYCOSIS FUNGOIDES. 
 
 Mycosis fungoides or granuloma fungoides is a pathologic condition of 
 the skin and subdermal structures having certain resemblances to sarcoma 
 and to some of the infectious inflammations. 
 
 Etiology. — Very little is known regarding the causes of this disease. 
 Various bacteria, principally micrococci, have been discovered in the 
 lesions, but none of these has been shown to be pathogenic. A few ob- 
 servers have found bodies resembling protozoa; but it is not certain that 
 these were really animal organisms. 
 
 Appearance. — The disease frequently presents distinct stages. First, 
 the skin becomes somewhat swollen and red and presents eczematous 
 lesions. In some cases the appearance is that of an erysipelatous inflam- 
 mation. In the next stage nodular elevations occur, and finally tumors of 
 considerable size, sometimes as large as an orange, and more or less fungoid 
 in appearance. Necrosis is frequent and watery or bloody liquid is dis- 
 charged. The tumors may have an angry, red appearance and have been 
 likened to tomatoes. Rapid disappearance and reappearance of the tumors 
 are a peculiar feature. 
 
150 
 
 TEXT-BOOK OF PATHOLOGY 
 
 Any part of the body may be affected and usually the lesions are mul- 
 tiple. 
 
 Structure. — Microscopically the structure of the tumors is allied to that 
 of lymphadenomata. There is a proliferation of connective-tissue cells 
 about the blood-vessels and glands at the base of the papillse of the skin, 
 forming a network or reticulum in which round (lymphoid) cells are em- 
 bedded. Epithelioid cells and giant-cells may occur. The tumors are 
 poorly supplied with blood-vessels, and to this is attributed the tendency to 
 central necrosis. Inflammatory infiltration of polymorphous leukocytes is 
 not observed to any considerable degree, excepting in the later stages 
 around and in the areas of necrosis. Mast-cells are often abundant, 
 
 Associated Conditions. — In some cases enlargement of the lymphatic 
 glands, liver, and spleen has been observed, and has suggested the term 
 pseudoleukemia cutis. Occasionally the blood presents leukemic char- 
 acters. 
 
 Nature. — The disease presents many resemblances to sarcoma or lymph- 
 adenoma, and it has frequently been described as multiple sarcoma of the 
 skin. In other respects it is allied to the infectious inflammations, though 
 there is much less evidence of true inflammatory infiltration than in these. 
 The relationship to leukemia and pseudoleukemia is unsettled. 
 
 This tumor 
 ameer, resembles cancer very 
 
 ENDOTHELIOMA. 
 
 which is also sometimes designated endothelial 
 closely in histologic appearances in 
 
 *jmm 
 
 Nr* 
 
 -Endothelioma of pleura: the pleural cavity was distended with effusion and the 
 lung was compressed and Invaded by secondary m ' 
 
 ■ nodules. 
 
PROGRESSIVE TISSUE-CHANGES. 
 
 151 
 
 some cases. It appears, however, to be purely endothelial in 
 origin, and therefore rather of the connective-tissue group or sar- 
 comata. It affects the pleura, peritoneum, and membranes of the 
 brain most frequently, but may be found in the skin, walls of the 
 blood-vessels, and elsewhere. The serous membranes when affected 
 become greatly thickened, tough, and white in color (Fig. 58), and 
 irregular elevations or nodules may occur. Metastasis is infre- 
 quent, but the adjacent organs are sometimes involved, and 
 occasionally more distant structures. 
 
 Fig. 59.— Microscopic section from the above (Fig. 58). 
 
 Histologically the tumor is characterized by more or less 
 tubular or acinus-like aggregations of endothelial cells. The 
 latter vary in character from those which are distinctly endo- 
 thelial to the most differentiated, which may be almost typical 
 cylindrical epithelium (Fig. 59). Between these cellular columns 
 or acini the connective tissue of the part affected may be seen in a 
 normal state, though it is more frequently thickened by prolifera- 
 tion. Careful inspection of microscopic sections shows that the 
 columns of epithelioid cells occupy lymph-channels, and it may be 
 possible to demonstrate that the endothelium of the latter has been 
 the starting-point of the cellular proliferation. In cases of carci- 
 noma with penetration into the lymphatic channels it is notable, 
 on the other hand, that the endothelial lining of the channels is 
 uninvolved. 
 
 GLIOMA. 
 
 Definition. — The term glioma is applied to tumors composed 
 of neuroglia. It is difficult to distinguish between the circum- 
 
152 TEXT-BOOK OF PATHOLOGY. 
 
 scribed tumors of this structure and the diffuse neuroglial* hyper- 
 plasia or gliosis met with in certain cases. (See section on Diseases 
 of the Nervous System.) 
 
 Etiology. — It is probable that congenital defects of develop- 
 ment play some part in the causation of these tumors, particularly 
 in the forms more frequently spoken of as gliosis. 
 
 Appearance. — A typical glioma is usually a solitary tumor, 
 rounded in outline, though its limits are difficult to determine, as 
 it merges gradually into the surrounding nervous tissue. Gliomata 
 are somewhat harder than the normal brain-substance, and often 
 the color is a little different, either more grayish or pink or red- 
 dish. Sometimes they are quite vascular and dark red. The 
 normal shape of the part may be a little disturbed, or there may 
 be indefinite elevation. In size the tumor varies up to masses as 
 
 i 
 
 Fig. 60.— Glioma of the corpora quadrigemina (Perls). 
 
 large as a lemon. Diffuse gliosis causes a swelling of the affected 
 parts, sometimes quite regular, at other times irregular. When 
 the spinal cord is affected its thickness may be considerably 
 increased. On section the area of gliosis is rather firm and 
 grayish in color. Nearly always there is a tendency to exca- 
 vation or cyst-formation. In the cord this leads to the develop- 
 ment of considerable cavities, as a rule communicating with the 
 central canal. 
 
 Seats. — Gliomata occur in the brain and less frequently in 
 the spinal curd. In rare cases the cranial nerves have been in- 
 volved. Glioma of the eyeball will be referred to below. Diffuse 
 gliosis is particularly common in the cord. It is usually met with 
 in the vicinity of the cavities of the brain or cord. 
 
 Structure. — A glioma consists of cells containing rounded or 
 oval nuclei with very little protoplasm and fine protoplasmic 
 extensions which interlace and form an intercellular reticulum, 
 giving the sections a granular appearance when viewed with low 
 powers of the microscope. Special staining and higher powers 
 may demonstrate the filamentous prolongations of the cells (Fig. 
 60). The number of cells and the density of the intercellular 
 network vary greatly. As a rule, the cells are larger than the 
 normal neuroglia-cells, and sometimes they contain several nuclei. 
 
PROGRESSIVE TISSUE-CHANGES. 153 
 
 The tumor is generally quite vascular and occasionally telangiec- 
 tatic vessels may be observed. Secondary hemorrhages are prone 
 to occur in the latter case. Softening may occur, and occasionally 
 sarcomatous transformation has been described. 
 
 Diffuse gliosis has similar microscopic appearances, though the 
 tissue is likely to be more compact and less vascular. In the 
 spinal cord the process begins as a subepithelial proliferation of 
 the glia at the posterior raphe of the central canal, the lining 
 epithelium of this at the same time undergoing a certain amount 
 of proliferation. Subsequently the gliosis increases and cavities 
 form within. These may be lined with epithelial or epithelioid 
 cells which are occasionally ciliated. Gliosis may also present 
 itself in the form of scattered nodular hyperplasias of the neu- 
 roglia. 
 
 Nature. — Glioma is essentially benign. It is dangerous 
 mainly on account of the pressure it exerts. Sarcomatous trans- 
 formation may possibly occur, but is exceedingly rare. The 
 growth of the tumor is rather slow. 
 
 Glioma of the eyeball is a form of tumor that is sometimes considered 
 true glioma. It is, strictly speaking, a round-celled sarcoma. It springs 
 from the retina and resembles in structure the granular layer of the retina. 
 It occurs most frequently in children, particularly in early life (two to four 
 years), and often on both sides simultaneously. Family predisposition, in 
 some cases, is very striking. Extension along the optic nerve or externally, 
 and a tendency to recurrence after removal, indicate the malignant char- 
 acter of the growth. 
 
 Glioma Ganglionare. 
 
 Definition. — This term indicates a form of mixed tumor composed of 
 neuroglia and nerve-fibers with large ganglionar nerve-cells. 
 
 Etiology. — Probably congenital abnormality of development furnishes 
 the groundwork for the subsequent development of these tumors. 
 
 Appearance. — A ganglionar glioma may resemble the ordinary glioma, 
 occurring as a solitary tumor, the outlines of which are difficult to dis- 
 tinguish from the surrounding tissue. More frequently it occurs in the 
 form of multiple nodular condensations scattered through the brain or 
 cord. The contour of the affected parts may not be altered, and on section 
 the growths may be recognized only by the light-colored patches and areas 
 of increased density. A few cases of ganglionar gliomata of the spinal or 
 sympathetic ganglia have been described. In these cases the tumors ap- 
 pear as rounded enlargements of the affected ganglia. Occasionally the 
 nerve-roots are seats of these tumors; the suprarenal capsules may also 
 be affected. 
 
 Structure. —The definition indicates the usual structure. The glia- 
 fibrils are generally conspicuous in number, the nuclei being comparatively 
 few. Traversing the tumor there may be more or less abundant nerve- 
 fibers with or without medullary sheaths. Large ganglionar cells may be 
 found in considerable abundance or in small number. The vascularity of 
 the growths differs greatly. 
 
 Nature. — The nature of these tumors is the same as that of the ordi- 
 nary glioma. 
 
154 TEXT-BOOK OF PATHOLOGY. 
 
 NEUROMA. 
 
 Definition. — Strictly speaking, neuroma is the term applied 
 to tumors composed of nerve-fibers. Ordinarily, however, the 
 name is given to fibrous growths springing from the perineurium or 
 endoneurium of nerves. The terms true and false neuroma dis- 
 tinguish between the two forms. True neuromata are exceed- 
 ingly rare. 
 
 Etiology. — Very little is known regarding the causation. 
 Injury may play a part, as in the case of amputation-neuromata. 
 
 Appearance. — False neuromata occur as nodular thickenings 
 along the course of nerves. They may be fusiform or elongated, 
 may extend considerable distances along the nerves, and may 
 form networks of ridges or elevations when the peripheral nerves 
 are involved (Plexiform Neuroma). As a rule they are multiple, 
 and sometimes occur in exceedingly great numbers scattered over 
 the entire body or involving a single part of the body, as the 
 nerves of the arm or leg. After amputations rounded thickenings 
 may occur at the ends of the nerves, constituting painful conditions 
 of the stump. 
 
 Seats. — The peripheral nerves are most frequently involved, 
 but the nerves may be implicated near their roots, or the terminal 
 fibers within the organs may become affected. 
 
 Structure. — Ordinary false neuroma consists of fibrous tissue 
 in the form of reticular connective tissue with greater or less 
 abundance of cells pushing aside or surrounding the nerve-fibers 
 proper. The latter are prone to degenerate in consequence of the 
 pressure. Proliferation of the nerve-fibers has sometimes been 
 described, but it is doubtful whether such actually occurs. More 
 probably the existing fibers increase in length and form a mass 
 by curling at the end. True neuromata of two kinds are de- 
 scribed : those composed of medullated and those consisting of 
 non-medullated nerve-fibers. The former are called myelinic, the 
 latter amyelinic. 
 
 Nature. — Neuromata are painful tumors, but benign in a 
 pathologic sense. Their growth up to a certain point is often 
 rapid. 
 
 LEIOMYOMA. 
 
 Definition. — Leiomyoma, or myoma lsevicellulare, is a tumor 
 containing smooth muscle-fibers. Nearly always there is a cer- 
 tain amount of fibrous tissue associated, and in the most com- 
 mon form, myomata of the uterus, there is always considerable 
 fibrous tissue, and the term fibromyoma is appropriate. Occasion- 
 ally a few unstriped muscle-cells may be seen in tumors of other 
 kinds. 
 
 Etiology. — Some of the myomata of the uterus exhibit 
 glandular acini in the interior and suggest a congenital origin. 
 
PROGRESSIVE TISSUE-CHANGES. 155 
 
 This, however, is by no means certain. In other cases there are 
 features suggesting that irritation is the important cause, though 
 this also remains to be proved. 
 
 Appearance. — Leiomyomata are usually rounded growths, 
 varying in size from minute nodules to huge solid masses weighing 
 as much as sixty to seventy pounds. The largest (heaviest) solid 
 tumor I have ever seen was a degenerated fibromyoma weighing 
 eighty pounds. Leiomyomata are surrounded by a capsule more or 
 less well developed and are generally quite hard, though secondary 
 degeneration at times alters the consistency, making the tumor quite 
 soft in the case of mucous transformation, or stony-hard when cal- 
 cification has occurred. On section through the growths the 
 stratified or fasciculated arrangement of the cells is visible to the 
 naked eye. Concentric layers may be apparent, or a more wavy 
 irregularity may be seen. They are grayish or flesh-colored, or in 
 rare instances quite red (myoma cavernosum) in consequence of en- 
 larged vascular channels. Central softening may lead to cystic 
 change (myoma cysticum). 
 
 When the myomata spring from the submucous or subserous 
 tissues they may become polypoid, hanging from a point of attach- 
 ment by a narrow pedicle. In rare instances the latter is 
 severed and the tumor becomes a free body. Submucous myo- 
 mata of the uterus may thus eventually be discharged after a 
 spurious labor. Subserous myomata may become free in the 
 peritoneal cavity. 
 
 Myomata of the uterus may have three situations — submucous, sub- 
 serous, or interstitial. In the latter, the tumor occupies the wall of 
 the uterus without any tendency to project particularly toward either sur- 
 face. Uterine myomata are usually multiple, occur during the third and 
 fourth decades of life, continuing their growth until the menopause and 
 usually decreasing after that epoch. They endanger life by their pressure 
 and by the copious uterine hemorrhages which they occasion. Very fre- 
 quently salpingitis is associated, and recently attention has been called to 
 degenerated conditions of the myocardium in patients suffering from uterine 
 fibroids. 
 
 Myomata of the skin occur in younger patients, even in childhood, and 
 are generally multiple and often painful (tubercula dolorosa). 
 
 Seats. — The common situations are the uterus, the gastro- 
 intestinal tract, and the ovaries ; the less common seats are the 
 walls of the blood-vessels, the skin, and the nipple. In all situa- 
 tions the tumor springs from pre-existing unstriped muscle-fiber. 
 In most cases, according to some authors, the origin is in the walls 
 ■of the minute blood-vessels, but direct origin from the muscular 
 layer of the affected organs, or from the erectores pilorum in the 
 case of the skin, cannot be denied. Myomatous metaplasia of the 
 connective tissue, as in the case of myomata originating in the 
 areas of old pleural thickening, has been assumed, but is im- 
 probable. 
 
156 TEXT-BOOK OF PATHOLOGY. 
 
 Structure. — As has been said, association with fibrous tissue 
 is usual. Microscopically the tumor presents a characteristic 
 appearance. Bundles of muscle-cells are seen running in different 
 directions. Those cut longitudinally show cylindrical nuclei as 
 the most conspicuous feature, the outlines of the cell being indis- 
 tinct (Fig. 61). Where the cells are transversely cut the nucleus 
 
 Fig. 61.— Leiomyoma of uterus. 
 
 presents a circular outline with clear protoplasm surrounding it. 
 The picture of a leiomyoma is often suggestive of sarcoma, but 
 may lie distinguished by the greater regularity in direction of the 
 cells in different bundles and by the more distinctly cylindrical out- 
 line of the nucleus. The cells of leiomyomata may be isolated by 
 maceration of the sections in 20 per cent, solution of nitric acid 
 for twenty minutes, or in 30 per cent, solution of caustic potash for 
 fifteen minutes. They are spindle-shaped structures containing a 
 nucleus about one-third the length of the entire cell. 
 
 Leiomyomata arc generally poor in blood-vessels, but may 
 show a telangiectatic condition of the vessels. The lymphatic 
 spaces may similarly dilate, forming cystic spaces containing 
 spontaneously coagulable material. 
 
 Of the degenerative changes calcification is the most common, 
 particularly in the uterine fibromyomata. This begins in the 
 center of the tumor, but may eventually involve the whole mass. 
 Myxomatous change may occur in myomata containing much 
 fibrous tissue, and sarcomatous transformation has been described, 
 but is rare. 
 
 Nature. — The nature is eminently benign. Myomata of the 
 digestive tract may cause occlusion or strangulation, or by their 
 weight may exercise serious traction. Uterine myomata are dan- 
 gerous in the ways already indicated. The growth is usually 
 slow. 
 
PROGRESSIVE TISSUE-CHANGES. 157 
 
 RHABDOMYOMA. 
 
 Definition. — Rhabdomyoma, or myoma striocellulare, is a tu- 
 mor containing more or less striped muscle-fiber. Usually there 
 is but a small quantity of the latter, the bulk of the tumor being 
 of some other tissue, most frequently sarcomatous. 
 
 Etiology. — Congenital defective development seems an im- 
 portant cause, as the tumors occur in early life and in situations 
 in which striped muscle-fiber does not normally occur. 
 
 Appearance and Seats. — The rhabdomyomata of the kid- 
 ney (the most frequent seat) present themselves as large rounded 
 or irregular masses, more or less encapsulated. In the testicle 
 they are similar, though of smaller size. A few cases have been 
 described in which irregular tumors of the retroperitoneal tissues 
 have contained muscle-fibers. 
 
 Structure. — The microscopic appearance is usually that of a 
 spindle-celled sarcoma, containing more or less striped muscle-fibers. 
 These are elongated spindle-shaped cells, partly striated, and sug- 
 gesting embryonal muscle-tissue and rarely more fully developed 
 muscle-fibers. Large areas of the tumor may contain no muscle- 
 fiber at all, while certain portions are richly supplied. Adenoma- 
 tous elements are not rarely associated. The tumors of the kidney 
 Avhich contain striped muscle-fibers are in the main sarcomatous or 
 adenosarcomatous. 
 
 Nature. — These tumors are malignant in proportion as the 
 sarcomatous element is predominant. Metastasis is, however, 
 infrequent. General cachexia and hemorrhages reduce the vitality 
 and lead to fatal termination. 
 
 PAPILLOMA. 
 
 Definition. — The term papilloma indicates a tumor arising 
 from the surface and covered with epithelium representing more 
 or less accurately the structure of the papillae of the skin. 
 
 Etiology. — It is difficult to draw a line between certain papil- 
 lomatous growths that are the result of chronic irritation and others 
 that arise in a seemingly spontaneous manner. It would appear 
 that irritation is an important factor in most, if not all, cases, but 
 there is also no doubt some form of predisposition. Whether this 
 resides in structural peculiarities or not is difficult to determine. 
 A peculiar form of inflammatory growth resembling the sponta- 
 neous papillomata is that known as venereal wart. It occurs about 
 the genitalia or anus and especially after gonorrhea. Another 
 form of inflammatory papillomata is that found in the mucous 
 membranes surrounding carcinomata or chronic ulcerations of 
 syphilitic or other kinds. 
 
 Appearance. — The most familiar form of papilloma is that 
 which occurs in the skin and which is commonly called wart. 
 
158 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 PlG. 62.— Papillomata of the 
 
 vocal cords ii'nmia specimen 
 in the Museum of the Phila- 
 delphia Hospital). 
 
 Warts or papillomata may be single, but more frequently occur in 
 groups, and there may be many growths in widely scattered areas 
 of the body. A wart may be simply a 
 smooth hemispherical elevation, or it may 
 have a cauliflower appearance. The epi- 
 dermis covering it is, as a rule, somewhat 
 more granular or rough than is that of the 
 normal skin. The size of these growths 
 varies from minute points to nodules as 
 large as a walnut. On the mucous surfaces, 
 especially where the epithelial covering is 
 columnar, the papilloma presents itself as 
 a soft and more distinctly cauliflower 
 growth (Fig. 62). It is red in color, or, 
 if the epithelium is stratified and squamous, 
 grayish or pink. The growth is usually 
 comparatively hard when covered by 
 squamous epithelium. 
 
 Two varieties are sometimes distin- 
 guished. The hard papillomata, such as 
 those which occur in the skin, and the 
 soft papillomata, or the form usually seen 
 in the mucous membranes. 
 Seats. — Papillomata occur in the skin of the neck, hands, 
 back, and other parts, and in the mucous membranes, particularly 
 in the bladder, larynx, nasal chambers, and gastro-intestinal tract. 
 Small papillomatous outgrowths may spring from the lining mem- 
 brane of glandular ducts, as in the breast or ovary. These may 
 lead to subsequent cystic change in the organ, or they may arise 
 after cystic change has begun by proliferation of the lining mem- 
 brane of the cyst. 
 
 Structure. — The essential parts of papilloma are the center 
 or groundwork of connective tissue containing blood-vessels and 
 the epithelial covering. In the skin the growth imitates the nor- 
 mal papillae, all portions of the latter, however, being greatly 
 exaggerated. When there is tendency to cauliflower appearance 
 the papilloma shows a branching form' on vertical section. Each 
 of the branches contains a connective-tissue framework with an 
 epithelial covering. The latter consists of stratified, squamous cells 
 and shows a decided tendency to horny change. Distinct concen- 
 tric whorls of horny epithelium, such as occur frequently in epi- 
 theliomata of the skin, may be met with in papillomata. In some 
 cases the amount of connective-tissue groundwork in the papilloma 
 is excessive ; in others the new-growth consists almost entirely of 
 proliferated epithelium. In some of these latter cases the resem- 
 blance to epithelioma may be quite suggestive, but a distinction 
 can be made by observing that the tumor tends to grow outward 
 
PROGRESSIVE TISSUE-CHANGES. 159 
 
 rather than into the deeper structures, and always shows some 
 connective-tissue stroma at least. The papillomata of the mucous 
 membranes differ according to their situation. In the larynx and 
 other portions covered with squamous epithelium they may present 
 much the same appearance as that seen in the skin, though the 
 epithelium, as a rule, remains softer. There are cases, however, 
 in which a distinct pachydermatous change is found in the epi- 
 thelial covering of papillomata. In the gastro-intestinal tract and 
 in the bladder papillomata are prone to be soft and villous in 
 appearance and are covered with a scantier epithelial coating. 
 Cystic change is not unusual as a result of degenerative processes 
 or of distention of the mucous glands. 
 
 Nature. — The nature of these tumors is benign, but they may 
 be destructive of the general health in consequence of repeated 
 hemorrhages or by interfering with the function of the organ or 
 part in which they are situated. In some cases they are supposed 
 to become malignant, but this has not been definitely proved. 
 
 ADENOMA. 
 
 Definition. — Adenoma is the term applied to a new-growth 
 corresponding more or less in structure with certain epithelial 
 glands, and therefore presenting acini or tubules containing 
 glandular epithelial cells (cylindrical or polyhedral) and a reticu- 
 lum of connective tissue and blood-vessels. It is difficult to 
 separate simple glandular hyperplasia on the one hand and carci- 
 noma on the other hand from true adenoma. This will be dis- 
 cussed in referring to the structure. 
 
 J$tiology. — The causation of adenoma is obscure. In some 
 cases congenital misplacements of tissue-elements appear to play 
 a part, as is seen in the cases of adenomata of the kidney having 
 the structure of suprarenal bodies. These tumors which, it is true, 
 some authorities refuse to consider as adenomata, have a general 
 resemblance to adenomata and spring from remnants of suprarenal 
 tissues embedded in the kidney-substance. Traumatism may be 
 a factor in the etiology by exciting the proliferation of such mis- 
 placed tissue-elements. In other cases the ordinary glandular 
 structures seem to be stimulated to abnormal hyperplasia and 
 tumor-growth in consequence of continued irritation. 
 
 Appearance. — The appearances of adenomata vary greatly 
 with their seat. On the mucous surfaces there may be a simple 
 thickening or more or less diffuse and irregular elevation of the 
 surface, or in other cases distinct papillomatous outgrowths and 
 rarely definite nodular tumors. In some of these cases the condi- 
 tion is purely one of inflammatory hyperplasia; in other cases 
 there is undoubted tumor-growth. No sharp demarcation can be 
 established. In the substance of the organs adenomata occur as 
 
160 TEXT-BOOK OF PATHOLOGY. 
 
 nodular tumors, usually singly and well circumscribed, and not 
 rarely surrounded by a fibrous capsule. They are moderately 
 firm, and on section whitish or pink in color. Sometimes cystic 
 change occurs as the result of dilatation of the glandular acini or 
 in consequence of degenerative softening; in these cases the con- 
 sistence is correspondingly altered. 
 
 Seats. — Among the situations in which adenoma is frequent 
 may be mentioned the mucous membranes, the skin, and certain 
 organs, notably the mammary gland, liver, kidney, suprarenal 
 bodies, thyroid gland, and ovaries. Clinically important seats are 
 the pylorus, the duodenal papilla, the rectum, and the uterus. In 
 these situations adenomata spring from the epithelial tubules or 
 mucous glands. In the skin the points of origin are the sebaceous 
 and sweat-glands. 
 
 Structure. — The definition in general indicates the structure 
 of these tumors. They are more or less typical; that is to say, 
 there are acini of normal appearance presenting a single layer of 
 columnar epithelium, with perhaps in places a tendency to heaping 
 up the several rows of epithelial cells. These acini are well in- 
 closed by a surrounding connective-tissue reticulum, and the 
 appearance of normal gland-tissue is thus produced. Unlike 
 normal glands, there are no excretory ducts, or at most imper- 
 fectly developed ducts. 
 
 Two varieties of adenoma are sometimes distinguished, the 
 tubular and the racemose or alveolar. In the former the glandu- 
 lar system is simple and consists of tubular formations lined with 
 columnar epithelial cells ; in the latter the appearance is that of 
 more complicated glands with closely aggregated acini of circular 
 outline containing columnar and often cubical or polyhedral cells. 
 The number of varieties may be carried further, however, for in 
 the liver the adenomata resemble the normal liver-structure rather 
 than the ordinary glandular formation above described, while in 
 the suprarenal capsules and kidney the appearance is that of 
 slightly atypical suprarenal structure, or in other cases that of 
 embryonal renal tubules. 
 
 With the further growth of adenomata the appearance may be 
 little changed. In other cases considerable variations occur, and 
 there is a tendency, more marked in some situations than in 
 others, to active proliferation of the epithelium, which may cause a 
 considerable alteration in the appearance of the tumor, and event- 
 ually transformation into definite carcinoma. In other cases the 
 structure from the beginning is so atypical and the epithelial pro- 
 liferation so irregularly active that the term adenocarcinoma is 
 applicable. 
 
 The connective-tissue stroma of adenomata may be moderate 
 in quantity or may be considerable. In some adenomatous 
 proliferations of the mucous membranes the number of gland- 
 
PROGRESSIVE TISSUE-CHANGES. 161 
 
 acini or tubules may be relatively small, while the interglandular 
 connective tissue shows active round-cell infiltration to a very 
 considerable degree. Sometimes the interglandular tissue is dis- 
 tinctly sarcomatous (adenosarcoma). In other instances the bulk 
 of the tumor may consist of connective tissue of fibrous character 
 in which are embedded a relatively small number of glandular 
 alveoli. In all of these cases it is difficult to determine whether 
 the connective-tissue process was primary and the epithelial sec- 
 ondary, or the reverse. 
 
 Secondary changes are common, the adenomata of the stom- 
 ach and uterus being particularly prone to change their char- 
 acter to that of carcinoma. In these cases there may be noted 
 active proliferation of the epithelial cells, so that the acini or 
 alveoli become completely filled, or that the ends of the tubular 
 structures become blocked up. There is a tendency to extension 
 of epithelial infiltration beyond the limits of the acini, cancerous 
 outgrowths being the result. In other cases the malignancy is 
 manifested by the excessive epithelial proliferation in the form of 
 new acini of irregular character (Fig. 63). This form is known 
 
 
 
 ■ I; 
 
 Fig. 63.— Destructive adenoma (Beyea). 
 
 as destructive adenoma, adenoma destruens, or adenocarcinoma. 
 Eventually the tumor may become purely carcinomatous ; in 
 other cases, however, it continues to increase in size, always re- 
 taining its adenocarcinomatous appearance, but never becoming 
 typically carcinomatous. 
 
 Degenerative changes may be met with as in other tumors. 
 Hyaline transformation or production may give the tumor an 
 
162 TEXT-BOOK OF PATHOLOGY. 
 
 appearance justifying the term " cylindroma " or " cylindro-aden- 
 oma." Such cases are rare. Myxomatous and even calcareous 
 change may sometimes be observed. The connective-tissue stroma 
 may proliferate actively and assume sarcomatous appearances — 
 adenosarcoma. Cystic change may result from gradual dilata- 
 tion of the glandular acini or from distention of normal ducts 
 or alveoli of the gland in which the tumor occurs. In these cases 
 the term cystic adenoma or cyst-adenoma is applicable (Fig. 64). 
 
 
 &&<&&?*&. 
 
 
 Fig. 64.— Adenoma of the mammary gland, with cystic enlargement of acini and abundant 
 interglandular hyperplasia of connective tissue. 
 
 Nature. — Adenomata are benign tumors. In some cases, 
 however, a pure adenoma may give rise to metastasis. Those of 
 the liver, for example, not rarely cause secondary deposits in the 
 spleen and less frequently elsewhere. The adenomata of the 
 thyroid gland similarly cause metastasis, though it is less certain 
 that these are to be considered as pure adenomata. Destructive 
 adenomata or adenocarcinomata are malignant in proportion to 
 the amount of carcinomatous transformation. 
 
 The effect of adenomata on the general health is variable. 
 They do not contribute to the organic metabolism as far as is 
 known, though occasionally biliary pigmentation of the adenomata 
 of the liver and the secretion of milk-like fluid in mammary 
 adenomata evidence the partial preservation of function by the 
 cells. The general health may be unfavorably influenced by 
 
PROGRESSIVE TISSUE-CHANGES. 163 
 
 adenomata of the mucous surfaces in consequence of their inter- 
 ference with normal functions or in consequence of secondary 
 ulceration and hemorrhage. 
 
 CARCINOMA. 
 
 Definition. — The term carcinoma or cancer may be applied to 
 tumors in which epithelial proliferations in the form of solid blocks 
 or columns, or in the form of atypical acini, separated by more or less 
 connective tissue, present themselves, the epithelial proliferation 
 showing a tendency to extend beyond normal anatomic limits. 
 It is extremely difficult to construct a definition that will be 
 universally applicable. Some have regarded the tendency of the 
 epithelial proliferation to break through the normal limits and 
 extend beyond the confines of the epithelial structures from which 
 it rises, as the important fundamental element of carcinoma. 
 Others have held that there is a peculiar atypical character in the 
 epithelial cells themselves, shown by irregular cell-division, hyper- 
 ■ehromatosis, and other features. The older authors believed that 
 polymorphism and certain irregularities of cell-contour suffice to 
 distinguish carcinoma-cells from normal cells or those of other 
 tumors ; but this polymorphism is now recognized to be the result 
 entirely of compression in the growth of the tumor, and to be 
 therefore accidental. Some have believed that the term car- 
 cinoma should include all epithelial tumors giving rise to metas- 
 tasis, but this necessarily restricts the term too greatly on the one 
 hand, and, on the other hand, includes certain tumors probably 
 purely adenomatous. I prefer to regard as carcinoma any 
 epithelial growth atypically reproducing certain glandular or 
 other structures and showing a manifest tendency to irregular 
 extension. 
 
 Etiology. — The causes and nature of carcinoma are still 
 obscure. A number of theories have been offered. These may be 
 considered under different headings. 
 
 (a) Congenital Theory. — The theory of Cohnheim regarding the 
 etiology of tumors in general is less applicable to cancer than to 
 certain other growths. There are a few examples, however, which 
 would seem to prove that misplaced epithelial cells undergo car- 
 cinomatous proliferation ; for example, there are cases of appar- 
 ently primary carcinoma springing from bones which would seem 
 to require this explanation. It is not always certain, however, 
 "that such cases are actually primary. They may represent metas- 
 tases from small primary growths which have escaped notice. 
 The rarity of carcinomata in early life would seem to negative 
 the congenital theory, and at all events would show that other 
 influences of importance are requisite. Of late, a number of 
 hypotheses that in a measure contain the idea of congenital 
 
164 TEXT-BOOK OF PATHOLOGY. 
 
 origin have been put forward to explain the formation of car- 
 cinoma. 
 
 In these there are assumed some form of peculiar irregularity 
 in cell-multiplication and a tendency to independent proliferation 
 supposed to originate in faulty development. These hypotheses 
 arc vague and uncertain. 
 
 {/>) Traumatic Theory. — Clinicians everywhere incline to give 
 great weight to this. A single traumatism probably has little 
 importance, though women frequently state that they recall 
 distinct injuries from which carcinoma of the breast has 
 seemed to originate. It must be recalled that such injuries are 
 sustained by practically every woman, and the presence of car- 
 cinoma would readily be attributed to a preceding hurt. In cases 
 of epitheliomata of the lip in pipe-smokers, in the careinomata of 
 tin- scrotum and limbs in chimney-sweeps and paraffin- workers, 
 and in cases of uterine careinomata following laceration of the 
 cervix, the effect of chronic irritation would seem to be impor- 
 tant. 
 
 (c) Parasitic Theory. — The peculiar growth of cancer, its de- 
 struetiveness of the general health, and its metastasis readily 
 suggest an infective origin. Bacteriologists sought to isolate 
 micro-organisms without success; later investigators have turned 
 their attention to low forms of animal life, protozoa. (For further 
 discussion, see Animal Parasites.) A few successful experiments 
 have been made at implantation from man to animals, or from one 
 animal to another ; but as Hanau, one of the few successful ex- 
 perimenters in this work, himself states, these experiments do not 
 prove infectiousness. The secondary growths in the second ani- 
 mal may be simply of the nature of metastasis, due to implantation 
 of the cancer-cells and subsequent proliferation. Occasionally an 
 endemic occurrence of carcinoma has been claimed, and some au- 
 thors have even referred to houses in which carcinoma frequently 
 arose. 
 
 Age plays an important part in the formation of carcinoma, 
 as this tumor is essentially one of advanced years. Among 275 
 cases collected by Lubarsch, 55.6 per cent, occurred between the 
 ages of forty-live and sixty-five. There were a few instances in 
 childhood and early life. Between fourteen and nineteen there 
 were 1.46 per cent.; between twenty and twenty-five, 1.8 per 
 cent.; between twenty-six and twenty-nine, 1.1 percent. The 
 frequency in later life was formerly ascribed to some alteration in 
 the vitality of the epithelial cells, rendering them more liable to 
 abnormal proliferation. The nature and cause of such alteration, 
 however, remain obscure and theoretical, though there is certainly 
 a greater tendency to cancer-growth as age increases. 
 
 Tumor-dyscrasia. — This indefinite term is supposed to indicate 
 a tendency to cancer-growth probably due to peculiarities of the 
 
PROGRESSIVE TISSUE-CHANGES. 
 
 165 
 
 liquids of the body. No proof of the existence of any definite 
 dyscrasia has ever been furnished, though it is apparent on study 
 that some form of disposition to this growth acts as the predis- 
 posing cause, even if traumatism, infection, or other factors are 
 the immediate cause. 
 
 Heredity was formerly regarded as of great importance. Cer- 
 tainly in some cases there seems to be hereditary transmission of 
 the tendency to develop carcinoma. 
 
 Appearance. — Carcinomata differ considerably in appearance 
 in different parts of the body. Those of the surfaces present 
 themselves as more or less nodular, flat elevations. In the skin 
 the nodules may remain hard and rather smooth, or they may 
 soften upon the surface, forming unsightly ulcerations. In the 
 mucous membranes the growths are more frequently soft and poly- 
 poid or cauliflower-excrescences (Fig. 65). Ulceration may occur 
 
 Fig. 65.— Carcinoma of the duodenal papilla (modified from Kast and Rumpel). 
 
 on the surface of such elevations, or from the first the tumor may 
 be of ulcerative character, causing spreading excavations limited 
 by thickened projecting edges. Carcinomata of the glandular 
 organs form more or less nodular tumors or irregular infiltrations. 
 These vary greatly in consistency, some being almost stony hard, 
 others soft in consequence of their preponderating cellular char- 
 acter or of secondary degenerations. On section the tumor is found 
 to be white or grayish in color, generally somewhat translucent 
 and glistening, and milky liquid may ooze from the surface. Cap- 
 sule-formation is rarely seen, though in occasional instances the 
 normal connective tissue of the organ is pressed outward by the 
 growth of the tumor, and thus forms an imperfect capsule. The 
 primary growth is nearly always solitary. Occasionally instances 
 are observed in which two separate masses develop simultaneously 
 
166 TEXT-BOOK OF rATHOLOGY. 
 
 and apparently independent of each other : as in the two breasts. 
 More Frequently apparent multiplicity is caused by the early ap- 
 pearance and rapid growth of metastases. 
 
 Secondary carcinomata are nodular in character and nearly 
 always multiple. The larger are often distinctly encapsulated. 
 Central softening or contraction of connective tissue may give the 
 surface of the nodule an umbilicated character (Fig. 66). The 
 
 
 
 ^f j :■■ ^^^m. 
 
 p 
 
 
 
 iif.# 
 
 
 Fig. 66.— Metastatic nodules of carcinoma on the surface of the liver (Hanot and Gilbert). 
 
 number varies greatly, from a few large or small nodules to innu- 
 merable tubercle-like forms in general carcinomatosis. In some 
 situations, as in bones, secondary carcinoma has an infiltrating 
 character. 
 
 Seats. — The situations in which carcinomata occur are very 
 numerous ; they invariably arise from pre-existing epithelial 
 structures. In the rare instances in which a presumably primary 
 carcinoma has occurred in bone or other connective tissues, the 
 presumption is warranted that the tumor originated from remnants 
 of epithelial tissue left by faulty development. Among the fre- 
 quent places of origin the most important are the uterus, the skin, 
 the gastro-intestinal tract, particularly the esophagus, pylorus, and 
 rectum, the mammary gland, the ovaries ; less frequently the liver, 
 kidney, thyroid gland, prostate, or testicle may be the starting- 
 point. Secondary carcinomata curiously do not often affect parts 
 in which the primary growth is frequent. Of the many seats 
 of secondary carcinoma, the lymphatic glands, the liver, spleen, 
 lungs, heart, and serous membranes are the most important. Sec- 
 ondary carcinoma of the bones is specially frequent after carcinoma 
 of the breast or the thyroid gland. 
 
 Structure. — The histology of carcinoma varies greatly in dif- 
 ferent situations and in different forms. There are two distinct 
 
PROGRESSIVE TISSUE-CHANGES. 
 
 167 
 
 elements involved — viz., epithelial cells and a connective-tissue 
 stroma. The epithelial cells are medium-sized or large cells of 
 epithelial appearance, having a rather large and clear nucleus ; 
 the shape of the cell, however, differing widely. In epithe- 
 liomata of the skin the cells are large and of a squamous variety. 
 In carcinomata of mucous membranes they are more often cylin- 
 drical or columnar, and there is a tendency to the formation 
 of cuboidal or polyhedral epithelium. The last-named forms are 
 habitually present in the cancers of glandular organs. The mutual 
 compression exercised may occasion a polymorphous character, 
 and the older writers regarded this as a distinctive feature by which 
 a carcinoma-cell could be recognized as such. Secondary changes 
 may occasion wide variations in the appearance of the cells ; thus 
 the epithelia of cancers of the skin tend to become arranged in 
 concentric whorls and at the same time to become somewhat 
 glistening from horny transformation (Fig. 67). The nucleus 
 
 llftiliillliail::!!;' 
 
 Fig. 67.— Epithelioma of skin, showing concentric arrangement and degeneration of cells. 
 
 may be clear and quite structureless, or may show a distinct 
 nucleolus and a definite chromatin network. Karyokinetic fig- 
 ures may be quite abundant and are frequently atypical. Degen- 
 erative changes (dropsical infiltration, myxomatous change, fatty 
 degeneration) may alter the nucleus as well as the body of the 
 cell. 
 
 The epithelial cells are usually grouped in the form of acini ; 
 
168 TEXT-BOOK OF PATHOLOGY. 
 
 either completely filled so as to form epithelial clumps or columns, 
 or in alveoli with a central lumen surrounded by epithelial cells 
 in a number of layers. In the last respect the alveoli differ strik- 
 ingly from those of adenoma, and there is the further difference 
 that cellular outgrowths may be seen at the periphery of the acini, 
 the "ells having broken through the retaining wall (basement- 
 membrane) and proliferated outside to form new clumps (Fig. 68). 
 
 ■^K, 
 
 «*• 
 
 
 Vx-;< <"$' ^r- : ; -■".:■<;•.-' '/• f -rK-~ 
 
 ■// 
 
 
 Fig. 68. — Carcinoma of uterus. 
 
 On examination of the epithelia within the acini it is found that 
 those of the peripheral layer frequently retain the columnar char- 
 acter seen in the normal alveoli of the gland from which the tumor 
 springs. The connective-tissue stroma of carcinoma is more or 
 less dense, but practically is always of fibrous character. It is 
 arranged in such manner as to form hollowed spaces or columns 
 in which the epithelial structures already described are embedded. 
 Frequently infiltrating leukocytes and plasma-cells or mast-cells 
 are seen within the stroma, and the latter also bears the vascular 
 channels that supply the tumor. 
 
 The above description applies to the ordinary carcinoma of 
 glandular organs. Differences are observable in the cancers of 
 the skin and other external surfaces. In these the structure is 
 rather that of much enlarged papilla? penetrating into the deeper 
 tissues. The cells are similar to those of the deeper layers of the 
 skin, are larger than those of glandular cancers, and more translu- 
 cent. Hollowed alveoli are exceptional. 
 
 Degenerative Changes. — Carcinomata are quite prone to 
 
PROGRESSIVE TISSUE-CHANGES. J 69 
 
 degenerations. In nearly all cases in which the tumor has reached 
 considerable size more or less fatty degeneration of the cells 
 becomes apparent. Preceding this or associated with it may be 
 cloudy swelling or dropsical infiltration of the cells, rendering the 
 nuclear outline less distinct and sometimes causing vacuolations. 
 Irregular and multiform nuclear degenerations are met with, and 
 probably occasion some at least of the structures known as para- 
 sites of cancer. The epitheliomata of the skin are particularly 
 prone to a horny transformation, this occurring first and most 
 prominently in the concentric whorls already described. In the 
 adenocarcinomata of the ovaries and other genital organs of women 
 the degenerated epithelial cells frequently undergo calcareous infil- 
 tration, and psammomata are thus formed. Colloid degeneration 
 of the epithelial cells is a rare event, and the term colloid cancer is 
 generally a misnomer, the real degeneration in most of these being 
 myxomatous, affecting the connective tissue principally, though 
 the epithelial cells are to a certain extent involved. Complete 
 degeneration by myxomatous or associated myxomatous and fatty 
 change may destroy all of the characteristics of the original tumor. 
 In some cases cystic transformation occurs in organs the seat of 
 cancer, or in the cancer itself. This may be due to occlusion and 
 subsequent dilatation of the ducts of the organ or of the acini in 
 the tumor, the cystic spaces becoming filled with mucoid or 
 gelatinous material. In some instances cystic carcinomata are 
 secondary developments originating in cystic adenomata. Hyalin- 
 change and pigmentation are rare in cancer. 
 
 Inflammatory processes are quite common. Cancers on free 
 surfaces are prone to undergo ulceration in consequence of irrita- 
 tion and infection. Among the micro-organisms discovered in 
 such instances the staphylococcus and streptococcus are conspicu- 
 ous. A distinct erysipelatous inflammation may occur in cancers 
 as in other structures. Invasion of tubercle-bacilli and the 
 deposit of miliary tubercles in carcinoma are rare events, though 
 they sometimes occur. Associations of carcinoma and tuberculosis 
 or syphilis may in other cases result from the secondary growth 
 of cancer in pre-existing gummatous or other syphilitic lesions or 
 in lupus. Practically all carcinomata show some leukocytic infil- 
 tration. The amount of this, however, varies greatly. 
 
 Nature. — Carcinoma is essentially malignant, the degree of 
 malignancy depending, however, upon the seat and upon certain 
 peculiarities of disposition of the individual. Sometimes a small 
 growth may remain practically latent for a long time, until acci- 
 dental circumstances, like traumatism, intercurrent disease, preg- 
 nancy, or the like, stimulate active growth. 
 
 Carcinoma exhibits all the elements of malignancy : the ten- 
 dency to recur after removal, metastasis, and general destruction 
 of the health. Recurrence after removal is most readily explained 
 
170 TEXT-BOOK OF PATHOLOGY. 
 
 upon the assumption that the entire growth had not been re- 
 moved. Microscopic studies show that the area of infiltration is 
 usually much greater than the naked-eye appearances would indi- 
 cate, and this explains why the surgeon cannot well remove the 
 whole disease. Metastasis, as a rule, follows the lymphatic chan- 
 nels, and thus primarily involves the lymphatic glands in the 
 neighborhood of the growth. The process may be explained as 
 follows : some of the epithelial cells in their advancing prolifera- 
 tion penetrate the lymphatic channels and are carried in the 
 lymph-stream to the nearest lymphatic gland, where they again 
 proliferate and form secondary nodules ; from these a similar 
 extension occurs, and eventually widespread metastasis results. 
 Less frequently the primary growth penetrates the walls of a vein 
 and metastasis occurs through the circulation. This is quite com- 
 mon in the case of cancers of the stomach or intestines. The 
 metastatic foci first spread through the portal circulation to the 
 liver. In still other instances secondary growths result from 
 mechanical transportation in the movements of the body ; thus 
 in carcinomata of the abdominal organs the peristaltic move- 
 ments may transfer particles to different parts of the abdominal 
 cavity. 
 
 Pathologic Physiology. — The general health of patients suffer- 
 ing with carcinoma is affected very profoundly, though the man- 
 ner in which this occurs remains obscure. It would seem to be 
 of the nature of a toxemia. Emaciation and loss of strength are 
 habitual, though often, perhaps, in large part the result of inter- 
 ference with organic functions, as, for example, in carcinoma of 
 the stomach. Progressive anemia may make its appearance, the 
 red corpuscles becoming less abundant and the quantity of hemo- 
 globin falling decidedly. There is usually a moderate amount of 
 leukocytosis, the large mononuclear forms increasing particularly. 
 Toward the end of life the tissue-destruction increases greatly, 
 though the excretory products of such may not be notably in- 
 creased in the excretions in consequence of failing circulation and 
 imperfect renal function. At this stage the accumulation of such 
 products in the blood may lead to sudden death from coma (see 
 Acid-intoxication). Hemorrhages and ulcerations may also con- 
 tribute to the impairment of health in cases of cancer. 
 
 Varieties of Carcinoma. 
 
 There are several forms of cancer sufficiently different to re- 
 quire separate description. The classification of these is generally 
 based upon the character and arrangement of the epithelium. We 
 may distinguish ( 1 ) carcinomata composed of surface-epithelium, 
 either (a) squamous or (b) cylindrical, and (2) glandular carcino- 
 mata, having either (a) more or less distinct adenomatous structure 
 
PROGRESSIVE TISSUE-CHANGES. 
 
 171 
 
 or (6) solid plugs or columns of epithelial cells, or (c) a mixture 
 of acini and solid columns. 
 
 Epithelioma. 
 
 This form, which consists of surface-epithelium, is of two 
 varieties, the squamous and the cylindrical. 
 
 Squamous epithelioma occurs in the skin or mucous mem- 
 branes, where squamous epithelium exists normally. Among the 
 frequent seats are the lips, the esophagus, the larynx, and the cer- 
 vix uteri. Occasionally squamous epithelioma arises in parts nor- 
 mally covered by other kinds of epithelium ; as, for example, in 
 the fundus of the uterus. In these instances there is probably a 
 primary metaplasia of the epithelium followed by carcinomatous 
 growth. Squamous epitheliomata present themselves as nodular, 
 wart-like elevations of the skin or mucous membrane, tending to 
 become ulcerated on the surface. Those of the mucous surfaces 
 are more elevated and softer. Histologically there are seen branch- 
 ing columns of epithelial cells extending downward from the pa- 
 pillae of the skin into the deeper structures. These consist of 
 large translucent squamous cells which show a tendency to arrange 
 themselves in certain places concentrically to form epithelial 
 perles. The latter frequently undergo a horny transformation 
 and sometimes even calcareous change (Fig. 69). The same 
 
 Fig. 69.— Squamous epithelioma, showing whorls of epithelial cells with central degen- 
 eration (from a photograph by Dr. W. M. Gray). 
 
 structures occasionally occur in benign papillomata, but much less 
 frequently. Metastasis is frequently seen in the neighboring 
 lymphatic glands, but the malignancy is less marked than in 
 glandular carcinomata. 
 
 Cylindrical Epithelioma.— This form is composed of co- 
 lumnar or cylindrical epithelium, and arises in the mucous mem- 
 branes, especially in the gastro-intestinal tract and the uterus. 
 
172 TEXT-BOOK OF PATHOLOGY. 
 
 The epithelial cells of the tubular glands or sometimes those 
 of the surfaces form the starting-point of the growth. More 
 or less acinus-like tubular structures, composed of a layer of 
 epithelial cells, or more frequently of a number of layers of epi- 
 thelia, the outer layer being often distinctly columnar, constitute the 
 characteristic feature of the tumor (Fig. 70). In the later stages 
 
 
 -'•"- ' • "•]■'''■' ^'V-li 'ST ' - ■ ASIA'S '"!?£' ■o'''-« '•■■''■ ' ■ 
 Fig. 70.— Cylindrical epithelioma of the intestine (Perls). 
 
 the acini become filled with proliferated epithelial cells of various 
 shapes and the cylindrical or tubular character of the acini is lost. 
 Carcinomata of the kidney, liver, and mammary gland, though not 
 originating from surface-epithelium, strictly speaking, may be of 
 the cylindrical form. Cylindrical epitheliomata are more nearly 
 like the glandular carcinomata in their malignancy and general 
 behavior than the squamous variety. 
 
 Glandular Carcinoma. 
 
 This term includes the carcinomata that have a resemblance 
 to racemose glands in their histologic structure. They consist 
 of acini or alveoli containing epithelial cells, usually in several 
 layers or completely filling the lumen, and a stroma of connective 
 tissue. Some authors distinguish three forms: the simple, the 
 medullary, and the scirrhous. These are simply variations of the 
 same tumor. In the simple form there is a combination of epi- 
 thelium and stroma in about the proportion seen in normal glands. 
 The tumor is therefore neither strikingly hard nor soft. In the 
 
PROGRESSIVE TISSUE-CHANGES. 
 
 173 
 
 medullary or soft carcinoma the amount of epithelium is excessive 
 and the tumor has a soft character (Fig. 71); while the scirrhous, 
 
 Fig. 71.— Medullary carcinoma of breast. 
 
 or hard, cancer is an indurated form, due to excess of fibrous tissue 
 and deficiency of the epithelium (Fig. 72). 
 
 The glandular cancers are more or less nodular or infiltrating 
 
 *fc 
 
 
 
 % 
 
 —Scirrhous cancer of brea 
 
 ,st (Warren; 
 
 
 growths varying in consistency in different cases, but having on 
 section a glistening white color with a certain amount of translu- 
 
174 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 cency. Milky liquid exudes from the surface on section. This 
 is composed of albuminous fluid containing degenerated epithe- 
 lium and free oil-droplets. Among the seats in which these forms 
 occur the most important are the pylorus and other mucous sur- 
 faces, the mammary gland, the pancreas, kidneys, ovaries, and 
 testicles. Widespread metastasis and other features of malignancy 
 are noted. In the case of the scirrhous form the primary tumor 
 may be strikingly small in comparison with the amount of meta- 
 static deposit. 
 
 Colloid Cancer. 
 
 This term is usually a misnomer, as most of the colloid cancers 
 contain no colloid material. The name gelatinous would be more 
 appropriate, but has not been generally accepted. Colloid cancers 
 are met with in the stomach and intestinal tract, in the mammary 
 gland, and in the ovaries. The tumor has a peculiar transparent, 
 glistening appearance. The entire mass maybe uniformly jelly- 
 like, or only portions of it are aifected. Microscopically mucous 
 degeneration of the connective tissue as well as of the epithelial 
 cells is discovered (Fig. 73). In some cases no trace of carcinom- 
 
 FlG. 73.— "Colloid cancer" of the breast, showing myxomatous change in the stroma and 
 fatty degeneration and partial disappearance of the epithelial cells (Perls). 
 
 atous tissue may be discoverable, the whole tumor having under- 
 gone degeneration. Sometimes the process involves the epithelium 
 rather than the connective tissue. ( !< illoid cancers frequently spread 
 by direct extension, and the entire abdominal cavity may become 
 filled with gelatinous material, representing degenerated secondary 
 growths. Occasionally the same kind of peritoneal growths seem 
 to originate primarily in the peritoneum, springing from fetal rem- 
 nants of epithelial tissue (Fig. 74). 
 
 True colloid cancer — that is, carcinoma with colloid degenera- 
 tion of the epithelium — is sometimes seen, though it is very rare. 
 It occasionally causes a gross appearance resembling that of sar- 
 
PROGRESSIVE TISSUE-CHANGES. 
 
 175 
 
 comatous cylindroma, and the term carcinomatous cylindroma has 
 been applied. 
 
 Fig. 74.— Colloid cancer of the peritoneum (modified from Birch-Hirschfeld). 
 
 SYNCYTIOMA MALIGNUM. 
 
 This term is applied to a form of tumor originating at the 
 placental site during pregnancy or the puerperium. It has also 
 been called deciduoma malignum, sarcoma deciduocellulare, 
 destructive epithelial tumor of the placental site, and chorio- 
 epithelioma. 
 
 The tumor occurs as a hemorrhagic infiltrating growth, some- 
 what resembling placental tissue in gross appearance, and fre- 
 quently gives metastasis by breaking into the blood-vessels. The 
 metastatic nodules are found in the external genitalia, frequently 
 in the lungs, less often in the liver, spleen, or other organs. The 
 growth is rapid, the uterine wall being quickly invaded and met- 
 astasis occurring in a short time. 
 
 The nature of this tumor is still the subject of some contro- 
 versy. Two types of cellular elements are recognized in its struct- 
 ure. One of these consists of irregular masses of protoplasm con- 
 taining dark nuclei. The nuclei probably multiply by direct 
 division. These protoplasmic masses are arranged in islands or 
 in branching columns which form a network. In the meshes of 
 this network are blood-spaces containing thrombi or masses of 
 blood-corpuscles. Sometimes masses like those above described are 
 found within the blood-spaces. The second form of cells consists 
 
176 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 of smaller irregular-shaped elements, which are unusually rich in 
 glycogen, and in which cell-division by karyokinesis is observed. 
 These cells lie in masses, of greater or less size, between and beside 
 the larger protoplasmic areas before described. In the later stages 
 of the growth obliterative thrombosis of the vessels leads to necro- 
 sis of the cellular constituents, particularly of the columns of large 
 epithelium-like cells. These are converted into homogeneous 
 fibrinous masses, and even the thrombi themselves may degen- 
 
 Fig. 75.— a, Fibrin, with numerous small round cells caught in the meshes : b, cells 
 resembling decidual cells, probably a proliferation of the Langhan's cells ; d, protoplasmic 
 masses containing large free nuclei. 
 
 erate. The view of Marchand regarding the nature of these 
 tumors is most widely accepted. He holds that the larger cells 
 are derivatives of the syncytium (a structure composed of epithe- 
 lial cells, probably of fetal origin), while the smaller cells are 
 formed from the epithelial covering of the chorion villi (Langhan's 
 cells). The tumor, therefore, is epithelial in nature, and it has 
 malignant properties. It differs, however, from ordinary epithe- 
 lioma and from carcinoma in its peculiar structure and in its clin- 
 ical course and dissemination. 
 
 CYSTS. 
 
 -This term includes pathologic formations of 
 Some are true tumors ; others are of quite dif- 
 
 Definition. 
 
 varied character, 
 ferent nature. 
 
 The term cyst is applied to pathologic formations consisting of 
 a more or less well-defined wall and enclosing liquid or semiliquid 
 contents of different character from the surrounding parts. This 
 definition is not entirely applicable, as certain structures that do 
 
PROGRESSIVE TISSUE-CHANGES. Ill 
 
 not present a definite capsule are sometimes termed cysts. Ac- 
 cordingly we may distinguish between true cysts and cyst-like 
 formations or cystoids, the former being enclosed by a capsule 
 lined with epithelium or endothelium ; the latter merely present- 
 ing a circumscribed collection of softened material. 
 
 Classification. — According to the method of formation, we 
 distinguish retention-cysts, softening-cysts, cysts due to the pres- 
 ence of foreign bodies, and proliferation-cysts. 
 
 Retention-cysts are formed when the excretory ducts of a gland 
 become occluded and the secretions accumulate and cause disten- 
 tion of the acini or of parts of the duct. Among such cysts may 
 be named the distended sebaceous glands of the skin in the forma- 
 tions called wens; the cysts of the salivary or small mucous 
 glands or ducts under the tougue, called ramdce ; retention-cysts 
 formed in the' uriuiferous tubules, the tubules of the ovary, or in 
 the parovarium, in the acini and ducts of the mamma?, pancreas, 
 and other glands. An entire organ may become converted into a 
 cyst, as in cases of distention of the kidney (hydronephrosis) from 
 obstruction of the ureter. 
 
 These cysts are distinguished by the fact that they have a dis- 
 tinct connective-tissue wall lined with epithelium or endothelium. 
 The contents of the cyst depend upon the part in which the forma- 
 tion has taken place. 
 
 Softening-cysts occur in consequence of degenerative softening 
 of normal or pathologic tissues. They are not rarely the result 
 of hemorrhage, the blood-clot first becoming inspissated and then 
 serous exudation occurring in the area of hemorrhage. Softening- 
 cysts are very common in tumors of different kinds. 
 
 Cysts due to foreign bodies are in part softening-cysts. The 
 tissues in the immediate vicinity may be injured and undergo 
 necrotic softening, while connective-tissue reaction produces a 
 capsule. This form of cyst is most frequently the result of in- 
 vasion of parasites, and the cyst-contents may be composed of 
 the parasite or the parasite and tissue-elements more or less 
 degenerated. 
 
 Proliferation- cysts. — This term is applied to formations more 
 closely analogous to true tumors than those mentioned before. 
 They merit more extended description than the other forms of 
 cysts, and may be designated as epithelial cysts. 
 
 Epithelial Cysts. 
 
 Definition. — In certain glandular organs, notably the ovary 
 and mammary gland, cystic formations occur which present strik- 
 ing appearances ; and though perhaps they represent adenomatous 
 or carcinomatous new growths, are so striking as to deserve special 
 mention. 
 
178 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 Ktiology. — These growths, in part at least, result from ob- 
 struction of excretory ducts and subsequent irritation by retained 
 secretions. Congenital abnormalities of structure may possibly 
 play a part in their causation. 
 
 Appearance. — Cystomata may be single or multiple, the 
 entire tumor being composed either of a single cyst or of one large 
 cyst subdivided into many smaller, or again of numerous separate 
 and unconnected cysts of varying size. On section the cystic 
 cavities are found to contain more or less serous or gelatinous 
 liquid, and sometimes hemorrhagic fluid is observed. Most fre- 
 quently the liquid is gelatinous or ropy, and is commonly spoken 
 of as colloid material. The inner lining of the cyst may be 
 smooth, like a serous or mucous surface, or elevated irregularly in 
 the form of polypoid outgrowths into the cavity of the cyst. The 
 entire cyst may thus be tilled with papillomatous elevations from 
 the epithelial lining. The term papuliferous or proliferative cyst- 
 omata is given to these forms (Fig. 76). The size of cystomata 
 
 
 Fig. 76.~Papilliferous adenocystoma of the kidney (Karg and Sehmorl). 
 
 varies from minute tumors not larger than a pea to enormous 
 masses weighing as much as sixty or eighty pounds. Secondary 
 degenerations may occur in the form of softening, hemorrhage, or 
 calcification. 
 
 Seats. — The mammary gland and ovary are the principal 
 situations in which tumors of this description are met with, but 
 analogous growths may make their appearance in any of the 
 glandular organs. 
 
 Structure. — Microscopically these growths present cystic 
 cavities lined with typical or modified columnar epithelium and a 
 stroma or reticulum of connective tissue. The amount of the 
 
PROGRESSIVE TISSUE-CHANGES. 179 
 
 latter and the appearance of the cysts themselves vary in different 
 cases. At times the stroma is very abundant and takes the form 
 of well-organized fibrous tissue, while the cysts and acini are small 
 and few in number. In these cases the appearance suggests a 
 primary proliferative connective-tissue process with secondary 
 implication of the epithelial elements. Such cases occur particu- 
 larly in the mammary gland, and there is difficulty in separating 
 them sharply from instances of chronic interstitial mastitis or dif- 
 fuse fibroma. In other instances the process manifestly begins 
 with the formation of epithelial acini, and the hyperplasia of 
 the connective tissue is certainly secondary. The acini in these 
 cases present themselves as hollow spaces of varying shape and 
 size, often branching, and lined with columnar epithelium in a 
 single layer or sometimes with several layers of more or less dif- 
 ferentiated columnar epithelium. 
 
 Nature. — These cystic growths often have a decided tendency 
 to malignancy. They may remain benign throughout; but fre- 
 quently they undergo carcinomatous change and spread widely or 
 give rise to metastasis. The malignancy is generally in propor- 
 tion to the amount of the epithelial proliferation and papuliferous 
 change, but there are instances in which metastasis occurs from 
 adenocystomata having regular gland-acini lined with single layers 
 of typical columnar cells. The cystomata of the ovary not rarely 
 extend to the surface of the organ, break through the capsule, and 
 present upon the surface as papillary growths, and frequently 
 they extend to the peritoneum and neighboring structures. The 
 entire abdomen may be involved. At the same time, or in other 
 cases independent of such direct extension, metastatic deposits 
 may be seen in nearby lymphatic glands. Somewhat the same 
 conditions may be observed in cystoma of the breast, but in this 
 situation the tumor is much more frequently confined within the 
 capsule of the organ. 
 
 TERATOMA. 
 
 Definition. — The term teratoma is applied to tumors of pecu- 
 liar mixed character, representing different elements of complex 
 tissues or structures in a situation in which these do not normally 
 occur. For example, the most frequent form of teratoma contains 
 various epidermal structures, such as hair, teeth, etc., and occurs 
 in internal organs. 
 
 Ktiology. — The causation of teratoid tumors or teratomata is 
 to be sought in congenital misdevelopments. We may, with Klebs, 
 distinguish endogenous forms, in which inclusions of superficial 
 tissues are retained in internal parts by a process of constriction ; 
 and eetogenous forms, in which a separate fetal deposition is the 
 origin of the tumor. The latter form represents a separate and 
 
180 TEXT-BOOK OF PATHOLOGY. 
 
 ill-developed fetus within the developed organism — a. fetus infetu. 
 A regular gradation may be traced from distinct teratoid tumors 
 having irregular mingling of tissue-elements, to malformations in 
 which a more or less systematic outgrowth, somewhat approaching 
 double monstrosities, occurs. Of the distinct teratoid tumors the 
 most frequent is the dermoid cyst. 
 
 Dermoid Cyst. 
 
 This tumor presents itself as a cystic formation with a con- 
 nective-tissue membrane and an inner lining resembling the skin. 
 This may present all the elements of the skin, such as stratified 
 epidermis, a papillary layer, and even subcutaneous connective 
 tissue. Hair-follicles and sebaceous glands are frequent, and 
 habitually long, light-colored hairs are found within the contents, 
 and teeth may be found in the lining membrane or free in the 
 contents of the cyst. The cyst is filled with a semifluid, cheesy 
 mass consisting of epithelial cells, fatty matter, and other detritus. 
 Occasionally dermoid cysts may contain nerve-tissue, muscle, or 
 structures resembling intestine. 
 
 The dermoid cysts vary in size from minute bodies no larger 
 than a pea to huge masses, the latter being most frequent in the 
 ovaries. Among the situations in which dermoids occur the 
 ovaries are most common ; less frequently they are found in the 
 testicles, in the peritoneum, in the membranes of the brain, about 
 the eye, in the neck, floor of the mouth, and elsewhere. Growth 
 is very slow, and they may remain practically latent through life. 
 
 The nature of these tumors is usually benign, though carcinom- 
 atous change may occur, and in the ovaries cystoma is prone to 
 be associated, and the latter may be malignant. 
 
 Other Teratoid Tumors. 
 
 Nodular masses may appear about the head or neck or in vari- 
 ous parts of the body, consisting of mingled tissues of various 
 kinds, such as glandular tissues, connective tissues, nerve, mus- 
 cle, etc. These can be classified as teratoid growths. Sometimes 
 they resemble some definite organ, as in the case of growths 
 appearing at the umbilicus of the new-born and simulating the 
 structure of normal intestine. 
 
 In the neck there are sometimes seen more or less cystic 
 growths lined with epithelium and having in their walls muscle- 
 fibers, lymphoid tissue, cartilage, etc. These growths probably 
 spring from remnants of the embryonal branchial clefts. The 
 mixed tumors of the parotid gland (sec Sarcoma) are allied to 
 these. 
 
 Cholesteatoma. — This tumor is characterized by glistening, whit- 
 ish, or pearly bodies composed of concentric layers of cells resem- 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 181 
 
 bling epithelium (Fig. 77). Sometimes crystals of cholesterin are 
 found in the center of these bodies, whence the name choles- 
 teatoma. Cholesteatomata are found in the membranes or sub- 
 stance of the brain, and present themselves as single or multiple 
 nodules. They are usually soft and glistening in appearance. 
 
 
 ® 
 
 
 i Ma 
 
 
 Fig. 77.— Cholesteatoma from the membranes of the brain. 
 
 Some authors consider them endotheliomata, but Ziegler has 
 found hair-follicles and hairs in certain specimens, and from this, 
 as well as from the horny change to which the cells in the pearly 
 bodies are prone, classifies them among the teratoid growths. 
 
 Somewhat similar tumors occur in the pelvis of the kidneys, in 
 the testicles, parotid glands, ovaries, and middle or external ear. 
 
 CHAPTER VII. 
 
 BACTERIA AND DISEASES DUE TO BACTERIA. 
 
 History. — Although for many centuries there had existed the 
 idea that disease and decay are due to the action of minute or- 
 ganisms, it was not until the use of the lens enabled the Dutch 
 naturalist Leeuwenhoeck actually to demonstrate their presence in 
 water and in human intestinal contents that the hypothesis of a 
 " contagium vivum " became more than mere guesswork. He 
 discovered, even with his imperfect instruments, short rods, curved 
 and straight, and described their motility. Muller (1785), by the 
 use of the compound microscope, attempted a more systematic 
 
182 TEXT-BOOK OF PATHOLOGY. 
 
 classification of these micro-organisms, and from this time many 
 investigators have added much to our knowledge of microbes, 
 that group of organisms which had been denominated by Linnaeus 
 by the term Chaos. To the German Henle is due the credit of 
 having first introduced an idea of order into this disorder. He 
 held that fermentation was the result of organic life, and that the 
 action of a contagium was analogous to that of a ferment. The 
 earliest systematic experimental work was that of Pasteur, in which 
 he established beyond doubt this relation between fermentation 
 and the life and development of bacteria. The first definite ideas 
 of the physiology of these micro-organisms are found in his experi- 
 ments on lactic-acid fermentation, and those of their pathogenesis, 
 in his demonstration of the microbic origin of the silkworm-disease 
 (1869). Davaine and Bayer about the same time established the 
 causal relation of a bacillus found in the blood of a sheep dead 
 of anthrax to that disease. 
 
 CLASSIFICATION. 
 
 Bacteria (schizomycetes, or cleft fungi) is the name given to a 
 branch of the lowest and simplest of the orders of the vegetable 
 kingdom. They are small, unicellular organisms, generally free 
 of chlorophyll, and colorless; they possess a cell-membrane albu- 
 minoid in composition and homogeneous protoplasmic cell-contents. 
 Some varieties are motile. Nuclei are absent, though in the opin- 
 ion of some the whole cell may be regarded as a nucleus. Bac- 
 teria multiply by cell-division, sexual distinctions being absent. 
 In many species resistant forms — spores — occur. 
 
 The simple elementary forms that occur are of three kinds : 
 the coccus, the bacillus, and the spirillum (Fig. 78). 
 
 7 
 
 6 
 
 m ^ '¥ M 
 
 Piq. 78.— Various forms of bacteria : 1 and 2, round and oval micrococci : 3, diplococcl; 
 ■1. tetracocci, or tetrads ; •">. Btreptococci ; ('•. bacilli ; 7, bacilli in chains, the lower showing 
 Bpore formation; 8, bacilli showing spores, forming drumsticks and Clostridia; 9 and 10, 
 spirilla; 11, spirochete. 
 
 COCCUS. — This is a spherical cell, varying in size up to 1 fi in 
 diameter. It takes the anilin-stains readily. Spore-formation 
 and motility are rare. When the cocci are found in groups, the 
 individuals being entirely separate, they arc termed staphylococci, 
 from the resemblance of the groups to a bunch of grapes; when 
 in pairs, diplococci ; when in chains, streptococci ; when in groups 
 of four, tetrads or merismopedia ; when in packets, sarcinae. 
 
 Bacillus. — A rod-shaped, cylindrical cell of varying length 
 and thickness. Spore-formation and motility are common. Most 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 183 
 
 of the group stain easily with the anilin dyes, but some require 
 special methods of staining. 
 
 Spirillum. — A cylindrical, rod-shaped cell, curved or spiral, 
 sometimes motile. It stains readily. 
 
 Many other classifications, all of them being to a certain extent arti- 
 ficial, have been made by different authors. Probably one of the most 
 useful and scientific is that of Migula : 
 
 I. Coccaceae. — Spherical cells dividing in one, two, or three directions. 
 
 Endospores rare. 
 
 1. Streptococcus. — Division in one direction, the individuals cohering 
 
 to form chains. Motility absent. 
 
 2. Micrococcus. — Division in two directions, the individuals when 
 
 coherent forming groups of four. Flagella absent. 
 
 3. Sarcina. — Division in three directions, forming packets of eight, 
 
 twenty-seven, or more cells. Motility absent. 
 
 4. Planococcus. — Division in two directions, as in the micrococcus. 
 
 Motility present. 
 
 5. Planosarcina. — As the sarcina. Motility present. 
 
 II. Bacteriaceae. — Rod-like, cylindrical cells, dividing at right angles to 
 
 the long axis. 
 
 1. Bacterium. — Cells without flagella, often with spores. 
 
 2. Bacillus. — Cells with peritrichous flagella, often with spores. 
 
 3. Pseudomonas. — Cells with polar flagella ; spores rare. 
 
 III. Spirillaceae. — Cells cylindrical, curved, bent, or spiral. Division as 
 
 in II. 
 
 1. Spirosoma. — Cells rigid, without flagella. 
 
 2. Microspira. — Cells rigid, with one, rarely two or three, polar flagella. 
 
 3. Spirillum. — Cells rigid, with five to twenty polar flagella. 
 
 4. Spirocheta. — Cells flexible, motile, but without flagella : perhaps 
 
 possessing an undulating membrane. 
 
 IV. Chlamydobacteriaceae. — Cells united in a simple unbranched fila- 
 
 ment. Division in one direction. Forms non-motile; conidia. 
 
 1. Slreptothrix. — Cells united in a simple unbranched filament. 
 
 Division in one direction. Forms non-motile ; conidia. 
 
 2. Cladothrix. — Cells united in a filament, with a false branching. 
 
 3. Crenothrix. — Cells united in an unbranched filament, and dividing 
 
 in three directions into small rounded cells. 
 
 4. Phragmodiothrix. — Cells at first united in an unbranched filament, 
 
 and dividing in three directions. Later the separate cells break 
 through the thin membrane and grow out as branches. 
 
 5. Thiothrix. — Cells united in an unbranched filament contained in a 
 
 thin membrane. Division in one direction. Cells contain gran- 
 ules of sulphur. 
 
 V. Beggiatoacese. — Cells united in a filament without sheath. Motile, the 
 
 movement being due to an undulating membrane. 
 
 MORPHOLOGY. 
 
 Cell -contents. — The body of the organism in unstained con- 
 ditions appears as a perfectly homogeneous protoplasmic mass. On 
 staining with anilin dyes a granular appearance is often observed, 
 which under high powers is resolved into a hyaline mass contain- 
 ing numerous chromophilic granules. Vacuolations also are often 
 
184 TEXT-BOOK OF PATHOLOGY. 
 
 present. Some modern observers (Biitschli et «L) have made out a 
 network immediately within the membrane and surrounding a 
 central body which readily stains with the nuclear dyes. This 
 latter they regard as a nucleus. Others, however, affirm that this 
 appearance is due to a concentration of the cell-protoplasm (endo- 
 plasm), the result of the rather complicated method of staining. 
 The question of the presence or absence of a nucleus is still an 
 open one. In many organisms, as the Bacillus diphtherias from a 
 blood-serum culture, for example, there exist certain transparent 
 refractive bodies which stain differently from the rest of the 
 microbe. These metachromatic bodies, as they are called, were 
 regarded by Ernst as nuclear in character. ( )thers look upon 
 them as possibly the primary state of spore-formation. 
 
 Spore. — The spore is a non-vegetative resistant form that the 
 microbe assumes when the conditions for growth are unfavorable. 
 The endoplasm seems to concentrate and become a small, oval, 
 highly refractive body, separated from the bacterial protoplasm by 
 a membrane of its own. It is generally of the same diameter or 
 somewhat smaller than the bacillus itself, and is situated either in 
 the middle (equatorial) or at the end of the microbe (polar spore). 
 It may be larger in diameter than the microbe and cause a swell- 
 ing at that point. When in the center of the rod this gives rise 
 to the form known as Clostridium ; when polar, to the so-called 
 drumstick-form (as in the Bacillus tetani). 
 
 Such intracellular spores <>r endospores occur among many 
 bacilli. Among the micrococci they are rare ; but it is supposed 
 that certain individual cocci become larger and more refractive in 
 appearance and assume the spore-state. These are called arthro- 
 spores. Whether these can be regarded as true spores is still 
 doubtful. 
 
 The spore is extremely resistant to conditions to which the 
 vegetative form readily succumbs ; to the action of certain chemi- 
 cal reagents, light, heat, etc. Bacteria that are grown on media 
 poor in nutrient material tend to become asporogenous. A certain 
 temperature is also necessary for spore-formation. Thus, although 
 the anthrax bacillus develops well at a temperature of 14° C. 
 (57° F.), it does not form spores below 18° C. (64° F.). To obli- 
 gate aerobes oxygen is necessary for their development, and anae- 
 robic cultures present them only in the absence of that gas. 
 Placed under conditions favorable to its vegetation the spore loses 
 its clearness, absorbs water, and swells. A small prominence pre- 
 sents at the side or end, which gradually lengthens and develops 
 into a young bacillus. The membrane of this new microbe is 
 formed from the inner layer of the spore-membrane (endospoHum), 
 while the outer layer (exosporium) is cast off. In not all of the 
 varieties of bacilli does sporulation take place, and even where it 
 does occur there may, under certain conditions, as in growth at 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 185 
 
 high temperatures, arise races which have lost this power (aspo- 
 rogenous races). 
 
 The spore does not stain readily with the ordinary anilin 
 stains, and special methods have been devised for coloring it. 
 
 Cell-membrane. — Surrounding each organism is a membrane 
 (ectoplasm) denser and more highly refractive than the cell-con- 
 tents (endoplasm). In some cases this is not to be differentiated 
 from the endoplasm ; but in others it is larger, and under certain 
 conditions becomes a gelatinous mass. In this case it is easily 
 seen, especially after appropriate staining. This is called the 
 capsule. In general this occurs only when the bacteria develop 
 within the animal organism, and not upon artificial culture-media. 
 It is probable that the ectoplasm is not a mere protective envelop, 
 but has to do with the functional activity of the bacterium. The 
 fact that the flagella, to which is due the motility of certain mi- 
 crobes, are directly continuous with and are simply prolongations 
 of this membrane, points to this view. 
 
 The cell-membrane is not easily colored by ordinary methods. 
 
 Flagella. — Motility is often a property of bacteria. It is 
 manifested in different ways, and is often characteristic of the 
 several varieties of bacteria. Some move slowly forward across 
 the field, others with great rapidity ; others again dart hither and 
 thither, slowly or so quickly as to be with difficulty observed. 
 They may at the same time have a rotary movement around their 
 long or their short axes. 
 
 After appropriate staining the cause of this motility is seen to 
 be the presence of slender, whip-like prolongations, originating 
 directly from the ectoplasm (Babes). They may be twenty times 
 as long as the body of the bacterium, and are arranged in the dif- 
 ferent species in different ways. Bacteria that possess no flagella 
 are termed Gymnobacteria ; those that have these organs, 
 Trichobacteria. There may be but one flagellum, situated at the 
 pole (monotrichous), or a number may be present (lophotrichous). 
 When they are situated at both poles the microbe is termed amphi- 
 trichous ; when distributed over the whole body of the bacteria, 
 peritrichous. The presence and the activity of flagella depend on 
 many factors : on the condition of the medium, bacteria grown from 
 liquid media being more active than those from solid ; on tem- 
 perature ; on presence of air ; on light ; and on the age of the 
 culture. They are easily broken off from the microbe, and care 
 must be used in staining them. A special method is employed. 
 
 Invollltion-forms. — By involution-form is meant the irreg- 
 ular appearance a microbe often assumes when its conditions of 
 growth are unfavorable. Numerous bacteria melt together and 
 become irregular chains, or they appear pear- or club-shaped. 
 The protoplasm becomes retracted and irregular staining takes 
 place. Sometimes the microbes lose all characteristic appearances. 
 
186 TEXT-BOOK OF PATHOLOGY. 
 
 Sometimes forms with branching projections are discovered. 
 These have often been described as involution-forms, but are now 
 more commonly regarded as normal, though unusual, structures. 
 This applies to tubercle bacilli, diphtheria bacilli, and some 
 others. This true branching (dichotomy) must not be confounded 
 with false or pseudodichotomy, due to mere apposition of separate 
 organisms, as seen in various bacilli, streptococci, etc., and habitu- 
 ally in the cladothrices. 
 
 Chemistry. — The bacterial cells are of variable composition, 
 depending to a great extent upon the kind of nutrient matter. It 
 consists mainly of water (85 per cent.). The chief solid material 
 is albumin. This varies according to the medium of growth, and 
 has been given the general name of mycoprotein (Nencki). Fat 
 is also present. The nuclein-bases, xanthin, guanin, adenin, and 
 cellulose, have been found by some. Some contain certain color- 
 ing-matters, bacteriopurpurin and a green substance similar to 
 chlorophyll. Organic acids and ferments of different kinds are 
 also found. In some special forms — the sulphur bacteria — sul- 
 phur is present. 
 
 DEMONSTRATION. 
 
 The success of the microscopic examination of bacteria in 
 the several fluids and tissues of the diseased body and in pure 
 cultures depends upon the differentiation of the microbes from the 
 surrounding substances by certain chemical reagents. The process 
 is twofold : to render more transparent the non-bacterial elements 
 and to render more visible the bacteria themselves. Thus a 1^- 
 per cent, solution of sodium hydrate dissolves the histologic ele- 
 ments except the fatty, elastic, pigmentary, and amyloid substances 
 and bacteria. 
 
 Methods of this sort have been entirely superseded by the use 
 of the anilin dyes. We can with these render bacteria more visi- 
 ble and at the same time differentiate them from the surrounding 
 tissue by means of contrast- or counter-stains. 
 
 Microbes, generally, stain with dilute aqueous or alcoholic 
 solutions of the anilin colors, but they differ greatly in the readi- 
 ness with which they take the stain and the tenacity with which 
 they hold it after treatment. To stain some it is necessary to 
 employ heat or to add some chemical substance to act as a mor- 
 dant and enable the stain to pass through the cell-membrane. 
 The most important of these are potassium hydrate, anilin oil, 
 alcohol, carbolic acid (1-5 per cent.), acetic acid (0.5-1 per cent.). 
 
 Some bacteria decolorize easily, even with Mater ; others 
 can be placed in alcohol, and some in strong solutions of mineral 
 acids, without losing their color. Those bacteria that stain easily 
 are the most readily decolorized. 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 187 
 
 Among the more frequently used of the anilin dyes are : 
 methylene-blue, dahlia, fuchsin, vesuvin, gentian-violet and thi- 
 onin. The following are useful formulae : 
 
 Loffler's methylene-blue : 
 
 Saturated alcoholic solution of methylene-blue . 30 cc. 
 Aqueous solution of potassium hydrate (0.01 
 
 per cent.) 100 cc. 
 
 Carbolized ihionin: 
 
 Saturated alcoholic solution of thionin . . . . 10 cc. 
 Carbolic-acid solution (1 per cent.) 100 cc. 
 
 Bacteria stained with these upon cover-glasses need no after- 
 treatment, but tissues are to be decolorized with alcohol. With 
 Loffler's solution the decolorization must be stopped at a point 
 where the protoplasm is colorless and the nuclei are faintly stained. 
 The bacteria remain a bright blue. Bacteria stained with thionin 
 retain a reddish tinge, however, even after prolonged action of 
 the alcohol. 
 
 ZiehVs solution is the best known stain for the Bacillus tuber- 
 culosis : 
 
 Fuchsin 0.25 gm. 
 
 Alcohol 10 cc. 
 
 Carbolic-acid solution (5 per cent.) 100 cc. 
 
 Treated with this for some three to five minutes (for tissues 
 longer) and with heat, the bacilli retain their red color after the 
 use of strong mineral acid solutions (sulphuric, nitric, or hydro- 
 chloric acid, 25 per cent.). A counter-stain, to color the decolorized 
 cellular elements, is used, and methylene-blue is generally em- 
 ployed. Gabbett mixes the contrast-stain with the sulphuric-acid 
 solution. 
 
 Gram's Method. — Another important differential stain is that 
 devised by Gram. The specimen is treated for some minutes in 
 an anilin-water solution of gentian-violet. Anilin-oil (4 cc.) is 
 well shaken up with 100 cc. of distilled water, filtered, and to this is 
 added 1 cc. of saturated alcoholic solution of the violet. The 
 specimen, stained a few minutes with this, is treated with an 
 iodid-iodin solution (iodin, 1 gm. ; potassium iodid, 2 gm. ; water, 
 300 cc), which fixes or in some way modifies the stain in the 
 bacteria and decolorizes other elements. The further action of 
 alcohol decolorizes certain varieties of bacteria stained in this, 
 while others it leaves unchanged. Bacillus anthracis, tuberculosis, 
 tetani, lepra?, diphtherias, rhinoscleromatis ; Staphylococcus aureus, 
 albus, and citreus ; Streptococcus pyogenes ; Pneumococcus ; 
 
188 TEXT-BOOK OF PATHOLOGY. 
 
 Micrococcus tetragenus ; and Actinomyces hominis are the most 
 important species that retain the stain. The Gonococcus ; Bacil- 
 lus pneumonia?, typhi abdominalis, coli communis, mallei ; and 
 Spirillum cholera? Asiatics arc among those that are decolorized. 
 
 Staining sections is more difficult : it takes longer time and 
 must often be aided by heat. This results in overstaining, and 
 decolorization is necessary. Many substances have the power 
 of decolorizing the tissue-elements in the following order : the 
 first to lose the color is protoplasm, then the nuclei, and lastly 
 the bacteria. For such differential decolorization alcohol, anilin 
 oil, or acid alcohol is the most used, the point aimed at being to 
 stop the decolorization as soon as the nuclei have begun to lose 
 their color. Some stains are not removed by this means, as 
 Gram's and thionin. 
 
 To stain .spores, the specimen is fixed by passing through the 
 flame and then put for a half to one hour in fuchsin, either an 
 aqueous or alcoholic solution, or in Ziehl's solution. The bacterial 
 protoplasm is then decolorized by alcohol or very dilute nitric acid 
 and counter-stained with Loffler's blue. 
 
 The capsule is colored with Ziehl's stain and the cell-contents 
 decolorized with dilute acetic acid (1 drop to 5 cc. of water). 
 Ribbert saturates with dahlia the following: distilled water, 100 
 cc. ; alcohol, 50 cc. ; acetic acid, 12.5 cc), and stains but a few 
 seconds. A very useful method is to stain the bacilli with 
 Loffler's blue for a few minutes and wash for the same time with 
 anilin-gentian-violet. The bacilli are blue against a reddish back- 
 ground, the capsule standing out uncolored. This is especially 
 useful in staining sputa. 
 
 Flagella are still more difficult to stain. The cover-glasses 
 must be carefully cleansed from all dust and grease. After fixa- 
 tion they are treated with a mordant Avhile hot : 
 
 Aqueous solution of tannin (20 gm. to 80 cc.) . . 10 cc. 
 
 Aqueous solution of ferrous sulphate 5 cc. 
 
 Alcoholic solution of fuchsin 1 cc. 
 
 The stain is a saturated solution of fuchsin in anilin-water. As 
 used by Loffler, a certain quantity of alkali or acid is added to 
 the mordant, according to the species of bacteria, but this has 
 been found to be unnecessary. 
 
 BIOLOGY. 
 
 Bacteria may be divided into two great classes : those that 
 live only on dead organic matter are termed saprophytes; those 
 that develop in and at the expense of the living organism, para- 
 sites. These latter by their growth cause certain pathologic con- 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 189 
 
 ditions in the host, and are called pathogenic. By obligate sapro- 
 phytes or parasites we mean those that can exist only under the 
 conditions named ; by facultative saprophytes and parasites, those 
 that can develop under both conditions. 
 
 Conditions of Growth. — Certain surrounding conditions 
 are necessary to bacteria, and any marked change in them will 
 inhibit the growth or totally destroy it. 
 
 Mechanical Conditions. — A slight shaking of a liquid culture 
 seems to help the development of bacteria, while a more violent 
 and long-continued agitation, destroys them. 
 
 Physical Conditions. — Electrical currents destroy the growth, 
 but probably by the action of certain products of the electrolysis, 
 and not by direct action. 
 
 Light. — Diffused daylight inhibits the growth of bacteria : sun- 
 light and, to a less extent, electric light destroy them. 
 
 Heat. — A certain temperature is necessary, the degree varying 
 with the species of microbe. Most of the water bacteria and sapro- 
 phytes grow between 0° and 30° C. (32° and 86° F.), the optimum 
 being 15°-20° C. (59°-68° F.) (Psychrophilic). The pathogenic 
 flourish between 10° and 45° C. (50°-113° F.), best at the 
 body-temperature, 37° (98.6° F.) (Mesophilic). There are some 
 that develop well at 40°-70° C. (±04°-158° F.) (Thermophilic). 
 Above these limits the members of the several groups are killed, 
 and each bacterium has its own thermic death-point. That of 
 most of the pathogenic varieties lies between 50° and 60° C 
 (122° and 140° F.). Below the lower limit the growth is in- 
 hibited only; very low temperatures ( — 250° C. ; — 418° F.) hav- 
 ing been used without preventing the future development of the 
 microbe. 
 
 Spores are extremely resistant to higher temperatures. While 
 no bacterium can live after exposure to 100° C. (212° F.), the 
 spores of some of the earth microbes are killed only after exposure 
 for an hour to steam heated to 115° C. (239° F.)/ 
 
 Chemical Conditions. — The essential substances for the growth 
 of bacteria are water, carbon, nitrogen and oxygen, and certain 
 salts. For the carbon, they require already prepared carbon com- 
 pounds, as the sugars, glucose, saccharose, lactose, etc., mannite, 
 glycerin — in fact, most of such as are soluble in water. Most of 
 the proteids and many simpler substances, even such as ammonium 
 carbonate, furnish the nitrogen. Free oxygen is necessary for 
 many microbes. Those for which this is absolutely required are 
 termed obligate aerobic. Facultative aerobes are those that grow 
 best in the presence of oxygen, but may develop in its absence. 
 Anaerobic microbes are those that grow best without oxygen and 
 are also obligate and facultative. It has been found possible to 
 produce races which, although naturally obligate anaerobic, 
 develop also in an atmosphere of oxygen. 
 
190 TEXT-BOOK OF PATHOLOGY. 
 
 Artificial Cultivation. — It is difficult and often impossible 
 to study the growth of bacteria in their natural habitat. Hence 
 we have recourse to artificial media, upon which we can study the 
 growth and morphology of the organisms and the various phe- 
 nomena that it brings about in different substances. 
 
 Media for Cultivation. — Usehinsky's fluid is a non-albuminous 
 medium : 
 
 Water 1000 cc. 
 
 Glycerin 30-40 gm. 
 
 Sodium chlorid 5-7 gm. 
 
 Calcium chlorid 0.1 gm. 
 
 Magnesium sulphate 0.2-0.4 gm. 
 
 Calcium phosphate 2.5-3 gm. 
 
 Ammonium lactate 6-7 gm. 
 
 Sodium asparaginate 3-4 gm. 
 
 Bouillon. — Water, 1000 cc. ; lean beef or veal, 500 gm. ; salt, 
 10 gm. ; peptone, 5 gm. The beef is soaked in water and then 
 filtered. To the filtrate are added the salt and peptone, and the 
 whole boiled for some fifteen to twenty minutes. It is then 
 rendered slightly alkaline and filtered and sterilized. Ordinary 
 beef-extract may be substituted for the fresh meat. Growths of 
 bacteria in this medium are not especially characteristic, but in 
 some species important differences appear. The liquid may become 
 clouded or remain clear, the growth settling to the bottom of the 
 tube as a flocculent deposit. The presence or absence of any 
 growth on the surface of the bouillon (a membrane or mycoderm) 
 is noted, as is also any change in the reaction. 
 
 Peptone solution, prepared in the same way, but omitting the 
 beef, is of use in the determination of the indol-reaction (see 
 Bacillus typhi abdominalis). 
 
 Liquid blood-serum is rarely employed. 
 
 Milk, slightly alkaline and to which a small quantity of litmus 
 or lacmoid may be added, is employed in determining changes of 
 reaction and the action of caseating ferments. 
 
 Extracts of many vegetable substances are also used, as hay, 
 potato, brewer's malt, etc. 
 
 Potato-extract, prepared by rubbing up 500 gm. of potato in 
 500 cc. of water, decanting and diluting to 1000 cc, and adding 
 40 <«•. of glycerin, is a good culture for the Bacillus tuberculosis. 
 
 Solid undid. — The two most important solid media are gelatin 
 and agar-agar. These are used in 10 per cent, and 1 per cent, 
 solutions, respectively, in bouillon. Many bacteria produce a pro- 
 teolytic ferment that liquefies gelatin. Other distinctions also are 
 met with in cultures upon this media. 
 
 Blood-serum is placed in test-tubes, slanted and sterilized for 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 191 
 
 one to two hours on five consecutive days at 60° C. (140° F.). 
 The temperature is then raised to the point of coagulation of the 
 albumin and the serum is thus solidified. Loftier mixes with the 
 liquid serum one-third part of bouillon containing 1 per cent, of 
 glucose. A more rapid way is carefully to solidify the serum on a 
 water-bath or in the hot-air sterilizer, and then sterilize in steam 
 on three separate days. 
 
 Glucose, lactose, or saccharose, added to these media, may be 
 used to study the action of the various ferments. 
 
 Glycerin (5-6 per cent.) added to agar-agar forms good media 
 for the growth of the tubercle-bacillus. 
 
 Potatoes and other vegetables, cut in the form of half cylin- 
 ders, are also used. 
 
 Inoculation of Media. — In studying the growth of micro- 
 organisms a portion of the culture-fluid, or other substance to be 
 examined, is transferred to the various culture-tubes. To do this 
 an inoculating-needle (ose) is employed. This is most conveniently 
 made with a piece of platinum wire one to one and a half inches in 
 length, either straight or with looped end, and fastened into the 
 extremity of a glass rod. It should be an invariable rule to 
 sterilize this needle in the naked flame both before and after it is 
 used. In inoculating liquid media the transference of a loopful 
 of the culture or other substance is made to the culture-tube. 
 When solid media are employed a straight puncture may be 
 made into the medium, or this latter may be solidified in a 
 slanted position and the needle drawn along the surface. Due 
 regard must be had for the richness in bacteria of the substance 
 examined. With pure cultures but a minute quantity is trans- 
 ferred ; with blood, however, large amounts, even |- to 1 cc, is 
 often used. 
 
 To study the appearance of the separate colonies cultures on 
 gelatin or agar plates are made. The medium is melted and then 
 cooled to a temperature not destructive to the bacteria ; 40° C. 
 (104° F.) for agar, lower for gelatin. The liquid medium is in- 
 oculated carefully and poured into sterilized shallow glass dishes. 
 Those devised by Petri are useful. They are from three and a 
 half to four inches in diameter and half an inch or less deep. 
 Each microbe is supposed to form by its growth a separate 
 colony, and in this way different species can be easily isolated 
 and reinoculated on fresh tubes. When cultures are used, or 
 when the bacteria are very numerous, the requisite dilution may 
 be made by inoculating a second tube from the first, and in like 
 manner a third from the second. Esmarch, instead of pouring 
 plates, quickly rolled the tubes on a piece of ice or in ice-water, 
 thereby forming a thin coating of the solid medium on the inner 
 surface of the tube. If it is necessary to make a numerical esti- 
 mation of the bacteria, definite quantities of the medium and 
 
192 TEXT-BOOK OF PATHOLOGY. 
 
 culture must be employed in the dilution. Sterilized pipettes 
 are used in the process of diluting. 
 
 Anaerobic Cultures. — These arc made by growing the inocu- 
 lated tubes or plates in the absence of oxygen, either by exhaust- 
 ing the air or by replacing it by some inert gas, preferably 
 hydrogen. Many tubes have been especially devised for this 
 purpose. A more convenient method is to make a deep puncture 
 in a gelatin or agar tube, and then preventing the absorption of oxy- 
 gen by nearly filling the tube with melted sterile medium. It has 
 been also proposed to inoculate the surface of such a tube with a 
 culture of a strict aerobic microbe. Glass tubes of small caliber 
 and a foot or more in length, and filled with inoculated melted 
 media and sealed in a flame, give good results. 
 
 Aerobic cultures grown in the absence of oxygen do not form 
 spores, and may be destroyed by a subsequent temperature of 80° 
 C. (176° F.), thus permitting the sporogenous anaerobic forms to 
 develop in pure culture. 
 
 FUNCTIONS AND PRODUCTS OF BACTERIA. 
 
 The study of the substances that result from the action of the 
 life of bacteria and the changes that they produce in their various 
 media of growth is really a branch of organic chemistry. The 
 function of bacteria is essentially a destructive one. They split 
 up the higher nitrogenous and non-nitrogenous compounds into 
 simpler substances. 
 
 The various substances that are found in the media of bacterial 
 growth comprise : (1) the components of the bacterial cell proper, 
 as the proteins; (2) the secretions of the cell, as the ferments; 
 and (3) substances that are the result of the action of microbes 
 upon the medium of growth. 
 
 (1) The first group has already been spoken of (see page 186). 
 The proteins may produce suppuration {jjyogeiue) or fever 
 
 (pyrogenic), or they may be the cause of an inflammatory process 
 ( phlogogenic). The best known examples are mallein, derived 
 from the bacillus of glanders, and tuberculin, from that of tuber- 
 culosis. These are pyrogenic when injected into animals suffering 
 respectively from glanders or tuberculosis, but have no, or at least 
 very slight, effect upon healthy subjects. Other proteins are shown 
 to have similar effects on tuberculous animals. In practice the 
 curative effect of these has not proved of much worth. 
 
 (2) The second group of products includes the ferments and 
 possibly the toxins. 
 
 Ferments. — A ferment is a complex body about which we 
 know but little except the effects that it produces. By its pres- 
 ence, and probably without entering into intimate chemical com- 
 bination, it possesses the power of breaking up more highly organ- 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 193 
 
 ized nitrogenous and non-nitrogenous compounds into simple, 
 and more diffusible molecules. They are termed enzymes or un- 
 formed ferments in contradistinction to the bacteria themselves, 
 which are called formed or living ferments. That the action of fer- 
 ments is not due directly to the microbe is shown by the facts that 
 bactericidal substances, such as phenol (5 per cent.), chloroform, 
 ether, etc., have no effect on them, and that cultures freed from 
 bacteria by filtration still possess fermentative power. The 
 action of ferments is termed fermentation, but the term is more 
 especially limited to their effect upon non-nitrogenous compounds, 
 particularly the carbohydrates. The result of fermentation upon 
 nitrogenous material is called putrefaction, which generally occurs 
 with, though often without, the formation of odorous gases and 
 other substances. 
 
 The principal bacterial ferments are : 
 
 Proteolytic Ferments. — These transform albumins into more 
 soluble and diffusible substances. One form very often met with 
 is that which liquefies gelatin. This acts in an alkaline medium, 
 and is therefore akin to the animal ferment trypsin. This lique- 
 faction of the gelatin affords a means of distinguishing many species 
 of microbes. 
 
 Diastatic Ferments. — These transform the starches into sugars, 
 and are found in many bacterial cultures, as of Bacillus mallei, 
 Bacillus pneumonia?, etc. 
 
 Inverting Ferments. — These change the non-fermentiscible su- 
 gars into those that undergo direct fermentation. Such ferments 
 are found, for instance, in cultures of Spirillum cholera? and 
 Metschnikowi. 
 
 Emulsifying Ferment. — This is formed by but few microbes. 
 One example is Micrococcus pyogenes tenuis. 
 
 Coagulating Ferment. — One of the means of differentiation of 
 bacteria is the coagulation of milk used as a culture-medium for 
 the bacteria under observation. This coagulation is due not to 
 acidity produced in the medium, but to the action of a ferment. 
 
 Some varieties of microbes produce a ferment that has the 
 power of dissolving this coagulum when formed (casease) ; and 
 still others produce both ferments — the coagulating and the dis- 
 solving. 
 
 Hydrolytic ferments are such as break up urea into ammonium 
 carbonate and hippuric acid into glycocol and benzoic acid. 
 
 Fat-splitting ferments split the fats into glycerin and the fatty 
 acids. 
 
 Oxidizing and nitrifying ferments are other less important 
 forms. 
 
 Effects of Ferments. — The single or combined action of 
 these various ferments causes certain special kinds of fermentation 
 distinguished by the principal substance produced. Alcoholic, 
 
194 TEXT-BOOK OF PATHOLOGY. 
 
 lactic-acid, and butyric-acid fermentation of the sugars, acetic- 
 acid fermentation of alcohol (Bacillus acidi lactici, Bacillus butyri- 
 cus, Bacillus acidi butyrici, Bacillus aceticus, etc.) ; cellulose fer- 
 mentation with the production of carbonic-acid gas and ammonia ; 
 nitrification, due to the oxidation of ammonium and the production 
 of nitrates (Winogradsky's nitromonas) and nitrites; mucoid fer- 
 mentation of glucose and invert-sugar are examples. 
 
 (3) Substances produced by bacteria from the culture-media 
 and tissues are varied and numerous. Besides those produced by 
 the various fermentative processes there are : the products of 
 digestion of albumin, albumoses, peptone, etc. ; the ptomains ; ni- 
 trogenous substances, as leucin and ty rosin, methyl-, dimethyl-, 
 trimethyl-j ethyl-, propylamins ; organic fatty acids, formic, acetic, 
 propionic, butyric, margaric, lactic, etc. ; certain aromatic com- 
 pounds, as indol, phenol, kresol, skatol, mercaptan, hydrochinon, 
 etc. ; and finally, hydrogen, carbonic dioxid, hydrogen sulphid, 
 ammonium, water, etc. 
 
 Toxins. — Further, the pathogenic bacteria produce both by 
 analysis and synthesis certain toxic substances which are akin to 
 the poisonous venom of certain serpents and other animals, and to 
 certain poisonous principles of plants, as abrin and ricin. These 
 are of indefinitely determined character, and act deleteriously upon 
 the organism only after the lapse of a certain time — a period of 
 incubation. They are considered the specific toxins of the several 
 bacteria. According to some, these give all the reactions of 
 albumin, and have been termed toxalbumins (Brieger). It is 
 probable, however, that a toxalbumin is but an impure form of 
 the true toxin, a combination of it and various substances derived 
 from the medium of growth. Some authors regard it as an albu- 
 minose; others, as a peptone. Most recent investigators look 
 upon the toxin as a ferment akin to the diastatic or hydrolytic 
 ferments. Roux and Yersin, in their monograph on the Bacillus 
 diphtheria;, hold this view. Many facts seem to support this 
 theory. The analogous pathologic action of the toxins and fer- 
 ments, their common origin in the bacterial cell, their destruction 
 (oxidation) in the presence of light, their precipitation by alcohol, 
 their precipitation from solutions by colloid bodies, their long and 
 imperfect dialysis, all point to this. High temperatures affect 
 both similarly, both being destroyed at from 60° to 100° C. 
 (140° to 212° F.). Chemical substances that have no effect 
 (chloroform, ether, etc.) on the ferments are without action upon 
 the toxins; and, vice versd, those that destroy the ferments 
 (formaldehyd) are also injurious to toxins. Both may be ab- 
 sorbed with impunity through the intestines, although pathogenic 
 when injected suhcutaneously or intraperitoneally. AVhen the 
 microbe is grown in some inorganic medium, or in a non-albu- 
 minous one (as Uschinky's solution), the toxic principle obtained 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 195 
 
 corresponds in its chemical reactions to a ferment. Most import- 
 ant is the fact that extremely minute doses are effective. Fer- 
 ments act without regard to the mass employed, and it would 
 seem that toxins act in almost imponderable amounts. It has 
 been estimated that T oVo S m - °f tetanus toxin will kill a horse 
 weighing 600 kg. — six hundred million times its weight ; and 
 that y^o o" m S- °^ tuberculin causes a reaction in a diseased man 
 weighing 60 kg. — sixty trillion times its weight. Finally, both 
 act only after a definite period of incubation. Courmont and 
 Doyon found that by increasing the amounts of tetanus toxin 
 injected into a dog they were not able to diminish beyond a defi- 
 nite limit this latent period. Blood taken from the animal during 
 the subsequent convulsions caused, when injected into another 
 animal, an immediate tetanic attack. According to these authors, 
 the ferment, possibly not toxic in itself, is capable of elaborating 
 within the body or culture-medium the tetanizing substance. 
 
 Fate of Toxins. — It is certain that there exist in various cells 
 of the animal organism certain oxidizing ferments by which the 
 toxin is destroyed. Not all of the toxin is thus oxidized. A part 
 is eliminated unchanged through the kidneys in the urine and to 
 some extent through the liver in the biliary secretion. Beside 
 these there is still another method of defence of the organism 
 against the action of toxin — the antitoxin (q. v.). 
 
 ChromogenesiS. — Many bacteria form colors which give to 
 the culture a characteristic appearance. Some attempt has been 
 made to classify those pigments according to their solubility in 
 alcohol, ether, etc. The pigment-forming bacteria themselves are 
 called chromophobe when the pigment is a component of the bac- 
 terial cell itself; chromopario, when the coloring-matter is an 
 excretion and the microbe remains colorless ; and parachromo- 
 phorie when both conditions exist. The production of the pig- 
 ment depends to some extent upon the constitution of the medium, 
 and it is possible to produce cultures and even races of pigment- 
 forming bacteria by the use of appropriate media. 
 
 PhotogenesiS. — The phenomenon of phosphorescence ob- 
 served in decaying fish is due to the action of bacteria. This 
 production of light is observed in many of the cholera-group of 
 vibriones. 
 
 THE LOCAL EFFECTS OF BACTERIA. 
 
 These may be either (a) mechanical or (6) histologic, the me- 
 chanical effects being least in importance, (a) Sometimes masses 
 of micro-organisms more or less completely occlude small blood- 
 vessels and occasion secondary changes in the tissues in this 
 mechanical way. In other cases the obstruction is incomplete, 
 but occasions thrombosis in the blood-vessel and various conse- 
 
196 TEXT-BOOK OF PATHOLOGY. 
 
 quentiaJ disorders, (b) The histologic changes occasioned by 
 bacteria arc proliferative and destructive, among the latter being 
 various degenerations and necrosis. The proliferative changes 
 may be non-specific or specific — that is, there may be simply 
 proliferation such as occurs from any irritation ; or there may be 
 special forms of proliferation more or less characteristic in extent, 
 distribution, and nature of the individual micro-organism. This 
 is seen in the characteristic lesions of tuberculosis, glanders, 
 rhinoscleroma, etc. The cellular degenerations and necroses occur 
 coincidentally or subsequent to the proliferative changes. On the 
 contrary, in many eases the first etfects of bacterial invasion seem 
 to be degeneration or necrosis of the tissues immediately around 
 the organisms. 
 
 EFFECT OF TOXIC PRODUCTS OF BACTERIA. 
 
 Bacteria usually gain entrance into the animal body through 
 some lesion of the epithelial layer, often the result of traumatism. 
 Sometimes the microbes find in certain cavities of the body favor- 
 able conditions for growth, as in the pulmonary or alimentary 
 tracts, and there develop and elaborate their toxins. 
 
 Intoxication and Infection. — In one class of diseases the 
 infecting microbe remains localized at the point of inoculation, and 
 is never or only exceptionally found in the fluids of the body, the 
 general symptoms of the disease being due to absorption of the 
 toxic products. Such are true Intoxications. In other cases the 
 microbe is found circulating in the blood throughout the body 
 and finds lodgement in most of the organs. These are called In- 
 fections. Tetanus is the type of the first class ; anthrax, of the 
 second. There is, however, no distinct line to be drawn, for the 
 symptoms of all infections are due to the toxins and other toxic 
 products. While some bacteria always produce pure intoxications 
 (tetanus), most of them may, under varying conditions, cause 
 either intoxications or infections. This diiference is due to a 
 relative lack of virulence. Either the microbe is weak in toxin- 
 producing power or the resistance of the tissue too great. The 
 toxin is essentially negatively chemotactic (see Inflammation), and 
 thus prevents the phagocytic action of the leukocytes ; while 
 many other bacterial products and the bacterial proteins (Buchner) 
 are positively chemotactic. When a pathogenic microbe is want- 
 ing in virulence, there is a determination of leukocytes to the 
 point of inoculation and Suppuration results. A virulent microbe 
 in the strict sense, then, is one that easily invades the animal body 
 and there produces its more or less powerful toxin ; an avirulent 
 one produces but little, if any, toxin and is destroyed by phago- 
 cytosis, either with or without suppuration. 
 
 Sapremia, Septicemia, and Pyemia. — From local sup- 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 197 
 
 purative foci toxic products may be absorbed into the general 
 circulation, and a condition known as Sapremia results. The 
 infecting bacterium itself may invade the blood-current without 
 giving rise to any secondary collection of pus. This is termed 
 Septicemia. When, however, the microbe is carried to various 
 parts of the body and there gives rise to secondary suppuration, 
 the condition is called Pyemia. 
 
 The destruction of leukocytes that takes place in the formation 
 of pus is due probably to bacterial proteins. From this point of 
 view suppuration is not specific, and its production by various 
 chemical substances proves this. 
 
 IMMUNITY. 
 
 Definition. — In the present state of our knowledge of the 
 condition of immunity it is most difficult to give a precise defini- 
 tion of this term. It denotes that condition of an organism which 
 enables it to resist the attacks of bacteria and their toxic secre- 
 tions. In one sense it is the reverse of susceptibility. An animal 
 that is not susceptible to an infection is said to be immune, and 
 the term immunization is applied to the process by which an 
 animal becomes thus refractory. 
 
 Varieties. — Immunity may exist in an animal naturally as 
 an inheritance from immune ancestors (Natural Immunity). While 
 absolute immunity is rare, examples of relative immunity are com- 
 mon. It may be individual or racial. Thus dogs and Alge- 
 rian sheep are refractive to anthrax, while other species of sheep 
 are extremely susceptible to this infection. The lower animals in 
 general seem to be perfectly immune against certain diseases 
 common to man, such as syphilis. Immunity may be produced 
 by a previous infection (Natural Acquired Immunity), or by arti- 
 ficial means (Artificial Acquired Immunity). It may be the result 
 of injections of cultures of the specific microbes, the virulence of 
 which has been naturally or artificially reduced, as in the vaccines 
 of variola and anthrax ; or of cultures, the living organisms hav- 
 ing been destroyed by heat or other means ; or of filtered cultures, 
 as in the production of diphtheria-serum ; or of the serum of ani- 
 mals that have been rendered immune by these methods. In the 
 first three cases the condition is more lasting and seems to be a 
 permanent adaptation of the organism (Active Immunity), while in 
 the last case it is but temporary (Passive Immunity). 
 
 In many cases immunity asserts itself against both the infect- 
 ing microbe and its specific toxin, as in the rat with regard to the 
 diphtheria-bacillus and its toxin ; but more often an animal is 
 resistant to the infection, though susceptible to the toxin. An 
 example of this is the action of the guinea-pig toAvard tetanus 
 (Vaillard). The reverse may be true, and we see an injection of 
 
198 TEXT-BOOK OF PATHOLOGY. 
 
 tuberculin without effect upon a healthy animal that is very 
 susceptible to tuberculous infection. Most commonly natural 
 immunity exists toward the infecting microbe and not its toxin. 
 
 Mechanism of Immunity. — In many cases the fluids of 
 the animal organism prevent the growth {inhibitory action), or 
 wholly destroy the bacteria [bactericidal action). Thus the blood 
 of the naturally immune rat is bactericidal to the anthrax bacillus. 
 Very many examples of this coexistence of immunity and bacteri- 
 cidal power of the blood can be given, and some authorities suppose 
 this to be the general explanation of the mechanism of immunity. 
 According to Buchner, this action is due to the presence in the 
 blood and fluids of the body of certain albuminous bodies, which 
 he terms Alexins. These are probably leukocytic in origin, and 
 arc not specific in their action, but protective toward all micro- 
 organisms. This coexistence of bactericidal action and immunity, 
 however, is by no means universal. Rabbits, for instance, possess 
 a bactericidal blood-serum, but are not naturally immune to 
 anthrax ; while, on the contrary, the adult dog is immune to this 
 disease, though its serum has no effect upon the Bacillus anthracis. 
 
 Another theory asserts that the inhibitory effect of the serum 
 causes some change in the vital properties of the bacteria. Cul- 
 tures of bacteria in the serum from immune animals seem to show 
 some such effect, but this is probably due rather to the immuniz- 
 ing action of the serum in which they are suspended, as bacteria 
 freed from this by filtration may show no such physiologic 
 degeneration. 
 
 The theory that has influenced our ideas of immunity more 
 than any other is that of Phagocytosis of Metschnikow. He holds 
 that the destruction of the microbes in the animal body is to be 
 explained, not by the conditions of the body-fluids, but by purely 
 cellular activity. The infecting microbes are taken up by certain 
 cells of the organism and are destroyed by intracellular digestion. 
 These cells — phagocytes — are of two kinds: the mobile macro- 
 phages including the mononuclear and polymorphonuclear leu- 
 kocytes ; and the fixed macrophages, including the vascular endo- 
 thelial cells, the cells of the bone-marrow and spleen, certain 
 connective-tissue cells and liver-cells, and even those of the nerve- 
 and muscle-tissue. After injection of a culture into the subcu- 
 taneous tissue of an animal, naturally or artificially immune, he 
 noticed that the bacteria were all taken up by the leukocytes. 
 Thai these microbes were still living and virulent, and were not 
 taken up as mere dead matter, Metschnikow regards as fully estab- 
 lished. One proof he cites is the fact that an exudate containing 
 no free bacteria, but all intracellular, is capable of producing 
 cultures on artificial media and causing infection in susceptible 
 animals. 
 
 To these facts Pfeiffer opposes the experiment of injecting 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 199 
 
 cholera vibriones into the peritoneum of artificially immune guinea- 
 pigs. He observed a complete destruction of the microbe by the 
 peritoneal fluid — an agglutination into masses and a gradual degen- 
 eration. There were few, if any, leukocytes present, and he there- 
 fore claimed that such destruction was entirely extracellular and 
 humoral in character. However, if a preliminary injection of 
 some substance that determines a local leukocytosis is made, there 
 occurs, instead of the reaction of PfeifFer, a true phagocytosis. 
 Metschnikow interprets Pfeiffer's phenomenon as the result of a 
 dissolution of the leukocytes by bacterial action and solution in the 
 peritoneal fluid of the destructive substances. It " is not a gene- 
 ral phenomenon, and occurs only after intraperitoneal injections, 
 and then only inconstantly." 
 
 Both schools now agree that the bactericidal substances are 
 derived from the leukocytes : the one, however, holding that 
 phagocytosis is but a secondary and infrequent phenomenon ; the 
 other, that it is the fundamental principle of immunity. 
 
 Whether or not phagocytosis is the only essential element in 
 immunity, many points have been established by corroborative 
 investigations. It is certain that phagocytosis does occur after 
 subcutaneous injection ; that this is much more marked in resist- 
 ant and immune animals than in susceptible ones ; that such intra- 
 phagocytic bacteria, at least in the early stages of the process, are 
 still living and virulent; and that the same phenomenon takes 
 place even in the peritoneum after a preliminary injection of a 
 positively chemotactic substance. 
 
 As has been said, the blood-serum and fluids of animals arti- 
 ficially immunized are often capable of producing a passive im- 
 munity when injected into other animals. It is probable that the 
 substances producing this are the result of the destruction of the 
 phagocytes (phagolysis), either within the animal body or after 
 the withdrawal of the serum. 
 
 Toxin-immunity; Antitoxin. — Immunity is manifested in two 
 ways, against the microbe or against the toxin ; and the sub- 
 stances that so act are therefore anti-infectious or antitoxic. One 
 theory explains the condition of immunity by supposing that the 
 cells of the body become accustomed to the poison (the old theory 
 of Chauveau). A blood-serum, however, may be extremely anti- 
 infectious without having any antitoxic properties, and numerous 
 examples of this prove that the theory just mentioned cannot be a 
 sufficient explanation. 
 
 The term antitoxin is applied to the serum of an animal that 
 protects against a specific disease, and it is generally both anti- 
 toxic and anti-infectious. The two best known examples are the 
 tetanus and diphtheria antitoxins, although in the laboratory anti- 
 toxic sera have been prepared for many of the infections of man 
 and of the lower animals. 
 
200 TEXT-BOOK OF PATHOLOGY. 
 
 Toxin-immunity exists naturally in some individuals against 
 certain animal poisons, such as the poisons of snakes, scorpions, 
 etc., and chemical poisons and alkaloids, as arsenic, abrin, ricin, 
 etc. Jt may also be developed by frequent exposure to such 
 poisons. Similarly, immunity against the toxin of a bacterium is 
 produced by the injection of gradually increasing doses of the 
 microbe and its products. Either a culture which has been steril- 
 ized by filtration or by heat, or one containing bacteria of very low 
 virulence, is used for the first injection. Preferably, small doses 
 of the toxin freed from microbes by filtration are used. The doses 
 are then increased until the animal is able to react against a small 
 injection of the pure culture, and this is then given in increasing 
 quantities. An animal thus treated is often able to withstand tre- 
 mendously large doses of culture. Curious and at present unex- 
 plainable conditions often arise. For instance, the antitoxin may 
 disappear from the blood of an animal thus artificially immunized 
 without any loss of immunity, and some animals die from the dis- 
 ease whose blood is still extremely antitoxic, a condition, as it is 
 called, of supersusceptibility. These few facts seem to point out that 
 immunity cannot be due to the antitoxic action of blood-serum. 
 
 Formerly Behring explained all toxin-immunity as, a histogen- 
 ous immunity : that is, that the tissues of the body become accus- 
 tomed to the toxin, a sort of Mithridatization. Later, however, 
 he regarded acquired immunity, both active and passive, as an 
 hematogenous immunity and due to the action of an antitoxin. 
 
 Antitoxin is probably a modification of the toxin by cellular 
 action, or a substance elaborated by the cells under the stimulation 
 of the toxin. 
 
 Electrical Prorhiotio)). — Some investigators have been able to 
 produce antitoxin in vitro by the action of either the continuous 
 current or the rapidly interrupted direct current on the toxin. If 
 this is so, the fact would point toward a direct modification. 
 
 Action of the Antitoxin.— -It was at first thought that the reaction 
 between toxin and antitoxin was a purely chemical one, but prob- 
 ably, as in bacterial immunity, it is an indirect one. A mixture of 
 snake-toxin and its antitoxin which has no effect when injected into 
 an animal, if previously heated to 70° C. (158° F.), may cause the 
 death of the animal. It is supposed that the antitoxin is destroyed 
 Hi thai temperature, while the toxin is not. The death of super- 
 susceptible animals cannot be due to any lack of antitoxin, but 
 may be explained by a want of reaction of the body-cells. 
 
 On the other hand, however, there are many experiments that 
 seem to show the reverse ; that the neutralization may take place 
 in the test-tube, and that it is really a chemical and not a physio- 
 logic reaction. 
 
 The protective substances present in the bodv, normal and im- 
 mune, are the defensive proteids of Hankin or the alexins of 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 201 
 
 Biichner. The former further subdivides them into sozins — those 
 proteids present in the normal animal body, and the phylaxins — 
 those in the body of the immune animal. The former are bacteri- 
 cidal and globulicidal, destroying the red and white blood-cor- 
 puscles ; and are easily destroyed by light and a temperature of 
 55° C. (131° F.). The phylaxins, the true antitoxins, are neither 
 bactericidal nor globulicidal, and withstand a temperature of from 
 70° to 80° C. (158° to 176° F.). In their other chemical reactions 
 they are similar to the toxins. 
 
 Hankin further divides the sozins and phylaxins, according to 
 whether they act against the microbe itself or its toxin, into myco- 
 and toxo-sozins and myco- and toxo-phylaxins. 
 
 There is a certain amount of immunity that can be produced 
 by the injection of substances that have an attractive power for 
 microbes (positive chemotaxis), such as salt-solution, peptone, ex- 
 tracts of certain organs. 
 
 This immunity, however, is not specific, but acts toward all 
 varieties of bacteria. It is found that even the so-called specific 
 antitoxins are active against other kinds of toxins, as tetanus-anti- 
 toxin is partially preventive against snake-poison. It is therefore 
 difficult to draw a distinct line between the specific and non-specific 
 forms of antitoxin. Indeed, it is questionable if our present 
 knowledge on the whole subject is sufficient to allow us to formu- 
 late a definite theory of immunity. 
 
 Elimination. — Antitoxin is probably eliminated through all of 
 the secretory organs. It has been found in the urine and to a 
 large extent in the milk. Brieger and Ehrlich obtained a quite 
 concentrated form of antitoxin by precipitation of the casein by 
 ammonium sulphate and purification by dialysis. As in the case 
 of toxins, the whole of the antitoxin seems to be carried down by 
 the precipitated colloid casein. 
 
 DISEASES DUE TO BACTERIA. 
 
 The bacterial diseases form a large and increasing group. In 
 some cases it has been shown by the positive application of Koch's 
 rules (see page 30) that the suspected micro-organisms are the 
 actual causes of the diseases under consideration ; in more numer- 
 ous instances all of the rules cannot be applied, but other consid- 
 erations go far toward establishing the specific nature of- certain 
 bacteria ; in still other cases the evidence warrants a strong suspi- 
 cion of the pathogenicity of bacteria found in connection with cer- 
 tain diseases, but there is nothing approaching actual demonstration. 
 
 Division of infectious diseases into those of certain and those 
 of uncertain bacteriology must cause differences of opinion. It is 
 adopted only for convenience, the merits of each individual case 
 being considered in the discussion of the individual diseases. 
 
202 TEXT-BOOK OF PATHOLOGY. 
 
 DISEASES OF CERTAIN BACTERIOLOGY. 
 
 SUPPURATIVE DISEASES. 
 
 Definition. — Under this heading we include for the present 
 various forms of suppurative inflammation, such as furunculosis, 
 abscess-formation, and allied diseases, like osteomyelitis, endocar- 
 ditis, etc. 
 
 Htiology. — A variety of organisms have been found to have 
 the power of producing suppuration. Among these the staphylo- 
 coccus group is most important. The Streptococcus pyogenes seu 
 erysipelatis is also of great significance ; less frequently the Dip- 
 lococcus pneumonia;, the Pneumobacillus of Friedlander, the Ba- 
 cillus pyocyaneus, the typhoid bacillus, the Bacillus coli communis 
 or the Bacillus pyogenes foetidus, the gonococcus, and others. 
 Some cases are due to a single organism ; in many there is double 
 infection. 
 
 1. The Staphylococcus Group. — Among these have been de- 
 scribed three important forms, the Staphylococcus pyogenes 
 aureus, albus, and citreus. 
 
 The Staphylococcus pyogenes aureus is a minute, rounded 
 body about ^5- to 1 // in diameter, having no motility and not 
 forming spores. When found in the tissues the cocci are apt to 
 be associated in clusters, whence the term staphylococcus (Fig. 79). 
 
 Fig. 79.— Staphylococcus pyogenes albus (Jakob). 
 
 Sometimes they are grouped in pairs, and may thus present a re- 
 semblance to gonococci. The opposed surfaces, however, are flat 
 instead of concave, as is the case with the gonococci. The 
 staphylococcus may be stained with ordinary anilin solutions and 
 is beautifully demonstrated by Gram's method. Cultures are 
 easily obtained upon the ordinary media. The most characteristic 
 growth is that upon agar. Along the line of inoculation a moist 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 203 
 
 colony develops, with at first a whitish but soon an orange-yellow 
 color. The growth in gelatin causes rapid liquefaction and the 
 precipitation of orange-yellow particles. The growth is best ob- 
 tained at oven-temperatures, but may be secured at lower degrees. 
 
 Distribution. — The Staphylococcus aureus is frequently found 
 upon the skin or in the various external secretions of healthy in- 
 dividuals. It does not seem to nourish anywhere apart from the 
 bodies of man or animals, but may remain in an active state in the 
 dust of rooms or upon clothing and the like. It has been found 
 in various lesions of the body ; notably, however, in furuncles, ab- 
 scesses, and carbuncles, and in ulcerative conditions of the exterior 
 or of the mucous membranes. It is also frequent in internal suppu- 
 rative inflammations, such as malignant endocarditis, osteomyelitis, 
 appendiceal abscesses, etc. In many of these lesions other organ- 
 isms may be associated. 
 
 Pathogenicity. — When pure cultures are injected into animals 
 abscesses are produced and a fatal termination may follow. In 
 the latter cases diffusion through the blood is found, and infarcts 
 of the kidneys, lungs and other organs caused by bacterial emboli 
 are discovered. Multiple abscesses may be seen. The organism 
 readily loses its virulence, as in the case of those found, upon the 
 skin of healthy persons, and in other accidental situations. When 
 rubbed in a virulent state into the skin of man it produces ab- 
 scesses or boils. 
 
 Staphylococcus Pyogenes Albus. — This organism is practi- 
 cally identical with the last-named in morphology, but in culture 
 produces a white instead of a yellow growth. It has been found 
 as a frequent harmless parasite of the skin (Staphylococcus epiderm- 
 idis albus of Welch). It occurs in abscesses and various suppu- 
 rative diseases, but rarely alone. As a rule, it is associated with 
 the golden staphylococcus or other organisms. It is distinctly less 
 virulent than the aureus. 
 
 Staphylococcus Pyogenes Citreus. — This form is the least 
 important of the three. It is not so common and, as a rule, less 
 virulent. It differs in the brilliant lemon color obtained upon 
 culture in various media. 
 
 2. The Streptococcus Pyogenes seu Erysipelatis. — The Streptococ- 
 cus pyogenes was first studied by Rosenbach in cases of suppuration. 
 A similar organism was afterward described as the Streptococcus 
 erysipelatis by Fehleisen. It would seem, however, that these 
 two organisms are identical. At all events, there are no distin- 
 guishing features which we can point out. The streptococcus is a 
 small spherical organism of variable size, frequently associated in 
 chains of from three to twenty or more individuals (Fig. 80). It 
 is easily stained with ordinary anilin solution or by Gram's 
 method. The cocci are not motile. Spore-formation has not 
 been observed, but occasionally in chains one of the individual 
 
204 TEXT-BOOK OF PATHOLOGY. 
 
 members is larger than the rest, suggesting arthrospores. Upon 
 artifieial media scanty hut rather characteristic growths are ob- 
 tained. On the gelatin plate there are formed small, translucent, 
 whitish or yellowish colonies of irregular outline. The gelatin is 
 
 Streptococcus pyogenes (Jakob). 
 
 not liquefied. Upon agar a very thin, transparent growth forms 
 around the line of inoculation. It consists of separate colonies 
 which do not become confluent. 
 
 The distribution of the streptococcus is much the same as that 
 of the staphylococci, though it is less commonly discovered about 
 the healthy body. It may, however, be found upon the mu- 
 cous membranes or in the various secretions or excretions of the 
 body. It is probably a strict parasite, multiplying only within 
 the living organism. 
 
 In disease it has been found in various forms of suppuration, 
 such as phlegmonous forms of inflammation of the subcutaneous 
 or submucous tissues, cither alone or in association with other 
 organisms. It occurs occasionally in focal suppurations, such as 
 abscesses, though these are more commonly due to staphylococci 
 alone. The streptococcus occurs at times in ulcerative endocarditis, 
 and not rarely in infectious endometritis. Streptococcic inflam- 
 mations of* the throat are of great interest. They may occur in 
 persons previously in good health, or in the course of infectious 
 diseases, like scarlatina, measles, or influenza. To the clinician, 
 the resulting lesion may be indistinguishable from that of diph- 
 theria; bacteriologic examination alone serves to establish the 
 diagnosis. The streptococcus is found in all cases of erysipelas, 
 in the tissues, and in the serum or other exudations. 
 
 Pathogenesis. — When cultures of streptococci derived from 
 suppurative diseases or from erysipelas are injected into rabbits 
 erysipelatous inflammation may result. Subcutaneous injections, 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 205 
 
 however, may cause no local or general symptoms in mice or rab- 
 bits. It would seem that animals are rather resistant. 
 
 Pathologic Physiology. — When injected into the subcu- 
 taneous tissue the staphylococcus produces local effects. The 
 organism may become liberated, gain entrance to ihe circulation, 
 and produce widespread results ; but it does not seem to produce 
 toxins that cause generalized results. The effects of the staphylo- 
 coccus seem to be due rather to a certain poisonous body con- 
 tained in the organism itself. This has been termed the bacterial 
 protein, and it seems to belong to the group of alkaline albumin- 
 ates. This body by its chemotactic effect causes the leukocytic 
 accumulations found in suppurative inflammations. The same 
 body, or perhaps others, appears to have a simultaneous irritative 
 and stimulating influence upon the fixed connective tissue of the 
 part, leading to proliferation. The staphylococcus also leads to 
 liquefaction in the tissues, as in gelatin, but whether directly or 
 through the accumulation of bodies derived from leukocytes is 
 uncertain. The defence of the organism against the staphylococ- 
 cus is partly mechanical and partly vital. The leukocytes prob- 
 ably swallow a certain number of organisms and cause their 
 destruction, while soluble bactericidal bodies, probably albumin- 
 ous in character, seem to be produced in the course of the infec- 
 tion. These have been termed alexins, and are largely derivatives 
 of the leukocytes. 
 
 The streptococcus would seem to be more active in the produc- 
 tion of soluble toxins than the staphylococci. The toxin has been 
 made by inoculating small quantities of bouillon with virulent 
 cocci, allowing these to grow for several weeks, and then destroy- 
 ing the organisms by heat. The injection of the toxins thus 
 produced leads to local and general reaction. An antistreptococcic 
 serum has also been produced, and seems to possess some power to 
 combat infection with the organism in question. 
 
 Other Organisms of Lesser Importance. 
 
 The Bacillus pyocyaneus is an occasional pathogenic organism found in 
 pus having a bluish or greenish color. The bacillus is small in size, fre- 
 quently occurring in chain-formation, and is actively motile. 
 
 Upon artificial media it produces colored growths and a soluble pig- 
 ment, which gives to the culture-medium for some distance from the growth 
 a greenish, or in some cases a dark-blue, coloration. The organism in pure 
 culture is highly virulent, producing intense suppurative inflammations. 
 
 The Bacillus pyogenes foetid us is probably identical with the Bacillus coli 
 communis, or is at least a close relative. These organisms, as well as the 
 typhoid bacillus, the Diplococcus pneumoniae, the Diplococcus meningitidis, 
 and the Pneumobacillus of Friedlander, are referred to elsewhere. 
 
 Micrococcus Tetragenus. — This form is a micrococcus from 1 to 2 ji in 
 diameter, and receives its name from the peculiar association in groups of 
 four. It occurs in the sputum and contents of cavities in pulmonary 
 phthisis, and occasionally elsewhere. It may give rise to general sepsis. 
 
206 TEXT-BOOK OF PATHOLOGY. 
 
 GONORRHEA. 
 
 Definition. — Gonorrhea is an infectious inflammation of the 
 urethral or other mucous membranes due to a specific organism, 
 the gonoooccua of Neisser. 
 
 Btiology. — There is no doubt that the gonococcus is the 
 specific cause of gonorrhea. This organism is a micrococcus, 
 usually arranged in pairs, the opposed surfaces of each being 
 slightly concave. This arrangement has suggested the designa- 
 tion " biscuit-shaped " diplococcus (Fig. 81). Sometimes groups 
 
 Fig. 81.— Pus from gonorrhea, showing gonococci (Jakob). 
 
 of four or more are found, while in other cases the cocci occur 
 singly. The organisms are abundant in the pus of acute gonor- 
 rhea, less abundant in advanced stages, in the pus of gonorrheal 
 salpingitis or other conditions, and may not be discovered at all. 
 They generally occupy the pus-cells, lying in the protoplasm, and 
 occasionally within the nucleus, in small numbers or so abun- 
 dantly as to fill the cell uniformly. In the tissues the same intra- 
 cellular position is usual, but here, as in the free pus, some organ- 
 isms may generally be found between the cells. The gonococcus 
 stains readily with ordinary solutions of anilin dyes, but is readily 
 decolorized by drain's method. 
 
 Cultivation of the gonococcus is difficult. Growths may, how- 
 ever, be obtained upon media consisting of human blood-serum 
 and agar-agar, upon acid gelatin or albuminous urine. The 
 growth in blood-serum consists of small colonies of grayish color 
 that coalesce and form a film on the surface of the medium ; around 
 the colony may generally be seen an irregular and inconspicuous 
 extension. 
 
 The gonococcus cannot be positively distinguished by its 
 morphology nor by the intracellular position. Other organisms 
 may in certain stages of their growth show a typical biscuit-form 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 207 
 
 (staphylococci and others) ; and the intracellular position is not 
 rarely assumed by a variety of bacteria. The failure to stain by 
 Gram's method and the failure to grow on ordinary media are 
 strong points in favor of the gonococcus. Typical cultures alone 
 settle the diagnosis. 
 
 Pathogenicity. — It has been demonstrated by direct implanta- 
 tion of pure colonies upon the healthy urethra that this organism 
 will cause characteristic gonorrhea. Urethritis may, however, be 
 due to other organisms ; the specific form termed gonorrhea is 
 probably always due to the gonococcus. Secondary lesions, such 
 as salpingitis, oophoritis, arthritis, peritonitis, conjunctivitis, endo- 
 carditis, etc., may also be due to this organism, no other form of 
 bacteria being present. Sometimes, however, complications, such 
 as periurethral abscesses, suppurative adenitis, etc., are due to 
 secondary infectious. 
 
 Pathologic Anatomy. — The lesions of gonorrhea will be 
 considered elsewhere. Suffice it to say in this place that the 
 organism causes suppurative catarrh of the mucous surfaces with 
 which it comes in contact. There is abundant round-cell infiltra- 
 tion, and the organisms tend to penetrate deeply into tissues. 
 
 Pathologic Physiology. — Gonorrhea is in most cases a 
 purely local disease. Little is known of its power to produce 
 soluble toxins. The distant lesions are in all cases, as far as we 
 definitely know, dependent upon deposit of the specific organism. 
 These have been found in the effusions of arthritis and in the 
 vegetations of gonorrheal endocarditis, as well as in the blood in 
 the last named condition. 
 
 CROUPOUS PNEUMONIA. 
 
 Definition. — There are a number of forms of inflammation 
 of the pulmonary tissues to which the term pneumonia is appli- 
 cable. The most definite form of disease is that spoken of as 
 croupous, fibrinous, or lobar pneumonia. In its typical form this 
 is a specific and well characterized disease. It is infectious, more 
 or less contagious, and caused by a specific organism. 
 
 Btiology. — The organism most likely the cause of croupous 
 pneumonia is the Dijplococcus pneumoniae. This organism is also 
 called the pneumococcus and the pneumobacillus. In reality the 
 last name is most applicable, but has not found general favor. 
 The diplococcus of pneumonia was recognized in the saliva of 
 healthy persons by Sternberg and Pasteur, but its relation to 
 croupous pneumonia was demonstrated by Frankel, and later by 
 Weichselbaum. The individual organism has a somewhat elon- 
 gated, lanceolate shape, and therefore deserves the name bacillus, 
 though it does not always show this bacillary shape distinctly 
 (Fig. 82). In the sputum and lungs, and in the blood of inocu- 
 
208 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 lated animals, it is commonly found in pairs ; the broader end of 
 the organisms adjacent, and the pointed ends projecting outward ; 
 
 Fig. 82.— Diplococcus pneumoniae in the blood (Frankel and Pfeiffer). 
 
 and the group is surrounded by a transparent capsule, which does 
 not take stains and therefore becomes conspicuous (Fig. 83). 
 Sometimes a number of the organisms are 
 grouped in chains, so that the name Strep- 
 tococcus pneumoniae has been suggested. 
 The capsule is not seen when the organ- 
 ism is obtained from cultures. The dip- 
 lococcus does not possess individual motil- 
 ity and has no flagella. It does not seem 
 to produce spores. 
 
 It may be readily demonstrated in the 
 sputum or in the tissues by staining with 
 the ordinary anilin dyes or by Gram's 
 method. 
 
 Cultivation. — The diplococcus grows 
 readily upon ordinary media, excepting potato. It forms charac- 
 teristic colonies upon agar-agar plates or in gelatin. Upon the 
 surface of the agar there appear transparent drop-like colonies 
 hardly visible to the naked eye, which under the microscope have 
 a finely granular appearance. I" jx>n gelatin plates similar growths 
 are produced, while in gelatin punctures the growth occurs along 
 the path of the wire as granular whitish spots separated from each 
 other. The organism tends to die out very readily in cultures, 
 and also loses its pathogenic property when propagated for several 
 generations. It is most luxuriant at 37° C. (98.6° F.). 
 
 Pathogenicity. — The specific character of this organ has not 
 been definitely proved according to the rules of Koch, but it is 
 
 Fig. 83.— Diplococcus pneu- 
 moniae: d, cocci, without cap- 
 sules ; b, single and paired 
 cocci, with capsules ; c. chain- 
 form ; d, colony of cocci (Zieg- 
 ler). 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 209 
 
 highly probable that it is the usual cause of pneumonia. The 
 diplococcus is frequently found in the saliva of healthy persons. 
 When this is introduced into animals, particularly rabbits, the 
 animal dies, with evidences of rapid sepsis. The post-mortem 
 shows some fibrinous exudate and occasionally a little pus at the 
 point of inoculation. The spleen is enlarged, and bacteria of dis- 
 tinct lanceolate-form and with capsules are widespread throughout 
 the body. Injections of lung-tissue or of pneumonic sputum pro- 
 duce similar results, and the organism in pure culture likewise 
 causes this form of septicemia. It has been claimed that injection 
 of the diplococci into the trachea will produce true pneumonia in 
 susceptible animals. This remains to be proved more definitely. 
 
 Besides the diplococcus there are certainly other elements which 
 contribute to the causation of the disease, else the frequent occur- 
 rence of the micro-organism in question in the saliva would make 
 pneumonia a much more common affection. The nature of the 
 contributing causes are, however, obscure. Exposure to cold, 
 general depression of the system, traumatism, alcoholism, and 
 other causes certainly predispose or help to determine the occur- 
 rence of the disease. These causes may act by temporarily 
 increasing the virulence of the diplococcus or by lowering the 
 resistive power. 
 
 Pathologic Anatomy. — (See Diseases of the Lungs.) 
 
 Pathologic Physiology. — The diplococcus produces, in the 
 first place, local lesions of the lungs ; and, in the second place, 
 systemic intoxication by toxins of uncertain character. The 
 organism itself, however, gains access to the blood and may pro- 
 duce secondary lesions in other organs. Infection with the diplo- 
 coccus of pneumonia causes a pronounced reaction on the part of 
 the blood in the form of leukocytosis. This is not invariable, but 
 is usually seen. After the attack of pneumonia there is temporary 
 immunity, and it has been claimed that animals may be immun- 
 ized for considerable lengths of time. This, however, is uncertain. 
 No definite antitoxic substance has thus far been secured. 
 
 The Diplococcus in Other Diseases. — The Diplococcus 
 pneumoniae has been found in various conditions complicating 
 pneumonia, and occasionally without the existence of a previous 
 croupous pneumonia. Among other lesions, meningitis, pleurisy, 
 and other inflammations of the serous surfaces, abscesses, otitis 
 media, and arthritis have been found to be due to this organism ; 
 or, at least, this organism alone has been found in some of these 
 cases. 
 
 OTHER FORMS OF PNEUMONIA. 
 
 Among other varieties of pneumonia may be mentioned the 
 catarrhal or lobular form, the tubercular form, and various irreg- 
 ular pneumonias, partly cellular, partly fibrinous, partly purulent 
 
210 TEXT-BOOK OF PATHOLOGY. 
 
 or hemorrhagic. A number of different organisms may be found 
 in such cases, and some of these may be of etiologic importance 
 in certain cases. 
 
 The Bacillus Pneumoniae of Friedlander. — This organism was 
 regarded at one time as the cause of croupous pneumonia. It is 
 probably in most eases an accidental associate, though it may 
 occasionally be the cause of catarrhal or irregular forms of pneu- 
 monia. It occurs as a distinct bacillus, 
 usually in pairs and surrounded by a cap- 
 sule like that of the diplococcus (Fig. 84). 
 Sometimes it may form chains of three, four, 
 or more organisms. It stains well with the 
 anilin dyes, but is decolorized by Gram's 
 method. A characteristic culture is ob- 
 ' li;:a"ilr;!f : Fd!"iia!Xr.~ tained in gelatin. The puncture-culture is 
 characterized by a luxuriant growth at the 
 top and a considerable vegetation all along the track. This leads 
 to a nail-shaped growth. The gelatin does not liquefy. Upon 
 agar a considerable whitish or yellowish growth occurs upon the 
 surface. There is formation of gas in media containing glucose, 
 and often also on potato. 
 
 In catarrhal pneumonia this organism may be discovered, or 
 the various forms of staphylococcus or the Streptococcus pyogenes ; 
 more rarely the influenza-bacillus, the Bacillus coli communis, the 
 typhoid bacillus, and others are discovered. In some of these 
 enses the disease may be the result of double infection. 
 
 Tubercular pneumonia, in which a uniform pneumonic process 
 is found in the lungs, may be due to simple infection with the 
 tubercle-bacillus, or to mixed infections. 
 
 Irregular pneumonias may be of varying pathologic type, and 
 may be occasioned by a great variety of organisms. No satis- 
 factory classification can be attempted, as the limitations of the 
 term pneumonia can scarcely be established. 
 
 RHINOSCLEROMA. 
 
 Rhinoscleroma is a disease affecting the skin about the anterior 
 nares and adjacent parts, and probably caused by a specific bacil- 
 lus. The disease has been especially observed in central Europe. 
 If presents itself in the form of nodular thickening of the skin of 
 the nose and lip, and sometimes spreads to the neighboring mu- 
 cous membranes — mouth, pharynx, or larynx. In the latter situa- 
 tions ulceration of the surface is frequent; the lesions of the skin 
 rarely ulcerate. Histologically the growth consists of round 
 granulation-tissue cells. Frequently the cells suffer hyaline de- 
 generation, forming rounded hyaline bodies. The bacilli may be 
 found between the cells and within these, especially such as pre- 
 
BACTERIA AND DTSEASES DUE TO BACTERIA. 211 
 
 sent hyaline degeneration. The micro-organism resembles the 
 bacillus of Friedlander, but, unlike this, stains well by Gram's 
 method, and when cultivated upon blood-serum or agar retains its 
 capsule. In other respects the two forms are identical. Inocu- 
 lation-experiments have thus far failed to produce the disease in 
 animals. 
 
 DIPHTHERIA. 
 
 Definition. — Diphtheria is an infectious and contagious dis- 
 ease caused by a specific bacillus. 
 
 Etiology. — The Bacillus diphtheria? was discovered by Klebs, 
 and more accurately studied by Loffler, and is therefore called the 
 Klebs-Loffler bacillus. This organism is a rod about the length 
 of the tubercle-bacillus and twice its thickness, with somewhat 
 swollen ends. It is readily demonstrated in the local lesions of 
 the mucous membranes or skin, where it may be quite abundant ; 
 the individual bacilli, however, are separate from one another. 
 The organism is peculiar in its great irregularity of shape and 
 size, particularly in cultures (Fig. 85). Frequently one end is 
 
 
 ^. 
 
 
 I 
 
 fly, ^ f sx 
 
 Fig. 85.— Bacillus diphtheria; from a pure culture. 
 
 especially large, giving a club-shaped appearance ; some of the 
 bacilli are very large ; some present rounded granules at either 
 end, the so-called polar granules. The bacillus is readily stained 
 with aqueous solutions of basic stains, especially with those rendered 
 slightly alkaline. (Loffler's stain — saturated aqueous solution of 
 methylene-blue, 30 cc. in aqueous solution of potassium hydrate, 
 1 : 10,000, 100 cc. — is the favorite stain.) The stained specimen 
 shows the morphology of the bacillus very clearly. The rounded 
 ends generally stain more deeply than the shaft of the bacillus, so 
 that the appearance somewhat suggests a diplococcus. Not rarely 
 transverse fractures give the organism the appearance of disjointed 
 segments. There are no flagella and the bacillus is not motile. 
 Spores have not been demonstrated. 
 
 Cultivation. — The most characteristic cultures are obtained 
 
212 TEXT-BOOK OF PATHOLOGY. 
 
 upon blood-serum, especially such as contains a small amount of 
 glucose. Upon this medium there is formed within six, twelve, or 
 twenty-four hours a thin, whitish or yellowish-white layer of ir- 
 regular outline, and often showing separate smaller colonies around 
 the edge. A small portion of the colony may be removed and 
 stained, and the diagnosis thus established with ease in a short 
 time. Other organisms found in the throat are slower in growth, 
 and do not therefore interfere with the diagnosis. 
 
 Pathogenicity. — When cultures in bouillon are injected beneath 
 the skin of a guinea-pig a fibrinous inflammation with more or less 
 widespread edema results, and the animal dies in from twenty-four 
 to thirty-six hours. Necrotic foci in the liver and other organs 
 are found post-mortem ; the neighboring lymphatic glands are 
 enlarged. If the animal survive, paralysis may make its appear- 
 ance, as in human beings recovering from the disease. 
 
 Non-pathogenic diphtheria bacilli are found in the pharynx of 
 healthy individuals in some cases, as well as upon the hands, hair, 
 or other parts of the body. These may differ from the virulent 
 bacilli in being somewhat shorter and in growing more luxuriantly. 
 Their distinctive character, however, is their harmlessness when 
 injected into animals. The term pseudodiphtheria bacillus is un- 
 fortunate, as it is probably the same organism, but one having lost 
 its virulence by growth in an unfavorable situation. Moreover, 
 the name pseudodiphtheria bacterium was formerly applied to 
 various organisms having nothing whatever in common with 
 the Klebs-Loffler bacillus. 
 
 Klebs-Loffler bacilli may be found in the pharynx of a person 
 showing no indication of disease. This means that the organism 
 has not found a favorable soil for its development or no abrasion 
 or opening into tissues that will support its growth. The bacil- 
 lus may, however, thrive and multiply for a considerable time 
 upon the mucous membrane of such a throat, as it may upon food, 
 clothing, or other infected materials. 
 
 Predisposing Causes. — Some predisposition is necessary for the 
 development of the disease. In part this is personal, some indi- 
 viduals being highly susceptible, others scarcely at all. In part, 
 accidental conditions, such as pharyngitis, laryngitis, abrasions, 
 etc., furnish a favorable opportunity for the infection. 
 
 The diphtheria of birds, calves, and certain other animals is 
 distinct from the human disease ; and the organisms are in no 
 way related. Human diphtheria may occur in cats, and these 
 animals may propagate epidemics. 
 
 Distribution of the Bacilli. — The organisms are abundant in the 
 pseudomembranes of diphtheria, but are only exceptionallv found 
 in the blood or internal organs. The visceral or nerve-lesions are 
 due to the toxins, and not to the bacillus. The same is true of 
 experimental diphtheria. The internal lesions may be produced 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 213 
 
 by injection of the toxin obtained by filtering a bouillon-culture 
 through a Pasteur filter. 
 
 Pathologic Anatomy. — Diphtheria is primarily a local dis- 
 ease of the pharynx (pharyngeal), of the larynx (laryngeal), of 
 the nose (nasal), or of the skin (dermal). The bacillus lodges in 
 the mucous membrane or skin, and produces a pseudomembrane. 
 This consists of fibrinous exudation in the form of fine granular 
 material or a fibrillar network, in which are embedded the epi- 
 thelial cells and other tissue-elements and infiltrating leukocytes. 
 The epithelial cells rapidly undergo coagulation-necrosis or granu- 
 lar degeneration, as do also the connective tissues when the pro- 
 cess extends beneath the mucosa. The blood-vessels become 
 obstructed by thrombosis or compression, and the tissue is there- 
 fore avascular. Nearly always the pseudomembrane thus formed 
 is attached to the underlying tissues, and when removed a raw 
 and bleeding surface is exposed. The depth of involvement, 
 however, varies ; sometimes the submucosa is soon involved ; 
 more often the disease is practically confined to the mucosa. 
 
 The macroscopic appearance is that of a whitish, dirty-yellow- 
 ish, or brownish membrane upon the mucous lining of the throat. 
 This begins as one or several patches upon the tonsil, and spreads 
 rapidly to the neighboring parts. In other situations the appear- 
 ance is much the same. Inflammatory swelling beneath and 
 around the diseased area is habitual. It is of great clinical im- 
 portance to recognize that true diphtheria may occur in the form 
 of typical follicular tonsillitis. 
 
 Internal or visceral lesions may occur in the course of diph- 
 theria or during convalescence. They are due to the action of the 
 toxin, and not of the bacillus. Necrotic foci in the liver, showing 
 advanced cellular degeneration of the cells with hyperchromatosis 
 of the nuclei, and similar lesions of other organs, may be seen in 
 the human body, as in animals killed with the organism or its 
 toxin. Myocarditis and myocardial degeneration, renal degenera- 
 tion and nephritis, and, most interesting of all, degeneration of the 
 peripheral nerves and neuritis, may be met with. All of these 
 will be described elsewhere. 
 
 Pathologic Physiology.— As has been said, the disease is 
 primarily local, and the bacilli nearly always remain localized in 
 the superficial lesions. The general manifestations — fever, pros- 
 tration, and the visceral lesions — are caused by poisonous sub- 
 stances elaborated by the growth of the bacilli. There are prob- 
 ably several substances of this sort, but one in particular — the 
 toxin — is most important. This may be obtained by filtering 
 bouillon-cultures through porcelain, and by its injection the con- 
 stitutional and some of the local manifestations of the disease may 
 be induced in animals. Successive introduction of increasing 
 doses of toxin causes the development of antitoxic substances that 
 
214 TEXT-BOOK OF PATHOLOGY. 
 
 may finally accumulate in the blood to such extent that the ani- 
 mal becomes immune to the most virulent bacilli. The antitoxic 
 substance or substances, or antitoxin, found in the blood and the 
 blood-serum of immunized animals, will render other animals im- 
 mune for a time, or combat and overcome the disease if already 
 existing. Simultaneous injection of antitoxin and of many times 
 the ordinarily fatal dose of toxin or diphtheria-cultures leaves an 
 animal unharmed. Later, when the immunity has passed off, a 
 small dose of toxin or culture without the antitoxin will kill the 
 same animal. The value of the antitoxin in animal experimenta- 
 tion is beyond doubt. In the human being there is scarcely any 
 doubt of its potency, though, of course, crucial experiments cannot 
 be made. 
 
 After an attack of diphtheria there is temporary immunity, 
 but this passes off and successive attacks may thus occur in the 
 same person. 
 
 TYPHOID FEVER. 
 
 Definition. — Typhoid fever is an infectious disease, with 
 characteristic lesions of the intestines, and due to a specific 
 bacillus. 
 
 Etiology. — Certain predisposing features make individuals 
 more liable at one time than another to this disease. It occurs in 
 adolescence and the young, though rarely also in the old. Cli- 
 matic conditions are supposed to play some part, and doubtless do 
 have an influence. Typhoid fever is especially a disease of the 
 temperate zones, and is most abundant in the autumn. Drainage 
 and other conditions affecting the surroundings of persons may 
 influence the predisposition. One attack usually confers immunity 
 for the rest of life ; exceptions, however, are met with. 
 
 The Bacillus. — The Bacillus typhi abdominalis, the specific 
 organism, was discovered by Eberth and isolated by Gaffky. It 
 is a short bacillus, from 1 to 4 // in length and 0.5 to 0.8 // in 
 thickness. The ends are rounded and often somewhat plump. In 
 culture these rods or bacilli occasionally form long chains, but in 
 the tissues they are never so arranged. The organism is actively 
 motile, this being due to flagella, of which there are eighteen or 
 twenty attached to the periphery (Fig. 86). When stained with 
 alkaline methylene-blue or other stains there are sometimes seen 
 dark-colored spots at the ends of the organism. These were 
 formerly regarded as spores, but are now recognized as areas of 
 condensation. Under certain circumstances the condensation is 
 Been in the center and vacuole-like formations are found at the 
 ends. The organism is readily stained, but decolorizes very 
 easily, and is therefore difficult to demonstrate in tissue. Pro- 
 longed staining, however, and rapid decolorization sometimes give 
 beautiful results. The bacilli are, as a rule, found in clusters. 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 215 
 
 These groups may, however, be few in number, and thus difficult 
 to detect in the organs. 
 
 Cultivation. — Artificial cultures of the bacillus have been ob- 
 tained from the spleen and other organs, as well as directly from the 
 stools and urine of patients suffering from the disease. They grow 
 very .well upon the ordinary culture-media, such as agar-agar, gel- 
 atin, and potato, the temperature of the body being most favorable, 
 
 ***■ 
 
 Fig. 86.— Bacillus tvphi abdominalis, from an agar-agar culture six hours old, showing the 
 flagella' stained by Loffler's method ; X 1000 (Frankel and Pfeiffer). 
 
 but some growth occurring at the ordinary temperature of the 
 room. Upon gelatin and agar there are formed irregularly whitish 
 films, which on close inspection with the lens show a granular 
 appearance. This growth, however, is not distinctive. Upon acid 
 potato a characteristic transparent pellicle is formed. This may 
 be invisible except to the trained eye, but on scraping the surface 
 with a platinum wire the pellicle can be raised, and on micro- 
 scopic examination it is found to be composed of bacilli. Some- 
 times the pellicle is yellowish or brownish. When cultivated in 
 milk there is slight acidity, but coagulation does not occur. When 
 grown in agar containing a little glucose practically no fermenta- 
 tive gas results. Another feature of importance is the absence of 
 indol-reaction, the addition of potassium nitrite and sulphuric acid 
 to bouillon-cultures causing no rose color, such as occurs with 
 some other organisms. 
 
 Pathogenicity. — Animal-experimentation has thus far been un- 
 satisfactory. A few observers have succeeded in producing intes- 
 tinal lesions and illness by feeding animals with typhoid cultures, 
 particularly after the stomach and intestines have been rendered 
 alkaline with soda and peristalsis has been checked with opium. 
 
216 TEXT-BOOK OF rATHOLOGY. 
 
 In most cases injection of the typhoid bacillus has produced sep- 
 ticemic manifestations. The constant occurrence of the germ, its 
 absence from other conditions, and the absence of any other germ 
 as a constant accompaniment of typhoid fever, have led to the 
 general acceptation of this as the specific cause. Moreover, its 
 properties are such that the spread of the disease in the acknowl- 
 edged ways is entirely compatible with the acceptance of the 
 bacillus as the specific cause. 
 
 The diagnostic features of the bacillus are plainly distinctive, 
 except that the Bacillus coli communis has a puzzling resemblance. 
 The latter, however, grows upon acid potato as a yellowish or 
 brownish film, coagulates milk promptly and causes decided acid 
 reaction, and is an active gas-producing organism when grown in 
 glucose-agar. The serum-reaction of Widal is a recent and im- 
 portant distinguishing mark. The serum from typhoid patients 
 must not, however, be relied upon absolutely, as it may contain 
 substances produced by the Bacillus coli as well as those produced 
 by the typhoid germ (see Widal reaction). 
 
 Distribution. — The typhoid bacillus occurs both within and 
 without the human body, and doubtless multiplies greatly in the 
 external world when the conditions are favorable. It occurs in 
 the lesions of the intestines and in the intestinal contents, espec- 
 ially during the second and third weeks of the disease. It is 
 usually less abundant, but often present in the spleen, liver, and 
 kidneys ; it may occur in considerable abundance in these organs 
 when there are local complications. It also occurs in the lungs, 
 in the parotid gland, and in other organs, and post-typhoidal ab- 
 scesses may contain the organism in abundance. Complicating 
 lesions of other organs may be dependent solely upon the specific 
 bacillus, this being capable even of acting as a pyogenic organism, 
 or they may be dependent upon secondary or mixed infections. 
 The bacillus is not found in the blood in abundance, but has been 
 demonstrated in the blood derived from the macular spots in the 
 skin. 
 
 The typhoid bacillus is peculiarly resistant, and may thrive 
 upon clothing, in soil, and in water for a long time. Cold has no 
 effect, the germ being virulent after freezing and thawing several 
 times. Carbolic acid in strengths that prove destructive to most 
 organisms has little effect on this germ. These features explain 
 the spread of the disease and its general prevalence. The organ- 
 i - 1 1 1 - are discharged from the body of a patient suffering from the 
 disease mainly in the stools, but in part also in the urine, sweat, 
 and other excreta. If they are not at once destroyed, contami- 
 nation of clothing, soil, water, etc. may occur, and subsequent 
 infection of susceptible individuals takes place through drinking- 
 water or food with which the infected water or other matters have 
 come in contact. It is possible that infection may occasionally 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 217 
 
 take place through the lungs by inhalation of dust. This must be 
 very rare. Intra-uterine infection undoubtedly occurs in some 
 instances in which the mother is suffering from typhoid fever. 
 
 Pathologic Anatomy. — The lesions of typhoid fever are 
 considered with the diseases of the intestines. It is important, 
 however, to add in this place that widespread changes may occur 
 in this disease as a result of the action of the bacillus, but especially 
 of toxins. Thus there may be focal necroses in the spleen and 
 liver, degenerative changes in the kidneys and muscles, and inflam- 
 matory changes in various glandular organs, the periosteum, the 
 bones, or the connective tissues, the result of the direct action of 
 the bacillus. 
 
 Sometimes typhoid infection occurs without specific lesions of 
 the intestines, the disease in these cases presenting itself as a form 
 of cryptogenetic sepsis. In cases of intra-uterine infection this 
 form is habitual, intestinal lesions being exceptional. 
 
 Pathologic Physiology. — The typhoid bacillus produces 
 by its local action toxic substances which give rise to fever and 
 other general symptoms as well as to secondary lesions. Brieger 
 and Frankel claim to have separated a specific toxalbumin. 
 Whether this be the poison or not, there is no doubt that some 
 form of toxin is present. During the existence of the disease the 
 system reacts in some way as yet unknown to check its progress 
 and to bring it to a termination at the end of four weeks, and 
 permanent immunity is usually conferred. Whether or not there 
 are distinct antitoxic substances remains to be determined. 
 
 A reaction of importance is that studied by Gruber and per- 
 fected by Widal. These observers showed that the serum of typhoid 
 blood in certain dilutions causes the bacillus in culture to clump or 
 form small masses and to lose its motility. If the serum be added 
 to the bouillon-culture, the uniform turbidity of the latter is lost 
 and the bacilli fall to fche bottom as a sediment. Under the micro- 
 scope the uniform distribution of the motile bacilli is destroyed, 
 clumps being rapidly formed and the motility of the bacilli in the 
 clumps rapidly or gradually subsiding. This reaction was found 
 in 2283 cases of typhoid fever reported by various writers, and 
 was absent in 109 cases of typhoid fever. It was absent in 
 1365 non-typhoid cases, and present in 22 non-typhoid patients. 
 It was therefore found in 95.5 per cent, of the typhoid cases, 
 and was absent in 98.4 per cent, of the non-typhoid cases ; 
 or, taking the entire 3779 cases, the correct result for diagnosis 
 was arrived at in 96.5 per cent. The reaction sometimes persists 
 for some years after the attack of typhoid fever. Sometimes it 
 occurs in cases in which there is typhoid infection without typhoid 
 fever in the ordinary sense. These facts may explain some of the 
 positive results obtained in non-typhoid cases. The serum must 
 be diluted with nineteen parts or more of water. Reactions with 
 
218 TEXT-BOOK OF PATHOLOGY. 
 
 stronger serum or partial reactions may be deceptive. Whether 
 the Widal reaction is produced by a substance connected with the 
 infection, or by substances concerned with immunization, is not as 
 vet determined. The latter seems more probable. 
 
 BACILLUS COLI COMMUNIS. 
 
 Synonyms. — Bacterium coli commune. A number of organ- 
 isms described under different names are probably identical. 
 Among these are Bacillus Neapolitanus of Emmerich; Bacillus 
 pyogenes foetidus of Passet. 
 
 Morphology. — The Bacillus coli communis is an organism 
 almost exactly like the typhoid bacillus in appearance. It is rod- 
 shaped, but sometimes elongated and filamentous, at other times 
 (young forms) short and rather rounded — coccus-like. It is 
 actively motile, and has llagella attached to the periphery of the 
 bacillus. The nagella are less numerous than are those of Eberth's 
 bacillus (three to ten), and the motility of the organism is less uni- 
 form and active. It may be stained by ordinary solutions of anilin 
 dyes, particularly with alkaline or carbolized solutions. It is de- 
 colorized by Gram's staining-method. The stained bacillus shows 
 light-colored or unstained portions like those of the typhoid bacil- 
 lus. True spores have not been detected. 
 
 Cultivation. — The organism grows luxuriantly upon ordinary 
 media. The most distinctive growth is obtained upon acid potato. 
 An elevated brownish colony is produced, which is usually easily 
 distinguished from the typhoid culture in the same medium. 
 When cultivated in gelatin or agar containing glucose active gas- 
 production results. In liquid media (bouillon) a peculiar odor is 
 developed. Addition of nitrites and pure hydrochloric or sulphuric 
 acid causes a rose-red color — indol-reaction. 
 
 Distribution and Pathogenicity. — The coli bacillus is a 
 normal inhabitant of the gastro-intestinal tract. In certain in- 
 flammatory diseases of the intestines, however, it seems to increase 
 in numbers and doubtless also in virulence. The organism may 
 be found outside the body in various situations, particularly in 
 water. 
 
 The bacillus coli is capable of producing inflammatory condi- 
 t ions in different situations. Injected into the peritoneal cavity 
 of animals it gives rise to acute flbrinopurulent peritonitis, and in 
 other parte of the body has analogous effects. 
 
 It has been found in various diseases of the gastro-intestinal 
 tract, of the biliary passages, of the urinary system, and of other 
 ] »arts, and is doubtless the direct cause of some of these, as the 
 conditions present are practically the same as those produced by 
 experimental inoculation of pure cultures. 
 
 Among the gastro-intestinal troubles it has been found in sus- 
 picious abundance in various forms of enteritis, in the distended 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 219 
 
 and suppurating appendix, and even in Asiatic cholera. It is 
 known that the strangulation of a knuckle of intestine by a liga- 
 ture leads to rapid increase of virulence of the contained bacilli. 
 It is possible that in appendicitis and in other intestinal diseases 
 similar conditions lead to increased infectivity, and thus cause an 
 ordinarily harmless organism to become virulent. In the cases of 
 Asiatic cholera in which this organism has been found the specific 
 germ of cholera has probably been overlooked or has disappeared 
 during the rapid multiplication of the saprophytic Bacillus coli. 
 
 Peritonitis may result from escape of the bacillus through a 
 ruptured intestine or directly through the wall of the bowel. The 
 latter is particularly prone to occur in cases of strangulation of the 
 intestines. 
 
 Various inflammatory diseases of the urinary tract, such as 
 cystitis, pyelitis, and pyelonephritis, seem to be occasioned by 
 this same germ. 
 
 Finally, there are cases of peritonitis secondary to enteritis, 
 pleurisy, endocarditis, and other inflammatory diseases, apparently 
 caused by this organism. 
 
 Pathologic Physiology. — Little is known of the toxic 
 effects of coli-infection. There is doubtless some toxic sub- 
 stance produced. A reaction similar to the Widal reaction 
 obtained with the typhoid germ has been found to occur when 
 cultures of the coli bacillus are subjected to the action of serum 
 from an animal inoculated with this organism or from a person 
 suffering with appendicitis or other diseases, either due to coli- 
 infection or accompanied by such. Occasionally the coli bacilli 
 agglutinate and their motility is checked by typhoid serum. The 
 explanation of this may be that in certain cases of typhoid fever 
 the coli bacillus is also active in the intestines, and in conse- 
 quence a mixed form of infection is present. 
 
 CHOLERA. 
 
 Definition. — Cholera is an acute infectious and contagious 
 disease caused by a spirillum or vibrio. 
 
 Etiology. — The specific cause of cholera is the Spirillum or 
 Vibrio cholera? Asiaticse. This organism is frequently spoken of 
 as the comma-bacillus of Koch. It is a short rod, from 0.8 to 
 2 [x in length, and usually somewhat curved. The term comma- 
 bacillus is applied to it on account of the latter fact. It is found 
 abundantly in the rice-water discharges of choleraic patients, and 
 is not rarely arranged in rows, though the vibriones are not actu- 
 ally attached to one another (Fig. 87). It is motile, the motility 
 being due to a single flagellum attached at one end. In artificial 
 cultures the organisms are actually joined to form spirals of greater 
 or less length, and these may present a rapid rotary movement. 
 
220 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 The demonstration of the cholera-spirillum is usually easy, as 
 ordinary stains color it intensely. Even the rlagellum may be 
 
 
 9* - 
 
 *3 
 
 
 
 Fig. 87.— Spirillum of Asiatic cholera, from a bouillon-culture three weeks old, showing 
 numbers of long spirals ; X 1000 (Frankel and Pfeiffer). 
 
 stained by the ordinary stains, though more definitely shown by 
 
 special methods. 
 
 Cultivation. — The cultivation of the spirillum is usually easy. 
 Cultures may be obtained upon agar-agar, blood- 
 serum, or other media, but the gelatin-culture is 
 most characteristic. In puncture-cultures the 
 growth occurs along the entire length of the 
 puncture, but particularly at the top, where the 
 supply of oxygen is abundant ; and the gelatin 
 becomes liquefied. This give rise to a peculiar 
 nail-shaped or funnel-shaped formation (Fig. 88). 
 In plate-cultures the growths first appear in the 
 lower strata of the gelatin as small granular whit- 
 ish spots which extend toward the surface, liquefy 
 the gelatin, and thus produce excavations. The 
 appearance to the naked eye suggests small air- 
 bubbles in the media. Under low powers of the 
 microscope the culture is seen to be coarsely 
 granular, the size of the granules varying with 
 the age of the culture. The bottom of the growth 
 presents an appearance like that of a surface 
 sprinkled with powdered glass. 
 
 When grown in bouillon or other liquid media 
 the cholera-microbe produces nitrites and indol, 
 
 so that the addition of a little pure sulphuric acid or hydrochloric 
 
 Pig. 
 
 -Punct- 
 
 ure-culture in gel- 
 atin of spirillum of 
 
 cholera ; sixty hours 
 Old (Shakespeare). 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 221 
 
 acid leads to a reddish coloration. This may be extracted with 
 chloroform or benzol, and " cholera-red " may be thus obtained. 
 
 The cultures of cholera grow best at a temperature about that 
 of the body, but they may thrive at much lower degrees of heat. 
 Exposure to a temperature of 52° C. (125.6° F.) for four minutes 
 may cause their destruction, but ten or fifteen minutes' exposure 
 at 55° C. (131° F.) does not always prove destructive. They 
 may thrive in distilled water, or in water containing saline 
 matter ; in or upon various forms of food ; upon clothing and the 
 like. The resistance, however, is not very great, and this has 
 been urged as an objection to the likelihood of the organism being 
 the cause of a disease having such evident tenacity. 
 
 Pathogenicity. — The pathogenicity of the cholera-spirillum is 
 now admitted universally. Injected into the peritoneum of ani- 
 mals it causes a rapid fall of temperature, abdominal tenderness, 
 and collapse. The peritoneum shows signs of beginning inflam- 
 mation, and the organisms are found in abundance within the 
 cavity. It has been possible also to produce intestinal changes 
 almost, if not, identical with those of human cholera in animals by 
 arresting the peristalsis of the intestines with injections of opium, 
 rendering the liquids of the stomach alkaline with sodium carbonate, 
 and then feeding cultures. In man a few auto-infections have 
 been practised, the experimenter swallowing cholera-cultures. In 
 one case at least typical cholera Avas admitted by Pettenkofer, the 
 most important opponent of the acceptance of this germ as the 
 specific cause. 
 
 Other Causes Operating in Cholera. — Certain climatic conditions 
 favor the development of the disease. Thus it is constant in cer- 
 tain regions of India, and spreads thence when the conditions 
 become favorable. The evidence shows that the germ is carried 
 by individuals, or by infected food and the like. The disease 
 flourishes in warm seasons of the year, and an epidemic is usually 
 brought to a close by winter frosts. 
 
 Individual disposition plays a part in the occurrence of the 
 disease, for the germ is easily destroyed by the acid gastric secre- 
 tions, and infection is therefore most likely to occur when gastro- 
 intestinal derangements furnish a favorable predisposition. 
 
 Pathologic Anatomy. — The lesions of this disease are 
 found in the intestinal tract, and will be described in the appro- 
 priate section. 
 
 Secondary lesions of other organs are met with in severer 
 cases, and result from the circulation of toxic substances produced 
 by the bacillus. 
 
 Pathologic Physiology. — A number of toxins have been 
 isolated from the blood of cholera-patients and from cultures. 
 The exact nature of these and the relations of the several forms 
 remain to be determined. It is certain, however, that toxins pro- 
 
222 TEXT-BOOK OF PATHOLOGY. 
 
 duced in tho intestinal tract give rise to many of the symptoms 
 of the disease. The human or animal organism in some way de- 
 velops immunizing or protective substances in the course of infec- 
 tion, and it has been found possible by a process of vaccination 
 with cultures of gradually increasing virulence to protect animals 
 and human beings from the disease. Pfeiffer found that the serum 
 of animals so vaccinated had a distinct action upon cholera-spirilla, 
 causing their agglutination or destruction, and probably in this way 
 exercising a protective influence. This, or a similar, reaction has 
 now been perfected in the ease of typhoid bacilli, and forms the 
 basis of the well-known Widal test. The same test is applicable 
 to Asiatic cholera. The rapid and copious intestinal discharges of 
 cholera lead to considerable inspissation of the blood, and doubtless 
 contribute to the causing of some of the symptoms of the disease. 
 Examination of the blood during the height of the malady may 
 show greatly increased numbers of red blood-corpuscles. 
 
 Organisms Resembling the Cholera=vibrio. 
 
 Spirillum of Finkler and Prior. — This organism was discovered 
 by the investigators, whose names it bears, in the stools of a case 
 of cholera nostras. It resembles the vibrio of Asiatic cholera in 
 its shape and somewhat in its manner of growth and its produc- 
 tion of the indol-reaction. It differs, however, in being somewhat 
 longer and more slender and in coagulating milk when this is used 
 as the culture-medium. The growth upon gelatin is more rapid, 
 so that within twenty-four hours in the case of a puncture-culture 
 the liquefaction has proceeded so far all along the puncture that an 
 elongated sac-like excavation is formed, in which turbid liquid is 
 contained. It has not yet been proved positively whether or not 
 this organism has an etiologic relation to cholera nostras. 
 
 Spirillum Tyrogenicum. — This is an organism discovered in old 
 cheese by Denecke. It resembles the last-named variety very 
 closely, and differs from the vibrio of cholera in liquefying gelatin 
 quickly, though the rapidity is not so great as in the case of the 
 Finkler and Prior organism. 
 
 Spirillum Metschnikowi. — This organism was discovered by 
 Gamaleia in the intestines of chickens affected with choleriform 
 disease. It is somewhat shorter and thicker than the cholera- 
 spirillum. In culture it resembles the vibrio of cholera very 
 closely, though the trained bacteriologist can easily distinguish 
 them. The organism is non-pathogenic for man, but chickens, 
 pigeons, and guinea-pigs are highly susceptible. 
 
 Besides these spirilla or vibriones which have been discovered 
 in various diseases, a number of organisms that resemble closely 
 the spirillum of cholera have been found in the water of streams 
 supplying the drinking-water of cities. Among these Neisser 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 223 
 
 described the Spirillum Berolinensis, obtained from the water of 
 the Spree in 1893. Dunbar and Oergel isolated a similar organ- 
 ism from the water of the Elbe, and a number of others of like 
 character are known. The relations, however, of the different 
 forms to each other and the differentiation of these varieties have 
 not as yet been definitely determined. 
 
 Pathogenicity. — Some of the forms described produce violent 
 gastro-intestinal disturbance and death in a certain proportion of 
 animals prepared by injection of opium and alkali nization of the 
 intestinal tract with soda and then fed with pure cultures of the 
 organisms. They are evidently highly irritating bacteria, and 
 some remote relationship seems to exist between them. This, 
 however, cannot be positively asserted. 
 
 TUBERCULOSIS. 
 
 Definition. — The term tuberculosis refers to various condi- 
 tions due to infection with the tubercle-bacillus, no matter what 
 the form or individual peculiarities of the case. The name was 
 originally employed because of the occurrence of small nodules 
 or "tubercles." It must be remembered, however, that other 
 diseases show small miliary nodules, perhaps indistinguishable to 
 the naked eye from miliary tubercles, and that tuberculosis some- 
 times occurs without a single tubercle. 
 
 Etiology. — Tuberculosis is infectious and contagious, the ba- 
 cilli being transferred by the secretions and excretions from dis- 
 eased persons to a susceptible individual through the air, food, 
 drink, or in other ways. The infectious character of the disease 
 was long suspected, but Avas definitely proved by Villemin in 
 1865, and in 1880 Koch succeeded in isolating the infective ba- 
 cillus. Predisposing causes are of some importance. Formerly 
 family susceptibility was thought an all-important cause, and the 
 disease was supposed to be transmitted directly in families. At 
 the present time we recognize the transmission of susceptibility, 
 and very rarely transmission of the disease itself, from parent to 
 child. Susceptible persons frequently show delicate organization 
 with poor development of the body, particularly of the chest. 
 Besides inherited susceptibility, acquired predisposition may result 
 from occupations which lower vitality, from grief, prolonged ner- 
 vous strain and exhaustion ; and some one of the organs may be 
 specially predisposed by injuries, as in cases of tuberculosis occur- 
 ring in the lungs of those inhaling sharp particles of metal, coal, 
 and the like. Such mechanical lesions prepare a place of lesser 
 resistance, and tubercle-bacilli more easily gain a footing than in 
 normal tissues. 
 
 The tubercle-bacillus is a rod-shaped organism about 1.5 to 3.5 // 
 in length and from 0.2 to 0.5 p. in breadth. It often occurs in 
 
224 TEXT-BOOK OF PATHOLOGY. 
 
 pairs or in groups, arranged end to end, but not rarely overlapping 
 somewhat, and evidently not closely attached one to the other. 
 A beaded appearance is caused by the alternation of portions 
 well stained and intervening parts with little or no stain (Fig. 
 
 / ' 
 
 Fig. 89.— Tubercle-bacilli in the sputum ; Zeiss's homog. immersion Vs, Oc. 4 ; magnified 
 about 1000 diam. 
 
 89). These light areas were formerly regarded as spores (Koch), 
 but are now believed to be the result of fragmentation of the 
 bacillus and retraction of the substance of the organism, causing 
 vacant areas. In other words, they are phenomena of degenera- 
 tion. They are almost certainly not spores. The tubercle-bacillus 
 is not motile and does not have flagella. It is therefore trans- 
 ported by outside agencies entirely. 
 
 Artificial culture of the Bacillus tuberculosis w T as first success- 
 fully accomplished by the use of blood-serum as a medium. 
 The bacillus grows very slowly ; after ten days or two weeks 
 the surface of the medium shows dry flakish deposits, somewhat 
 resembling the scales in certain skin-diseases (Fig. 90). The 
 edges of these flakes tend to elevate themselves a little, and the 
 substance of the growth has a crumbled appearance. Placed under 
 a cover-glass in mass and examined with the microscope these flakes 
 are found to be composed of contorted masses of bacilli (Fig. 91). 
 Pure cultures are best obtained from the lymphatic glands of ani- 
 mals artificially infected and destroyed before the tuberculous 
 foci have advanced to the stage of necrotic change. Cultures 
 may be obtained with some difficulty from the sputum or other 
 excreta. At the present time blood-serum is less frequently used, 
 as it has been found that agar-agar slightly acidulated and con- 
 taining a large proportion of glycerin, and bouillon containing gly- 
 cerin, serve as useful media. Even potato and other simple sub- 
 Btances are found to be satisfactory media. The bacillus requires a 
 rather even temperature for its growth ; it flourishes best at 37.5° 
 C. (99.5° F.), and does not grow below 29° C. (84° F.), or above 
 42° C. (107.6° F.). Exposure to higher temperatures (75° C.) 
 (167° F.) rapidly destroys it; and strong sunlight is destructive. 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 
 
 225 
 
 It requires considerable air and always grows upon the surface of 
 the medium in which it is cultivated. Prolonged cultivation upon 
 artificial media lessens its virulence. 
 
 Demonstration. — The demonstration of the tubercle-bacillus by 
 staining-methods is extremely easy and satisfactory. It has been 
 found that this organism, like that of lepra and the smegma-bacil- 
 lus, does not readily stain, but after receiv- 
 ing a stain retains it despite the action of 
 strong mineral acids. Upon this principle 
 the methods of staining are based. Koch 
 used as a stain a gentian-violet solution con- 
 taining anilin-oil, the latter playing the part 
 of a mordant or an agent to fix the stain in 
 resistant bacilli. The specimen was then 
 
 m 
 
 
 Fig. 90.— Culture of tubercle- 
 bacilli on glycerin-agar. four 
 weeks old (Frankel and Pfeiffer). 
 
 Fig. 91.— Bacillus tuberculosis : adhesive cover- 
 glass preparation from a fourteen-day-old blood- 
 serum culture : X 100 (Frankel and Pfeiffer). 
 
 decolorized by treating it with a solution of a mineral acid, which 
 removes the stain from everything but the tubercle-bacillus. A 
 counter-stain might then be used to render the detection of the 
 bacilli more easy. 
 
 The most convenient method is the following : sputum is 
 spread in a film upon thin cover-glasses or slides. These are 
 allowed to dry in air and then thoroughly fixed by drawing the 
 specimen through a Bunsen flame three times ; a drop or two of 
 Ziehl's solution of carbol-fuchsin (see p. 187) are added and heated 
 until the liquid steams. After two or three minutes the stain is 
 washed off with water and a few drops of Gabbett's solution 
 (methylene-blue, 2 ; sulphuric acid, 25 ;■ water, 75) placed upon it 
 
226 TEXT-BOOK OF PATHOLOGY. 
 
 and allowed to remain a minute or two. The specimen is again 
 washed with water, and should then be uniformly blue ; if not, a 
 little more Gabbett's solution is added as before. In this method 
 the oarbol-fuchsin stains everything, including the tubercle-bacil- 
 lus ; the sulphuric acid of the second solution decolorizes every- 
 thing but the tuberele-bacillus ; and the methylene-blue at once 
 stains the cells and other elements, leaving the bacilli dark red. 
 Even more satisfactory results may be obtained by allowing the 
 carbol-fuchsin to stain at ordinary temperatures for twelve hours ; 
 and in the staining of bacilli in tissues this prolonged cold staining 
 is particularly desirable. Gram's method gives positive results. 
 
 Distribution of the Tubercle-bacillus. — This organism is prob- 
 ably a pure parasite, occurring and multiplying only in the body 
 or excreta of diseased individuals, human or animal. Sputa or 
 other excreta containing the bacillus may dry and retain the 
 bacillus in a dormant though still potential form for long periods 
 of time, outside the body. Multiplication of the organism, how- 
 ever, probably very rarely occurs, except within the body. The 
 bacillus is found in the lesions of all parts of the body. 
 
 Modes of Infection. — The bacillus may gain access to the body 
 either by direct inoculation, by the inhalation or swallowing of 
 the germs, or by intra-uterine transference through the placenta. 
 Direct inoculation through external wounds is perhaps more fre- 
 quent than is believed. Definite lesions of the skin have been 
 caused by vaccination, and are not infrequent upon the hands of 
 anatomists, in the form of the so-called anatomic tubercles. In 
 some of the cases of scrofulous or tuberculous glands of the 
 neck in children, it is likely that the bacillus gains entrance 
 through abrasions of the skin or of the mucous membrane of the 
 mouth or pharynx. Genital tuberculosis is quite possibly fre- 
 quently produced by direct implantation. The most common 
 form of infection is through the inspired air. The breath of 
 phthisical patients does not ordinarily contain bacilli, but the dust 
 of rooms in which tuberculous patients have lived may contain 
 numerous bacilli in a dry state, and these readily become mixed 
 with the air and are thus inhaled. Tuberculosis of the lungs, or 
 more rarely of other parts of the respiratory tract, is thus produced 
 in susceptible persons. The swallowing of tuberculous material 
 may lead to tuberculosis of any part of the gastro-intestinal tract 
 by the direct inoculation that results. Thus intestinal tuberculosis 
 in particular is produced. Sometimes, however, the bacilli pass 
 through the wall of the intestine and cause a primary lesion in the 
 lymphatic glands of the abdomen. The bacilli are swallowed 
 with milk or meat, or they may gain access to the mouth, in the 
 form of dust or particles of various kinds, and be swallowed with 
 the saliva. The milk and meat of infected cattle frequently con- 
 tain bacilli, and undoubted instances of infection in this way have 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 227 
 
 been proved. The intra-uterine transmission of tuberculosis is 
 rare, but does occur. Most of the cases, however, of tuberculosis 
 in early life may be explained as post-natal infections through 
 milk, inspired air, etc. 
 
 Relations of Human to Animal Tuberculosis. — The lower ani- 
 mals are liable to tuberculosis in varying degrees. The disease is 
 very common among cattle and less frequent in hogs, goats, 
 horses, dogs, cats, sheep, rats, guinea-pigs, and rabbits. Animals 
 become more susceptible when kept in confinement. Captive 
 monkeys are particularly liable. Birds and fowl of various kinds 
 are susceptible, though the disease is somewhat different in them 
 from that seen in man. 
 
 Animals may become infected from man, and may further 
 spread the infection by their discharges or excretions. In the case 
 of cattle the danger of dissemination is particularly great, as 
 tainted milk is liable to produce intestinal tuberculosis, and meat 
 if insufficiently cooked may similarly cause infection. 
 
 Pathologic Anatomy. — Tuberculosis is characterized by the 
 eruption of small nodules varying in size from one or two milli- 
 meters in diameter to that of a small pea. These are known 
 as miliary tubercles. As already mentioned, the latter in gross 
 appearance are not distinctive of tuberculosis, as similar nodules 
 are met with in other diseases. Besides the tubercle there are 
 inflammatory lesions occurring between the tubercles and varying 
 with the anatomic character of the organs affected. Thus in the 
 lungs the tubercle may be inconspicuous, whereas the pneumonic 
 infiltration of the lung-tissue surrounding the tubercles and filling 
 in the spaces between them gives the organ its most striking 
 anatomic characters. There are instances of tuberculosis in which 
 the whole process runs its course without the development of any 
 definite tubercles. For example, in the lungs the inhalation of 
 tubercle-bacilli in considerable number may be followed by rapid 
 tuberculous pneumonia without definite tubercles, and in other 
 situations similar results may be produced. In the further prog- 
 ress of a case of tuberculosis caseous change is important. This 
 may present itself in the form of areas of considerable size having 
 a dull, opaque, lusterless, grayish or whitish character, and not 
 inaptly likened to the appearance of cheese. These centers of 
 caseous necrosis may finally become liquefied, and cavity-forma- 
 tions may result. These changes are particularly frequent in 
 tuberculosis of the lungs, less frequent in bones, skin, glands, 
 kidneys. In connection with tuberculosis of bones there may 
 be formed small or large cavities filled with liquefied caseous 
 or puriform material. These may involve the surrounding tis- 
 sues as well as the bones themselves. The term cold abscess 
 is applied to them. Small tubercular areas and sometimes even 
 large foci are prone to be surrounded by reactive fibrous-tissue 
 
228 TEXT-BOOK OF PATHOLOGY. 
 
 hyperplasia, and thus a complete encapsulation may result. Small 
 foci mav be uniformly transformed by organization of proliferating 
 connective tissue and mav be thus entirely healed. In other cases 
 simple encapsulation occurs, the tuberculous mass within perhaps 
 undergoing calcification. These changes will be more particularly 
 referred to below. 
 
 Tuberculous lesions of the mucous membranes frequently begin 
 with the formation of distinct tubercles occupying the deeper 
 layers of the mucosa or the submucosa. These by confluence may 
 form considerable areas of tuberculous disease, while at the same 
 time reactive inflammation of the surrounding tissues adds to the 
 mass. Sooner or later ulcerative changes upon the surface make 
 their appearance and irregular, more or less necrotic, ulcers re- 
 sult. The caseous appearance of these and the occurrence of 
 distinct tubercles in the edges or base manifest the character of 
 the process. 
 
 Structure and Evolution of the Tubercle. — When the tubercle- 
 bacillus is received into any tissue or organ its first effect, accord- 
 ing to the investigations of Baumgarten, is to stimulate or irritate 
 the fixed connective-tissue elements and cause a proliferation of 
 round cells, which resemble in their abundance of protoplasm the 
 epithelial cells, and are therefore known as epithelioid cells. These 
 
 :•- ..... •' ,'?<£* "'Ul-: ''Ate 
 
 Fig. 92.— Miliary tubercles in the liver, showing abundant round cells in the peripheral 
 parts, epithelioid and giant-cells within. 
 
 have usually a single nucleus, of rather clear vesicular appear- 
 ance, not deeply staining, and a relatively large amount of proto- 
 plasm. They may be produced in greater or less abundance, as 
 the first reactive change of the tissues to the irritation of tubercle- 
 bacilli. Next there follows an infiltration with leukocytes from 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 229 
 
 the surrounding blood-vessels, and the focus of irritation thus 
 becomes surrounded with numerous small round cells mostly 
 mononuclear, with darkly staining nucleus and a small protoplas- 
 mic body (Fig. 92). Some of the cells are polynuclear. This 
 leukocytic infiltration represents the reaction of the vascular sys- 
 tem to the tubercular irritation or infection. The number of small 
 round cells varies greatly in different instances. Sometimes, as in 
 certain tubercles of lymphatic glands, they may be relatively few, 
 while the epithelioid cells are present in abundance. In other 
 cases the leukocytes are so quickly attracted and in such num- 
 bers that the tubercle seems composed of these cells alone, no 
 epithelioid cells appearing in view. These tubercles are known 
 as the lymphoid. In the later stages the round cells may disap- 
 pear by degeneration, exposing the previously hidden epithelioid 
 cells to view. 
 
 At the stage of the tubercle when it is composed mainly of 
 epithelioid and lymphoid cells it appears to the naked eye as a 
 grayish, somewhat translucent pearly body. It is avascular, no 
 tendency toward formation of new blood-vessels being apparent. 
 In the further evolution of the lesion degenerative changes take 
 place. These are coagulation-necrosis, fatty change, and eventually 
 a transformation into cheesy material, the so-called caseous necrosis. 
 These changes result from the specific action of the living tubercle- 
 bacillus, though in part also from the avascular condition of the 
 tissue. Avascularity alone, however, is not the cause of caseous 
 necrosis. One of the first changes noted is a granular change 
 in the cell-protoplasm which lessens the affinity of the cell- 
 protoplasm and of the nucleus for ordinary stains. There may 
 be seen among the cells of the tubercle here and there indi- 
 viduals which show this beginning necrosis. These are usually 
 grouped in the center of the tubercle, though at times also at dif- 
 ferent points. The outlines of these cells become less distinct and 
 they are progressively less deeply stained, until with advanced 
 necrosis the cell is broken down into particles or debris (Fig. 93). 
 In the early stages of necrosis the epithelioid cells tend to run 
 together, forming large, irregular giant-cells with many nuclei 
 arranged either around the periphery or frequently at either pole 
 of the cell. Some observers believe that giant-cells result from 
 rapid multiplication of nuclei within the epithelioid cells. This is 
 very rare. Others have supposed that the running together of 
 leukocytes or lymphoid elements of the tubercle causes the for- 
 mation of giant-cells. This does not seem ever to occur. The 
 giant-cell is not characteristic of tuberculosis, as it may be found 
 in many of the specific inflammations and also in foci of chronic 
 irritation due to foreign bodies, as well as in tumors. In no con- 
 dition, however, are they so abundant or so conspicuous as in 
 tuberculosis. In some cases they may not be seen in the tubercles 
 
230 TEXT-BOOK OF PATHOLOGY. 
 
 at any stage. In other cases they are very numerous. The giant- 
 cell falls an early victim to the advancing necrosis, and the pro- 
 toplasm becomes granular and opaque, and eventually breaks down 
 completely. This change usually occurs at the opposite side of 
 the cell from that in which the nuclei are gathered ; or in cases in 
 which the nuclei surround the cell the necrotic changes begin in 
 the center. Finally, a tubercle undergoes almost complete necrosis 
 and is transformed into a cheesy mass, the surrounding connective 
 tissue perhaps still showing proliferative changes which may 
 
 >V :. - 
 
 '-'" '...- 
 
 &£#* 
 
 •*£ 
 
 
 &'*>&$£ 
 
 Fig. 93.— Large tubercle of the lung, showing cheesy necrosis in the center ; the epithe- 
 lioid and giant-cells around the cheesy center are more or less degenerated. 
 
 eventually cause encapsulation of the tubercle. Calcification may 
 ensue in the cheesy mass and thus lead to permanent destruction 
 of the nodule. 
 
 In the growth of tuberculosis the normal tissue-elements of the 
 part affected are pushed aside, or may be softened and destroyed by 
 the disease-processes. The connective-tissue fibers of the part, 
 however, are longest retained, and remain as a reticulum or tuber- 
 cle-stroma long after the other elements of the tissue have dis- 
 appeared or been pushed aside. 
 
 Tubercles tend to coalesce, forming larger tubercular masses, 
 and sometimes distinct tuberculous tumors are so produced. In 
 the lower animals, particularly in cattle, such tubercular tumors 
 of the serous surfaces are not uncommon. They may simply 
 stud the membranes, or they may hang as polypoid masses; the 
 term "pearl disease" is applied to these cases. Somewhat similar 
 tubercular tumors are met with in human tuberculosis, especially 
 in the brain. As a rule, however, increasing areas of tuberculous 
 disease of organs are only partly composed of tubercles, the bulk 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 
 
 231 
 
 of the diseased area presenting evidences of ordinary or peculiar 
 inflammatory changes to which the presence of the tubercles has 
 stimulated the tissues. 
 
 The tubercle-bacilli in the earliest stages of the tubercle may 
 be seen lying in the tissue and perhaps between the epithelioid 
 cells first formed. With the evolution of the disease they are 
 more and more abundant, are largely within the cells, and the 
 giant-cells in particular may contain large numbers (Fig. 94). As 
 
 Fig. 94.— Giant-cell containing bacilli (from a photograph made by Dr. Wm. M. Gray). 
 
 the necrotic changes increase the bacilli become less conspicuous, 
 and eventually none may be visible. The existence of the bacilli 
 or their spores, however, cannot be doubted, since injection of 
 portions of such tubercles produces the disease in guinea-pigs. 
 
 After the establishment of the local lesion of tuberculosis in 
 any part of the body two opposing tendencies struggle for suprem- 
 acy, the tendency of the tuberculous disease to spread and the 
 tendency of the normal tissues to encapsulate or limit the spread 
 of the invading disease. In most cases the former succeeds and 
 the secondary tubercles first appear in adjacent parts, the transpor- 
 tation of the bacilli from the primary to the secondary focus being 
 accomplished either by the flow of the lymph or juices of the body, 
 or by the phagocytic activity of leukocytes. The latter take from 
 the edges of the tubercle some of the bacilli and transport them 
 either by their own ameboid activities or in the lymph-stream to 
 neighboring parts, where they themselves fall victims to the organ- 
 isms they have appropriated, and thus deposit the germs of new 
 foci of disease. The dissemination of tubercles to more distant 
 parts may occur in various ways. In the case of tuberculosis of 
 the mucous membranes bacilli may be cast off from the surface 
 and spread to other parts of the mucous tracts with the contents 
 of these, as in the case of tuberculosis of the gastro-intestinal 
 tract. In the case of pulmonary lesions the ulcerative processes, 
 
232 TEXT-BOOK OF PATHOLOGY. 
 
 or attacks of coughing, may loosen infected particles from lesions 
 of the bronchi, and the deep inspiratory efforts following the 
 cough, or the ordinary inspirations, may carry the bacilli into 
 the finer bronchioles, where new foci arise. If the tubercular 
 lesion involves the walls of the lymphatics, particularly the larger 
 lymph-channels, like the cervical or thoracic ducts, bacilli may 
 gain access to the lymph-stream and thus be transported to the 
 venous circulation, and then through the heart to the lungs or 
 perhaps to other organs. When the tuberculous lesion invades the 
 wall of a vein the dissemination of the bacilli is even more rapid 
 and widespread, as the organisms find their way to the heart by a 
 more direct route. In rare instances an artery is invaded and the 
 organisms are scattered through the terminal distribution of this. 
 Upon surfaces the disease may spread by direct continuity or by 
 the movements of the body. Thus lesions of the peritoneum may 
 become almost universal in consequence of the peristaltic move- 
 ments, though more frequently the extension occurs along the lym- 
 phatic channels. 
 
 The condition which results from general infection and forma- 
 tion of tubercles in various situations is known as miliary tubercu- 
 losis. In these cases the progress is usually rapid and a fatal 
 termination is not long delayed. The tubercles therefore remain 
 small, and at autopsy are still typically gray miliary tubercles. 
 Sometimes, however, miliary tuberculosis may assume a more 
 chronic form, perhaps in consequence of the gradual admission of 
 bacilli to the circulation and the formation of small crops of 
 tubercles during a considerable period of time. 
 
 Miliary tuberculosis may be local or general. In the former 
 case the bacilli are admitted to the vascular distribution of a re- 
 stricted area only ; in the latter widespread dissemination through 
 the blood occurs, and practically all parts of the body may be in- 
 volved. Localized miliary tuberculosis is most frequent in the 
 lungs. 
 
 Seats of Tuberculosis. — Among the frequent situations 
 in which tuberculosis makes its appearance are the lungs, the 
 lymphatic glands, the bones and joints, the mucous membranes, 
 particularly those of the larynx and intestines, the serous mem- 
 branes, the prostate, testicle, ovaries, Fallopian tubes, kidneys, 
 uterus, suprarenal capsules, brain, liver, spleen. In some of these 
 situations the lesions arc practically always secondary, as, for ex- 
 ample, in the liver and spleen. In others they are most frequently 
 primary, as in the lungs. The occurrence of primary tuberculosis 
 in the internal organs may be difficult to explain. It is possible, 
 however, for the bacilli to gain access to the lymphatic or blood- 
 circulation without causing a lesion at the point of entrance. Their 
 deposit in some internal organ then occasions the first or primary 
 focus of disease. Thus primary tuberculosis of the mesenteric 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 233 
 
 glands, of the lymphatic glands of the neck, or of the post- 
 bronchial glands, may occur without primary disease of the intes- 
 tines, of the mouth or skin, or of the lungs in the several instances. 
 Similarly primary tuberculosis of the kidney or of the suprarenal 
 capsule may occur without any evidence of the point of entrance 
 of the micro-organisms. In some cases, of course, the primary 
 lesion may be so small and in such a hidden situation that it 
 escapes notice. 
 
 After the discovery of the tubercle-bacillus a number of diseases 
 not previously recognized as tuberculous became identified as 
 forms of this disease. Among these is Lupus Vulgaris of the skin. 
 The histologic examination shows numerous tuberculous granula- 
 tions, sometimes arranged in striate fashion along the small blood- 
 vessels of the skin and containing epithelioid and lymphoid cells 
 and giant-cells. The presence of the bacilli and the proved infec- 
 tiousness of the tissue, with the histology, render the nature of this 
 disease certain. The warty formations frequently acquired by 
 anatomists at points of injury have likewise been shown to be in 
 many cases due to tuberculous infection. Scrofula, which was 
 formerly regarded as a special condition predisposing strongly to 
 tuberculosis, is now regarded as tuberculosis occurring in different 
 forms and situations. The scrofulous glands of the neck consti- 
 tute tuberculous adenitis, the infection in many cases gaining 
 access through the mucous membranes of the mouth and pharynx 
 or through the skin. Scrofulous rhinitis and sinuses have simi- 
 larly been shown to be forms of tuberculous disease. Many cases 
 of joint-disease regarded as scrofulous or otherwise are dependent 
 upon the action of the tubercle-bacillus. 
 
 Latent Tuberculosis. — A tuberculous lesion may become encap- 
 sulated and limited in its extent before it has invaded tissues 
 widely, and may so remain for years without giving rise to mani- 
 fest clinical symptoms. Subsequently, however, the encapsulating 
 membrane may be penetrated and widespread infection, local or 
 general, may occur. Such latent tuberculosis is particularly fre- 
 quent in the post-bronchial glands. These glands are often found 
 enlarged at autopsies in which no tuberculous disease of other 
 organs is found. Injections of emulsions of such glands in a nota- 
 ble proportion of cases produce tuberculosis in guinea-pigs, and 
 thus it has been determined that the glands in question are fre- 
 quently the seat of latent tuberculous disease. The existence of 
 such lesions explains the cases of sudden generalized miliary 
 tuberculosis, in which no primary focus of the disease was recog- 
 nized during life. 
 
 Pathologic Physiology. — The effect of tuberculosis upon 
 the general health varies greatly. Undoubtedly the bacillus is 
 capable of producing toxins that have an effect upon the general 
 organism ; the nature of these, however, still remains undeter- 
 
234 TEXT-BOOK OF PATHOLOGY. 
 
 mined. The tuberculin of Koch, a glycerin-extract from cultures 
 of the tubercle-bacillus, produces fever with general symptoms 
 such as are frequently associated with pyrexia and local reactive 
 changes in existing tuberculous lesions. Among the latter redness 
 or increased vascularization of the tubercles, and softening or ne- 
 crosis of the cells surrounding the bacilli, are most important. The 
 last-named change deters the growth and multiplication of the 
 bacilli themselves, but at the same times makes their escape from 
 the focus of disease more easy and thus exposes the individual to 
 the liability of general infection. The active substance contained 
 in tuberculin is probably an albuminous body. It does not act 
 upon the tubercle-bacillus directly and is not an antitoxin. In 
 addition to this the tubercle-bacillus in its dead state contains 
 some body or bodies capable of influencing the organism, as was 
 shown by the experiments of Prudden and Hodenpyl, who were 
 able to produce nodular lesions and small local abscesses by in- 
 jecting dead bacilli into the circulation of animals. These lesions, 
 of course, are not strictly tuberculous, though they possess some 
 elements of the natural tubercle. It is altogether probable, how- 
 ever, that in addition to the tuberculin of Koch and the chemo- 
 tactic substances contained in the body of the tubercle-bacilli, 
 there are other poisonous substances produced by the growth and 
 multiplication of the bacilli in the tissues, that lead to a general 
 deterioration in the health of victims of this disease. 
 
 Tuberculosis is primarily a local process, but influences the 
 general organism by its direct effect upon the organic functions of 
 the parts in which it is located by the development of these as yet 
 unknown toxic substances, and later by the widespread infection 
 of the organism. The mechanism of defence against tuberculosis 
 is only partly known. In the case of local lesions of the lungs or 
 other parts the reaction of the tissues probably resulting from the 
 activity of chemotactic substances in the body of the bacilli them- 
 selves, or of similar substances produced by the cellular necrosis, 
 leads to the formation of an embankment of cellular or fibrous 
 tissue that serves to hold the disease in check. Subsequently the 
 disease may be wholly eradicated by degenerative changes termi- 
 nating in calcification. That such favorable results are not 
 uncommon is proved by the frequent occurrence at autopsies of 
 small sclerotic or calcareous areas in the lungs. Tuberculosis is 
 frequently cured in these early stages, but after it has reached the 
 degree of intensity or the widespread character that makes it recog- 
 nizable by <»ur present methods of physical examination, the reactive 
 processes are usually no longer able to cope with its progress. 
 
 PSEUDOTUBERCULOSIS. 
 
 This name has been applied to conditions occasionally met 
 with in which nodular lesions resembling tubercles, but containing 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 235 
 
 micro-organisms of different kinds, have been found in the liver, 
 kidneys, and other organs. One of the best studied of the organ- 
 isms in question is a bacillus, motile and easily stained by methods 
 which do not color the tubercle-bacillus. Pure cultures inoculated 
 in other animals give rise to the same lesions. Pseudotuberculosis 
 is probably not a specific form of disease ; a variety of conditions 
 may present this appearance. 
 
 FOWL=TUBERCULOSIS. 
 
 Tuberculosis of various forms of fowl or birds (Avian Tuber- 
 culosis, Tuberculosis Gallinarum) is a disease similar to, but not 
 identical with, human tuberculosis. The spontaneous disease of 
 birds occurs most frequently in the liver. There are nodules 
 composed of round cells, but showing no tendency to coagulation- 
 necrosis or to the formation of giant-cells. The bacillus, which is 
 found in abundance, resembles the human tubercle-bacillus and 
 may be stained by the same methods, but differs from this organ- 
 ism in the fact that it grows upon ordinary media and not upon 
 potato, and is more resistant to heat, at least as far as its retention 
 of virulence is concerned. When inoculated in rabbits abscesses 
 result at the point of inoculation, and later lesions of the lungs 
 develop. The lungs are never primarily involved in the spon- 
 taneous disease of birds. Many believe this disease a variety of 
 tuberculosis modified by its occurrence in birds. 
 
 LEPROSY. 
 
 Definition. — Leprosy, Lepra, or Elephantiasis Grsecorum, is 
 an infectious and mildly contagious disease, caused by a specific 
 bacillus, the Bacillus lepras, discovered by Hansen. 
 
 Etiology. — The essential cause of leprosy is a bacillus which 
 closely resembles the tubercle-bacillus, though it is less frequently 
 curved and is somewhat more easily stained. Further, it differs 
 in its grouping in the tissues and in its failure to grow satisfactorily 
 on artificial media. The organism is usually found in large num- 
 bers in the leprous lesion, and is readily stained by any of the 
 methods applicable for tubercle-bacilli or by Gram's method. It 
 frequently shows light areas like those of the tubercle-bacillus, 
 and these have been regarded as spores ; more probably they are 
 produced by fragmentations, as in the case of tubercle-bacillus. 
 Attempts at culture have thus far been unsuccessful, though Neis- 
 ser claims to have obtained cultures on blood-serum containing 
 gelatin and on coagulated egg-albumin. Others have claimed 
 definite results with similar media, but cultivation at the present 
 time is not ordinarily possible. 
 
 The specific nature of the bacillus has not been demonstrated, 
 as it is almost, if not entirely, impossible to produce the disease 
 
236 TEXT-BOOK OF PATHOLOGY. 
 
 in animals. Some successful experiments have been made by 
 inoculating portions of leprous tissue in the anterior chamber of 
 the eye or other parts of animals; but definite generalized leprosy 
 has not been thus far produced. In one case the disease has been 
 given to a condemned criminal by direct inoculation. 
 
 Besides the specific bacillus other conditions are important in 
 the etiology. Thus the disease flourishes in certain localities 
 extensively and little in other places. It is uncommon in the 
 United States, but some of the Gulf States, particularly Louisiana, 
 have considerable colonies, and in the Northwest and on the Pacific 
 Coast it is met with among the Norwegian and Chinese immi- 
 grants. In Mexico, South America, Norway and Sweden, India, 
 and other Asian countries it is common, and the Sandwich Islands 
 are particularly affected. During the Middle Ages it flourished in 
 Europe as a universal scourge, unsanitary conditions probably 
 acting as the predisposing cause. Certain articles of diet are 
 believed to occasion it, particularly fish ; this view, however, lacks 
 proof. 
 
 The disease must be regarded as contagious, though less so 
 than tuberculosis. Intimate association for a long time seems to 
 be necessary for its transference. It is probably transmitted from 
 parent to offspring in rare instances. 
 
 Pathologic Anatomy. — Leprosy presents itself in two 
 forms, the tubercular and the anesthetic form. In the former there 
 are developed in the skin of the face, the extensor surfaces of the 
 elbows and knees, about the hands, or less frequently elsewhere, 
 small or large nodular elevations. These at first are reddish in 
 color, with apparent inflammatory reaction. Later they lose their 
 redness and remain as indolent lesions that grow very slowly or 
 remain stationary. They may break down, forming ulcerations 
 which do not readily heal, or they may be gradually converted 
 into fibrous cicatricial tissue, causing unsightly deformities of the 
 skin. The appearance of the patient's face is highly characteristic, 
 and is known as leontiasis leprosa (Fig. 95). The mucous mem- 
 branes and some of the internal organs may be involved. The 
 anesthetic form is usually marked by less conspicuous lesions, but 
 subjective symptoms, such as hyperesthesia and neuralgic pains, 
 and later ulcerations partly trophic in nature, may make it a more 
 serious variety. In the skin there are found whitish or brownish 
 spots, slightly if at all elevated or altered in consistency. Later, 
 ulcerations may appear. Very commonly the anesthetic and 
 tubercular varieties are coexistent. 
 
 The nodules occurring in the liver, spleen, and testes in this 
 disease are admitted to be similar to the nodules of the skin ; 
 those found in the lungs, kidneys, and intestines, as well as those 
 of the serous surfaces, are believed by many to be tuberculous and 
 the result of secondary infection. These two diseases are certainly 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 237 
 
 frequently associated ; probably 40 per cent, of the cases of lepra 
 become tuberculous. 
 
 Other forms of secondary infection occur, thus injuries of 
 superficial lesions may allow pyogenic infection, and extensive 
 ulcerations and gangrenous necrosis may ensue. The terms lepra 
 
 Fig. 95.— Nodular leprosy (Goldschmidt). 
 
 mutilans and lepra gangrenosa are applied to such ; and various 
 micrococci and saprophytic organisms have been discovered in 
 such cases. 
 
 Structure of the Leprous Lesions. — The nodule or leproma is a 
 somewhat indurated growth resembling the tubercle, but differing 
 from it in its greater vascularity and in the absence of the ten- 
 dency to cheesy necrosis. Microscopically it is composed very 
 largely of proliferated connective-tissue cells of different forms, 
 and leukocytes. New blood-vessels are discovered in more or less 
 abundance, and a tendency to complete organization with the 
 formation of fibrous tissue may be seen in the character of the 
 cells and the presence of fibrous intercellular material. The 
 
238 TEXT-BOOK OF PATHOLOGY. 
 
 bacilli occur within the cells and possibly also between them. 
 They are always found in groups and usually in large numbers. 
 They multiply within the cells, the protoplasm of the latter at the 
 same time undergoing a process of swelling and degeneration. 
 This at first spares the nucleus, but finally the nucleus itself is 
 broken down and the cell is thus converted into a sac containing 
 degenerated protoplasm and abundant bacilli (Fig. 96). The 
 term lepra-cell has been given to these. 
 Giant-cells may be formed, though they 
 are not frequent and are rarely typical. 
 Secondary infections or injuries may lead 
 to suppurative or other forms of soften- 
 ing, and the final termination either with 
 or without previous softening may be 
 cicatrization. The lesions of the internal 
 organs met with in some leprous cases, 
 notably those of the lungs, intestine, kid- 
 ney, and serous surfaces, are avascular, 
 lepra^eiUKargwid^chmOTi)* show more tendency to necrosis, and con- 
 tain more giant-cells ; in some cases inoc- 
 ulation has showed that the lesions contained the tubercle-bacilli. 
 Whether they are strictly tubercles, or whether they are lepro- 
 mata with secondary infection with tubercle-bacilli, cannot be 
 decided. They are certainly not pure leprosy, and more probably 
 are purely tuberculous. 
 
 The anesthetic areas and pigmented or light-colored spots of 
 the anesthetic form present somewhat the same histologic features 
 as the leprous nodule, though in a diffuse form. Formerly these 
 lesions were considered entirely the result of trophic changes. 
 In these cases the more conspicuous lesion is that of the nerves. 
 These may show nodular thickening of the perineurium with inflam- 
 matory and degenerative changes of the nerve itself. The bacilli 
 are present in these lesions. Changes in the spinal cord have 
 occasionally been discovered. 
 
 Pathologic Physiology. — Infection with the lepra-bacillus 
 leads to local rather than general disturbances. The toxins of the 
 disease, if such there be, are not of great virulence, and constitu- 
 tional symptoms are therefore wanting as a rule. In the later 
 stages fever and other systemic disorders may be occasioned by 
 secondary infections. A supposed antitoxic substance has been 
 prepared and has been largely used. It is impossible to claim or 
 disclaim the antitoxic nature of this, as no toxins have as yet been 
 isolated or obtained in any form, and the supposed antitoxic sub- 
 stances cannot therefore be tested. 
 
 In the anesthetic form it was formerly customary to regard the 
 pigment or light-colored spots as a result of trophic disturbance, 
 and more destructive lesions, such as ulceration and gangrene, 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 239 
 
 received a similar explanation. Recent investigations, however, 
 seem to show that in these cases there is usually from the first a 
 leprous change in the tissues, and that secondary infections fre- 
 quently play a part, though trophic disturbances must still be 
 admitted to a certain extent. 
 
 GLANDERS. 
 
 Definition. — Glanders is an infectious and contagious disease 
 of horses and asses, sometimes communicated to other animals and 
 to man, and caused by a specific bacillus. 
 
 etiology. — The Bacillus mallei was discovered by Lb'tHer and 
 Schiitz. It is an organism resembling the tubercle-bacillus, 
 though somewhat shorter and thicker. It occurs in the lesions of 
 the disease singly or in clumps, and has been found in the blood. 
 The bacillus is non-motile and does not possess flagella. Stained 
 specimens show parts that do not receive the stain. These have 
 been regarded as spores, but are more generally thought to be areas 
 of degeneration. Ordinary solutions of anilin dyes, and especially 
 alkaline solutions, stain the organism very well. The demonstra- 
 tion of the bacillus in the tissues requires prolonged staining and 
 rapid decolorization. 
 
 Cultivation. — Cultures are best obtained from softened nodules 
 of guinea-pigs inoculated with infected pus, or from the testicles 
 after injection of infective matter into the peritoneal cavity. The 
 organism grows quite readily upon ordinary media, but the most 
 characteristic culture is seen upon boiled potato. The colony 
 first appears as a honey-like layer, which becomes brownish in 
 color. The potato itself becomes greenish-brown beneath and 
 around the colony. The cultivation is most successful between 
 30° and 40° C. (86° and 104° F.). 
 
 Drying and elevated temperatures rapidly destroy the organ- 
 ism, and antiseptics kill it quite readily. The bacillus is a pure 
 parasite, multiplying only in the body of infected animals or 
 man. 
 
 Pathogenicity. — The specific character of the bacillus is unques- 
 tionable. Inoculation of guinea-pigs, rabbits, field-mice, or other 
 animals with infected pus or with pure cultures leads to nodular 
 lesions at the point of introduction, with subsequent softening and 
 ulceration. After death nodules are found in the liver, spleen, 
 kidneys, or other organs, and these contain the bacilli. In horses 
 and asses characteristic lesions of the mucous membranes have 
 been produced experimentally ; while in man accidental infection 
 of hostlers or others coming in contact with diseased animals, and 
 of bacteriologists working with cultures, has been repeatedly 
 observed. In one case in my own knowledge a man was infected 
 in a stable in which a glandered horse was kept, and the bacteri- 
 
240 TEXT-BOOK OF PATHOLOGY. 
 
 ologist who isolated the organisms from the patient accidentally 
 infected himself with the cultures. 
 
 Pathologic Anatomy. — In horses glanders presents charac- 
 teristic lesions of the mucosa of the nose. At first there are found 
 slightly elevated nodules, which have a marked tendency to soften, 
 forming irregular ulcerations that become confluent. The floor 
 and edges of the ulcers are yellowish and necrotic in appearance, 
 and discharge more or less purulent matter. The lymphatic glands 
 of the neck and elsewhere enlarge and may suppurate. In the 
 skin the lesions are much the same, but more sluggish. Nodules 
 are not rarely met with in the lungs. These are grayish or pink- 
 ish in color, and tend to rapid necrosis. More rarely nodules or 
 ulcers arc found in the mucosa of the gastro-intestinal tract. 
 
 In man similar nodules and ulcerations may be found in the 
 nose, larynx, or trachea ; and external lesions resembling small or 
 large carbuncles are found. 
 
 Histologically the lesions of glanders consist of aggregations 
 of round cells of lymphoid or polymorphonuclear type. There is 
 a marked tendency to suppurative or necrotic softening, and some- 
 times hemorrhagic infiltration may be pronounced. 
 
 Pathologic Physiology. — A toxic substance called mallein 
 (a bacterial protein) has been obtained from cultures of the bacilli. 
 Injected into infected animals this acts somewhat as does tubercu- 
 lin in tuberculosis. A special toxin is probably active in the pro- 
 duction of the general symptoms of the disease. By repeated 
 dosage with mallein it is claimed that immunity may be conferred. 
 
 MALIGNANT EDEMA. 
 
 Definition. — Malignant edema is a form of intense infective 
 inflammation and necrosis observed in certain animals and in man, 
 and is due to a specific micro-organism. The condition has fre- 
 quently been described by clinicians as gaseous gangrene, traumatic 
 gangrene, gangrene foudroyante, etc. Infectious emphysema (q. v.) 
 has doubtless often been mistaken for this disease. 
 
 Etiology. — The micro-organism of malignant edema was de- 
 scribed by Pasteur and named theVibricm septigue. Koch showed 
 that it docs not flourish in the blood, and that the name given by 
 Pasteur is therefore not appropriate. He named it therefore Ba- 
 cillus cedematis maligni. This organism is widely distributed. It 
 is very commonly present in the soil, particularly in garden-earth, 
 and is often found in dust and in the intestinal contents of animals. 
 Introduced into the subcutaneous tissue of animals it multiplies 
 greatly and sets up a violent local process. The bacilli are readily 
 obtained from the diseased area, and may be stained with the ordi- 
 nary anilin dyes, but not by Gram's method. The bacillus resem- 
 bles the anthrax-bacillus very closely, but is somewhat more 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 
 
 241 
 
 slender. It is prone to occur in long chains, the organisms being 
 apparently in contact end to end. Movement of the organisms is 
 frequently observed, and flagella are found by appropriate stains. 
 In the spore-formation the center of the organism swells and the 
 spore is developed within. 
 
 Cultivation. — The cultivation of this organism is generally easy. 
 White mice or other susceptible animals are first infected by intro- 
 ducing powdered garden-earth into a subcutaneous sac. Direct 
 infection of the open wound will not succeed, as the organism is 
 strictly anaerobic. 
 
 From the pus in the subcutaneous tissues growths may be ob- 
 tained upon the surface of gelatin in an atmosphere of hydrogen, 
 or in puncture-cultures in gelatin from which oxygen has been 
 excluded. On the surface of the gelatin are formed small grayish- 
 white bodies, which increase in size with advancing age. Portions 
 removed from these and stained show masses of bacilli in the form 
 of long filaments. In the gelatin-tube there are formed whitish 
 spherical colonies of a somewhat cloudy appear- 
 ance. These consist of a turbid liquid, the 
 gelatin undergoing liquefaction. There is also 
 some gas-production, the gas formed having a 
 peculiar and unpleasant odor. This is marked 
 when the medium contains glucose (Fig. 97). 
 
 Distribution. — The bacillus of malignant 
 edema occurs only in the subcutaneous tissues 
 near the point of inoculation, in the muscles, 
 and in the peritoneal cavity at the time of death. 
 It does not invade the blood, as the amount of 
 oxygen there present prevents its growth, and 
 it flourishes in the subcutaneous tissue because 
 this is least accessible to oxygen. In bodies 
 dead some time the organism may spread to the 
 blood and the organs of the body. The distri- 
 bution of the organisms outside the body has 
 been referred to. 
 
 Pathogenicity. — The bacillus of malignant 
 edema is undoubtedly the cause of the disease 
 in question, as has been proved by inoculations 
 upon mice, guinea-pigs, and other animals. 
 Cats and dogs are less susceptible than other 
 animals ; cattle seem to be almost wholly im- 
 mune. 
 
 Pathologic Anatomy. — The lesions of 
 malignant edema consist of various forms of 
 rapid suppuration and necrotic inflammation 
 of the subcutaneous tissues. There may rapidly form emphy- 
 sematous and gangrenous alterations of the subcutaneous tissues, 
 
 Fig. 97. —Bacillus 
 of malignant edema 
 growing in glucose- 
 gelatin (Frankel and 
 Pfeiffer). 
 
242 TEXT-BOOK OF PATHOLOGY. 
 
 with sometimes pus-formation, at other times extensive hemor- 
 rhagic infiltration. 
 
 Pathologic Physiology. — Toxins are doubtless formed, but 
 these have not as yet received special attention. A few cases of 
 malignant edema have been reported in man ; some following in- 
 jection of musk in the course of typhoid fever ; some occurring in 
 the puerperium, and some apparently without external injury. 
 Infection in the latter probably occurred from the mucous sur- 
 faces. In all cases the general vitality of the patient was reduced 
 by some previous disease. 
 
 ANTHRAX. 
 
 Definition. — Anthrax is a specific infection due to a charac- 
 teristic bacillus. It occurs most frequently in cows and sheep ; it 
 may affect other animals and man. Dogs, cats, birds, and cold- 
 blooded animals are quite immune. In animals it is called splenic 
 fever ; in man, malignant pustule and wool-sorters' disease. 
 
 Etiology. — The Bacillus anthracis is a non-motile rod-shaped 
 organism that has a decided tendency to form long chains. The 
 individual bacillus is from 5 to 20 fi in length and from 1 to 1.25 p. 
 in thickness. The chains appear as threads, with often a little 
 thickening at the ends of the individual bacilli showing the points 
 of contact. The ends are squared or often slightly concave. In 
 
 
 Fig. 98.— Bacillus anthracis, stained to show the spores (Frankel and Pfeiffer). 
 
 artificial cultures in the presence of oxygen spores are formed 
 within the bacilli. These are elliptical or oval in shape, and do 
 not alter the configuration of the bacillus (Fig. 98). 
 
 The organism is easily stained with the simple anilin dyes, and 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 243 
 
 may be demonstrated in the blood or the tissues by Gram's or 
 Weigert's stains. There are no flagella. 
 
 Cultivation. — The anthrax-bacillus may be obtained in pure 
 culture from the diseased organs upon various media. The cul- 
 ture in gelatin is most characteristic. Upon plates there are 
 formed whitish colonies, which under low powers of the micro- 
 scope show a tufted, irregular character at the edges and upon the 
 surface, suggesting bunches of twisted wool-fibers. The gelatin is 
 slightly liquefied. The tufts may be removed by pressing a cover- 
 glass against the surface of the colony, and when stained are found 
 to consist of curved parallel chains of bacilli. In puncture- 
 cultures filaments project at right angles to the puncture toward 
 the sides of the test-tube, and the growth at the surface, where 
 oxygen is abundant, is luxuriant, while that in the depth is com- 
 paratively sparse. 
 
 Pathogenicity. — The infectiveness of the bacillus is undoubted. 
 A small portion introduced into a susceptible animal gives rise to 
 marked symptoms in twelve or twenty-four hours, and death soon 
 follows. The bacilli may be demonstrated in the blood and in 
 various organs in great abundance. When the bacillus is killed 
 and the spores are introduced into the body similar results follow. 
 
 Distribution. — The anthrax-bacillus occurs in all of the local 
 lesions, and from these extends into the blood and into the organs, 
 particularly the spleen, liver, kidney, and lungs, where they are 
 found in the capillaries in immense numbers. The structure of 
 these organs is, as a rule, little affected, probably because death 
 occurs before changes may take place. The organisms are dis- 
 charged from the body in the stools, urine, and other discharges, 
 and thus conveyed to other animals. At one time it was sup- 
 posed that they are scattered about by earth-worms obtaining 
 them from cadavers. This is scarcely probable. Multiplication 
 of the organisms outside the body does not occur to any extent, 
 but the organisms, and particularly the spores, may live a long 
 time, and may be conveyed to great distances in infected mate- 
 rials, particularly wool, hides, bristles, and the like. 
 
 Mode of Infection. — In animals infection most frequently occurs 
 through the gastro-intestinal tract, the bacilli being swallowed 
 with fodder that has been contaminated. The organisms may, 
 however, gain entrance through the lungs or through external 
 abrasions. The latter form of infection is most common in 
 man ; though gastro-intestinal and pulmonary infection sometimes 
 occurs. 
 
 Pathologic Anatomy. — The lesions produced by anthrax 
 are more or less local, but occasion general septicemia. In man, 
 after infection of the skin through abrasions in persons handling 
 the hides or wool, or other materials from diseased animals, a 
 swelling of greater or less size develops. This is intensely in- 
 
244 TEXT-BOOK OF PATHOLOGY. 
 
 flammatory, often covered and surrounded by slight bullous vesi- 
 cles, and attended with considerable edema. Erosion of the sur- 
 face may take place and sanious liquid may be discharged, with 
 the formation of crusts. Histologically the process consists of 
 rapid infiltration of the corium and papillary bodies with leuko- 
 cytes. The bacilli are found in abundance between the cells, and 
 hemorrhagic infiltration and sero-sanguinolent edema are observed. 
 Necrosis subsequently occurs, though not to a considerable extent. 
 When infection takes place through the gastro-intestinal tract, as 
 is sometimes observed in man and very commonly in animals, 
 lesions somewhat like the above are formed in the mucosa 
 and submncosa of the small intestine, less frequently of other 
 parts. At first these lesions appear as hemorrhagic extravasa- 
 tions, then swelling follows, and finally the surface ulcerates, leav- 
 ing irregular excavations with blood-stained bases and edges. 
 Profuse diarrhea with bloody discharges may occur. Infection 
 through the lungs occurs in men engaged in handling infected 
 ■wool (wool-sorters' disease), and in persons working in paper-fac- 
 tories, where infected rags carry the germs. In these instances 
 the bacilli lodge in the alveoli of the lungs, causing rapid cellular 
 exudation with considerable edema and hemorrhagic infiltration. 
 The process is lobular in character, but large areas of the lungs 
 may be simultaneously involved. Serosanguinolent pleurisy, swell- 
 ing of the lymphatic glands of the mediastinum, and hemorrhagic 
 extravasations of the mediastinum are not unusual. 
 
 Pathologic Physiology. — The presence of the anthrax- 
 bacillus leads to the formation of toxic materials in the blood, and 
 a poisonous albumose has been obtained from cultures. The 
 general symptoms, however, are probably in large measure the 
 result of dissemination of the bacilli themselves and their local 
 effects. 
 
 It has been found possible by cultivation at high temperatures 
 and by introducing the organisms into insusceptible animals, and 
 also by adding chemical agents to cultures, to alter the pathogenic- 
 ity of the bacillus to such an extent as to make it harmless, even 
 to white mice. By introduction of such cultures and subsequent 
 successive inoculation with cultures of increasing virulence pro- 
 tection has been afforded . Antitoxic substances have been obtained 
 from the blood of protected animals, but the method of successive 
 vaccinations rather than the use of antitoxic serum is at present 
 relied upon to combat the disease. 
 
 INFECTIOUS EMPHYSEMA. 
 
 Definition. — This term is provisionally applied to a form 
 of infection that has been described under various names, such as 
 gaseous gangrene, gas-phlegmon, emphysematous necrosis, and the 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 245 
 
 like. Undoubtedly it has been mistaken for malignant edema in 
 certain cases. The disease is caused by the Bacillus aerogenes 
 capsulatus of Welch and Nuttall. 
 
 Ktiology. — The bacillus in question is a non-motile organism 
 of variable size, 3 to 6 p. in length and about the thickness of an 
 anthrax bacillus, with adjacent ends slightly rounded or square 
 cut, and occurring singly, in pairs, clumps, or sometimes in short 
 chains. Very rarely it occurs in long threads. It is easily stained 
 with the ordinary anilin dyes or Gram's stain. A capsule is some- 
 times demonstrable in specimens obtained from the body or 
 from agar-cultures. The bacillus does not form spores. It is 
 probably identical with the Bacillus phlegmones emphysematosse 
 of Frankel. 
 
 Cultivation. — The organism is anaerobic, no growth occurring 
 on the surface of solid media in the presence of oxygen. In 
 media containing fermentable material gas-formation is regularly 
 observed. The colonies in agar are grayish- white or slightly 
 brownish ; those in the depth appearing as ' small spheres or ovals 
 slightly flattened, with knob-like or feathery projections. The 
 cultures in gelatin show slight and slowly developing liquefac- 
 tion. 
 
 Pathogenicity. — By experiments on animals exactly the same 
 lesions are produced as those found in man. 
 
 Pathologic Anatomy. — The lesions of this infection are 
 "widespread. At the point of inoculation there may be found 
 edematous infiltration, with blood-stained fluid, and emphysema 
 due to gas-formation. Eapid necrosis or gangrenous soften- 
 ing of the tissue may occur. The entire surface of the body 
 sometimes becomes emphysematous, and at the autopsy the organs, 
 especially the myocardium, kidneys, liver, and spleen, present a 
 characteristic appearance. They are lighter in color, and on in- 
 spection are found to be filled with minute vacuoles or gas-bub- 
 bles. The blood of the heart and vessels presents a foamy condi- 
 tion, due to the gas-formation. Practically any of the tissues of 
 the body may be affected. Microscopically, the occurrence of gas- 
 vesicles with numerous bacilli in their walls is the most striking 
 feature. 
 
 Regarding the mode of infection, it seems likely that in all 
 cases the organisms enter through some injury or abrasion con- 
 nected with the external world. Some cases have followed trau- 
 matic injuries, others occur in connection with disease marked by 
 ulcerations of the surface of mucous membranes, and at least one 
 instance has been carefully studied in which the disease occurred 
 during the puerperium, probably due to uterine infection. It is 
 not improbable that many of the cases of supposed air-embolism 
 from douching of the uterus after labor are in reality cases of 
 this form of infection. 
 
246 TEXT-BOOK OF PATHOLOGY. 
 
 TETANUS. 
 
 Definition. — Tetanus is an acute infectious disease due to a 
 specific bacillus. The bacillus of tetanus was discovered by Xico- 
 laier and isolated by Kitasato. 
 
 Etiology. — The bacilli occur in the form of cylindrical rods, 
 which are frequently swollen at one end, due to the presence of a 
 rounded spore (Fig. 99). They are non-motile, or but slightly 
 
 & 
 I 
 
 c ■■>.■■ -> 
 
 / 
 
 ? v v 
 
 v * 
 
 0. 
 
 r 
 
 \ 
 
 / ^ 
 
 Fig. 99— Bacillus tetani ; X 1000 (Frankel and Pfeiffer). 
 
 motile, although they may have flagella. They usually occur 
 singly, though occasionally a few may be seen end to end. They 
 occur in the local lesions from which traumatic tetanus takes its 
 origin, and may sometimes be readily demonstrated by spreading 
 some of the pus or exudate upon a cover-glass and staining with 
 the ordinary anilin stains. They also stain by Gram's method. 
 The bacillus does not diffuse itself through the body, but in a few 
 cases it has been found in the central nervous system. The organ- 
 ism is readily destroyed by heat, but its spores are quite resistant. 
 
 Cultivation of the tetanus-bacillus is difficult. It is obtained 
 from garden-earth or the pus of infected wounds by submitting 
 the material to sufficient heat to destroy other organisms, even the 
 bacillus of tetanus itself, leaving the spores uninjured. With this 
 material animals are inoculated, and from the products of the local 
 lesions or directly from the original material cultures are made in 
 gelatin. 
 
 The organism is strictly anaerobic. The typical culture is 
 obtained in the depth of gelatin. Deep beneath the surface there 
 are formed along the line of puncture pointed processes stand- 
 ing out at right angles from the puncture. After a week lique- 
 faction of the gelatin occurs, and an accumulation containing 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 247 
 
 grayish-white turbid liquid is formed. When the growth is formed 
 on the surface of gelatin in an atmosphere of hydrogen a similar 
 radiating structure is found in the colonies, the centers of which 
 are rather dense. Liquefaction of the gelatin subsequently takes 
 place. Considerable gas with a pungent odor is produced in the 
 growth of this bacillus. 
 
 Distribution. — The tetanus-bacillus is found very frequently in 
 garden-earth, in the intestinal discharges of animals, and upon 
 various articles about stables. Infection occurs in human beings 
 or animals through punctures made by nails, splinters, and the like. 
 
 Pathogenicity. — The bacillus placed upon an open wound may 
 not give rise to the disease, from the fact that the presence 
 of oxygen prevents its growth. Subcutaneous inoculation, how- 
 ever, causes rapid destruction of animals with typical symptoms. 
 The period of incubation may be only a few hours, or one or two 
 days, or it may be several weeks. The association of certain 
 other organisms, such as the pus-producing organisms, seems to 
 favor the development of the disease by preventing phagocytic 
 action of leukocytes, or by consuming oxygen and thus allowing 
 the tetanus-bacillus to flourish. 
 
 Pathologic Anatomy. — No characteristic lesions are found 
 in this disease. Locally a wound or injury through which inocu- 
 lation has taken place may be discovered ; but this is only excep- 
 tionally extensive. Sometimes no local injury can be discovered, 
 and it is supposed that infection at times occurs through the gastro- 
 intestinal tract, or through other mucous membranes. Intense 
 congestion of parts of the nervous system may be found at the 
 autopsy, but this is not characteristic. 
 
 Pathologic Physiology. — Tetanus is essentially a toxemic 
 disease. The bacillus produces, at the point of its growth, poisons 
 of almost inconceivable power. Two distinct substances have 
 been isolated, tetanin and tetanotoxin. These occur in the blood, 
 urine, and probably other fluids of the body. The bacilli are 
 not found in these fluids. When the toxin of tetanus is intro- 
 duced into animals in gradually increasing quantity immunity is 
 developed and the serum is found to have antitoxic power. The 
 antitoxin may be precipitated from the blood by alcohol, and kept 
 in a dry state. In practical medicine the antitoxin of tetanus has 
 not proved as useful as experiments seemed to promise. This may 
 be due to the fact that the intoxication is generally so extensive 
 by the time the disease is recognized that treatment comes too late. 
 
 ACTINOMYCOSIS. 
 
 Definition. — Actinomycosis is a chronic infectious process 
 characterized by inflammatory reaction of the tissues with a ten- 
 dency to the formation of suppurative foci, and due to the specific 
 action of a micro-organism, the Actinomyces bovis seu hominis. 
 
248 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 Etiology. — Actinomycosis is a disease of cattle, horses, swine, 
 and occasionally of man, being communicated to the latter from 
 animals directly or indirectly. 
 
 The specific cause of the disease, the actinomyces, is an organ- 
 ism which occurs in the tissues in the form of clusters having a 
 radiate structure, and it has therefore been termed the "ray 
 fungus." These clusters may he so small as to be invisible to the 
 naked eye, or they may reach considerable dimensions by their 
 growth and aggregation. The central part of the cluster fre- 
 quently has a granular appearance, suggesting a mass of micro- 
 cocci. Reaching out from this may be seen more or less regu- 
 larly diverging stria? or rays, and the periphery is composed of 
 what appear to be bulbous extremities of the rays (Fig. 100). 
 
 
 
 
 
 
 
 
 
 ■ 
 
 
 
 
 
 *.♦ *'*•.. -.» 
 
 • 1 \l'i 
 
 
 ' 'HJim 
 
 9*mB&L- v 
 
 
 > • i^jHL.^ 
 
 .. « 'j^wByt 
 
 )k^' Wr\ 
 
 - fid BS3 i 
 
 ^telfe- *»■ 
 
 « -•Ha 
 
 JBLWr 
 
 
 reP ••■ 
 
 
 . v ^Bw 
 
 W?T?'* i •;••' 
 
 -.•vP 
 
 ■^ *w ,> • ►*.*'.•• • 
 
 . - -X, ■ w 
 
 
 Fig. 100.— Actinomyces cluster (Karg and Schmorl). 
 
 The exact biologic position of the organism has not yet been 
 determined. By some it is regarded as one of the hyphomycetes ; 
 others place it among the bacilli. 
 
 Pure cultures of the organisms have been obtained from the 
 lesions in animals, but are only developed with difficulty from the 
 human disease. The infectiousness of actinomycosis has been 
 abundantly demonstrated by inoculation-experiments. The cult- 
 ures may be obtained upon ordinary media, such as agar-agar, with 
 or without glycerin, and form firm points, small in size and some- 
 times almost cartilaginous in consistency. The characteristic 
 striate or ray-like structure is not seen in cultures as in the origi- 
 nal clusters, but the organism may present a somewhat branched 
 appearance. 
 
 The manner of infection with the actinomycoses is not com- 
 pletely determined. It is quite likely, however, that the parasite 
 is carried to the tissues by various vegetable substances, particu- 
 larly the spears of the oat-seed and other grains. Sometimes these 
 have been found embedded in the lesions; in other cases splinters 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 249 
 
 of wood have been discovered. It seems possible that the specific 
 agent is conveyed into the tissues by these foreign bodies. 
 
 Pathologic Anatomy. — The pathologic changes induced by 
 the actinorayces consist of round-celled infiltration and prolifera- 
 tive changes in the connective tissue surrounding the parasite, and 
 sometimes secondary softening, necrosis, or suppuration. In cattle 
 the disease affects the lower jaw, less frequently the upper jaw or 
 other bones ; the tissues of the neck, the tongue, and other parts. 
 In man it is met with in the gums and floor of the mouth, in the 
 lungs, intestines, and other internal organs. The naked-eye 
 appearance of the lesions may first be simply that of a hard red 
 papular formation, with more or less induration surrounding it ; 
 later this tends to increase in size and may break down, forming 
 necrotic or suppurative excavations. The process of repair or 
 cicatrization may proceed in some parts to the extent of almost 
 complete repair, while the suppurative or necrotic change advances 
 in other directions, and thus cavities and irregular communicating 
 sinuses are established. The part in which the disease exists may 
 be considerably disfigured and much enlarged. The pus or 
 necrotic material within the lesions has a peculiar granular charac- 
 ter, the grannies or actinomycosis-bodies frequently containing a 
 group of the organisms. Occasionally calcification of the diseased 
 area may take place. When the jaw-bone is affected the disease, 
 as a rule, begins about carious teeth, fistulse communicating with 
 the roots of teeth. 
 
 In the case of disease of the lungs some have observed a pre- 
 liminary catarrhal inflammation of the bronchi. More frequently, 
 however, there are from the first nodular areas of bronchopneu- 
 monia, which tend to undergo changes similar to those already 
 described. The surrounding lung-tissue frequently becomes indu- 
 rated from interstitial pneumonitis. Extension may occur to the 
 pleura, pericardium, and mediastinal tissues. 
 
 In the case of actinomycosis of the intestinal tract there are 
 first elevations of the mucous membrane, the disease involving the 
 mucosa and the submucosa. Subsequent softening of these leads 
 to the formation of ulcerations. Extension to the peritoneum and 
 to the other organs of the abdomen may take place. 
 
 In any case of actinomycosis a penetration of the blood-vessels 
 or lymph-channels may lead to metastases. Thus in actinomyco- 
 sis of the abdominal cavity the liver is frequently involved ; and 
 other parts of the body may be similarly affected. Actinomycotic 
 lesions of the brain (abscesses) are sometimes seen in such in- 
 stances. In other cases of cerebral involvement there may be no 
 evidence of the original focus or point of entrance of the germ. 
 
 Microscopically the characteristic feature of this disease is the 
 parasite itself surrounded by lymphoid cells in considerable num- 
 bers, with some epithelioid cells and occasionally giant-cells. 
 
250 TEXT-BOOK OF PATHOLOGY. 
 
 When the process tends to a favorable termination by cicatrization 
 fibrous-tissue formation proceeds in the usual manner. 
 
 Pathologic Physiology.— The actinomyces is mainly active 
 as a local parasite, the general disturbances of health being com- 
 paratively slight. There is a marked tendency to limitation or 
 retardation of the disease, and sometimes this is effected com- 
 pletelv. 
 
 MYCETOMA. 
 
 Mycetoma, or Madura-foot, is an infectious disease occurring in 
 India and elsewhere, and caused by an organism of an uncertain 
 biologic class. The disease is not infrequent in Madura, Delhi, 
 and other parts of India, and has been observed in Africa, South- 
 ern Europe, and America. 
 
 Etiology and Pathologic Anatomy.— As its name indi- 
 cates, the disease affects the foot, and usually follows injuries, par- 
 ticularly thorn-wounds. In rare cases the hands or other parts 
 are affected. At first there is nodular inflammatory swelling, be- 
 ginning on the plantar surface or dorsum of the foot and spread- 
 ing to the sides. These swellings 
 r*'" s" .Y: : ':'"'V r 'r -~-;.—y_— - arc hard and painless. Later, 
 
 softening occurs and rupture 
 takes place. Thin, watery pus 
 #§£>■• ,~ ( is discharged, and this contains 
 
 grayish or reddish granular bod- 
 ies or black granules resembling 
 particles of gunpowder. In the 
 former case the term pale myce- 
 \$* w - '. toina is applied ; the latter vari- 
 
 ety is called black or melanoid. 
 In the later stages of the disease 
 discharging sinuses may remain, 
 while newer nodules in turn are 
 formed and soften. Finally, the 
 member affected becomes greatly 
 deformed, the portions not in- 
 volved growing thin, while the 
 diseased part increases in size. 
 Death occurs from exhaustion or 
 complications. 
 
 Histologically the nodules re- 
 semble large tubercles, but are 
 fig. loi.-streptothrix Ma"d7r* iiTalec- highly vascular. The bulk of 
 tion of diseased tissue (Vincent). the growth consists of granula- 
 
 tion-tissue cells, those in the cen- 
 ter being small, those near the outer edge often large and contain- 
 ing two or more nuclei. True giant-cells are rare. In the center 
 may be found a branching micro-organism, called Streptothrix Ma- 
 
 psf" >; 
 
 
 
 : }&2 
 
 
 
 
 
 
 l */ . 
 
 
 *© m 
 
 
 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 251 
 
 durce (Vincent). This stains by Gram's method, and sometimes 
 shows somewhat bulbous swelling of the ends of the threads and 
 their branches (Fig. 101). Around the organism may be seen an 
 area of degeneration, having a striate arrangement suggesting that 
 seen in actinomycosis. Extensive degeneration and pus-formation 
 occur in the center of the diseased areas in the later stages ; and 
 hemorrhage may occur from the new blood-vessels. Histologic 
 examination of the granules in the pus shows the micro-organisms 
 in the form of interlacing threads. Bodies resembling spores have 
 occasionally been described. 
 
 The organism has not as yet been definitely classified. It is 
 certainly allied with the actinomyces, but probably not identical. 
 It has been cultivated upon various media, particularly infusions 
 of hay and the like, rendered slightly acid in reaction. It forms 
 small nodular and hard growths, which become rose-red in color 
 when they cling to the sides of the test-tube near the surface of 
 the liquid, or brownish when they sink to the bottom. Upon 
 agar isolated grayish or later rose-red clusters are formed. In- 
 oculation-experiments have thus far met with little success. 
 Local reaction has been so produced, but not a definite disease. 
 
 RELAPSING FEVER. 
 
 Definition. — Eelapsing fever, or typhus recurrens, is an in- 
 fectious and contagious disease, probably caused by a specific organ- 
 ism which is found in the blood. 
 
 Etiology. — The Spirochseta Obermeieri is a spiral organism, 
 in length several times the width of the red corpuscle (16 to 40 //). 
 It is found in the fresh blood, and presents active movements due 
 to flagella (Fig. 102). The organism stains well with ordinary 
 anilin dyes. The relation of this spi- 
 rillum to the disease can hardly be ^n© ..Q m . 
 questioned, as it is invariably present ^ © ^^f £§t 
 and appears in the blood during the /J^N-v 
 paroxysms of fever and disappears in q // ^ </ Q 
 the intervals, thus showing its relation q2P 
 to the symptoms of the disease. The 
 organism has not as yet been cultivated, 
 but by inoculation with blood a num- o - 
 ber of investigators have transferred €&>© Cpt® 
 the disease to monkeys and human © 
 
 beinffS. Fig. 102.— Spirochseta Obermeieri 
 
 J? ... * . . , m! in the blood (von Jaksch). 
 
 Pathologic Anatomy. — The 
 
 spleen becomes greatly enlarged ; it frequently presents a varie- 
 gated appearance on section, due to areas of anemic infarction and 
 necrosis or fatty degeneration alternating with deeply congested 
 portions. 
 
 //« 
 
TEXT-BOOK OF PATHOLOGY. 
 
 Pathologic Physiology.— The peculiar feature of relapsing 
 fever and the one that has given it its name is the recurring par- 
 oxysms of fever. The cause of this periodicity is as yet unknown, 
 though it is likely that the development of the spirochseta is such 
 as to determine the relapses. 
 
 INFLUENZA. 
 
 Definition. — Influenza is an infectious disease occurring in 
 widespread epidemics and caused by a specific bacillus. 
 
 Etiology. — The Bacillus influenza? was discovered by Pfeif- 
 fer and Canon in 1892. The bacilli are extremely small and 
 usually occur singly, though they are occasionally united by the 
 ends, forming short chains. They may be stained with the ordi- 
 nary anilin dyes, especially with carbof-fuchsin, but are decolorized 
 by Gram's method. The ends of the bacillus are somewhat swol- 
 len and usually stain rather more deeply than the shaft. This 
 gives the organism somewhat the appearance of a diplococcus or 
 dumbbell-shaped bacillus. It is not motile. It has been culti- 
 vated upon glycerin-agar and upon blood-serum, forming minute 
 drop-like colonies, seen with difficulty with the naked eye, but 
 clearly with the aid of a lens. The colonies do not coalesce. The 
 appearance of the growth is somewhat like that of condensed 
 moisture on the surface of the culture-medium. 
 
 The bacilli occur abundantly in the sputum of the disease, de- 
 creasing in quantity as the case advances. When purulent expec- 
 toration ceases the bacillus disappears entirely. In fatal cases it 
 has been found in abundance in the tissues of the lung, particu- 
 larly in cases in which complicating pneumonia has existed. It 
 does not occur in other diseases. Animal experimentation has thus 
 far been unsatisfactory, though the organism has proved patho- 
 genic for certain animals. Definite results have not, however, 
 been reached, and the specific character of the organism is inferred 
 rather than demonstrated. 
 
 Pathologic Anatomy. — There are no specific lesions in this 
 disease. The organisms provoke intense catarrhal processes and 
 doubtless at times pneumonia. In some cases the pneumonia of 
 grip is caused by mixed or secondary infection. 
 
 Pathologic Physiology.— Very little is known regarding 
 the mode of activity of the bacteria.' The constitutional" symp- 
 toms ^suggest toxemia, but the nature of the poison is obscure. 
 The immunity from the disease must be exceedingly short, as re- 
 curring attacks and relapses may be frequent and succeed one 
 another rapidly. Certain complications and sequels, such as in- 
 flammations of the serous surfaces and neuritis, indicate general- 
 ized infection and intoxication. 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 253 
 
 BUBONIC PLAQUE. 
 
 Definition. — The bubonic plague, or pest, is an infectious 
 disease due to a peculiar bacillus. 
 
 Etiology. — The bacillus of bubonic plague was discovered 
 by Yersin and Kitasato independently in 1894. In blood drawn 
 from a puncture of the skin and in pus from the affected glands 
 may be found small bacilli somewhat resembling the influenza- 
 bacillus. These organisms may be stained readily, and are then 
 seen to be swollen somewhat at the ends and more deeply stained 
 at the poles than in the center (Fig. 103). This gives them an 
 
 
 &&&>: 
 
 *2l 
 
 Fig. 103.— Bacillus of bubonic plague (Yersin). 
 
 appearance resembling that of the diplococci, and in specimens 
 from the blood or tissues there is an indistinct capsule. The 
 bacillus is feebly motile, but flagella have not been detected. 
 Pure cultures have been obtained upon various media. Upon 
 glycerin-agar moist, rounded, whitish or bluish-white colonies are 
 formed. Portions of such colonies removed for examination show 
 the bacilli ranged in chains. 
 
 Pathogenicity. — The bacillus has been found pathogenic for 
 mice, rats, guinea-pigs, and rabbits, and the symptoms produced 
 by pure cultures are the same as those induced by inoculating ani- 
 mals with blood or portions of tissue from diseased persons. The 
 lymphatic glands may be swollen and petechial hemorrhage may 
 occur as in the human disease. 
 
 Distribution. — In the human being suffering from bubonic 
 plague the bacilli are found in the local lesions of the lymphatic 
 glands, the buboes ; and also in the blood and various organs. 
 Rats and mice frequently die during epidemics, and doubtless help 
 to spread the disease by infecting the soil and dust about dwell- 
 ings. Yersin showed that flies die of the disease, and succeeded 
 in obtaining the bacillus from their dead bodies. 
 
254 TEXT-BOOK OF PATHOLOGY. 
 
 Pathologic Anatomy. — The organism produces swellings 
 and suppuration of lymphatic glands, particularly those of the 
 groin, and secondarily lesions of internal organs. The lymphatic 
 glands swell quickly, become tender and congested, and then 
 soften, forming a rather thick pus. This is sometimes somewhat 
 blood-tinged. Petechial hemorrhages and blood-stained effusions 
 into the serous cavities may occur. Petechia? of the skin are apt 
 to develop as a result of slight traumatisms. Thus the bite of an 
 insect, instead of producing its usual results, may cause distinct 
 ecchymoses in persons suffering from the disease. 
 
 Pathologic Physiology. — It seems that the distribution of 
 the bacillus in the blood, as well as toxic substances, contributes 
 to the general disturbance of health. By successive inoculation 
 immunity has been produced, and toxins and antitoxins have been 
 obtained from the serum. The importance of these latter, how- 
 ever, is still under investigation. 
 
 DISEASES OF UNCERTAIN BACTERIOLOGY. 
 
 SYPHILIS. 
 
 Definition. — Syphilis is a specific contagious disease of man, 
 of uncertain etiology. The disease has never been observed in 
 any of the lower animals. 
 
 Utiology. — The attempts to find a specific cause of this dis- 
 ease have not as yet met with definite success. The organism 
 which at the present time has the best claim to recognition is that 
 observed by Lustgarten. This resembles the tubercle-bacillus 
 very closely. It is 3 to 7 // long, and often somewhat curved and 
 swollen at the ends. It stains with difficulty, and a complicated 
 method was suggested by the discoverer. The bacilli are found 
 in the diseased areas in small numbers, lying within the cells and 
 partly between them. It has also been claimed that they occur in 
 the blood. The organism has never been isolated or cultivated 
 upon artificial media. Furthermore, it is difficult to distinguish 
 this supposed specific germ from other bacilli, notably the smegma- 
 bacillus, by the staining-methods suggested. 
 
 Whatever the nature of the organism, it is quite certain that 
 the disease is definitely infective. In the great majority of cases 
 infection occurs by direct inoculation in sexual intercourse. It 
 may, however, be conveyed in many other ways. Physicians are 
 sometimes infected in performing surgical operations or in exam- 
 ining syphilitic cases ; persons have frequently been inoculated in 
 the process of tattooing or vaccination when saliva or vaccine- 
 lymph from diseased individuals was employed. Infection may 
 be caused by kissing, or indirectly by the use of drinking-vessels 
 which have been employed by the diseased. The new-born may 
 be syphilitic in consequence of disease of the father or mother ; and 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 255 
 
 healthy wet-nurses may be infected by syphilitic nurslings. In 
 addition to the specific cause, surrounding conditions and individ- 
 ual susceptibility doubtless play a part. During the Middle Ages 
 this disease at times and in certain places almost attained the char- 
 acter of a universal scourge. Its manifestations were severe, its 
 course rapid, and in every sense its nature was malignant. Cases 
 of this description are exceedingly rare at the present day. 
 
 Pathologic Anatomy. — The pathologic course of this dis- 
 ease may be divided into three stages : the initial stage, the second- 
 ary stage, and the tertiary stage. 
 
 Chancre. — In the initial stage there is formed at the point of 
 inoculation a primary lesion, commonly termed chancre. This 
 may make its appearance first as a somewhat red and inflamed 
 papule, or as a vesicle which ruptures and thus produces an ero- 
 sion. When it begins as a papule the surface soon becomes eroded, 
 and thus a superficial ulceration is established. The peculiar feat- 
 ure of this lesion, to which Hunter called particular attention, is 
 its hardness or induration, and it is by this feature largely that it 
 is distinguished from the soft chancre or chancroid. The initial 
 or primary lesion may remain indolent or as a small erosion for a 
 long time, or it may soon cicatrize and leave a more or less definite 
 scar. The chancre occurs upon the glans penis or prepuce, or 
 within the urethra of the male ; and in the vagina, urethra, or upon 
 the cervix uteri and external genitalia of the female. Extrageni- 
 tal chancres may be observed in the rectum or anus, on the lips 
 or tongue, tonsils or pharynx, the fingers, or other parts. 
 
 Secondary Lesions. — At the end of a variable period of time 
 after the eruption of the initial sore secondary manifestations of 
 the disease make their appearance. The first among these, as a 
 rule, are swelling and induration of the neighboring lymphatic 
 glands (syphilitic bubo). Later the superficial lymph-glands of 
 the entire body become swollen and, like those in the neighbor- 
 hood of the lesion, indurated. At the same time eruptions upon 
 the skin and mucous membranes make their appearance. The 
 interval between the primary and the secondary manifestations is 
 variable. Sometimes it is but a few weeks (three or four), at other 
 times it may be several months. The manifestations of the sec- 
 ondary stage may begin with fever and constitutional symptoms, 
 suggesting sudden and recent infection, and at the same time 
 changes in the blood (rapid reduction of red corpuscles, moderate 
 leukocytosis) make their appearance. Among the lesions of the 
 skin various forms of papules, macules, and scaly eruptions are 
 most frequent and characteristic. The lesions are usually sym- 
 metrically arranged on the two sides of the body and cause but 
 little irritation. The color of the skin is frequently said to be 
 somewhat coppery. On the mucous membranes and neighboring 
 skin the most characteristic lesion of this stage is the condyloma 
 
256 TEXT-BOOK OF PATHOLOGY. 
 
 latum, or mucous patch. This appears as a somewhat elevated 
 patch with superficial erosion or ulceration. The surface has a ne- 
 crotic appearance, and may be covered with more or less secretion. 
 
 Tertiary Lesions. — These may take the form of ordinary in- 
 flammatory changes of the mucous membranes or of other parts, 
 with a pronounced tendency to fibrous-tissue overgrowth and 
 thickening, or of definite nodules — the syphilitic gummata, or 
 sypMlomata. Among the diffuse syphilitic changes of the tertiary 
 stage may l>e ranked atheromatous thickening of the intima of the 
 blood-vessels, certain changes in the liver, spleen, kidneys, and 
 heart-muscle, and doubtless also similar alterations in the nervous 
 system. 
 
 The localized lesions of the tertiary stage — the gummata — are 
 most frequent in the bones (tibia, sternum, and skull) ; and in the 
 internal organs, such as the liver, lungs, kidneys, heart, and brain. 
 
 The gumma presents itself as a nodular mass, varying in size 
 from small tubercle-like formations (miliary gummata) to tumors 
 the size of an orange, or larger (Fig. 104). It is hard, and has 
 
 Fig. 104.— Gummata of the liver. 
 
 frequently an elastic character, which has suggested the name 
 gummy tumor or gumma. On section the substance is frequently 
 found to be gelatinous or mucoid in appearance ; but there is 
 nearly always considerable induration, either peripheral, in the 
 form of a capsular enclosure, or striate, in the form of Viands 
 extending from the center to the periphery and into the sur- 
 rounding tissue. Occasionally gummata soften very rapidly and 
 become converted more or less completely into puriform collections. 
 When situated in the mucous membranes or adjacent to the sur- 
 faces of the body, suppurative, fatty or necrotic softening may 
 lead to the formation of superficial ulcerations. These may re- 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 257 
 
 main indolent, or may gradually become cicatrized. Sometimes a 
 gummatous lesion disappears entirely by absorption without leav- 
 ing a trace of its existence. 
 
 Histology. — In syphilitic processes of all kinds and in all of 
 the stages there is a tendency to accumulation of the round cells 
 and proliferation of connective-tissue cells, the processes being 
 first manifest around the smaller blood-vessels, but subsequently 
 extending to other parts of the tissue. The walls of the blood- 
 vessels themselves are frequently involved, and thickening of the 
 inner or of all the coats may be observed. Complete destruction 
 of the vascular channels is not rarely the consequence. In the 
 subsequent course of the disease there is a tendency to the forma- 
 tion of distinct cicatricial connective tissue, giving rise to indurated 
 scars or diffuse sclerosis ; and a less pronounced tendency to the 
 occurrence of degenerations, mucoid and fatty, causing areas of 
 degenerative softening. 
 
 The Chancre. — The initial lesion first presents small areas of 
 round-cell infiltration in the deeper layers of the skin or mucous 
 membrane, and as a rule in the neighborhood of the blood-vessels. 
 The connective tissue at the same time undergoes proliferative 
 change, and spindle-shaped cells or irregular embryonal connec- 
 tive-tissue cells are found mingled with the round lymphoid cells, 
 or surrounding the foci of the latter. Thickening of the blood- 
 vessels may be observed in the later stages or from the very first. 
 The tissue-elements of the skin and of the subcutaneous tissue are 
 usually separated by infiltrating liquid, and the latter may loosen 
 the tissues of the surface and cause exfoliation of the superficial 
 epidermis, and thus lead to the development of the primary vesicle 
 or the erosion so commonly seen. The induration of the chancre 
 is probably the result of the sclerosis of the vessels and the gen- 
 eral connective-tissue hyperplasia, as well as in part due to the 
 tense infiltration of serous liquid. 
 
 The Mucous Patch. — The condyloma latum is very similar in 
 structure to the initial lesion. There is, first, round-cell infiltra- 
 tion of the deeper layers of the mucous membrane, with serous 
 exudation and erosion of the surface. Later, there is a tendency 
 to connective-tissue hyperplasia, though this is less marked than 
 in the case of the chancre. 
 
 The Tertiary Lesions. — The gumma is composed in large part 
 of round cells derived from the blood-vessels and proliferated 
 connective-tissue cells having a spindle-shape or various irreg- 
 ular forms. Epithelioid cells are less abundant, and giant-cells, 
 though occurring at times, are usually few in number. The 
 blood-vessels are nearly always more or less affected, the intima 
 particularly being thickened ; there is also new formation of blood- 
 vessels, the lesion in this respect differing from the nodular lesion 
 of tuberculosis (Fig. 105). Secondary changes are almost always 
 
258 TEXT-BOOK OF PATHOLOGY. 
 
 seen in gummata of considerable dimensions. Among these may 
 be recognized a gradual necrotic transformation of the cells in the 
 center of the lesion, with distinct fatty degeneration or myxoma- 
 tous change. The degenerated tissue may be infiltrated by leuko- 
 cytes in a state of fair preservation. 
 
 In the diffuse tertiary lesions of syphilis the tissues of the 
 affected organ are indurated, the connective tissue showing more 
 
 Fig. I05.—Gummatous meningoencephalitis (Ziegler). 
 
 or less pronounced hyperplasia. These processes cannot be 
 certainly distinguished by their microscopic or general features 
 from sclerosis due to other causes. 
 
 Pathologic Physiology. — Syphilis is one of the most per- 
 sistent of the infectious diseases, and occasions widespread changes 
 that are doubtless toxic in character. The nature of the toxic 
 principles, however, is entirely unknown. In the tertiary stage 
 pronounced anemia (cachexia) is frequent ; and in the secondary 
 stage rapid chloro-anemia with leukocytosis is quite common. 
 
 Congenital Syphilis. 
 
 Syphilitic lesions may be found in the new-born, or may 
 develop some time after birth. Not rarely they occur in the new- 
 born fetus, and cause its premature death. Frequently there is 
 maceration of the fetus prior to expulsion. Among the lesions 
 observed, sclerotic changes in the lungs, liver, spleen, pancreas, 
 and other organs are conspicuous ; and a certain condition of the 
 bones is quite characteristic. The latter consists of a hypeq)lasia 
 of connective tissue and fatty degeneration at the junction of the 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 259 
 
 epiphyses of the long bones with the shafts. Various superficial 
 lesions of the skin in the form of vesicles or bullae, fissure, and 
 the like may be observed. The blood may present considerable 
 excess in the number of leukocytes. An almost distinctive con- 
 dition of second dentition is that ,*«»«ii&»^& ei 
 known as Hutchinson's teeth. This 
 consists of a notched indentation of 
 the cutting surface of the upper cen- 
 tral incisors. In addition, the tooth FlG . loe.-Hutchinson's teeth, 
 is often wedge-shaped and peg-like 
 
 (Fig. 106). All cases of inherited syphilis do not present this 
 condition, and it occasionally occurs in non-syphilitic children. 
 
 SOFT CHANCRE. 
 
 Definition. — The soft chancre or chancroid is an infectious, 
 venereal sore appearing upon the external genitalia. Its probable 
 cause is the bacillus of Ducrey. 
 
 Etiology. — The soft chancre occurs almost exclusively upon 
 the genital organs or the surrounding parts. It is always caused 
 by direct contagion. 
 
 The bacillus of Ducrey and Unna is a rod-shaped organism 
 about 1.8 jut in length and 0.5 jx in thickness, and is somewhat 
 compressed in the middle, so that it has a figure-of-8 shape. The 
 ends are rounded and the organisms often occur in chains, or later 
 in the disease in pairs as a diplobacillus. 
 
 The demonstration of the bacillus in the pus is comparatively 
 easy. The specimen is stained with alkaline solutions of methyl- 
 ene-blue and quickly decolorized with weak acetic-acid solution. 
 In the tissues the demonstration is more difficult. 
 
 The cultivation of the bacillus has not thus far proved success- 
 ful, though certain bacteriologists claim they have succeeded. 
 
 The bacillus is found in the pus of the soft chancre, as well as 
 in the deeper parts, lying between the cells and frequently within 
 the leukocytes. It has also been discovered in the pus and walls 
 of ulcerating buboes, but is generally absent in the pus of un- 
 opened buboes. 
 
 Mixed Injection. — Various other organisms have been found 
 associated with the bacillus, including streptococci, staphylococci, 
 the gonococcus, and bacilli of uncertain nature. 
 
 Pathologic Anatomy. — The soft chancre is an ulcer of 
 variable character. Usually it is a simple ulcer, with suppurating 
 base and edges, not differing from ulcers due to other causes. 
 Sometimes the ulceration seems more malignant and takes on a 
 phagedenic or serpiginous character (see Ulceration). The neigh- 
 boring lymphatic glands are usually enlarged and sometimes 
 undergo suppurative softening (bubo). 
 
260 TEXT-BOOK OF PATHOLOGY. 
 
 Pathologic Physiology. — Little is known of the existence 
 of special toxic bodies in this disease. It is believed, however, 
 by BOine that toxins are produced by the bacilli, and that these are 
 capable of producing secondary lesions (bubo) without the presence 
 of the bacilli themselves. 
 
 YELLOW FEVER. 
 
 Definition. — Yellow fever, or typhus icteroides, is now recog- 
 nized as infectious and contagious, and it is probably caused by a 
 specific bacillus recently isolated. 
 
 Etiology. — The Bacillus icteroides was discovered in 1897 by 
 Sanarelli. This is a small bacillus from 2 to 4 /jl in length, with 
 rounded extremities. It is frequently united in pairs, and is actively 
 motile, the motility being due to from four to eight lateral flagella. 
 The organism is pleomorphous. It is readily stained by the ordi- 
 nary anilin dyes, but is decolorized by Gram's method. 
 
 Cultivation. — Sanarelli succeeded in obtaining cultures upon 
 the ordinary media, but the growth on the surface of agar is most 
 distinctive. When incubated for twelve hours at 37° C. (98.6° F.) 
 and then allowed to develop further at lower temperatures there 
 will be found, first, semitransparent rounded colonies, and, later, 
 enlargement of these with the formation of a thick white border, 
 giving the appearance of a drop of sealing-wax. The character- 
 istic growth is thus obtained in twenty-four hours. 
 
 Distribution. — Sanarelli found the bacillus in the various organs 
 as well as in the blood. He succeeded in obtaining cultures in 58 
 per cent, of the cases studied. Failure in a large proportion of 
 cases he attributed to the small number of bacilli present. 
 
 Pathogenicity. — The pathogenic role of this organism is becom- 
 ing quite widely recognized. The discoverer succeeded in produc- 
 ing in animals lesions and symptoms very analogous to those of the 
 human disease. The dog responded most satisfactorily. Injected 
 into the veins of a dog there is active emesis, then hemorrhages 
 throughout the body, and finally extensive fatty degeneration of 
 the liver and kidneys. In one case extreme jaundice developed. 
 
 Other Micro-organisms. — Previous to Sanarelli's work a great 
 variety of organisms had been described. Among others a bacil- 
 lus by Richardson, a micrococcus by Finlay and Delgado, a 
 bacillus by Gibier, and other organisms by Freire and Carmona 
 and by Sternberg. None of these organisms appears to have im- 
 portance, or to be the same as that discovered by Sanarelli. The 
 organisms isolated by Havelberg about the same time as Sanarelli's 
 appear to be of no importance. 
 
 Pathologic Anatomy. — The lesions of this disease are 
 mainly those of the internal organs — liver and kidneys. In the 
 liver extensive fatty degeneration leads to some swelling and light 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 261 
 
 color of the organ, and on section there may be mottled appear- 
 ance due to the alternation of healthy and fatty areas. In the 
 kidneys degenerative changes of the parenchyma and extravasation 
 of blood are associated in varying proportions. The appearance 
 may be that of an acute hemorrhagic nephritis, or more particu- 
 larly that of degenerative nephritis. Hemorrhages in the mucous 
 and serous surfaces are frequent, particularly extravasation of the 
 mucosa of the stomach. 
 
 Pathologic Physiology. — The organism of yellow fever 
 probably produces abundant toxin. Small numbers of the bacilli 
 seem at times to give rise to violent symptoms. Sanarelli has 
 claimed that antitoxic serum is obtainable from immunized 
 animals. Recently an agglutinative reaction, like that of Widal 
 for the typhoid germ, has been described. 
 
 MEASLES. 
 
 Measles, or rubeola, is an infectious and contagious disease in 
 all probability due to some micro-organism. A number of micro- 
 organisms have been discovered, but none as yet has been defi- 
 nitely proved to be the cause. Several observers (Canon and Pie- 
 licke, Czajkewski) have found a bacillus somewhat resembling 
 that of influenza, but the matter is still unsettled. Doehle de- 
 scribed a protozoan organism occurring in the blood. 
 
 SCARLET FEVER. 
 
 Scarlet fever, or scarlatina, is an infectious and contagious 
 disease probably due to a micro-organism. A variety of organ- 
 isms have been discovered in cases of scarlet fever, but none as 
 yet has proved to be specific. The weight of evidence seems to 
 suggest the pyogenic micrococci (streptococci) as probable etiologic 
 agents. Protozoan organisms have also been described (Doehle). 
 
 MUMPS. 
 
 The bacteriology of mumps is uncertain. Charrin and Capitan 
 isolated a number of organisms, mainly micrococci and motile 
 bacilli. A number of other authors subsequently obtained simi- 
 larly indefinite results. Laveran and Catrin in 1893 found a 
 diplococcus. 
 
 WHOOPING=COUGH. 
 
 A short bacillus was discovered in the expectoration of pertus- 
 sis by Afanassiew in 1887. He injected cultures of this into the 
 trachea and lungs of dogs, and found that the animals became ill 
 and died, after presenting convulsive cough with bronchitis similar 
 
262 TEXT-BOOK OF PATHOLOGY. 
 
 to that of whooping-cough. Wendt confirmed these results ; but 
 Ritter found a diploeoccus in his cases, and Cohn and Neumann 
 found small cocci, often arranged as diplococci or more rarely as 
 short chains. Czaplewski and Hensel describe a bacillus resem- 
 bling the influenza-bacillus, and believe that the organisms of 
 Cohn and Neumann were identical with theirs. Others have dis- 
 covered organisms similar to the ordinary pyogenic micrococci ; 
 and some have described protozoa in the blood. 
 
 TYPHUS FEVER. 
 
 A number of micro-organisms have been discovered in this 
 disease, including strepto-bacilli (Hlava), small granular bodies 
 growing to thread-like organisms (Thoinot and Calmette ; Lewa- 
 scheff), diplococci (Dubief and Briihl). Lewascheff has more 
 recently concluded from a study of 158 cases that the micrococci 
 of Dubief and Briihl, which have also been described by others, 
 are the important agents, and proposes the name Micrococcus exan- 
 tlicmaticus. 
 
 RABIES. 
 
 Hydrophobia is doubtless an infectious malady, but the bac- 
 teriology is still obscure. Micrococci and bacilli of different 
 kinds have been described. Memrao isolated a form of blasto- 
 mycetes, and claims to have produced the disease in dogs with 
 pure cultures of this. 
 
 THE HEMORRHAGIC DISEASES. 
 
 The hemorrhagic diseases constitute a group of affections of 
 probably quite divergent character, which, however, are similar 
 in presenting hemorrhages in and from the mucous membranes, in 
 the skin, serous surfaces, and in the deeper tissues or organs. 
 
 The general causes of hemorrhage must be considered in con- 
 nection with these diseases. Among the causes capable of pro- 
 ducing hemorrhages such as occur in the hemorrhagic diseases are 
 mechanical conditions, as atheroma or other diseases of the walls 
 of the blood- vessels ; toxic conditions, such as poisoning by the 
 venom of animals and by various blood-poisons, and probably 
 obscure poisons produced in the course of anemic or other dis- 
 eases ; infectious conditions, such as occur in hemorrhagic variola, 
 scarlatina, etc. ; and nervous conditions, as are illustrated in the 
 hemorrhages following injuries to the brain and those accompany- 
 ing certain states of cerebral excitation. 
 
 Clinically the hemorrhagic diseases or purpuras may be classi- 
 fied as primary and secondary, the former occurring without any 
 definite preceding disease ; the latter being symptomatic of various 
 
BACTERIA AND DISEASES DUE TO BACTERIA. 263 
 
 disorders. Among the primary there are : (1) infectious forms, 
 including, with more or less probability, purpura, scurvy, and 
 various forms of cryptogenetic sepsis; (2) toxic forms, as those due 
 to drugs and venom of animals ; (3) mechanical forms, as hemo- 
 philia. Among the secondary purpuras are : (1) infectious forms, 
 as scarlatina, variola, and the like ; (2) mechanical forms, as those 
 due to cardiac and arterial diseases, or embolism ; (3) toxic forms, 
 as those resulting from intestinal auto-intoxications, jaundice, 
 pernicious anemia, etc. ; and (4) nervous forms, as those due to 
 hysteria, diseases of the brain, etc. 
 
 The infectious purpuras interest us particularly in the present 
 place. Various micro-organisms have been found in different 
 forms of hemorrhagic disease. Kolb described a bacillus patho- 
 genic for animals, which occurred in five cases of hemorrhagic 
 purpura. Babes and Oprescu isolated a bacillus from one case of 
 hemorrhagic septicemia, and others have found various micrococci, 
 especially the streptococcus. It is not unlikely that many of the 
 micro-organisms may assume a peculiar virulence and acquire the 
 power to produce hemorrhages under certain circumstances. 
 
 In scurvy several micro-organisms have been described, but 
 the one which has the best claim for consideration is that discov- 
 ered by Babes, a delicate bacillus occurring in the gums. Strepto- 
 cocci were found in association with it. 
 
 RHEUMATISM. 
 
 Definition. — Acute articular rheumatism is probably an in- 
 fectious condition ; the nature of the infectious agent, however, is 
 uncertain. 
 
 Etiology. — The manifestations of rheumatism agree very well 
 with those of infectious diseases, and some of the lesions frequently 
 complicating the disease, such as endocarditis, are invariably in- 
 fective. The relationship between tonsillitis and rheumatism has 
 been explained by some as that between primary and secondary dis- 
 order. It is supposed that the infectious agents effect an entrance 
 into the body through the tonsils, causing primary tonsillitis and 
 secondary general infection, with localization in the joints. In 
 other cases it has been held that the organisms enter through 
 abrasions of the skin or in other ways. 
 
 Guttmann, one of the first to maintain the infectious origin, 
 described a Staphylococcus pyogenes flavus discovered in one of 
 his cases. Sahli found an organism which he classified as Staphylo- 
 coccus pyogenes citreus. He enunciated the theory that rheuma- 
 tism represents a form of staphylococcic infection, the organisms, 
 however, being of a low grade of virulence. They are not found 
 abundantly in the exudations in the joints, as they remain fixed in 
 the synovial tissues. Hence, they are difficult of discovery. 
 
264 TEXT-BOOK OF PATHOLOGY. 
 
 Other organisms, including various forms of bacilli, have been 
 described. 
 
 Very recently Achalnie has described a bacillus which he and 
 others have found in a number of eases of acute articular rheuma- 
 tism. It is a large baciUus resembling that of anthrax ; sometimes 
 it is motile ; it stains well with anilin dyes and with Gram's stain; 
 may have a capsule ; and forms polar spores much' larger than the 
 bacillus. This organism is obligate-anaerobic, growing best in 
 liquid media, in which it forms small bubbles of gas. Thioroloix 
 claims to have produced typical symptoms in the rabbit; and the 
 inoculation-experiments of others have given suggestive results. 
 This bacillus was obtained from the blood in a number of cases; 
 and from the pericardial fluid and blood in a state of purity in one 
 case. The organisms have been found in sections of the heart- 
 muscle and valves. 
 
 MALTA FEVER. 
 
 Synonyms. — Mediterranean Fever ; Gibraltar Fever ; Febris 
 Undulans. 
 
 Definition. — This disease has been described as a form of 
 irregular fever occurring in various places along the Mediter- 
 ranean coasts. It has been regarded as an aberrant form of 
 typhoid fever, but is probably independent and due to a special 
 micro-organism. 
 
 Btiology. — The micro-organism discovered by Bruce, and 
 designated Micrococcus Maltensis, is by many regarded as the 
 specific cause. This is an oval micrococcus about ^ fi in diameter, 
 occurring singly or sometimes in pairs, but never in chains. It 
 has no motility of its own. It may be stained with ordinary solu- 
 tions of anilin dyes, but not by Gram's method. It occurs abun- 
 dantly in the spleen, but not in the blood. Pure cultures have 
 been obtained, and inoculation in monkeys has seemed to give 
 positive results. Malta fever is not contagious. The micro- 
 organisms seem to enter the body through the respiratory or the 
 intestinal tract. 
 
 Pathologic Anatomy. — The mucous membrane of the small 
 intestine is red and the solitary follicles and Peyer's patches are 
 sometimes swollen. The mucosa of the large intestine is generally 
 dark red and presents small round or larger irregular ulcerations, 
 from which intestinal hemorrhages occur. In some cases lesions 
 of the ileum resembling those of typhoid fever have been de- 
 scribed ; but it is doubtful if the cases in which these occurred 
 were Malta fever, and not typhoid. The spleen is enlarged and 
 hyperemia 
 
 Pathologic Physiology. — Malta fever is characterized by 
 irregular febrile movements. The cause of this irregularity and 
 the nature of the toxic substance generated in the disease are un- 
 
ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 265 
 
 known. Recently a serum-reaction, like that of Widal for typhoid 
 fever, has been obtained with the serum and cultures of Malta 
 fever. 
 
 BERI=BERI. 
 
 Definition. — This disease is an infection due to undetermined 
 causes. It occurs in tropical and subtropical countries, and is 
 characterized by muscular weakness, generalized muscle-pains, 
 dropsy, and cardiac failure. The essential lesions seem to be 
 degeneration and inflammation of the peripheral nerves. 
 
 Etiology. — Beri-beri occurs among young persons and usually 
 affects numbers of people. It is most frequent along ocean coasts 
 and great- rivers, and is most prevalent during damp seasons of 
 the year. It does not seem to be contagious. 
 
 Various micro-organisms have been described, including a 
 number of bacilli and micrococci, as well as organisms resembling 
 the malarial hematozoa. One observer (Taylor) was able to 
 produce the disease in animals by the injection of blood from a 
 diseased person. 
 
 Pathologic Anatomy. — Among the lesions observed are 
 punctate hemorrhages in the serous surfaces ; parenchymatous and 
 fatty degeneration of the heart-muscle ; enlargement of the liver 
 and spleen. Degeneration and inflammation of the peripheral 
 nerves are constant and important conditions. 
 
 CHAPTER VIII. 
 
 ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 
 
 PROTOZOA. 
 
 AMCEBA COLI. 
 
 Description. — This organism, first accurately described by 
 Losch, is an ameboid body from 20 to 30 ju in diameter, consist- 
 ing of a clear protoplasmic outer portion and a finely or coarsely 
 granular protoplasm within (Fig. 107). It frequently shows vacu- 
 oles and sometimes a nucleus. It presents active ameboid move- 
 ments when studied on a warm stage of the microscope ; and fre- 
 quently contains foreign bodies, such as bacteria, pigment-particles, 
 and portions of blood-corpuscles or other cells. 
 
 In the movements of the organism pseudopodia are projected 
 from some part of the periphery. These at first draw upon the 
 clear peripheral zone, but after their formation the granuloplasm 
 
266 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 flows into the projected pseudopods. When in unfavorable sur- 
 roundings the organism undergoes a form of change called the 
 encysted state. In this the body becomes spherical, and the wall 
 is eventually stiff* and firm and usually presents a double contour. 
 
 Fig. 107.— Amoeba coli in intestinal mucus, with blood-corpuscles and bacteria (Losch). 
 
 The division into a clear and a granular protoplasm is lost, the 
 organism being uniformly granular. 
 
 Distribution and Pathogenesis. — The organism in ques- 
 tion has been found abundantly in the stools of patients suffering 
 from dysentery. It is readily detected in the necrotic particles or 
 the mucus of the stools, and has also been found in the tissues of 
 the bowel-wall adjacent to the dysenteric ulcers and abundantly in 
 the liver-abscesses secondary to dysentery. 
 
 It has, however, been found in the dejections from cases other 
 than dysentery, and even in the stools of healthy individuals. 
 
 The pathogenic importance of this organism cannot be positively 
 established until cultures are obtainable. Thus far, attempts to 
 secure pure cultures have failed. The injection of mucus contain- 
 ing the ameba into the rectum of cats and other animals has occa- 
 sionally produced typical dysentery, but this does not prove the 
 pathogenicity of the ameba. The regularity of the occurrence of 
 the organism in certain forms of dysentery and its relations to the 
 lesions are the strongest evidences in favor of its pathogenic role. 
 
 OTHER AMCEB/E. 
 
 Several other amoebae of lesser importance have been discov- 
 ered. Among these are the Amoeba urinalis, found in the urine in 
 cases of cystitis, and several forms met with in the mouth, espe- 
 cially about the teeth. 
 
ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 267 
 
 HEMATOZOON MALARI/E. 
 
 The organism which is now recognized as the cause of malaria 
 is an animal organism of the protozoan group, the exact biologic 
 position of which, however, remains undetermined. Most authors 
 regard it as one of the sporozoa. It occupies the blood and the 
 vascular channels of the various organs, deriving its nourishment, 
 for the most part, directly from the blood-corpuscles. The mode 
 of infection and the life-history of the organism outside the human 
 body are unknown. It seems most probable that the organisms 
 are conveyed to man through the air. Many clinicians, however, 
 hold that the infection may be conveyed by drinking-water. 
 Direct contagion does not occur, but it has been shown that the 
 blood is infectious when introduced into the circulation of a 
 healthy person. The drinking of the blood does not give rise to 
 the disease. Certain external conditions are favorable or necessary 
 to the development of the disease, and probably are important in 
 fostering the development of the organisms outside the body. These 
 external conditions are moist, marshy soil, atmospheric humidity, 
 and high temperature. The disease occurs in the lowlands or 
 bottomlands, and very rarely in high and dry ground. Extensive 
 excavations and the like may cause the appearance of the disease 
 or increase it, and, on the other hand, suitable drainage may cause 
 its diminution or disappearance. 
 
 The Hematosoon. — Three forms of malarial parasites have 
 been distinguished ; and it is likely that these are three definite 
 species, although some still maintain they are merely alterations 
 of the same organism. 
 
 The Parasite of Tertian Fever. — Examination of the fresh blood 
 of a patient some hours after a tertian chill shows in some of the 
 red corpuscles small hyaline bodies, having ameboid movement 
 and often assuming cross- or star-shapes. These are the so-called 
 plasmodia. Later, the plasmodia have pigment about their pe- 
 riphery, and finally the amount of pigment may become consid- 
 erable. During this time the organism grows and the red cor- 
 puscle becomes paler. Eventually the ameba may almost com- 
 pletely fill the corpuscle. At this stage, which occurs just prior 
 to the paroxysm, segmentation begins. The pigment, which pre- 
 viously has shown active movements, collects toward the center and 
 becomes motionless, and lines of radiate striation are formed in the 
 organism, giving it a rosette-like figure composed of twelve to 
 twenty parts. Segmentation proceeds until each of the segments 
 becomes a small spherule. The corpuscle then bursts and the 
 spherules or spores escape, probably to begin their cycle of develop- 
 ment from the start by entering new red corpuscles as minute 
 plasmodia. This cycle of development requires forty-eight hours. 
 
 The Organism of Quartan Malaria. — This is similar to the last 
 
268 TEXT-BOOK OF PATHOLOGY. 
 
 named, but differs in the fact that the pigment-granules are much 
 less abundant and coarser. The red corpuscle is not decolorized, 
 as in the case of the tertian, but assumes a somewhat greenish 
 hue. In about seventy-two hours segmentation occurs, six to ten 
 segments and then spherules being formed. 
 
 The Parasite of Irregular Malaria. — In the irregular malarial 
 fevers of the summer and foil (the estivo-autumnal fevers) the 
 organism is smaller than in the other cases, and rarely presents 
 much pigment. The plasmodium frequently presents itself as a 
 ring-shaped body, highly refractive and with a shaded central 
 part. A few pigment-granules may be seen, but rarely more. 
 The organism itself does not become larger than about one-third 
 the diameter of the corpuscle in which it occurs. The red cor- 
 puscle itself is greenish, as in the quartan variety. Segmentation 
 is not observed in the circulating blood, though centrally placed 
 pigment may be seen. The segmentation takes place in the spleen, 
 bone-marrow, and other parts. The duration of the cycle of 
 development is indefinite. 
 
 Other Types Assumed by the Malarial Hematozoa. — Besides the 
 regular forms described there is a flagellate variety, which is seen 
 only in the blood kept for a little while outside the body. This is 
 formed by the projection of thread-like processes which have 
 active thrashing-movements. The pigment of the body itself is 
 in the central part and is actively motile. These ciliated hema- 
 tozoa may be found in tertian or quartan fever, but especially in 
 irregular malaria. Recent observations on the blood of birds, as 
 well as the studies of Manson and Ross in malaria, .seem to show 
 that the formation of these flagellated bodies is important in the 
 reproduction of the organism. 
 
 In the estivo-autumnal fevers a very curious form of the hema- 
 tozoa is found ; this is the crescent form described by Laveran. It 
 occurs in cases of some weeks' duration, and is developed within 
 the corpuscles ; first, as a somewhat oval body, which becomes 
 more and more cresccntic, the pigment at the same time clumping 
 in the center. The red corpuscle may entirely disappear, with the 
 exception of a small portion seen in the concave part of the cres- 
 cent as a mere shadow. 
 
 The Organism Chddde the Human Body. — It has been impossi- 
 ble up to the present time to discover the malarial organism in 
 soil or water, and only a few uncertain observations of its occur- 
 rence outside the body have been made. Recently Manson sug- 
 gested that the mosquito is the probable carrier of the contagion. 
 
 Pathologic Anatomy. — The most important fact in malarial 
 infection is the destruction that it occasions in the blood. Rapid 
 anemia with liberation of the hemoglobin (hemoglobinemia) and 
 the appearance of granular pigment in the blood are among the 
 results. The pigment accumulates in the spleen, liver, bone- 
 
Plate i. 
 
 3 4 
 
 %y/ ^p 
 
 8 9 
 
 
 77 
 
 7^ 
 
 r 
 
 23 
 
 ,<?■ 
 
 
 (? 
 
 i>i> 
 
 , 
 
 ^) 
 
 -?<? 
 
 Various forms of malarial parasites (Thayer and Hewetson) : Figs. 1 to 10, in- 
 clusive, tertian organisms; Figs. 11 to 17, inclusive, quartan organisms; Figs. 18 to 
 27, inclusive, estivo-autumnal organisms. 
 
 Fig. 1.— Young hyaline, form ; 2, hyaline form with beginning pigmentation ; 
 3, pigmented form ; 4, full-grown pigmented form ; 5, 6, 7, 8, segmenting forms ; 9, 
 extracellular pigmented form ; 10, flagellate form. 
 
 Fig. 11. — Young hyaline form; 12, 13, pigmented forms; 14, fully-developed 
 pigmented form; 15, 16, segmenting forms; 17, flagellate form. 
 
 Figs. 18, 19, 20. — King-like and cross-like hyaline forms; 21, 22, pigmented 
 forms ; 23, 24, segmenting forms ; 25, 26, 27, crescents. 
 
ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 269 
 
 marrow, and in other situations. Congestive enlargement of the 
 spleen and, after long-continued attacks, cirrhotic changes may be 
 observed. Thrombi of the capillaries and arterioles are not rare, 
 and to these, in part at least, are due the focal necroses observed 
 in the liver and elsewhere. 
 
 Pathologic Physiology. — The curiously paroxysmal seiz- 
 ures of malaria are probably the result of the liberation of toxic 
 substances. The periodicity depends upon the duration of the 
 cycle of development of the organism. A single group of tertian 
 organisms cause a tertian fever (a paroxysm every other day). 
 Infection with two groups of tertian organisms, maturing on alter- 
 nate days, produces a quotidian fever (a paroxysm every day). 
 One group of quartan organisms causes quartan fever (a paroxysm 
 every third day) ; these groups (maturing on successive days) cause 
 quotidian fever. 
 
 COCCIDIUM OVIFORME. 
 
 Description. — The coccidia are small bodies from 30 to 40 [i 
 in length and from 1 5 to 20 fi in width, having a thick and rather 
 glistening capsule. The body is filled with granular material, 
 which is not rarely aggregated in the center. Outside the body 
 sporulation takes place. The granular protoplasm divides into 
 four rounded capsulated spores, each containing a granular resting- 
 body lying in the concavity of a sickle-shaped daughter-spore. 
 Sometimes endogenous sporulation is said to occur, the parasite 
 simply breaking up into a large number of sickle-shaped bodies. 
 The term psorospermice is applied to the rounded spores found in 
 the coccidium (Fig. 108). 
 
 Occurrence and Pathogenesis. — The coccidium is a fve- 
 
 Fig. 108.— Coccidia from the human liver (Leuckart). 
 
 quent parasite of rabbits and certain other animals. It leads to 
 the formation of yellowish nodules in the liver. It is an intra- 
 cellular parasite, first invading the cells of the biliary passages 
 and afterward the surrounding hepatic cells as well (Fig. 109). 
 Less frequently it occurs in the intestinal tract, giving rise to 
 nodular thickenings or ulcerations. 
 
 The parasite escapes from the body in the stools and then un- 
 dergoes sporulation. Other animals are probably infected by 
 ingestion of the spores or sporulating coccidia. Occasionally the 
 disease decimates rabbits or guinea-pigs kept in confinement. The 
 
270 TEXT-BOOK OF PATHOLOGY. 
 
 animals become languid, lose their appetite, emaciate, and have 
 fever. Later they suffer from convulsions, stupor, or coma, and 
 die in this condition. 
 
 A few cases of coccidial disease of the liver have been observed 
 in man. The lesions present themselves as cystic nodules spring- 
 ing from the bile-ducts, or less commonly as a diffuse involvement 
 
 
 7 
 f 
 
 Fig. 109.— Coccidia in the wall of the bile-duct and the adjacent hepatic structure of a 
 rabbit. 
 
 of the liver with cirrhosis and causing jaundice. Coccidial lesions 
 of the intestines have also been discovered in man, and less com- 
 monly invasion of the heart, of the kidneys, and other parts. 
 
 The close association of the organism with the lesions, and the 
 number of organisms discovered in the tissues, justify the belief 
 that it is the specific cause of the lesions. 
 
 The coccidium of the intestinal tract is generally smaller and 
 the sporulation more rapid than that of the hepatic form. It was 
 therefore supposed by Leuckart to be a special variety, and has 
 been called Goccidiwm p&rforans. More recently this has been 
 regarded as identical with the ordinary form. 
 
 ANIMAL PARASITES AND CARCINOMA. 
 
 The theory that carcinoma and other malignant tumors are due 
 to some form of infection is by no means of recent origin. Bac- 
 teriologists sought to isolate micro-organisms without success; and 
 later observers have turned their attention to certain structures 
 supposed to be animal organisms. 
 
 In 1889 Thonui found in the protoplasm and nuclei of carci- 
 noma-cells bodies which he regarded as coccidia ; and about the 
 
ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 271 
 
 same time Malassez and Albarran found similar structures in the 
 cells of an epithelioma of the maxilla. Darier found bodies of 
 the same kind in Paget' s disease of the nipple, and many sub- 
 sequent investigators have described more or less similar forma- 
 tions. 
 
 Among these supposed protozoan organisms some are intranu- 
 clear, some extranuclear, and some wholly extracellular. Among 
 the intranuclear and extranuclear cell-inclosures Sj orb ring de- 
 scribed round bodies which tend to grow and eventually spor- 
 ulate, forming cystic bodies containing twenty to thirty spores 
 (spore-cysts). These structures resemble the parasites of silk- 
 worm disease, and are classified by Sjorbring as microsporidia. 
 Sudakewitsch and others have described bodies more closely 
 resembling coccidia in their sharp, double contour and the pres- 
 ence of peculiar, sometimes sickle-shaped, bodies within. Pod- 
 wyssozki and Sawtschenko described forms differing from coccidia 
 in the absence of a distinct capsule, and resembling rather the 
 amebae, such as those occurring in the blood of birds and in 
 malaria. The views of these authors, particularly Sawtschenko, 
 have, however, undergone some modification in their several con- 
 tributions. Puffer, Plimmer, and Walker described structures 
 occurring only in the protoplasm of the cells, and resembling 
 coccidia, but forming neither spores nor sickle-shaped bodies, but 
 multiplying by direct division (Fig. 110). Many of the investi- 
 gators lay stress upon the behavior of the supposed parasites 
 
 Fig. 110.— Inclusions in cancer-cells : a and b, early stages of " parasitic " bodies ; c, 
 late stages, showing division by segmentation; d, cancer-cell containing leukocytes 
 (Ruffer). 
 
 toward stains. Thus Puffer and his collaborators point out that 
 the nuclei of their parasites do not receive basic stains like cell- 
 nuclei, but the acid-stains, and the body of the parasite is scarcely 
 at all stained. This point, however, has certainly been overesti- 
 mated as an indication of the parasitic nature of the bodies. De- 
 generated cells notoriously vary from normal ones in this respect. 
 The supposed spores of Sjorbring and others are very probably 
 products of degeneration, as Puffer and others contend ; and it 
 lias not yet been shown by anyone that all of these supposed para- 
 sites are not degenerated leukocytes or epithelial cells included 
 within the cancer-cells or simple products of cell-degeneration. 
 
272 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 Some authorities have advanced a theory quite different from 
 the above, holding that the cancer-cells themselves are parasitic 
 organisms. Korotneff distinguishes three kinds of organisms in 
 carcinoma : amebse, eoccidia, and gregarinidse. The ameboid form, 
 which he calls Amoeba caehexica, has a granular protoplasm and a 
 clear nucleus. It is actively motile, and may leave the epithelial 
 cells to enter the connective tissue. After establishing itself it 
 becomes encysted, the nucleus breaking up and the protoplasm 
 becoming more dense. Zobids and sporozooids result, the former 
 going on to the formation of a gregarina(Rhopalo- 
 cephalus carcinomatosus) (Fig. Ill), or a coccid- 
 ium, the latter forming new amebae. Some of 
 the structures figured by Korotneff are undoubt- 
 edly merely cancer-cells. A few authors claim 
 to have found parasites of various kinds in the 
 blood of cases of carcinoma. 
 
 A close study of the so-called parasites of 
 carcinoma shows that they are probably the re- 
 sult of cell-degenerations. This is evident in 
 part from the fact that they are most abundant 
 in degenerated carcinomata or in degenerated 
 areas of carcinomata, and from the very diver- 
 gent character of the forms described. Further- 
 more, similar structures occur in other tumors, 
 some of them eminently benign, and even in 
 ordinary inflammatory tissue. Russell, in 1890, 
 described certain rounded bodies that stain intensely with fuchsin, 
 and occur in or between the cells. These " fuchsin-bodies " are 
 certainly not parasites, but cell-productions. 
 
 Recently it has been urged that certain blastomyeetes, resembling 
 the ordinary yeast-fungus, if not identical with it, are the actual 
 cause of cancer, and that many of the bodies formerly regarded as 
 protozoa are blastomyeetes. This view lacks confirmation. 
 
 Fig 111.— Rhopa- 
 locephalus carcino- 
 matosus (Korotneff). 
 
 ANIMAL PARASITES AND MOLLUSCUM CONTAGIOSUM. 
 
 Definition. — Molluscum, or Epithelioma Contagiosum, is an 
 infectious disease of the skin marked by the appearance of white 
 and pink papules. 
 
 Etiology. — The cause of this disease is, no doubt, a micro- 
 organism of some sort. Its contagiousness is evidenced by the 
 occurrence of epidemics in houses or asylums, by the occurrence 
 nf accidental inoculations, and by direct experiments. The incu- 
 bation-period seems to be a long one — sometimes extending to- 
 several months. The lesions have been found to contain small 
 bodies whose resemblance to eoccidia was long ago pointed out 
 by Virchow. It is uncertain whether these are really parasites or 
 

 ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 273 
 
 epithelial degenerations. Some authors are positive regarding the 
 parasitic nature of the bodies ; others are equally convinced of 
 their nonparasitic character. 
 
 Appearances. — The disease occurs as single or, more fre- 
 quently, multiple papules, at first quite small, but later becoming 
 nodules of considerable size. In the larger a central depression or 
 umbilication is seen, and on pressure cheesy matter may be ex- 
 pressed from this. After reaching about 3 or 4 mm. in diameter 
 they remain stationary, or undergo softening and suppuration. 
 In exceptional cases the tumor may reach the size of a small 
 orange. 
 
 Seats. — The disease occurs on the face, neck, chest, genitals, 
 or sometimes scattered over the whole body, sparing only the 
 palms and soles. The lesions have occasionally been found on the 
 mucous membranes. 
 
 Structure. — Microscopically the lesions of this disease are 
 found to consist of epithelial proliferations having a somewhat 
 acinous arrangement, a hair-follicle occupying the center of each 
 group of cells. The interior of the nodules is filled with soft, 
 cheesy matter which may be expressed. The epithelial cells are 
 arranged in several layers, the upper being normal cells with large 
 nuclei, the deeper layers showing beside the nucleus small drop- 
 lets, or rounded spherules, the so-called molluseum-bodies. These 
 bodies grow in size, and may be so large as to fill the cell, pushing 
 the protoplasm and nucleus to one side. In this process the cell- 
 wall and protoplasm become horny, and practically the entire 
 body consists of the enlarged molluscum-corpuscle. Certain 
 granulations and more or less definite segmentations within these 
 bodies have been described as sporulating conditions. The nature 
 of these bodies is very doubtful ; they may be coccidia, gregarin- 
 idse, or ameboid bodies ; but they may also, as some contend, be 
 the results of epithelial degenerations. 
 
 VARIOLA AND VACCINIA. 
 
 A number of bacteria have been described from time to time 
 in these diseases, and various micrococci in particular have been 
 found in the pustules, but none of these can be considered as 
 specific. Several bacilli have been recently described. 
 
 In 1887, Pfeiffer and van der Loeff independently described a 
 protozoan parasite of the order sporozoa, which occurs in the cells 
 of the rete. This organism was found in variola as well as in vac- 
 cinia. Pfeiffer, Guarnieri, and other investigators found that by 
 inoculation of the cornea of rabbits large numbers of the supposed 
 parasites make their appearance in the epithelial cells. These organ- 
 isms are rounded bodies lying in the protoplasm of the cells, some- 
 times singly, sometimes in groups of two or three. Slow ameboid 
 
 18 
 
274 TEXT-BOOK OF PATHOLOGY. 
 
 movements are visible aud the organisms present one or more 
 nuclei. Spore-formation has been observed by several investiga- 
 tors. Guarnieri suggested the name ( 'ytoryctes variolce sen vaccinae. 
 The nature and the significance of these supposed organisms have 
 not vet been positively determined. Some authorities look upon 
 them as products of cell-degeneration. 
 
 Secondary infections with various micrococci or other organ- 
 isms are common in small-pox and vaccination, and may play an 
 important part in pustulation, and in the more definite complica- 
 tions, such as septicemia, pneumonia, hemorrhagic septicemia, ery- 
 sipelas, and the like. 
 
 VARICELLA. 
 
 The etiology of chicken-pox is even less definitely determined 
 than that of small-pox. Pfeiffer discovered the same organism 
 described by him in vaccinia and variola. Bacteria of one sort or 
 another have been occasionally found. 
 
 MEASLES, SCARLET FEVER, AND OTHER DISEASES. 
 
 Certain investigators have discovered bodies having some of 
 the appearances of protozoa in measles, scarlet fever, pernicious 
 anemia, leukemia, sarcomata of various sorts, and in a number of 
 other diseases. These observations, however, do not merit further 
 discussion in this place. Future investigations must decide whether 
 they have been accurate or not. 
 
 CERCOMONAS INTESTINALIS. 
 
 This organism is a pear-shaped body with a sharp anterior 
 extremity provided with a delicate short cilium. The broader 
 posterior end is provided with a long, tail-like flagellum. A 
 larger and a smaller variety have been described (Fig. 112). The 
 
 Fig. 112. — Cercomonas intestinalis : a, larger, 6, smaller variety (Davaine). 
 
 former is the variety usually found, and is from 10 to 12 u in 
 length. A minute oval aperture has been found at the anterior 
 extremity. 
 
 Significance. — The organism has been discovered in great num- 
 bers in various diarrheal conditions, especially in cholera. It is 
 not known to have pathogenic powers. 
 
ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 275 
 
 CERCOMONAS COLI HOMINIS. 
 
 A single observation of this organism was made by May. The 
 body of the parasite was not quite the size of a red corpuscle ; 
 rather granular and glistening and slightly greenish. It was 
 spindle-shaped, the anterior end more blunt than the posterior. 
 Four cilia were found attached to this end, and upon one side of 
 the organism was seen an undulating membrane. In the same 
 case smaller bodies, less developed and probably younger para- 
 sites, were discovered. The patient suffered from carcinoma of 
 the stomach and chronic diarrhea. 
 
 TRICHOMONAS INTESTINALIS. 
 
 This organism is pear-shaped ; from 10 to 15 fi in length 
 and 7 // in breadth (Fig. 113), The anterior end is blunt; the 
 posterior end is prolonged into a sharp, tail-like projection. 
 
 Fig. 113.— Trichomonas intestinalis (Zunker). 
 
 The body is granular and contains one or two bodies resembling 
 vacuoles. Near the anterior end at one side may be seen a row 
 of ten or twelve cilia, which give the organism active motility. It 
 has also ameboid movements. 
 
 Significance. — This organism has been found in cases of diar- 
 rhea, but its significance is doubtful. 
 
 TRICHOMONAS VAGINALIS. 
 
 This form is rather smaller than the last, with an attenuated 
 caudal end and a more blunt anterior portion, provided with three 
 flagella ; there is a lateral undulating membrane with six or seven 
 short cilia. 
 
 Significance. — The organism has been found in cases of vagini- 
 tis due to various causes, but also in the absence of evident 
 disease. 
 
 OTHER FORMS OF TRICHOMONAS. 
 
 Sternberg has found several forms in the mouth, and especially 
 about the teeth. These have been termed Trichomonas flagellata, 
 Trichomonas caudata, and Trichomonas elongata. 
 
276 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 BALANTIDIUM COLI. 
 
 Balantidium or Paramecium coli is a rounded body from 
 7 to 10 (i in length and slightly less in breadth (Fig. 114). It 
 is surrounded by a coat of cilia closely set. 
 There is an oral aperture at one end and an anal 
 opening at the other. The substance of the 
 parasite is granular, and contains a nucleus and 
 two contractile vacuoles besides various foreign 
 matters. Encysted forms with a thickened capsule 
 have been described. 
 
 Significance. — The hog is the natural host of 
 this parasite. Man is probably infected through 
 drinking-water or contaminated food-stuffs. It is 
 found particularly in northern countries of Europe, 
 and occurs in cases of diarrhea principally involv- 
 ing the large intestine. Chronic catarrhal inflam- 
 mation and dysenteric lesions have been described. The organism 
 is probably irritating, but whether pathogenic or not is unknown. 
 
 Fig. 114.— Balan 
 tidium coli (Malm 
 sten). 
 
 MEGASTOMA ENTERICUM. 
 
 This organism in its active state is irregularly pear-shaped, and 
 presents at its broad end a cup-shaped depression situated obliquely 
 at one side (Fig. 115). On the anterior edge of the depression are 
 
 Fig. 115.— Megastonia eutericum from the intestines of a mouse (Grassi and Schewiakoff). 
 
 attached two long cilia, and at one point of the posterior lip are 
 two pairs of cilia. In the base of the depression are seen two 
 vesicular structures (nuclei) united by a band. The protoplasm 
 
ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 277 
 
 is finely granular and is surrounded by a delicate capsule. When 
 free the organism is capable of rather rapid motion, but in the in- 
 testine it is attached to the epithelial cells by its cup-shaped 
 depression. The organism exists in this form in the duodenum 
 and jejunum. In the colon or other unfavorable situations it 
 forms oval encysted bodies showing the nuclei and cilia within. 
 Significance. — Megastoma is a frequent parasite of the mouse, 
 but has been found in the intestines of other animals, and occasion- 
 ally in man. It has been found especially in chronic diarrheal 
 conditions, and at times appears in the stools in immense numbers. 
 No definite lesions have been found, and the pathogenicity of the 
 germ is uncertain. 
 
 CESTODES OR TAPE=WORMS. 
 
 General Biology. — The life-history of the different forms 
 of tape-worms is much the same. They have two states of exist- 
 ence, the larval, which is generally found in one species of ani- 
 mals, and the adult state, usually occurring in another species. It 
 is supposed that in the case of one or two tape-worms an inter- 
 mediary host is unnecessary, but this is doubtful. The adult 
 worm, or tape-worm, occupies the intestinal tract of man or the 
 
 1 2 
 
 Fig. 116 —Segments of (1) Taenia saginata, (2) Bothriocephalus latus, and (3) Taenia solium, 
 showing arrangement of uterus. 
 
 lower animals. It consists of a head, by which the worm fastens 
 itself to the mucous surface ; and after the head, a neck of greater 
 or less size and length, and a body consisting of separate links or 
 
278 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 proglottides. The latter represent complete organisms, containing 
 . a complicated genital apparatus, hermaphroditic in nature, which 
 produces numerous eggs. The eggs are partly discharged from 
 the segments in the intestinal tract through a genital j>ore, but 
 especially escape into the outer world when the ripe segments are 
 separated from the body of the worm, are discharged from the 
 bowel, and subsequently rupture and scatter the contained ova 
 (Fig. 116). The egg or ovum encloses an immature larval organism, 
 which, when received into a suitable host, penetrates the walls of 
 the stomach or intestine and finds its way to the muscles or organs, 
 where it imbeds itself and forms the well-known measles (see Figs. 
 11(3 and 117). These are seen with the naked eve as small cvst- 
 
 Fig. 117.— Eggs of various worms found in the alimentary canal of man: a, Ascaris 
 lumbricoides ; b, c, Oxyuris vermicularis ; d. Trichoeephalus dispar ; e, Anchylostoma 
 duodenale; f, Distoma hepaticum ; G, Distoma lanceolatum ; h, Taenia solium: i, Taenia 
 saginata; K, Bothrioeephalus latus ; X 400. 
 
 like bodies lying between the muscle-fibers. They contain a scolex 
 or head, like that of the adult-worm, inverted into a sac filled with 
 clear, watery liquid. When the measles or cysticen-i occur in hol- 
 low cavities, such as the ventricles of the brain, they may reach 
 considerable size. They differ somewhat in different forms of 
 tape-worm, as will be described in connection with the individual 
 species. When flesh infested with larval tape-worms is eaten by 
 man or some suitable animal, the cysts are dissolved and the scolex 
 fastens itself upon the mucous membrane of the intestine. The 
 body of the worm is then slowly or rapidly formed. 
 
 Man is the host of tape-worms of adult or of larval type ; most 
 frequently the former. In one case, the Taenia echinococcus, only 
 the larval worm occurs in the human body, in the form of hydatid 
 cysts. 
 
ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 279 
 
 TAENIA SOLIUM. 
 
 This form occurs in the adult state in man as a worm two or 
 three meters in length ; and in the hog or rarely in man in its 
 larval condition. The head is about the size of a pin-head and 
 very dark. Anteriorly it has a rostellum armed with a double 
 row of from twenty-six to thirty hook- 
 lets. At the sides of the head are four 
 suckers (Fig. 118). Attached to the 
 head is a neck of thread-like appearance, 
 which terminates in the immature seg- 
 ments of the anterior part of the body. 
 The segments at first are broad and 
 short, but become longer in proportion 
 to the breadth toward the posterior end. 
 The sexually mature segments are found 
 at the middle and the posterior end of 
 the worm. They contain a uterus consist- 
 ing of a median tube and six to twelve 
 lateral branches (Fig. 116). The genital 
 pore is found at one side of the segment, fig. us.— Head of Taenia solium 
 
 f iii, , • • • (Mosler and Peiper). 
 
 irregularly alternating m successive pro- 
 glottides. The eggs, which may be squeezed from the segments 
 or obtained free in the feces, are rather oval or spherical, from 30 
 to 35 [x in diameter, and consist of a peripheral striated zone and 
 a central granular portion, showing indistinctly six lines represent- 
 ing hooklets (Fig. 117). Groups of segments may be discharged 
 from time to time, but this is not frequent ; the discharge of 
 single segments is less frequent. The proglottides have indepen- 
 dent movement, and may sometimes be seen to move about upon 
 the bed-clothes. 
 
 The I^arval State in Man. — When the ova are taken into 
 the stomach the shell is digested and the embryo with its six 
 hooklets is set free. This penetrates the wall of the stomach or 
 intestine, and in some uncertain manner reaches the muscles or 
 organs, where it effects a lodgement. The hooklets are discarded 
 and a little cyst containing clear liquid is formed, and at one point 
 may be found a bud-like projection into the sac. This develops 
 a scolex or head, which eventually becomes identical with the head 
 of the fully formed worm. The cyst may be surrounded by a 
 wall of reactive connective tissue. The duration of this process 
 of formation of the cysticercus varies somewhat (five to ten or 
 twelve weeks). The size of the cysts in the muscles varies from 
 minute points to that of a pea. In the ventricles of the brain 
 the cysticerci may be as large as a small cherry. Occasionally 
 compound or racemose cysticerci are met with. 
 
 Among the seats of special interest are the brain, the muscles, 
 
280 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 especially the peripheral muscles, tongue, and heart-muscle, and 
 the subcutaneous tissues. 
 
 The Adult Worm in Man. — When measled meat (hog, occa- 
 sionally that of deer, sheep, and other animals) is eaten in insuf- 
 ficiently cooked form by man the capsules 
 of the cysticerci (Fig. 119) are dissolved, 
 the scolex attaches itself to the mucous 
 membrane of the small intestine, and the 
 worm is developed. Usually there is but 
 one worm ; occasionally several occur in the 
 same case. The worm may remain in the 
 intestine for years, despite repeated eiforts 
 to dislodge it. In other cases it is spon- 
 taneously discharged. Reverse peristalsis 
 may cause portions to be carried to the 
 stomach, whence they may be discharged 
 by vomiting. 
 
 Geographical Distribution. — The 
 Taenia solium is an exceedingly rare para- 
 site in America. It seems to be more 
 common in certain parts of Europe. 
 
 Fig. 119.— Measled pork ; two- 
 thirds the natural size (Leuck- 
 art). 
 
 T7EN1A SAQINATA. 
 
 This form is the common tape-worm of man. It is larger than 
 the preceding form, being from four to eight meters in length. 
 The head is large (2 mm. broad), cuboidal, and provided with 
 four suckers. There is an abortive rostellum, but no hooklets 
 (Fig. 120). The neck is short, and the segments rapidly become 
 
 
 1*10. 120.— Head of Tenia saginata 
 (Mosler and Peiper). 
 
 Fir.. 121.— Cysticercus Ta-nire sagi- 
 natoe ; natural size (Leuekart). 
 
 broader than long, but in the posterior half of the worm, where 
 the sexually mature proglottides are found, the segments are longer 
 than broad. The uterus is formed like that of the Taenia solium, 
 but the lateral branches are more numerous (twenty to thirty, and 
 
ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 281 
 
 often dichotomously branched) (Fig. 116). The eggs are rather 
 more oval and larger than those of Taenia solium, but otherwise 
 closely resemble the latter. 
 
 The larval form, or cysticercus, occurs in the ox and some- 
 times in the giraffe. The measles are found in the muscles, liver, 
 lungs, and occasionally in other organs (Fig. 121). 
 
 The adult form occurs only in man, and occupies the small 
 intestine. The presence of the worm does not seem to occasion 
 any definite disease of the intestines, except in rare cases, when a 
 number are found present in a coiled mass, or when one worm is 
 similarly coiled. This may cause intestinal obstruction, and pos- 
 sibly in exceptional instances rupture of the bowel. 
 
 The symptoms ascribed to tape-worms are some of them doubt- 
 less reflex ; but it is noteworthy that they are often absent until 
 the patient discovers segments in the stools. (Further refer- 
 ence to possible pathologic results is made in the discussion of 
 Bothriocephalus latus.) It is an exceedingly 
 common parasite in certain countries (Africa 
 and the East), but is more or less commonly 
 found in all parts of the world. 
 
 TVENIA NANA. 
 
 This form, sometimes called the dwarf 
 tape-worm, in its adult state is about 2.5 cm. 
 in length (Figs. 122 and 123). It has a 
 rounded head, with a rostellum that may be 
 protruded or retracted and that bears a single 
 circle of twenty-two to twenty-seven hook- 
 lets. The mature segments of the posterior 
 end of the worm have a yellow color. The 
 genital pore is on the same side in all the 
 segments. The eggs are oval in shape, 
 whitish and transparent ; they are from 47 
 to 48 n long and 38 to 
 
 139 fj. broad. 
 The intermediary host 
 of this form is not cer- 
 tainly known, but is sup- 
 posed to be some form 
 of insect or snail. The 
 adult parasite alone oc- 
 curs in man. The head 
 fig. 122.— Taenia nana, attaches itself deeply in FlG 123 _ T8enia nana 
 
 fe^andPefper) ^ (M ° S " the mucOUS membrane mu /h enlarged (Mosler 
 f j?.ii i i and reiper). 
 
 oi the bowel and may 
 cause considerable local disturbance. There are usually sev- 
 
282 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 eral or many worms associated ; sometimes there may be several 
 thousands. 
 
 T/ENIA ELLIPT1CA. 
 
 This form is identical with Tcenia cucu- 
 merina. It is a common parasite of dogs 
 and cats. The length is from 15 to 30 cm. ; 
 the head is provided with a rostellum bear- 
 ing sixty booklets ranged in four rows ; the 
 rostellum may be protruded or retracted. At 
 the junction of the segments there is a consid- 
 erable contraction of the diameter of the worm, 
 giving the body a markedly linked character 
 (Fig. 1 24). The mature segments have a red- 
 dish-brown color from the presence of the eggs. 
 Each proglottide has a double sexual appa- 
 ratus with a genital pore at each side. The 
 intermediary host is probably the louse of 
 the dog and occasionally the flea. The adult 
 worm usually occurs in numbers in the intes- 
 tinal tract, and in some cases seems to pro- 
 Fl (kosiel T ana PefpS ica duce inflammatory disturbances. 
 
 T/ENIA FLAVOPUNCTATA. 
 
 This form (probably identical with Taenia diminuta) is from 
 20 to 30 cm. in length ; the head is elongated and verges gradu- 
 ally into the neck. The suckers are small, but there is neither 
 rostellum nor hooklets. The segments are marked by a yellowish 
 spot which represents the male genital organs. 
 
 T/ENIA MADAGASCARIENSIS. 
 
 This form is from 25 to 30 cm. in length ; the head is marked 
 by four large suckers and a rostellum bearing hooklets. 
 
 OTHER FORMS OF T/ENIA. 
 
 Besides these more or less satisfactorily described forms, a 
 number of uncertain varieties have been reported, such as the 
 Tcenia tenella, Tcenia AJgeriana, etc. 
 
 T/ENIA ECHINOCOCCUS. 
 
 The Taenia echinococcus in its adult form occurs in the intes- 
 tinal tract of the dog, the larval condition occurring in man and in 
 some of the lower animals. The mature worm is about 4 or 5 
 mm. in length, and consists of four segments (Fig. 125). The 
 head, which constitutes the first, is provided with four suckers and 
 a rostellum bearing fourteen to twenty-five hooklets in a double 
 
ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 283 
 
 row. The second segment is about the breadth of the head, but 
 somewhat shorter. The third is considerably larger; and the 
 fourth is the largest of all, constituting about 
 one-half or two-thirds of the entire worm. The 
 uterus consists of a median portion with few 
 lateral branches. The eggs are oval, from 17 
 to 30 [x in diameter, and the shell is rather 
 thinner than in the eggs of other tape-worms. 
 
 The adult worm occurs in great numbers in 
 the small intestine of the dog. It is also found 
 in the wolf and fox, and occasionally in other 
 animals. 
 
 The Bchinococcus Cyst. — This term is 
 applied to the structure in which the larval 
 worm is embedded. Three varieties have been 
 distinguished. 
 
 (a) Echinococcus Scolicipariens. — When the 
 eggs reach the stomach of man the embryo is 
 freed and penetrates the mucous membrane. It is carried by the 
 blood or lymphatic stream to the liver or other organs, where it 
 develops an eehinococcus-cyst (Fig. 126). 
 
 Fig. 125.— Taenia echi- 
 nococcus ; enlarged 
 (Mosler and Peiper). 
 
 Fig. 126.— Echinococcus-cyst of the liver (from a specimen in the Museum of the Phila- 
 delphia Hospital.) 
 
 The wall of the cyst is composed of two layers, an outer cuticular 
 and an inner parenchymatous, granulocellular layer. The paren- 
 chymatous layer is important as a budding or brood-membrane. 
 After some weeks there may be seen upon its surface small buds 
 or projections, which later become hollowed by a central excava- 
 tion and form a small cyst ; secondary budlets spring from the 
 surface of this and gradually form embryonal heads or scolices 
 (Fig. 127). When mature these are retracted or inverted into 
 the cavity or cyst of the original bud. In this manner a large 
 number of heads are formed upon the inner wall of the original 
 
284 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 Fig. 127.— Formation of 
 buds upon the parenchyma- 
 tous layer (Leuckart). 
 
 echinococcus-cyst, the cavity of the cyst at the same time increas- 
 ing in size and being distended with characteristic liquid. This 
 is a clear fluid, having a specific gravity of 
 from 1009 to 1015 and a neutral or alka- 
 line reaction, and containing no albumin or 
 only traces, but a considerable quantity of 
 chlorid of sodium. Sugar is sometimes 
 found in the fluid. 
 
 (b) Echinococcus Hydatidosus. — Besides 
 this form of simple cyst with buds attached 
 to the inner wall, there are cases in which 
 daughter-cysts and even granddaughter- 
 cysts are formed. The daughter-cysts are found within the original 
 cyst, and are probably produced by cystic degeneration of the buds 
 already described ; and possibly in some cases by simple separation 
 of the buds. They are variable in size, sometimes becoming as 
 large as a nut or egg, and when granddaughter-cysts are contained 
 within them the size may be even greater. To this form the term 
 Echinococcus hydatidosus or Echinococcus endogenes is applicable. 
 
 In a subvariety of this form secondary cysts are produced out- 
 side the original wall. These are formed by a process of soft- 
 ening in the cuticular wall, with gradual projection of the paren- 
 chymatous layer toward the exterior and eventual rupture, with 
 formation of secondary cysts outside. 
 
 (c) Echinococcus Multilocularis. — In a third form of echinococ- 
 cus-disease there are numerous small cysts, from the size of a 
 grape-seed to that of a pea, embedded in connective tissue, and 
 altogether forming a more or less definite tumor-mass. On sec- 
 tion this presents an alveolar appearance, the cysts containing 
 somewhat gelatinous material. Careful examination of the inner 
 walls of the small cysts shows them to contain pigment and cal- 
 careous particles. Scolices, however, are absent for the most part, 
 
 Fig. 128.— Echinococcus multilocularis (Luschka). 
 
 the cysts being generally sterile. The term Echinococcus multi- 
 locularis is applied to this variety of disease (Fig. 128). Its forma- 
 tion is explained by the assumption that there are secondary pro- 
 
ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 285 
 
 liferations in an outward direction from the original cyst, rather 
 than a deposit of large numbers of ova or embryos. The whole 
 mass presents the appearance of a tumor, and not rarely central 
 necrosis and softening occur as in tumors. 
 
 Echinococcus cysts may continue to grow until they have reached 
 huge dimensions without undergoing any secondary changes. In 
 other cases the parasite may die and the growth may cease, 
 or active proliferation of the tissues around the cyst may lead to 
 early destruction. In still other cases suppurative change occurs 
 in the cyst or its wall. In all cases when the cyst reaches a cer- 
 tain size the tissues around produce a connective-tissue capsule of 
 greater or less thickness. When the parasite dies inspissation of 
 the liquid occurs, and it may eventually disappear or be converted 
 into a thick whitish material ; the cyst-walls and the connective- 
 tissue capsule at the same time shrivel and present peculiar con- 
 centric lamellations that are very characteristic. Eventually cal- 
 cification of the wall of the cyst and to a certain extent of its 
 contents takes place. 
 
 Seats. — Echinococcus cysts are most frequent in the liver. 
 They also occur in the lungs, kidneys, spleen, and omentum, and 
 less frequently in the brain or other parts of the nervous system. 
 The pathologic effects are produced by direct mechanical pressure. 
 
 The geographical distribution is extensive, but the dis- 
 ease is common only in restricted localities, especially in northern 
 countries (north of Europe, Iceland). 
 
 BOTHRIOCEPHALIC LATUS. 
 
 The Bothriocephalic latus is the largest tape-worm of man, 
 reaching the length of from 5 to 9 m. The head is flattened 
 and club-shaped and presents two groove-like suckers at its sides 
 (Fig. 129). The neck is thin and gradually increases in diameter. 
 The ripe segments are quadrate, and are dis- 
 tinguished by a rosette-like formation of the 
 uterus, which is plainly visible in the center of 
 each proglottid (Fig. 116). The genital pore is 
 upon the flat surface of the segment and always 
 upon the same side of the worm. The eggs are 
 oval in shape and enclosed in a shell present- 
 ing a hinged lid at one pole. The intermedi- 
 ary host is some form of fish, most frequently 
 the pike. The eggs first undergo a certain 
 amount of development in water, the embryo neC k ^f ^othriocepli^ 
 becoming free and floating about or being pro- lus latus (Leuckart). 
 pelled by a ciliated outer covering and then 
 entering the digestive tract of fish. 
 
 The geographical distribution is comparatively restricted. 
 
286 TEXT-BOOK OF PATHOLOGY. 
 
 It is frequent in certain northern countries, as in Sweden, and in 
 parts of central Europe, especially in Switzerland. It is only 
 occasionally met with in America in immigrants. 
 
 Pathologic Physiology. — Local disturbances of the intes- 
 tines are not observed ; but persons harboring Bothriocephalus 
 sometimes suffer from profound anemia. This has been attributed 
 to poisonous substances elaborated by the worm, or resulting from 
 decomposition of its segments. Similar anemia occasionally ac- 
 companies other forms of tape-worm. 
 
 BOTHRIOCEPHALUS CORDATUS. 
 
 This variety is much smaller than the last, the maximum being 
 from 1 to 1.25 m. The head is short, broad, and heart-shaped, 
 and the suckers are placed upon the flat surface. The uterine 
 structure differs from that of Bothriocephalus latus in being nar- 
 rower and more elongated, and also in having lateral branches. 
 The body of the worm contains granular calcareous matter. 
 
 BOTHRIOCEPHALUS CRIST ATUS. 
 
 This form is about 3 m. in length, and is distinguished by two 
 crest-like projections upon the head. These are covered with 
 numerous small papilla?. There are no definite suckers, and the 
 head contains abundant granular calcareous matter. 
 
 BOTHRIOCEPHALUS LIGULOIDES. 
 
 This variety occurs only in the larval form in man. It has 
 been found in the region of the loins and in the tissues about the 
 eyes. The head of the worm is distinguished by a papilla-like 
 projection. 
 
 NEMATODES, OR ROUND=WORMS. 
 
 ASCARIS LUMBRICOIDES. 
 
 The Ascaris lumbricoides, or ordinary round-worm, is one of 
 the most frequent intestinal parasites. The male may reach a 
 length of 25 cm. and a thickness of 2 to 4 mm. ; the female is 
 longer, up to 40 cm., and thicker, up to 5 or G mm. The body 
 of the worm is brownish or sometimes pinkish in color, and pre- 
 sents parallel ridges or rings somewhat like those of the earth- 
 worm. The head is provided with three rounded prominences or 
 lips, between which the mouth is placed (Fig. 130). The male 
 shows two chitinous spicules at the cloaca. The eggs of the worm 
 are produced in great numbers; they are covered with a tough 
 shell, and surrounding this is a clear material in an irregular mass. 
 The contents of the eggs consist of agranular material, sometimes 
 showing the linear outlines of an embryo. 
 
ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 287 
 
 The ascaris develops in man from swallowing of the 
 infested drinking-water or food. The parasites may be 
 singly or in numbers. They occupy the 
 small intestine, but frequently migrate, 
 entering the gall-ducts, the stomach, the 
 esophagus, and even the larynx or nasal 
 cavities. They may give rise to violent 
 symptoms by obstruction of these pas- 
 sage-ways, or when in numbers or 
 united in masses even intestinal obstruc- 
 tion may be caused. Occasionally abscess- 
 cavities containing lumbricoids are found 
 in connection with ulcerations and per- 
 foration of the intestines. These abscesses 
 were believed by older authors to be 
 caused by the worms ; at the present time 
 it is more generally held that the worms 
 play no important part, their presence 
 being due only to their coincidence in the 
 intestine. 
 
 ASCARIS MYSTAX. 
 
 This form, which is common in cats 
 and dogs, is rarely met with in man. It 
 is much smaller than the ordinary round- 
 worm, the male reaching a length of 45 or 
 60 mm., and the female 120 or 130 mm. 
 The head is distinguished by two lateral 
 wing-like projections composed of chitin- 
 ous material. 
 
 eggs in 
 present 
 
 ASCARIS MARATIMA. 
 
 Fig. 130.— Ascaris lumbri- 
 coides : A, female : B, male ; C, 
 
 This form has been observed but once, ffitf$Xffi™'$tev3£i 
 and the female alone was found. 
 
 OXYURIS VERMICULARIS. 
 
 The oxyuris, seat- worm, or pin-worm, is one of the commonest 
 parasites of man. The male is 2.5 to 5 mm. in length ; the female, 
 10 to 12 mm. (Fig. 131). The posterior end of the male is blunt 
 and curved upon itself; in the female it is elongated. The eggs 
 of the oxyuris, which are produced in great numbers, are oval or 
 elliptical and about 5 p. long. The embryo is visible within as 
 a lobulated body. The parasite is developed directly from the 
 eggs. When these are swallowed the outer coating is dissolved 
 in the stomach and the embryos escape, to reach their full de- 
 velopment in the small intestine. The impregnation occurs in 
 the small intestine and within a short time after the swallowing 
 
288 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 of the eggs. After impregnation and ripening the female para- 
 sites move toward the rectum and may be discharged, or may 
 leave by their own movements. The life 
 of the worm is short, but there is always 
 the possibility of reinfection. 
 
 Oxyuris is especially common in child- 
 hood. It is probable that the worms 
 sometimes cause inflammatory troubles. 
 In cases in which they accumulate in num- 
 bers a form of verminous diarrhea may be 
 produced. In female children vaginitis 
 frequently results from the migration 
 of the parasites into the vagina. 
 
 Fig. 131.— Oxyuris vermicu 
 laris : a, female ; b, male (Mos 
 ler and Peiper). 
 
 TRICHINA SPIRALIS. 
 
 The Trichina spiralis occurs in its larval form in the muscles 
 or organs of man and in the lower animals ; in the adult form it is 
 found in the intestines of man or animals. 
 
 The adult male is about 1.5 mm. in length and 0.14 mm. in 
 thickness. At the posterior end there is a retractile cloaca flanked 
 by two projections. The female is 2 to 4 mm. in length and 0.6 
 mm. in thickness. The eggs are provided with a very thin shell, 
 and the embryos escape from this within the uterus. They are 
 produced in immense numbers. The young embryos found in the 
 intestinal tract are from 0.1 to 0.16 mm. in length, the anterior 
 end thicker than the posterior. In part they escape with the 
 feces, and die ; the greater part pene- 
 b trate the intestinal wall and are car- 
 
 ried to various parts of the system, 
 embedding themselves especially in 
 the muscles, where they undergo 
 further changes. Here the organism 
 coils itself and becomes surrounded 
 with a capsule, which is at first trans- 
 parent, but may subsequently undergo 
 calcareous change and become opaque 
 (Fig. 132). 
 
 Trichina? are acquired by man by 
 eating improperly cooked ham. The 
 capsules are digested and the larval trichinae set free. In the 
 small intestine they reach their maturity in about three days, dis- 
 charging the embryos, some of which die or escape with the feces, 
 while others bore their way into the mucous membrane. They 
 are disseminated throughout the body by their own migrations or 
 with the lymph- and blood-streams. 
 
 The favorite seat is the striated muscle-tissue, and they lie 
 
 Fig. 132— Trichina-capsule with 
 its connective-tissue covering: a, 
 early stage; b, calcined (Leuckart). 
 
ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 289 
 
 within the muscle-bundles themselves or less frequently between 
 them. They reach their destination in ten days after the primary 
 invasion, but subsequent crops are deposited as the young continue 
 to mature in the intestines. In two or three weeks they begin to 
 become encysted in the muscles. 
 
 When the embryos are liberated in the stomach and intestines 
 they occasion violent gastro-intestinal irritation, with vomiting, 
 diarrhea, and often more or less pronounced collapse. In their 
 later migration the worms set up intense muscular pains of rheu- 
 matoid character, with edematous swelling and fever. 
 
 Trichiniasis is common in all parts of the world, but has been 
 largely reduced by greater care in the cooking of pork. 
 
 
 ANKYLOSTOMA DUODENALE. 
 
 The Ankylostoma duodenale, or Dochmius duodenalis, is a 
 cylindrical worm, the female being from 7 to 16.5 mm. in length ; 
 the male, from 7 to 11.2 mm. The head is rounded, and is armed 
 with six sharp, hook-like teeth. The female is usually of a brown- 
 ish or reddish color, due to absorption of coloring-matter of the 
 blood. The eggs are easily distinguished, being elliptical-shaped, 
 from 0.056 to 0.063 mm. in length and 0.036 to 0.04 mm. in 
 thickness. The shell is separated from the contents, and the latter 
 have a granular appearance, are brownish, and in the state of 
 segmentation. The eggs may appear in the stools in great num- 
 
 Fig. 133.— Anchylostoma duodenale: a, male, natural size ; b, female, natural size ; c.male 
 magnified ; d, female magnified ; e, head, greatly magnified ; /, eggs (von Jaksch). 
 
 bers. The embryo is fully developed outside the body, and entering 
 the stomach and intestines of man there undergoes full develop- 
 ment (Fig. 133). 
 
 The adult worm occupies the small intestine. It may be 
 
 19 
 
290 TEXT-BOOK OF PATHOLOGY. 
 
 present in small or large numbers, and is usually rather firmly 
 attached to the mucous membrane. Changes in the latter, how- 
 ever, are not pronounced. 
 
 Patients harboring this parasite frequently become intensely 
 anemic. It was this parasite which Mas found in many cases of 
 Egyptian chlorosis, and it is the same organism that produced the 
 intense anemias (pernicious anemia) of the laborers engaged in 
 building the St. Gotthard tunnel. 
 
 ANGUILLULA INTESTINALIS AND RHABDITIS STERCORALS. 
 
 The Anguillula intestinalis occupies the intestinal tract and the 
 ducts communicating with it. It is an actively motile, cylindrical 
 organism about 1 mm. in length, the male somewhat smaller than 
 the female. In the latter the posterior extremity is drawn out to 
 a fine point and straight ; in the former it is thicker and curled 
 upon itself. Besides this distinction the male bears two spicules 
 projecting from the cloaca. The eggs are ellipsoid, 0.17 mm. in 
 length and 0.45 mm. in thickness, and present evidences of seg- 
 mentation or the formation of embryo within. The larval organ- 
 ism escapes from the egg and lives a certain length of time as a 
 nonparasitic body ; then becomes quiescent, until it is taken into 
 the intestinal tract. 
 
 Associated with this parasite and often in greater numbers is a 
 second form, the Anguillula, or Rhabditis stercoralis. This differs 
 from the Anguillula intestinalis in being smaller and less organ- 
 ized in structure. 
 
 These organisms have been found with special frequency in 
 Cochin China and other eastern countries, occurring in the 
 intestinal tract in cases of severe diarrhea. It is doubtful whether 
 they have definite pathologic significance. 
 
 TRICHOCEPHALUS DISPAR. 
 
 The anterior portion of this parasite is thin and thread-like, 
 while the posterior portion is thicker. The length of the worm is 
 
 Fig. 134.— Triehocephalus dispar ; natural size (Heller). 
 
 from 4 to 5 cm., the male being somewhat the smaller. The 
 thicker part of the male is curled upon itself and blunt at the 
 end, while that of the female is straight and more pointed. The 
 
ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 291 
 
 eggs are very characteristic, being brownish in color, covered with 
 a thick capsule, and having at either pole a button-like projection 
 (Fig. 117). The length of the egg is about 0.55 mm. 
 
 The parasite occupies the cecum in man, occasionally the vermi- 
 form appendix, and sometimes the small intestine. It is particu- 
 larly frequent in children in Syria and Egypt. It does not, as a 
 rule, produce serious disturbance. Recently it has been claimed 
 that the parasite causes considerable disturbance by abstracting 
 blood. 
 
 FILARIA MEDINENSIS. 
 
 The Filaria or Dracunculus Medinensis is a round-worm in- 
 festing the subcutaneous tissues and the skin. The male has 
 never been discovered. The female sometimes reaches a length 
 of 60 to 80 cm. ; it is yellowish in color and exceedingly elas- 
 tic. In general appearance it resembles a string of catgut. 
 The body of the worm contains a highly developed uterus, 
 which practically fills the cavity of the worm, the intestinal 
 tube being crowded to one side. The uterus is found to con- 
 tain innumerable small embryos ; these escape when the parasite 
 is ruptured. 
 
 The organism occurs very abundantly in tropical countries of 
 the old world, notably Arabia, along the coast of the Caspian Sea, 
 in Abyssinia, and Guinea. The parasite is sometimes called the 
 Guinea-worm. 
 
 The parasite infests the subcutaneous tissues, particularly those 
 of the lower extremities, and gives rise to inflammatory lesions 
 resembling carbuncles. The method of invasion and the life- 
 history of the organism are obscure. It is not improbable that 
 the embryos occur in water of swamps and enter directly through 
 the skin. Some authorities believe that the invasion occurs 
 through the gastro-intestinal tract. 
 
 FILARIA SANGUINIS HOMINIS. 
 
 Several varieties of filariae have been found in the blood and 
 are included under this generic term. The discovery of the 
 organism, or rather of the embryos, was made by Wucherer, in a 
 case of hematuria. 
 
 The embryos appear in the blood, urine, the lymph, and the 
 tissues as thread-like structures, varying in size in the different 
 varieties. The ordinary form has a thickness of about the 
 diameter of a red corpuscle, and is as much as 0.2 to 0.5 mm. 
 in length. It consists of a transparent sheath, almost completely 
 filled with the embryo, the ends, however, projecting a little 
 beyond the organism, in a sac-like fashion (Fig. 135). The em- 
 bryo is actively motile, squirming, thrashing, or curling and un- 
 
292 TEXT-BOOK OF PATHOLOGY. 
 
 curling itself rapidly, and thus producing more or less agitation 
 of the corpuscles or solid bodies in its vicinity. 
 
 The number of the embryos found in the blood varies greatly ; 
 in many cases a search through several cover-glass preparations 
 may be necessary to detect a single one. Usually they are more 
 
 
 ,-v- 
 
 SSiil 
 
 % 
 
 t ; 
 
 Fig. 135.— Filaria embryo, alive in the blood (F. P. Henry). 
 
 abundant. A feature of importance is that they occur only during 
 the night, unless the patient reverses the usual conditions and rests 
 during the day. 
 
 The adult worm is found only in the lymphatic channels ; it 
 reaches a length of 38 mm., and has a rounded oral orifice at the 
 anterior end. It produces embryos in great abundance, and these 
 are carried along in the circulation. 
 
 Fllariasis is particularly common in the warmer climates, but 
 is occasionally met with in this country, especially in the Southern 
 States. One of its most frequent forms is characterized clinically 
 by hematochyluria. The embryos in these cases may be found in 
 the blood and also in the chylous urine. Pathologically no gross 
 changes may be found, but there may be in other cases evident 
 distention of the lymphatic channels and blood-vessels of the 
 pelvis of the kidneys, ureters, or bladder; and the embryos may 
 be found in the substance of the kidneys or in the walls of the 
 blood-vessels. Another form of fllariasis is elephantiasis. In 
 these cases there is obstruction of the lymphatic vessels in con- 
 sequence of the presence of the parasites, of thrombi, or of inflam- 
 matory lesions, and as a result of these conditions dilatation of the 
 peripheral lymphatic vessels occurs. The skin may be ruptured 
 and chylous liquid may exude. The embryos may be found in 
 this on microscopic examination. 
 
 Manson has described three varieties of filari* — the original 
 form, or Filaria nodurna ; a second variety, in which the embryos 
 are found at any time, night or day, called Filaria perstans, which 
 he believes the cause of the sleeping-disease of Africa as well as 
 of certain skin diseases (Craw-Craw) ; and a third form, the Filaria 
 dittnia, which appears in the blood only during the day. 
 
ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 293 
 
 OTHER FORMS OF FILARI^E. 
 
 The Filaria loa is a small thread-like form met with in Africa 
 and sometimes in tropical America. It invades the eye, lying 
 beneath the conjunctiva. The Filaria lentis was found in the lens 
 in a case of cataract. The Filaria labialis was discovered in a 
 pustule on the lip of a student in Naples ; and the Filaria hominis 
 oris was found by Leidy in the mouth of a child. The Filaria 
 imrnitis is the common filaria of the dog, and has been found in 
 man. The Filaria bronckialis was found in bronchial lymphatic 
 glands in a case of phthisis, and has also been found in the trachea 
 and bronchi. 
 
 ECHINORRHYNCHUS GIQAS. 
 
 This is a large round-worm, the body being marked by distinct, 
 transverse, parallel rings. The male may be from 7 to 10 cm. in 
 length, the female from 31 to 50 cm. There is a retractile rostel- 
 lum, with six rows of hooklets, at the anterior end, each row com- 
 posed of eight spicules. The parasite occupies the small intestine • 
 of the hog, and has been found occasionally in man. The inter- 
 mediate host seems to be the grub of the cockchafer and the June- 
 bug. 
 
 Other varieties of echinorrhynchus have been described, but 
 are not well-determined species. 
 
 EUSTRONQYLUS GIQAS. 
 
 The female of this species may reach a length of 1 m. ; the 
 male is but one-third this size. The anterior end of the worm 
 is retracted, and the mouth surrounded by six papillae. The 
 posterior end is expanded, and provided with a spicule projecting 
 from the cloaca. The color of the worm is brownish or blood-red. 
 The parasite is found in the pelvis of the kidneys, ureters, and 
 bladder of dogs, horses, cattle, and other animals, and rarely in 
 man. Among its results are enlargement of the pelvis of the 
 kidney and atrophy of the kidney-substance. 
 
 STRONQYLUS LONGEVAGINATUS. 
 
 This parasite was found in the lungs of a child. It resembles 
 the strongylus met with in the lungs of sheep and other animals. 
 
 TREMATODES, OR FLUKE=WORMS. 
 
 The fluke-worms are usually flattened organisms, somewhat 
 tongue-shaped and provided with powerful suckers and occasion- 
 ally also with hooklets. The intestinal canal begins in the oral 
 orifice anteriorly, but is closed at the posterior extremity. Repro- 
 
294 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 duction may take place directly or by the formation of an inter- 
 mediate organism which is parasitic to certain lower animals. In 
 this stage they are actively motile, swimming about in water, and 
 are known as the cercarise. 
 
 DISTOMA HEPATICUM. 
 
 The Distoma hepaticum, or liver-fluke, is from 15 to 35 mm. in 
 length and 6 to 20 mm. broad ; it is pointed at either end, and an- 
 teriorly is provided with two suckers, one 
 at the head and one upon the ventral sur- 
 face, somewhat posterior to the first (Fig. 
 136). The genital pore lies between the 
 two suckers. The eggs are oval in shape, 
 0.14 to 0.15 mm. in length, and provided 
 with a lid at one pole. 
 
 The adult organism occupies the biliary 
 ducts and is a frequent parasite of sheep. 
 It is occasionally met with in man, usually 
 occurring in considerable numbers. It 
 gives rise to obstruction of the biliary 
 passages and consequent enlargement, con- 
 gestion, and later degeneration of the 
 liver. The gall-ducts above the point 
 of obstruction have sometimes been found considerably dilated or 
 cystic. Clinically ascites and jaundice have been found, with 
 gastro-intestinal symptoms and distoma-eggs in the stools. 
 
 Fig. 136.— Distoma hepati- 
 cum; two-thirds the natural 
 size (Mosler and Peiper). 
 
 DISTOMA LANCEOLATUM. 
 
 This form is smaller than the last, 8 to 10 mm. in length and 
 2 to 2.5 mm. in breadth. The two suckers are far apart, and the 
 genital pore lies between them (Fig. 137). 
 The eggs are 0.04 to 0.05 mm. in length 
 and 0.03 mm. in breadth. 
 
 This form is frequently associated with 
 the last, and occupies the biliary passages of 
 sheep and cattle. It is occasionally met 
 with in other animals and in man. 
 
 D 
 
 Fig. 137.— Distoma lan- 
 ceolatum ; two-thirds the 
 natural size (Mosler and 
 Peiper). 
 
 DISTOMA HEMATOBIUM. 
 
 This organism occurs in sexually distinct 
 forms ; the male and female, however, oc- 
 curring together. The male is 12 to 14 mm. in length and 1 mm. 
 thick, and the posterior part is somewhat flattened and curved 
 ventralward to form a groove, in which the female is attached 
 
ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 295 
 
 
 (Fig. 138). The latter is 16 to 18 mm. long, and 0.13 mm. thick. 
 The eggs are 0.12 mm. long and 0.04 mm. broad, and drawn out 
 
 Fig. 138.— Distoma hematobium, with eggs (von Jaksch). 
 
 *m 
 
 to a point at one end. The adult parasite occupies the portal vein 
 and the veins of the spleen, mesentery, and the plexuses of the 
 bladder and rectum. The eggs of the 
 organism may be found in any of the 
 organs, notably in the liver, in the intes- 
 tinal walls, and in the mucous mem- 
 branes of the urinary passages. They 
 probably occupy the vascular system 
 ordinarily, but cause rupture of the walls 
 of the vessels and thus escape into the 
 tissues. 
 
 The pathologic changes caused by 
 this parasite are most strikingly seen in 
 the ureters and bladder in acute cases. 
 Hyperemic spots or small hemorrhages 
 may be seen in the mucous membrane, 
 and the surface is covered with blood- 
 stained mucus containing the eggs. In 
 cases of longer standing roughness of the 
 mucous membranes and usually small 
 ecchymotic elevations or outgrowths, 
 suggesting papillomata, are observed 
 (Fig. 139). Section through these shows 
 that they consist of proliferated cells 
 with enlarged blood-vessels, from which 
 the adult worm may be removed. The 
 
 vessels may contain eggs in enormous numbers. The mucous 
 membrane is frequently covered with a calcareous deposit com- 
 posed of urate and oxalate of sodium, and the excrescences may 
 be converted into calcified polyps. Among the final results may 
 be cicatricial strictures of the ureter, pyelitis, and distention of 
 the pelvis of the kidney, with atrophy of the kidney-substance. 
 Similar pathologic processes may be found in the rectum. When 
 the portal vein is occupied the eggs of the distoma may be abun- 
 dant in the liver-substance. Distoma hematobium is a parasite 
 occurring with enormous frequency in Northern Africa and 
 
 If 
 
 Fig. 139.— Papillary thicken- 
 ing of the mucous membrane 
 of the bladder, showing dis- 
 toma-eggs in site (Mosler 'and 
 Peiper). 
 
 tissues surrounding the 
 
296 TEXTBOOK OF PATHOLOGY. 
 
 neighboring countries. It is comparatively rare in other parts of 
 the world. 
 
 DISTOMA PULMONALE. 
 
 This organism is from 8 to 10 mm. in length and from 5 to 6 
 mm. in breadth. The eggs are brownish, and from 0.08 to 0.1 
 mm. in length. The worm occurs in the lungs, occupying exca- 
 vated spaces, usually near the periphery of the organ. These 
 cavities contain reddish or quite hemorrhagic mucopurulent liquid 
 and abundant eggs. The cavities are in communication with the 
 bronchi, and clinically the disease is marked by cough and hemor- 
 rhagic expectoration or even repeated hemoptysis. This parasite 
 occurs very frequently in Japan, China, and Corea. 
 
 OTHER FLUKE=WORMS. 
 
 Among other forms of distoma of less importance are Distoma 
 crassum, met with a few times in the intestine ; Distoma hetero- 
 phyes; Distoma ophthalmobium, found in the lens of the eye; Dis- 
 toma sinese, found in the liver; Distoma conjunctum, also occurring 
 in the liver ; and the Monostoma fentis, occurring in the eye. The 
 Amphistoma hominis occurs in the intestinal tract. Two forms, 
 the Hexathyridium venarum and Hexathyridium pinguicola, are 
 possibly forms of encapsulated Distoma hepaticum. 
 
 ANNELIDES. 
 
 Two forms of leeches are of some pathologic importance. The 
 Hirudo Ceylonica is a form occurring with great frequency in 
 Ceylon and other islands and in parts of South America. It is 
 found in vegetation, and attaches itself to the skin of the legs and 
 to other parts of man by means of a sucker and its short teeth. 
 It may give rise to painful ulcerations when removed. The 
 Hirudo vorax is met with in parts of Europe and Africa. It gains 
 access to the mucous membranes of the mouth, larynx, trachea, or 
 nasal chambers, and leads to inflammatory troubles. It is not able 
 to effect a lodgement upon the skin. 
 
 ARTHRO PODIA. 
 
 A number of parasites belonging to the groups Arachnoidea 
 and Insecta are met with in man. Most of these, however, are 
 purely external parasites, and are fully described in works upon 
 diseases of the skin. There are two forms, however, that merit 
 brief description here : the Pentastomum denticulatum, the larval 
 form of Pentastomum tsenioides ; and the larvae of various flies, 
 the presence of which in the gastro-intestinal tract and other parts 
 of the body is termed myiasis. 
 
ANIMAL PARASITES AND DISEASES CAUSED BY THEM. 297 
 
 PENTASTOMUM DENTICULATUM. 
 
 This parasite is occasionally found in the liver and rarely in 
 the spleen, intestinal walls, lungs, and kidneys of man. It is dis- 
 covered in small nodular lesions, which consist of the more or less 
 degenerated parasite lying in a cheesy or semicalcified material, 
 surrounded by a fibrous or calcareous capsule. The parasite is 
 from 4 to 5 mm. in length and 1.5 mm. in breadth ; has a rather 
 rounded body, which is encircled by parallel rings armed with 
 spicules ; and is provided with two pairs of stout chitinous hook- 
 lets, one pair lying on either side of the mouth. The adult form, 
 Pentastomum tcenioides, resembles its larva in structure, but is 
 considerably larger, the male being from 16 to 18 mm. long, the 
 female from 60 to 85 mm. This form lodges in the nasal cavities 
 and frontal sinuses of the dog and other animals, and produces 
 eggs containing the embryos, which escape with the nasal secretion 
 and eventually gain access to the alimentary tract of other animals 
 or of man. 
 
 MYIASIS. 
 
 A number of flies, of the orders Estridse, Musca, Lucilia, and 
 Sarcophaga, may deposit their eggs in wounds or in cavities of the 
 body to which they gain access, such as the nasal or pharyngeal 
 chambers and the communicating passages. The eggs so deposited 
 are hatched, and the larval insects may be retained and may occa- 
 sion intense irritation. Sometimes the larva? are found in the gas- 
 trointestinal tract, the eggs having been swallowed with food. 
 Immense numbers may be discharged from the intestines, and in 
 some cases the larvae seem to occasion intestinal irritation. The 
 term myiasis is given to the invasion of these larval insects. 
 
 
PART II. 
 SPECIAL PATHOLOGY. 
 
 CHAPTER I. 
 
 DISEASES OF THE BLOOD. 
 
 ANATOMY. 
 
 The blood is a liquid tissue composed of corpuscles or cells 
 and a fluid intercellular substance. The cells are of three kinds : 
 the red corpuscles, or erythrocytes ; the white corpuscles, or leuko- 
 cytes ; and the blood-plaques, or hematoblasts. The fluid element 
 of the blood, the liquor sanguinis, or plasma, is an albuminous and 
 saline liquid of a slightly varying composition. The blood as a 
 whole is red in color, rather viscid, and alkaline in reaction. The 
 total quantity is about one-thirteenth of the body-weight. 
 
 The erythrocytes, or red corpuscles, are biconcave disks 
 about 7 fi in diameter and having a yellowish or amber color. 
 They are quite uniform in size and regularly rounded. Histo- 
 logically they are composed essentially of an albuminous substance 
 containing hemoglobin embedded in a delicate stroma. The 
 hemoglobin is the important element, and constitutes 95 per cent. 
 by weight of the corpuscles. In early fetal life most of the red 
 corpuscles are nucleated, but the nucleated forms later decrease in 
 number and are comparatively scanty at the time of birth. 
 Within the first few months of post-fetal life all of them dis- 
 appear, and in subsequent years nucleated corpuscles are present 
 only in cases of disease. 
 
 There are about 5,000,000 corpuscles in the cubic millimeter 
 of the blood of normal individuals. The figures vary slightly at 
 different times in the same individual, and many influences con- 
 tribute to the production of more lasting changes in number (see 
 page 313). The volume of the red corpuscles in the blood is 
 dependent upon the number of corpuscles and upon their size. 
 Observers have reached varying results in studying the volume, 
 but it may be placed at between 40 and 50 per cent, of the total 
 bulk of the blood. 
 
 The leukocytes, or white corpuscles, are rounded or 
 spherical bodies presenting a more or less granular appearance in 
 
DISEASES OF THE BLOOD. 
 
 299 
 
 the fresh state. They vary in size from the diameter of the red 
 corpuscles to several times the size of the latter. The leukocytes 
 are identical with the lymph-corpuscles. They are of several more 
 or less distinct varieties ; the classification, however, is exceedingly 
 difficult, as transitional forms are abundant. The classification 
 most frequently adopted is that of Ehrlich and of his pupils, and 
 while it is not entirely satisfactory, it has one advantage over 
 others, viz., that of simplicity. Ehrlich distinguishes (Fig. 140) : 
 
 
 
 i "3P&&' 
 
 Fig. 140.— Various forms of blood-corpuscles : a, lymphocyte ; b, lymphocyte approach- 
 ing c; c, large mononuclear; d, transitional ; e, polymorphonuclear neutrophile; /.poly- 
 morphonuclear eosinophile ; g, broken eosinophile ; h, neutrophilic myelocyte ; i, eosino- 
 philous myelocyte; j, basophile, mast-cell; k, red corpuscles; I, nucleated red corpuscles. 
 
 1. Small mononuclear leukocytes, or lymphocytes. These are 
 smaller than the red corpuscles, or about the same size, are spher- 
 ical, and contain a relatively large nucleus, the protoplasm often 
 forming a scarcely visible band around the nucleus. The latter is 
 rich in chromatin and stains deeply. Sometimes cells considerably 
 larger than the typical lymphocyte may resemble them in other 
 respects, and it may be difficult to determine whether these are 
 lymphocytes or large mononuclear cells (Fig. 140, 6). The proto- 
 plasm of lymphocytes normally contains no granular matter when 
 stained by the ordinary methods. Deep staining with methylene- 
 blue with the aid of heat does, however, frequently lead to the 
 detection of a slightly granular character in the protoplasm. 
 
 2. Large mononuclear leukocytes. These forms are larger than 
 the lymphocytes, being from two to three times the diameter of 
 the red cells. They are often oval in outline, and the nucleus is 
 poorer in chromatin than that of the lymphocyte, so that it appears 
 comparatively pale in the stained blood. The protoplasm is 
 usually free of granules, but it may show fine and very pale gran- 
 ules when stained with intense basic stains like methylene-blue. 
 
 3. Transitional leukocytes. These are similar to the last, but 
 
300 TEXT-BOOK OF PATHOLOGY. 
 
 differ in that the nucleus is often a little indented or horseshoe- 
 shaped. It is very often impossible to determine satisfactorily 
 whether a certain cell is a large mononuclear or a transitional 
 form, and the two maybe considered as practically the same. The 
 protoplasm, as a rule, contains no granules, but neutrophilic 
 granules (see page 301) have occasionally been detected, and 
 eosinophile granules are more frequently present. 
 
 4. Polymorphonuclear leukocytes ; polynuclear leukocytes ; neu- 
 trophils. These are the most numerous forms, and probably 
 represent the fully developed white blood-cell. They are some- 
 what smaller than the large mononuclear elements, and are dis- 
 tinguished by a polymorphous nucleus which is richer in chroma- 
 tin than that of the large mononuclear form, though perhaps less 
 rich than that of the lymphocyte. The nuclei are elongated, and 
 variously curved or distorted so as to resemble the letters S, U, 
 V, Z, etc., and in some cases they are wreath-shaped. Frequently 
 parts of the nucleus are so thin that they are scarcely visible, or 
 actually become broken, and the term polynuclear was therefore 
 applied. This name is, however, less appropriate than the term 
 polymorphonuclear. The amount of chromatin in the nucleus 
 varies greatly, and the size of the nucleus is correspondingly 
 variable. The protoplasm usually contains fine granules, which 
 are closely set and almost completely fill the cell. These granules 
 have a strong affinity for neutral mixtures of anilin or other stains, 
 and have therefore been called the neutrophilic granules (see page 
 301 ). A small proportion of the polymorphonuclear leukocytes 
 of the blood contain eosinophile granules. These cells are usually 
 larger than the neutrophilic forms, and the nucleus is more nearly 
 like that of the typical transitional leukocyte. 
 
 5. Myelocytes ; mast-cells. These are large cells identical with 
 the large granular cells of the bone-marrow. They are often 
 three or four times the size of the red corpuscles, and are dis- 
 tinguished by a large, pale, oval nucleus. The protoplasm usually 
 contains neutrophilic granules, but occasionally contains eosino- 
 phile granules. The nucleus is frequently somewhat irregularly 
 outlined and not rarely suffers degenerative change. Smaller cells, 
 resembling the typical myelocyte in the character of the nucleus 
 and protoplasm, are sometimes observed, and are difficult to clas- 
 sify. Myelocytes occur in exceedingly small numbers, if at all, 
 in normal blood. They are abundant in certain forms of leukemia, 
 and also occur in pernicious anemia and various infectious and 
 systemic diseases. 
 
 The granules of the leukocytes are classified according to their 
 behavior with the anilin stains. We may distinguish four impor- 
 tant types of granules (Figs. 140 and 141) : 
 
 1. rt-granules, eosinophile granules, or oxyphile granules. These 
 are coarse granules giving the appearance in the unstained blood 
 
DISEASES OF THE BLOOD. 301 
 
 of minute fat-droplets ; they are highly refractive, and have been 
 shown to be composed of albuminous material. They are dis- 
 tinguished by their strong affinity for acid stains/ and in particular 
 for eosin. This circumstance has given rise to the name eosino- 
 phil and oxyphile (Fig. 147). 
 
 The eosinophile granules in the normal blood occur only in 
 polymorphonuclear leukocytes. 
 
 2. y-granules ; mast-cell granules. These are intensely baso- 
 
 «&> 
 
 -.:v: e*?-/-^ '•X'.-'V.^.- 
 
 Fig. 141.— Leukocytes, showing various forms of granulations : a, Neusser's basophilic, 
 perinuclear granules ; b, large mononuclear cells with 6-granules ; c, mast-cell granules : 
 d, basophilic lymphocytes, 6-granules ; the stain in b, c, and d was a mixture of eosin and 
 hematoxylin, the cover-glass being kept in the stain several hours at 37° C. (98.6° F.). 
 
 philic, coarse granules, occurring in mononuclear cells. They are 
 present in small proportions in the normal blood (Fig. 141). 
 
 3. ^-granules are fine basophilic granules occurring in the 
 lymphocytes or large mononuclear cells (Fig. 141). 
 
 4. e-granules ; neutrophilic granules. These are the most abun- 
 dant and the most important of all the forms. They occur as 
 fine granulations filling up the protoplasm of the polymorphous 
 cells, and they are occasionally present in transitional leukocytes. 
 They are distinguished by their affinity for the neutral mixtures 
 
 1 The term acid stain is here used in a sense somewhat different from that of 
 the chemist. A stain in which the acidulous part of the compound carries the 
 coloring-principle is known as an acid stain, while one in which the basic ele- 
 ment is the staining-principle is called basic. For example : picrate of am- 
 monium is an acid stain because the picric acid is the staining-element. Mixt- 
 ures of certain acid with basic stains may be prepared so that tissue-elements 
 having a strong acid affinity will select the acid stain, those having a basic affinity 
 the basic stain, while other elements without such special affinity receive a mixed 
 or neutral stain. 
 
302 TEXT-BOOK OF PATHOLOGY. 
 
 of Ehrlich (Fig. 147). It must be recognized, however, that these 
 granules are in reality faintly oxyphilic, receiving the acid stains, 
 such as eosin or acid fuchsin, more readily than basic stains. In 
 a few instances I have found them distinctly basophilic. 
 
 The nature of the granules of the blood is still obscure. They 
 are undoubtedly connected in some way with the specific function 
 of the leukocytes, but whether they are of the nature of a secre- 
 tion or not is unknown. 
 
 The chemical composition of the leukocytes is of considerable 
 importance, but is difficult to determine from the impossibility of 
 obtaining large numbers free from other elements. It is known, 
 however, that these cells contain among other bodies leukonuclein, 
 histon, lecithin, and cholesterin. They also contain more or less 
 abundantly glycogen and fats ; and saline constituents including 
 potassium salts in particular. The leukonuclein is a combination 
 of the phosphorus-containing nucleinic acid and an albumin. It 
 is present in the nuclei of nucleated red corpuscles and in other 
 nuclei, but especially in those of the leukocytes. It is more or 
 less intimately combined with histon, a body resembling the albu- 
 moses. 
 
 The number of leukocytes in the normal blood varies consider- 
 ably. The average number, however, is probably between 6000 
 and 10,000. Alterations in the number under various circum- 
 stances w T ill be discussed below. 
 
 Proportions of the Different Forms. — The relative proportions of 
 the different leukocytes are determined by counting large numbers 
 and calculating the percentage proportion of each form. Approxi- 
 mately there are 25 per cent, lymphocytes, 65 to 75 per cent, 
 polymorphonuclear forms (neutrophiles and eosinophiles), 5 to 8 
 per cent, transitional and large mononuclear. About 1 to 3 or 5 
 per cent, of all of the leukocytes contain eosinophile granules, and 
 occasionally a larger proportion is met with in normal blood. 
 
 Blood-plaques. — These are small disks somewhat resem- 
 bling the red corpuscles, though smaller and without the charac- 
 teristic biconcavity of the latter. They rarely exceed 3 fi in 
 diameter, and are often much less. They are viscid, and tend to 
 adhere to the other corpuscles or to become agglutinated in clusters. 
 The total number has been estimated at from 150,000 to 500,000 
 per cubic millimeter. The term hematoblast was applied by 
 Hayem in the belief that the plaques are the progenitors of the 
 red corpuscles. 
 
 The plasma of the blood is an albuminous liquid containing 
 serum-albumin and scrum-globulin and various saline compounds. 
 The relative proportion of serum-globulin to serum-albumin is as 
 1 to 1 or 1^-. Of the saline constituents sodium salts are most 
 important, the phosphates, carbonates, sulphates, and chlorids 
 being most abundant. Various other nitrogenous and non-nitro- 
 

 DISEASES OF THE BLOOD. 303 
 
 genous substances are present in small proportions. Reference 
 will be made to some of these below. 
 
 BLOOD=FORMATION. 
 
 The process of blood-formation is still obscure in some particu- 
 lars. In early fetal life blood-corpuscles are undoubtedly formed 
 in the mesoblastic columns in which the blood-vessels are devel- 
 oped. At a later stage the liver is active in their production. 
 Subsequently the spleen and the bone-marrow seem to assume the 
 principal role. According to Neumann and Bizzozero, the red 
 corpuscles are developed from nucleated hemoglobin-containing 
 cells of the bone-marrow, which lose their nuclei by a process of 
 gradual disintegration. Others have held that the nuclei are ex- 
 truded from the nucleated cell. According to these views, all of 
 the red corpuscles are derived from nucleated red cells, or eryth- 
 roblasts. Other observers, however, hold that the red corpuscles 
 and leukocytes originate from a common parent-cell free from 
 hemoglobin. This parent-cell gives rise to two series of descend- 
 ants, one series containing hemoglobin and leading to the formation 
 of red corpuscles, while the other series is free from pigment and 
 forms the leukocytes. The principal place of formation of the 
 red corpuscles during adult life seems to be the bone-marrow, but 
 the spleen and the lymphatic tissues probably also play a part. 
 French writers, following Hayem, hold that the progenitor of the 
 red corpuscle is the blood-plaque. This view, however, is not 
 sustained by sufficient evidence. 
 
 The white corpuscles undoubtedly originate in the bone-marrow, 
 lymphatic tissues, and spleen. The lymphocyte is the youngest 
 form, and the other varieties probably are secondary developments 
 from this, the completion of their development occurring in the 
 blood-making organs, notably the marrow. 
 
 PATHOLOGIC CHANGES IN THE RED CORPUSCLES. 
 
 The si^e of the red corpuscles varies in diseases of different 
 kinds. There may be dwarf corpuscles, 2 to 4 or 5 [jl in diameter 
 (microcytes) ; or, on the other hand, giant-cells (megalocytes), from 
 9 to 15 [x or even 20 fi in diameter. The small forms frequently 
 have a spherical shape rather than the disk-like form of the nor- 
 mal corpuscle, and may be deeply pigmented. The large corpus- 
 cles are often irregular in shape, and are prone to be paler than 
 normal corpuscles (Fig. 142). Some observers have found that 
 the average size of the red corpuscle is greater in certain diseases 
 than in health. This is probably the result of hydropic conditions. 
 
 The Shape of the corpuscles often suffers great change, and 
 many forms of irregularity may be observed. The term poikiloey- 
 tosis is applied to this condition (Fig. 142). Some of the poikilo- 
 
304 TEXT-BOOK OF PATHOLOGY. 
 
 cytes may be exceedingly small and may present active movements. 
 These have been termed pseudo-bacilli by Hayem. These changes 
 of form in red corpuscles are regarded by many authorities to be 
 
 mm |lV J), 
 
 , <m 
 
 Fig. 142.— Blood from a case of- pernicious anemia: a, megalocytes : 6, microcytes ; c, poi- 
 kilocytes; d, nucleated *ythrocytes ; e, normal erythrocytes ; /, leukocytes. 
 
 the result of degenerative changes in the protoplasm with conse- 
 quent ameboid movement which occasions irregular projections. 
 The small forms are doubtless in many cases the result of frag- 
 mentation. Ehrlich used the term schistocyte to indicate this fact. 
 
 Dust-corpuscles. — Miiller recently described certain small 
 spherical bodies somewhat resembling the leukocytic granules, but 
 lying free in the plasma and often actively motile. These he 
 termed hemokonice, or dust-corpuscles. They occur in normal blood 
 as well as in that of various diseases. A number of theories have 
 been offered regarding the nature of these bodies. My own belief 
 is that they are fragments of red corpuscles, similar to those that 
 may be produced by heating fresh blood under a cover-glass to 
 destructive temperatures. Under these circumstances small, bud- 
 like processes are formed on the periphery of the red corpuscles, 
 and some of these may break off and float free in the plasma. 
 
 Visible ameboid movements may sometimes be observed 
 under the microscope, especially in severe anemias, such as per- 
 nicious anemia. 
 
 Nucleated red corpuscles, or erythroblasts, occur in the 
 severe anemias as in the fetal blood. They are more frequent in 
 the severest cases, and in particular in the anemias of children. 
 Some are exceedingly small (microblasts), some about the size of 
 the normal red corpuscle (normoblasts), and some large and irregu- 
 lar (megaloblasts). The smaller forms appear first and in the more 
 moderate anemias ; occasionally they occur in great numbers or 
 crops from time to time (blood-crises). 
 
DISEASES OF THE BLOOD. 305 
 
 Karyokinetic figures are occasionally seen in the nuclei of 
 erythroblasts, especially in certain anemias of children. 
 
 Shadow corpuscles are red corpuscles that have lost their 
 color almost completely and are scarcely visible. They may be 
 observed in severe anemias, and especially in cases of intoxication 
 with blood-poisons. 
 
 Polychrotnatophilia. — The normal red corpuscle has a spe- 
 cial affinity for acid stains. In diseased conditions it may develop 
 an affinity for basic stains, and when colored with mixtures of acid 
 and basic stains may present tints combining all the stains employed. 
 Thus in staining with eosin and hematoxylin the degenerated 
 corpuscles may present a purplish or violet color, instead of a 
 pink. 
 
 Vacuolation and pigmentation of the red corpuscles are 
 rare forms of degeneration. The pigmentation is due to separa- 
 tion of the hemoglobin in the form of irregular granules. 
 
 Alterations of Isotonicity. — All forms of cells have cer- 
 tain osmotic relations, in consequence of which they retain their 
 constituent elements in the presence of surrounding liquids of 
 certain kinds. If the osmotic relations vary or the surrounding 
 liquids are altered, the constituents of the cell may be extruded. 
 In the case of blood-corpuscles distilled water rapidly abstracts 
 the hemoglobin and other substances, but saline solutions of cer- 
 tain strengths do not so affect the corpuscle. The exact strength 
 of a certain saline solution may be determined which will preserve 
 the corpuscle, and this is known as the isotonic strength of the 
 corpuscle expressed in percentage-terms of the saline used. De- 
 generated corpuscles more readily yield their constituents, and the 
 isotonic saline solution is therefore of higher percentage. In 
 normal blood the isotonicity of the red corpuscle is generally 0.46 
 to 0.48 per cent. NaCl ; that is, solutions of common salt of this 
 strength do not affect the red corpuscles. In anemic diseases the 
 isotonic solutions may be from 0.5 to 0.6 per cent. 
 
 PATHOLOGIC CHANGES IN THE LEUKOCYTES. 
 
 Very frequently degenerations of the nuclei of the leukocytes 
 t are observed in the form of fragmentations or karyolytic change. 
 Attention has recently been called (Neusser) to the presence of 
 basophilic granules about the nucleus in certain forms of disease, 
 such as leukemia, gout, and lithemia in its widest sense. These 
 granules are supposed to be significant of disintegration of the 
 nuclei in the process of uric-acid formation. Their nature and 
 significance, however, are unsettled. Occasionally vacuolization 
 and fatty degeneration of leukocytes are observed, and glycogen 
 may be found in abnormal quantities. In cover-glass preparations 
 
306 TEXT-BOOK OF PATHOLOGY. 
 
 the leukocytes are sometimes found broken or fragmented, and this 
 doubtless occurs to some extent in the circulating blood. 
 
 PATHOLOGIC CHANGES IN* THE PLASMA. 
 
 Various disorders of the plasma have been studied. These are 
 mainly of a chemical sort, and consist of the presence of abnormal 
 substances or of normal constituents in excessive quantity. Urea 
 is present in large quantities in some cases of nephritis and uremia, 
 and older authorities believed the symptoms of uremia due to the 
 presence of this substance. This view is no longer held. Uric 
 acid occurs in small quantities in health ; but in large quantities 
 in gout, leukemia, leukocytosis, and other disorders of the blood. 
 The xanthin bases may be present in considerable quantities in the 
 same cases. Glycogen or grape-sugar is found in excessive quan- 
 tities in diabetes and, according to some observations, in cases of 
 carcinoma. Levulose and other carbohydrates are rare constitu- 
 ents of the plasma. Fatty acids may be present in leukemia, dia- 
 betes, acute yellow atrophy of the liver, and some other diseases. 
 The quantity of sodium in the plasma increases in anemic diseases. 
 
 Certain changes occur in the plasma or serum in anemic dis- 
 eases, as a result of which the globulicidal character is increased. 
 The nature of these changes is obscure. The presence of toxic 
 substances the result of bacterial action is referred to in the dis- 
 cussion of bacteria. 
 
 Hypertonieity of the serum is a term indicating that the salinity 
 of the plasma or serum is such that the blood may be somewhat 
 diluted without destruction of the corpuscles. By graduated dilu- 
 tions the degree of hypertonieity may be estimated, and is found 
 less in certain diseases than in health (see Isotonicity of the Red 
 Corpuscles). 
 
 Hyperinosis and hypinosis are terms designating increased and 
 decreased capability for fibrin-formation. The former is met with 
 at times in chlorosis, leukemia, or other anemic affections, and in 
 certain infectious diseases. The latter is notably present in leu- 
 kemia and some cases of hemolysis. There has been much the- 
 orizing in regard to these conditions, but very little knowledge of 
 practical importance has been acquired. 
 
 PLETHORA. 
 
 Plethora is the name applied by the older writers to a condition 
 in which the total quantity of blood was supposed to be excessive. 
 It is now recognized that plethora is much less frequent and per- 
 manent than was formerly believed. Several varieties were de- 
 scribed. 
 
 Plethora vera was the name given to the condition in which 
 the quantity of the blood was supposed to be increased without 
 
DISEASES OF THE BLOOD. 307 
 
 change in its quality. Persons supposed to have this condition 
 are described as robust, with high color and vigorous circulation. 
 They are generally individuals living in luxury. The term " full- 
 blooded " is still applied, but it is recognized that the fulness of 
 the superficial vessels is the result of peculiarities of the circulation 
 rather than of increase in the quantity of blood. 
 
 Plethora apOCOptica is the term given to conditions in 
 which there is local increase in the blood. 
 
 Plethora hydremica is a condition in which the total quan- 
 tity of the blood is increased by dilution. This was regarded as 
 frequent in cases of cachexia after hemorrhages, etc. 
 
 Experimental evidence might be referred to to substantiate the 
 view that plethora in the strict sense does not often occur as a 
 lasting condition. Temporary plethora is produced by the drink- 
 ing of large quantities of liquid, but the excretory organs soon 
 dispose of this excess. 
 
 OLIGEMIA. 
 
 Oligemia is a term indicating reduction in the quantity of blood. 
 This is met with temporarily after hemorrhage, but very soon 
 serous liquid from the tissues enters the blood-vessels and restores 
 the original quantity. At the time of the hemorrhage the quantity 
 may be immediately reduced to a very great degree without caus- 
 ing death. Serious consequences are averted by the activity of 
 the vasomotor system, the blood-vessels accommodating them- 
 selves by contraction to the reduced quantity of blood. Subse- 
 quently when liquid of the tissues is absorbed into the blood- 
 vessels the latter dilate and their natural volume is soon restored. 
 The blood, however, becomes hydremic, or watery. Oligemia or 
 quantitative anemia may possibly occur in certain cachectic and 
 anemic diseases, but this has not been proved, and the relative 
 proportion between the mass of blood and the weight of the body 
 is certainly not much disturbed in any case. 
 
 HYDREMIA AND ANHYDREMIA. 
 
 Hydremia, a diluted or watery condition of the blood, may 
 occur from excessive consumption of water, but active excretion 
 of liquid soon restores the blood to its previous condition. Hemor- 
 rhage leads to hydremia in the manner above described ; and in 
 the chronic anemias there is possibly some dilution of the serum. 
 It has never been shown, however, in any of the many experiments 
 made to determine this point, that the plasma in anemias is less 
 rich in solid constituents than normal plasma. The reduction in 
 solid matter in the blood as a whole is due to the diminution in 
 the number of red corpuscles and changes in their composition. 
 
 Anhydretnia is a condition in which the plasma of the blood 
 
308 TEXT-BOOK OF PATHOLOGY. 
 
 is thickened by the loss of watery elements. This may occur in 
 consequence of excessive sweating or excessive discharge of water 
 from the bowels, kidneys, etc. The number of red corpuscles in 
 a given bulk of blood increases. The specific gravity and the 
 solid residue of the plasma of the blood as a whole increase corre- 
 spondingly. 
 
 LIPEMIA. 
 
 Lipemia is a pathologic condition in which fat occurs free in 
 the blood-plasma. Fat is always present as a normal constituent 
 of blood, and is in slight excess during the process of digestion. 
 Lipemia occurs in cases of chronic nephritis, diabetes, pulmonary 
 tuberculosis, alcoholism, and some other conditions, and may reach 
 marked grades of severity. The blood may have a milky appear- 
 
 Fig. 143.— Blood from a case of lipemia, stained with osmie acid: upper half of field 
 cleared with oil of turpentine; lower half shows the fat-droplets and granules stained 
 with oamic acid between the blood-corpuscles; enlargement, 100 diameters (after Gum- 
 precht: Deutsch med Woch., Sept. 27, 1894). 
 
 ance to the naked eye, and under the microscope highly refractive 
 droplets or granules are observed. The latter stain black with 
 osrnic acid (Fig. 143). 
 
 MELANEMIA. 
 
 This condition is distinguished by the occurrence of dark pig- 
 ment or granular matter in the circulating blood. It occurs in 
 cases of malaria and certain other fevers. The pigment may be 
 
DISEASES OF THE BLOOD. 309 
 
 free in the plasma in the form of yellowish or blackish granules ; 
 or may be found as small particles in the leukocytes. 
 
 HEMOCYTOLYSIS-HEMOGLOBINEMIA. 
 
 Definition. — Hemocytolysis is the term applied to the condi- 
 tions in which the red blood-corpuscles are destroyed. The name 
 hemolysis is generally employed in the same sense, though it refers 
 to destruction of all of the elements of the blood. In this condi- 
 tion hemoglobin is liberated and is dissolved in the plasma. To 
 this the term hemoglobinemia is applicable, but the name met- 
 hemoglobinemia is more appropriate, as the hemoglobin is usually 
 present in the serum in this altered form. 
 
 Ktiology. — Hemolysis constantly takes place in the liver, the 
 coloring-matter of the blood being converted into bile-pigments. 
 Pathologic hemolysis results from the action of various infectious 
 and toxic agents. It occurs in the course of severe malaria, re- 
 lapsing fever, pneumonia, and various hemorrhagic infections ; and 
 is occasioned by many poisons (see Blood-poisons). Excessive 
 cold may be a contributing cause, as seems to be the case in some 
 instances of paroxysmal hemoglobinuria (q. v.). 
 
 Pathologic Anatomy. — The blood may present striking 
 morphologic changes in the red corpuscles, such as microcyto- 
 sis, megalocytosis, poikilocytosis, fragmentation, and vacuolation. 
 Shadow-corpuscles may be abundant, and in the later stages of 
 the process beginning regeneration of the blood causes the pres- 
 ence of nucleated red corpuscles. The blood as a whole is often 
 quite dark in color. 
 
 Associated changes are frequently met with in the liver, kid- 
 neys, and skin. The hepatic cells are often swollen and more or 
 less degenerated and bile-stained. Excessive production of bile 
 (polycholia) may occur. This over-production, with the swelling 
 of the hepatic cells and the consequent obstruction of the biliary 
 channels, occasions reabsorption . of bile and consequent jaundice 
 (so-called hematogenous jaundice). The excess of hemoglobin, 
 which cannot be disposed of by the liver, may be excreted in the 
 urine (hemoglobinuria). Sometimes hemoglobin-infarcts are met 
 with in the renal tubules ; and thrombosis of the renal or other blood- 
 vessels is occasionally observed. Acute nephritis is a rare result. 
 
 Pathologic Physiology. — Hemocytolysis leads to more or 
 less pronounced disturbance of the internal or tissue respiration, 
 as the altered hemoglobin is incapable of carrying oxygen. Dysp- 
 nea and various nervous symptoms are the result. The liberation 
 of cellular constituents (from destruction of the red and white 
 corpuscles) occasions increased coagulability of the blood and the 
 formation of thrombi (ferment-intoxication). Fever and other 
 general symptoms may be due to the same cause. 
 
3 1 TEXT-BOOK OF PA THOLOG Y. 
 
 POLYCYTHEMIA. 
 
 Polycythemia, or erythrocytosis, the condition in which the num- 
 ber of red corpuscles in a given bulk of blood is increased, may be 
 actual or relative. Actual polycythemia is that in which there is 
 over-production of red corpuscles ; this is probably rare. Relative 
 polycythemia is due to decrease in the quantity of the plasma. It 
 is met with in a variety of conditions, including certain cardiac 
 diseases, with slow failure of compensation, and especially in con- 
 genital cyanosis ; in residents of high altitudes ; in the new-born ; 
 and in cases of cholera or other diseases in which liquid discharges 
 cause inspissation of the blood. The explanation of the increased 
 number of corpuscles in some of these conditions has occasioned 
 considerable controversy. Some have held that the number of 
 corpuscles (at high altitudes, for example) increases actually rather 
 than relatively, for the purpose of furnishing a greater oxidizing 
 surface, but this has not been proved. It is more likely that the 
 increased number of corpuscles is caused by changes in their dis- 
 tribution in the circulation. In evidence of this it may be pointed 
 out that the number of corpuscles in dependent parts, such as the 
 foot, is greater than normal. In cardiac disease and in persons 
 living at high altitudes it is not improbable that similar stagnation 
 of the corpuscles in the peripheral tissues takes place. 
 
 LEUKOCYTOSIS. 
 
 The term leukocytosis is given to a more or less transient in- 
 crease in the number of leukocytes, the polymorphonuclear forms 
 being usually in excess. Sometimes leukocytosis is continuous or 
 chronic, and sometimes the excessive number of leukocytes is due 
 to increase in the mononuclear elements rather than the polymor- 
 phonuclear. 
 
 Etiology. — The causes of leukocytosis are varied. It is 
 generally observed as a normal condition in the new-born, the 
 number of corpuscles remaining in slight excess during the first 
 year of life. It also occurs in many cases of pregnancy ; and is 
 quite constant during the period of digestion in healthy persons, 
 proteid food being more striking in the effect than a farinaceous 
 or mixed diet. In some diseases of the stomach post-digestive 
 leukocytosis seems not to occur. 
 
 Inflammatory and Infectious Leukocytosis. — Among the strictly 
 pathologic forms of leukocytosis the most important are those due 
 to inflammations and infections of various kinds. Croupous 
 pneumonia occasions considerable increase of leukocytes in most 
 cases, and this is continuous until the final decline of the fever. 
 Suppurations of all kinds act in a similar manner. Inflammations 
 of the serous membranes — peritonitis, pleurisy, meningitis — may 
 
DISEASES OF THE BLOOD. 311 
 
 be attended by moderate or severe leukocytosis. Among the acute 
 infectious fevers there are some in which leukocytosis occurs and 
 others in which this is wanting, and this fact often proves valu- 
 able to the clinician. Among those in which the leukocytes do 
 not increase in number are typhoid fever, influenza, malaria, and 
 acute miliary tuberculosis. 
 
 Cachectic leukocytosis occurs in a variety of marantic conditions, 
 and toward the end of life in any case of wasting disease there may 
 be a great increase in the number of leukocytes. This agonal 
 or terminal leukocytosis is either cachectic (toxic) in nature or it 
 may be due to terminal infections. 
 
 Malignant tumors. frequently cause leukocytosis. 
 
 Hemorrhage may occasion increase in number of the white cor- 
 puscles, more or less in accordance with the quantity of blood lost. 
 
 Mechanical and Thermal Causes. — Massage and cold baths fre- 
 quently cause increase in the number of leukocytes for a time. 
 
 Medicinal leukocytosis, or that due to the introduction of various 
 drugs, is probably allied to infectious and cachectic leukocytosis 
 in the manner of its production. 
 
 Pathogenesis. — The nature of leukocytosis is still the sub- 
 ject of some controversy. Formerly it was held that the in- 
 creased number of leukocytes is wholly due to overproduction ; 
 later, some investigators claimed that diminished destruction is the 
 important cause. The explanation which seems most acceptable 
 at the present day is that of Golscheider and Jakob. These 
 observers hold that infectious and toxic leukocytosis is due to the 
 attractive influence of the toxic substances upon the leukocytes in 
 the blood-making organs, and to a certain extent to the stimu- 
 lating influence upon those organs, leading to increased production 
 of leukocytes. There are at all times large numbers of leuko- 
 cytes in the lymphatic tissues and throughout the other tissues of 
 the body which may be drawn into the circulation by chemotactic 
 substances. When, however, leukocytosis is prolonged it is likely 
 that new formation of leukocytes takes place, as the supply would 
 otherwise soon become exhausted. 
 
 Character of the Blood. — The blood in leukocytosis varies 
 considerably in character. The number of leukocytes may be 
 only moderately increased (10,000 to 20,000) or may be excessive 
 (50,000 to 100,000). The older writers distinguished between 
 leukocytosis and leukemia by the number of leukocytes present. 
 This distinction is no longer admitted, as there are cases of leuko- 
 cytosis with very marked increase in the number of the leuko- 
 cytes and cases of leukemia with leukocytosis temporarily or con- 
 tinuously of more moderate degree. 
 
 In the majority of cases of leukocytosis the polymorphonuclear 
 elements are in relative as well as actual excess, the mononuclear 
 elements being actually increased in number, but relatively defi- 
 
312 TEXT-BOOK OF PATHOLOGY. 
 
 cient (Fig. 144). The proportion of polymorphonuclear elements 
 is frequently 80 to 85 per cent., and sometimes 90 or 95 per cent., 
 instead of 65 to 70 per cent. In the leukocytosis of the new-born, 
 in hemorrhagic leukocytosis, cachectic leukocytosis, and that due 
 
 6° ° 
 
 Fig. 144.— Septic leukocytosis, showing marked increase of polymorphonuclear leukocytes. 
 
 to malignant tumors, the mononuclear elements frequently pre- 
 ponderate. Occasionally myelocytes have been observed, and 
 karyokinetic figures may occur in the nuclei. 
 
 Pathologic Physiology. — Leukocytosis certainly exercises 
 some profound influence upon the system, but the exact nature of 
 this influence is unsettled. Those who contend in favor of the 
 phagocytic theory of immunity claim, more or less directly, that 
 the increase of leukocytes is a protective process, the purpose 
 being the removal and destruction of irritants. Others believe 
 that leukocytosis is part of the cellular processes concerned in the 
 production of immunizing substances. There is certainly more 
 active destruction of leukocytes in leukocytosis than in health, as 
 is evidenced by the increase of xanthin bases and uric acid in the 
 urine ; and it may be that in this destruction protective substances 
 are liberated. 
 
 HYPOLEUKOCYTOSIS. 
 
 Hypoleukocytosis, or leukopenia, is the condition in which there 
 is deficiency in the number of leukocytes. This is met with in 
 moderate degree in various diseases, such as tuberculosis, typhoid 
 fever, some cases of pneumonia, cachexia, inanition, progressive 
 pernicious anemia, etc. The nature of hypoleukocytosis is not 
 always clear. Some have held that it is due to destruction of 
 leukocytes (leukolysis), while others claim that it is the result of 
 altered distribution of the leukocytes. It has been shown by 
 experimenters that the injection of certain micro-organisms or 
 toxic substances will produce, first, a decrease in the number of 
 
DISEASES OF THE BLOOD. 313 
 
 leukocytes, and then an increase. The primary hypoleukocytosis 
 is explained by some as the result of active destruction of leuko- 
 cytes, but the conditions of the urine do not give evidence of such 
 active destruction, and others have shown that the capillaries of 
 the lungs, liver, and other organs are overfilled with leukocytes 
 during this stage. The assumption is therefore warranted that 
 hypoleukocytosis is the result of disturbance in the distribution of 
 the leukocytes. 
 
 ANEMIA. 
 
 Definition. — This term includes a variety of conditions in 
 which the blood is reduced in quality in one direction or another. 
 The term oligocythemia indicates a reduction in the number of red 
 corpuscles, while the name oligochromemia indicates a reduction in 
 the coloring-matter of the corpuscles. Usually these conditions 
 are associated. 
 
 Classification of Anemias. — It is not as yet possible to 
 offer a strictly scientific classification, but for ordinary purposes the 
 old division into primary and secondary anemias may be retained. 
 The term primary anemia may be given to forms in which 
 the anemia is the striking pathologic condition. The older 
 writers used the name to indicate that the anemia was an essen- 
 tial disease and dependent upon no preceding affection, excepting 
 possibly a disturbance of the hematopoietic organs. The term 
 secondary anemia, or symptomatic anemia, may be used to desig- 
 nate anemic conditions in which some underlying disease that has 
 occasioned the anemia is conspicuous. According to the classi- 
 fication here offered, all anemias are recognized as secondary in 
 the strict sense, but those in which the underlying disease is not 
 conspicuous are classified as primary, and those in which the origi- 
 nal disease is conspicuous as secondary. 
 
 SECONDARY ANEMIA. 
 
 Etiology. — Various unsanitary conditions may influence the 
 character of the blood by the constant disturbance of the organic 
 functions. A cause of immediate anemia is hemorrhage. This 
 first leads to reduction in the quantity of blood ; and later by 
 absorption of liquid from the tissues to dilution of the blood, or 
 hydremia. Finally, after a variable period the character of the 
 blood is restored by regeneration of corpuscles and of coloring- 
 matter. Parasites of various sorts may lead to anemia. Among 
 the more important are the intestinal worms, Anchylostoma 
 duodenale, Bothriocephalus latus, and Anguillula intestinalis. The 
 mode of action of these is not entirely clear. Some have held 
 that they cause anemia by loss of blood through the intestine, and 
 this is probably true in the case of Anguillula, but marked anemia 
 
314 TEXT-BOOK OF PATHOLOGY. 
 
 may occur from the presence of Bothriocephalic or Anchylostoma 
 without much hemorrhage taking place. An explanation worthy 
 of consideration in these cases is that the parasites generate 
 poisons either in their ordinary life or by their death and decom- 
 position, and that these poisons are the cause of the anemia. 
 Other intestinal parasites may occasion more or less anemia 
 directly or indirectly. The parasites occurring in the blood itself, 
 notably the malarial organism, may cause extreme anemia. Infec- 
 tiou8 diseases frequently lead to impoverishment of the blood. In 
 the acute febrile diseases, such as typhoid fever, rheumatism, and 
 pneumonia, the anemia may not be conspicuous during the prog- 
 ress of the disease, but becomes apparent after the fever has sub- 
 sided. This may be explained by the assumption that increased 
 respiration and sweating cause inspissation of the blood and 
 relative increase in the number of red corpuscles during the exist- 
 ence of fever, so that the anemia is unnoticed. In chronic infec- 
 tions, such as syphilis and tuberculosis, marked anemia may occur. 
 Among the poisons capable of producing anemia are lead, arsenic, 
 phosphorus, and the like, and experimentally pyrogallol, nitro- 
 benzol, and similar substances have been used to produce anemia. 
 The anemias of various infectious diseases are undoubtedly toxic in 
 character, and very probably those occurring in gastro-intestinal 
 and nutritional diseases are similarly the result of the action of 
 poisons generated within the body. Organic diseases and new 
 growths of various sorts may occasion anemia by the general dis- 
 turbance of health, by toxic products generated in the course of 
 disease, by hemorrhage, etc. 
 
 Pathologic Anatomy. — The condition of the blood in sec- 
 ondary anemias varies with the duration and grade of the anemia. 
 In moderate cases the number of red corpuscles decreases slightly 
 (4,000,000 to 3,000,000), and the hemoglobin is correspondingly 
 reduced, though often somewhat more strikingly than the corpus- 
 cles. The fresh blood may show no visible changes under the 
 microscope, and even in stained preparations the appearance may 
 be normal. More marked anemia is distinguished by greater re- 
 duction, the number of corpuscles sinking to 2,500,000 or 2,000,000 
 per cu.mm. in extreme cases. The hemoglobin is usually reduced 
 more markedly than the corpuscles. Examination of the fresh 
 blood shows pallor of the corpuscles and various irregularities in 
 size (microcytes and megalocytes) and shape (poikilocytes). Nu- 
 cleated red corpuscles may be present in small numbers, the 
 microblasts and normoblasts predominating. The stained blood 
 may disclose degeneration of the corpuscles by the presence of 
 polychromatophilic forms. The leukocytes do not play an essen- 
 tial part in this form of anemia. Their number may be normal 
 or reduced ; in other cases leukocytosis is present. The relative 
 proportions of the different forms is usually about normal. In 
 
DISEASES OF THE BLOOD. 315 
 
 severe cases the lymphocytes may increase relatively and actually, 
 at the expense of the polymorphonuclear forms. Myelocytes are 
 occasionally present. 
 
 Associated changes in various organs may be met with. Among 
 these are parenchymatous and fatty degeneration of the heart, 
 kidneys, and liver. These conditions have often been ascribed to 
 reduced oxidation, which was supposed to be due to poverty in he- 
 moglobin. Physiologic studies, however, do not establish the ex- 
 istence of a reduction in the respiratory exchange of gases. It is 
 likely that toxic conditions of the blood occur in anemia, and that 
 the poisons act directly upon the affected organs. 
 
 Pathologic Physiology. — The process of oxidation is of 
 particular interest in anemia, and, as has been stated, recent in- 
 vestigations show that the consumption of oxygen and elimination 
 of carbon dioxid are normal. To accomplish this result more 
 active circulation and greater energy of the tissues are required. 
 Partly in consequence of the latter, diseases of the organs named 
 in the last paragraph result ; and at the same time some of the 
 characteristic symptoms (palpitations, dyspnea) are produced. In 
 severe secondary anemias increased tissue-waste occurs, and nitro- 
 gen is discharged in excess of that ingested. 
 
 THE PRIMARY ANEMIAS. 
 
 The conditions included under this title are chlorosis, progres- 
 sive pernicious anemia, leukemia, and Hodgkin's disease. The 
 term simple primary anemia is sometimes used to designate a form 
 of anemia without distinct cause, and characterized by moderate 
 oligocythemia. There are, it is true, occasional cases of moderate 
 anemia in which no definite precedent disease can be discovered ; 
 but these are exceptional cases, and are to be considered as sec- 
 ondary anemias in which the underlying disease is latent. Cases 
 of this sort do not conform to a definite type, and cannot there- 
 fore be considered as illustrating a special form of anemia. 
 Another term frequently used is splenic anemia. This is even 
 less satisfactorily defined. Splenic enlargement may occur in 
 any of the primary anemias, and may in some cases be excessive. 
 Moreover, some of the distinctly secondary anemias (as those of 
 rickets, syphilis, and malaria) are very often attended with splenic 
 enlargement. It has not been proved that there is a special form 
 of anemia with splenic enlargement as the conspicuous lesion, and 
 cases of so-called splenic anemia are to be considered as secondary 
 or primary anemias in which splenic enlargement happens to be 
 marked. 
 
 CHLOROSIS. 
 
 Definition. — Chlorosis is a primary anemia due to retarded 
 hemogenesis, characterized by a peculiar pallor and marked reduc- 
 
316 TEXT-BOOK OF PATHOLOGY. 
 
 tion in the percentage of hemoglobin, and occurring almost exclu- 
 sively in young girls and women. 
 
 Etiology. — Chlorosis is most frequent at the time of begin- 
 ning menstruation and during the years immediately following 
 this. A form of late chlorosis has been described in women above 
 thirty years of age and at the menopause ; but the nature of this is 
 doubtful. Chlorosis in the male is still more doubtful, though a few 
 cases have been described by competent observers. Hereditary 
 tendencies are of etiologic importance. The disease occurs more 
 frequently in families in which tuberculosis is common than in 
 those not so affected. Constitutional predisposition is also an 
 important factor, poorly developed girls, and particularly those of 
 delicate mould, being especially liable to the disease. Virchow 
 found hypoplasia of the heart and great vessels, and Rokitansky 
 the same condition in the generative organs, and pathologists 
 have been inclined to regard these as important factors in the 
 development of the disease. 
 
 Various exciting causes have been considered as of more or less 
 importance. Emotional excitement was regarded as a prime cause 
 by ancient authorities, and in consequence such terms as icterus 
 seufebris amantium were applied. Home-sickness, grief, etc., are 
 causes of moment. Intestinal auto-intoxication has been regarded 
 as the essential factor by many, but physiologic chemists fail to 
 find evidences of the existence of such intoxication. Menstrual 
 disturbances are important as symptoms, and have often been re- 
 garded as causes. The hypoplasia of the genital organs adds some 
 probability to this view, but more definite evidence is wanting. 
 
 At the present time it seems most likely that chlorosis is due 
 to faulty development, and especially to a want of proper hemo- 
 genetic power. 
 
 Pathologic Anatomy. — The hypoplasia of the vascular and 
 generative systems has been referred to. These are primary 
 lesions, and possibly causal. Various secondary diseases may be 
 encountered, as in other anemias. Among these, myocardiac de- 
 generation and dilatation are most important, though they do not 
 attain high grades of severity. The spleen is frequently a little 
 enlarged. Peculiar yellowish or greenish pigmentation of the 
 skin is a striking feature. The pigment is doubtless altered 
 hemoglobin, but its exact nature is unknown. 
 
 The Blood. — The blood is paler than normal, and watery. The 
 specific gravity decreases progressively, and the solid matter 
 is deficient. Increased coagulability is sometimes observed. The 
 number of red corpuscles may be normal, even in well-developed 
 cases, but the proportion of hemoglobin sinks progressively. 
 In prolonged cases the corpuscles become reduced in number, 
 but the deficiency of hemoglobin continues to be excessive. 
 Severe cases of chlorosis frequently show 3,000,000 or 2,000,000 
 
DISEASES OF THE BLOOD. 317 
 
 red corpuscles per cu.mm. and 30 per cent, to 20 per cent, of 
 hemoglobin. The red corpuscles may be little altered in ap- 
 pearance in the early stages ; later, irregularities in size and 
 shape are frequent, and nucleated red corpuscles (especially small 
 forms) make their appearance. The latter sometimes occur in 
 great numbers in crops (blood-crises). The leukocytes are usually 
 normal in number and kind ; but in some cases myelocytes have 
 been met with. 
 
 During the process of recovery from chlorosis the red corpus- 
 cles increase in number before any change occurs in the percentage 
 of hemoglobin. 
 
 Pathologic Physiology. — Chlorosis resembles the second- 
 ary anemias in most particulars, as far as its influence on the general 
 health is concerned. Some of the symptoms (cardiac and men- 
 strual) are doubtless due to primary abnormalities of structure. 
 The preservation of the subcutaneous fat despite advancing anemia 
 is a striking feature. It is explained by von Noorden by the 
 assumption that the quiet and warmth which chlorotics find neces- 
 sary to their comfort lead to accumulation of fat. Decreased 
 oxidation is certainly not the cause. 
 
 PROGRESSIVE PERNICIOUS ANEMIA. 
 
 Definition. — Progressive pernicious anemia is a form of 
 extreme anemia tending to increase in severity to a fatal end. It 
 may be apparently causeless, or more or less adequate causes may 
 be discovered. It is characterized by excessive oligocythemia 
 and marked changes in the red corpuscles. 
 
 etiology. — The disease was described by Addison as a wholly 
 causeless anemia — that is, an anemia independent of precedent 
 disease of any sort. In recent years, however, causes of various 
 sorts have been discovered. Pernicious anemia may occur in 
 childhood or old age, but is usually met with at or after middle 
 age. Depressing emotions, fright, exposure, and unsanitary sur- 
 roundings may act as contributing causes. Among the more 
 definitely active influences are : pregnancy and lactation, gastro- 
 intestinal diseases, and intestinal parasites. Pregnancy and lacta- 
 tion are frequent causes, but their manner of operation is obscure. 
 Gastro-intestinal diseases of various sorts have been found in cases 
 of pernicious anemia, including atrophy of the gastric and duo- 
 denal mucosa, ulcerations, carcinoma, etc. The manner of opera- 
 tion of these is obscure, though recent experimental work, tending 
 to show that pernicious anemia is hemolytic in nature, suggests 
 that poisons are generated in the gastro-intestinal tract, and, gain- 
 ing access to the blood, cause its destruction. Among the evi- 
 dences favoring this hemolytic theory, beside that furnished by 
 direct experimental intoxication, are the peculiar pigmentation of 
 
318 TEXT-BOOK OF PATHOLOGY. 
 
 the liver and the excess of coloring-matter in the urine. Of the 
 intestinal parasites that occasion a pernicious form of anemia, the 
 Anchylostoma duodenale and Bothriocephalus latus are important. 
 Other parasites occasionally cause severe anemia, but rarely, if 
 ever, forms suggesting true pernicious anemia. The manner of 
 production of anemia by parasites is still obscure. Some have 
 held that the loss of blood (especially in the case of Anchylostoma) 
 is the important cause ; but there are instances in which but 
 little blood is lost. Others believe that the parasites generate 
 poisons in their life or by decomposition after their destruction, 
 and that these poisons act as hemolytic agents. 
 
 In addition to the above, hemorrhages, systemic diseases (ma- 
 laria, syphilis, and tuberculosis), and various kinds of infection 
 have been considered as causes. Among the infectious agents 
 various bacteria and protozoan organisms have been described. 
 None of these seems to be of importance. 
 
 Pathologic Anatomy. — Various secondary changes are met 
 with, those in the blood-making organs being most important. 
 The bone-marrow of the long bones is red and softened and 
 often quite hemorrhagic (for details, see Bone-marrow). This 
 change was formerly regarded as a primary and causal one. At 
 the present time it is looked upon as secondary and reactive to 
 the severe anemia. It represents the effort of the bone-marrow to 
 compensate for the active blood-destruction. The spleen is some- 
 times enlarged, and may be considerably so. (Pigmentation of 
 the spleen will be referred to below.) 
 
 The liver, kidneys, and especially the heart suffer degenerative 
 changes (fatty) in severe cases. Similar alterations in the blood- 
 vessels may cause punctate hemorrhages (especially in the retina), 
 or larger hemorrhages in various situations. The lesions of the 
 gastro-intestinal tract have been referred to. Some of them are 
 doubtless secondary to the anemia; others may be primary. 
 
 Degenerations of the posterior and lateral columns of the spinal 
 cord are frequent. They seem to be due to a toxic agent rather 
 than to hemorrhages. 
 
 Pigmentation of the liver, spleen, kidneys, and other organs is 
 a significant condition in evidence of the active hemolysis supposed 
 to occur in this disease. The pigmentation of the liver is most 
 important, and seems to be characteristic. It occurs in the hepatic 
 cells of the periphery of the lobules and in the endothelial cells of 
 the lymphatic channels and capillaries in the same situation. The 
 pigment is iron-containing, and may be well demonstrated by ap- 
 plying the iron reactions (sulphid of ammonium ; hydrochloric acid 
 and ferrocyanid of potassium — forming Prussian blue). 
 
 The Blood. — The color of the blood is often strikingly pale ; 
 though it may be dark in spite of marked anemia. The specific 
 gravity is reduced. The marked feature of the disease is pro- 
 
DISEASES OF THE BLOOD. 319 
 
 noimced oligocythemia. This progresses rapidly, and in ordinary 
 cases the number of red corpuscles sinks to 1,000,000 or less per 
 cu.mm. : at the same time changes in size (microcytes and megalo- 
 cytes) and in shape (poikilocytes) make their appearance, and 
 reach grades rarely attained in other diseases (see Fig. 145). "Nu- 
 
 O 
 
 
 Fig. 145.— Blood in pernicious anemia, showing irregularity in the size and shape of 
 the red corpuscles ; one nucleated red corpuscle (megaloblast) and two leukocytes ; stained 
 with Ehrlich's triple mixture. 
 
 cleated red corpuscles are always present in some number and 
 are usually abundant (Fig. 145). The larger forms (megaloblasts), 
 as a rule, predominate ; but in some cases the smaller forms are 
 more abundant. Karyokinetic figures may be found in the nuclei. 
 Polychromatophilia is generally present. The leukocytes may be 
 decreased or normal in number ; in the late stages leukocytosis is 
 not uncommon, and it may become extreme. The larger mono- 
 nuclear leukocytes are usually more abundant than in health, and 
 myelocytes often occur in considerable numbers. In the terminal 
 leukocytosis of pernicious anemia the lymphocytes often predomi- 
 nate. 
 
 The fibrin-factors have been found in increased quantity in 
 chemical examinations, and albumoses (peptone ?) and excessive 
 quantities of xanthin-bodies have been detected in some cases. 
 
 Pathologic Physiology. — Pernicious anemia has many 
 characteristics of an intoxication, and there are undoubtedly toxic 
 bodies in the blood, whether these be essential or incidental. Some 
 investigators claim to have obtained putrescih and cadaverin from 
 the urine. There is more active metabolic tissue-consumption than 
 in health ; but the relations of oxidation to some of the secondary 
 lesions of the disease require further study. 
 
 Leukemia. 
 
 Definition. — Leukemia is a disease of hemogenesis, character- 
 ized by increase in the number of leukocytes in the circulating 
 
320 TEXT-BOOK OF PATHOLOGY. 
 
 I dot id and by pathologic changes in the bone-marrow, spleen, and 
 lymphatic glands. 
 
 Htiology. — Various diseases (malaria, syphilis, rickets, etc.) 
 have been regarded as predisposing causes. The same is true of 
 pregnancy, lactation, traumatism, exposure, and other influences. 
 Sometimes heredity seems to be an important element. 
 
 Infection has been suspected as the direct cause of leukemia by 
 many observers, and various forms of bacteria have been discovered 
 in the blood and tissues. There are certainly some very striking 
 facts in favor of an infectious nature, the most important being the 
 apparent contagiousness in a few cases. The various micro-organ- 
 isms need not be enumerated, as none of them has been proved to 
 be pathogenic. Bodies resembling protozoa have been found in 
 the blood and in the organs (lymphatic glands), but the nature and 
 significance of these are uncertain. 
 
 The relations of the lymphatic lesions to the condition of the 
 blood requires consideration. Virchow held that active prolifera- 
 tive change in the lymphadenoid tissues is the pathologic foun- 
 dation of the disease and the source of the increased numbers of 
 leukocytes in the blood. This view was strongly supported by 
 Flemming's discovery of karvokinetic changes in the cells of the 
 lymphatic glands and spleen. Another school of pathologists 
 maintained that the increased proportion of leukocytes results 
 from retardation in leukocytic destruction, and that the peculiar 
 lesions of the lymphadenoid tissues result from the deposit of the 
 leukocytes from the blood. Most authorities agree that there is some 
 deposition of this kind, but hold to the view of Virchow that the 
 enlargement of the organs comes in the main from primary disease 
 of the affected organs. 
 
 Pathologic "Anatomy. — The lesions of the solid organs 
 principally affect the spleen, the bone-marrow, and the lymphatic 
 glands, and the terms lienal or splenic, medullary or myelogenous, 
 and lymphatic leukemia are applied. In the majority of cases the 
 spleen and bone-marrow are involved, and the name lienomedul- 
 lary leukemia is used. Pure lymphatic leukemia is comparatively 
 rare, but involvement of the lymphatic glands with the spleen 
 and bone-marrow is common. A few cases of pure myelogenous 
 leukemia have been described, but their nature was not certainly 
 determined. 
 
 (The changes met with in the lymphatic structures are discussed 
 in the appropriate sections and in the chapters on Tumors.) 
 
 In a few instances the primary lesion was lymphadenoma of 
 the thymus gland or its remnant. Occasionally the primary dis- 
 ease is in the lymphadenoid tissues of the gastro-intestinal tract. 
 Primary dermal leukemia has been described (lymphodermia 
 perniciosa), but is not satisfactorily established. 
 
 Among the secondary lesions are lymphoid infiltrations of the 
 
DISEASES OF THE BLOOD. 
 
 321 
 
 liver, kidneys, lungs, heart, and other tissues. The organs show 
 areas of light color, or a streaked or mottled appearance, due to 
 the deposition of masses of lymphoid cells (Fig. 146). Secondary 
 
 Fig. 146.— Lymphoid infiltrations between the renal tubules, from a case of leukemia. 
 
 degenerations of the heart, liver, and kidneys may result from the 
 lymphomatous deposits, or from the impoverished state of the 
 blood and the presence of toxic substances. Scleroses of the 
 spinal cord may be met with, as in pernicious anemia. 
 
 The Blood. — The blood is often light in color and may be quite 
 milky in appearance. The specific gravity is lowered. The 
 alkaline reaction is less decided than normal, and in some cases 
 the reaction has been found acid, probably from rapid change after 
 removal from the body. Coagulation is slow. This has been 
 attributed to the presence of albumoses in the blood. 
 
 The conspicuous feature in the blood is the increased number 
 of leukocytes. In moderate cases there are from 100,000 to 300,- 
 
 000 white corpuscles per cu.mm. In severe cases the number is 
 greater ; while in mild or beginning cases, or in cases under active 
 treatment, the number may for a time be normal or subnormal. 
 
 1 have at the present time under observation a case in which the 
 leukocytes have fallen to 3,000 from 500,000 per cu.mm. Rapid 
 fluctuations in number are very common. 
 
 The study of the blood led Virchow to distinguish two forms 
 of leukemia : that in which small forms of leukocytes pre- 
 dominate (lymphemia), and that marked by the excessive number 
 of large cells (splenemia). This distinction may still be made, 
 but the significance attributed to it as an indication of the organs 
 primarily affected cannot now be sustained. It is true that in 
 lienomedullary leukemia large cells usually predominate, while 
 Lymphocytes are conspicuous in lymphatic forms of leukemia ; but 
 
322 TEXT-BOOK OF PATHOLOGY. 
 
 transitional cases rob the distinction of its practical importance. 
 It is here retained for the sake of convenience of description. 
 
 Lienomedullary Type. — The blood presents a great excess of 
 white corpuscles and more or less decided poverty in red cells. 
 The proportion of white to red corpuscles is often 1 : 3, 1 : 2, or 
 even 1:1. The larger mononuclear leukocytes (including normal 
 mononuclear and transitional elements and myelocytes) predomi- 
 nate over the lymphocytes and polymorphonuclear elements (Fig. 
 147). The latter two forms, however, are actually increased. 
 
 
 
 
 
 
 
 @ 
 
 
 •$# 
 
 Fig. 147.— Blood in lienomedullary leukemia, showing several mononuclear neutro- 
 philes (myelocytes), one polymorphonuclear neutrophile, and an eosinophile : a nucle- 
 ated red corpuscle and a lymphocyte are seen in the lower part of the illustration ; stained 
 with Ehrlich's triple mixture. 
 
 Myelocytes are usually found in great numbers, and are an evi- 
 dence of implication of the bone-marrow. There is usually an 
 actual increase in the number of eosinophile elements, but the 
 percentage-proportion is rarely increased. Basophilic leukocytes 
 (mast-cells and finely basophilic forms) are present in numbers 
 greatly in excess of those found in health. The red corpuscles 
 present the usual features of anemic blood, and nucleated forms 
 are particularly abundant. This is regarded as an evidence of 
 disease of the bone-marrow. 
 
 A peculiar constituent of the blood are the Charcot-Neumann 
 crystals. These are polyhedral, needle-shaped crystals of un- 
 certain composition, met with in the blood after death or some 
 time after removal from the body, and exceptionally in the fresh 
 blood. They were first detected in the bone-marrow. 
 
 Lymphatic Type. — The leukocytosis is less marked than in the 
 lienomedullary type. The lymphocytes predominate (Fig. 148), 
 but actual excess of large mononuclear forms and polymorpho- 
 nuclear leukocytes is observed. Myelocytes occur in small num- 
 bers ; exceptionally in considerable proportion. The number of 
 red corpuscles is decreased, and nucleated red cells may be present. 
 
DISEASES OF THE BLOOD. 323 
 
 Pathologic Physiology. — Leukemia is usually a progres- 
 sively destructive disease. The nature of the disturbances, how- 
 ever, is only partly known. The blood contains toxic substances 
 generated by leukocytic destruction (xanthin-bodies) and acids 
 (lactic, acetic, etc.). Albumoses are present in varying propor- 
 
 o^ # °^ °o 
 
 b% 
 
 Fig. 148.— Lymphatic leukemia, showing excess of lymphocytes. 
 
 tions, and probably play an important part in the pathology. The 
 urine frequently contains excess of xanthin-bases and uric acid. 
 
 Acute I/euketnia. — In a certain number of cases leukemia 
 seems to run an acute course, terminating in from a few weeks to 
 a few months. The characters of the blood are much the same as 
 in ordinary chronic leukemia (especially the lymphatic type), and 
 the lesions are similar. Gastro-intestinal lesions (ulcers in the 
 mouth, stomach, or intestines) and petechial hemorrhages (pur- 
 pura) are frequent. In several instances distinct contagiousness 
 was noted. The exact pathology of this condition remains obscure ; 
 it is very probable that there is some form of acute infection. 
 
 Hodgkin's Disease. 
 
 Pseudoleukemia, or Hodgkin's disease, resembles leukemia in 
 the lesions of the solid organs, but differs in that the blood does 
 not present increase in the number of leukocytes. The lymphatic 
 glands enlarge more quickly than in leukemia and the spleen and 
 marrow are less frequently involved, but otherwise no distinction 
 can be made. Cases of Hodgkin's disease sometimes become con- 
 verted into leukemia, and the reverse has been known to take 
 place. It has been held by some that Hodgkin's disease repre- 
 sents an aleukemic stage of the same disease. 
 
 Pseudoleukemia Infantum. 
 
 Under this name von Jaksch described a form of leukocytosis, 
 with enlargement of the spleen and liver, occurring in children. 
 
324 TEXT-BOOK OF PATHOLOGY. 
 
 There is rapid and excessive oligocythemia, and the leukocytosis 
 is pronounced. Leukocytes of all types are present, and give to 
 the blood a curiously variegated appearance. There is no striking 
 difference, however, from the characters of the blood met with in 
 other cases of leukocytosis in infancy. Rickets and congenital 
 syphilis seem to be closely related to this form of disease. 
 
 The enlargement of the spleen and liver is not of the nature 
 of that seen in leukemia or Hodgkin's disease, but is simply a 
 chronic hyperplastic condition. 
 
 FOREIGN BODIES AND PARASITES. 
 
 Foreign Bodies in Blood. — Various kinds of particles may 
 gain access to the blood-current and may be carried to peripheral 
 parts of the circulation. In anthracosis a lymphatic gland may 
 attach itself and, after softening, rupture into a vein. The parti- 
 cles of carbon are thus distributed in the blood. Small portions 
 of tumors, of the heart-valves, calcareous particles from atherom- 
 atous plates, and portions of thrombi are frequently transported by 
 the blood. Charcot crystals are met with in leukemia, and pig- 
 meut-matter, due to disintegration of the blood itself, is seen in 
 malaria. 
 
 Parasites in the Blood. — Among the animal parasites are 
 the malarial plasmodium, which occurs within the red corpuscles 
 or free in the plasma ; the Distoma haematobium, which occupies 
 the portal vein ; and the embryos of the Filaria sanguinis hominis. 
 (These are more fully described in the section on Parasites.) Por- 
 tions of hydatid cysts or of cysticerci and trichinae are occasionally 
 conveyed in the circulation. 
 
 Vegetable Parasites. — Mould-fungi sometimes gain entrance 
 into the circulation and lead to serious embolism, as does also the 
 actinomyces. Of the pathogenic bacteria, the spirillum of relaps- 
 ing fever and the bacillus of anthrax are most abundant in the 
 blood. Other micro-organisms are more difficult of demonstration, 
 though micrococci of suppuration, the bacillus of influenza, and 
 even tubercle-bacilli have been detected. 
 
 METHODS OF EXAMINING THE BLOOD. 
 
 The purely clinical examinations, such as the enumeration of 
 the corpuscles and the estimation of the percentage of hemoglobin, 
 need not be here described. The microscopic examinations alone 
 will be considered. 
 
 Examination of the Fresh Blood. — A drop of blood is 
 obtained from a prick into the end of a finger or the lobe of the 
 ear. The finger or ear is first cleansed, then pricked with a lancet, 
 and the first few drops of blood wiped away. A small drop is 
 then received upon a carefully cleansed thin cover-glass, and this 
 is laid on an equally clean and slightly warm glass slide. The 
 
DISEASES OF THE BLOOD. 325 
 
 blood spreads into a thin film from the weight of the cover-glass. 
 If prolonged examination is to be made, a ring of vaselin around 
 the edges preserves the specimen for some hours. 
 
 The examination should be made with an oil-immersion lens. 
 Malarial parasites, the spirocheta of relapsing fever, and filarise 
 are quite readily detected in such specimens ; and the size and 
 shape of the red corpuscles and the ameboid movements of the 
 leukocytes can be determined. For the last purpose a warming- 
 stage is requisite if a prolonged examination is to be made. 
 
 Examination of Fixed Preparations. — Thin cover-glasses 
 are carefully cleaned with soap-water, then with clear water, and 
 finally with alcohol. A drop of blood is placed upon one of the 
 glasses and a second glass is laid upon it. The blood spreads into 
 a thin film, and the cover-glasses are then slid apart and allowed 
 to dry in air. 
 
 Fixation of the blood may be accomplished by immersing 
 the prepared cover-glass in a mixture of equal parts of absolute 
 alcohol and ether for from five to thirty minutes. For certain 
 stains (notably the neutrophilic mixture) a better method of fixa- 
 tion is the employment of heat. The most accurate method of 
 heating is to place the cover-glass in an oven at 120° C. (248° F.) 
 for an hour ; but I find that drawing the cover-glass rapidly through 
 a Bunsen flame three times accomplishes the purpose almost as well. 
 Special methods of fixation, as with bichlorid of mercury, picric 
 or osmic acid, etc., are rarely necessary. 
 
 Staining. — A useful stain to determine the morphology of the 
 corpuscles is Gollasch's mixture : 
 
 Eosin crystals 0.5 
 
 Hematoxylin 2.0 
 
 Glycerin 
 
 Distilled water 
 
 Absolute alcohol da 100.0 
 
 Glacial acetic acid 10.0 
 
 Alum slight excess. 
 
 The solution must be allowed to " ripen " by exposure for sev- 
 eral weeks in a light place. The specimen is stained for two or 
 three minutes, washed in water, and examined. The various 
 pathologic conditions of the red corpuscles are brought out, and 
 the morphology of the leukocytes is well shown. The oxyphilic 
 granules stain sharply with the eosin. 
 
 Similar results are obtained with the following mixture : 
 
 Methylene-blue, saturated aqueous solution 40 
 
 Eosin, j per cent, solution in 75 per cent, alcohol 20 
 
 Distilled water 40 
 
 The specimen may be stained for from three to five minutes, 
 but better results are obtained by placing the stain containing the 
 
326 TEXT-BOOK OF PATHOLOGY. 
 
 cover-glass preparation in an oven at 37° C. (98.6° F.) for an hour. 
 The morphology and changes in the red corpuscles are clearly 
 shown, and the oxyphilic and basophilic granules of the leukocytes 
 are well stained — the former red, the latter blue. The basophilic 
 granules of the leukocytes are especially distinct. 
 
 Neutrophilic granules are best stained with Ehrlich's triple 
 stain : 
 
 Orange Gr, saturated aqueous solution 120 to 135 
 
 Acid fuchsin, saturated aqueous solution 80 to 165 
 
 Methyl-green, saturated aqueous solution 125 
 
 Distilled water 300 
 
 Absolute alcohol 200 
 
 Glycerin 100 
 
 The first two stains are mixed, and the third is added gradu- 
 ally, stirring constantly. The water, alcohol, and glycerin are then 
 added. Aery often less acid fuchsin and more methyl-green give 
 better results. The fixed preparation is stained for three minutes 
 and washed in water. The red corpuscles take the orange stain ; 
 the nuclei of white and red corpuscles and basophilic granules 
 take the green ; the oxyphilic granules take the red ; and the 
 neutrophilic granules take the violet or purple of the mixture. 
 
 Staining of Parasites. — The malarial parasites may be 
 satisfactorily examined in unstained specimens, but it is sometimes 
 desirable to study them after staining. Cover-glass preparations 
 are made as before described, and fixed by heat or by immersion 
 in the absolute alcohol-ether mixture for from thirty minutes to 
 several hours. The staining maybe accomplished with any of the 
 various eosin-methylene-blue mixtures, but Plehn's solution has 
 been specially recommended for the purpose : 
 
 Methylene-blue, saturated aqueous solution 60 c.c. 
 
 Eosin, \ per cent, solution in 75 per cent, alcohol 20 c.c. 
 
 Distilled water 40 c.c. 
 
 Potassium hydrate, 20 per cent, solution 12gtt. 
 
 This stains the malarial organisms blue, the red corpuscles red. 
 Similar solutions stain filaria? satisfactorily, and are useful in 
 demonstrating various bacteria in the blood. 
 
 CHAPTER II. 
 
 DISEASES OF THE LYMPHATIC TISSUES. 
 
 THE SPLEEN. 
 
 Anatomic Considerations. — The spleen is practically a 
 complicated Lymphatic gland with close relations to the circula- 
 tion. It is enclosed in a fibrous capsule, from which trabecular 
 
DISEASES OF THE LYMPHATIC TISSUES. 327 
 
 enter into the substance of the organ and give off subdivisions 
 that unite and form a framework, in the meshes of which lym- 
 phoid tissue is embedded. The splenic artery enters at the hilum 
 and subdivides into numerous branches which traverse the tra- 
 becule. Side branches are given off from the trabecular arterioles ; 
 these penetrate the splenic pulp and are surrounded by denser 
 aggregations of lymph-cells, which are visible to the naked eye as 
 the Malpighian bodies. All of the terminal arteries discharge 
 their blood directly into the spaces of the splenic pulp, from which 
 it is re-collected into the veins. The spaces contain, in addition 
 to lymphoid cells and red blood-corpuscles, larger cells often con- 
 taining pigment-granules or even small blood-corpuscles. 
 
 The weight of the spleen in the adult varies from 140 to 
 200 gm. 
 
 The splenic function remains in doubt. It seems to have some 
 connection with the process of manufacture of leukocytes, and is 
 one of the sources of red blood-corpuscles. It may also be the 
 place of destruction of red corpuscles, and in cases of general 
 hemolysis, or blood-destruction, the blood-pigment and fragmented 
 corpuscles are especially arrested in this organ. 
 
 Pathologic Physiology. — The relations of diseases of the 
 spleen to the general health are still obscure. It has been held 
 by some pathologists that this organ plays an important part in 
 the process of immunization or combating infectious diseases. The 
 fact that bacteria and foreign bodies circulating in the blood are 
 arrested in the spleen to such a large extent warrants the suspicion 
 that this organ is important in arresting irritants, and thus pre- 
 venting their gaining access to more vital parts. Experimenters, 
 however, have found no uniform increase of susceptibility to micro- 
 organismal inoculation on the part of desplenetized animals. For 
 the present, therefore, we can only suspect that removal or disease 
 of the spleen renders individuals more vulnerable to infections. 
 
 The effect of removal of the spleen in human beings is sur- 
 prisingly slight. A certain amount of anemia and general deteri- 
 oration of health follow the operation, but seem to be the result 
 of the operation per se, rather than of removal of the organ. Sub- 
 sequently, complete health is regained. 
 
 ABNORMAL DEVELOPMENT AND SITUATION. 
 
 Complete absence of the spleen has sometimes been noted in 
 children that lived for several years. More commonly slighter 
 defects, such as unusual smallness or excessive lobulation, occur. 
 Very often small accessory spleens, the size of a pea or a marble, 
 are found. 
 
 Movable Spleen. — The organ may be quite movable, either as 
 a congenital condition or as the result of enlargement and resulting 
 
328 TEXT-BOOK OF PATHOLOGY. 
 
 traction upon its attachments. Downward displacement and 
 movability are frequently found in cases of splanchnoptosis. 
 Twisting of the pedicle of a movable spleen may lead to stran- 
 gulation of the circulation and consequent necrosis. 
 
 CIRCULATORY DISTURBANCES. 
 
 Anemia may occur in cases of general anemia resulting from 
 hemorrhage or inanition. The spleen presents a contracted appear- 
 ance, the capsule being wrinkled, and on section the substance is 
 found to be lighter in color and the fibrous stroma is more prom- 
 inent than normal. 
 
 Hyperemia may be active or passive. Active hyperemia is a 
 physiologic condition during digestion, when the spleen increases 
 somewhat in size. Intense congestion occurs in a number of dis- 
 eases, but so commonly passes into inflammation that it will be 
 described under that heading. Passive congestion is most marked 
 in cases of cirrhosis of the liver, but also occurs in association 
 with hyperemia of other organs as the result of cardiac failure, of 
 emphysema, or of other diseases obstructing the larger venous 
 channels. The spleen is greatly enlarged and of a dark-red color, 
 and the capsule is often tensely distended ; the Malpighian bodies 
 are less visible than normally. After long continuation of the 
 process hyperplasia of the trabecular and the fibrous stroma gen- 
 erally takes place. The spleen may be greatly enlarged and very 
 dense at this stage. Subsequently contraction of the newly-formed 
 fibrous tissue may lead to atrophy of the proper splenic substance 
 and increased induration of the organ [cyanotic induration). Con- 
 siderable pigmentation is found in such cases from the destruction 
 of the stagnated blood. 
 
 Hemorrhages in the spleen may be the result of traumatism, 
 when large hematomata may form, especially just beneath the cap- 
 sule. Small areas of hemorrhage are not infrequent in intense in- 
 fections with splenitis, but it is difficult to draw a line between 
 hemorrhage and the overfilling of the spaces by congestion, since 
 the blood under normal conditions enters directly into the splenic 
 pulp. 
 
 Embolism of the splenic artery is very common in cases 
 of endocarditis or thrombosis in the left heart or aorta. As the 
 spleen contains abundant " terminal arteries," infarction is the 
 common result. The area may remain light colored, constituting 
 an anemic infarct ; or it may become overfilled with blood, when 
 hemorrhagic infarction results. In either case there is a wedge- 
 shaped lesion, with the base toward the surface of the organ and 
 the apex within, harder than the surrounding tissue, and usually 
 somewhat elevated. The swelling and elevation in the case of 
 anemic infarction are partly due to a zone of hyperemia which 
 
DISEASES OF THE LYMPHATIC TISSUES. 329 
 
 usually surrounds it. Complete resolution may occur, but more 
 commonly the area involved undergoes coagulation-necrosis and 
 softening, and as absorption takes place fibrous overgrowth gives 
 rise to the formation of a scar. There may be numerous infarcts 
 of small size, or a single large one sometimes occupying as much 
 as half of the organ. (Septic infarction and its results are dis- 
 cussed under Abscess of the Spleen.) 
 
 Thrombosis of the splenic vein may occur in association with 
 thrombosis of the portal vein. It causes intense passive hypere- 
 mia of the spleen. Occasionally calcification of thrombi gives 
 rise to the formation of splenic 
 
 INFLAMMATION OF THE SPLEEN, OR SPLENITIS. 
 
 Splenitis occurs in a variety of conditions, and may present 
 itself in several forms, among which the acute enlargement of the 
 spleen of infectious diseases and localized splenitis, or abscess of 
 the spleen, are the principal. 
 
 Diffuse Splenitis. — The splenic enlargement of infection 
 occurs particularly in typhoid fever, malaria, septicemia, typhus, 
 and relapsing fevers ; and less markedly in pneumonia, scarlet 
 fever, small-pox, and influenza. In the earlier stage the spleen is 
 simply congested and presents a dark-red color ; is firm, and the 
 capsule more or less distended. On section the Malpighian bodies 
 are usually obscured, and there may be visible areas of hemorrhagic 
 extravasation. Microscopically at this stage the blood-vessels are 
 all found overdistended, and the spaces within the splenic pulp are 
 filled with red and white blood-corpuscles. If the process has con- 
 tinued for some time, pigment-masses and degenerated corpuscles 
 are visible, but there are as yet no evidences of inflammatory 
 hyperplasia of the splenic pulp or stroma. 
 
 As the process advances the spleen may become softer and may 
 be quite diffluent. On section the substance is now found to be 
 lighter in color, the Malpighian bodies are distinct, and, particu- 
 larly in violent septic cases, are decidedly prominent, presenting 
 themselves as yellowish-gray punctae, somewhat resembling miliary 
 tubercles. The capsule of the organ may still be tensely distended, 
 but in other cases is wrinkled, as if some shrinkage of the spleen 
 had occurred in the change from the first stage of congestion to 
 that of well-defined inflammation. Microscopically there are now 
 apparent great increase of the cells of the splenic pulp, and particu- 
 larly of those constituting the Malpighian bodies. That this in- 
 crease is partly at least due to active proliferation is known from 
 the abundance of mitoses. There is also hyperplasia of the stroma 
 and trabeculse, and of the endothelial cells of the spaces. 
 
 In still later stages signs of degeneration may become promi- 
 nent. This is apparent in the increasing softening of the organ, 
 
330 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 while under the microscope there are found cellular degenerations 
 leading to the formation of detritus, to fragmentation of the nuclei 
 of the cells, and to pigmentation by disintegration of red blood- 
 corpuscles. 
 
 Terminations. — Most frequently complete resolution occurs. 
 Sometimes, however, persistence of the inflammation is noted ; 
 and, when repeated attacks of the infection occasion repeated 
 attacks of splenitis, chronic inflammatory hyperplasia is the result. 
 This is especially marked in the " ague-cake" spleen of malaria. 
 Spontaneous rupture or rupture from slight trauma may result 
 from the softened and distended condition of the organ. Finally, 
 suppuration may ensue, either in the form of a diffuse softening 
 and purulent infiltration of the entire organ, or in the form of a 
 localized abscess beginning at the point of greatest involvement. 
 
 Circumscribed Splenitis, or Abscess of the Spleen. — 
 This may be the termination of an acute diffuse splenitis, particu- 
 larly in septicemia and typhoid fever ; or it may be caused by 
 extension of diseases of neighboring structures, by septic embo- 
 
 Fig. 149.— Embolic abscess of the spleen (from a specimen in the Museum of the Philadel- 
 phia Hospital). 
 
 lism, or traumatic injuries. In the last case, the mechanical 
 injury of the spleen merely furnishes suitable conditions for the 
 action of bacteria conveyed to it through the circulation, or the 
 spleen is actually penetrated and infected. Occasionally abscess 
 may result from the perforation of gastric ulcers or from the ex- 
 tension of other inflammations in the vicinity. An important 
 
DISEASES OF THE LYMPHATIC TISSUES. 331 
 
 group of oases is that in which the abscesses are embolic and 
 metastatic (Fig. 149). Such cases are met with in malignant 
 endocarditis or thrombosis of the heart or aorta, and in cases of 
 pyemia following other infective conditions. The first effect of 
 the embolism is an hemorrhagic or anemic infarction, but this soon 
 undergoes suppurative softening, beginning at the apex of the in- 
 farct. Metastatic abscesses are most common near the surface of 
 the organ and are usually multiple, though a single cavity occupy- 
 ing the greater part of the organ may occur. Small collections 
 may become absorbed or inspissated, leaving a necrotic or cheesy 
 collection as a residue. Larger collections may be discharged by 
 perforation into the stomach or intestines, or they may break into 
 the peritoneal or pleural cavity, causing septic peritonitis or 
 pleuritis. 
 
 Chronic Inflammation or Chronic Hyperplasia of the 
 Spleen. — Attention has already been called to the slow hyper- 
 plasia of the connective tissue and sometimes of the splenic pulp 
 occurring in consequence of chronic passive congestion and of re- 
 peated attacks of acute splenitis. The spleen is large in size and 
 firm. The capsule is often tensely distended and may be greatly 
 thickened. The thickening is either diffuse or circumscribed, 
 patches of almost cartilaginous hardness occurring in the latter 
 case. Attachments by fibrous adhesions may fix the spleen to the 
 diaphragm or the neighboring organs. On section the spleen is 
 found dark in color from the presence of abundant pigment, and 
 the excess of fibrous tissue may be visible to the naked eye. Mi- 
 croscopically, increased thickness of the fibrous trabecule and of 
 the walls of the small blood-vessels and pigmentation with altered 
 blood-pigment are the conspicuous features. 
 
 A somewhat different form of chronic hyperplasia is dependent 
 upon syphilis, especially upon the congenital form. In this the 
 appearances are much the same as in the cases following splenitis 
 or congestion, but, as a rule, the color is somewhat lighter from 
 the fact that the process is a slowly hyperplastic one without acute 
 inflammatory or congestive manifestations. Somewhat similar 
 appearances result from rickets. 
 
 ATROPHY AND DEGENERATIONS. 
 
 Atrophy of the spleen is very common in old age. The cap- 
 sule is usually wrinkled and somewhat thickened, and on section 
 the organ is more fibrous in appearance on account of atrophy of 
 the splenic pulp and proliferation of the stroma. Thickening of 
 the capsule sometimes appears in the form of white plates of 
 cartilaginous hardness, which result from inflammatory over- 
 growth of the capsule (perisplenitis eartilaginea). 
 
 Amyloid degeneration occurs more frequently in the spleen 
 
332 TEXT-BOOK OF PATHOLOGY. 
 
 than in any other organ. The causes are those which lead to amyloid 
 disease elsewhere. Jn most cases the degeneration begins in the 
 Malpighian bodies, affecting the walls of the blood-vessels (Plate 
 2) and the lymphoid elements. On section in such a case there 
 are seen small round areas about the size of a currant-seed, of 
 gelatinous, translucent appearance. These have been likened to 
 grains of boiled sago, and the term sago-spleen is not inappropriate. 
 In other cases a more uniform involvement of the whole organ is 
 noted, and the section presents the appearance of boiled ham or 
 dried beef. Considerable enlargement of the organ is noted in 
 such instances, and the tissue is much harder than normal. 
 Beginning amyloid degeneration may be difficult to determine 
 microscopically, but is readily demonstrated by the microscopic 
 staining-reaetions (see Amyloid Degeneration). 
 
 Hyaline degeneration has been observed in association 
 with amyloid and independent of the latter. It affects the small 
 blood-vessels and the reticulum more particularly. 
 
 Pigmentation is a very common result of chronic congestion 
 as well as of repeated acute splenitis ; the spleen in cases of 
 cirrhosis of the liver and in chronic malaria is therefore habitually 
 pigmented. The deposit occurs first in the walls of the blood- 
 vessels and later throughout the splenic structure, either within the 
 cells or lying free in the tissue. Occasionally pigment-particles 
 derived from the external world are deposited in the spleen. This 
 is especially true of dust-particles which have reached the circu- 
 lation from softened bronchial glands. In cases of diseases of 
 other kinds leading to discharge of foreign bodies or tissue-ele- 
 ments into the circulation, the arrest not rarely occurs in the 
 spleen, and reactive congestion or inflammation with enlargement 
 of the spleen may result (spodogenous splenitis). Pigmentation of 
 the spleen is seen in progressive pernicious anemia and other con- 
 ditions in which hemolysis occurs. The pigments resulting from 
 the destruction of red corpuscles are deposited in the liver, spleen, 
 and other organs. * 
 
 Calcification occurs in the thickened capsule of chronic 
 splenitis and in old infarcts, tubercular or syphilitic areas, and 
 occasionally in thrombi of the splenic vein. Parasitic cysts may 
 be surrounded by calcification. 
 
 TUMORS AND PARASITES. 
 
 I/ymphadenoma of the spleen, as it occurs in the diseases 
 leukemia and pseudoleukemia, like the alterations of the lym- 
 phatic glands occurring in the same diseases, may properly be in- 
 cluded among the tumors rather than among simple hyperplasia?. 
 The disease is appropriately designated lymphadenoma or lympho- 
 sarcoma. The spleen may be affected primarily in leukemia (lienal 
 
Plate 2. 
 
 ftif^i 
 
 
 Amyloid degeneration of the spleen, showing a degenerated Malpighian hody; 
 specimen stained with hematoxylin and eosin. 
 
DISEASES OF THE LYMPHATIC TISSUES. 
 
 333 
 
 or splenic leukemia), or it may be involved after the bone-marrow 
 (myelogenous leukemia) or the lymphatic glands (lymphatic 
 leukemia). The appearances of the organ in leukemia and in 
 Hodgkin's disease are identical. In the earlier stages the spleen 
 is enlarged and soft. On section there is evidence of intense con- 
 gestion, while at the same time light-colored areas, representing 
 enlarged Malpighian bodies, are visible throughout its structure. 
 Subsequently the hyperplasia of the lymphoid structures increases 
 and the organ becomes lighter-colored and- harder than normal. 
 The pressure exerted on the splenic pulp causes anemia, and 
 granular or pigmentary degeneration of the cells, while anemic 
 and hemorrhagic infarctions with subsequent necrosis are likely to 
 form near the surface of the organ. The section of such a spleen 
 presents a peculiarly variegated appearance, while the microscopic 
 examination exhibits wide variations from the normal. The 
 Malpighian bodies are found greatly enlarged, and are composed 
 of aggregations of the ordinary lymphoid cells, together with 
 larger round cells. Mitoses have frequently been demonstrated. 
 The splenic pulp is degenerated, exhibiting large cells enclosing 
 pigment-granules or red corpuscles and detritus. 
 
 Sarcoma and Carcinoma. — Primary sarcoma of the round- 
 celled, or fibro-sarcomatous, variety has been 
 observed. Secondary sarcoma, particularly 
 melanotic sarcoma, and secondary carcinoma 
 are more common than primary growths. 
 
 Cysts are occasionally discovered. They 
 are small, and are probably due to dilatation 
 of the lymphatic spaces or to atrophy and 
 cystic degeneration of the Malpighian fol- 
 licles. 
 
 Fibroma, angioma, and lymphan- 
 gioma are very rare. 
 
 Parasites. — Pentastomum denticula- 
 tum, echinococcus cysts, and cysticerci have 
 been observed. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis of the spleen may occur 
 in the form of minute miliary tubercles, 
 which have a grayish translucent appear- 
 ance and are usually present in large num- 
 bers, especially near the capsule. They may 
 be distinguished from enlarged Malpighian 
 bodies by their greater opacity and their grayish rather than yel- 
 lowish color. Tuberculosis also occurs in the form of larger 
 caseous nodules, especially in children (Fig. 150). In these cases 
 
 Fig. 150.— Large caseous 
 tubercles in the spleen of a 
 child (Orth). 
 
334 TEXT-BOOK OF PATHOLOGY. 
 
 there are seen nodular masses the size of a pea or cherry studding 
 the surface and deeper structure of the spleen. This form is called 
 Affcutuberculoae by the Germans, from the resemblance of the large 
 nodules to tubercles met with in monkeys. Histologic examination 
 proves the nodules to be composed of aggregations of tubercles 
 undergoing caseation. 
 
 Primary tuberculosis of the spleen has never been observed. 
 
 Syphilis may present itself in the form of syphilitic gummata, 
 which are usually multiple and may be either small or large. They 
 are distinguished by their central degeneration or by the fibrous- 
 tissue striatums at the exterior. 
 
 Diffuse hyperplasia of the spleen is a frequent or almost con- 
 stant lesion of congenital syphilis. 
 
 THE LYMPHATIC GLANDS. 
 
 Anatomic Considerations. — The lymphatic glands con- 
 sist of accumulations of lymphadenoid tissue surrounded by a 
 connective-tissue capsule. There may be distinguished an outer 
 cortical and an inner medullary portion, the former consisting of 
 spherical masses or follicles of lymphoid cells enclosed in a con- 
 nective-tissue reticulum springing from the trabecular, the latter 
 being composed of medullary cords similar to the former in struct- 
 ure, but of elongated form. The afferent lymphatics enter the 
 glands at the hilum and discharge the lymph into the cortical 
 spheres ; the liquid filters slowly toward the medullary cords, 
 where it eventually enters the efferent lymphatics. The medullary 
 cords are surrounded by spaces lined with endothelial cells, the 
 lymph-spaces. 
 
 ATROPHY. 
 
 Atrophy of the lymph-glands occurs in old age and in various 
 marasmic conditions. The glands suffer considerable diminution 
 in size, the cellular elements being particularly affected ; they are 
 therefore hard, dry, and often irregular in shape. Fatty infiltra- 
 tion may occur simultaneously with atrophy, the gland in such 
 cases preserving its size and having a decidedly fatty appearance. 
 
 HYPERTROPHY. 
 
 This is so closely allied to the conditions designated by the 
 name of lymphadenoma that it is difficult to separate the cases 
 which might be considered as strictly hypertrophy. 
 
 DEGENERATIONS. 
 Fatty infiltration is sometimes seen in cases of general 
 obesity and also, as before mentioned, in atrophy of the glands. 
 Amyloid degeneration is met with in cases of general amyl- 
 
DISEASES OF THE LYMPHATIC TISSUES. 335 
 
 oid disease, and particularly in the cases in which the intestines 
 are affected. The lymphatic glands may, however, be independ- 
 ently involved in cases of tuberculosis attended with suppuration. 
 In such instances the adjacent lymphatic glands are most likely to 
 suffer amyloid change. The morbid process rarely leads to marked 
 alteration of the glands, but the amyloid material may be demon- 
 strated by the staining-reactions peculiar to it. The connective 
 tissue of the trabecular and around the blood-vessels is first 
 affected ; later, the endothelial cells. 
 
 Hyaline degeneration has been described. It affects the 
 blood-vessels and connective tissue of the glands. 
 
 Calcification not infrequently forms the terminal condition 
 in cases of necrosis or induration of the glands in consequence of 
 tuberculous or simple inflammation. There may be small calca- 
 reous granules scattered through the gland, or the entire gland 
 may be infiltrated. 
 
 Necrosis may occur in consequence of tuberculous or syphilitic 
 affections, or of simple inflammation. In the former cases, particu- 
 larly in tuberculosis, the center of the gland or the entire gland 
 becomes cheesy and soft, often liquefying and discharging the 
 contents by rupture of the capsule. In consequence of simple 
 inflammation, as in certain infectious fevers (typhoid, diphtheria, 
 scarlet fever), a different form of necrosis is met with, areas of the 
 gland becoming soft, pultaceous, and sometimes putrid. The 
 gland may rupture, discharging its contents, or absorption of the 
 liquid with inspissation and a pseudocaseous form of degeneration 
 may result. Finally, the degenerated area may become calcareous. 
 
 Pigmentation may follow acute inflammations or traumatic 
 
 S23S|Ff 
 
 Fig. 151.— Anthraeosis of a bronchial lymph-gland (Orth). 
 
 injury of the glands, the extravasations of blood occurring in such 
 conditions leading to hematogenous pigmentation. The blood- 
 pigment occurs in granular masses within the cells of the stroma 
 or within the lymphatic cells themselves. Blood-pigmentation 
 
336 TEXT-BOOK OF PATHOLOGY. 
 
 may also occur in the glands adjacent to areas of hemorrhagic 
 extravasation, the pigment in such cases reaching the glands 
 through the lymphatic vessels and being deposited in the lymph- 
 sinuses, or even in the follicles and cords. Analogous pigmen- 
 tation from external sources may result from tattooing, and occurs 
 regularly in the bronchial glands as the result of the inhalation of 
 various dust-particles which penetrate the walls of the bronchioles 
 and alveoli and eventually find their way to the bronchial glands 
 through the lymphatic stream (anthracosis) (Fig. 151). The 
 glands may be completely black in such cases, and the lymphatic 
 circulation through them may be obliterated. Secondary inflam- 
 matory changes result in most eases (see page 337). 
 
 INFLAMMATION ; LYMPHADENITIS. 
 
 Acute lymphadenitis is commonly secondary to inflamma- 
 tions in the neighborhood, the irritants being carried by the 
 afferent lymphatics. Sometimes direct extension of inflammation 
 by contiguity of structure may lead to involvement of the 
 lymphatic glands. Occasionally lymphadenitis is seemingly pri- 
 mary in cases in which the infective irritants have caused no 
 lesion at the portal of entrance to the body. 
 
 Pathologic Anatomy. — The glands become enlarged, hyperemic, 
 and considerably infiltrated with liquid. When the inflammation is 
 intense there may be minute hemorrhages. Microscopically the 
 lymph-sinuses are found distended with cells — leukocytes, red 
 blood-cells, and proliferated and desquamated endothelial cells 
 from the lining membrane of the sinuses. The follicles and cords 
 are increased in size from infiltration and probably also from pro- 
 liferation of the lymphoid cells. The process may become arrested 
 and resolution to the normal condition may ensue. If mild inflam- 
 mation of this character has continued for a great length of time, 
 or if the condition is repeated, hyperplasia of the trabecular con- 
 nective tissue, of the blood-vessels, and of the capsule of the gland 
 may lead to a termination in chronic enlargement and induration 
 of the glands. 
 
 In cases of greater intensity of the infective cause necrotic or 
 suppurative changes may occur. In the cases of necrosis such as 
 occur in typhoid fever and in diphtheria there maybe noted small 
 spots of yellowish-white color in the hyperemic glands, and subse- 
 quently these undergo well-marked necrosis. Complete necrotic 
 softening and even rupture of the gland may ensue, or, if the 
 necrosis remains limited in extent, inspissation and sometimes 
 calcification may terminate the process. 
 
 Suppurative lymphadenitis is not uncommon. It is seen 
 in the glands below Poupart's ligament in cases of infective wounds 
 of the leg; in the inguinal glands as a result of chancroid or gon- 
 
DISEASES OF THE LYMPHATIC TISSUES. 337 
 
 orrheal urethritis ; in the glands of the neck in association with 
 diphtheritic, scarlatinal, or other inflammations of the throat, or 
 following erysipelas ; in the axillary glands as a result of wounds 
 of the arm ; and in the internal lymphatics in various infective dis- 
 eases. The term bubo is applied to suppurative lymphadenitis of 
 superficial glands. Of particular interest is the tendency to this 
 condition in the Plague of the East, or the bubonic plague (q. v.). 
 
 Pathologic Anatomy. — The changes noted in the gland at the 
 outset are similar to those in the simple inflammations, but under 
 the microscope a greater accumulation of leukocytes is apparent, 
 and the gland tends to soften, with the formation of more or less 
 creamy pus. The capsule may prove resistant for a time, and 
 reactive inflammation around may establish an additional wall. 
 A single gland of a group may be affected, but more commonly 
 the several glands are together involved. Eventually rupture 
 may take place, but in instances in which the process has been 
 circumscribed inspissation of the pus and finally calcification may 
 occur. 
 
 In the most intense forms of lymphadenitis hemorrhagic or 
 gangrenous conditions are developed. 
 
 Chronic lymphadenitis leads to induration with enlarge- 
 ment. It occurs as the result of repeated acute attacks or in con- 
 sequence of long-continued irritation by particles carried to the 
 lymphatic glands from some focus of disease. 
 
 Pathologic Anatomy. — As a rule, the process affects the con- 
 nective-tissue elements of the gland in particular, and there 
 results a considerable amount of induration, sometimes associated 
 with atrophy or necrosis of the proper lymphoid structure. Occa- 
 sionally, however, the lymphoid elements themselves are hyper- 
 plastic, and the normal relation of fibrous tissue, follicles, and 
 medullary cords is preserved. 
 
 Microscopically the overgrowth of the connective tissue spring- 
 ing from the trabecular, from the blood-vessels, and from the 
 reticulum of the lymphoid portions, is apparent. This may consist 
 of round cells and fibrous connective tissue, or there may be a 
 tendency to the formation of epithelioid cells and even giant-cells. 
 
 Pathologic Physiology. — Inflammations of the lymphatic 
 glands are the result of the arrest of irritants of various sorts 
 carried to the glands in the lymphatic channels. This arrest not 
 unlikely serves the purpose of a protection against general dis- 
 semination of irritants, and may be of great importance in this 
 way. Complete occlusion of the lymph-sinuses by deposition of 
 solid particles (as coal-dust), or by disease of the glands, may 
 obstruct the lymphatic flow entirely, and a retrograde inflammatory 
 process may result from the damming back of infected lymph or 
 from extension of disease along the lymphatic channels. 
 
338 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis of the lymphatic glands is due in nearly all 
 cases to infection by bacilli reaching the gland through the affer- 
 ent lymphatics, though occasionally it would seem that hemato- 
 genous infection occurs. Under the heading tuberculosis we must 
 include what the older writers designated as scrofulous glands, for 
 in the majority of such cases, if not in all, the disease is essentially 
 tuberculosis, though the mode of infection is not always apparent. 
 Morbid Anatomy. — The first visible change is the formation of 
 small grayish nodules in the gland, and sometimes the eruption of 
 these is attended with hyperemia and inflammation. Later, these 
 tubercles increase in size and undergo caseous 
 changes (Fig. 152) as elsewhere, and eventu- 
 ally the entire gland may be converted into 
 a cheesy mass, which may liquefy and not rare- 
 ly discharges through the ruptured capsule. 
 Microscopically, the first appearance is that of 
 gray tubercles containing giant-cells and 
 epithelioid cells, surrounded by a zone of 
 round cells (Fig. 153). Later, the character- 
 istic appearances of hyaline transformation 
 and of caseation are observed. Sometimes 
 the glands in tuberculosis become enlarged and harder than normal, 
 and present areas of grayish color, but do not tend so markedly to 
 
 Fig. 152.— Cheesy lymph 
 gland (Orth). 
 
 Fig. 153.— Tuberculous lymphatic gland : a, recent tubercle with giant-cell (c) ; a,, inferio: 
 i giant-cell (c,) ; b, lymphadenoid tissu«- ; <l, epithelioid cell (Ziegler). 
 
 caseous tubercle with | 
 
 undergo necrosis. In these instances the microscopic examination 
 presents foci composed for the most part of epithelioid cells, and 
 
DISEASES OF THE LYMPHATIC TISSUES. 
 
 339 
 
 much less abundant in round cells than are tuberculous tissues as 
 a rule (Fig. 154). 
 
 
 Fig. 154.— Tuberculous lymphatic gland : a, lymphadenoid tissue ; 6, large round cells 
 (epithelioid) ; e, large spindle-cells (Ziegler). 
 
 Scrofula. — The tuberculous nature of scrofulous lymphadenitis 
 was first demonstrated by the infectiousness of the softened 
 
 
 
 
 i i 
 
 H& 
 
 y 1 
 
 Fig. 155.— Tuberculous lymphadenitis of the cervical glands (from a case in the Children's 
 Hospital). 
 
340 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 glandular material when injected into animals. The micro-organ- 
 isms themselves may be demonstrable in the earlier stages in the 
 epithelioid or giant-cells, or lying between these ; but when the 
 process is at all advanced it is extremely difficult or impossible to 
 demonstrate bacilli. 
 
 Individual Groups of Glands. — Among the more commonly 
 affected groups of glands are the cervical (Fig. 155), the bronchial, 
 and the mesenteric. Tuberculous cervical glands occasion consider- 
 able tumors in the neck, and it is these in particular that have 
 been classified as scrofulous. Not rarely they advance to complete 
 softening, and rupture on the surface. Sometimes, however, they 
 penetrate deeply, and may rupture into the trachea or esophagus, 
 or into the pleural cavity. The mode of infection is rarely 
 apparent, but in many cases no doubt the micro-organisms enter 
 through the mucosa of the mouth or pharynx, or the tonsils, where 
 they may or may not first occasion specific lesions. 
 
 The bronchial glands are affected very frequently in cases in 
 which the bacilli, entering through the lungs, have left no trace of 
 tuberculous disease at the portal of entrance ; while in cases of 
 actual tuberculosis of the lungs the bronchial glands are quite 
 constantly involved (Fig. 156). The glands are usually cheesy and 
 
 Fig. 156.— Tuberculous lymphatic glands at the bifurcation of the trachea (from a speci- 
 men in the Museum of the Philadelphia Hospital). 
 
 may become calcareous, but softening not rarely occurs. Perfora- 
 tion of one of the bronchi may lead to acute bronchogenetic tuber- 
 
DISEASES OF THE LYMPHATIC TISSUES. 341 
 
 culosis of the lungs ; or the softened gland may discharge into a 
 large vein and thus occasion miliary tuberculosis. 
 
 The mesenteric glands are especially involved in children, this 
 condition being known as tabes mesenterica. The infection occurs 
 through the intestinal tract ; and has sometimes been found due 
 to the ingestion of infected milk or meat. The intestines may 
 first suffer, or the bacilli may penetrate the intestinal mucosa with- 
 out causing local lesions. 
 
 Syphilis. — Enlargement of the lymphatic glands may occur in 
 the vicinity of the initial lesion during the primary period ; and 
 is habitually present in all parts of the body during the second- 
 ary period, the post-cervical, axillary, inguinal, and epitrochlear 
 groups being most characteristically involved. The glands are 
 hard, and do not tend to soften or suppurate. Microscopically 
 there is found proliferation of the connective-tissue elements 
 throughout the gland. 
 
 In the tertiary period gummata {bubo tertiaris) may be ob- 
 served, especially in the lymphatic glands adjacent to the diseased 
 viscera. 
 
 I/eprosy, actinomycosis, and other infections occasion- 
 ally involve the lymphatic glands (see General Pathology). 
 
 TUMORS. 
 
 I^ymphadenottia ; lymphosarcoma. — The term lymph- 
 adenoma has been applied to certain enlargements of the lymphatic 
 glands in which the appearance and structure resemble closely 
 those of the normal gland. The nature of many of such cases is 
 obscure, and very likely widely varying diseases have been in- 
 cluded. In some instances repeated irritation has occasioned a 
 functional hypertrophy or chronic inflammation of the gland, 
 while in others, doubtless, infectious diseases (especially tuberculo- 
 sis) may have been mistaken for tumors. We may restrict the 
 term lymphadenoma to apparently causeless enlargements of the 
 lymphatic glands in groups. In some cases the disease tends to 
 involve the glands in all parts of the body, as well as to invade 
 the spleen, the liver, the kidneys, and other organs. Enlarge- 
 ments of this sort occur in leukemia and Hodgkin's disease (Fig. 
 157). In cases of localized enlargements of the lymphatic glands; 
 it is likely that local irritation, as a rule, plays a prominent part 
 in causation. 
 
 Pathologic Anatomy. — Two forms of lymphadenoma have been 
 described, the hard and the soft. In the former the glands of the 
 group are enlarged and hard, the capsule is thickened, and the 
 trabecular increased. Microscopically there is evidence of exces- 
 sive proliferation of connective tissue, though overproduction of 
 lymphoid elements may occur at the same time. In soft lymph- 
 
342 
 
 TEXT-BOOK OF PATHOLOGY, 
 
 adenoma the gland has much of its natural appearance, although 
 it is somewhat more opaque and grayish. There is no tendency 
 to soften or suppurate, and the individual glands of a group, 
 though closely held together, do not fuse entirely. The distinction 
 of lymph-sinuses, follicles, and medullary cords is less marked than 
 normally, and the appearance is that of a uniform lymphoid 
 
 Fig. 157.— Hodgk in's disease, showing marked enlargement of the glands of the right 
 axilla, with consequent dropsy of the arm; less marked involvement of the submaxillary, 
 cervical, and inguinal lymph-glands. 
 
 tissue composed of a cellular reticulum in which small round cells 
 are embedded. From an anatomical standpoint the term lympho- 
 sarcoma is applicable, and still more from the fact that nodular 
 infiltrations with enlargement are usually found in the spleen as 
 well as in organs which do not normally contain lymphatic tissue, 
 such as the liver, the kidneys, and the heart. In some cases of 
 lymphosarcoma the blood contains excess of leukocytes. These 
 cases are known as leukemia. In other cases, though anatomical 
 differences are not detectable, the blood contains no excess of 
 leukocytes. These cases may present the clinical features of a 
 
DISEASES OF THE LYMPHATIC TISSUES. 343 
 
 progressive anemia, and are known as Hodgkin's disease, or 
 pseudoleukemia. In occasional instances transformation of Hodg- 
 kin's disease into leukemia, or the reverse, takes place, and there 
 seems to be no well-established dividing-line between the two 
 conditions (see, also, Lymphadenoma, in Part I.). 
 
 Sarcoma. — Other forms of sarcoma are sometimes met with 
 as primary localized new growths of the lymphatic glands. Such 
 are not rarely seen in the mediastinum. In these instances the 
 capsule of the gland is penetrated and local extension to neigh- 
 boring glands and other surrounding structures is commonly 
 observed, but the entire group of glands is not, as a rule, affected. 
 General metastasis may occur, but affects the larger organs rather 
 than the lymphoid tissues. Round-cell, spindle-cell, and alveolar 
 sarcoma are the forms described. Secondary sarcoma occasionally 
 involves the lymphatic glands. 
 
 Carcinoma is always secondary, the lymphatic glands being 
 the most frequent seat of secondary cancer. 
 
 BONE-MARROW. 
 
 Anatomic Considerations. — The marrow of the bones is 
 a lymphadenoid tissue consisting of a reticulum of connective- 
 tissue cells, supporting a rich network of capillaries and venules 
 of unusual width. The cells proper of the marrow are rounded 
 and vary greatly in size. They contain a clear nucleus, and many 
 of them neutrophilic granules. In addition to these marrow-cells 
 there are occasional giant-cells lying near the bony trabecular ; and 
 more frequently cells containing pigment-granules ; also nucleated 
 red corpuscles, non-nucleated red corpuscles, and large cells en- 
 closing corpuscles. After the first few years of life the marrow 
 of the long bones loses its reddish color and becomes more or less 
 yellow, and there is then found, microscopically, a great pre- 
 ponderance of fat-cells. 
 
 DEGENERATIONS. 
 
 Fatty Infiltration. — The fat which occurs normally in the 
 marrow may be excessively developed in conditions of general 
 obesity, but also at times in marantic individuals, or as a result of 
 atrophy of the bony tissues. 
 
 Mucoid degeneration is occasionally seen, and necrosis 
 may form a part of the processes of inflammation. 
 
 Pigmentation occurs in the bone-marrow in cases of destruc- 
 tion of blood, as in malaria or various hemolytic toxemias, as the 
 bone-marrow is one of the filtering organs for the blood. 
 
344 TEXT-BOOK OF PATHOLOGY. 
 
 ATROPHY. 
 
 Atrophy of the bone-marrow is not infrequent in old age or in 
 marasmic conditions. 
 
 HYPERTROPHY. 
 
 Hypertrophy of the bone-marrow occurs in various anemic 
 diseases. Strictly speaking, there is atrophy or disappearance of 
 the fat-eel Is of the yellow marrow of the long bones and hyper- 
 plasia of the true lymphoid elements. The bone-marrow, there- 
 fore, assumes more and more the appearance of the red or lym- 
 phoid marrow of early life. The highest grades of this transfor- 
 mation are met with in progressive pernicious anemia (Plate 3, 
 Fig. 1 ) and iu leukemia, but similar changes occur in cancer, tuber- 
 culosis, and various other cachectic conditions. The marrow be- 
 comes soft and red in color, and in extreme cases may be dark- 
 red and liquid. 
 
 Microscopically the fat-cells are much reduced in number and 
 may be wholly wanting. In their place are found marrow-cells 
 of various sizes, many of them containing neutrophilic and eosino- 
 philic granulations. Cells containing pigment-granules or red 
 blood-corpuscles, and nucleated red blood-corpuscles of different 
 sizes, are seen in varying numbers. 
 
 In leukemia the marrow often has a mottled appearance, light- 
 colored areas composed largely of white corpuscles arrested in the 
 marrow or formed in loco by active proliferation, alternating with 
 darker areas of congestion or hemorrhagic extravasation (Plate 3, 
 Fig. 2). The light-colored areas may predominate and may pre- 
 sent a puriform appearance (pyoid marrow). More rarely the ap- 
 pearance of the marrow in leukemia is similar to that seen in the 
 other anemic diseases. Microscopically a curious constituent is 
 discovered — the Charcot- Neumann crystals (see Leukemia). It 
 has been held that leukemia is dependent primarily upon the dis- 
 ease of the bone-marrow (myelogenous leukemia), but the marrow- 
 changes, in some eases at least, arc secondary. 
 
 INFLAMMATION. 
 
 Osteomyelitis, or inflammation of the marrow, is infectious 
 in nature, and may occur in the course of various diseases, such as 
 typhoid fever, relapsing fever, small-pox, septicemia, and the like; 
 or as a result of traumatism and direct infection. The marrow- 
 disease may be the only expression of an infection which has 
 arisen in an obscure manner (infectious osteomyelitis). In the 
 cases occurring in the course of infectious diseases, the changes are 
 comparable to those which occur in the spleen under the same cir- 
 cumstances. The marrow assumes a redder color than normal, 
 and it may be studded with punctate hemorrhages. In other 
 
Plate 3. 
 
 3 s 
 
DISEASES OF THE LYMPHATIC TISSUES. 345 
 
 cases areas of necrosis and granular degeneration of the cells may- 
 be present, and increased numbers of lymphoid cells or white 
 blood-corpuscles may be discovered. Sometimes the marrow is 
 quite purulent (see Diseases of Bone). 
 
 INFECTIOUS DISEASES AND TUMORS. 
 
 (These will be referred to in the discussion of Diseases of the 
 Bones.) 
 
 THE THYMUS GLAND. 
 
 Anatomy and Development. — The thymus gland at its 
 earliest period consists of endodermic epithelium arranged some- 
 what like that of an epithelial gland. Later, mesoblastic lymphoid 
 cells and connective tissue infiltrate it ; and at birth and for several 
 years thereafter it is composed largely of lymphoid tissue arranged 
 like the follicles of lymphatic glands. Here and there in the cen- 
 ter of these may be seen concentric whorls (the corpuscles of 
 Hassall), the remains of the original epithelial cells. After the 
 second year of life retrogressive changes take place, and by the 
 age of adolescence the gland is converted into a mass of fatty con- 
 nective tissue. 
 
 Congenital Abnormalities. — Complete absence or various 
 minor irregularities of the thymus may occur ; at times it is found 
 enormously hypertrophied. In the latter case the root of the 
 great vessels, the pericardium, and heart may be covered over by 
 the enlarged thymus, and sudden death seems at times due to this 
 cause. Thymic asthma, so-called, is rarely, if ever, due to enlarge- 
 ment of the thymus. 
 
 Circulatory Disturbances. — Intense congestion and punc- 
 tate hemorrhages may be found in cases in which death has occurred 
 from asphyxia. 
 
 Inflammation of the thymus as a primary disease is of doubt- 
 ful occurrence, but abscesses may occur in cases of general pyemia, 
 or from extension of suppurative affections of adjacent parts. 
 
 Infectious Diseases. — Syphilis occurs in the form of gum- 
 mata, especially in the new-born. Caseation and softening of the 
 gumma may occur, and a resemblance to abscess is thus produced. 
 Miliary or caseous tuberculosis occasionally invades the thymus gland. 
 
 Tumors. — The thymus or its remnant is not infrequently the 
 place of origin of lymphosarcoma of the anterior mediastinum 
 (see Fig. 47). Tumors having this origin may be recognized by 
 their shape and by the regularity of their outlines, the lympho- 
 sarcomata (lymphadenomata) of the lymphatic glands of the 
 anterior mediastinum having a more irregular lobulated appear- 
 ance. Ordinary round-celled sarcoma has been described, and 
 epithelioma springing from the corpuscles of Hassall has been 
 seen in a few cases. 
 
346 TEXT-BOOK OF PATHOLOGY. 
 
 CHAPTER III. 
 DISEASES OF THE CIRCULATORY SYSTEM. 
 
 THE HEART. 
 
 Development of the Heart— At the earliest period of fetal life the 
 heart is represented by a hollow tube, lying toward the ventral aspect of 
 the neck. Later this assumes an S-shape, and still later a transverse con- 
 striction marks the position which the auriculoventricular grooves subse- 
 quently occupy. Finally, vertical grooves divide the lateral halves into 
 the respective auricles and ventricles ; and the truncus arteriosus, which is 
 at one of the ends of the primitive tube, becomes divided into two parts, 
 forming the pulmonary artery and aorta. The separation of the cavities 
 within is accomplished by the outgrowth of septa springing from the walls 
 of the primary cavities. The septum dividing the ventricles is the first to 
 appear, and springs forward from the posterior wall. Next a budding is 
 seen in the position which is later occupied by the tissue between the 
 auriculoventricular orifices of the two sides; still later the auricular cavity 
 is divided into two parts by a process beginning at the lower and posterior 
 part. The septum which divides the truncus arteriosus is essentially con- 
 nected with or is a part of the septum which separates the ventricles. All 
 of these changes begin from the seventh to the ninth or tenth week of 
 fetal life. 
 
 Anatomic Considerations. — The heart consists of three 
 layers, the endocardium, muscular layer, and pericardium. The 
 endocardium is the inner lining of the organ, and is composed 
 of a layer of endothelial cells resting upon a stratum of connective 
 tissue. It is continuous with the lining membrane of the arteries, 
 and by duplications forms the valves. The muscle of the heart is 
 arranged in lamella?. The fibers of the heart-muscle are peculiar 
 in being branched and in being devoid of a sarcolemma. The 
 pericardium resembles the endocardium in structure. 
 
 The blood-vessels supplying the heart-muscle are branches of 
 the coronary arteries. They divide and subdivide, and afford 
 abundance of blood proportionate to the needs of so active an 
 organ. The lymphatic system is equally developed. The ner- 
 vous system includes numerous ganglionic centers in the furrows 
 between the ventricles and between the auricles and ventricles. 
 Other ganglion-cells are found within the muscle itself. 
 
 Details regarding the gross structure of the organ need not be 
 mentioned here. The weight of the heart in the adult male is 
 about 300 g., in the adult female about 250 g. The volume of 
 the entire organ in the adult male is about 290 to 310 cu.cm., in 
 the adult female about 260 to 280 cu.cm. 
 
 CONGENITAL DISEASES AND DEFORMITIES. 
 
 Abnormalities of the heart may be discovered in the new-born, 
 and are the result of developmental defects, or less commonly of 
 
DISEASES OF THE CIRCULATORY SYSTEM. 347 
 
 fetal endocarditis and myocarditis. The older pathologists at- 
 tributed many of the conditions to inflammatory changes, which 
 more accurate knowledge of the development of the heart clearly 
 indicates are the result of defects in development. 
 
 Abnormality of Position. — The heart may retain its posi- 
 tion high up toward the cervical region, and may even be entirely 
 in the neck. Occasionally it is completely exposed, or, merely 
 covered with pericardium, lies immediately beneath the skin, 
 the sternum in such cases being divided in the middle line. 
 Sometimes it lies beneath the skin of the abdomen. 
 
 Abnormality in Sise. — Congenital smallness, or hypojilasia, 
 of the heart and aorta is occasionally observed. Particular atten- 
 tion has been called to this condition in cases of chlorosis (see p. 368). 
 
 Defective Development. — There may be complete absence 
 of the heart in acardiac monsters. Sometimes the septa dividing 
 the auricles and ventricles are wholly wanting and a bilocular 
 heart results ; or the auricular septum alone is absent, when the 
 organ is trilocular. More commonly than these conditions, the 
 organ is completely reversed, lying on the right side of the body 
 and having the blood-vessels entering it and leaving it reversed, 
 so that the general venous blood enters the left auricle, the pul- 
 monary blood the right auricle, while the aorta springs from the 
 right ventricle and the pulmonary artery from the left. The 
 abdominal viscera may be reversed at the same time, the liver 
 being on the left, and the spleen on the right, side. This condi- 
 tion is spoken of as dextrocardia. Other abnormalities in the 
 arrangement and origin of the great blood-vessels, such as an 
 undivided truncus arteriosus, are rare. 
 
 Stenosis and atresia of the pulmonary artery result from abnor- 
 mal situation of the septum which divides the truncus. Com- 
 plete atresia is very rare. Stenosis is one of the commonest 
 developmental defects, of the heart, and in some cases is due to 
 fetal myocarditis about the orifice. It may involve the root, the 
 conus, or the trunk of the vessel. The septum of the ventricles 
 is usually defective and the foramen ovale remains patulous. 
 When the stenosis is considerable the pulmonary circulation is 
 maintained by the persistence of the ductus arteriosus Botalli ; and 
 the right ventricle is greatly hypertrophied. 
 
 Stenosis and atresia of the aorta are less frequent than the same 
 conditions affecting the pulmonary artery. They arise from the 
 same cause, and are usually accompanied by the same defects of 
 the septa and patency of the ductus arteriosus. Stenosis of the 
 trunk of the aorta at the isthmus — i. e., at a point between the left 
 subclavian artery and the mouth of the ductus arteriosus — is not 
 infrequent in moderate degree. More rarely there may be almost 
 complete atresia, or the aorta may be entirely wanting at this 
 point. The circulation is maintained by collateral anastomosis 
 
348 TEXT-BOOK OF PATHOLOGY. 
 
 of the branches of the subclavian with the descending aorta. 
 Id all of these cases hypertrophy of the left ventricle is usually 
 present. 
 
 Defects of the ventricular septum may he unaccompanied by other 
 abnormalities; but, as a rule, they are of secondary importance, 
 occurring in cases of abnormality of the pulmonary artery or aorta. 
 The septum may be completely wanting, or there may be partial 
 defects, these latter usually lying anteriorly and above, in what is 
 known as the membranous portion, or the undefended space. 
 Very frequently a patulous condition of the foramen ovale is 
 present. * 
 
 Defects of the auricular septum are comparatively rare, but a 
 patulous condition of the foramen ovale is one of the mostfrequent 
 of congenital affections of the heart. It is due to the failure of 
 the valve of the foramen to unite at the edges, as normally occurs 
 -nine time after birth. Slit-like openings are seen very frequently 
 in post-mortem examinations, while more decided patency is occa- 
 sionally observed without other cardiac abnormalities. This is 
 especially likely to occur when congenital atelectasis or some other 
 pulmonary affection causes continuance of high blood-pressure in 
 the right heart after birth. 
 
 Stenosis and atresia of the auriculoventricular orifices are rare 
 congenital conditions; and in the former fetal endocarditis doubt- 
 less plays an important part. When there is complete atresia the 
 auricular septum must remain widely open and the septum of the 
 ventricle is usually deficient and the ductus Botalli patulous. 
 
 Patulous Ductus Botalli. — This condition is frequent in cases of 
 stenosis of either the aorta or pulmonary artery, and serves to con- 
 vey the blood from the patulous artery into that which is obstructed. 
 Like the patulous foramen ovale, it may occur as an independent 
 condition resulting from congenital atelectasis of the lung which 
 leads to the continuance of the fetal conditions of circulation. 
 
 Valvular Defects. — Not rarely there may be but two semilunar 
 valves at the aorta or pulmonary orifice, and, on the other hand, 
 four may be observed, the latter being a relatively common condi- 
 tion. Similar numerical abnormalities occur at the auriculoven- 
 tricular valves. Abnormal length or shortness of the leaflets may 
 also be observed, or the segments may be united, forming a com- 
 plete ring. The latter condition must not be mistaken for the 
 agglutination of endocarditis. 
 
 Pathologic Physiology. — Congenital heart-diseases occa- 
 sion serious disturbances of the circulation, leading to overfilling 
 of the venous channels and often abnormal mixture of the arte- 
 rial and venous blood. In consequence of these conditions blue- 
 aess or cyanosis is a common symptom, and the terms congenital 
 cyanosis and morbus ccervUeus are applied. The imperfect oxida- 
 tion of the blood doubtless causes profound effects, but these 
 
DISEASES OF THE CIRCULATORY SYSTEM. 
 
 349 
 
 have not as yet received accurate study. The imperfect circu- 
 lation causes certain changes in the tissues, notable among which 
 
 Fig. 158.— Congenital cardiac disease, showing peculiar thickness of lips and nose 
 (Eichhorst). 
 
 are thickness of the lips and nose, giving rise to a peculiar facial 
 expression (Fig. 158) and "clubbing" of the finger-ends (Fig. 
 
 Fig. 159.— Clubbing of the fingers in congenital cardiac disease ; from same case as 
 Fig. 158 (Eichhorst). 
 
 159). The blood in congenital cyanosis often contains an excess 
 of red blood-corpuscles (see Polycythemia). 
 
350 TEXT-BOOK OF PATHOLOGY. 
 
 CIRCULATORY DISTURBANCES. 
 
 Thrombosis of the cavities of the heart results from 
 the causes which induce thrombosis elsewhere in the circulatory 
 system. These are mainly slowing- of the current of blood, some 
 roughness or disease of the endocardial lining, and diseased con- 
 ditions of the blood itself, which render it more liable to coagula- 
 tion. Slowing of the circulation is the most frequent cause of 
 intracardiac thrombosis, and leads to the formation /)f the clots 
 found post-mortem in cases of gradual death. If the circulation 
 has been slow for a considerable length of time, there may be 
 found more or less grayish or white thrombi in the auricular 
 appendages of the auricles or in the ventricles between the muscu- 
 lar trabecular especially near the apex. The formation of these 
 is explained by the gradually decreasing rapidity of the current 
 of blood, which leads to the deposit of the leukocytes and blood- 
 plaques upon the endocardium and their conversion into fibrin. 
 The color may be almost completely white; but if the current is 
 almost stagnated, admixture of red corpuscles occurs and pinkish 
 or quite red clots (currant-jelly clots) are formed. Of this latter 
 sort are the thrombi formed in the heart during the agonal 
 period and post-mortem. They are further distinguished from 
 the thrombi formed intra vitam by the fact that they are not 
 closely attached to the endocardium and between the trabecular 
 muscles. 
 
 Among the diseases in which the circulation is prone to be 
 sluggish, and which are frequently accompanied by cardiac throm- 
 bosis, pneumonia, tuberculosis of the lungs, the asthenic fevers, 
 and diseases of the muscle of the heart may be named. Dilata- 
 tion of the chambers of the heart and cardiac aneurysm lead to 
 thrombosis by their effect upon the rapidity of the circulation 
 either in the general heart-cavity in the first, or in the aneurysmal 
 dilatation in the second. Among the endocardial lesions which 
 occasion thrombosis the most important is acute endocarditis. In 
 this condition there is habitually deposited upon the affected part 
 of the valves or mural endocardium a capping of fibrin deposited 
 from the blood passing over the diseased area. In chronic endo- 
 carditis, especially when there are irregular calcareous deposits 
 rendering the surface rough and uneven, considerable thrombotic 
 deposit may occur. 
 
 Pathologic Anatomy. — Cardiac thrombi, formed some time before 
 death, usually appear as deposits upon the heart-wall of a yellow- 
 ish or whitish color and rather firmly attached between the muscu- 
 lar trabecules. Occasionally they have a stratified appearance, due 
 to the fact that the circulation varied in rapidity during the for- 
 mation of the thrombi. Secondary changes are not rare, the 
 most striking being softening of the fibrinous mass in places, with 
 
DISEASES OF THE CIRCULATORY SYSTEM. 
 
 351 
 
 Fig. 160.— Thrombosis in cardiac 
 chambers, showing cyst-like struct- 
 ure (Orth). 
 
 the formation of cyst-like cavities varying in size from a split pea 
 to a cherry (Fig. 160). Sometimes thrombi project from the 
 endocardial surface in a polypoid form, 
 and these may present the appearance 
 of fibroid tumors. A curious form 
 occurs in the auricles, the thrombus 
 presenting itself as a round mass 
 attached to the endocardium by fine 
 pedicles or lying entirely free [ball- 
 thrombi; globular thrombi). 
 
 Lesions in Other Organs. — Throm- 
 bosis of the heart may occasion serious 
 disturbance of the circulation by weak- 
 ening the heart-muscle or by obstruct- 
 ing the valvular orifices. The latter 
 is especially common in the case of the 
 globular thrombi or the polypoid 
 thrombi of the auricles. Passive con- 
 gestion of the various organs and the 
 secondary changes due to this con- 
 dition follow. Thrombosis may lead 
 to another and more serious danger, that of embolism. When 
 portions of the thrombus are broken off they are carried into the 
 circulation and lodge in the small arteries of the spleen, the 
 kidney, the brain, the lungs, or elsewhere, causing infarctions, or, 
 in case micro-organisms be present in the original thrombus, 
 metastatic abscesses and pyemia. 
 
 Thrombosis and Embolism of the Coronary Artery. — 
 The former condition is much the more common, as the coronary 
 arteries are frequently the seat of advanced atheromatous con- 
 traction and roughening, which predispose strongly to thrombosis ; 
 and, on the other hand, the mouths of the coronary arteries are 
 so placed that emboli are unlikely to enter. The lodgement of an 
 embolus seriously compromises the heart's action, as has been 
 shown experimentally in animals, and marked pathologic change 
 is therefore unlikely to occur before death ensues. When a 
 partially obstructing embolus lodges or a thrombus is formed there 
 results almost complete anemia of the area supplied by the artery 
 affected, and in consequence an anemic infarct. The muscle-fibers 
 of the affected area become hyaline or granular, and do not take 
 the stain when subjected to ordinary histologic examination. To 
 the naked eye the diseased portion presents itself as a white, and 
 later as a yellowish, area of softening, and the condition is spoken 
 of as myomalacia eordis. It is found most frequently in the 
 anterior or posterior wall of the left ventricle, near the apex, from 
 the fact that the descending branch of the left coronary artery is 
 most commonly involved. Next in frequency to these points the 
 
352 TEXT-BOOK OF PATHOLOGY. 
 
 anterior portion of the septum is found to be affected. Small 
 areas may heal by absorption of the degenerated tissue, and by 
 infiltration and proliferation of connective tissue. In this manner 
 a sear is formed, which may remain, or may subsequently lead to 
 aneurysmal dilatation. On the other hand, rupture of the heart 
 may be occasioned either with or without the formation of an acute 
 aneurysmal dilatation at the degenerated area. 
 
 DISEASES OF THE ENDOCARDIUM. 
 INFLAMMATION. 
 
 Inflammation of the endocardium, or endocarditis, may be acute 
 or chronic, though the latter is in most cases merely a continuation 
 of the former. 
 
 Acute endocarditis affects the endocardium of the valves 
 in the great majority of cases, but it is sometimes found in the 
 endocardium of the cavities of the heart, when it is spoken of as 
 mural endocarditis. 
 
 Etiology. — Endocarditis is practically always a secondary pro- 
 cess, and is in nearly all, if not all, cases due to the action of 
 micro-organisms. Cold and traumatism, upon which the older 
 writers insisted as causal factors, act merely as predisposing 
 causes. Endocarditis occurs most frequently in association with 
 acute articular rheumatism. Next to this cause scarlet fever, 
 pneumonia, and puerperal sepsis are most important, but in any 
 case of suppurative or infectious disease endocarditis is a possible 
 complication. It occurs at times also in Bright' s disease and in 
 conditions of great malnutrition, such as carcinoma and certain 
 nervous affections. These cases have been cited as opposing the 
 view that endocarditis is always infectious and due to micro- 
 organisms. It may be that toxic substances resulting from 
 improper metabolism act upon the endocardium as do micro- 
 organisms, or that portions of the endocardium suffer degeneration 
 as a result of depressed nutrition, but it is also possible that ter- 
 minal or intercurrent infection from some hidden source may occur 
 in these chronic diseases, with resulting endocarditis. 
 
 As to the micro-organisms themselves, the most important are 
 the Staphylococcus pyogenes annus, the Streptococcus pyogenes, and 
 the Diplococcus pneumoniae. But there are many forms which 
 have been less frequently detected. Among such are the Staphy- 
 lococcus pyogenes albus, the Micrococcus endocarditidis capsulatus 
 and rugatus, the Bacillus endocarditidis griseus and capsulatus, 
 Bacillus pyogenes foetidus or Bacillus coli communis, the Bacillus 
 diphtherial, and the bacillus of typhoid fever. The tubercle- 
 bacillus has been found in a few cases, but it is generally believed 
 that its presence is explainable as a secondary deposit rather than 
 
DISEASES OF THE CIRCULATORY SYSTEM. 353 
 
 as the cause of the endocarditis. Recently the gonococcus has 
 been recognized as one of the organisms capable of causing endo- 
 carditis. 
 
 The micro-organisms reach the point of disease from the blood 
 passing over the endocardium, and not through the coronary cir- 
 culation. This is proved by the fact that the aortic and pulmo- 
 nary leaflets are frequently involved, and they are not supplied 
 with blood-vessels, and also by the experimental production of 
 endocarditis by injections of micro-organisms into the blood after 
 the valve has been mechanically injured. In such cases there is 
 a direct deposit of micro-organisms upon the heart-valves. 
 
 Pathologic Anatomy. — It was customary formerly to distinguish 
 two varieties, a simple or verrucose, or benign endocarditis, and an 
 ulcerative, septic, mycotic, diphtheritic, or malignant form; but it 
 seems unnecessary at the present time to maintain strictly such a 
 distinction. The cases vary in anatomical appearance and in 
 malignancy, but there is no essential difference and no sharp 
 dividing-line. 
 
 The most common seats, in order of frequency, are the mitral 
 valve, the aortic valve, the pulmonary valve, and the endocardium 
 of the left ventricle, the left auricle, and the right ventricle. The 
 part of the valves first involved is a line running across the leaf- 
 let at about a distance of 2 mm. from the free edge. It is along 
 this line that the valves impinge in closing, and it is probable 
 that the mechanical injury sustained predisposes to endocarditis. 
 In the cavities the lesions are frequently found upon the chordee 
 
 Fig. 161.— Section through a segment of the aortic valve and adjacent parts of the aorta 
 and heart, showing vegetations on the aortic valve (magnified) : 6, aortic valve segment; 
 c, c, vegetations ; /, calcareous particles in the base of the aortic valve (Bramwell). 
 
 tendineae, and of the parts of the mural endocardium proper most 
 apt to be affected may be mentioned the portion of the left ven- 
 tricle near to the septum and the aortic valves, and the endocar- 
 dium of the left auricle on the posterior and outer wall above 
 the posterior mitral leaflet. 
 
 23 
 
354 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 The first appearance of endocarditis is that of an area of opacity 
 or slight roughness extending in a line across the valve or involv- 
 ing the endocardium elsewhere. Later, small nodular elevations, 
 not unlike ;t row of small beads, may form ; and finally there is a 
 distinct, irregular, and wart-like fibrinous elevation (Fig. 161). To 
 cases of this character the name verrucose endocarditis has been 
 given ; or from the usually benign character, the name simple 
 endocarditis j or from its most frequent cause, rheumatic endo- 
 carditis. In other cases the mass of fibrinous deposit is more 
 abundant (Fig. 162) and more irregular, while in still others the 
 
 Fig. 162.— Endocarditis of the aortic and mitral valves, showing vegetations (fibrin- 
 deposits) of considerable size (Kast and Rumpel). 
 
 deposit of fibrin does not take place, or, if so, is soon detached, 
 while necrotic changes occur in the endocardium, leading to the 
 formation of irregular ulcers. Secondary deposits of fibrin may 
 cover an ulcer after its formation, or its edges may be heaped 
 with fibrin ; and not rarely the active necrotic process in the 
 endocardium is not visible until the fibrinous coating, which is 
 usually considerable in such cases, is removed. These forms of 
 endocarditis are those that have been termed malignant, diph- 
 theritic, septic, mycotic, or idcerative. They are especially frequent 
 after puerjieral sepsis or other septic diseases and in pneumonia, 
 but there is no well-established dividing-line between the benign 
 eases and the severe cases, either in etiology, in morbid anatomy, 
 or in the clinical course and termination, so that I prefer to re- 
 gard them as varying grades of the same general process. 
 
 .Microscopically the endocardium beneath the coat of fibrin 
 
DISEASES OF THE CIRCULATORY SYSTEM. 
 
 355 
 
 shows desquamation of the endothelial cells, with frequently some 
 hyaline degeneration or coagulation-necrosis of the latter. Below 
 this there are round-cell infiltration and, as the process continues, 
 proliferation of fibroblastic cells. The fibrinous covering of the 
 valve itself consists of flakes or granular masses, or a fibrillar net- 
 work. By the proper staining-methods masses of bacteria may 
 frequently be demonstrated in the superficial layers of the endo- 
 cardium or in the fibrinous deposit. 
 
 The simple differs from the malignant forms of endocarditis 
 merely in the lesser activity of the necrotic changes in the endo- 
 thelium and the greater prominence of reparative processes (round- 
 cell infiltration, proliferation of connective tissue). 
 
 Results. — Simple endocarditis may be healed by the gradual 
 absorption or breaking off of the fibrinous deposit and its dis- 
 semination in the circulation, with coincident thickening of the 
 endocardium at the point of disease by the formation of fibro- 
 blastic cells and sclerotic connective tissue. When the process 
 is very limited, and especially when the mural endocardium 
 is affected, merely a white spot of thickening on the endo- 
 cardium results. When . the process is deep there may be 
 
 Fig. 163.— Aneurysm of the mitral valve, with rupture of the valve-cusp, seen from 
 the auricular surface : a, wall of left auricle ; 6, anterior segment of the mitral valve, the 
 chordae tendineee have heen cut short ; c, aneurysm with triangular opening (Bramwell). 
 
 decided distortion by contraction of the new-formed connective 
 tissue. When the deposit of fibrin is large it frequently under- 
 goes calcification, and remains as an irregular, calcareous mass 
 attached to the valve. In the severer or malignant cases destruc- 
 tion of an entire valve or of one of the chordae tendinese may 
 occur. When one of the layers of the valves alone is penetrated 
 
356 TEXT-BOOK OF PATHOLOGY. 
 
 acute valvular aneurysm may be formed by a pouching of the 
 other layer of the valve (Fig. 163). 
 
 Mural endocarditis of malignant type may lead to myocarditis 
 of a purulent character, and may even penetrate to the pericardium 
 and set op a purulent pericarditis. 
 
 Lesions in Other Organs. — The most serious danger of endo- 
 carditis is embolism. Small fragments of the fibrinous deposits 
 are liable to be carried off into the peripheral circulation, and in 
 ulcerative cases fragments of the valves themselves may be so con- 
 veyed. They are prone to lodge in the arteries of the spleen, 
 kidneys, and brain, forming hemorrhagic infarcts or metastatic 
 abscesses, according to the non-infective or infective character of 
 the embolus. 
 
 Chronic Endocarditis usually affects the valves of the heart 
 and leads to the distortions of the valves constituting chronic 
 valvular heart disease. Clinically, there are signs of disturbances, 
 and eventually more or less complete failure of the circulation. 
 
 Etiology. — Chronic endocarditis may be merely the continuation 
 of acute endocarditis, or it may occur as an insidious process, 
 chronic from the outset. In the former group of cases the causes 
 are, of course, those of acute endocarditis, and it is particularly 
 the rheumatic form that is likely to pass on to a chronic condition. 
 The severer grades, or those commonly spoken of as malignant 
 endocarditis, are usually fatal, though occasionally they may termi- 
 nate by reparative overgrowth of fibrous tissue. The group of 
 cases in which the disease is chronic from the start has much in 
 common with arteriosclerosis and atheroma, as far as etiology is 
 concerned. These cases occur more frequently in persons of 
 advanced years and in those whose occupation has been laborious. 
 Chronic alcoholism, gout, lead-poisoning, syphilis, and diabetes are 
 among the recognized causes. Not rarely the endocardial disease 
 is secondary to the arteriosclerosis, and it may be directly due to 
 it, resulting from the constant elevation of blood- pressure due to 
 that disease. Laborious occupations act in a similar manner. 
 
 Pathologic Anatomy. — In brief, the changes that occur in the 
 endocardium arc overgrowth of fibrous tissue, causing thickening 
 with subsequent contraction and distortion of the valves. The 
 chorda? tenuinese are frequently involved and become converted 
 into sclerotic cords of a whitish color, and less frequently white 
 elevations are seen upon the mural endocardium. 
 
 Microscopically there are found the characteristic appearances 
 of new-formed connective tissue with occasionally, in the earlier 
 stages, the appearances of granulation-tissue. New-formed blood- 
 vessels may be found within this tissue, though frequently these 
 are degenerated (hyaline and obliterated). Subsequently other de- 
 generations take place. The area of thickening becomes more 
 translucent and hyaline, then opaque and soft ; coagulation-necrosis 
 
DISEASES OF THE CIRCULATORY SYSTEM. 357 
 
 and fatty degeneration take place, and there may thus be formed 
 beneath the endocardial surface a lesion somewhat resembling a 
 minute abscess. This may rupture upon the endocardial surface, 
 forming a so-called atheromatous ulcer, upon which fibrinous 
 deposits may collect ; or it may be slowly inspissated and con- 
 verted into a calcareous patch. In cases in which acute endo- 
 carditis with thrombotic deposits passes into chronic endocarditis 
 the fibrinous masses of the surface may be rendered calcareous at 
 the same time that the sclerotic processes are taking place in the 
 valve. Subsequently the same degenerative changes and calcifi- 
 cation may occur in the tissue of the valve itself, as are seen in 
 the atheromatous form of the disease. In the late stages it is 
 often quite impossible to determine whether the case began as an 
 acute endocarditis, or whether it was chronic from the first. 
 
 The segments of the valves are frequently greatly shortened 
 and rounded, so that they become mere stumps, or they may be 
 curled upon themselves or drawn back and firmly adherent to the 
 wall of the aorta, pulmonary artery, or the ventricular cavity. 
 The individual segments may be agglutinated and united as a ring 
 or diaphragm projecting from the valvular orifice. 
 
 The valvular function is interfered with in two ways : first, 
 obstruction may be offered to the outflow of blood by the rigid pro- 
 jecting valves, a condition to which the term stenosis is applied ; 
 or, on the other hand, the valves may be so distorted, shortened, 
 or drawn backward that they are no longer able to close, and in- 
 sufficiency results. The semilunar valves are particularly prone to 
 be shortened and thickened and recurved, and insufficiency is 
 therefore most likely to occur. The mitral valve is frequently 
 thickened and converted into a funnel-like formation by agglutina- 
 tion of the edges of the anterior with those of the posterior segment. 
 There may thus be merely a slit-like orifice (button-hole mitral), 
 which occasions great obstruction to the outflow of blood from the 
 auricle. Somewhat similar changes are met with at the tricuspid 
 valve. The pulmonary valve is rarely affected in later life, but is 
 sometimes the seat of fetal endocarditis, leading to permanent 
 changes. 
 
 Resulting Changes in the Heart. — The valvular defects can be 
 overcome in only one way — by increase of the power of the heart- 
 muscle. Hypertrophy is therefore the natural result. This affects 
 first the cavity upon which excessive work falls as the result of 
 the regurgitation of blood in cases of insufficiency, or as the result 
 of the excessive strain placed upon the heart- wall to force the blood 
 through the narrowed orifice in stenosis. The amount of hyper- 
 trophy varies with the condition of the general health of the indi- 
 vidual and with the seriousness of the heart-lesion itself. When 
 the general health is good there is apt to be commensurately ade- 
 quate hypertrophy, and when the lesion is not of sufficient gravity 
 
358 TEX1-B00K OF rATHOLOGY. 
 
 to interfere with the circulation in the coronary arteries, and the 
 heart is therefore constantly supplied with a sufficiency of blood, 
 hypertrophy is well maintained. Eventually as the result of con- 
 tinued overwork and of continuously increasing embarrassment of 
 the circulation or of intercurrent diseases, the heart-muscle suffers 
 fatty or fibroid degeneration, the cavities dilate, and the circulation 
 foils. 
 
 Changes in Other Organs. — The passive congestions result- 
 ing from failure of the muscle of the heart are often extreme, and 
 may lead to profound changes in various organs, notably the lungs, 
 liver, and kidneys. These are discussed in the appropriate sections. 
 Embolism is a not infrequent accident in chronic endocarditis, the 
 emboli being parts of the valvular deposits or parts of thrombi in 
 the cavities of the heart. 
 
 Pathologic Physiology. — Endocarditis, acute and chronic, 
 leads to various disturbances of the circulation and of the general 
 health. In acute endocarditis the lesions may become the center 
 of dissemination of infectious material, and the disease may run 
 its course with all the manifestations of an obscure septicemia. 
 This is particularly true of the cases usually designated as malig- 
 nant. .Serious disturbance of the heart-action occurring in acute 
 eases is sometimes difficult to explain. The lesions upon the 
 valves may be seemingly very insignificant, and yet the heart may 
 be very irregular in action and exceedingly weak. In part this 
 may be reflex and in part it is probably the result of associated 
 disease of the myocardium. Some recent investigations, made 
 according to modern methods, have shown the heart-muscle impli- 
 cated more often than has been suspected. Acute myocarditis and 
 diseases of the blood-vessels of the myocardium (thrombosis) have 
 been discovered. 
 
 In chronic endocarditis the disturbances of health are largely 
 the resull of mechanical disorders of the circulation. In large 
 part these are brought about by the valvular defects themselves, 
 but in the later stages associated degenerations and weakness of 
 the myocardium are of great importance. At any stage of the 
 disease the state of the heart-muscle determines the seriousness of 
 the disease ; marked defects of the valves may be compensated 
 for by a powerful myocardium, while, on the contrary, apparently 
 trivial defects may occasion serious results when the heart-muscle 
 is diseased. Metabolic disturbances of various sorts may occur in 
 consequence of the imperfect circulation. The respiratory ex- 
 change of gases, in some cases at least, is reduced, though the 
 degree of cyanosis cannot be taken as an index of the reduced 
 oxidation. In man cyanosis is dependent upon stagnation of cir- 
 culation rather than reduced oxidation. The products of metab- 
 olism excreted in the urine may indicate the reduction in oxygen 
 in the tissues. The metabolic consumption of the proteids of the 
 
DISEASES OF THE CIRCULATORY SYSTEM. 359 
 
 body seems to be increased, but the explanation of this fact has 
 not yet been satisfactorily determined. Some regard it as a con- 
 sequence of molecular necrosis due to insufficiency of the supply 
 of oxygen. The excretion of nitrogenous elements may, however, 
 be reduced when transudates are forming. This is due to the 
 storing up of metabolic products in the transudates. The urine 
 may present albumin as a result of chronic congestion and second- 
 ary renal disease ; the hepatic functions are disturbed by congestion 
 and jaundice may result ; and in the more severe instances hydro- 
 bilinuria occurs. The condition of the blood is of special inter- 
 est. During periods of failing compensation the concentration of 
 the blood is increased or normal, and the number of blood-corpus- 
 cles may be excessive. In part, at least, these conditions are 
 explained by the assumption that the corpuscles are retained in 
 the peripheral parts of the circulation in greater measure than the 
 fluid elements (see Polycythemia). When the cardiac compensa- 
 tion is well maintained some anemia may be apparent, especially 
 in cases of aortic disease. 
 
 CIRCULATORY DISTURBANCES. 
 
 Anemia of the heart-muscle may be part of a general 
 anemia. It may occur in cases of narrowing or obstruction of 
 the coronary arteries, and it may be the result of the pressure of 
 pericardial effusions. When long continued it leads to fatty 
 degeneration of the heart, but is itself of little consequence. 
 
 Hyperemia of the heart-muscle may occur when there is 
 obstruction to the return of the blood to the right heart through 
 its venous channels. It may be part of a general hyperemia in a 
 failing compensation of valvular or muscular diseases of the heart. 
 The heart-muscle assumes a dark-red color, and the veins are seen 
 under the epicardium as dilated bluish vessels. 
 
 Hemorrhages in the heart- muscle may result from ob- 
 struction of the coronary arteries, when the hemorrhage assumes 
 the form of an infarct. There may also be hemorrhages in cases 
 of intense myocarditis or surrounding abscesses of the heart-mus- 
 cle, and finally points or streaks of hemorrhagic infiltration may be 
 seen between the muscle-fibers in persons who have died with 
 some form of hemorrhagic diathesis, from sepsis, or from various 
 intoxicants. 
 
 DEGENERATIONS. 
 
 Parenchymatous degeneration, or cloudy swelling of the 
 heart, was designated by Virchow as parenchymatous myocarditis. 
 It is essentially a degenerative process and should be so described, 
 though it forms a not inconsiderable part of the pathologic changes 
 occurring in the heart in acute myocarditis. 
 
 Etiology. — The immediate cause is infection. It is met with 
 
360 TEXT-BOOK OF PATHOLOGY. 
 
 in the course of diphtheria, typhoid fever, scarlet fever, rheuma- 
 tism, and other infections. It may be that elevation of the tem- 
 perature alone suffices to bring it about, and in these cases no 
 doubt abnormal substances resulting from disordered metabolism 
 are the direct toxic agent, but as a rule it is the specific toxins of 
 the infections that occasion the myocardial disease. Localized 
 parenchymatous degeneration may be found in the heart-fibers ad- 
 jacent to areas of endocarditis or pericarditis, and doubtless the 
 same etiologic factors are at work in this as in more generalized 
 instances. 
 
 Pathologic Anatomy. — The changes are more marked in the left 
 ventricle than elsewhere ; though any part of the heart may be 
 affected. As a rule, parenchymatous degeneration occurs as a 
 diffuse process, but there may be only limited areas here and 
 there. The myocardium becomes pale in color and often has a 
 turbid appearance ; it is softer than normal, the heart-walls are 
 usually flabby, and the cavities somewhat dilated. Microscop- 
 ically, the fibers are found to be filled with fine granules of albu- 
 minous nature, which may completely obscure the striations and 
 even the nuclei, but which may be cleared up by the addition of 
 acetic acid. Multiplication of the nuclei and round-cell infiltra- 
 tion of the intermuscular connective tissue may be observed, but 
 these are inflammatory changes rather than degenerative, and are 
 not, therefore, strictly a part of the disease in question. Paren- 
 chymatous degeneration may be complicated by a form of hyaline 
 degeneration, the affected fibers becoming converted into cylin- 
 ders of waxy appearance. When cloudy swelling persists fatty 
 degeneration is often the terminal ehange. 
 
 Amyloid degeneration results from the causes which induce 
 amyloid disease in other organs. It is not infrequently found in 
 minute areas here and there, but only rarely has it been seen as a 
 widespread process affecting the connective tissue between the 
 muscle-fibers and beneath the endocardium and pericardium. In 
 such cases the same wax-like appearance is seen as in the liver or 
 spleen, and the characteristic reaction with iodin may be demon- 
 strated. 
 
 Hyaline degeneration is sometimes associated with amy- 
 loid, and gives rise to a glassy or waxy transformation of the con- 
 nective tissue. It is usually seen in small areas, but may be quite 
 widespread. Zenker described a form of hyaline disease of the 
 muscle-fibers themselves as occurring in typhoid and other infec- 
 tious fevers, and affecting the heart-muscle as well as the muscles 
 of the abdominal wall. This is usually associated with parenchy- 
 matous degeneration and occurs in limited areas. Microscopically 
 there may be seen small hyaline masses or globular areas embedded 
 in the muscle-fiber, the rest of the fiber showing the appearances 
 of cloudy swelling. 
 
DISEASES OF THE CIRCULATORY SYSTEM. 361 
 
 Fatty infiltration, or obesitas cordis, is but an increase 
 of the normal condition. In the normal heart there is a certain 
 amount of fatty deposit beneath the epicardium, especially in the 
 furrows and along the lines of the blood-vessels. In disease this 
 may become enormously increased and there may be penetration 
 of the adipose tissue into the wall of the heart between the mus- 
 cle-fibers, sometimes as far as the subendocardial fibrous layer. 
 
 Etiology. — The causes are those which induce general obesity. 
 Thus, it may be the consequence of an hereditary tendency or 
 sedentary habits, with overeating and drinking'; it is more com- 
 mon in advanced years than in early life. Very frequently it is 
 met with in women who have grown stout at the menopause ; 
 sometimes, however, considerable deposit about the heart may 
 occur in persons otherwise presenting no tendency to fatness. 
 
 Pathologic Anatomy. — The adipose tissue beneath the visceral 
 pericardium may be slightly increased in amount, or the heart may 
 be embedded within an enormous deposit of fat, which may involve 
 not alone the epicardium, but the parietal layer and the medias- 
 tinum as well. On section through the heart-wall, trabecule of 
 adipose tissue may be seen passing through the heart's substance, 
 and sometimes subendocardial deposits may be seen as a uniform 
 infiltration beneath the endocardium or as localized deposits pro- 
 jecting into the heart beneath the endocardium. Microscopically 
 fatty infiltration presents the ordinary appearances of adipose cells 
 lying between the heart-muscle fibers (Fig. 164). The fibers 
 themselves are not involved ; but they may become atrophic from 
 
 Fig. 164.— Fatty infiltration of the heart, from a section through the wall of the right 
 auricle (Bramwell). 
 
 pressure, and in such instances present a more yellowish or brown- 
 ish color than normal, and microscopically show an abundance of 
 
362 TEXT-BOOK OF PATHOLOGY. 
 
 granules. In other eases pronounced fatty degeneration is seen in 
 the muscle-fibers. 
 
 Results. — Weakening of the heart-muscle must necessarily 
 result from the mechanical impediment imposed upon the muscle. 
 Circulatory disturbances are therefore met with as in valvular 
 disease or fatty degeneration. Occasionally rupture of the heart 
 occurs, and is due to the atrophic condition of the muscle proper 
 and a want of resisting power of the infiltrating adipose tissue. 
 It is especially prone to occur when the disease is localized. 
 
 Fatty degeneration affects the muscle-fibers themselves. 
 
 Etiology. — Fatty degeneration results from malnutrition or 
 from toxic agencies. The most frequent cause is anemia, either 
 local or general. Local anemia is due to sclerosis and narrowing 
 of the coronary arteries ; or it may be the consequence of improper 
 circulation in the coronary vessels attending the final stages of 
 valvular disease of the heart. Fatty degeneration is therefore a 
 terminal condition in arterial sclerosis affecting the coronary ves- 
 sels and in valvular disease. The remote or antecedent causes 
 are those which bring about arteriosclerosis. We find it therefore 
 in elderly persons of the male sex who have had syphilis, who 
 have used alcohol excessively, or have gout or chronic Bright's 
 disease. The fatty degeneration of the heart resulting from gen- 
 eral anemia is most typically seen in pernicious anemia, in which 
 the most extreme grades of fatty disease are sometimes witnessed. 
 Of the cases which are due to toxic agents we may distinguish 
 those resulting from specific infections and those occurring in 
 various chemical intoxications. In the specific fevers, in which 
 intense parenchymatous degeneration occurs, and among these 
 diphtheria is most prominent, fatty degeneration is sometimes the 
 terminal condition. Among the external poisons capable of 
 producing the disease phosphorus and arsenic are important. 
 
 Pathologic Anatomy. — Fatty degeneration may be a localized 
 or a diffuse process. As a rule, a considerable portion of the 
 heart is affected, but only isolated fibers or groups of fibers are 
 involved. There results a somewhat speckled or mottled condi- 
 tion, which is especially visible beneath the endocardium. Streaks 
 or lines of a yellowish or whitish color alternate with the darker 
 portions of normal muscle. When the process is uniform the 
 entire muscle assumes a yellowish hue. It is softer than normal, 
 the cavities tend to dilate, and the walls may be considerably 
 thinner than normal. 
 
 Microscopically the muscle-fibers are found to be filled with 
 small granules of a dark color or with small droplets of high 
 refractive power (Fig. 165). These may completely obscure the 
 nucleus, or they may be arranged in groups at the poles of the 
 nucleus. Sometimes distinct vacuolization of the fibers is seen, 
 especially in cases in which fibroid myocarditis accompanies the 
 
DISEASES OF THE CIRCULATORY SYSTEM. 
 
 363 
 
 fatty change. The nature of the granules and droplets within the 
 fibers is well demonstrated by treating the section with osmic acid, 
 when the fat-droplets become intensely black. 
 
 Fig. 165.— Fatty degeneration of the heart in a case of pernicious anemia ; some of the 
 fibers in the lower part of the illustration are normal (Birch-Hirschfeld). 
 
 Associated Conditions. — In cases of coronary sclerosis, or valvu- 
 lar heart disease with failure of compensation, fatty degeneration 
 is rarely the sole pathologic condition. As a rule, fibroid myo- 
 carditis accompanies it, and the latter may be the more extensive 
 and important condition of the two. Fatty infiltration is often 
 met with as an associated condition, and may be the direct cause 
 of the degeneration by the pressure exerted upon heart-muscle 
 fibers by the infiltrating fat. Rupture of the heart may occur in 
 cases in which fatty degeneration affects localized areas, as is often 
 the case near the apex of the heart. 
 
 Fig. 166.— Marked general segmentation with great diastasis of the pieces ; X 120 (from 
 the American Journal of the Medical Sciences) (Hektoen). 
 
 Segmentation of the Fibers. — This is an interesting con- 
 dition occasionally observed, especially in cases in which sudden 
 
364 TEXT-BOOK OF PATHOLOGY. 
 
 death has taken place. It consists in a transverse splitting of the 
 fibers, by which they are converted into columns of varying length 
 separated by transverse fissures (Fig. 166). It has been described 
 under the name of etat segmentaire, or myocardite segmentaire, by 
 French writers. A considerable discussion as to its significance 
 has arisen, some holding that it is a condition of clinical as well as 
 pathologic importance ; others, that it occurs during the death- 
 agony or post-mortem. Whether the latter statement be true or 
 not, the segmentation seems to indicate a degree of fragility of the 
 fibers, and in particular of the cement-substance, wholly abnormal, 
 though it may not be demonstrable by our present means of exam- 
 ination. This fragility may be due to digestive action of bacteria 
 or bacterial products, as has been suggested. 
 
 Degeneration of the intracardiac ganglia has been 
 noted by a number of observers in myocarditis and in cases of 
 angina pectoris without gross cardiac alteration. The change^ 
 observed are swelling, or granular, fatty, and hyaline degeneration 
 of the ganglion-cells, and infiltration of round cells with sclerotic 
 formation between the nerve-cells. The importance of these 
 changes has not been determined. 
 
 Pathologic Physiology. — The functional disorders in de- 
 generations of the myocardium may be due to the direct injury of 
 the fibers, or to disturbances of the nervous mechanism of the 
 heart. The latter seems to be the case in instances in which 
 marked cardiac irregularity, or arrhythmia, occurs. The disease 
 of the fibers explains the weakness of the heart -action ; and this is 
 especially marked in cases (of fatty and fibroid disease) in which 
 the circulation through the coronary arteries is insufficient. Some- 
 times the heart is arrested and sudden death occurs in cases of 
 myocardial degeneration due to infectious fevers (diphtheria). 
 This was formerly ascribed to heart-clots, but is now recognized 
 as a form of sudden and complete asystole due to the myocardial 
 disease or to associated nervous disorders, organic (in the intra- 
 cardiac ganglia or in the cardiac nerves) or reflex. The disturb- 
 ances of the general circulation in myocardial disease and their 
 results are similar to those met with in valvular disease. 
 
 INFLAMMATION. 
 
 Inflammation of the heart-muscle, or myocarditis, may be either 
 acute or chronic, diffuse or circumscribed. 
 
 ■ Acute myocarditis Mas designated carditis by the older 
 writers, though the same term was applied to endocardial and 
 pericardial inflammations as well. It may be circumscribed or 
 diffuse, the former appearing in the form of abscesses of the 
 heart-muscle. 
 
 Acute circumscribed myocarditis, or abscess of the heart, 
 
DISEASES OF THE CIRCULATORY SYSTEM. 
 
 365 
 
 may occur in connection with penetrating endocardial lesions or in 
 association with pericarditis. More frequently the infection takes 
 place through the coronary circulation, and the metastatic abscesses 
 of the heart are but a part of a general pyemic disease (Fig. 167). 
 
 Fig. 167.— Embolic abscess of the myocardium (Karg and Schmorl). 
 
 This occurs in cases of puerperal sepsis, in osteomyelitis, and other 
 intensely septic diseases, but particularly in cases of malignant 
 endocarditis. 
 
 Pathologic Anatomy. — When the infectious emboli are large a 
 single abscess or a few abscesses result, while in cases of finely 
 disseminated infectious particles the heart-substance may be 
 studded with innumerable suppurating points. These are more 
 common in the left ventricle and in the anterior wall than else- 
 where. At first the lesion may present itself as a minute, hemor- 
 rhagic, or necrotic area, but soon the focus softens and forms a 
 purulent collection. In size the abscesses vary from the merest 
 points to cavities the size of a cherry, and as much as an ounce of 
 pus has been removed from a single cavity. Perforation may take 
 place into the heart itself, and acute cardiac aneurysm or even 
 rupture of the heart may ensue. On the other hand, the abscess 
 may discharge into the pericardial sac, or without such rupture 
 may set up purulent pericarditis. Occasionally the pus becomes in- 
 spissated and fibrous overgrowth causes its complete encapsulation, 
 or finally the area may be rendered calcareous. Such terminations, 
 however, are rare, the patient usually perishing of the pyemic pro- 
 cess, as a part of which the abscesses in the heart occur. « 
 
 In suppurative myocarditis occurring from extension in conse- 
 quence of malignant endocarditis communicating sinuses may be 
 established between the chambers of the heart. 
 
 Acute diffuse myocarditis occurs in various forms of infec- 
 
366 TEXT-BOOK OF PATHOLOGY. 
 
 tious fevers. It was first recognized in typhoid fever, but is more 
 common in diphtheria and scarlet fever, and is met with in acute 
 rheumatism, puerperal septicemia, and various other infections. 
 It is most likely that the toxins of the infectious diseases named 
 are the immediate causes, and not the specific bacteria themselves. 
 The process may be entirely diffuse, but in most cases the left 
 ventricle is more seriously involved than other parts, and often 
 there are merely localized areas of myocarditis scattered about in 
 various parts of the ventricular wall. 
 
 Pathologic Anatomy. — The affected heart-muscle is soft and 
 often distinctly friable. In the earlier stages there may be spots 
 of hemorrhagic infiltration, but as a rule the color is rather lighter 
 than that of the normal organ. It may be noticeable that the 
 bundles of fibers easily separate from one another. The cavities of 
 the heart are frequently dilated, particularly the left ventricle. 
 
 Microscopically the important changes are diffuse infiltration of 
 round cells in the connective tissue between the muscle-fibers (Fig. 
 168), and proliferation of the connective tissue itself, with forma- 
 
 %mn 
 
 m 
 
 Fig. 168.— Acute diffuse myocarditis. 
 
 tion of rounded or spindle-shaped fibroblastic cells. There is no 
 tendency to suppuration. The blood-vessels are usually somewhat 
 distended with blood, and there may be distinct proliferative thick- 
 ening of their walls. Degenerative changes of the muscle-fibers 
 themselves are rarely, if ever, absent, and it is most probable that 
 the first stage in the process is a toxic degeneration of the muscle- 
 fibers, and that the intermuscular infiltration and proliferation are 
 consequent upon the primary degeneration. The fibers become 
 granular and opaque, the striations are indistinct; occasionally 
 there may be vacuolization, and sometimes the segmentation to 
 which so much attention has been directed of late. Proliferation 
 or swelling of the nuclei of the muscle-fibers is frequent, and the 
 hyaline transformation of Zenker is sometimes observed. 
 
DISEASES OF THE CIRCULATORY SYSTEM. 367 
 
 Results. — Under entirely favorable conditions acute, diffuse, 
 and non-suppurative myocarditis usually terminates in complete 
 resolution. It is, however, quite likely that the proliferative 
 changes noted in the intermuscular connective tissue often ad- 
 vance to complete organization and formation of localized areas 
 of sclerosis. Death from dilatation of the cavities and cardiac 
 failure is not uncommon. 
 
 Chronic myocarditis, or fibrous myocarditis, like the acute 
 form, may be diffuse or localized, though in this case the circum- 
 scribed form is the more common. 
 
 Etiology. — It is not unlikely that many cases are consequent 
 upon acute diffuse myocarditis, as has been already suggested. 
 In such cases the myocarditis may be looked upon as a pri- 
 mary affection. More commonly the process is secondary, and is 
 dependent upon primary disease of the coronary arteries or dis- 
 turbances of the circulation in the coronary arteries. It is there- 
 fore very common to find areas of sclerosis in cases of atheroma of 
 the coronary arteries or in valvular disease of the heart in which 
 the coronary circulation has finally become deficient. Among the 
 remote antecedent causes are the conditions which are prone to 
 occasion arteriosclerosis, such as old age, alcohol, gout, syphilis, 
 and the like. The connection between the arterial disease and the 
 resulting myocardial sclerosis has been the subject of considerable 
 dispute. No doubt, in some instances, the circumscribed areas of 
 fibrous overgrowth met with in the distribution of branches of the 
 coronary artery represent the scars of healed infarctions. In other 
 cases, however, it would seem more likely that a slow degenerative 
 change with gradual overgrowth of the connective tissue occurs in 
 consequence of the disturbed circulation through the damaged 
 coronary vessels, and it has been urged that in these instances the 
 fibroid disease of the heart is degenerative, and not in reality an 
 inflammatory process at all. Diffuse sclerosis may be associated 
 with hypertrophy in cases of valvular disease and other conditions 
 causing cardiac enlargement. 
 
 Localized myocarditis with fibroid overgrowth is very com- 
 monly met with at the tips of the papillary muscles in association 
 with chronic endocarditis and disease of the chordae tendinese. 
 
 Superficial myocarditis of a fibroid character may be seen 
 beneath the pericardium or endocardium which has been thick- 
 ened by chronic inflammation. 
 
 Pathologic Anatomy. — The characteristic change is the forma- 
 tion of sclerotic areas in the muscle-substance. These appear 
 either as more or less irregular spots, or as streaks or lines running 
 in the direction of the fibers of the heart. They are most com- 
 mon in the anterior wall of the left ventricle, near the apex, in the 
 septum, and at the tips of the papillary muscles ; but the entire 
 substance of the heart may be involved and thickening of the walls 
 
368 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 may result. The impediment offered to the muscle of the heart 
 by the intermuscular sclerosis may lead to true hypertrophy, but 
 more commonly there is degeneration of the fibers in consequence 
 of the pressure of the new-formed tissue, and yellowish areas of 
 fatty degeneration are frequently observed. 
 
 Microscopically the diseased areas are found to consist of more 
 
 Fig. 169.— Edge of an area of fibrous myocarditis, showing replacement of the fibers by 
 connective tissue (Orth). 
 
 or less well-organized connective tissue lying between the muscle- 
 fibers and pressing them far apart, or taking the place of atrophic 
 muscle-fibers (Figs. 169 and 170). 
 
 
 
 Sometimes certain portions show the earlier stages of the 
 process, round-cell infiltration and proliferation of the connective 
 
DISEASES OF THE CIRCULATORY SYSTEM. 
 
 369 
 
 tissue being the important features (Fig. 171). As a rule, how- 
 ever, the diseased areas are found in a completely organized con- 
 
 •v ;->;&>£ 
 
 Fig. 171.— Endomyocarditis, showing, a, thickened endocardium ; b, bands of muscle- 
 fibers with interstitial infiltration of round cells and proliferated connective tissue 
 (Bramwell). 
 
 dition. The muscle-fibers themselves suffer granular and fatty 
 degeneration, and not infrequently distinct vacuolization is ob- 
 served. 
 
 Results. — In cases in which a considerable area of chronic 
 myocarditis is developed, as is not uncommonly observed at the 
 apex in consequence of thrombotic or embolic obstruction of the 
 anterior coronary artery, an aneurysm of the heart may result 
 from gradual stretching of the fibroid area. In cases in which the 
 process is diffuse the heart-muscle may at first undergo hyper- 
 trophy in consequence of the excessive labor imposed upon it, but 
 eventually degeneration from pressure upon the fibers gains the 
 ascendency, dilatation of the cavities ensues, and general failure 
 of the circulation is the terminal result. 
 
 It is not unusual to find diffuse arteriosclerosis and fibroid 
 disease of other organs associated with chronic myocarditis. In 
 such cases the antecedent cause is the arterial disease, which in 
 turn may be dependent upon some systemic disorder. 
 
370 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 HYPOPLASIA AND ATROPHY. 
 
 Hypoplasia of the heart is a congenital condition in which 
 the heart is insufficiently developed and remains undersized 
 throughout life. This condition is frequently associated with 
 hypoplasia of the aorta and other large vessels, and sometimes 
 with a similar condition of the generative organs. Persons hav- 
 ing a predisposition to tuberculosis and women who develop 
 chlorosis not rarely present the conditions referred to. These in- 
 dividuals are often of delicate structure, with feeble or unstable 
 circulation, and, in the case of males, of effeminate nature and 
 appearance. The heart is small in size, and, as a rule, uniformly 
 affected in all parts. The epicardium may be somewhat wrinkled, 
 and this condition, no doubt, has often led to the description of 
 eases of this sort as instances of atrophy. 
 
 Atrophy of the heart is usually described as occurring in 
 two varieties, simple and brown atrojrfiy. It is very doubtful, how- 
 ever, if simple atrophy ever occurs. Many of the cases so desig- 
 nated were doubtless hypoplasia, and other cases probably brown 
 atrophies. 
 
 Etiology. — Atrophy of the heart usually occurs in persons of 
 advanced age ; but is occasionally met with in the young. It 
 results from simple senility, or from 
 various cachectic or wasting diseases, 
 such as tuberculosis, carcinoma, and 
 the like. 
 
 Pathologic Anatomy. — The heart 
 is small in size, sometimes weighing 
 but a third or fourth of its normal 
 weight. The capsule, or epicardium, 
 is wrinkled, and may be somewhat 
 thickened by fibrous-tissue over- 
 growth or by fatty or mucoid change. 
 
 1 
 
 m 
 
 :1 
 
 1 
 
 + [ 
 
 
 i 
 
 U '' 
 
 m 
 
 V T *m 
 
 l trophy c 
 Been from the front (two-thirds 
 natural size) (Bramwell). 
 
 Fig. 173.— Brown atrophy of 
 the heart- muscle. 
 
 The vessels are conspicuously tortuous (Fig. 172). 
 flabby and often quite dark in color. 
 
 The muscle is 
 
DISEASES OF THE CIRCULATORY SYSTEM. 371 
 
 Microscopically the fibers are found smaller than normal, and 
 contain excess of pigment. The latter is brownish or black, and 
 at first situated at the poles of the muscle-nuclei (Fig. 173). Later 
 the whole fiber may be uniformly pigmented. Sometimes the mus- 
 cle-fiber is converted into a hollow sheath, containing scattered 
 pigment-granules and more or less fragmented nuclei. Complete 
 destruction of the fiber may lead to the apparent occurrence of 
 pigment between the muscle-fibers. The pigment does not con- 
 tain iron, and seems to be a derivative of the albuminous con- 
 stituents of the fibers. 
 
 Localized atrophy of the fibers may occur around areas of 
 disease of the heart-muscle, such as foci of myocarditis, tubercles, 
 gummata, etc. The fibers present the same appearances as -those 
 just described. 
 
 Pathologic Physiology. — Atrophy of the heart-muscle does not 
 often occasion striking results or symptoms, as the process is in 
 most cases commensurate with the general emaciation and de- 
 creased demand. Occasionally irregular action of the heart is 
 noted, and sudden death has sometimes occurred. 
 
 HYPERTROPHY AND DILATATION. 
 
 Hypertrophy and dilatation are usually associated and result from 
 the same causes, the degree of hypertrophy or of dilatation present 
 in a given case depending upon the suddenness of action or the 
 intensity of the cause, and upon the state of the heart itself. A 
 sudden strain may cause immediate dilatation ; repeated strains of 
 less severity cause hypertrophy in a well-nourished heart, or in- 
 creasing dilatation in one the seat of myocardial weakness or 
 degeneration. 
 
 Etiology. — The influence of valvular diseases (q. v.) of the heart 
 in developing hypertrophy has been sufficiently discussed. Vari- 
 ous other causes may lead to overwork or cardiac strain, and occa- 
 sion hypertrophy or dilatation. We may classify the causes in 
 accordance with their operation upon one or the other, or both 
 ventricles. 
 
 Causes Acting on the Left Ventricle. — All forms of arterial 
 disease, but especially diffuse arteriosclerosis, increase the work of 
 the left ventricle notably, and may cause marked changes in it. 
 Aneurysms of the aorta, however, have surprisingly little effect. 
 Chronic Bright' s disease, especially the interstitial form, is a well- 
 known cause. It probably acts in several ways : partly by the 
 associated arterial disease, partly by vascular contraction due to 
 toxic products, and partly by the direct stimulation of cardiac 
 action by the same causes. Excessive exercise or laborious occu- 
 pations (mining, blacksmithing, etc.) may act upon the whole 
 heart, but especially upon the left ventricle. 
 
372 TEXT-BOOK OF PATHOLOGY. 
 
 Causes Acting on the Right Ventricle. — Diseases of the 
 lungs and pleura, such as emphysema, fibroid phthisis, and pleural 
 synechia?, are frequent causes of hypertrophy and dilatation of the 
 right ventricle. 
 
 Causes Acting on the Heart as a "Whole. — General func- 
 tional overstimulation may cause uniform enlargement of the 
 organ. This may be seen in cases of hysteria, exophthalmic 
 goiter, and other diseases in which the overaction is due to ner- 
 vous influences. Excessive eating and drinking affect the left more 
 than the right ventricle, but influence both sides to some extent. 
 Habitual, excessive beer-drinking is most striking in its effects, 
 and doubtless acts through the constantly recurring overdistention 
 of the blood-vessels, as well as through the excess of nutriment 
 and direct stimulus conveyed to the organ. Pericardial adhesions 
 may occasion continuous overaction of both ventricles. 
 
 Any of the causes named may occasion hypertrophy or dilata- 
 tion, or both. The degree of hypertrophy is dependent upon the 
 previous integrity of the heart-muscle, the state of the general 
 health, and the manner of action of the cause. Sudden strains 
 are more likely to cause dilatation, and pure dilatation may result 
 if the muscle of the heart is degenerated. This is illustrated by 
 cases of acute dilatation of the heart in the course of infectious 
 fevers. 
 
 Pathologic Anatomy. — Four forms of enlargement of the heart 
 may be distinguished. First, the walls are thickened, and the 
 cavities are smaller than normal; this is known as <%mcenJbri& 
 hypertrophy, but it is likely that the decreased size of the cavities 
 is due to post-mortem contraction ; second, hypertrophy of the 
 walls with normal cavities is spoken of as simple hypertrophy ; 
 third, hypertrophy with cavities of increased size is known as 
 eccentric hypertrophy, or hypertrophy with dilatation; and, fourth, 
 there may be pure dilatation without hypertrophy. In hyper- 
 trophy the muscle-substance is darker than normal and is increased 
 in consistency. Microscopically the fibers are increased in thick- 
 ness, and there is probably also increase in the number of the 
 fibers. The nuclei of the muscle are swollen and multiply ; myo- 
 cardial degeneration (fibro-fatty) is often associated. When dila- 
 tation is present the heart-muscle is usually softer, more flabby, 
 and generally somewhat lighter in color, due to associated degen- 
 eration. 
 
 The shape of the heart varies from the normal. When the 
 left ventricle is hypertrophied the organ is increased in length 
 and extends further to the left than normal (Fig. 174). When 
 the right ventricle is hypertrophied the organ assumes a rounded 
 shape ; its apex is less sharp, and the transverse measurement of 
 the organ is greatly increased. The weight and size of the heart 
 may increase enormously, and the term cor bovinum is often highly 
 
DISEASES OF THE CIRCULATORY SYSTEM. 373 
 
 appropriate. Weights of from 500 to 800 g. are not infrequent, 
 and may be greatly exceeded. Stokes recorded a case in which 
 the weight was 1980 g. 
 
 Pathologic Physiology and Results. — Hypertrophy is a rel- 
 ative process which serves to counterbalance the valvular or 
 
 Fig. 174.— Hypertrophy of the left ventricle (Ziegler). 
 
 other impediments to the circulation. Occasionally there may be 
 excessive hypertrophy, but, as a rule, it is merely sufficient to 
 maintain the circulation under ordinary conditions with less re- 
 serve power than is met with in health. In consequence valvular 
 lesions or arteriosclerosis may occasion no symptoms for a long 
 time, provided the individual leads a quiet life. Eventually, 
 however, when intercurrent diseases have determined cardiac 
 weakness, or when the impediment to the circulation has grown 
 progressively to an excessive degree, dilatation ensues and fail- 
 ure of the circulation is the consequence. When the left ventri- 
 cle is at fault congestion of the pulmonary system occurs, and 
 edema, hemorrhage from the lungs, or thrombosis with infarction 
 of the lungs may take place. When the right ventricle fails 
 general systemic congestion, cyanosis, and dropsy are the conse- 
 quence. 
 
 Great hypertrophy, while it results from arterial disease, very 
 frequently reacts upon the arteries and increases existing arterial 
 disease, or occasions arterial disease when it has not previously 
 existed. This is due to the increased force with which the blood 
 is projected from the ventricular cavity and the increased dis- 
 tention which the arteries suffer in consequence. 
 
374 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 ANEURYSM. 
 
 Aneurysm of the heart is a rare condition. It is usually found 
 in the anterior wall of the left ventricle, near the apex, but may 
 affect any part of the auricles or ventricles. Sometimes it is diffi- 
 
 Fig. 175.— Aneurysms of the left ventricle : the sac through which the prohe was passed 
 was situated posteriorly; the unopened aneurysm on the right was anterior; the heart 
 is somewhat twisted out of its usual shape to show both sacs in the illustration (Sailer). 
 
 cult to distinguish simple dilatation from aneurysm. The usual 
 cause of aneurysm is coronary obstruction, with resulting degen- 
 eration of localized areas of the wall of the heart. First, there is 
 softening (myomalacia), and this may occasion acute aneurysmal 
 dilatation and even rupture of the heart. In other cases the 
 degenerated area becomes fibrous and subsequently dilates. Acute 
 aneurysm of the heart-wall may similarly occur in cases of mural 
 endocarditis. Rupture in such chronic cases is a rare termination. 
 
 WOUNDS AND RUPTURE OF THE HEART. 
 
 Non-penetrating and even penetrating wounds of the heart- 
 wall are sometimes recovered from, the injury being repaired by 
 scar-tissue or fibrous myocarditis. As a rule, penetrating injuries 
 occasion rapid death by hemorrhage into the pericardium. Spon- 
 taneous rupture of the heart may be occasionally the result of 
 
DISEASES OF THE CIRCULATORY SYSTEM. 375 
 
 severe strain of a normal heart, but, as a rule, it occurs when 
 there is myocardial disease. Myomalacia cordis, fatty degenera- 
 tion, malignant endocarditis, and abscess are the conditions most 
 likely to occasion rupture. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis may occur in the form of acute miliary tuber- 
 culosis, affecting either the endocardium, myocardium, or peri- 
 cardium ; while caseous tubercles result from extension of tuber- 
 cular adenitis from the anterior or middle mediastinum. 
 
 Syphilis is rare, but may occur in the form of gumma or of 
 diffuse infiltration. Gummata may lie immediately beneath the 
 pericardium or endocardium, and after softening by degeneration 
 may rupture on the surface. 
 
 Actinomycosis may involve the heart by extension from the 
 mediastinum or by embolism. White or grayish nodules are 
 formed, and subsequently degenerate. 
 
 NEW GROWTHS AND PARASITES. 
 
 Primary tumors of the heart are extremely rare. Sarcoma, 
 fibroma, lipoma, myxoma, and myoma have been met with, and 
 usually occur in the form of wart-like growths projecting into the 
 cavities beneath the endocardium. Organized pediculated thrombi 
 have frequently been mistaken for tumors. 
 
 Secondary tumors are more common. Sarcomata of the 
 mediastinum may involve the pericardium, or even the heart-wall, 
 by direct extension, while secondary carcinomata and sarcomata 
 may affect the myocardium by metastasis. In the latter instances 
 nodular formations are seen embedded in the heart-muscle. 
 
 Parasites. — Echinococcus cysts are occasionally seen beneath 
 the endocardium or pericardium, and may rupture into the cavities 
 of the heart, with resulting embolism. The cysticerci of Taenia 
 solium and of Taenia saginata have occurred in man, but are more 
 common in animals. The larval Pentastomum denticulatum is a 
 rare parasite of the heart. 
 
 THE PERICARDIUM. 
 
 The pericardium is a membranous sac enclosing the heart and 
 the root of the great blood-vessels. It is composed of a fibrous 
 outer layer, and is lined within by flat endothelial cells. Normally 
 it contains from 5 to 50 cc. of clear serous liquid. 
 
 Partial or complete absence of the pericardium is sometimes 
 seen, especially in cases of ectopia of the heart. Occasionally 
 diverticula are present congenitally. 
 
376 TEXT-BOOK OF PATHOLOGY. 
 
 CIRCULATORY DISTURBANCES. 
 
 Hyperemia of the pericardium may occur in valvular heart- 
 disease or in cases of tumor or aneurysm causing intrathoracic 
 pressure. 
 
 Hemorrhages. — Extreme passive congestion with ecchy- 
 motic hemorrhages is found post-mortem in cases of death from 
 asphyxia. Small punctate hemorrhages are also occasioned by 
 various infectious diseases and by certain poisons, as phosphorus. 
 They are also seen in pernicious anemia, scurvy, purpura, and 
 other blood diseases. 
 
 Hemopericardium is a term applied to accumulation of 
 blood in the pericardial sac. It may result from rupture of the 
 heart or of aneurysms of the aorta, pulmonary artery, or coronary 
 arteries. The serous effusion of inflammatory conditions of the 
 pericardium may sometimes contain considerable blood which has 
 escaped from the small blood-vessels in the inflammatory tissue. 
 This is more common in inflammatory effusions of the pericardium 
 than of other serous membranes, and is particularly true of tuber- 
 culous and cancerous cases. 
 
 Hydropericardium, or dropsy of the pericardium, may occur 
 when passive congestion is continued, or as a part of a general 
 anasarca. Occasionally the liquid is milky {chylous hydrojieri- 
 eardium). 
 
 INFLAMMATION. 
 
 Inflammation of the pericardium, or pericarditis, is 
 
 the most important pathologic process affecting this part of the 
 body. 
 
 Etiology. — Pericardial inflammations may be primary or sec- 
 ondary. In the former the irritants are conveyed to the pericar- 
 dium through the blood, while in the latter the inflammation 
 results from extension. Primary pericarditis occurs in association 
 with various infectious diseases, notably acute rheumatism, scarlet 
 fever, small-pox, influenza, and intense septic infections. It is 
 also met with in the course of nephritis, either acute or chronic. 
 Secondary pericarditis may result from extension of inflammation 
 from the pleura, the lung, the mediastinal glands, the sternum, the 
 esophagus, and stomach, or from the heart itself. 
 
 In many instances, even where the pericarditis has occurred in 
 the course of an infectious disease, micro-organisms are not dis- 
 covered in the exudate ; this may be due to the arrest of the 
 micro-organisms in the pericardial tissues ; staphylococci, strepto- 
 cocci, pneumococci, and tubercle-bacilli have all been found. 
 
 Pathologic Anatomy. — Several varieties may be distinguished, 
 though one form may merge into another. 
 
 Fibrinous or Dry Pericarditis. — The first change noted in 
 
DISEASES OF THE CIRCULATORY SYSTEM. 377 
 
 pericarditis is a dulness or lusterless condition of the surface of 
 the membrane. Somewhat later distinct granulations, or a thin 
 coating of fibrin, appear upon the surface, and this may increase 
 until the deposit has a notable thickness. The movements of the 
 heart may give the latter a marked roughness or rugosity, and the 
 term applied by older writers, cor villosum, is not inappropriate 
 
 Fig. 176.— Acute pericarditis (Bramwell). 
 
 (Fig. 176). Microscopically there is seen a deposit of granular or 
 fibrillar fibrin upon the surface, whilst the endothelial cells are 
 loosened and partly degenerated, and the subendothelial tissues 
 are infiltrated with round cells. The blood-vessels are generally 
 widely dilated, and punctiform hemorrhages may be observed. 
 
 Serofibrinous Pericarditis. — The pericardial exudate rarely 
 remains purely fibrinous in character. Usually there is seen some 
 serous outpouring, and the sac becomes distended with more or 
 
378 TEXT-BOOK OF PATHOLOGY. 
 
 less abundant turbid, serous liquid, in which flakes of fibrin are 
 suspended. In such cases the fibrinous deposit is generally slight. 
 Later the fluid may be reabsorbed, leaving a simple fibrinous 
 pericarditis. 
 
 Purulent pericarditis, or pyopericardium, may begin as a 
 fibrinous or serofibrinous process, or it may assume the suppura- 
 tive form from the very start. In these cases the cause of the 
 pericarditis is usually some intense general infection, as in puer- 
 peral pyemia and septicemia, or it may be a local infection, as in 
 casts in which an esophageal or gastric ulceration has ruptured 
 into the pericardium, or in which a caseous tubercular focus or 
 purulent pleurisy has found a similar discharge. The pericardial 
 sac is filled with more or less purulent or seropurulent liquid, and 
 the pericardium itself is covered with fibrinopurulent exudate. 
 The superficial layers of the myocardium are frequently involved 
 by inflammatory edema, myocarditis, or fatty degeneration. 
 
 Hemorrhagic pericarditis is met with in individuals of low 
 vitality and in persons suffering from scurvy, purpura, and similar 
 affections. Pericarditis accompanying tuberculosis or cancer of 
 the pericardium is specially prone to assume a hemorrhagic type. 
 Usually the exudate is serous, but distinctly colored with blood ; 
 sometimes it is almost completely hemorrhagic. 
 
 Terminations of Acute Pericarditis. — Any of the forms described 
 may persist for a considerable length of time without change, but 
 usually certain alterations are noted. In the fibrinous variety, or 
 in the serofibrinous form, after the liquid has been reabsorbed, the 
 visceral and the parietal pericardium lie in contact and are aggluti- 
 nated by the exudate. Gradually the inflammatory processes 
 beneath the fibrinous exudate extend into the fibrinous coating ; 
 connective-tissue hyperplasia and new formation of blood-vessels 
 follow, and granulation-tissue unites the adjacent layers of pericar- 
 dium. At the same time the fibrinous exudate is reabsorbed and 
 subsequently organization of the granulation -tissues is completed. 
 Fibrous adhesions binding the two layers of the pericardium 
 together ensue, and at times complete obliteration of the sac is the 
 consequence (Figs. 177 and 178). In cases in which the inflam- 
 mation is slight, or in which the layers are kept apart by persist- 
 ent serous exudate, the areas of inflammation gradually become 
 thickened by new-formed fibrous tissue, and there remain upon 
 the surface of the pericardium sclerotic spots, often spoken of as 
 "milk spots." Occasionally portions of the fibrinous exudate re- 
 main unabsorbed, and together with the thickened membrane 
 itself and the adhesions suffer calcareous infiltration. The 
 heart may thus be encased in calcareous plates of considerable 
 thickness. 
 
 Purulent pericarditis may terminate by discharge of the exu- 
 date into the esophagus, stomach, pleura, or even into the bronchi, 
 
DISEASES OF THE CIRCULATORY SYSTEM. 
 
 379 
 
 and by the subsequent adhesion of the two layers of the sac. In 
 other cases gradual inspissation of the pus takes place and the 
 cheesy residue may remain or eventually become calcareous. 
 
 Fig. 177.— Adhesive pericarditis, showing fibrin-deposit, with new blood-vessels extending 
 upward into it (Perls). 
 
 Associated Conditions. — While, on the one hand, pericarditis 
 often follows inflammatory processes in the surrounding parts, it, 
 
 ~"-A'- ; ■-'■•■■ fJ U" ■■■• ■■: ■•£'■<■' 
 
 Fig. 178.— New blood-vessels and fibroblastic cells in a beginning adhesion of the 
 pericardial layers. 
 
 on the other hand, not infrequently occasions disease of the adja- 
 cent structures. In most cases of severe acute pericarditis there 
 
380 TEXT-BOOK OF PATHOLOGY. 
 
 is some associated inflammation of the mediastinal structures and 
 of the pleura contiguous to the pericardium. Cases which termi- 
 nate with the formation of fibrous adhesions within the pericardial 
 sac usually present, also, mediastinal and pleural adhesions with 
 the external surface of the pericardium {pericarditis interna et 
 externa). Myocarditis extending to a depth of 1 or 2 mm. is seen 
 in nearly every case of pericarditis. In cases in which considerable 
 pericardial exudate is present the heart-muscle is pressed upon and 
 impeded in function, so that venous congestions are commonly 
 observed. Adhesive pericarditis leads to hypertrophy and, later, 
 dilatation of the chambers of the heart. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis of the pericardium may result from the exten- 
 sion of pulmonary or pleural tuberculosis, or of tubercular affec- 
 tions of the mediastinal glands. More rarely direct infection may 
 occur through the medium of the circulation. Miliary tubercles 
 are formed in the subserous and serous layers of the membrane, 
 while the surface is covered with fibrinous exudation. The attend- 
 ant pericarditis may be entirely fibrinous and the tubercles may 
 be hidden from view by a thick deposit. In other cases there is 
 serous or hemorrhagic or purulent exudation, the latter especially 
 in cases in which caseous vomica? have ruptured into the pericar- 
 dial sac. Tuberculous pericarditis may terminate by gradual ab- 
 sorption of the exudate and fibrous adhesion, sometimes with 
 calcareous infiltration. In other cases the necrotic and destructive 
 changes characteristic of tuberculous processes elsewhere gain the 
 ascendency, and the disease proves fatal by the seriousness of the 
 cardiac involvement. 
 
 Syphilis is an extremely rare condition. Certain indurative 
 changes in the pericardium have, however, been met with in asso- 
 ciation with syphilis of the heart. 
 
 Actinomycosis may result from extension of actinomycosis 
 of the mediastinum or of the lungs. 
 
 TUMORS AND PARASITES. 
 
 Primary tumors, such as lipoma and fibroma, are extremely 
 rare. Secondary carcinoma and sarcoma are more frequent. 
 They result from similar growths in neighboring structures. 
 Hydatid cysts and cysticerci are occasionally met with. 
 
 PNEUMOPERICARDIUM. 
 
 Pneumopericardium (air in the pericardium) may result from 
 perforation of the sac in cases of fracture of the ribs or from pene- 
 tration of foreign bodies through the esophagus into the pericar- 
 
DISEASES OF THE CIRCULATORY SYSTEM. 381 
 
 dium. It also results from rupture of gastric or esophageal ulcers, 
 and a certain amount of gaseous accumulation complicates purulent 
 pericarditis when the exudate undergoes decomposition. The 
 association of air and pus (pneumopyopericardium) more often 
 results from secondary purulent inflammation after the develop- 
 ment of pneumopericardium. 
 
 THE ARTERIES. 
 
 Anatomic Considerations. — The arteries and veins consist 
 of three coats, called, respectively, the intima, or inner coat, the 
 media, or middle coat, and the adventitia, or external coat. The 
 intima consists of a layer of endothelial lining-cells, below which 
 there is a thick fibrous layer and then an elastic membrane. The 
 middle coat consists of smooth muscle-fibers, while the outer coat 
 is composed of the fibro-elastic tissue. Small blood-vessels, the 
 vasa vasorum, ramify through the adventitia and media, but the 
 intima is avascular. 
 
 CONGENITAL DEFECTS. 
 
 Certain defects of distribution and of origin of the larger 
 trunks have been referred to in the discussion of congenital defects 
 of the heart. Very commonly there are anomalies in the arrange- 
 ment of the peripheral branches, but these are of merely anatom- 
 ical interest. 
 
 Hypoplasia. — A condition of importance is congenital small- 
 ness, or hypoplasia. This may affect the aorta and larger vessels 
 together with the heart, or it may be confined to the blood-vessels, 
 the heart being normal. Vascular hypoplasia has been especially 
 met with in chlorotic girls, and also occurs in persons of tubercu- 
 lous habit. The aorta is sometimes so small that it barely admits 
 the little finger, and the walls are usually correspondingly decreased 
 in thickness. Decided elasticity of the coats of the vessels may 
 be observed. 
 
 HYPERTROPHY. 
 
 This occurs when a collateral circulation is established in con- 
 sequence of obstruction of an artery. Similarly in the new for- 
 mation of tissue the blood-vessels first formed are delicate vascu- 
 lar channels, which subsequently hypertrophy and are converted 
 into well-developed arterioles. In this case there is a uniform 
 overgrowth of each of the component parts of the blood-vessel, 
 and not a mere hyperplasia of one or another coat. 
 
 ATROPHY. 
 
 Atrophy may occur in a part which is undergoing general 
 atrophy, or in consequence of pressure and anemia of certain 
 
382 TEXT-BOOK OF PATHOLOGY. 
 
 areas. Degeneration of the walls usually takes place in such 
 cases, and the conditions are therefore more properly considered 
 among degenerations. 
 
 DEGENERATIONS. 
 
 Fatty Degeneration. — Any one of the coats may be affected, 
 but the process is most common in the intima. Fatty degenera- 
 tion is one of the important factors in atheroma ; more rarely it 
 occurs as an independent affection of the blood-vessels. In the 
 latter case disturbances of circulation and toxic agencies in the 
 blood are the immediate causes. Small white or yellowish spots 
 or streaks may be seen in the endothelium, and microscopically 
 the endothelial cells may be found granular or filled with oil- 
 drops. In cases of greater severity there may be actual erosion 
 of the endothelial surface. In cases in which the media is affected 
 the muscle-cells undergo fatty degeneration. Fatty degeneration 
 may occasion rupture of the blood-vessels, or calcareous infiltra- 
 tion may ensue. 
 
 Calcareous infiltration is the common termination of athe- 
 roma, but sometimes calcification of the intima or media, or even 
 of the entire wall of the vessel, may be observed without arterio- 
 sclerosis. The process is most common in the intima and media, 
 and, aside from the instances in which it is a part of atheroma, it 
 may occur in consequence of circulatory disturbances, or as the 
 result of bone-disease, with destruction of osseous tissue and sur- 
 charge of the blood with earthy salts. 
 
 Hyaline degeneration is a condition, the nature and uniform 
 character of which remain in doubt. A form of hyaline degenera- 
 tion is very common in the hyperplastic tissue of arteriosclerosis, 
 and is generally the first evidence of beginning degeneration. It 
 is met with in small blood-vessels which are obstructed by thrombi, 
 or which are subjected to destructive pressure by inflammatory 
 new growths or other causes. Not infrequently it is due to infec- 
 tious fevers or intoxications, and in these cases the small arteries 
 and the capillaries are prone to be affected. Hyaline degeneration 
 of the blood-vessels is the striking feature of certain cylindromata 
 (see Fig. 54). The artery may show a uniform or a more nodular 
 glass-like thickening, and under the microscope the subendothelial 
 tissue or the adventitia, or the entire wall of the blood-vessel may 
 be found converted into vitreous substance. Rupture of the 
 affected vessel is a not infrequent result. 
 
 Amyloid degeneration commonly begins in the blood-ves- 
 sels of the parts of the body in which this disease is found. In the 
 kidneys the capillary tufts of the Malpighian bodies and in the 
 spleen the capillaries within the lymphoid nodes are first affected. 
 In these cases the entire wall of the vessel is involved, and pre- 
 
DISEASES OF THE CIRCULATORY SYSTEM. 383 
 
 sents the characteristic appearances of the disease. Amyloid disease 
 is sometimes found in the intima of the larger blood-vessels, occur- 
 ring in small linear or punctate areas, and scarcely to be recog- 
 nized excepting by chemical tests. 
 
 INFLAMMATION. 
 
 Inflammation of the arteries may affect the inner, the middle, 
 or the outer coat, and in a strict anatomical sense the terms 
 endarteritis, mesarteritis, and peri-arteritis are justified ; but, as a 
 rule, all three coats are more or less involved at the same time, 
 and no practical distinction can be drawn. There may be acute 
 or chronic inflammation. 
 
 Acute Arteritis. 
 
 Acute arteritis may be of two kinds : a suppurative, or necrotic, 
 form, and a productive form. 
 
 Acute suppurative arteritis occurs in the arteries travers- 
 ing areas of suppurative inflammation, and results from the exten- 
 sion of the suppurative process. It may also occur in consequence 
 of the lodgement of infected emboli or as a result of infection of 
 thrombi within the vessels. 
 
 When the process extends from without, the adventitia and 
 then the media are infiltrated with round cells, and in cases of 
 some of the larger vessels there may be visible points or collec- 
 tions of pus. The process may extend as deeply as the intima, 
 and may completely perforate the wall of the vessel, leading to 
 hemorrhage. The intima itself is not directly involved by the 
 suppurative process from the lack of independent blood-supply, 
 but the emigrated leukocytes may infiltrate it, and degenerative 
 changes are common in the endothelium. Where the process 
 begins by infection within, as through softened thrombi or infectious 
 emboli, there is first necrotic or degenerative destruction of the 
 intima, and subsequently infiltration of the media and adventitia 
 with emigrated round cells. 
 
 A form of infectious arteritis resembling malignant endocarditis 
 has been observed in association with that condition in a few 
 instances. Ulcerated patches are seen in the intima of the aorta, 
 and acute aneurysmal dilatation or even perforation has been met 
 with. 
 
 Acute productive arteritis is most commonly the result 
 of tissue-changes surrounding the arteries, and is therefore con- 
 stantly met with in diseases of organs leading to overgrowth 
 of connective tissue. The condition is chronic rather than acute 
 in such instances. Acute productive arteritis occurs as a conse- 
 quence of thrombosis within the blood-vessels when the latter are 
 
384 TEXT-BOOK OF PATHOLOGY. 
 
 not infected. The terra thrombo-arteritis has been applied to these 
 cases. It is by thrombo-arteritis that wounds of vessels are closed 
 and the lumen of the blood-vessels at the point of ligation perma- 
 nently obliterated. 
 
 The changes affect mainly the intima and the adventitia, both 
 of which coats are densely infiltrated with round cells. The 
 thrombus, which was the original cause of the arteritis, or which 
 has resulted from the arteritis, becomes similarly infiltrated with 
 round cells, and as the process advances is found to be penetrated 
 by fibroblastic cells, which probably take origin from proliferation 
 of the endothelial-lining cells or from other connective-tissue cells 
 in the walls of the vessels. New blood-vessels spring from the 
 vasa vasorum and penetrate the thrombus, and a lesser number of 
 new vessels may enter the thrombus directly from the lumen of 
 the occluded vessel itself (see Fig. 7). The process of organization 
 takes place as in the serous surfaces generally, and, as new connec- 
 tive tissue is formed, the thrombus is gradually removed and the 
 lumen of the vessel may become completely obliterated. Less ex- 
 tensive involvement of the vessel may lead to the formation of 
 bands of adhesion passing from one side of the vessel to the other, 
 and causing considerable deformity and distortion. In other cases 
 there may be merely thickening of the intima as a final result, the 
 thrombus having been washed away or absorbed. The media 
 usually takes very little part in the process, being merely infil- 
 trated with round cells, but the entire wall of the vessel may 
 become fibroid in the terminal stages and the separate coats may 
 be indistinguishable. 
 
 Peri-arteritis Nodosa. — Under this name has been described a form 
 of productive inflammation of the adventitia leading to the formation of 
 fibrous nodules. In some of these cases there is no doubt a different path- 
 ology, as in the instances in which the intima has been found to protrude 
 in a hernious manner through defects in the media, but in most cases the 
 disease is a productive peri-arteritis (see also under Aneurysm). 
 
 Arteriosclerosis. 
 
 Arteriosclerosis, or endarteritis chronica deformans, 
 
 is a chronic degenerative and inflammatory disease of the arterial 
 system. It may be confined to the arteries, or may be more 
 extensive, involving the capillaries as well, when the term artcrio- 
 capillary fibrosis (Gull and Sutton) is applicable. Sometimes the 
 veins also are involved, and for this condition the name angio- 
 8clero8is has been proposed. 
 
 Etiology. — Arteriosclerosis is a physiologic process of old age, 
 and probably begins as early as middle life in most persons. The 
 earlier occurrence of the disease or the more extreme grades of its 
 severity are dependent upon a variety of causes, among which cer- 
 tain chronic intoxications, viz., syphilis, gout, chronic alcoholism, 
 
DISEASES OF THE CIRCULATORY SYSTEM. 385 
 
 and chronic nephritis, are prominent. An important cause is 
 muscular exertion, and it is not uncommon to find marked in- 
 stances in persons whose life or occupation has subjected them to 
 unusual muscular strain. Cachectic conditions of various kinds 
 may piay a part, as in cases of carcinoma, tuberculosis, or inani- 
 tion ; and sometimes the chronic arterial disease follows after 
 acute infections, such as rheumatism, scarlet fever, typhoid fever, 
 and the like. 
 
 Pathogenesis. — Not a little difference of opinion has existed in 
 regard to the manner in which the recognized causes of arterio- 
 sclerosis operate. At first it was generally maintained that the 
 infectious and toxic agencies directly irritate the inner lining of 
 the blood-vessels and produce inflammatory thickening. This 
 view has, however, been quite generally abandoned, and it now 
 seems established that degenerative changes and loss of elasticity 
 in the vessel-wall are the result of the primitive causes, and that 
 the hyperplastic processes in the intima and other parts of the 
 arterial wall are the ultimate result. 
 
 In cases of arteriosclerosis occurring in old age, for example, 
 the first disturbance of the blood-vessel consists in the loss of 
 elasticity in the muscularis and the overdilatation of the blood- 
 vessels. Secondarily, in consequence of this loss of elasticity, 
 there is a hyperplasia of the intima, which serves in some measure 
 to contract the lumen of the vessels and thus restore the vascular 
 channels to their normal condition. In cases of purely patho- 
 logic arteriosclerosis similar functional weakness of the muscularis 
 or more pronounced and demonstrable degenerative changes may 
 be the primary conditions, which in the end lead to arteriosclerosis. 
 In all cases the direct effect of elevations of blood-pressure may 
 play an important part, and in cases of muscular overwork or of 
 hypertrophy of the heart the increased vascular tension may be the 
 all-important cause. 
 
 Pathologic Anatomy. — Arteriosclerosis may be a diffuse process, 
 affecting more or less uniformly a large part of the arterial system, 
 or it may be a circumscribed or nodular condition. In the latter 
 instances, which are most common in the aorta and large vessels, 
 there are seen on the inner lining of the vessel nodular elevations, 
 varying in size from the merest points to that of a small coin. 
 These are raised a millimeter or two above the surface, and in 
 their earlier stages have a translucent grayish color ; they are 
 covered with smooth, unaltered endothelium. Later, degenerative 
 changes ensue and the nodule becomes dull white or yellowish in 
 color, and finally calcification may render it extremely hard (athe- 
 romatous plate). The focus may, on the other hand, soften com- 
 pletely by degeneration and may discharge into the lumen of the 
 vessel, leaving a necrotic, ulcerated patch (atheromatous ulcer). 
 Calcareous change may now occur, and the surface may be covered 
 
386 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 with thrombotic fibrinous deposits. These circumscribed areas of 
 arteriosclerosis may be few in number and widely separated. In 
 such cases the openings into the coronary arteries and the other 
 branches of the aorta are the favorite seats. In other cases the 
 plates may be so numerous and thickly set that the aorta is com- 
 pletely transformed. 
 
 Diifuse arteriosclerosis is especially frequent in elderly per- 
 sons, and is more common in the small vessels than in the aorta. 
 Sometimes it is associated with the nodular form; sometimes 
 the nodular change is completely wanting. 
 
 Microscopically the nodular elevations are found to consist of 
 dense sclerotic tissue in which deeply staining cells of elongated 
 character may be visible, the hyperplasia affecting the subendo- 
 thelial part of the intima in the earliest stages (Fig. 179). Sub- 
 
 179.— Transverse section of a cerebral vessel, in 
 Hirschfeld). 
 
 case of endarteritis nodosa (Birch- 
 
 sequently degeneration of the nodule becomes manifest. At first 
 the intercellular material assumes a hyaline character and becomes 
 glassy in appearance. The cells themselves may suffer fatty 
 degeneration from pressure. Later the whole area undergoes 
 myxomatous or •more particularly fatty degeneration, and breaks 
 down, forming a pultaceous detritus in which fat-drops and choles- 
 terin-plates are prominent (Fig. 180). Eventually calcareous 
 granules are deposited. 
 
 Fatty degeneration and calcification may also be apparent in 
 the media, and more or less hyperplastic connective-tissue over- 
 growth may lie seen in the adventitia. In cases of diffuse arterio- 
 sclerosis the media, as a rule, is thickened by hypertrophy of the 
 muscle-fibers as well as by sclerosis; but in the nodular forms the 
 media is usually distinctly thinner than normal. Koster pointed 
 out that round-cell infiltration surrounding the small branches of 
 
DISEASES OF THE CIRCULATORY SYSTEM. 387 
 
 the vasa vasorum in the media is the earliest change in some 
 instances. Considerable round-cell infiltration may be seen in the 
 deeper layers of the intima and in the media, and new formation 
 
 Fig. 180.— Atheromatous degeneration of a cerebral artery (Karg and Schmorl). 
 
 of blood-vessels may be quite pronounced. Such changes, how- 
 ever, are not usual and not characteristic. 
 
 Results. — In the smaller blood-vessels, particularly in those of 
 the brain, the hyperplastic process in the intima may proceed to 
 ;such a degree that the lumen of the vessels is almost completely 
 obliterated (endarteritis obliterayis). Complete obliteration may 
 take place by direct union of the opposite walls of the vessel, or 
 there may be first thrombosis, with subsequent organization of the 
 thrombus. In the aorta and in some of its larger branches the 
 loss of elasticity consequent upon the formation of fibrous tissue 
 and subsequent degenerations leads to gradual dilatation of the 
 blood-vessel walls, either in the form of diffuse ectasia or of local- 
 ized aneurysmal sacs. Sometimes the degeneration of the dis- 
 eased area occasions spontaneous rupture of the vessel. 
 
 Portions of the thrombotic deposits upon the roughened lining 
 of the vessels, or portions of the degenerative tissue itself, may be 
 discharged into the circulation, and may be carried to the periph- 
 eral parts as emboli. 
 
 Changes in Other Organs. — Diffuse arteriosclerosis places an 
 impediment upon the heart which leads to hypertrophy of its walls, 
 and in particular of the walls of the left ventricle. 
 
 When the process affects the small blood-vessels in the sub- 
 stance of the various organs, degenerative changes due to anemia 
 and reactive hyperplasia of connective tissue are common results. 
 
388 TEXT-BOOK OF PATHOLOGY. 
 
 Thus, in cases of* sclerosis affecting the cerebral vessels, cerebral 
 softening is commonly met with, while in cases in which the 
 branches of the coronary or of the renal arteries are affected, 
 degeneration and fibroid changes are seen in the heart and kid- 
 neys. 
 
 INFECTIOUS DISEASES. 
 
 Syphilis may involve the blood-vessels in a variety of ways. 
 No doubt, syphilitic infection is the most potent cause in the pro- 
 duction of arteriosclerosis, but more specific involvement of the 
 vessels occurs. Thus in areas of syphilitic infiltration and indura- 
 tion or adjoining gummata, the blood-vessels present noteworthy 
 changes. The intima and the adventitia, but particularly the 
 former, undergo great hyperplasia, and the lumen of the vessel 
 may be almost obliterated. The changes are first noted in the 
 intima, where large numbers of epithelioidal cells are formed, 
 while, later, infiltration of round cells is observed. The adven- 
 titia is similarly, but less extensively, affected. There is no his- 
 tologic or macroscopic feature by which the syphilitic nature of 
 the disease can be positively asserted. 
 
 Tuberculosis. — The arteries may become involved in areas 
 of tuberculosis, though, as a rule, they prove resistant for a long 
 time. Typical caseous degeneration may be seen in the walls 
 of the blood-vessels, beginning in the adventitia and gradually 
 advancing toward the interior. In the lungs these changes are 
 not infrequently seen in the walls of tuberculous cavities, and 
 as a result there may be small aneurysmal dilatations at the 
 points where the Avail of the vessel has become eroded and weak- 
 ened. It is from such vessels that the severe hemorrhages of the 
 late stages of phthisis take place. Sometimes the blood-vessels 
 of the tuberculous area present productive change leading to 
 great thickening of the adventitia and of the intima, and there 
 may be considerable narrowing of the lumen of the vessel. This, 
 however, is less common than the degenerative changes before 
 alluded to. 
 
 ANEURYSM. 
 
 Definition. — By aneurysm is meant a more or less localized 
 dilatation of the arterial walls. The term has, however, been 
 applied also to collections of blood outside of an artery enclosed 
 by an adventitious Avail and consequent upon a rupture of the ves- 
 sel. The name false or spurious aneurysm has been specially 
 applied to such cases, while the term true aneurysm is reserved for 
 such as conform to the first definition. It is preferable to confine 
 the single word aneurysm to the latter. 
 
 Btiology. — Aneurysms are always due to some Aveakness of 
 the A\ r alls of the blood-A'essel and to the distending force of the 
 
DISEASES OF THE CIRCULATORY SYSTEM. 
 
 389 
 
 blood within. It is therefore most common to find the disease in 
 persons beyond the age of forty or forty-five years, and particu- 
 larly in those who have acquired arteriosclerosis. Among the 
 remote causes, therefore, are the causes of arterial disease — syph- 
 ilis, gout, alcoholism, lead-poisoning, and other chronic intoxica- 
 tions. Sometimes it would seem that there is an hereditary weak- 
 ness of the arterial coats, and instances of aneurysm occurring in 
 successive generations have been recorded. Even congenital aneur- 
 ysms have been observed. As contributing causes may be ranked 
 all conditions which increase the blood -pressure. Thus laborious 
 occupations, hypertrophy of the heart, and diseases which occasion 
 constant excess of blood-pressure give rise to arterial degeneration 
 and also to dilatation of the vessel in a purely mechanical way. 
 Sudden aneurysmal dilatation of the weakened vessel may occur 
 after severe straining efforts, as in coughing, during labor, in the 
 straining of obstinate constipation, etc. Of all the causes, syphilis 
 is most important. 
 
 More acute degenerative changes in the blood-vessels may lead 
 to aneurysmal dilatations. Thus in the rare instances of acute 
 aortitis in association with malig- 
 nant endocarditis, small aneur- 
 ysmal dilatations and even rupture 
 of the aorta may occur. Embolism 
 plays a part in a similar manner. 
 Sometimes a calcareous embolus 
 from a diseased valve of the heart, 
 or from an atheromatous plate in 
 the aorta, may lacerate the walls 
 of the peripheral vessel, leading 
 to the formation of a dilatation. 
 In other cases infected emboli 
 (as in malignant endocarditis or 
 thrombosis with secondary de- 
 generation of the clot) lodge in 
 the peripheral vessels and occa- 
 sion acute inflammatory or de- 
 generative lesions of the walls, 
 and eventually aneurysmal dila- 
 tation. These cases are analogous 
 to the aneurysms of lower animals, 
 caused by animal parasites (Fig. 
 181). 
 
 The artery most commonly af- 
 fected is the aorta, and in particular the thoracic portion. A 
 majority of the aneurysms affecting the thoracic part of this 
 vessel arise from the ascending limb, and not rarely it is one 
 of the sinuses of Valsalva that first suffers dilatation. Next 
 
 Worm-aneurysm of the horse 
 (Leuckart). 
 
390 
 
 TEXT-BOOK OF rATHOLOGY. 
 
 to the aorta in point of frequency, the popliteal, femoral, carotid, 
 subclavian, innominate, axillary, and iliac vessels are affected. 
 
 An interesting form, and one of great frequency and clinical signifi- 
 cance, is that which affects the small blood-vessels of the brain, particularly 
 the branches supplying the lenticu- 
 lostriate body. This is the so-called 
 miliary aneurysm, which is commonly 
 the cause of cerebral hemorrhage 
 (Fig. 182). It is simply a small 
 saccular aneurysm due to weakening 
 of the blood-vessel walls by sclerosis 
 or degeneration. 
 
 In some cases of the condition de- 
 scribed as peri-arteritis nodosa (see 
 page 384) there has been discovered 
 a hernious projection of the intima 
 through defects of the media. These 
 have been recorded as instances of 
 congenital aneurysm ; but this expla- 
 nation does not suffice for all cases 
 (see Arteritis). 
 
 In phthisical lungs there are often 
 found somewhat similar hernious 
 aneurysms, due to erosion of the ad- 
 ventitia and media by the tubercu- 
 lous process ; and it is from these that 
 the severe hemorrhages of the late 
 stages of phthisis occur. 
 
 Fig. 182.— Miliary aneurysm of the brain. 
 
 Fig. 183.— Cylindrical and some- 
 what cirsoid aneurysm of the ab- 
 dominal aorta ; an opening has been 
 made to show the clot within (from 
 a specimen in the Museum of the 
 Philadelphia Hospital). 
 
 Pathologic Anatomy. — Aneurysms may be of three kinds : 
 ( 1 ) those in which there is quite general dilatation of all of the coats 
 of the vessel, and which therefore present themselves in the form 
 of a more or less uniform dilatation (edatic aneurysm) ; (2) those in 
 which a local weakening leads to the formation of a saccular pouch, 
 often communicating with the artery by a narrowed orifice (saccular 
 aneurysm) ; and (3) those in which a rupture of the intima, and 
 usually of portions of the media as well, has led to infiltration of 
 blood between the tunics of the vessel-wall (dissecting aneurysm). 
 
 1. Ectatic Aneurysm. — There is more or less uniform dilatation 
 in these cases, and there may be distinguished fusiform or spindle- 
 
DISEASES OF THE CIRCULATORY SYSTEM. 
 
 391 
 
 shaped and cylindrieal varieties, according to the shape assumed 
 (Fig. 183). In some instances the vessel is rendered tortuous by 
 the unequal involvement of different portions, and to this form the 
 term cirsoid aneurysm may be applied. The same term, as well as 
 the name anastomotic aneurysm, is given to certain conditions of 
 the arteries of the scalp and other parts which lead to the forma- 
 tion of tortuous vessels standing out prominently beneath the skin ; 
 but these are instances rather of hypertrophy of the coats, with 
 increase of length and thickness of the walls, without in reality any 
 aneurysmal dilatation at all. 
 
 In ectatic aneurysms the intima and adventitia are usually 
 thickened, and there are generally atheromatous patches in the 
 former. The media is generally thinner than normal, and may be 
 actually deficient in places. Ectatic aneurysms may show a cer- 
 tain amount of thrombosis in the form of laminated clots, when 
 there are pouchings or inequalities in the dilatation ; but very 
 frequently there is no thrombosis. 
 
 2. Saccular Aneurysm. — This is the most important variety. 
 According to Thoma and others, the first step in the process is the 
 
 Fig. 184.— Saccular aneurysm of the arch of the aorta, projecting forward and attached to 
 the ribs (Ziegler). 
 
 weakening or giving way of the media, followed by gradual dila- 
 tation of the intima and adventitia. There results a saccular 
 dilatation communicating with an artery, from which it arises by 
 a more or less narrow orifice (Fig. 184). The aneurysmal sac 
 
392 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 grows larger and larger, and may eventually rupture ; but even 
 then a secondary retaining wall may be formed by condensation 
 and reactive hyperplasia of the surrounding tissues. The wall of 
 the aneurysmal sac consists of thickened adventitia and intima, the 
 media being usually thinned and often completely wanting. The 
 intima is generally covered with atheromatous plates, and the cav- 
 itv, as a rule, contains more or less abundant laminated clots, 
 which tend to contract and organize, or to suffer subsequent 
 
 w 
 
 ■4 1 1 
 
 k 
 
 - vwbI 
 
 ... «Jf 1 
 
 ■ 
 
 Fig. 185.— Saccular and partly ectatic aneurysm of the descending part of the arch of the 
 aorta (from a specimen in the Museum of the Philadelphia Hospital). 
 
 degeneration. The aneurysm, if small, may be completely healed 
 by the organization of the clots within. 
 
 The tissues surrounding the aneurysm are pushed aside or 
 compressed, and may suffer extensive necrosis. In cases of 
 aneurysm of the thoracic aorta the sternum and ribs may be 
 eroded, and the aneurysm may project beneath the skin anteriorly 
 and eventually rupture (Fig. 187). In other cases the trachea, 
 bronchial tubes, or lungs are compressed, and rupture takes place 
 through the trachea or bronchi (Fig. 188). In still others the sac 
 projects posteriorly, erodes the bodies of the vertebra? and ribs, 
 and may compress the spinal cord or may project beneath the 
 
DISEASES OF THE CIRCULATORY SYSTEM. 393 
 
 tissues of - the back. Occasionally communication is established 
 with the large venous trunks, particularly the descending vena 
 cava. Complete arrest or cure of an aneurysm may take place 
 by organization of the clots contained, but such a result is rare. 
 3. Dissecting-aneurysm is most common in the aorta. As the 
 result of degenerative lesions or of mechanical injury, rupture of 
 the intima occurs, and the blood finds its way between the coats 
 of the artery, often burrowing to considerable distances. In a 
 case under my observation the walls of the aorta were dissected 
 
 Fig. 186.— Saccular aneurysm of the ascending part of the arch of the aorta (from a 
 specimen in the Museum of the Philadelphia Hospital). 
 
 as far as the bifurcation, where secondary ruptures had occurred 
 in the intima (Fig. 189). Usually the dissection takes place in 
 the media, which is thus separated into two parts. Subsequently 
 the adventitious canal may become lined with endothelium, and 
 in my case atheromatous plates had formed in the latter. 
 
 Associated Conditions in Other Parts. — Some hypertrophy 
 of the heart may occur when an aneurysm is situated near the root 
 of the aorta, and particularly in instances in which direct press- 
 ure is brought to bear upon the heart. As a rule, however, the 
 
394 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 amount of hypertrophy is much less than might be expected. 
 Pressure upon the venous channels is an early manifestation, and 
 
 Fig. 187.— Aneurysm of the aorta : erosion of the sternum and projection of the sac 
 beneath the skin. 
 
 leads to passive congestion and often to dropsy and cyanosis. 
 Necrosis of the parts which are directly compressed has already 
 
 Fig. 188.— The trachea, showing perforation of an aneurysm of the aorta (from a specimen 
 in the Museum of the Philadelphia Hospital). 
 
 been alluded to. Portions of the clot within the aneurysmal 
 cavity not rarely become separated, and are carried as emboli to 
 the peripheral parts of the circulation. 
 
DISEASES OF THE CIRCULATORY SYSTEM. 
 
 395 
 
 False or spurious aneurysms most commonly result from 
 traumatism, though sometimes spontaneous rupture of the vessel is 
 the immediate cause. The blood may find its way from the rupt- 
 ured artery into the surrounding tissues, forming a blood-tumor, 
 or hematoma, which becomes encapsulated by condensation of the 
 surrounding tissues and by reactive overgrowth of connective 
 tissue. The retaining wall thus formed may in some cases be 
 lined with endothelial cells, and secondary inflammatory thicken- 
 ing or atheromatous plates may form. When an artery and vein 
 
 Fig. 189.— Dissecting-aneurysm of the aorta : the aneurysm began near the aortic 
 valves and extended to the iliac branches, converting the aorta into a double tube: 
 a, transverse, b, longitudinal section. 
 
 are both injured, as is sometimes the case in phlebotomy, the blood 
 may enter the vein and distend this markedly. The term aneur- 
 ysmal varix is applied to such cases. In other instances the 
 artery and vein communicate by an intermediate sac formed by 
 the condensation of the intervening tissues, and for such the name 
 varicose aneurysm is used. 
 
 THE VEINS. 
 
 Anatomical Considerations. — The veins resemble the 
 arteries, excepting that the muscular coat is less well developed 
 and that most of the veins are supplied with endothelial redupli- 
 cations or folds, which act as valves and prevent the backward 
 flow of the blood. 
 
 CIRCULATORY DISTURBANCES. 
 
 Thrombosis of the veins is the most important condition. 
 This, however, is sufficiently considered under Thrombosis (p. 55). 
 
396 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 DEGENERATIONS. 
 
 Fatty degeneration of the intima and media may occur, as 
 in the arteries, but it is comparatively rare and unimportant. 
 
 Calcification is met with in veins which have become dilated 
 or varicose, or otherwise diseased. 
 
 INFLAMMATION, OR PHLEBITIS. 
 
 Acute phlebitis is a comparatively common affection. _ It 
 may occur as the result of inflammation, particularly infectious 
 inflammation, in the neighborhood of the vein. In such cases the 
 outer coat is first involved, and the term periphlebitis is properly 
 applied. This condition is met with in association with infected 
 wounds and phlegmonous inflammations of the subcutaneous 
 tissues. The veins beneath the skin may be distinctly visible as 
 blue streaks running in various directions. Microscopically there 
 is found to be an invasion of the adventitia with round cells, and 
 actual foci of suppuration are not uncommon. The cellular infil- 
 tration may extend to the media and sometimes to the intima, and 
 not rarely thrombosis occurs within. The thrombi thus formed 
 may secondarily become infected, soften, and occasion septic embo- 
 lism. _ ... , . 
 
 In another group of cases phlebitis begins from within, and is 
 the consequence of primary thrombosis of the vein (Figs. 190 and 
 191). To such the name thrombophlebitis is applicable. The 
 
 Fig. 190.— Thrombophlebitis of the femoral vein (from a specimen in the Museum of the 
 Philadelphia Hospital). 
 
 histologic changes are similar in these to those which occur in 
 thrombo-arteritis, and as terminal results localized thickening of 
 the venous wall or irregular contractions by the formation of 
 fibrous adhesions and even complete obliteration of the venous 
 channel may result. AVhen the thrombus is thus organized or 
 partially organized calcification may eventually occur, and in this 
 manner phleboliths, or vein-stones, are formed. 
 
 Chronic phlebitis, or phlebosclerosis, corresponds to 
 chronic arteritis or arteriosclerosis. A certain amount of chronic 
 inflammatory thickening of the vein ensues as a consequence of 
 thrombophlebitis. Phlebosclerosis may also be due to overdis- 
 
DISEASES OF THE CIRCULATORY SYSTEM. 
 
 397 
 
 
 tention of a vein resulting from thrombosis or other forms of 
 obstruction, and thus plays a secondary part in dilatation of the 
 veins, or phlebectasia. 
 
 Phlebosclerosis may, however, occur as a widespread affection 
 in association with arteriosclerosis, though rarely in equal degree, 
 in consequence of certain systemic conditions — syphilis, alcohol, 
 gout, etc. The changes occurring in the vein are practically the 
 
 
 
 
 Fig. 191.— Phlebitis and periphlebitis of the umbilical vein of the new-born : purulent 
 infiltration of the intima and adventitia; calcareous particles in the media (Birch- 
 Hirschfeld). 
 
 same as those in the artery, but the new-formed fibrous tissue in 
 the intima less commonly undergoes degenerative changes and 
 calcification than in arterial sclerosis. 
 
 In cases of congenital syphilis an interesting form of thicken- 
 ing of the intima, leading to stenosis or even complete obstruction, 
 has been found in the veins of the umbilical cord, and less fre- 
 quently in the portal vein. Similar hyperplastic endophlebitis has 
 been found in the veins of the extremities in syphilis of adults. 
 
 DILATATION OF THE VEINS ; PHLEBECTASIA ; VARICOSITY. 
 
 Etiology. — Dilatation of the veins occurs from mechanical 
 obstruction to the circulation or from weakness of their walls. 
 It presents itself more commonly in dependent portions of the 
 
398 TEXT-BOOK OF PATHOLOGY. 
 
 body, and is particularly frequent in the veins of the legs, of 
 the rectum, of the neck of the bladder, of the spermatic cord, 
 of the scrotum, and of the vagina. 
 
 Mechanical causes are most important. Thus in cases of 
 cirrhosis of the liver, of obstinate constipation, and of pelvic 
 tumors, dilatation of the veins of the rectum, causing hemor- 
 rhoids, is frequent. In cases of abdominal tumors, repeated 
 pregnancy, or other causes of obstruction to the venous return of 
 the blood from the lower extremities, varicosity of the veins of 
 the legs is frequently observed. Always, however, local disease 
 of the veins themselves tends to make the dilatations more pro- 
 nounced, and in addition systemic depression, and particularly 
 cardiac weakness, are contributing causes which operate by aiding 
 in the stagnation of the blood, which otherwise might pass by col- 
 lateral channels to its proper destination. 
 
 Pathologic Anatomy. — The veins in phlebectasia become 
 dilated and also elongated, so that they soon assume a tortuous 
 character. Not rarely masses of much-dilated veins lie closely 
 aggregated in groups or clumps beneath the surface of the skin ; 
 and communications may be established between the adjoining 
 pouches of dilatation, and thus a cavernous tissue is formed. The 
 walls of the dilated veins are usually considerably thickened 
 (phlebosclerosis), and even calcification may occur in the intima. 
 
 Results. — The circulation of the blood is slowed and throm- 
 bosis is therefore frequent. The thrombi may undergo organiza- 
 tion or calcification, or in other cases may soften and occasion 
 embolism. When varicosities are established in the veins of any 
 submucous tissue, catarrhal inflammation of the overlying mucosa 
 is occasioned and generally proves obstinate. At the same time a 
 certain amount of hyperplasia of the connective tissue between the 
 dilated veins takes place and thickening of the mucous membrane 
 results. When the subcutaneous veins are involved the skin is 
 prone to become thickened and to present eczematous inflamma- 
 tion, while the subcutaneous tissue may be greatly increased in 
 thickness and density (phlebectatic elephantiasis, or pachydermia). 
 Not rarely ulcerations of the skin of the lower extremity owe 
 their origin to varicosity of the veins, and such ulcers are prone 
 to prove indolent and obstinate. Hemorrhage may occur from 
 varicosities of the submucous veins, particularly in case of hem- 
 orrhoids and in the esophageal varicosities of drunkards. 
 
 TUMORS. 
 
 Tumors rarely begin in the walls of the veins, though myoma 
 and sarcoma have been described. More commonly the walls of 
 the veins are secondarily involved in cases of tumors surrounding 
 them. 
 
DISEASES OF THE CIRCULATORY SYSTEM. 399 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis not rarely attacks the veins, particularly those 
 of the lungs. Perforation of the wall may take place, and miliary 
 tuberculosis is a frequent consequence. 
 
 Syphilis of the veins has already been referred to. 
 
 THE LYMPHATIC CHANNELS. 
 
 Anatomic Considerations. — The lymphatic system begins 
 in the lymph-spaces, which are the spaces between the tissue- 
 elements in all parts of the body. These lymph-spaces unite to 
 form definite lymphatic capillaries, which are channels having 
 walls composed of a single layer of endothelial cells. The lym- 
 phatic capillaries unite to form larger vessels, and in these con- 
 nective-tissue coats support the endothelial lining. 
 
 INFLAMMATION. 
 
 Inflammation of the lymphatic vessels, or lymphan- 
 gitis, is always secondary to inflammatory affections of the parts 
 surrounding the lymphatics, or of those parts from which the lym- 
 phatics take their origin. In cases of infective lesions of the ex- 
 tremities red lines, indicating the position and course of the inflamed 
 lymphatics, may not infrequently be seen beneath the skin, extend- 
 ing upward to the nearest lymphatic glands. Histologically the 
 first change in such cases is swelling and ofttimes multiplication 
 of the endothelial cells of the lymphatic vessel ; later, there may 
 be accumulation of leukocytes within, and the lymphatic channel 
 may be uniformly filled with pus or distended at different points. 
 Usually a certain amount of perilymphangitis accompanies the 
 process, and in cases of violent septic infection the surrounding 
 tissues may become extensively involved in phlegmonous inflam- 
 mation. Thrombosis may take place within the lymphatic chan- 
 nel in cases of moderate severity, and obstruction ensue. The ter- 
 mination is either in resolution or suppuration, with more or less 
 widespread involvement of the surrounding tissues. Kesolution 
 may be only partial, the inflammatory changes going on to the 
 formation of connective tissue, which may obliterate the channels, 
 or the restitution of the wall of the lymphatic vessel may be im- 
 perfect, and subsequent dilatation results. 
 
 DILATATION OF THE LYMPHATICS, OR LYMPHANGIECTASIA. 
 
 This condition may be an acquired or a congenital affection. 
 
 Acquired dilatation of the lymphatics results from ob- 
 struction to the larger channels, as in cases of pressure upon or 
 thrombosis of the thoracic duct, or of obstruction of the lym- 
 
400 TEXT-BOOK OF PATHOLOGY. 
 
 phatic channels by filarise. In other cases it is due to inflamma- 
 tions surrounding the lymphatics and leading to weakness of their 
 walls. It is very commonly observed in the subcutaneous lym- 
 phatics, and constitutes the endemic elephantiasis of warmer coun- 
 tries. This condition is particularly common in the lower extrem- 
 ities, scrotum, and labia, but may affect other parts. The skin is 
 greatly thickened and the surface often of irregularly lobulated 
 character. On incision into it there is found an abundant exuda- 
 tion from the subcutaneous tissue of serous or of milky liquid. 
 
 Obstructive dilatation of the intra-abdominal lymphatics is not 
 unusual. Rupture of dilated branches in the genito-urinary tract 
 may lead to chyluria. 
 
 Congenital lymphangiectasia may take the form of a 
 diffuse condition affecting the lymphatics more or less regularly 
 in certain parts of the body, or it may appear in circumscribed 
 areas, often in situations in which the ordinary lymphatic supply 
 is not abundant. The diffuse form occasionally presents itself in 
 the new-born in the form of edematous or semicystic swellings of 
 the subcutaneous tissue, resembling those of elephantiasis. In the 
 same group of cases belong the instances of congenital enlargement 
 of the tongue (maeroglossia) and of the lips (maerocheilia). In some 
 of these instances the development of the condition does not occur 
 until some time after birth, though the process is in reality con- 
 genital. Localized lymphatic dilatations constitute the form of 
 new growth known as lymphangioma (see General Pathology). 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis. — The lymphatics play an important part in 
 the dissemination of tuberculosis within the organs, and they may 
 themselves be involved in the disease. This is beautifully illus- 
 trated in cases of intestinal tuberculosis with ulceration. In such 
 cases the lymphatic channels in the serous coat may be seen radi- 
 ating from a point opposite the ulceration toward the mesentery, 
 and small miliary nodules are seen in their course. 
 
 Syphilis. — The lymphatics may be involved in syphilitic proc- 
 esses in their vicinity, but the changes are not characteristic. 
 
 TUMORS. 
 
 In addition to the lymphangioma^ referred to, the lymphatic 
 vessels are the primary seat of tumors resulting from multiplica- 
 tion of the lining endothelial cells, which are known as endothdio- 
 rnata. These tumors are especially common in the serous surfaces, 
 but may also be met with in the skin and elsewhere. The lym- 
 phatics bear an important relation to the metastasis of malignant 
 tumors, particularly of carcinomata. The carcinoma-cells enter 
 
DISEASES OF THE CIRCULATORY SYSTEM. 401 
 
 the lymphatics and are carried by the stream to distant parts of 
 the body ; sometimes the lymphatics near carcinomata are found 
 densely packed with cancer-cells. 
 
 PARASITES. 
 
 The adult of the Filaria sanguinis hominis resides in the lym- 
 phatic vessels, and the embryos may be present in large numbers 
 (see General Pathology). 
 
 THE THORACIC DUCT. 
 
 Pathologic processes involving the thoracic duct resemble in 
 general character those of the other lymphatic vessels, but the size 
 of the duct and its anatomical relations make the diseases affect- 
 ing it of somewhat greater significance than the same diseases when 
 occurring in the smaller lymphatics. 
 
 Thrombosis may occur in association with inflammation of 
 the duct or without such, and there may be a permanent occlusion 
 in consequence. Dilatation of the lower parts of the duct, as 
 well as of the lymphatic vessels of the abdomen, may ensue, and 
 sometimes the receptaculum or other portions of the duct may 
 become cystic. Chylous ascites may likewise result. More com- 
 monly collateral circulation re-establishes circulation and serious 
 consequences are not observed. 
 
 Dilatation of the thoracic duct may also result directly 
 from cardiac failure with engorgement of the greater veins. The 
 outflow of lymph is impeded, and in some cases the backward 
 pressure of the blood through the superior cava may fill and dis- 
 tend the upper part of the thoracic duct with blood. 
 
 Inflammation occurs in consequence of various inflammatory 
 diseases of the abdomen or of the pelvis, by the invasion of irri- 
 tants through the lymph received from the affected areas. There 
 may also be direct extension of inflammation in cases of abdominal 
 disease, or in pleurisy or other intrathoracic affections. 
 
 Tuberculosis affecting the abdominal portion of the duct is 
 sometimes observed in cases of intestinal or mesenteric tubercu- 
 losis, and may occasion secondary miliary tuberculosis, particu- 
 larly the form in which the disease is subacute or chronic in its 
 course (Weigert). 
 
 Tumors. — Primary tumors are sometimes observed, and sec- 
 ondary carcinoma is more commonly met with. 
 
402 TEXT-BOOK OF PATHOLOGY. 
 
 CHAPTER IV. 
 DISEASES OF THE RESPIRATORY SYSTEM. 
 
 THE NASAL CAVITIES. 
 
 Anatomic Considerations. — The mucous membrane of the 
 nose is unusually prominent, especially over the lower turbi- 
 nated bone, where it is 4 mm. thick. In the lower, or respiratory, 
 parts of the nose the epithelium is stratified ciliated columnar. 
 The submucosa is replete with a venous network, giving it, par- 
 ticularly over the inferior turbinated bone, the appearance of 
 erectile tissue. In the olfactory regions non-ciliated columnar 
 cells, which become attenuated at the inner end, line the surface. 
 Between the filiform prolongations within lie round and tapering 
 olfactory cells. Small tubular and racemose serous and mucous 
 glands are freely distributed in the mucosa. 
 
 CONGENITAL ABNORMALITIES. 
 
 Deviations of the septum and other slight anomalies are com- 
 mon. Atresia, absence of the septum or other parts, or complete 
 absence of the nose, are rare defects. Harelip and cleft palate 
 frequently involve the nasal cavities. 
 
 CIRCULATORY DISTURBANCES. 
 
 Active congestion occurs in consequence of exposure to 
 great heat or cold, or of ascending elevations ; and when the heart 
 is overstimulated. 
 
 Passive congestion may be due to cardiac weakness, obstruc- 
 tive diseases of the lungs, and local pressure on veins. 
 
 Hemorrhage. — In either passive or active congestion hemor- 
 rhage (epiztaccis) may occur. Bleeding may, however, result from 
 blood-diseases (hemophilia, pernicious anemia, leukemia), from 
 disease of the blood-vessels (arteriosclerosis), or in a paroxysmal 
 form from obscure causes. Epistaxis is a frequent prodromal 
 symptom of typhoid fever ; less frequently it occurs in influenza 
 and other infections. 
 
 Hdema of the mucous membrane may be associated with in- 
 flammation. 
 
 INFLAMMATIONS. 
 
 Acnte nasal catarrh (acute rhinitis ; coryza) commonly 
 results from exposure to cold. Irritant fumes may cause it; often 
 it seems infectious and contagious. It may occur as an associated 
 
DISEASES OF THE RESPIRATORY SYSTEM. 403 
 
 condition in various infections, as grip, typhoid fever, measles, etc. 
 The mucosa is at first intensely red and dry ; then an irritating 
 serous, followed by mucous and finally mucopurulent, exudation 
 is discharged. Herpes or eczematous eruptions of the lip are 
 common. Considerable inflammatory edema of the mucous mem- 
 brane of the nose and accessory cavities may occur. 
 
 Chronic rhinitis follows repeated acute attacks, especially 
 in scrofulous, tuberculous, or syphilitic persons. The mucosa, 
 especially over the inferior turbinated bone, becomes thickened 
 (hypertrophic rhinitis) and may remain so, or undergo atrophy 
 (rhinitis atrophica). In the latter the exudate is scanty and ap- 
 pears as dry, greenish crusts, which sometimes occasion extensive 
 ulcerations and become horribly offensive. To such cases the term 
 ozena is applied. Various forms of bacilli and micrococci have 
 been discovered, the most frequent being an organism resembling 
 the bacillus of Friedlander. Fetid discharges may also occur in 
 syphilitic or tuberculous diseases of the nose (ozcena syphilitica s. 
 tuberculosa). 
 
 INFECTIOUS DISEASES. 
 
 Diphtheritic rhinitis is usually secondary to pharyngeal 
 diphtheria. Non-specific diphtheritic rhinitis is a very rare con- 
 dition. 
 
 Syphilis in the secondary stage and in congenital cases some- 
 times occasions simple catarrhal rhinitis. Mucous patches may 
 occur, or gummata springing from the mucous membrane or from 
 the periosteum or perichondrium. The latter tend to ulcerate and 
 cause destruction. The purulent discharge may be fetid. 
 
 Tuberculosis may occur as disseminated or aggregated 
 tubercles of the mucous membrane, or as ulcers and carious pro- 
 cesses. These are all rare, but " scrofulous catarrhs " of children, 
 probably often tuberculous, are common. Lupus of the face may 
 extend to the nose. 
 
 Glanders occasions intense purulent and hemorrhagic rhinitis, or nodu- 
 lar growths with ulceration. Nodules and ulcers in lepra, and irregular 
 swelling and induration of the mucous membrane of the nose and the 
 adjoining skin in rhinoscleroma are rare conditions. 
 
 TUMORS. 
 
 The commonest form of tumors is the polyp, which is some- 
 times distinctly the result of hypertrophic rhinitis, at other times 
 obscure in origin. Polyps present the ordinary structure of the 
 nasal mucosa, with a tendency to cystic change from occlusion of 
 the glands, or to adenomatous appearances from proliferation of 
 the glandular elements. Fibroid, myxomatous, and sarcomatous 
 polyps also occur. In all cases there is a tendency to recurrence 
 
404 TEXT-BOOK OF PATHOLOGY. 
 
 after removal. A rare form of hairy polyp has been recently 
 described. Chondromata, osteomata, sarcomata, and epithelial or 
 glandular cancers may be found. 
 
 PARASITES AND FOREIGN BODIES. 
 
 Larva? of various flies may occur in the nasal chambers and set 
 up serious inflammatory lesions. Foreign bodies may become 
 incrusted with lime-salts and lead to the formation of rhinoliths. 
 
 THE LARYNX. 
 
 Anatomic Considerations. — The lining epithelium of the 
 larynx is stratified squamous as far as the false vocal cords. 
 Below these and throughout the ventricles it is stratified ciliated 
 columnar, and thus continues into the trachea and bronchi, ex- 
 cepting over the true vocal cords, which are covered with strati- 
 fied squamous epithelium. The tunica propria contains much 
 yellow elastic fiber, and the submucosa is quite loose, especially 
 over the base of the epiglottis and the aryepiglottic folds. 
 
 CONGENITAL ABNORMALITIES. 
 
 Minor defects in shape of the constituent parts of the larynx 
 are not rare. Congenital fistula? communicating with the exterior, 
 and dilatation of the ventricles similar to the normal pouching 
 found in certain monkeys, are occasionally met with. Abnormal 
 largeness and smallness, the latter especially in persons having 
 poorly developed sexual organs and those castrated early in life, 
 are more frequent conditions. 
 
 CIRCULATORY DISTURBANCES. 
 
 Anemia may occur in general anemia, and is sometimes found 
 in tuberculous and chlorotic subjects in pronounced degrees. 
 
 Active hyperemia follows exposure, overuse of the voice, 
 and irritation by gases, dust, and the like. 
 
 Passive hyperemia occurs in heart-diseases, intrathoracic 
 tumor, and other conditions obstructing the venous circulation. 
 In active congestion the larynx is bright red ; in passive con- 
 gestion it is dark red in color, and distended veins may be 
 prominent. 
 
 Hemorrhages are seen in the mucosa after death from 
 asphyxia, in cases of purpura or other hemorrhagic conditions, as 
 well as in intense inflammation of the larynx. Large hemor- 
 rhages may occur in cases of cancer. 
 
 fedema of the epiglottis, the aryepiglottic folds, and other 
 parts of the larynx may be part of a general anasarca in Bright's 
 
DISEASES OF THE RESPIRATORY SYSTEM, 405 
 
 disease or heart-disease, or may result from local pressure upon 
 the veins. The parts become greatly swollen, and of an anemic, 
 translucent appearance. Great stenosis of the larynx commonly 
 results. Generally " edema of the larynx " is inflammatory in 
 nature (see below). 
 
 INFLAMMATIONS. 
 
 Acute catarrhal laryngitis results from chemical or 
 mechanical irritation ; it accompanies whooping-cough, measles, 
 small-pox, typhoid fever, and other infections. The mucous 
 membrane is bright red and swollen. A scanty mucous or muco- 
 purulent exudate is usually noted. Intense laryngitis is attended 
 with small hemorrhagic ecchymoses or erosions ; true ulcers are 
 rare. Follicular ulcers are sometimes seen, and rarely small 
 vesicles arise upon the surface (herpetic laryngitis). 
 
 Acute laryngitis may cause considerable disturbance of breath- 
 ing by the swelling of the mucous membrane, and in children 
 often leads to spasmodic contraction of the laryngeal muscles, 
 with paroxysmal dyspnea (false croup). 
 
 Chronic catarrhal laryngitis may follow the acute form, or 
 begin gradually. Overuse of the voice and exposure to cold or 
 irritating gases or dust are the common causes. The mucous 
 membrane is usually thickened and somewhat granular, or even 
 papillomatous. There is a tendency for the epithelium to assume 
 a squamous or epidermoid character, especially on the vocal cords 
 {pachydermia laryngis). In the later stages atrophic changes 
 may ensue. 
 
 Edematous laryngitis is generally known as edema of the 
 larynx. Nearly always it is a true inflammatory edema, due to 
 violent irritation, general or local infection, or severe local lesions 
 of a chronic nature, such as tuberculous or syphilitic ulceration 
 and perichondritis. The looser submucous tissues at the base of 
 the epiglottis and over the aryepiglottic folds become greatly 
 swollen, and the surface is more or less translucent. Sometimes 
 the edematous infiltration is yellowish, or even quite purulent, 
 especially in cases in which phlegmonous suppurations have ex- 
 tended from neighboring parts (retropharyngeal abscess ; erysipe- 
 las). When circumscribed areas are affected abscess results. 
 
 Perichondritis, inflammation of the perichondrium of the 
 cartilages of the larynx, is usually secondary to serious laryngeal 
 diseases, as syphilitic or tuberculous ulcers, carcinoma, etc. It 
 may be primary in typhoid fever or other infections. Frequently 
 suppuration and necrosis of the cartilage result ; but merely local- 
 ized induration and swelling may occur. 
 
406 
 
 TEXT-BOOK OF PATHOLOGY, 
 
 INFECTIOUS DISEASES. 
 
 Diphtheritic and croupous inflammations may be part 
 of the anatomical changes in diphtheria, but may also occur in 
 
 typhoid fever, scarlet fever, 
 small-pox, or other infectious 
 diseases, or from violent irri- 
 tation by steam or the like. 
 The surface of the larynx is 
 covered with a more or less 
 adherent, grayish or yellowish 
 pseudomembrane, which con- 
 sists of a network or masses 
 of fibrin entangling degener- 
 ated round cells and epithe- 
 lium. The membrane is most 
 adherent where the epithelium 
 is squamous. Diphtheritic 
 laryngitis usually follows a 
 similar process in the pharynx 
 (see Diphtheria, Part I.). 
 
 Tuberculosis is nearly 
 always secondary to pulmo- 
 nary tuberculosis. Small lo- 
 calized tuberculous masses, or 
 more diffuse tuberculous infil- 
 tration, are found in the mu- 
 cosa and submucosa, especially 
 on the posterior wall of the 
 larynx. Early caseation and 
 ulceration are further charac- 
 teristics (Fig. 192). Simple 
 catarrhal inflammation, or hy- 
 pertrophic conditions of the mucous membrane between the 
 tuberculous masses, or edematous laryngitis and perichondritis, 
 may complicate the tuberculous lesions. Lupus of the nose and 
 pharynx may extend to the larynx, where it occasions nodular 
 thickenings and ulceration. 
 
 Syphilis may occasion simple catarrh of the larynx, or infil- 
 tration and erosion of the mucous membrane secondary to pharyn- 
 geal involvement. The latter conditions are most frequent in 
 the epiglottis, the posterior wall of the larynx, and the vocal 
 cords. Gummata may occur in the same situations independent 
 of pharyngeal syphilis, and lead to deeper ulcers. In the 
 healing of syphilitic ulcers irregular papillomatous elevations 
 of the healthy mucosa, or extreme contractions and deformities 
 of the larynx, may occur. 
 
 Fig. 192.— Tuberculous erosion and ulcer- 
 ation of the larynx, causing extensive de- 
 struction of the vocal cords (from a specimen 
 in the Museum of the Philadelphia Hospital). 
 
DISEASES OF THE RESPIRATORY SYSTEM. 
 
 407 
 
 I^epra and glanders sometimes occur in the form of nodular 
 swellings and ulcers. 
 
 Swelling and ulceration of the lymphatic follicles analogous to 
 the lesions in the intestines may occur in typhoid fever ; and in 
 small-pox there may be small areas of infiltration and epithelial 
 degeneration, or even pseudomembranes. 
 
 TUMORS. 
 
 Papilloma. — Over half of all tumors of the larynx belong to 
 the group of papillomata or papillomatous fibromata. These are 
 simply hypertrophied papillae covered with a thick mantle of 
 squamous epithelium (Fig. 193). The 
 stroma may be insignificant and the 
 epithelium considerable (hard papilloma), 
 or the stroma may be excessive, highly 
 vascular, and infiltrated with round cells, 
 while the epithelial covering is thin (soft 
 papilloma). Papillomata are most frequent 
 on the false vocal cords or on the other 
 parts of the larynx lined with squamous 
 epithelium. They usually occur in num- 
 bers, but may be solitary. Chronic in- 
 flammation often determines their occur- 
 rence ; and they are not infrequent around 
 chronic ulcers or carcinoma of the larynx. 
 Simple hyperplasia of mucous membrane, 
 of normal structure, occurs in various 
 chronic inflammatory conditions of the 
 larynx. 
 
 Fibroma. — Nodular, sessile, or poly- 
 poid fibromata constitute one-third of all 
 tumors. They are most frequent on the vocal cords and in the 
 upper part of the larynx. 
 
 Cystic dilatation of the glands may occasion mucous polyps. 
 Adenoma, lipoma, myxoma, sarcoma, and chondroma are rare 
 tumors. Tumor-like masses of heterotopic thyroid- gland tissue 
 have been found in the larynx. 
 
 Carcinoma may be primary, or less frequently secondary. 
 Primary carcinoma is usually of the squamous variety and occurs 
 about the vocal cords. Nodular thickening with ulceration results. 
 Papillomatous thickening of the mucous membrane frequently sur- 
 rounds the growth. Secondary involvement of the cervical glands 
 and esophagus may occur. 
 
 Of 1100 tumors of the larynx, collected by Bruns, 602 were papillo- 
 mata, 346 fibromata, 73 mucous polyps, and 27 cysts. Seventy-six per cent, 
 occupied the true cords, or the anterior commissure of the cords. Mackenzie 
 found 67 per cent, papillomata and 16 per cent, fibromata. 
 
 :.— Papillomata of 
 the vocal cords (from a speci- 
 men in the Museum of the 
 Philadelphia Hospital). 
 
408 TEXT-BOOK OF PATHOLOGY. 
 
 PARASITES AND FOREIGN BODIES. 
 
 The larval Trichina spiralis may infest the laryngeal muscles; 
 and lumbricoids occasionally enter from the pharynx. Eehino- 
 CQCCU8 cysts are very rare. 
 
 Large foreign bodies may cause death by suffocation. Smaller 
 bodies may rest in the larynx, especially the ventricles, for years, 
 becoming surrounded by hyperplastic mucous membrane or a cap- 
 sule of fibrous tissue. Calcareous concretions may form around 
 small foreign bodies, or spontaneously in the ventricles. 
 
 THE TRACHEA. 
 MALFORMATIONS. 
 
 Congenital Malformations. — Complete absence of the 
 trachea occurs in acephalic monsters. Congenital decrease in 
 length or diameter, in the number or completeness of the carti- 
 lages, and like minor deformities, are more common. An adven- 
 titious bronchus is occasionally seen, especially on the right side, 
 and fistulous communications with the exterior or with the esopha- 
 gus are rare congenital defects. Diverticula may be due to a 
 rudimentary condition of a supernumerary bronchus. Congenital 
 cysts may occur between the trachea and esophagus when fistulous 
 communications between them become closed at either end. 
 
 Acquired Malformations. — Dilatations of the trachea may 
 be diffuse or localized. They depend for their occurrence upon 
 weakness of the walls and some impediment to expiration. Sac- 
 cular dilatations are usually on the posterior wall. Narrowing of 
 the lumen may be due to pressure of tumors or aneurysms ; to 
 new growths or cicatricial contractions (especially syphilitic) or 
 to foreign bodies within. 
 
 CIRCULATORY DISTURBANCES. 
 
 Anemia and active and passive congestion result from the same 
 causes as in the larynx ; and the pathologic anatomy is the same. 
 
 INFLAMMATIONS. 
 
 Inflammations are usually associated with laryngitis or bron- 
 chitis, and are due to the same causes. Simple catarrhal and pseudo- 
 membranous inflammations are met with. Foreign bodies may 
 cause extensive and deep inflammation, leading to ulceration and 
 sometimes perforation. Chronic inflammation assumes a prolifera- 
 tive, and later an atrophic, character. Proliferative (polypoid) 
 inflammation is not infrequent after tracheotomy, and may occa- 
 sion serious obstruction. Ozena of the trachea may be associated 
 with nasal ozena. 
 
DISEASES OF THE RESPIRATORY SYSTEM. 409 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis and syphilis occur under the same circum- 
 stances as in the larynx. Syphilis may, however, affect the 
 trachea and bronchi independent of disease of the pharynx or 
 larynx. 
 
 TUMORS. 
 
 Primary tumors are rare. Secondary involvement by cancer, 
 extending from the esophagus or thyroid gland, or by sarcoma, 
 from the surrounding lymphatic structures or thymus gland, is 
 more frequent. Ecchondroses and osteomata may spring from the 
 cartilages, and multiple chondromata have been found in the mu- 
 cous membrane. Retention-cysts of the mucous glands are occa- 
 sionally seen on the posterior wall, protruding outside the trachea. 
 
 THE BRONCHI. 
 
 Anatomic Considerations. — The larger bronchi corre- 
 spond very closely to the trachea in structure. The smaller 
 divisions have thinner walls, being less provided with cartilagi- 
 nous rings, but having instead small cartilage-plates and greater 
 abundance of muscle-fibers. The tubes having a diameter less than 
 1 mm. are called the terminal bronchioles, and lead into yet smaller 
 tubes, the alveolar passages, which open into dilated infundibula, 
 and the last named are finally surrounded by air-sacs. The lining 
 epithelium is stratified columnar ciliated down to the terminal 
 bronchioles, where it becomes simple columnar. In the alveolar 
 passages there is first polygonal, then flat, epithelium ; while in the 
 infundibula and air-sacs there are practically only flat epithelial 
 
 CONGENITAL MALFORMATIONS. 
 
 These are rare and unimportant. Dilatations or narrowing and 
 anomalous division of the tubes have been noted (see Trachea). 
 
 CIRCULATORY DISTURBANCES. 
 
 Anemia and hyperemia occur under the same circumstances 
 as in the trachea and larynx. 
 
 Hemorrhage. — Intense congestion may occasion hemorrhages 
 into the mucous membrane or into the bronchi themselves. More 
 frequently hemorrhage is due to catarrhal inflammation, tuberculous 
 ulceration, or a general hemorrhagic tendency. Aneurysms of the 
 aorta (see Fig. 188) and the small aneurysms of the pulmonary 
 arterioles in tuberculosis of the lungs not infrequently rupture 
 through the bronchi. 
 
 INFLAMMATIONS. 
 
 Both acute and chronic bronchitis are common conditions, and 
 there are a variety of forms. 
 
410 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 Acute catarrhal bronchitis results from exposure, from 
 inhalation of irritating gases, and from downward extension of 
 tracheal catarrhs. The terminal bronchioles are frequently affected 
 secondarily in pulmonary diseases. Bronchitis is constantly asso- 
 ciated with some of the infectious fevers — typhoid fever, measles, 
 whooping-cough, etc. Various micro-organisms have been found 
 in bronchitis. Among these are the pyogenic micrococci, the 
 diplococcus of Frankel, the bacillus of Friedlander, and latterly 
 the Bacillus influenzae, the Bacilli coli, with many others. The 
 mucous membrane presents an intensely red color; at first it 
 is dry, but later a mucous or mucopurulent exudate is formed 
 
 W M 
 
 Fig. 194.— Acute bronchial catarrh (Thoma), 
 
 (Fig. 194). The exudation may be excessive in quantity, in which 
 case the condition is called bronchorrhea. This may be serous or 
 purulent, and is sometimes very offensive in odor (fetid bronchitis). 
 Microscopically the bronchial mucous membrane is infiltrated with 
 round cells, especially in the purulent eases ; the epithelial cells are 
 degenerated, many being converted into goblet-cells; and the 
 mucous glands are distended with mucus. The inflammatory 
 conditions may extend outward as far as the peribronchial tissue, 
 and occasionally there is some perichondritis. 
 
 Chronic catarrhal bronchitis occurs after repeated attacks 
 
DISEASES OF THE RESPIRATORY SYSTEM. 
 
 411 
 
 of the acute form, and especially in old persons or in those who 
 have some cardiac weakness which tends to cause congestion of 
 the bronchi. Chronic bronchitis is frequently associated with 
 chronic diseases of the lungs. 
 In chronic cases the mucous 
 membrane may undergo con- 
 siderable alteration. Fre- 
 quently the ciliated cells dis- 
 appear entirely and are re- 
 placed by columnar or polyg- 
 onal epithelium ; and hyper- 
 trophic conditions of the 
 mucous membrane are some- 
 times present. More fre- 
 quently the bronchus is uni- 
 formly thickened by cellular 
 infiltration and overgrowth 
 of fibrous tissue. 
 
 Fibrinous bronchitis 
 occurs under a variety of 
 conditions. It is most fre- 
 quent in association with fig 
 laryngeal and tracheal diph- 
 theria, but may also be due 
 to inhalation of powerful irritants 
 
 195— Lar 
 fibrin 
 
 nchitis (Vierordt) 
 
 Croupous inflammation of the 
 
 Fig. 196.— Sputum from a case of 
 asthma, showing Curschmann spirals, 
 Charcot-Leyden crystals, leukocytes, and 
 numerous free eosinophile granules; un- 
 stained specimen (Jakob). 
 
 Fig. 197.— Sputum from a case of 
 asthma, showing leukocytes, some con- 
 taining eosinophile granules ; free eosino- 
 phile granules ; and micrococci ; stained 
 with eosin and methylene-blue (Jakob). 
 
 finer bronchi occurs in both croupous and catarrhal pneumonia. 
 Finally, there is a form of chronic or essential fibrinous bronchitis, 
 
412 TEXT-BOOK OF PATHOLOGY. 
 
 characterized by periodical attacks, in which fibrinous casts of the 
 bronchi arc formed and discharged (Fig. 195). In all forms of 
 fibrinous bronchitis there arc often found in the sputa, on micro- 
 scopic examination, fine spirals wound about a central riber 
 (( Wschmann's spirals); and within these or associated with them 
 the small octahedral crystals described by Charcot and Leyden. 
 
 Bronchiolitis Exudativa. — This term was given by Curschmann to the 
 condition of the terminal bronchioles he assumed to be present in cases of 
 asthma. The sputa contain the spirals that bear his name, and Charcot- 
 Leyden crystals. The sputa in these cases are further characterized by the 
 abundance of eosinophile cells (Figs. 196 and 197). 
 
 Ulcers of the bronchi are met with in severe catarrhal inflammations, 
 but more frequently are tuberculous, syphilitic, or due to extension of ul- 
 cerative processes from neighboring parts. It is not unusual to find ulcera- 
 tion in the main bronchus opposite the point of pressure of an aneurysm. 
 
 Peribronchitis may occur from direct extension of inflammation from 
 within, or it may be due to extension along the lymphatic channels from 
 the pleura or interlobular septa of the lung. It is found most frequently 
 as a part of pulmonary tuberculosis, and may be fibrous, caseous, or purulent. 
 
 STENOSIS AND OBSTRUCTION OF THE BRONCHI. 
 
 The smaller bronchial tubes may be considerably occluded by 
 catarrhal swelling of the mucosa and accumulation of exudate 
 within. Clinically this is often so marked in bronchitis affecting 
 the terminal bronchioles as to have suggested the name suffocative 
 catarrh. (This capillary bronchitis is always merely a part of 
 bronchopneumonia, and will be considered under that head.) 
 More serious obstructions of the bronchi occur when old ulcers 
 have healed, leaving cicatrices ; or in cases of tumors of the bronchi 
 or pressure upon the outside. Foreign bodies are usually coughed 
 up, but may remain for long periods and occasion obstruction. 
 
 BRONCHIECTASIS, OR DILATATION OF THE BRONCHI. 
 
 This is due to increased pressure within the bronchi or to some 
 weakness of the walls, or to both. The weakening of the walls 
 is most frequently due to chronic bronchitis. If it is extreme, 
 simply the force of the inspired air may suffice to cause dilatation, 
 but the increased expiratory efforts of coughing may aid materially. 
 When a part of the lung is collapsed (atelectasis) the impediment 
 to the entrance of air leads to dilatations of the bronchi above the 
 collapsed area. This is especially noted in children. The weight 
 of accumulating secretions in the tubes is rarely the cause of 
 bronchiectasis. Finally, in fibrous pneumonia the traction of the 
 connective tissue, at (aching itself, on the one hand, to the outer 
 wall of the bronchus, and, on the other hand, to the pleura, may 
 bring about considerable dilatations. 
 
 The enlargement of the bronchus may be localized, when it 
 
DISEASES OF THE RESPIRATORY SYSTE3I. 
 
 413 
 
 is termed saccular bronchiectasis; or more uniform, when the 
 names cylindrical and fusiform are applied, according to the shape 
 of the bronchus (Fig. 198). The mucous membrane may be 
 almost normal in appearance in small dilatations, but more com- 
 monly is thickened and irregular on the surface. There may even 
 
 Fig. 198.— Bronchiectasis : a, saccular; b, cylindrical ; one-half natural size (Orth). 
 
 be actual polypoid outgrowths, and ulcerations may occur when 
 the secretions are specially abundant and irritating. Microscopi- 
 cally the epithelium is found to approach the squamous type ; while 
 the wall of the bronchus is generally infiltrated and cirrhotic. 
 The exudation is generally purulent and copious, and may be 
 very fetid. Occasionally it is thick and cheesy. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis of the bronchi is usually associated with pul- 
 monary tuberculosis, and appears in the form of miliary or larger 
 nodules in the mucosa or submucosa, which tend to break down to 
 form ulcers. 
 
 Syphilis sometimes occurs in the form of eruptions and ulcers. 
 There may be dense scar-formation and deformity in consequence 
 of the healing of such ulcers. 
 
 TUMORS. 
 
 Polypoid conditions of the mucosa occur in cases of chronic 
 bronchitis. Fibroma, chondroma, and lipoma are rare forms of 
 tumors. Primary cancers may spring from the mucous glands, 
 or from the surface-epithelium, but are very rare. Leukemic 
 nodules are seen in the bronchi at times, and lymphosarcomata are 
 not rarely found to spring from the peribronchial lymphatic tissues. 
 
 PARASITES AND FOREIGN BODIES. 
 
 Bronchiectatic cavities may contain a growth of aspergillus — 
 Mycosis aspergillina. Round worms may enter by migration, and 
 hydatid cysts are met with. 
 
414 TEXT-BOOK OF PATHOLOGY. 
 
 Foreign bodies from the exterior usually enter the right bron- 
 chus. They often lead to serious inflammation and suppuration, 
 unless they are coughed up. Bronchial concretions sometimes 
 form by inspissation of the secretions, especially in bronchiectatic 
 cavities. Very rarely cartilaginous or bony masses, derived by 
 outgrowth and' later separation from the bronchial cartilages, are 
 observed. 
 
 THE LUNGS. 
 
 Anatomic Considerations.— The structure of the lungs in 
 their unexpanded condition is very similar to that of an epithe- 
 lial gland, consisting of ducts, the bronchi ; and glandular tissue, 
 the pulmonary parenchyma. The terminal bronchioles divide 
 into several alveolar passages, which open into infundibula, and 
 these in turn are surrounded by air-sacs. The groups of infun- 
 dibula connected with a terminal bronchiole constitute an acinus. 
 Neighboring acini unite to form lobules, and the lobules unite to 
 form lobes. The epithelial lining-cells of the air-sacs are large, 
 flat plates, which resemble endothelial cells very closely. Beneath 
 these cells is a layer of elastic tissue, which gives the lungs their 
 characteristic elasticity, and in which is embedded a rich network 
 of capillaries, that carry on the proper respiratory function of 
 the lungs. These capillaries are the terminal ends of the pulmo- 
 nary artery. Another set of blood-vessels, the bronchial arteries, 
 serve only to nourish the walls of the bronchi and the structure 
 of the lungs themselves. The return circulation is mainly carried 
 on by the pulmonary veins, which receive the blood of the 
 pulmonary arteries and much of that of the bronchial arteries. 
 The distribution of the lymphatic vessels in the lungs is of the 
 greatest significance in pathologic anatomy, especially with regard 
 to the dissemination of infectious diseases in the lung itself. One 
 system of lymphatics begins in the lymph-spaces between the cells 
 of the intervesicular septa. These lymph-spaces deliver their 
 contents to lymphatic capillaries in the same region, and these in 
 turn follow the alveolar passages, surrounding the latter on all 
 sides. Where the several alveolar passages unite to form a ter- 
 minal bronchiole the smaller lymphatic capillaries also unite to 
 form larger branches, which follow the bronchioles. Other lym- 
 phatic vessels surround the pulmonary veins, constituting a peri- 
 vascular system. Still another system begins in small subpleural 
 capillaries, which unite and enlarge and penetrate the lung along 
 the interlobular septa. A portion of them also pass at once to the 
 peribronchial and perivesicular tissues. All of the lymphatic 
 trunks leave the lung at the root and eventually discharge into 
 the thoracic duct. 
 
 Collections of lymphoid cells are found in various places along 
 
DISEASES OF THE RESPIRATORY SYSTEM. 
 
 415 
 
 the lymphatics in the tissue of the lung. Near the root these are 
 of considerable size, and merit the name of lymphatic nodes or 
 glands. Still larger and more important ones are found surround- 
 ing the bronchi just outside the lungs, and around the end of the 
 trachea. 
 
 CONGENITAL DEFECTS. 
 
 Complete absence of the lungs has been noted in certain mon- 
 sters. One lung may be absent, or its parenchyma may be unde- 
 veloped, while the bronchi are dilated even to a cystic condition. 
 The opposite lung is compensatorily enlarged. Minor abnormali- 
 ties in the division of the lobes and the like are not rare ; and in 
 a few instances accessory lobes, wholly disconnected from the rest 
 of the lima;, have been observed. 
 
 CIRCULATORY DISTURBANCES. 
 
 Anemia of the lung occurs as a part of general anemia, from 
 pressure upon the lung, or from obstruction or obliteration of the 
 blood-vessels. The last is the cause of the great pulmonary 
 anemia in emphysema of the lungs. The lungs are pale in color 
 or of a mottled appearance in elderly persons, in whose organs 
 considerable pigment is usually present. 
 
 F • ■'*■>•£,** 
 
 m v *m&-i*ip, 
 
 , -.1 
 
 '* <$** 
 
 iSttff 
 
 
 tail- 
 
 
 : *u 
 
 
 ***"' JK, ** 
 
 **% 
 
 5 * i * ^»j 
 
 fi&i 
 
 
 ■ ■'■::-■ , 
 
 Ajjfe> t 
 
 %•*■ £~ ''."■'■* 
 
 ..iv*B 
 
 
 
 
 *\ 
 
 
 ■JL* 
 
 
 
 % J m> 
 
 * nSw 
 
 Fig. 199.— Acute congestion of the lung (Karg and Schmorl). 
 
 Active Hyperemia or Congestion. — Exercise constantly 
 leads to increased flow of blood to the lungs, and this may be ex- 
 treme, causing rapid death (apoplexia pulmonum vascularis). In 
 cases of irritation of the lungs by the inhalation of heated or cold 
 air, or of irritating gases, and in certain lesions of the base of the 
 brain, there may be more or less active congestion of the lungs 
 (Fig. 199). Collateral hyperemia occurs when the opposite lung 
 
416 TEXT-BOOK OF PATHOLOGY. 
 
 or some other part of the body becomes anemic. The lung in 
 active hyperemia has a dark-red color, and on section blood flows 
 from the surface of section. The alveoli may contain free blood, 
 and in marked eases there is blood in the sputa during life. 
 
 Passive hyperemia is for the most part a chronic condition, 
 due to causes which prevent the outflow of blood from the lungs. 
 The most frequent cause is valvular disease, particularly mitral 
 stenosis and regurgitation ; but weakness of the left ventricle 
 from fatty disease or fibroid degeneration acts in a similar manner. 
 Any local cause of hindrance to the outflow of the blood in the 
 veins leads to similar passive congestion. It is often found in 
 the dependent parts of the lungs in cases of great asthenia, as in 
 typhoid fever. This is called hypostatic congestion; not infre- 
 quently it leads to hypostatic pneumonia when irritants are inspired 
 or descend through the bronchi to the parts of the lung affected. 
 Post-mortem there is often a similar hypostatic congestion, but 
 without any evidences of catarrhal inflammation of the bronchi, 
 such as always occurs in the cases developed during life. 
 
 Fig. 200.— Phagocytic cells of the sputum, containing blood pigment, from a case of 
 cardiac congestion of the lungs (Jakob). 
 
 The lung in passive hyperemia is dark-red in color and heavy. 
 In the more acute cases it is moist on section, being infiltrated with 
 serous exudate and blood ; in chronic cases, as in slow heart-failure, 
 the tissue is dry and indurated. Microscopically the blood-vessels 
 in the alveolar walls are seen to be greatly distended, and project 
 into the alveoli. \iv(\ and white blood-corpuscles are seen within 
 the alveoli and in the interstitial tissues. In the later stages the red 
 corpuscles either re-enter the circulation or break down to form 
 dark pigment-granules within the alveolar epithelial cells, the leu- 
 kocytes, or lying free in the tissues of the alveolar walls. In such 
 cases there are at the same time considerable hyperplasia and indu- 
 
DISEASES OF THE RESPIRATORY SYSTEM. 417 
 
 ration of the connective tissue of the lung ; and the whole process 
 is called cyanotic induration. In cases of heart-disease with con- 
 gestion of the lungs there are very commonly found in the sputa 
 pigmented epithelial cells and leukocytes, such as those described 
 above (Fig. 200). They are of somewhat diagnostic importance. 
 
 Edema occurs most frequently as a result of passive hyperemia. 
 In other cases the edema is the consequence of general septic condi- 
 tions which lead to unusual permeability of the blood-vessels. Simi- 
 lar edema, not dependent on passive congestion, occurs in the parts 
 of the lung surrounding inflammatory areas, and in some cases 
 sudden pulmonary edema seems dependent on vasomotor relaxa- 
 tion. In the cases of edema due to passive congestion the lungs 
 are dark-red in color, and on section more or less serous fluid, ren- 
 dered frothy by admixture of air, exudes from the cut surface. In 
 the other forms of edema the lung may be quite light in color, 
 generally grayish, but on section the same frothy serum exudes 
 from the surface. 
 
 Hemorrhage. — Small punctate hemorrhages occur in cases 
 of severe congestion or inflammation, in the hemorrhagic or in- 
 fectious diseases, and in consequence of high blood-pressure, as in 
 death from asphyxia or in whooping-cough. When hemorrhage 
 from congestion is combined with serous effusion the lung assumes 
 an appearance not unlike that of a hyperemic spleen (splenization). 
 A form of apparent hemorrhage is seen in cases in which the blood 
 is aspirated from the bronchi. In such cases, lobular spots of 
 hemorrhagic infiltration are found at the bases. Large hemor- 
 rhages into the substance of the lungs may be traumatic, or they 
 may be due to rupture of an adjacent aneurysm into the lung. 
 Small or large pulmonary hemorrhages are at times due to lesions 
 of the nervous system, especially of the base of the brain. 
 
 Hemorrhage from the lungs, discharging externally through' the 
 bronchial tubes, is most commonly due to tuberculosis, and is 
 particularly frequent in the late stages, when cavities have formed. 
 The immediate source of the bleeding is generally an eroded ves- 
 sel in the wall of the cavity, and a small miliary aneurysm is 
 commonly found at the point of erosion. Hemoptysis may be the 
 first indication of the existence of pulmonary tuberculosis, but the 
 old belief that hemorrhages cause phthisis is ill-founded. A 
 hemorrhage or any other lesion of the lungs may, of course, add to 
 the liability to infection ; but, as a rule, the cases in question are in- 
 stances of hemorrhage occurring before the other evidences of the 
 pulmonary disease have become marked. Occasionally hemopty- 
 sis is due to congestion of the lungs, to erosion of small blood- 
 vessels from gangrene, abscess, or the like, or to vicarious men- 
 struation. 
 
 Hemorrhagic infarcts may occur in the lungs, as in other 
 places, from obstruction of the arteries by emboli. The latter 
 
418 TEXT-BOOK OF PATHOLOGY. 
 
 come from the right heart or from the general venous system, and 
 lodge in the smaller branches of the pulmonary artery, frequently 
 at their points of subdivision. Very often, however, emboli are 
 not found, or, if so, are so small as to have been unable to cause 
 obstruction without the associated thrombosis, or there may be 
 purely thrombotic occlusion. Valvular lesions and muscular 
 weakness of the heart aid greatly in the production of infarctions 
 by causing a sluggish circulation in the pulmonary vessels, and 
 thus encouraging thrombosis. Infarctions are occasionally due to 
 thrombosis of the pulmonary veins without obstruction of the 
 arteries ; more rarely they are caused by occlusion of one of the 
 bronchial tubes. The latter condition leads to collapse (atelectasis) 
 of the part of the lung associated with that tube, to consequent con- 
 gestion (see Atelectasis), and, sometimes, when the congestion is 
 severe, to hemorrhage. In addition, it is to be remembered that 
 hemorrhages into the lungs are likely to have the shape and appear- 
 ances of ordinary infarcts, because they occupy the area supplied by 
 the bronchus into which the blood finds its way. Infarctions are 
 most frequently found in the lower lobes and in the right lung ; they 
 
 Fig. 201.— Hemorrhagic infarction of the lung (from a photograph by Dr. Wm. M. Gray). 
 
 are usually multiple. They have the characteristic wedge-shape, the 
 base of the wedge directed toward the pleural surface. They are 
 hard, airless, dark -colored, and project above the other parts on 
 section and on the pleural surface. Microscopically there is seen 
 a uniform hemorrhagic infiltration of the tissues (Fig. 201), and 
 not infrequently hyaline thrombosis of the smaller blood-vessels. 
 Toward the apex of the infarct there is more fibrin in the blood- 
 vessels, and the main vessel may be found obstructed by an embo- 
 lus or thrombus. Small infarcts may be wholly removed through 
 the vascular and lymphatic channels after liquefaction and granu- 
 lar degeneration of the blood -clot. More commonly a pigmented 
 scar is left. Softening and cyst-formation may occur, or in cases 
 
DISEASES OF THE RESPIRATORY SYSTEM. 419 
 
 in which the original embolus was infected by micro-organisms, or 
 in which the infarct becomes infected through the bronchial tubes, 
 abscess or gangrene may result. 
 
 Embolism without infarction is not infrequent in the lungs. 
 An interesting form is fat-embolism, resulting from fracture of a 
 bone with disorganization of the marrow, and less frequently from 
 traumatic disturbances of other fat-tissues. When large branches 
 of the pulmonary artery are occluded in this way, or when numer- 
 ous vessels are obstructed, sudden death may result. In other 
 cases there are merely great dyspnea and oppression. Air-embo- 
 lism, embolism of hydatid cysts, and embolism of portions of 
 tumors are rare. Attention has been called to the embolism of 
 placental cells in certain cases of eclampsia. 
 
 HYPERTROPHY AND ATROPHY. 
 
 Hypertrophy. — True hypertrophy, in the sense of increase 
 of all the constituents of the lung-tissue, is extremely rare, and 
 probably only occurs when areas of the pulmonary tissue have 
 been rendered useless early in infancy or in fetal life. Cases have 
 been observed, however, in which a single lung occupied the entire 
 side of the thorax to which it belonged, and also a part of the 
 other side, where complete atrophy of the other lung had existed. 
 It may be that limited areas of hypertrophy occur more frequently 
 than we at present believe, but evidence is wanting. 
 
 Partial Hypertrophy. — The muscular tissue of the intervesicular 
 septa and of the smaller bronchioles not infrequently undergoes 
 proliferation or hyperplasia when there has been obstruction in 
 the air-passages, so that greater expiratory force was required. 
 Similarly the elastic tissues may become increased ; but these are 
 not instances of true hypertrophy. 
 
 Atrophy. — Aside from that which occurs as a part of emphy- 
 sema, atrophy does not take place. 
 
 EMPHYSEMA. 
 
 By this term is indicated an increase of the air contained within 
 the lungs, either in the normal tubes and alveoli, or in the inter- 
 stitial connective tissue. Two varieties of emphysema may be 
 distinguished by their essentially different nature. These are the 
 interstitial and the vesicular. 
 
 Interstitial emphysema of the lungs is similar to the em- 
 physema of the subcutaneous tissues — i. e., the term refers to the 
 existence of air within the fibrous tissue of the lung. This occurs 
 in the course of affections in which there is some obstruction to the 
 expiration, combined with severe coughing or forcible expiratory 
 efforts, leading to rupture of the intervesicular septa and extrava- 
 sation of air. Degenerative or inflammatory weakness of any part 
 
420 TEXT-BOOK OF PATHOLOGY. 
 
 of the pulmonary structure would, of course, act as a primary 
 cause. Interstitial emphysema is most commonly observed in 
 such diseases as whooping-cough and membranous croup ; it may 
 also result simply from straining efforts, as in women during labor, 
 or from forcibly blowing wind-instruments, etc. The air from the 
 ruptured air-vesicle finds its way into the interalveolar and inter- 
 vesicular septa, and, passing along these, eventually reaches the 
 subpleural connective tissue, where it is seen in the form of small 
 blebs, movable from place to place. The process may extend to 
 the roots of the lungs and even to the mediastinal tissues, or to 
 the subcutaneous tissues of the neck. When an air-vesicle near 
 the pleural surface ruptures pneumothorax may result. 
 
 Vesicular emphysema is the term used to designate over- 
 distention of the alveoli and air-sacs of the lung. Two factors 
 play a part in the causation of this condition : first, increase of the 
 pressure under which the air exists in the lung ; and, secondly, 
 degenerative or inflammatory weakness, with loss of elasticity of 
 the lung-structure itself. There are several varieties, and the 
 causes vary somew T hat in each. 
 
 (a) Acute vesicular emphysema results simply from excessive 
 air-pressure within the alveoli, and may be more or less wide- 
 spread. It occurs in cases in which inflammatory swelling or mu- 
 cous secretions within the bronchi obstruct the expiration of air, 
 but are not sufficient to impede the more vigorous inspiratory 
 force. There results overdistention of the alveoli and air-vesicles. 
 Somewhat similar conditions are present when the entrance of air 
 into certain parts is impeded by obstruction or disease of the 
 bronchi or by consolidations of the pulmonary tissue. Localized 
 emphysema of other parts results (Fig. 203) ; the term vicarious 
 emphysema is applied to such cases. This is not unusual in the 
 lobules of the lung surrounding areas of pneumonic or tuberculous 
 consolidation, and may affect an entire lobe or lung when the en- 
 trance of air into the other lobes or the other lung is prevented. 
 
 Pathologic Anatomy. — In these cases of acute and vicarious 
 emphysema there is simply overdistention of the alveoli, and the 
 tissue presents a paler color than normal and a cotton-like sensa- 
 tion when grasped in the fingers. Microscopically nothing beyond 
 overstretching of the septa and some anemia of the vessels is 
 apparent. If the causes continue to operate, changes similar to 
 those found in chronic vesicular emphysema ensue. 
 
 (b) Chronic vesicular emphysema is the ordinary form of emphy- 
 sema, and is sometimes spoken of as substantial emphysema. 
 
 Etiology. — Chronic vesicular emphysema commonly occurs in 
 elderly persons, and is predisposed to by attacks of broncho- 
 pneumonia and by the existence of other inflammatory and con- 
 gestive conditions of the lungs. These conditions lead to weak- 
 ness and loss of elasticity of the pulmonary tissue. Heredity 
 
DISEASES OF THE RESPIRATORY SYSTEM. 
 
 421 
 
 plays a part in the same direction, and it is supposed by some that 
 there is an abnormal lack of development of the elastic tissue in 
 the lungs of such persons, rendering them more susceptible to this 
 disease. The direct exciting cause of emphysema is increase of 
 the air-pressure within the alveoli, and much speculation has been 
 indulged in to discover whether inspiration or expiration plays the 
 more important part in increasing the pressure. It seems likely 
 that the expiratory force is the more important one, as in the case 
 of constant coughing in chronic bronchitis, the blowing of wind- 
 instruments, and the constant straining in certain pelvic disorders, 
 all of which may lead to emphysema. 
 
 Pathologic Anatomy. — The lung increases in size, and very 
 often remains distended when the thorax is opened post-mortem. 
 The edges are rounded ; the organ is light in color, and has a cotton- 
 
 Fig. 202.— Emphysema of the lungs (Karg and Schmorl). 
 
 like feeling when squeezed between the fingers. On section into it 
 the alveoli may be seen to be distended, and there may be cavities 
 of quite considerable size, often as large as a pea, and sometimes 
 even that of a cherry or plum (Fig. 202). Large spaces of this 
 kind are not unusual near the pleural surface ; the term bullous em- 
 physema has been used in reference to such cases. The pigment- 
 matter of the lung is very much lessened, and may be distributed 
 in radiating or parallel lines. This lessening of the pigment is 
 not alone due to its distribution over a greater space, but there is 
 also actual disappearance by removal through the lymphatic chan- 
 nels and through expectoration. 
 
 Chronic emphysema may be a general process affecting all 
 parts of both lungs, or it may be localized. In the latter case it 
 is the apex and anterior edges that are most commonly involved, 
 
422 TEXT-BOOK OF PATHOLOGY. 
 
 but spots of emphysema may be seen here and there in other parts 
 of the lung, interspersed with normal tissue. The involvement of the 
 apex and anterior portions is due to the fact that the expiratory 
 force is more apt to distend these portions of the lung than the 
 lateral and basal portions, which receive the uniform support of 
 the sides of the chest and the diaphragm as they contract against 
 the lung. 
 
 Microscopically emphysema is found to consist in enlarge- 
 ment of the vesicles and alveoli by distention and by atrophy 
 and disappearance of the intervesicular and interalveolar septa. 
 Studied from the earliest stage, there will be found, first, over- 
 distention of the air-sacs, then a gradual thinning, and finally 
 vacuolization of the intervesicular septa at their thinnest parts. 
 Coincidentally the small capillaries are compressed, and are finally 
 converted into hyaline cords. The anemia consequent upon this 
 determines additional atrophy and degeneration of the septa and 
 fatty degeneration of the loosened epithelium, so that eventually 
 the whole of the septum disappears. Later, adjacent alveoli inter- 
 communicate and large spaces are thus formed. 
 
 The obstruction to the pulmonary circulation due to the oblit- 
 eration of the capillaries leads to collateral hyperemia of the larger 
 branches supplying the bronchi, and thus prolongs the chronic 
 bronchitis, which in the first instance may have been the cause of 
 the emphysema. Subsequently collateral anastomosis between the 
 pulmonary arteries and the bronchial system of blood-vessels is 
 established. 
 
 Associated Conditions in Other Organs. — The shape of the 
 thorax in emphysema is characteristic. The chest is in a constant 
 state of extreme inspiration, the clavicles elevated, the sternum 
 protruded, the back arched. It has a shape well likened to that 
 of a barrel. The diaphragm is usually depressed, and the liver is 
 below its normal position ; the heart is almost or completely cov- 
 ered over in front and usually pressed somewhat backward from 
 the chest-wall. 
 
 Pathologic Physiology. — The effect of emphysema upon the 
 circulation is important. The obstruction of the pulmonary cap- 
 illaries leads to increase of pulmonary pressure, and eventually 
 hypertrophy of the right heart; later, dilatation of the right ven- 
 tricle ensues, and characteristic cardiac dropsy with general cyano- 
 sis may result. 
 
 (c) Senile emphysema is due to erosion of the intervesicular 
 septa, the result of the atrophic processes to which old age pre- 
 disposes. There is not necessarily any element of increased air- 
 pressure in the causation of this form of emphysema, and the 
 volume of the lung may not be notably increased, though the 
 tissue is lighter and the air-spaces are found to be increased. The 
 lung is light in color and often collapses readily. 
 
DISEASES OF THE RESPIRATORY SYSTEM. 423 
 
 ATELECTASIS. 
 
 The term atelectasis is applied to two distinct conditions, one 
 occurring as a congenital affection, in which the lung has never 
 been properly expanded by air ; the other occurring in after-life, 
 in which the lung is compressed or collapsed, so that the alveoli 
 and air-vesicles are rendered airless. 
 
 Congenital atelectasis is found in new-born babes in 
 whom the inspiratory power has been so deficient, as the result of 
 general weakness or compression of the thorax, or of compression 
 of the brain by cerebral hemorrhage, that the lungs, or parts of 
 them, have never been expanded. It may also take place in a 
 purely mechanical way by obstruction to the air-passages by 
 meconium or other foreign matter. 
 
 Pathologic Anatomy. — Congenital atelectasis commonly affects 
 the bases and posterior portions of the lung. The area of disease 
 is of a dark-reddish color ; it is rather tough, and on section pre- 
 sents a smooth appearance ; pressure gives no sign of crepitation. 
 If a portion be thrown into water, it sinks. Usually a con- 
 siderable part of the lung is involved, but sometimes merely 
 lobular areas are affected. By inserting a blowpipe into the 
 bronchi the lung may be inflated, and resumes its normal ap- 
 pearance, provided the condition has not persisted for any length 
 of time. If the child does not perish, secondary changes take 
 place. The epithelium of the alveoli degenerates, more or less 
 proliferation of the connective tissues of the septa occurs, and the 
 pleura over the diseased area is prone to become thickened. The 
 atelectatic portion of the lung in such cases remains collapsed ; it is 
 smooth on section, free of pigment, and can no longer be inflated. 
 Secondary dilatation of the bronchioles and bronchi may ensue. 
 
 It is of interest, in a medicolegal sense, to recognize that atelectasis re- 
 sembling the congenital form may be met with in the bodies of infants that 
 have lived, breathed, and even cried lustily. The explanation of this is 
 that the collapse ensued some time after birth, and that as the lung had 
 practically still its fetal characteristics, the resulting atelectasis is the exact 
 counterpart of the congenital form. 
 
 Atelectasis in later life occurs under a variety of condi- 
 tions. It may simply be the result of compression of the lung by 
 pleural effusions, by deformities of the chest, by tumors, aneur- 
 ysms, and the like. It may also be met with in cases in which 
 the bronchial tubes have become obstructed. The larger bronchi 
 may be occluded by the pressure of tumors or aneurysms, or by 
 foreign bodies, and the resulting atelectasis is of considerable 
 extent ; the smaller bronchi and bronchioles are frequently ob- 
 structed by intense catarrhal thickening of their mucosa, and in 
 consequence lobular areas of atelectasis are developed. The latter 
 
424 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 is especially frequent as one of the pathologic features of broncho- 
 pneumonia (q. v.). 
 
 The explanation of atelectasis as the result of bronchial ob- 
 struction has occasioned much discussion, and several theories 
 have been proposed. In some cases it is not unlikely that mucous 
 secretions within the bronchi may prevent inspiratory entrance of 
 air into the lungs without opposing any obstacle to expiration, so 
 that collapse is gradually developed. In other cases it is likely 
 that both inspiration and expiration are prevented, while the air 
 contained within the air-vesicles is gradually absorbed. It is 
 claimed that first the oxygen, later the carbonic acid, and finally 
 the nitrogen, are absorbed ; the col- 
 lapse of the alveoli then becomes 
 complete. It is possible, also, that 
 atelectasis may be developed as the 
 result of the failure of respiratory 
 motions on one side, or affecting a 
 certain part of the lung. As a re- 
 sult of this, the elasticity of the 
 pulmonary tissue would gradually 
 press the air out of the affected 
 area, while new air was not sup- 
 plied by inspiration. Such a con- 
 dition, however, must be rare. 
 
 Pathologic Anatomy. — The part 
 affected by atelectasis is dark in 
 color, and is much reduced in size, 
 so that when lobular areas are af- 
 fected the pleural surface may be 
 considerably depressed (Fig. 203). 
 On section the surface is smooth 
 and generally dry, though in some 
 instances passive hyperemia, which 
 is generally present to some extent, reaches such a grade that 
 bloody liquid flows freely from the surface of section. The term 
 splenization is properly applied to such cases, whereas the instances 
 in which the surface is dry are often spoken of as carnifieation. 
 The lung does not crepitate, and sinks when placed in water. In 
 the earlier stages the diseased portion may be inflated through the 
 bronchial tubes ; but when the condition has persisted, connective- 
 tissue overgrowth springing from the septa causes permanent 
 induration and permanent collapse. The lung in such cases is 
 hard and of a dark color, due to the deposit of hematogenous pig- 
 ment, the result of disintegration of the blood present. The 
 bronchi may be compressed, but sometimes atelectatic bronchi- 
 ectasis results. 
 
 Fig. 203.— Atelectasis due to bron- 
 chial obstruction : acute emphysema 
 of the unaffected portions of the lung 
 (Orth). 
 
DISEASES OF THE RESPIRATORY SYSTEM. 425 
 
 INFLAMMATION, OR PNEUMONIA. 
 
 Classification. — Inflammation of the lungs, pneumonia, or 
 pneumonitis, may arise in a variety of ways, and present itself in 
 a number of widely varying forms, both as to the distribution and 
 the nature of the pathologic changes in the pulmonary structure. 
 In all cases some irritant is conveyed to the lung either (a) from the 
 upper air-passages or external world through the bronchi ; (6) 
 from some other part of the body through the blood (hematogenic 
 pneumonia) ; or (c) from the pleura by direct extension or through 
 the lymph-channels (pleurogenic pneumonia). 
 
 Anatomically pneumonia is classified according to the nature 
 of the inflammatory products, and there are thus distinguished : 
 fibrinous pneumonia, in which the air-vesicles and terminal bron- 
 chioles contain an exudate especially rich in fibrin ; catarrhal, or 
 bronchopneumonia, in which the exudate is composed of an albumi- 
 nous liquid containing numerous epithelial cells and blood-cor- 
 puscles ; purulent pneumonia, in which pus-cells are the note- 
 worthy element in the exudate ; cheesy pneumonia, in which 
 cellular desquamation and cheesy necrosis are prominent ; and 
 productive, or fibrous pneumonia, in which there is overgrowth 
 of fibrous connective tissue. It is to be remembered, how- 
 ever, that mixed cases are of frequent occurrence. Thus in 
 many instances localized areas of decided fibrinous pneumonia are 
 found in the midst of larger areas of catarrhal pneumonia ; some 
 distinctly purulent exudation may be met with in many instances 
 of fibrinous or catarrhal pneumonia ; and more or less productive 
 inflammation and fibrous overgrowth may be seen in any of the 
 other varieties. Typical cases, however, present little mixture of 
 the lesions. 
 
 The terms parenchymatous and interstitial pneumonia are 
 sometimes employed, but are of doubtful significance. The proper 
 parenchyma of the lungs, the alveolar septa, and their contained 
 blood-vessels, are never the sole seat of inflammation, and the 
 term parenchymatous pneumonia, as usually applied to inflam- 
 mations of the lining epithelium of the air-vesicles, is therefore 
 misused. It is more proper to call the fibrous variety interstitial 
 pneumonia. 
 
 Fibrinous Pneumonia. 
 
 Definition. — Fibrinous, or croupous, or lobar pneumonia is 
 an acute infectious form of pneumonia, generally caused by the 
 Diplococcus pneumonias, and usually involving an entire lobe or 
 more of one or both lungs. Pathologically it is characterized by 
 an exudation within the air-vesicles and terminal bronchioles, 
 mainly composed of fibrin ; and clinically the disease is marked 
 by a definite and characteristic course. 
 
 Etiology. — The important factor in the causation of fibrinous 
 
426 TEXT-BOOK OF PATHOLOGY. 
 
 pneumonia is the Diplococcus pneumoniae (Frankel-Weichsel- 
 baum). This micro-organism is found in the sputa and in the 
 lungs of the great majority of cases, and is undoubtedly the cause 
 of the pneumonia ; but occasionally other micro-organisms seem 
 to occasion typical fibrinous pneumonia. Among these are the 
 pneumococcus of Friedlander, streptococci, staphylococci, the 
 bacillus of typhoid fever, the bacillus of influenza, and the Bacillus 
 coli communis. In some cases in which bacteria other than the 
 diplococcus are supposed to be the cause, there is doubtless mixed 
 infection ; but it must be accepted at the present time that a num- 
 ber of micro-organisms are capable of causing the disease. The 
 fibrinous pneumonia which occurs in the course of tuberculosis is 
 certainly due to secondary infection, and the same thing frequently 
 happens in the course of typhoid fever and influenza, though the 
 specific bacilli of these diseases may alone cause pneumonia. 
 
 The micro-organisms usually gain access to the lungs through 
 the bronchi. In the case of the Diplococcus pneumoniae the fre- 
 quent occurrence of this organism in the mouth and upper respira- 
 tory passages furnishes a ready explanation of one source of infec- 
 tion. More rarely the bacteria may be directly inspired from 
 without, or, exceptionally, they may reach the lungs through the 
 circulation. 
 
 There are certain predisposing factors which have long been 
 recognized clinically as causes of pneumonia. These probably act 
 by rendering the pulmonary tissues less resisting, or by increasing 
 the virulence of the diplococci of the mouth. Among these causes 
 are exposure to cold, injury of the lungs by traumatism, fatigue, 
 and systemic depression. 
 
 (For the description of the Diplococcus, see page 207.) 
 
 Pathologic Anatomy. — The lesions most frequently involve 
 the lower lobe of the right lung; next in order is the lower lobe 
 of the left lung ; the apices alone are least frequently involved. 
 In all cases there is a tendency to the involvement of a whole 
 lobe, and, as a rule, the entire area of disease is affected uniformly 
 and simultaneously. There are wide variations, however ; for, on 
 the one hand, typical fibrinous pneumonia may occasionally appear 
 as a more or less lobular disease (particularly in influenza), and, 
 on the other hand, the process may spread from one part of the 
 lung to another (pneumonia migrans). In typical cases, not only 
 is the process uniformly distributed, but it passes through distinct 
 stages : first, of congestion, then of consolidation, and finally of 
 resolution. 
 
 Stage of Congestion or Engorgement. — The affected area is dark- 
 red in color ; it is swollen and heavy, and on pressure crepitates 
 less than a healthy lung. The pleura over the diseased part is 
 dull and lusterless. On section through the lung bloody liquid 
 exudes, and when the part is compressed with the fingers this 
 
DISEASES OF THE RESPIRATORY SYSTEM. 
 
 427 
 
 liquid shows few air-bubbles. The condition is simply one of 
 intense congestion, with exudation into the alveoli and terminal 
 bronchioles of serous liquid and blood-corpuscles (see Fig. 199). 
 Microscopically the small blood-vessels of the septa are seen to be 
 greatly distended and project inward toward the alveoli. Within 
 the latter may be found many red corpuscles, a lesser number of 
 leukocytes, and some detached epithelial cells. 
 
 Stage of Consolidation, or Hepatization. — The diseased lung is 
 
 Fig. 204.— Red hepatization of the lung (from a photograph by Dr. Wm. M. Gray). 
 
 now completely solid and liver-like in consistency (hepatization). 
 It is swollen, and marked on the surface by indentations of the 
 
 Fig. 205.— Croupous pneumonia ; beginning gray hepatization (Karg and Schmorl). 
 
 ribs. The surface of section is at first red in color (red hepatiza- 
 tion, Plate 4), but later becomes white or gray, or in elderly 
 
428 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 persons (in whom the lungs are usually darkly pigmented from 
 inhalation of dust) of a variegated appearance, resembling granite 
 (gray hepatization, Plate 5). The cut surface is entirely dry, 
 and is finely granular on account of the projection of small 
 plugs of fibrin from the alveoli and bronchioles. The pleura 
 is generally covered with fibrinous exudation. Microscopically 
 the alveoli are found distended with a network or particles of 
 fibrin, in which the same cellular constituents as occur in the 
 stage of congestion are embedded. The fibrinous network is beau- 
 tifully demonstrated by staining the sections after the method 
 of Weigert (Fig. 204). The blood-vessels are less prominent than 
 
 Fig. 206. 
 
 -Advanced gray hepatization (from a photograph by Dr. Wm. M. Gray). 
 
 in the first stage. As the disease advances to the period of 
 gray hepatization the number of leukocytes within the exudate 
 increases and the blood-vessels become still less prominent (Figs. 
 205 and 206). 
 
 Stage of Resolution. — Gradually softening of the exudate occurs 
 and the lung becomes more moist. Puriform liquid may be 
 squeezed from the surface of section, or may be seen in the bron- 
 chioles and bronchi. Crepitation is re-established. Microscopi- 
 cally fatty degeneration of the cells of the exudate is apparent. 
 Softening is further contributed to by simple liquefaction. The 
 result of these processes is emulsification of the exudate, which is 
 finally carried off by the lymphatics or expectorated. 
 
 Before the process of resolution is completed the epithelial cells 
 of the alveoli and bronchioles proliferate, so as to repair the dis- 
 eased portions. At the same time proliferative changes may be 
 seen in the tissues of the septa. These conditions exist throughout 
 the disease to a slight extent, but become more apparent in the" 
 stage of resolution. Eventually the lung is restored to its pre- 
 vious condition. 
 
 Unusual Characters. — In some cases the pathologic changes 
 
Plate 
 
 Croupous pneumonia, stage of red hepatization (Bollinger). 
 
Plate <,. 
 
 Croupous pneumonia, stage of gray hepatization (Bollinger). 
 
DISEASES OF THE RESPIRATORY SYSTEM. 429 
 
 vary somewhat from the typical form described. Not rarely there 
 are considerable congestion and even edema of the lung through- 
 out the disease ; in drunkards or cachectic individuals the exudate 
 is more markedly hemorrhagic than is usually the case ; and some- 
 times, particularly in instances accompanied by streptococcous in- 
 fection, the exudate is more cellular than customary. In still 
 other cases proliferative changes in the septa are prominent. 
 
 Associated I^esions and Pathologic Physiology. — The 
 portions of the lung not involved by the pneumonic process are 
 usually somewhat emphysematous and congested ; and edema may 
 develop. The latter is, however, not so common as has often been 
 assumed. The larger bronchial tubes, as a rule, remain normal, 
 or at most become congested. The finer bronchi are more fre- 
 quently hyperemic, and excess of mucus coats the surface. In 
 practically every case there is a certain degree of fibrinous pleu- 
 risy, either on the external surface of the pleura or between the 
 lobes. Extensive pleurisy is rare and serous exudation is un- 
 common. The pleurisy is directly attributable to the micro-organ- 
 ism which has caused the underlying pneumonia. 
 
 Though fibrinous pneumonia is frequently an entirely local in- 
 fection, systemic intoxication is usually present, and general infec- 
 tion may further aid to develop widespread pathologic changes. 
 Leukocytosis is present in the great majority of cases ; its ab- 
 sence is generally significant of unusually intense systemic in- 
 toxication. White clots are often detected in fatal cases in the 
 chambers of the heart and in the large blood-vessels leaving the 
 heart. Cardiac and respiratory embarrassment, often ascribed to 
 mechanical causes, such as heart-clot or extensive consolidation, is 
 probably in many cases due to the action upon the nervous system 
 of the toxins of the disease. Myocardial degenerations aid in pro- 
 ducing circulatory weakness. The heart-muscle and the kidneys 
 may suffer parenchymatous degeneration, as in other febrile infec- 
 tions, and acute exudative inflammation (myocarditis, nephritis) 
 may occur in either of these organs. Albuminuria is not infre- 
 quent, and albumoses may be found in the urine, especially during 
 the stage of resolution. The chlorids of the urine are usually 
 diminished. The spleen is enlarged and soft. 
 
 Pericarditis is frequent, and endocarditis, either of the simple 
 or of the malignant type, is more common than in any other acute 
 infection, excepting rheumatism. Meningitis is occasionally noted. 
 
 Fibrinous or pseudomembranous bronchitis, laryngitis, gastritis, 
 colitis, and cystitis are sometimes met with. Inflammations of the 
 joints and abscesses in various organs may occur. 
 
 Unusual Terminations.— Secondary infection with pyogenic 
 micro-organisms may lead to termination in abscess ; or this result 
 may be due to the fact that the pneumonia was primarily caused 
 by such micro-organisms. The affected area may suffer gangrene 
 
430 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 even more commonly than suppuration. Gangrene is especially 
 prone to occur when the exudation is distinctly hemorrhagic and 
 in cases in which the circulation is specially weak. Finally reso- 
 lution may be delayed and productive changes may occur in the 
 
 Fig. 20".— Induration of Ihe lung (carnification) in a case of pneumonia of five weeks' 
 duration : a, new connective tissue of the septa ; b, intra-alveolar proliferation of connec- 
 tive tissue ; c, desquamated epithelium in the alveoli ; e, new blood-vessels ; /, lining epi- 
 thelium of the alveoli (Kaufmann). 
 
 septa and even within the alveoli. There results a solidification 
 (carnification) of the lungs, or, as it is termed, fibrous pneumonia 
 (Fig. 207). 
 
 Catarrhal Bronchopneumonia. 
 
 Definition. — Catarrhal bronchopneumonia, or lobular pneu- 
 monia, is an acute inflammatory affection of the pulmonary tissue, 
 occurring in localized areas and consequent upon inflammation of 
 the terminal bronchioles. In most, if not all, cases some species 
 of bacterium is the immediate cause. Pathologically it is charac- 
 terized by inflammation of the terminal bronchioles and by exuda- 
 tion into the alveoli of albuminous liquid containing desquamated 
 epithelial cells, together with more or less red blood-corpuscles 
 and leukocytes ; clinically the disease is marked by an indefinite 
 and irregular course. 
 
 Etiology. — Catarrhal pneumonia may be produced experi- 
 mentally in animals by causing them to inhale steam or various 
 irritating vapors. Still more characteristic lesions are produced 
 when the vapors inhaled hold decomposing organic matter in sus- 
 pension. The same result is accomplished by cutting the vagus 
 nerves, as a consequence of which the vocal bands and esophagus 
 are paralyzed and irritating secretions and particles of food are 
 conveyed into the lung by inspiration. In man tumors, en- 
 largements of the thyroid gland, or inflammatory exudation, 
 may compress the vagi and lead to forms of pneumonia similar 
 to the experimental pneumonia of dogs. Somewhat analogously, 
 
DISEASES OF THE RESPIRATORY SYSTEM. 431 
 
 in the late stages of various diseases particles of food and mucous 
 secretions may sink to the dependent parts of the lungs, or may- 
 be drawn in by the inspiratory air and set up catarrhal pneu- 
 monia in the parts already predisposed to inflammation by hy- 
 postatic congestion (hypostatic pneumonia). Of the same etio- 
 logic sort are the catarrhal pneumonias which occur in diphtheria, 
 epithelioma of the larynx, and inflammatory conditions of the 
 mouth and pharynx, in which irritating particles are carried to 
 the finer bronchi by inspiration (aspiration-pneumonia; deglu- 
 tition-pneumonia). Catarrhal pneumonia of this kind is not in- 
 frequent in the new-born as a result of vigorous inspiratory efforts 
 made while the head is descending through the vagina. 
 
 Most frequent, however, of all forms of catarrhal broncho- 
 pneumonia is that which occurs in the course of measles, whoop- 
 ing-cough, influenza, or other infectious fevers attended with 
 bronchitis. The manner of involvement of the alveolar structures 
 will presently be described ; for the present it may be said that 
 the inflammatory process extends from the bronchi by continuity 
 and contiguity, or by aspiration of irritating bronchial secretions. 
 
 The immediate cause of catarrhal pneumonia is, in the majority 
 of cases, some bacterium. The most frequent is the Diplococcus 
 pneumoniae, which occurs in over 50 per cent, of all cases, either 
 alone or in combination with the Streptococcus pyogenes, staphy- 
 lococci, the pneumococcus of Friedlander, the bacillus of influenza 
 or of typhoid fever, or the Bacillus coli communis. Any of the 
 other forms named, and especially the pyogenic micrococci, may 
 cause catarrhal pneumonia without the diplococcus of Frankel ; 
 but in the case of fevers (typhoid fever, influenza) in which the 
 specific micro-organisms are found, there is usually mixed infec- 
 tion with the Diplococcus pneumoniae. 
 
 Pathologic Anatomy. — The lesions vary somewhat in dif- 
 ferent cases, and we may distinguish three important types, the 
 simple, or ordinary catarrhal bronchopneumonia, the hypostatic 
 form, and aspiration-pneumonia. 
 
 1. Simple Catarrhal Bronchopneumonia. — The lung in such cases 
 presents more or less distinct external appearances. On the 
 pleural surface may be seen lobular areas of dark- or light-red or 
 grayish color, which are somewhat elevated and harder than the 
 normal lung. Surrounding these the pulmonary tissue is emphy- 
 sematous, while here and there may be seen dark-red or lead-col- 
 ered and somewhat depressed areas of pulmonary collapse (atelec- 
 tasis). The lung as a whole is crepitant, while the pneumonic and 
 atelectatic areas are consolidated and airless, and sink in water. 
 On section through the lungs the same general appearances are 
 visible, though the consolidated patches are most abundant near 
 the surface. Both lungs are, as a rule, involved, and any portion is 
 liable to the disease. The smaller and medium-sized bronchi and 
 
432 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 the bronchioles contain mucopurulent secretion, which may be 
 squeezed out; the areas of pneumonic consolidation are smooth 
 and moist on the surface of section, or exceptionally somewhat 
 granular as a result of admixture of some fibrinous pneumonia. 
 < focasionally there may be puriform liquid or small purulent col- 
 lections around the bronchiole in the center of the lobule. The 
 area of collapse (atelectasis) is dark-red, as a rule, and on pressure 
 bloody liquid exudes. 
 
 In the very earliest stages of the disease the lobules of con- 
 solidation and collapse may be inflated by inserting a tube into the 
 bronchus supplying the part and by blowing gently into it. Later 
 this is not possible, as the consolidation increases. At the same 
 time it is noted that the consolidated areas become lighter in color, 
 until at last they are grayish-yellow ; while the areas of collapse 
 become pneumonic and present a similar change of color. 
 
 Microscopically the terminal bronchioles and alveolar passages 
 present somewhat swollen walls and contain variable amounts 
 of mucous exudate containing desquamated cells. In the areas 
 
 
 *v* 
 
 : :'•'• 
 
 
 Fig. 208.— Catarrhal pneumonia (Karg and Schmorl). 
 
 of consolidation the alveoli and the air-sacs are filled with liquid 
 and variable numbers of epithelial cells, red corpuscles, and leuko- 
 cytes (Fig. 208). The liquid is albuminous in nature, as may 
 be readily demonstrated by boiling a portion of the tissue. The 
 epithelial cells are desquamated from the lining membrane either 
 singly or in groups, and there is evidence that active proliferation 
 is taking place as well. In most cases the number of red corpus- 
 cles and leukocytes is small, but in some instances, particularly in 
 cases in which streptococci and staphylococci are operative, the 
 exudation may be quite hemorrhagic, or later purulent. The alve- 
 
DISEASES OF THE RESPIRATORY SYSTEM. 433 
 
 olar septa regularly present considerable round-cell infiltration, 
 and the blood-vessels are surrounded by emigrated leukocytes. 
 The blood-vessels in the septa are distended and tortuous. 
 
 The atelectatic areas present even greater congestion of the 
 blood-vessels, and the alveolar cavities are obliterated by the col- 
 lapse of the walls, or contain at most a little hemorrhagic exudate. 
 The epithelial cells tend to lose their characteristic shape and 
 become cuboidal. 
 
 As resolution advances, the cellular exudate becomes lighter in 
 color as a result of fatty degeneration, and eventually it is absorbed 
 or expectorated. Coincidently the round-cell infiltration disap- 
 pears from the septa, and the pulmonary tissue returns to the 
 normal, excepting that the epithelial cells of the alveoli tend to 
 remain more or less cuboidal for a time. 
 
 Pathogenesis. — The manner of development of the lesions is 
 of considerable interest. In the ordinary catarrhal bronchopneu- 
 monia now under discussion there is always a primary bronchitis 
 of the terminal bronchioles, a bronchiolitis, or capillary bronchitis, 
 as it is termed. This may be spread to the alveolar structure in 
 several ways. In most instances, no doubt, the inflammation 
 travels downward along the bronchioles to their termination by 
 continuity, or outward through their walls to the surrounding 
 alveoli by contiguity. In either case there results a patch of 
 catarrhal pneumonia surrounding a terminal bronchiole. Less 
 commonly the affected lobule first becomes atelectatic and then 
 pneumonic. The atelectasis results from the obstruction of the 
 bronchioles by mucus or by their swollen walls, and is due to 
 the gradual absorption of the air contained within the alveoli and 
 the inability of more to enter (see Atelectasis). Subsequently the 
 collapsed area becomes inflamed by the entrance of micro-organisms 
 from the bronchioles or by extension of surrounding inflammation. 
 
 Unusual Characters. — Marked variations are seen in the nature 
 of the process and in its distribution. In some instances there is 
 but little pneumonic consolidation, while the bronchiolitis, or capil- 
 lary bronchitis, is a striking feature. In other cases the exudate is 
 decidedly hemorrhagic or purulent, and it may in certain areas be 
 quite fibrinous. Regarding the distribution, the most striking 
 variation is the tendency in some cases to lobar involvement by 
 confluence of the lobular areas (pseudolobar form). 
 
 Associated Lesions. — The constant association of bronchitis 
 has been sufficiently noted. Pleurisy is less common than in 
 fibrinous pneumonia, but the patches near the surface are regularly 
 covered with fresh pleural exudation. It has long been recognized 
 that purulent pleurisy is more apt to occur after pneumonia in 
 children than in adults, and in many of these cases the antecedent 
 pneumonia is catarrhal. Widespread toxic and infective lesions 
 may occur, as in fibrinous pneumonia. 
 
4o4 TEXT-BOOK OF PATHOLOGY. 
 
 Unusual Terminations. — In cases in which micro-organisms, 
 more virulent than usual, cause the pneumonia, suppuration and 
 gangrene may result. Fetid and pultaceous foci, or purulent 
 collections surrounded by considerable areas of congestion and 
 inflammatory edema, result. In other instances the process of 
 resolution is slow, and fibroid overgrowth of the septa and pro- 
 liferation of connective tissue within the alveoli ensue, with the 
 production of more or less extensive sclerotic hardening and con- 
 traction of the lung-structure. Within such areas the alveolar 
 exudate may lie for a long time as a fatty mass ; but this is very 
 unusual ; and true caseation, of which so much was formerly said, 
 does not occur. The instances in which this was supposed to 
 have occurred were cases of subsequent infection with tubercle- 
 bacilli, or cases of tuberculous pneumonia ab initio. 
 
 2. Hypostatic Pneumonia. — The bases and posterior portions of 
 the lungs are commonly involved in these cases. The process 
 occurs as a terminal affection in many diseases. It begins as an 
 intense hypostatic congestion and hemorrhagic edema of the de- 
 pendent parts of the lungs. Subsequently the irritants which 
 make their way to the congested area through the bronchi set up 
 a form of inflammation of the terminal bronchioles and air-vesicles 
 which is largely catarrhal, but more fibrinous than ordinary bron- 
 chopneumonia. The inflammatory process is also more diffuse, 
 and is at the most insignificant compared with the antecedent and 
 associated congestion and edema. 
 
 3. Aspiration-pneumonia. — Of the dust which we constantly in- 
 hale, the greatest part is arrested in the upper air-passages or in 
 the larger bronchi, and is expectorated. A part, however, reaches 
 the finer bronchi and bronchioles, and sets up a certain amount of 
 loeal irritation and congestion, with desquamation of epithelial 
 cells and emigration of leukocytes. Ordinarily these processes are 
 exceedingly trivial and can rarely be demonstrated. In persons, 
 however, whose occupations (e. g., steel-grinding, coal-mining, 
 marble-cutting, etc.) subject them to excessive dust-inhalation the 
 pulmonary changes are extensive and severe. This is one form 
 of aspiraiaon-bronchopneumonia, but the irritation rarely stops at 
 the point of catarrhal inflammation ; on the contrary, the irritant 
 particles penetrate the walls of the bronchioles and are distributed 
 by the lymphatics, causing fibroid changes of greater or less 
 extent. The pneumonia thus produced is therefore more properly 
 considered as a form of fibrous pneumonia (q. v.). 
 
 In the course of various affections of the pharynx, larynx, 
 trachea, and bronchi, as well as in cases in which through palsy 
 of the larynx, or through general depression, particles of food or 
 secretions of the mouth enter the air-passages, irritating matters 
 may be inspired or "aspirated" into the finer divisions of the 
 bronchial system. There results intense local irritation, with 
 
DISEASES OF THE RESPIRATORY SYSTEM. 435 
 
 catarrhal inflammation and consolidation. The exudate is largely 
 epithelial, but more often serous, hemorrhagic, or purulent than in 
 simple catarrhal pneumonia. The condition may be circumscribed 
 to small patches, but if large particles are aspirated and the larger 
 bronchial tubes are obstructed, widespread consolidation, of the 
 character described, results. The inflammatory process in these 
 cases of aspiration-pneumonia are habitually intense, and often 
 terminate in suppuration or necrosis, with considerable surround- 
 ing hyperemia and edema. 
 
 Cheesy or Tuberculous Pneumonia. 
 
 Definition. — Cheesy or tuberculous pneumonia is an acute or 
 subacute form of pneumonia caused by the tubercle-bacillus, and 
 involving lobular areas or, by confluence of such, an entire lobe or 
 lung. Pathologically it is characterized by proliferation and des- 
 quamation of epithelial cells, infiltration of the alveolar septa, 
 and finally by cheesy necrosis of the area of disease. Clinically 
 the disease presents itself as a more or less acute pneumonic 
 tuberculosis. Caseous pneumonia is frequently associated with 
 miliary or peribronchial tubercles, affecting the alveoli adjacent 
 to the tubercles. 
 
 Etiology. — Cheesy pneumonia as an independent condition is 
 more common in children than in adults. The immediate cause is 
 the tubercle-bacillus. Infection occurs by rupture of a tubercu- 
 lous gland or cavity into one of the bronchi and dissemination 
 of the infective material throughout the lung. Likewise, bacilli 
 may be inhaled from outside, or from tuberculous foci in the bronchi, 
 larynx, or nose. In cases of disseminated tuberculosis of the lungs 
 areas of caseous pneumonia are habitually encountered in the pul- 
 monary structure between the tubercles. Finally, infection may 
 take place through the blood, but the occurrence of caseous pneu- 
 monia rather than miliary tuberculosis in such cases is assuredly 
 rare. 
 
 Mixed infection with Diplococci pneumoniae is not infrequent, 
 hut it is not, as some investigators have maintained, essential to 
 the disease. 
 
 Pathologic Anatomy. — In its most typical form caseous 
 pneumonia is a lobular process beginning around the terminal 
 ends of the bronchioles, where the infective material lodges. The 
 lung presents on section areas of consolidation not unlike those 
 seen in catarrhal bronchopneumonia. At first these are congested 
 and red in color, but very soon degenerative changes cause a 
 grayish or yellowish color. The surface of section is usually 
 smooth, but often somewhat granular from associated fibrinous 
 exudation. When abundant infection has occurred the areas may 
 be thickly set, and a lobar form is thus established (Plate 6) ; or 
 
436 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 there may be a gradual involvement of new areas, receiving their 
 infection from those first formed, with a similar, but less uniform, 
 lobar pneumonia as the result. 
 
 Caseous pneumonia shows no tendency to resolution, but, on 
 the contrary, tends to progressive cheesy degeneration, and at last 
 to the formation of cavities. The entire lung may be riddled with 
 small excavations, presenting ragged, cheesy walls. Usually the 
 cavities are small, even though there be few ; exceptionally, large 
 ones are seen. Though resolution does not occur, limited areas 
 may be healed by reactive fibrous overgrowth springing from the 
 alveolar septa and encapsulating the diseased area, or penetrating 
 it, and transforming the whole into a fibrous mass. 
 
 Microscopically the exudation has many of the characters seen 
 in catarrhal bronchopneumonia. Essentially the exudate is cellu- 
 
 JSSS 
 
 Fig 209 -Peribronchial tubercle of the lung and caseous pneumonia of the adjacent 
 alveoli. 
 
 lar, and is principally composed of large epithelial cells. These 
 are the desquamated and proliferated lining-cells of the alveoli. A 
 smaller number of red blood-corpuscles and leukocytes is noted, 
 but they are unessential. Sometimes a fibrinous network may 
 be seen in the alveoli, but quite as often this is wholly wanting. 
 The blood-vessels are engorged at first, and the septa are infiltrated 
 with round cells and spindle-cells. The walls of the blood- 
 
Plate 6. 
 
 Subacute caseous (tuberculous) pueumouia (Bollinger). 
 
DISEASES OF THE RESPIRATORY SYSTEM. 437 
 
 vessels themselves may be thickened by proliferation of the con- 
 nective tissue. As the process advances, the cellular exudate and 
 the alveolar walls as well undergo cheesy degeneration, and pre- 
 sent a granular appearance under the microscope (Fig. 209). 
 
 Associated I^esions. — Cases of typical caseous pneumonia, 
 as above described, are rare ; as a rule, more specific tubercular 
 lesions are associated. These may result subsequent to the pneu- 
 monic process from the penetration of infective material into the 
 lymphatics and its dissemination along these channels ; or the 
 specific tubercles may antedate the associated caseous pneumonia. 
 The smaller bronchi are commonly attacked, and tubercular 
 bronchitis and peribronchitis tending to cheesy change result. The 
 pleura may be covered with inflammatory exudation, or may pre- 
 sent miliary tubercles over the area of disease. Associated pleural 
 involvement is especially common between the lobes. The lym- 
 phatic glands of the anterior mediastinum and around the bronchi 
 are frequently enlarged, and may be cheesy in the later stages. 
 
 Fibrous Pneumonia. 
 
 Definition.— Fibrous, or productive, pneumonia is a chronic 
 process resulting from continued irritation, and involving small or 
 large areas of the pulmonary structure. Pathologically it is 
 characterized by overgrowth of connective tissue, and clinically it 
 is marked by signs of more or less extensive mechanical impair- 
 ment of the pulmonary functions. 
 
 Classification. — Several quite distinct forms, depending upon 
 different modes of causation, may be described. The principal 
 varieties are : (1) the pneumonokonioses, or fibrous pneumonias, 
 due to dust-inhalation ; (2) the secondary indurative pneumonias, 
 such as sometimes follow croupous, catarrhal, or caseous pneu- 
 monia, or more frequently chronic congestion of the lungs or 
 atelectasis ; (3) pleurogenetic fibrous pneumonia, in which the 
 process arises by extension of chronic pleural disease ; and (4) 
 peribronchial and perivascular fibrous pneumonia, in which the 
 process follows the bronchi and pulmonary arteries. 
 
 1. Pneumonokoniosis. — Of the dust we constantly inhale, but 
 a small part reaches the finer divisions of the bronchial tree. 
 Most of it adheres to the walls of the upper respiratory tract and 
 is discharged with the sputa, either free or enclosed in leukocytes 
 or epithelial cells {dust-cells; staubzellen). When fine particles 
 reach the terminal bronchioles they occasion catarrhal inflamma- 
 tion, marked by proliferation of the epithelium and exudation of 
 leukocytes. These cells may envelop the irritant particles and 
 remove them through the expectoration. When, however, the 
 dust has sharp edges (as in coal-dust, iron-dust, marble-dust, etc.), 
 and especially when the quantity inhaled is considerable, removal 
 
438 TEXT-BOOK OF PATHOLOGY. 
 
 by expectoration becomes more difficult. In such cases the foreign 
 particles penetrate the walls of the bronchioles and alveoli, passing 
 between the epithelial cells. They may be arrested in the alveolar 
 septa and in the tissue surrounding the bronchioles by the for- 
 mation of a zone of inflammatory exudation, which eventually 
 organizes, forming a fibrous capsule. Some of the particles, how- 
 ever, move along the lymph-spaces into the lymphatic vessels, 
 being carried by leukocytes or floating free in the liquid. These 
 particles may be arrested at various points along the lymphatics, 
 and may occasion fibrous thickening of the vessels or of the peri- 
 lymphatic tissue. The greater portion, however, passes to the 
 lymphatic glands at the root of the lung and surrounding the 
 bronchi, and indurative enlargement of these structures results. 
 In exceptional instances the irritant particles may be conveyed 
 still further, being deposited in the glands about the smaller curva- 
 ture of the stomach and beneath the fissure of the liver. This 
 unusual distribution in a direction opposite the usual lymphatic 
 current is explained by the assumption that obstruction of the 
 larger pulmonary lymphatics causes a reversal of the current. 
 Metastatic distribution of dust-particles may also be due to 
 rupture of one of the affected lymphatic glands into a vein. 
 
 Pathologic Anatomy. — The appearance of the lung varies with 
 the amount of dust inhaled and with its nature. In cases of 
 moderate degree small areas of fibrous thickening, with puckering, 
 are the only abnormality. On section these are found to be hard 
 and of grayish color ; often, however, darkly pigmented, owing to 
 the character of the particles inhaled as well as on account of the 
 formation of hemorrhagic pigmentation. The fibrous tissue may 
 be arranged in a stellate fashion, or concentrically around a nucleus 
 of foreign matter. Secondary changes are not uncommon ; calci- 
 fication is frequently observed, and true bone-formation is occa- 
 sionally noted. Such areas of localized pneumonokoniosis are 
 very commonly met with near the apices. 
 
 More extensive induration is rare, and is rather more frequent 
 at the bases. Large areas of induration may completely de- 
 stroy the vesicular character of the lung-structure. Firm bands 
 of connective tissue may follow the bronchi and radiate into the 
 peripheral portions of the lung, or thickened trabecule may pass 
 from the pleural surface toward the anterior, or, again, a more 
 uniform sclerosis may exist throughout the organ. The organ is 
 contracted ; the pleura, as a rule, is thickened and drawn inward ; 
 and the bronchi may be widely dilated as a result of the traction 
 of the contracting connective tissue and as a consequence of accumu- 
 lating secretions within. Extensive adhesions to the chest-wall 
 often cause deformities of the chest, and the pericardium, heart, 
 and other mediastinal structures may be drawn from their normal 
 positions. 
 
DISEASES OF THE RESPIRATORY SYSTEM. 439 
 
 In rare cases the epithelium of the alveoli and finer bronchioles 
 proliferates, and later undergoes a certain amount of fatty degen- 
 eration, giving rise to an appearance not unlike caseation. In still 
 other cases necrosis and suppuration and cavities (non-tubercular) 
 are observed. 
 
 Microscopically. — In the beginning stages round-cell infiltration 
 and connective-tissue proliferation may be seen around the foreign 
 particles in the septa, and a certain amount of catarrhal inflam- 
 mation may be present in the alveoli. Sharp-edged particles often 
 occasion small hemorrhages. In the later stages dense sclerotic 
 tissue characterizes the process. Proliferative inflammation of the 
 epithelium of the alveoli may be present, but more often the cells 
 undergo atrophy and disappear. 
 
 Varieties. — Certain varieties, dependent upon the kind of dust 
 inhaled, have been described. The term anthracosis is applied to 
 those instances in which coal-dust is the irritant. To a moderate 
 extent this is seen at every autopsy on persons of adult age, but 
 the cases in which conspicuous sclerosis has occurred from this 
 cause are met with only in coal-miners and others of similar occu- 
 pation. The lung is of a marble-like or slate-like appearance, and 
 the lymphatic glands around the bronchi are intensely pigmented. 
 Siderosis is the designation of the cases of pneumonokoniosis due 
 to iron-dust, as seen in grinders, founders, etc. Chalicosis is the 
 term applied to the form due to stone-dust, as seen in potters, 
 marble-cutters, etc. 
 
 2. Secondary fibrous pneumonia sometimes occurs after croup- 
 ous or catarrhal pneumonia, or atelectasis, and in these cases 
 appears in the form of uniform or localized induration of the pul- 
 monary structure. It is due to reactive inflammation of the septa, 
 causing thickening of the latter, as well as proliferation within the 
 alveolar exudate. Similar reactive fibrous change is seen in some 
 cases of caseous pneumonia, and in chronic phthisis the cavities 
 are quite generally walled by fibrous tissue. Finally, chronic 
 congestion of the lung, such as occurs in valvular diseases of the 
 heart, particularly mitral disease, frequently leads to diffuse 
 sclerosis of the lung. Such cases are distinguished by dilatation 
 of the veins and by hemorrhagic pigmentation. 
 
 3. Pleurogenic fibrous pueumonia is an occasional consequence 
 of chronic pleurisy. The lung presents on section dense tra- 
 becule of fibrous tissue, which extend from the thickened and 
 sclerotic pleura deep into the pulmonary structure (Fig. 210). 
 
 4. Peribronchial and perivascular fibrous pneumonia may be 
 associated with the pleurogenic form, or the overgrowth of con- 
 nective tissue around the bronchi and vessels may start at the 
 root of the lung and extend toward the periphery. The latter 
 form has been described by some observers as especially liable to 
 result from syphilis. More moderate peribronchial and perivas- 
 
440 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 cular fibrous pneumonia occurs in association with other forms, as 
 the pneumonokonioses and secondary fibrous pneumonias, but in 
 these cases it is but a minor part of the process. 
 
 Fig. 210.— Fibrous pneumonia secondary to chronic pleurisy (Kaufmann). 
 
 Congenital Syphilitic Pneumonia. — A form of productive pneumonia, 
 as distinguished from fibrous pneumonia in the strict sense that the latter 
 is characterized by formation of sclerotic fibrous tissue, is met with in con- 
 genital syphilis. This is the, pneumonia alba of some writers. It is charac- 
 terized by great proliferation of round and irregular connective-tissue cells, 
 with more or less multiplication and degeneration of epithelial cells in the 
 alveoli and bronchioles. The lung is solid, airless, and white in color. 
 Gummata may be associated. 
 
 Purulent Pneumonia. 
 
 Definition. — Purulent pneumonia is an acute form of pneu- 
 monia caused by pyogenic micro-organisms. Pathologically it is 
 characterized by purulent and hemorrhagic exudation in the con- 
 nective tissue, lymphatic channels, or terminal bronchioles and 
 alveoli ; and clinically it is marked by evidences of intense septic 
 infection as well as of great pulmonary embarrassment. 
 
 The infection in purulent pneumonia may reach the lungs 
 through the bronchi (bronchogenic), the blood-vessels (hemato- 
 genic), or the subpleural lymphatics (pleurogenic or lymphogenic). 
 
 Bronchogenic purulent pneumonia has already been referred 
 to in the description of fibrinous pneumonia and catarrhal bron- 
 chopneumonia. It is particularly frequent in the latter, in some 
 cases of which considerable purulent exudation may be seen in 
 the alveoli or, in the form of small purulent collections, in the 
 
DISEASES OF THE RESPIRATORY SYSTEM. 441 
 
 intervesicular septa. These are instances of intense infection, and 
 the majority of such cases are due to the Streptococcus pyogenes 
 or to staphylococci. The pneumococcus may, however, be found 
 alone. The most decided purulent bronchopneumonia is seen in 
 instances of aspiration-pneumonia secondary to a suppurative proc- 
 ess in the upper respiratory passages, in which particles of infec- 
 tive material are inspired and lodge in the bronchioles. 
 
 Purulent pneumonia is rarely met in the course of fibrinous 
 pneumonia, but sometimes occurs as a terminal condition. Ab- 
 scesses of considerable size may be formed. 
 
 Hematogenic purulent pneumonia is secondary to suppurative 
 or gangrenous processes in other parts of the body, and is a 
 manifestation of pyemic infection. It is frequent in puerperal 
 septicemia, in suppurative osteomyelitis, and like conditions. 
 The micro-organisms are carried by the veins to the right heart, 
 and may first set up malignant endocarditis, from which embolism 
 takes place, or they may pass directly through the right heart to 
 the lungs. As a rule the micro-organisms in question are either 
 streptococci or staphylococci ; but in certain specific infections 
 (as typhoid fever) the specific organisms may alone occasion puru- 
 lent pneumonia. 
 
 When large embolic masses reach the lungs occlusion of larger 
 branches of the pulmonary artery occurs and hemorrhagic infarcts 
 are formed. In the earliest stages these appear as more or less 
 well-circumscribed areas of hemorrhagic infiltration of dark-red 
 color. Very soon change of color occurs, and the foci alter to a 
 grayish, then a yellowish, color, and finally liquefy, forming sup- 
 purative cavities, with irregular walls. The tissue around is in- 
 tensely engorged and edematous, and not rarely quite hemorrhagic. 
 Microscopically it presents the appearances of a catarrhal and 
 hemorrhagic pneumonia. The abscesses frequently break into the 
 bronchi and discharge their contents ; more rarely rupture into 
 the pleural sacs occurs. The pleura itself is intensely inflamed 
 over the embolic areas, and, as a rule, is covered with fibrino- 
 purulent exudate. Extensive purulent pleurisy (empyema) may 
 occur. 
 
 When the micro-organisms reach the lung in a more dissemi- 
 nated manner they pass at once to the smaller arterioles and capil- 
 laries. Embolic infarcts are wanting in such cases, but there is 
 diffuse serous, hemorrhagic, catarrhal, and purulent exudation, 
 which causes consolidation of a somewhat gelatinous character. 
 Small foci of suppuration may be seen, and the purulent process 
 may visibly extend to neighboring parts of the lung along the 
 lymphatic vessels. 
 
 Terminations. — In either of the above forms, the localized 
 embolic or the diffuse, necrosis or gangrene of the pulmonary tissue 
 may occur. Occasionally recovery takes place by absorption of 
 
442 TEXT-BOOK OF PATHOLOGY. 
 
 the purulent exudate or by its discharge. As a rule, the disease 
 is fatal. 
 
 Pleurogenic purulent pneumonia follows intense pleurisy, usu- 
 ally of purulent type. Infection of the subpleural lymphatics 
 first ensues, and later the purulent process extends into the lung 
 within and around these vessels {purulent lymphangitis &nd peri- 
 lymphangitis), in the form of yellowish streaks or bands, which 
 surround the veins and bronchi and follow the interlobular fibrous 
 tissue in various directions. The lobules of the lung may be so 
 pushed apart that the term pneumonia desiccans is quite applicable. 
 The proper substance of the lung adjoining the paths of purulent 
 invasion, and under the pleura, frequently shows the same form of 
 hemorrhagic and purulent pneumonia as occurs in the diffuse 
 hematogenic form. 
 
 Associated Lesions. — Widespread pyemic and toxic lesions 
 are often found in association with purulent pneumonia, but they 
 are often merely coincident results of the same primary disease 
 to which the pneumonia owed its origin, rather than the conse- 
 quences of the purulent pneumonia itself. Secondary infections 
 may, however, occur, such as malignant endocarditis of the left 
 side of the heart, septic nephritis, and the like. 
 
 GANGRENE. 
 
 Gangrene of the lung results from the action of putrefactive 
 micro-organisms in necrotic areas of the lung-tissue. It may be 
 the consequence of direct extension of carious conditions of the 
 ribs or other adjacent bony structures through the pleura into the 
 lung, or of the extension of necrotic processes from ulcers or can- 
 cerous disease of the esophagus or stomach. In other cases the 
 infective materials reach the lung through the inspired air, coming 
 from ulcerative processes in the upper air-passages, or from with- 
 out. When foreign bodies lodge in the bronchi, or the latter are 
 obstructed by the pressure of tumors or aneurysms, there may be, 
 first, more or less congestion and pneumonic consolidation, followed 
 by secondary infection and gangrene. In still other instances the 
 infective material reaches the lung through the blood, and, finally, 
 gangrene is sometimes a terminal process in pneumonia, tubercu- 
 losis, and hemorrhagic infarction of the lungs. Certain general 
 conditions predispose more or less to it. Thus in diabetic indi- 
 viduals congestions or pneumonia are prone to terminate in this 
 wav, and engorgement of the veins or passive hyperemia always 
 renders the lung more liable. 
 
 Pathologic Anatomy. — Gangrene may appear as a circum- 
 scribed or diffuse process. In the former instances more or less 
 extensive areas of lung present a dark, reddish, brownish, or even 
 greenish appearance, and are surrounded by a zone of intense con- 
 
DISEASES OF THE RESPIRATORY SYSTEM. 443 
 
 gestion or of pneumonic consolidation, often of purulent or hemor- 
 rhagic type. The diseased part is soft, pultaceous, and foul in 
 odor. Later it may break down into a putrid mass, and may dis- 
 charge through the bronchial tubes, severe pulmonary hemorrhages 
 sometimes occurring at the same time. The bronchi and the 
 blood-vessels often escape the process, and may pass through the 
 gangrenous area without being themselves materially affected ; 
 but usually the bronchi are penetrated, and the blood-vessels, after 
 they become occluded by thrombosis, suffer the fate of the other 
 tissues. The process may extend widely from a single focus, or 
 reactive inflammation may establish a fibrous capsule, and after 
 discharge of the gangrenous material through the bronchi, healing 
 by the formation of a scar may terminate the disease. 
 
 Diffuse gangrene does not differ much in its general appear- 
 ances, but is less intense and in general more widespread. The 
 affected area is of a dark-red or greenish-black color, soft, and edem- 
 atous, or sometimes dry, and has a somewhat fetid odor, as in 
 •the circumscribed form. Spots of hemorrhagic infiltration and of 
 softening, with formation of cavities, may be noted. 
 
 The sputa in gangrene are mucopurulent, of a yellowish-gray 
 or brownish color, and intensely fetid. When placed in a conical 
 vessel they separate into three layers : the upper frothy, the lower 
 puriform and brownish in color, and the middle layer more fluid 
 and yellowish. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis. 
 
 Tuberculosis of the lungs is generally a local disease, but 
 may be only part of a general tuberculosis. The specific cause, 
 the tubercle-bacillus, gains access to the lungs through the same 
 channels as the irritants that occasion pneumonia. The most fre- 
 quent method of infection is through the air-passages (broncho- 
 genie tuberculosis), the bacilli in such cases coming directly from 
 the outside world or from a tuberculous lesion of the nose, mouth, 
 pharynx, larynx, or bronchi. The latter lesions in turn are fre- 
 quently caused by bacilli inhaled from without, the bacilli owing 
 their presence in the inspired air to the desiccation and dis- 
 semination of sputa of phthisical patients (see Tuberculosis, in 
 Part I.). A second method of infection is that through the 
 blood (hematogenic tuberculosis). The pulmonary disease in 
 such cases is usually secondary to a tuberculous lesion elsewhere 
 which has perforated a vein and discharged its contents into the 
 blood. In such cases general tuberculosis results, and the lungs 
 are affected in common with other vulnerable structures. The 
 infected material may reach the blood in a more roundabout way, 
 when a tuberculous gland or other focus breaks into a lymphatic 
 
444 TEXT-BOOK OF PATHOLOGY. 
 
 vessel (commonly the thoracic ducts in cases of tuberculosis of the 
 abdominal or posterior thoracic lymphatic glands). Hematogenic 
 tuberculosis may in rare instances be limited to the lung, and be 
 secondary to an older tuberculous lesion of the lung itself. This 
 happens when a caseating nodule perforates a branch of the pul- 
 monary artery and the infective matter is carried to the peripheral 
 distribution of the artery. The third and last method of impli- 
 cation of the lungs is through the lymphatic vessels (lymphogenic 
 tuberculosis). This may be secondary to tuberculous pleurisy or to 
 caseous tuberculosis of the peribronchial lymphatic glands or of 
 the thoracic vertebrae. 
 
 Bronchogenic Tuberculosis. 
 
 The action of the tubercle-bacillus when inhaled may be likened 
 to the action of dust-particles entering the lungs in a similar 
 manner. Larger masses of infective material may lodge in the 
 bronchi or larger bronchioles and set up tuberculous ulcerations, 
 from which smaller particles may be secondarily aspirated into the 
 finer divisions of the bronchial tree. Such an occurrence, how- 
 ever, is extremely rare. More commonly the tubercle-bacilli are 
 inhaled in a state of extreme dissemination, and are not arrested 
 until they reach the point of division of the terminal bronchioles 
 into the alveolar passages. One of two results may occur at 
 this point : either there is set up a limited area (miliary nodule) 
 of caseous or tuberculous pneumonia, or the bacillus penetrates 
 between the epithelial cells and occasions more specific tubercular 
 changes in the peri-alveolar and peribronchial connective tissues 
 (miliary tubercles). It has been the occasion of some dispute 
 among pathologists to decide which of these processes is most apt 
 to arise when the infection occurs through the bronchial tubes. 
 Undoubtedly both kinds of change may take place, and it seems 
 likely that in nearly every instance there is a mixture of the two 
 forms. When the infective material is in great abundance and is 
 particularly virulent, and in cases in which the individual is 
 especially vulnerable, caseous pneumonia predominates over the 
 formation of tubercular nodules. On the other hand, a less 
 abundant infection or greater resisting power on the part of the 
 individual determines the greater liability to the formation of 
 nodules and the less likelihood of extensive caseous pneumonia. 
 In case of either manner of onset, however, there is soon added 
 the other form of disease. Thus in the instances in which caseous 
 pneumonia first occurs, the peribronchial involvement character- 
 istic of that condition leads to dissemination of the bacilli along 
 the lymphatic channels, and there are formed in the neighborhood, 
 or to considerable distances around, miliary nodules, which in turn 
 spread the infection to the alveolar structures in their vicinity. 
 
DISEASES OF THE RESPIRATORY SYSTEM. 445 
 
 In a similar manner, when the primary lesion is a tubercular 
 nodule surrounding the alveolar passages, the alveoli soon be- 
 come involved by caseous pneumonia. 
 
 At the same time that these processes are taking place and 
 spreading, degenerative and reparative changes are set on foot. 
 The areas of pneumonia, which began as grayish miliary nodules or 
 as larger areas of lobular tuberculous pneumonia, change their color 
 to a yellowish and become completely caseated ; while the second- 
 ary tubercles in the neighborhood, or those which were primarily 
 formed, similarly become opaque and lusterless, and finally yellow- 
 ish by caseation. This tendency to caseous necrosis is one of the 
 most prominent and characteristic features of tuberculous tissues, 
 and has occasioned no little investigation and controversy to 
 establish its causation. Little doubt now exists that two factors 
 play a part : first, the lack of adequate blood-supply, and, second, 
 the specific action of the tubercle-bacillus. The blood-vessels in 
 caseous pneumonia or in the tubercles are inadequate to supply 
 sufficient nourishment to the tissue. In the pneumonic areas this 
 is due to proliferative changes in the intima and to direct pressure 
 of the exudate, while in the tubercles it is due to hyaline and 
 other forms of degeneration with collapse of the walls. 
 
 Coincidently with the process just described round-cell infil- 
 tration and proliferative changes are manifest in the structures 
 surrounding the diseased areas. In the case of the areas of caseous 
 pneumonia infiltration and proliferation of the connective tissue of 
 the septa, as well as proliferative changes in the blood-vessels of 
 these parts, are observed. There is a wide variation in particular 
 instances in the degree of these reparative processes, and in gen- 
 eral it may be said that the more acute the disease the more apt 
 is degenerative caseation to take place and the less likely regener- 
 ation to occur. Similar overgrowth and infiltration may be seen 
 around the tubercles, and in favorable instances the latter may be 
 completely encapsulated or converted into a fibrous nodule. In 
 instances in which the reparative processes are very extensive 
 there may eventually be a preponderance of connective tissue over 
 caseous pneumonia or miliary tubercles. 
 
 Varieties. — We may distinguish all of the forms of broncho- 
 genic tuberculosis by the name of pneumonic tuberculosis, from the 
 fact that the element of caseous pneumonia is always an important 
 one, and separates them sharply from hematogenic and lympho- 
 genic tuberculosis, in both of which the formation of miliary 
 tubercles predominates over other processes. 
 
 Three forms of pneumonic tuberculosis are met with : the 
 acute, which is frequently spoken of as acute caseous phthisis, or 
 galloping consumption; the chronic, which is also known as 
 chronic ulcerative phthisis ; and the form in which fibrous over- 
 growth predominates, and which is therefore known as fibrous or 
 
446 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 fibroid phthisis. While typical instances of these forms are quite 
 distinct, there is no sharp dividing-line separating the groups, and 
 individual forms merge insensibly one into the other. 
 
 Acute pneumonic tuberculosis is more common in children than 
 in adults. Two elements play a part in its occurrence : first, a 
 high degree of susceptibility, and, second, abundant infection with 
 virulent bacilli. The latter may be derived from without the body 
 by direct inhalation, or may come from the discharge of older 
 caseous areas in the lungs, which have broken into the bronchial 
 tubes, or from some focus of tuberculosis in the upper air-pas- 
 sages. 
 
 Pathologic Anatomy. — This form of tuberculosis is lobular, 
 but very frequently by confluence of the aifected areas an entire 
 lobe may be involved. Either the base or the apex may be first 
 affected. On section the lung presents a more or less variegated 
 appearance in the earlier stages, due to the formation of miliary 
 patches and lobular areas of caseous pneumonia having a grayish 
 appearance, and the coincident congestion of surrounding portions 
 of the lung-tissue. Sections through the lung which cut a termi- 
 nal bronchiole in a longitudinal direction show it surrounded by 
 peribronchial caseation and more or less filled with cheesy exudate 
 
 Fig. 211.— Bronchogenic tuberculosis of the lung, showing the involvement of the tissues 
 surrounding the terminal bronchioles (Birch-Hirschfeld). 
 
 (Fig. 211). Transverse sections give the appearance of a section 
 through a large tubercle, but the lumen of the bronchiole may 
 usually be discovered in the center or to one or the other side. 
 Small miliary tubercles may be apparent in the edges of the pneu- 
 monic patches, and even for some distance around them, but the 
 tuberculous tissue is more apt to appear as diffuse infiltration along 
 the peribronchial and perivascular lymphatics than as distinct 
 tubercles. As the process increases the lung-tissue may be com- 
 pletely involved and uniformly gray or yellowish and consolidated 
 
DISEASES OF THE RESPIRATORY SYSTEM. 
 
 447 
 
 (Fig. 212). The cut section is generally somewhat granular in the 
 earlier stages from admixture of fibrinous exudation in the alveoli ; 
 but later progressively increasing caseation and softening render 
 the surface of section smooth 
 and moist. Not infrequently 
 complete destruction takes 
 place and cavities are formed. 
 These are usually small and 
 present no marked tendency 
 to the formation of an organ- 
 ized wall, but appear simply 
 as necrotic excavations with 
 irregular, ragged outlines. The 
 pleura over the surface of such 
 a lung is usually inflamed and 
 covered with more or less fibri- 
 nous or fibrinopurulent exuda- 
 tion, and not rarely with an 
 abundant crop of tubercles. 
 Occasionally a vomica may 
 rupture and cause pneumo- 
 thorax or pyopneumothorax. 
 
 When the process is less 
 active and the infection less 
 abundant confluence of the 
 lobular areas is less likely to 
 occur, and there are seen 
 merely disseminated patches 
 ■of caseous pneumonia scat- 
 tered through various parts 
 •of the lung, which is itself 
 more or less congested. In 
 .such instances, too, the evi- 
 dences of reparative change 
 are more decided. Complete encapsulation with subsequent calci- 
 fication may ensue, or fibrous overgrowth may convert the entire 
 area into a cicatricial mass. If the cheesy area is simply enclosed 
 with fibrous tissue, it may remain quiescent for a time, possibly 
 for years, and subsequently penetrate the enclosing wall and occa- 
 sion a fresh extension of the whole process. 
 
 Chronic pneumonic tuberculosis is the ordinary form of pulmo- 
 nary phthisis. It begins in the apices of the lungs in the great 
 majority of cases, though children are as likely to be first affected 
 at the bases as at the apices. While there is no doubt that chronic 
 ^phthisis is usually due to infection through the inspired air, it 
 must be admitted that occasionally the onset of the process is due 
 to infection through the blood or lymphatic channels. In the in- 
 
 Fig. 212.— Extensive bronchogenic tuber- 
 culosis (caseous pneumonia) of the base of 
 the lung (Orth). 
 
448 TEXT-BOOK OF PATHOLOGY. 
 
 stances of the latter kind there is first established a localized 
 lesion which caseates and penetrates a bronchial tube, discharging 
 its contents, and thus leading to widespread bronchogenic infec- 
 tion. The further development of the disease takes place in sev- 
 eral distinct ways (see below). 
 
 Pathologic Anatomy. — When there has been an existing bron- 
 chitis, adhesion of the bacilli may occasion tuberculous bronchitis 
 with ulceration and secondary involvement of the surrounding tis- 
 sues. More commonly the bacilli lodge in the finer bronchioles, as 
 in acute pneumonic phthisis, and give rise to lobular areas of caseous 
 pneumonia, surrounded by tubercles which are formed along the 
 course of the lymphatic vessels leading out from the first-formed 
 caseous areas. There is a tendency to a constant increase of the 
 area of disease by the discharge of caseous material into the 
 bronchi and its aspiration into other parts of the lung, and also 
 by dissemination of the infection along the lymphatic vessels 
 traversing the connective tissue around the blood-vessels and 
 bronchi. Section through the lung discloses more or less consoli- 
 dated tissue of an opaque, grayish or yellowish appearance, in 
 which the bronchi may be seen as open spaces or filled with muco- 
 purulent liquid. Little distinction between caseous pneumonia 
 and the tubercles can be made in the center of such an area, but 
 at the edges, where the process is seen in the earlier stages, such 
 distinction may be possible. 
 
 The same tendencies to degeneration and softening, on the one 
 hand, and to the processes of repair, on the other hand, are seen 
 in chronic pneumonic phthisis as are apparent in the acute form. 
 There is the difference, however, that these changes are less rapid, 
 and that, as a rule, proliferation of connective tissue with the for- 
 mation of fibrous tissue is more pronounced than in the acute 
 disease. 
 
 The degenerative and necrotic processes lead to a most charac- 
 teristic lesion of tuberculous lungs — the cavity. Cavities are formed 
 either through the dilatation of the bronchioles (bronchiectasis), 
 due to their ulcerated and weakened condition and to the pressure 
 of retained secretions, with subsequent ulceration and break- 
 ing down of the surrounding caseous tissue ; or, on the other 
 hand, to liquefaction of caseous areas not in connection with the 
 bronchial tube. In the latter case, however, communication with 
 the bronchi is frequently established by extension. A single 
 cavity may grow larger and larger by constant ulcerative proc- 
 esses, in which not alone the caseous tuberculous degeneration 
 takes a part, but also active ulcerative changes dependent upon 
 mixed infection through inspiration of pyogenic organisms. As a 
 rule, however, larger cavities are formed by the confluence of 
 separate smaller ones, and there may be found a series of ex- 
 cavations communicating more or less extensively with each 
 
■ DISEASES OF THE RESPIRATORY SYSTEM. 449 
 
 other. The cavity, or vomica, contains a variable amount of 
 ill-smelling, putrid secretion, consisting of broken-down cheesy 
 matter, pus-cells, degenerated epithelial cells, and libers of elastic 
 tissue, and containing tubercle-bacilli, pyogenic organisms, and 
 occasionally mould-fungi. The walls of the cavity are generally 
 formed by reparative fibrous proliferation, and are covered with 
 a pyogenic membrane, usually darkly pigmented. The inner 
 surface is very rough and ribbed by projecting bands. The latter 
 represent the trabecule and blood-vessels of the lung-tissue, which 
 have resisted ulceration more obstinately than the surrounding 
 structure of the lung. This resistance may continue to such an 
 extent that the blood-vessel is left as a cord passing directly 
 through the center of the cavity ; but, as a rule, the lumen of 
 the vessel is soon obliterated by thrombosis and the vessel itself 
 destroyed. Not infrequently examination of the blood-vessels in 
 the wall of the cavity or passing through it show small aneurysmal 
 dilatations which result from the weakening of the wall by the 
 surrounding necrotic process and from the pressure of the blood 
 within. It is from aneurysms of this character that the large and 
 often fatal hemorrhages of the later stages of tuberculosis take 
 place, though hemorrhage may also occur directly from the eroded 
 blood-vessel. The smaller hemorrhages of the early stages of 
 phthisis, which occasion only a streaking of the sputa with blood, 
 are due to early erosion of small vessels of the bronchioles or to 
 capillary ruptures dependent upon congestion. 
 
 Fibroid Phthisis. — The reparative or fibrous processes which 
 tend to counteract caseation and destruction may begin before 
 cavity-formation or after it. When beginning in the earlier stages 
 the caseous areas will be found to present a capsule of more or less 
 well-developed fibrous tissue, which may completely surround and 
 separate them from the neighboring tissue of the lung. The cap- 
 sule tends to contract and shrink, and the caseous material within 
 may become completely calcareous. In this manner a limited 
 focus of tuberculosis of the lungs not infrequently becomes com- 
 pletely arrested. When the capsule is not so firm, after a period 
 of quiescence or latency extending over even a number of years, 
 fresh extension may begin, the capsule may be perforated, and 
 acute pneumonic phthisis may be established, or the tubercu- 
 lous process may extend more slowly through the contiguous areas 
 as chronic ulcerative phthisis. 
 
 The fibrous capsules surrounding the cavities, which have 
 already been alluded to, may be of varying prominence. In case 
 of small vomicae with pronounced fibrous walls the contraction of 
 the latter may almost obliterate the cavities, leaving only narrow 
 and distorted spaces containing a small amount of putrid material 
 (cicatrices jisluleuse of Laennec). Complete healing of a cavity 
 of notable size probably never occurs. When the excava- 
 
450 TEXT-BOOK OF PATHOLOGY. 
 
 tions are of large size the reparative processes consist simply 
 in the formation of a thick wall of fibrous tissue, which prevents 
 the further extension, for a time, at least, of the tuberculous 
 process. 
 
 Complications in Bronchogenic Pneumonia. — Of first im- 
 portance in tuberculosis of the lung is the condition of the pleura. 
 In the acute pneumonic form the pleura adjoining the diseased 
 areas is generally more or less inflamed and may present consider- 
 able fibrinopurulent exudation, as in croupous pneumonia. Serous 
 or seropurulent exudation may likewise be present, and eruption 
 of miliary tubercles in the pleura is not unusual. The same proc- 
 esses may occur in chronic pneumonic tuberculosis or chronic 
 phthisis. More commonly there are found simply fibrous adhe- 
 sions binding the one surface of the pleura to the other, especially 
 at the apex. 
 
 Extension of the tuberculous process may also take place 
 directly upward along the air-passages, and is due for the most 
 part to direct infection by the sputa. There may thus occur tuber- 
 culous ulceration of the larger bronchi, of the trachea, of the 
 larynx, or of the pharynx. When the sputa are swallowed, as is 
 especially likely to happen in children, or in adults during sleep, 
 intestinal tuberculosis is apt to occur. 
 
 Finally, dissemination of the tuberculous disease through the 
 blood is frequent. A caseous area in connection with one of the 
 veins may penetrate the lumen of the vessel and discharge its 
 contents into the circulating blood, or may first occasion tuber- 
 culous proliferation in the intima of the vein or infectious throm- 
 bosis, from which the blood is secondarily infected. There results 
 general miliary tuberculosis, the tubercles occurring especially in 
 the spleen, the liver, the kidneys, the choroid coat of the eye, or in 
 the membranes of the brain or other serous membranes. 
 
 Acute pneumonia may accompany either acute or chronic pneu- 
 monic tuberculosis, and certain authors insist that in practically all 
 cases there is more or less mixed infection. This is probably not 
 the case, but complicating pneumonia is undoubtedly frequent. 
 In most of such cases localized patches of catarrhal bronchopneu- 
 monia are seen between the caseous lobules ; but sometimes a frank 
 fibrinous consolidation may occupy the lower lobe of a lung in 
 which the upper lobe presents beginning tuberculosis. Quite fre- 
 quently there are small areas of pneumonic consolidation of fibri- 
 nous character in the lobe which is itself the seat of tuberculous 
 involvement. Toward the end of life there is usually extensive 
 edema of the bases and posterior portions of the lungs. 
 
 The heart has interesting relations with tuberculosis of the 
 lungs. Early writers called attention especially to the fact that 
 phthisical subjects frequently present unusual smallness (hypo- 
 plasia) of this organ, and more recently attention has been directed 
 
DISEASES OF THE RESPIRATORY SYSTEM. 451 
 
 to the fact that congenital stenosis of the pulmonary orifice strongly 
 predisposes to tuberculosis of the lungs. Some have claimed that 
 there is an antagonism between cardiac disease and tuberculosis. 
 This view is not well founded, though it is probable that the 
 chronic congestion of cardiac disease renders the lung somewhat 
 less vulnerable to tuberculous infection than the normal lung. 
 Where there is a long-standing tuberculous consolidation hyper- 
 trophy, especially of the right ventricle, is likely to occur. Tuber- 
 culous pericarditis may be found in association with tuberculous 
 pleurisy ; and tubercles may also, though much more rarely, be 
 found upon the endocardial lining. The latter are due to infec- 
 tion through the blood. 
 
 Hematogenic Tuberculosis. 
 
 This form occurs when a focus of tuberculous disease ruptures 
 into a blood-vessel and the infective materials are disseminated in 
 the circulation. As a rule, hematogenic tuberculosis of the lungs 
 is only a part of a general tuberculosis of the entire body. The 
 points from which the primary infection may take place are, of 
 course, numerous, but caseous lymph-glands of the cervical or 
 peribronchial group, or old foci of tuberculosis at the apex of the 
 lung, are perhaps the most frequent. The organs and structures 
 of the body likely to be infected by general miliary tuberculosis 
 are the spleen, the liver, the kidney, the choroid coat of the eye, 
 the meninges, and, more prominently than any other organ, the 
 lungs. In the rare cases in which rupture of the vomica has 
 occurred into one of the branches of the pulmonary artery within 
 the lung, only one lung, or but a part of a lung, may be involved. 
 
 Pathologic Anatomy. — The pathologic feature of import- 
 ance in hematogenic tuberculosis is the formation of miliary tuber- 
 cles. These appear as gray or translucent areas, the size of millet- 
 seeds, around and involving the terminal arterioles or capillaries 
 in the intervesicular septa. At first they may be so small that the 
 naked eye scarcely discovers them, and they are so translucent that 
 oblique* light is necessary to make them appear to view. Later 
 they increase in size and become more grayish and opaque. Micro- 
 scopically there are the well-known characteristics of the miliary 
 tubercle embedded in the perivascular connective tissue (see Tuber- 
 culosis, Part I.). These tubercles, however, are prone to distin- 
 guish themselves from the characteristic tubercles seen elsewhere 
 by their more irregular outline and the more irregular arrangement 
 of their component histologic elements. When the tuberculous 
 process is particularly rapid and virulent giant-cells are few in 
 number, and the tubercle is composed mainly of proliferated 
 connective-tissue cells of the ordinary type, some epithelioidal 
 cells, and round infiltration-cells, all of them more or less granu- 
 
452 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 lar, and the entire nodule surrounded by a zone of caseous, 
 catarrhal, or even hemorrhagic pneumonia of the contiguous 
 alveoli of the lung (Fig. 213). The tubercles are rarely seen 
 
 Fig. 213.— Miliary tuberculosis of the lung, showing two tubercles with degenerated cen- 
 ters, and caseous pneumonia of the alveoli adjacent to the tubercles (Orth). 
 
 in the stage of advanced necrosis, but this may take place in 
 instances of a more chronic course in which the bacteria are 
 admitted to the lungs slowly and perhaps in a state of lesser viru- 
 lence than common. In those instances of what may be termed 
 chronic miliary tuberculosis there may be a considerable amount of 
 caseation of the tubercles, and the patches, as a rule, become decid- 
 edly larger than in the ordinary acute form (Fig. 214). An expla- 
 nation of this form of chronic miliary tuberculosis has been offered 
 by certain authors, who hold that these are instances of infection 
 through the thoracic duct and blood-vessels. The infective material 
 enters the thoracic duct from caseous lymphatic glands in the ab- 
 domen or thorax, and is discharged with the lymph into the veins 
 in a gradual manner, only a little being allowed to pass at a time. 
 The ordinary and typical acute miliary tuberculosis presents 
 itself clinically as an acute infectious disease, running its course 
 rapidly and causing early dissolution. The disease is rather a 
 general toxemia than a local process, and toxemic changes may be 
 present in various organs, such as occur in other infectious and 
 toxemic diseases. The heart, liver, the kidneys, and, in general, 
 the parenchymatous structures are prone to become degenerated, 
 and when the febrile infection continues there may be extensive 
 
DISEASES OF THE RESPIRATORY SYSTEM. 453 
 
 fatty degeneration. In addition to the eruption of miliary tuber- 
 cles in other organs, to which allusion has already been made, 
 there is also involvement of the pleura which belongs more prop- 
 
 Fig. 214.— Hematogenic tuberculosis, showing many scattered miliary tubercles and 
 several clusters (modified from Bollinger). 
 
 erly to the pulmonary process itself, and is simply a continuation 
 of the same infection which gave rise to the pulmonary involve- 
 ment. 
 
 Lymphogenic Tuberculosis. 
 
 It is possible for tuberculous infection of the lungs to occur 
 through the lymphatic channels in several ways. In speaking of 
 acute miliary tuberculosis, particularly of the more gradual type, 
 reference was made to the fact that infective material is sometimes 
 carried by the thoracic duct from the lymphatic glands of the 
 abdomen and posterior mediastinum, as well as possibly from 
 carious thoracic vertebrae to the blood-vessels, and thence distrib- 
 uted through the blood to the lungs as a hematogenic infection. 
 Direct infection, however, through the lymphatic channels may 
 take place. Thus tuberculous pleuritis, either primary or second- 
 ary to tuberculous disease of the vertebrae or ribs, sometimes 
 spreads directly into the lung through the lymphatic vessels trav- 
 ersing the interlobular connective tissue ; and in cases of caseous 
 tuberculosis of the peribronchial glands the infective material may 
 be conveyed into the lungs either by a reversal of the current of 
 
454 TEXT-BOOK OF PATHOLOGY. 
 
 lymph in the vessels running to these glands or by direct exten- 
 sion along the lymphatic walls. A form of lymphogenic tuber- 
 culosis of the lungs may also be referred to in which caseous 
 lymph-glands directly perforate the lung-tissue, but the actual 
 dissemination of the process in the lungs in these cases is usually 
 through the bronchial tubes into which the bacilli gain entrance. 
 Pathologic Anatomy. — It is characteristic of lymphogenic 
 tuberculosis to find small nodular areas which microscopically are 
 seen to be more or less characteristic tubercles. These are 
 scattered along the lymphatic vessels running in the interlobular 
 septa or surrounding the blood-vessels and bronchi. In the in- 
 stances of lymphogenic tuberculosis secondary to pleuritis sup- 
 purative lymphangitis and perilymphangitis (see Pneumonia) are 
 not infrequently associated. 
 
 SYPHILIS. 
 
 It has been the occasion of much dispute whether the many 
 forms of disease attributed to this cause can be really so classified. 
 Undoubtedly some of the conditions attributed to syphilis are 
 cases of tuberculosis, or of some other form of pulmonary disease. 
 But there are other varieties which can unquestionably be spoken 
 of as syphilitic. Among these are the diffuse infiltration of the 
 new-born and the tertiary gummata. 
 
 Diffuse syphilitic infiltration of the lungs is occasion- 
 ally met with in the newborn. As a rule, infants showing this 
 are stillborn. It manifests itself as a more or less lobar consoli- 
 dation and induration of the lung-tissue. On section the lung is 
 light gray or almost white in color, and completely airless, so, that 
 the name 'pneumonia alba, given by older writers, was highly 
 significant. Microscopically there are seen widespread round- 
 cell and spindle-cell infiltration and proliferation in the inter- 
 alveolar and interlobular connective tissues, with more or less 
 compression of the bronchioles and alveoli. The epithelium of 
 the latter may be somewhat proliferated and desquamated, and 
 shows a tendency to fatty degeneration and necrosis. In some 
 instances the degenerative changes do not take place, and the 
 proliferated epithelium of the alveoli is massed within the alveolar 
 lumen, and is for the most part of a cuboidal character. The 
 blood-vessels commonly show proliferation of the adventitia as 
 well as of the intima, and may be completely obliterated. Ac- 
 cording to Birch-Hirschfeld, syphilitic fetuses of the sixth or 
 seventh month sometimes present limited disease of this nature 
 and of such distribution that it is recognized to begin as a peri- 
 bronchial and peri-alveolar infiltration of lobular distribution. 
 
 Syphilitic gummata may be associated with the diffuse 
 form of congenital syphilis, or may be present in the new-born 
 
DISEASES OF THE RESPIRATORY SYSTEM. 
 
 455 
 
 without the latter. Gummata are occasionally seen in adults. 
 They are present most frequently near the root of the lung 
 beneath the pleura, but may be scattered through other parts of 
 the organ. As a rule, the number is limited. They appear as 
 more or less rounded nodules of a grayish to yellowish color, with 
 more or less fibrous overgrowth surrounding them and often 
 radiating from them into the surrounding lung-tissue. Central 
 necrosis may proceed to such extent that cavities are formed. 
 
 Occasionally the contents of a gumma may be discharged 
 through the bronchial tubes, or they may be absorbed and a 
 cicatricial puckering of the lung-tissue may mark the place 
 of the former disease. Microscopically there are seen in the 
 earlier stages the ordinary appearances of gummata (see Syphilis, 
 Part I.), with more or less diffuse infiltration surrounding them and 
 with thickening and hyaline degeneration of the blood-vessels. 
 
 Syphilitic fibrous induration of the lung, so-called, has 
 been described, and it seems likely that some of the cases embraced 
 
 Fig. 215.— Syphilis of lungs : a, thickened alveolar walls or stroma ; b, partly longi- 
 tudinal section of bronchus ; c, uninfiltrated alveoli ; d, new connective tissue infiltrated 
 with small round cells ; e, cells lining alveoli ; f, artery showing thickened walls ; g, des- 
 quamated lining cells (Linsley). 
 
 in the description are really syphilitic in nature. The process 
 begins, as a rule, at the root of the lungs, from which it radiates 
 
456 TEXT-BOOK OF PATHOLOGY. 
 
 through the tissue toward the pleura. The fibrous tissue, for the 
 most part, surrounds the bronchi and blood-vessels (Fig. 215). In 
 another group of cases the process spreads from the pleura and 
 occasions the formation of dense bands of fibrous tissue passing 
 inward into the lung-structure. In still other cases the fibroid 
 overgrowth is so diffuse that the appearance presented resembles 
 so closely that of pneumonokoniosis, that it is practically indis- 
 tinguishable. It is quite probable that many instances, in which 
 appearances such as these are met with, are not at all syphilitic ; 
 but the occurrence of changes of this description in association 
 with gummata, and, again, the occurrence of such changes without 
 gummata in undoubtedly syphilitic individuals, make it likely that 
 some at least are of this origin and nature. 
 
 GLANDERS. 
 
 Glanders occasionally affects the pulmonary tissue, the infec- 
 tion taking place either by inhalation from ulcerated lesions in 
 the nose or other portions of the upper air-passages, or more 
 rarely by distribution of the bacilli through the blood. The lesions 
 are of two kinds. There may be merely a grayish or purulent 
 infiltration of a diffuse character, with the formation of abscesses 
 and often with associated hemorrhagic infiltration. Considerable 
 areas of the lung may be consolidated in this manner, or the 
 process may be localized and lobular. In other cases nodular 
 patches varying from the size of a hemp-seed to that of a pea are 
 seen in various parts of the lung. These consist of masses of 
 round cells, and show an early tendency to degeneration. More 
 or less hemorrhagic and catarrhal inflammation of the alveoli 
 surrounding these nodules may be present. 
 
 ACTINOMYCOSIS. 
 
 Actinomycosis is a rare affection of the lungs. It may result 
 from the direct extension of actinomycosis of the lymphatic tissues 
 and cellular structures in the anterior or posterior mediastinum, 
 when there are formed in the pulmonary tissue fistulous necrotic 
 tracts containing more or less cheesy and purulent material, in 
 which the characteristic yellowish actinomycosis-granules are 
 found. The latter on microscopic study show the actinomyces. 
 The infection may also take place by a gradual descent of the 
 process from the mouth or upper respiratory passages along the 
 trachea and bronchi to the lung; or, more commonly still, by 
 aspiration of the infective agents. In the latter cases nodules 
 consisting of round cells are formed, and present themselves as 
 grayish or grayish-red patches varying in size from that of a pea 
 to that of a cherry, and showing a decided tendency to fatty de- 
 generation and purulent softening. The surrounding lung-tissue 
 
DISEASES OF THE RESPIRATORY SYSTEM. 457 
 
 is commonly consolidated, and presents the appearances of purulent 
 and catarrhal or even hemorrhagic pneumonia. In many cases 
 there is also a manifest tendency to productive changes, which lead 
 eventually to the formation of more or less fibrous tissue within 
 the alveoli and in the interalveolar and interlobular connective 
 tissues. Not rarely this indurative process completely surrounds 
 areas of degeneration and softening. 
 
 TUMORS. 
 
 The lungs are, comparatively speaking, a rare seat of tumors, 
 though a variety of both primary and secondary growths occur. 
 
 Connective-tissue Tumors. — Small nodular fibromata have 
 occasionally been observed scattered through the lungs in the peri- 
 bronchial connective tissue, and a few instances of similar nodules 
 of lipoma are recorded. Chondroma is more common than either 
 of these, and doubtless takes origin from the peribronchial carti- 
 lages. Secondary chondromata have been observed in cases of 
 chondroma elsewhere. True osteoma is rare, but more frequently 
 ossification of sclerotic areas is met with in instances of pneumono- 
 koniosis. 
 
 Sarcoma is the most frequent connective-tissue tumor of the 
 lungs. It may originate in the lymphatic glands surrounding the 
 bronchi in the roots of the lungs, from the lymphatic nodes sur- 
 rounding the smaller bronchi within the lungs, from the lymphatic 
 vessels themselves, or from the subpleural or other connective 
 tissue of the lung itself. Primary sarcoma is less common than 
 secondary. In one form it presents itself as rounded masses of 
 grayish or yellowish color lying around the bronchi in the root 
 of the lung (Fig. 216). On section through this it is seen to con- 
 sist of more or less enlarged and transformed lymphatic glands, 
 and there may be secondary nodules scattered through the lung. 
 This form of sarcoma is particularly common in pneumonokoniosis, 
 as seen in the fibroid lungs of the cobalt-miners of Schneeberg. 
 Primary sarcoma may also be of the form called endothelioma. The 
 lymphatic vessels in the peribronchial tissue become filled with 
 proliferated cells, and their ramification may be distinctly visible on 
 section as a network traversing the pulmonary tissue. Primary sar- 
 coma of the spindle-cell or round-cell variety may spring from the 
 subpleural connective tissue. Giant-cell sarcoma has been observed. 
 
 Secondary sarcoma is extremely common. It is seen in nearly 
 all instances in which metastasis has occurred from a primary 
 growth in any part of the body. In these cases there are found 
 well-defined nodules of varying size, situated for the most part 
 near the surface of the lung (Fig. 217). They are whitish in color 
 and tend to soften. The lung-tissue between may be congested, 
 and there may even be pneumonic consolidation. Secondary sar- 
 
458 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 coma of the lung may also occur from direct extension of mediasti- 
 nal sarcoma or of sarcoma in other of the surrounding structures. 
 An interesting type of secondary sarcomatous involvement of the 
 lungs occurs in what is teamed malignant lymphoma or lymph- 
 adenoma, either with or without leukemia. These may be consid- 
 ered as instances of generalized lymphosarcoma. The lungs are 
 found to contain small nodules, consisting of round cells embedded 
 in a more or less reticular matrix of stellate and spindle-cells. 
 
 Epithelial Tumors. — Carcinoma is practically the only form 
 to be considered, though adenoma of the lung has been described. 
 Carcinoma of the lung is certainly less frequent than was formerly 
 believed, sarcoma having been confused with it. Massive cancer 
 may start from the mucous glands of the larger bronchi near the 
 root of the lung. The tumor is irregular, soft, and tends to ulcer- 
 
 
 
 mm** \ i JOT 
 
 
 
 •- 
 
 Fig. 216.— Lymphosarcoma of the post-bronchial glands, invading the lung; the lung is 
 divided by a long incision and the halves laid open. 
 
 ate in the center, forming cavities. Secondary nodules within the 
 lung-tissue arc seen along the lymphatic vessels surrounding the 
 bronchi. Primary carcinoma may also start from the epithelium 
 of the finer bronchial tubes. The proliferation soon penetrates the 
 wall of the bronchus and extends along the lymphatic vessels in 
 the peribronchial connective tissue. In this manner bands of new 
 growth are seen traversing the lung. Occasionally squamous- 
 celled carcinoma may originate in the epithelium of the terminal 
 bronchioles and alveoli. 
 
 Secondary carcinoma of the lungs is less frequent than second- 
 
DISEASES OF THE RESPIRATORY SYSTEM. 
 
 459 
 
 ary sarcoma. It may occur by metastasis from cancer elsewhere, 
 and in these instances the appearance of the nodules is much the 
 same as that of sarcoma. Secondary cancer of the lung may also 
 result from extension of esophageal carcinoma or of cancer of the 
 
 Fig. 217.— Secondary sarcomata of the lung: the primary growth was attached to the 
 pleura: 
 
 breast penetrating the thoracic walls and pleura. Finally, in car- 
 cinoma of the upper respiratory passages or of the mouth inhalation 
 of cancerous particles may lead to secondary nodules in the lungs, 
 associated at times with areas of broncho-pneumonia. 
 
 Cysts. — Congenital cysts have been described, but they are 
 probably merely dilatations of the bronchi. Adenomatous pro- 
 liferation of the epithelial lining of such dilatations may take place. 
 Dermoid cysts are rarely encountered. They may discharge 
 through the bronchial tubes. 
 
 PARASITES. 
 
 Besides the specific and pathogenic micro-organisms that have 
 been referred to as occurring in tuberculosis, pneumonia, and 
 other infectious diseases, various forms of bacteria and mould- 
 fungi are met with as accidental and non-specific parasites. Such 
 
460 TEXT-BOOK OF PATHOLOGY. 
 
 micro-organismal collections are most frequent in areas of gan- 
 grene, in degenerated infarcts, and in dilated bronchi or tubercular 
 cavities. Sarcinre, a form of leptothrix resembling that seen so 
 frequently in the mouth, and several varieties of aspergillus, have 
 been noted. The general term Pneumonomy costs aspergillina is 
 applied to the occurrence of the last-named mould-fungi in the 
 lungs. Sometimes they are so abundant that they are readily dis- 
 covered in the sputa ; and it is likely that certain inflammatory 
 conditions of the lungs are directly due to such organisms. The 
 clinical course may suggest tuberculosis, and pathologically diffuse 
 or irregular consolidation of the lungs may characterize such cases. 
 Animal Parasites. — Of the lowest forms of animal life or 
 protozoa, the Monas lens, cercomonas, and paramecium have been 
 observed. These are entirely accidental, occurring in cases of 
 gangrene, putrid bronchitis, and similar conditions. The class of 
 vermes furnishes the more important parasitic affections of the 
 lungs. The Distoma pulmonale- is not infrequent in parts of Asia. 
 It occasions serious hemoptysis. The Strongylus longevaginatus, 
 cchinococcus-cysts, and Cysticercus ccllulosce are occasionally seen. 
 Pmtastomwm denticulatum has been observed. 
 
 THE PLEURA. 
 
 Anatomic Considerations. — The pleura is a membrane 
 composed of fibrillar connective tissue and elastic fibers, contain- 
 ing a rather abundant network of capillaries. It is lined on the 
 surface with a single layer of flat endothelial cells, between which 
 there are openings from the pleural cavity into the subpleural 
 lymphatics. The latter form a rich network in the subpleural 
 connective tissue and play an important part in the pathologic 
 processes affecting the pleura. 
 
 CIRCULATORY DISTURBANCES. 
 
 Passive hyperemia occurs in various diseases interfering 
 with the respiration, and still more intensely in cases in which 
 there is pressure upon the azygos veins or diffuse intrathoracic 
 pressure. 
 
 Petechial hemorrhages may occur when the congestion is 
 intense. They are particularly frequent and prominent in cases 
 of death from suffocation, but are also seen in various disorders 
 of the blood and hemorrhagic diatheses, such as pernicious anemia, 
 purpura, and intoxications of various kinds. 
 
 Hemothorax is the term applied to the presence of free blood 
 in the pleural cavity. It may be due to wounds of the chest-wall, 
 causing rupture of blood-vessels, to fracture of the ribs, and to 
 rupture of aneurysms into the pleural sac. If the pleura is in a 
 
DISEASES OF THE RESPIRATORY SYSTEM. 461 
 
 healthy condition and secondary infection does not take place, 
 more or less rapid absorption of the blood ensues. When infec- 
 tion occurs, secondary inflammations of the pleura and disorgani- 
 zation of the blood result. 
 
 Hydrothorax, or dropsy of the pleural cavity, may be but a 
 part of a general edema occurring in chronic kidney-disease or 
 heart-disease. It is usually bilateral, and the fluid presents the 
 ordinary characteristics of a serous effusion. Unilateral hydro- 
 thorax is, however, not infrequent in cardiac disease attended with 
 great enlargement of the organ. The hydrothorax in such cases 
 is generally right-sided, and is probably due to pressure upon the 
 azygos veins and the root of the right lung. The pleura itself is 
 not particularly disordered, but very frequently some opacity and 
 loss of luster is noted, and there may be edema of the subpleural 
 fibrous tissue. The lungs are pressed backward toward the root 
 and against the spinal column, and may be considerably com- 
 pressed. Unilateral hydrothorax may be due to pressure upon the 
 veins of one side by tumors or aneurysm. A small amount of 
 serous outpouring into the pleural sacs occurs quite commonly just 
 prior to death. 
 
 Hydrothorax causes compression of the lungs and displacement 
 of the other adjacent viscera. The seriousness of the results are 
 in proportion to the amount of effusion. 
 
 Pneumothorax designates the presence of air in the pleural 
 cavities. It may result from rupture of tuberculous vomicae, gan- 
 grenous areas, softened hemorrhagic infarcts, or abscesses of the 
 lungs, or rupture of emphysematous air-vesicles beneath the pleura, 
 allowing egress of air into the pleural sac. It may also occur after 
 an empyema has ruptured into the lung and established a fistu- 
 lous communication between the pleural sac and the bronchioles. 
 Very rarely it is due to a penetrating wound of the chest. The 
 pleural sac may be more or less tensely distended with air ; the 
 lung is pushed backward against the spine, is more or less gray- 
 ish or brownish in color, indurated and airless. The pleura 
 itself may present no abnormality, and the air may be absorbed ; 
 but very frequently infection takes place, and purulent exudation 
 from the pleura collects in the sac. The condition is then spoken 
 of as pyopneumothorax. The neighboring organs are often greatly 
 displaced, particularly the heart, the diaphragm, and the liver. 
 In left-sided pneumothorax the heart may be pushed far to the 
 right of the sternum, and when the right side is affected the liver 
 may be pushed downward considerably below the ribs. 
 
 INFLAMMATION. 
 
 Inflammation of the pleura, or pleuritis, is designated 
 by the clinical name pleurisy. 
 
462 TEXT-BOOK OF PATHOLOGY. 
 
 Etiology. — It may result from local or from general causes. 
 Among the local causes the most important are extension of inflam- 
 mation from the lungs in the various forms of pneumonia, in gan- 
 grene and tuberculosis ; extension from pericarditis or mediastinal 
 diseases, and extension from inflammatory affections of the spine, 
 of the ribs, or of the chest-walls. Less directly peritonitis, hepatic 
 abscess, and other abdominal affections may occasion pleuritis by 
 extension, and in rare cases perforation of esophageal or gas- 
 tric ulcers, or abscess of the spleen or liver, may be the 
 cause. 
 
 In the group of cases due to general causes the pleural inflam- 
 mation is the result of infection or intoxication involving the 
 pleura through the blood. Thus in pyemia and septicemia, in rheu- 
 matism, and in other acute infectious diseases, and in Bright's dis- 
 ease, acute inflammation of the pleura is not uncommon. Cold 
 and traumatism have long been regarded as important causes, but 
 their action is doubtless only a predisposing one, the immediate 
 cause being some infection for which the traumatism or the 
 exposure to cold has paved the way. 
 
 The micro-organisms found in pleurisy are quite numerous. In 
 the cases secondary to ordinary pneumonia, pneumococci are fre- 
 quently discovered, and these micro-organisms may be present 
 even though there be no pneumonia at all. In the instances 
 secondary to tuberculosis of the lungs, as well as sometimes 
 in cases of primary pleurisy without affection of the lungs, 
 tubercle-bacilli are discovered. In the purulent cases, as w r ell as 
 in some instances of simple fibrinous or serofibrinous pleurisy, 
 staphylococci and streptococci are detected. When there is 
 abundant liquid it is always difficult to discover the micro-organ- 
 isms, and in many instances in which bacteria have not been found, 
 it is probable that the difficulty of their demonstration, even by 
 animal experimentation, accounts for the failure to demonstrate 
 them, rather than their absence. A number of forms have occa- 
 sionally been seen, such as the Bacillus coli communis, the typhoid 
 bacillus, the bacillus of anthrax, and others. 
 
 Pathologic Anatomy. — Several forms of pleuritis may be recog- 
 nized, though one of these merges into the other, and a single case 
 may pass from one into another form at its various stages. It is 
 well, however, to separate these stages as distinct forms, since 
 many cases maintain a uniform character throughout. The forms 
 are the fibrinous, serofibrinous, purulent, and hemorrhagic ; after 
 any of these forms there may be left chronic pleural thickening or 
 adhesions of a fibroid character. 
 
 Fibrinous pleuritis begins with congestion and loss of luster 
 of the pleural surface, after which there soon follows exudation of 
 a fibrinous character, forming a thin, whitish pellicle on the sur- 
 face. This may become yellowish and increase in thickness, so 
 
DISEASES OF THE RESPIRATORY SYSTEM. 463 
 
 that the pleural surfaces become agglutinated, and when separated 
 present an appearance likened to the appearance of two pieces of 
 buttered bread separated after having been pressed together 
 (bread-and-butter pleurisy). This process may be confined to 
 small areas of the pleura, or it may be quite universal. Some- 
 times it is limited to the reflections of the pleura separating the 
 lobes of the lung. 
 
 Microscopically the exudate consists of fibrils or flakes or 
 granular masses of fibrin more or less infiltrated with round cells. 
 Beneath this the endothelium of the pleura is found to be some- 
 what thickened by proliferation and some of the cells are detached. 
 The connective tissue beneath the endothelium and the subpleural 
 connective tissue are infiltrated with round cells and the blood- 
 vessels are hyperemia In favorable cases and when the process 
 has been slight a gradual reabsorption of the exudate takes place, 
 and the integrity of the pleura may be restored completely. 
 When the exudate has been more extensive and the agglutina- 
 tion of the pleural surfaces has been considerable, new blood- 
 vessels from the capillaries of the pleura penetrate the fibrinous 
 exudate, fibroblastic cells develop from the older connective-tissue 
 cells, and gradually organization takes place, so that the adjacent 
 layers of pleura are bound together by connective tissue, the 
 fibrinous exudate gradually undergoing absorption and disappear- 
 ing. The adhesions thus formed are at first delicate and quite 
 cellular, but are later converted into dense, sclerotic bands. 
 When fibrinous pleurisy occurs repeatedly, as in tuberculosis 
 of the lungs, and is not sufficiently extensive to cause adhe- 
 sions, the surface of the pleura may become thickened and 
 opaque in spots from proliferation of the connective tissue. 
 In this way considerable chronic thickening of the pleura may 
 ensue. 
 
 Serofibrinous pleuritis may be simply a further stage of the 
 foregoing form, though in many instances it begins almost at once 
 as a serous exudation into the pleural sac. The liquid is heavier 
 than dropsical fluid and contains flakes and shreds of fibrin. 
 Microscopically it is found to contain white and red blood-corpus- 
 cles in small numbers, and occasionally detached endothelial cells. 
 Sometimes the number of red corpuscles increases considerably, 
 and there may be a gradual transition to the hemorrhagic form of 
 pleuritis. The amount of liquid varies from a few cubic centi- 
 meters to several liters ; and the pleura itself shows a more or 
 less extensive coating of fibrinous exudate. The lung is pressed 
 backward, as in pneumothorax or hydrothorax, and the adjacent 
 organs are similarly displaced. 
 
 Purulent pleuritis, or empyema, or pyothorax, is always the 
 result of micro-organismal infection. The process may begin as a 
 purulent pleuritis, or as a primary serofibrinous pleurisy, second- 
 
464 TEXT-BOOK OF PATHOLOGY. 
 
 ary infection occurring either from within the body or through 
 infected aspi rating-instruments from without the body. When a 
 transition of the latter kind occurs the exudate is seen to become 
 more and more turbid ; the number of pus-corpuscles gradually in- 
 creases until the liquid is quite purulent. Spontaneous discharge of 
 empyema most frequently takes place through the lung and bronchi. 
 More rarely rupture occurs through the chest-walls anteriorly be- 
 tween the ribs. When rupture has occurred through the lung 
 and bronchi the fistulous communication may remain open and 
 pneumothorax may ensue. 
 
 The pleura in empyema shows more or less abundant granula- 
 tions, which in case of discharge of the liquid serve eventually to 
 unite the costal and pulmonary pleura by firm fibrous adhesions. 
 Occasionally the pus may be completely absorbed, or it may 
 undergo gradual inspissation, remaining as a more or less cheesy 
 detritus, which may finally become calcareous. Such terminations, 
 however, are rare. 
 
 Hemorrhagic pleuritis is generally the result of tuberculous 
 infection or of malignant disease of the lungs and pleura. Pleu- 
 ritis may also take a hemorrhagic form in old and cachectic indi- 
 viduals, or in persons suffering from scurvy, purpura, and similar 
 diseases. As a rule, the liquid is serous, with considerable admixt- 
 ure of blood, but in tuberculous and malignant pleuritis it is 
 sometimes well nigh pure blood. 
 
 Associated Lesions in Other Parts. — Though pleuritis is fre- 
 quently the result of acute or chronic affections of the lung, it 
 often occasions secondary disorders in the latter organ. The sub- 
 pleural lymphatics are commonly distended with cells, and the 
 inflammatory process may extend for considerable distances along 
 these channels into the interlobular septa of the lung. In empy- 
 ema the resulting purulent lymphangitis and perilymphangitis 
 lead to striking pathologic appearances (see Pneumonia). The 
 lung also suffers from direct pressure in serous and purulent pleu- 
 ritis. If the compression to which it is subjected is not relieved 
 by absorption of the liquid, or by its removal by aspiration, the 
 alveolar epithelium degenerates and proliferative inflammation 
 takes place in the connective tissue, so that a permanent contrac- 
 tion of the lung results. The removal of the liquid at this stage 
 is not followed by the return of the lung to its proper size and 
 function. On the contrary, the removal or absorption of the liquid 
 in these cases, especially when they occur in young children, causes 
 a sinking in of the ribs and curvature of the spinal column, and 
 the heart and other adjacent organs may be permanently dis- 
 placed. Most remarkable deformities of the chest may occur. 
 Less extensive contraction of one side of the chest, or displace- 
 ment of the heart, may result from the contraction of bands of 
 adhesions, without marked collapse of the lung. 
 
DISEASES OF THE RESPIRATORY SYSTEM. 465 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis of the pleura, or tuberculous pleuritis, may be 
 either primary or secondary. Cases of the former are compara- 
 tively rare. In most instances the pleural disease is secondary to 
 tuberculosis of the lungs, or to tuberculosis of other adjoining 
 parts. Hematogenic infection may occur under the same con- 
 ditions as hematogenic infection of the lungs, and frequently the 
 lungs and pleurae arc studded with miliary tubercles at the same 
 time. 
 
 When the pleural disease is secondary to tuberculosis of the 
 lungs the appearances vary considerably. In many cases small 
 gray or yellow tubercles are found in the subpleural connective 
 tissue and in the pleura, and the surface may be coated with 
 fibrinous exudate, while the cavity of the pleura may be more or 
 less distended with serofibrinous, hemorrhagic, or purulent liquid. 
 Not rarely the liquid effusions are reabsorbed and dense adhesions 
 are formed, or great thickening of the pleura results. Sometimes 
 considerable calcification of the thickened pleura and of the in- 
 spissated exudate is the terminal result. The tubercle-bacilli are 
 often difficult to demonstrate in the liquid, even by injections into 
 animals, though they may be present in the pleura itself. 
 
 Syphilis of the pleura is a doubtful condition. Fresh pleuritis 
 may be found in the neighborhood of a syphilitic gumma ; and 
 there are cases of considerable pleural thickening in syphilitic 
 persons in which the disease may possibly be syphilitic, though 
 in these cases, as in similar indurative conditions in the lungs, 
 there is considerable doubt as to the essential nature of the disease. 
 
 TUMORS AND PARASITES. 
 
 Tumors of the pleura are comparatively rare. Fibromata 
 and lipomata are occasionally seen as small nodular masses in the 
 serous or subserous coat of the costal or visceral pleura. Chon- 
 dromata and even osteomata have been observed. More frequently 
 calcification and ossification of portions of the thickened pleura 
 take place after pleuritis. 
 
 Primary sarcoma may spring from the subpleural connective 
 tissue, and, according to Coats, is especially common in children, 
 and is most frequently of the spindle-cell variety. Primary endo- 
 thelioma of the pleura has been studied by a number of investiga- 
 tors. In a case under my observation it presented itself as a 
 more or less uniform thickening of the pleura of one side, involv- 
 ing the diaphragmatic reflection in particular. The cavity was 
 filled with hemorrhagic fluid, and there were some nodular enlarge- 
 ments on the surface (Figs. 218 and 219). This is the usual ap- 
 pearance presented. Metastasis may occur in the lung beneath 
 the diseased pleura, or even in more distant parts. 
 
 30 
 
466 
 
 TEXT-BOOK OF PATHOLOGY 
 
 Fig 218 -Endothelioma of pleura: the pleural cavity was distended with effusion, and 
 the lung was compressed and invaded by secondary nodules. 
 
 wm^^^^^^^^^^ 
 
 Fig. 2iy.— Microscopic section from the preceding illustration. 
 
 Secondary tumors of the pleura may occur by metastasis or by 
 direct extension. In the former manner sarcomata and carcmo- 
 mata sometimes involve this structure ; by the latter method of 
 
DISEASES OF THE GASTBO-INTESTINAL TRACT. 467 
 
 involvement mammary tumors and new growths of the medias- 
 tinum, the ribs, or other adjacent structures may extend to the 
 pleura. 
 
 Parasites. — Echinococcus cysts may originate in the sub- 
 serous connective tissue of the costal or the visceral pleura, and 
 may rupture into the pleural cavity. Psorospermise have been 
 found in pleural effusions. The Amoeba coli has been found in 
 the pus of empyema following hepatic abscess. 
 
 CHAPTER V. 
 DISEASES OF THE GASTROINTESTINAL TRACT. 
 
 THE MOUTH. 
 
 CONGENITAL ABNORMALITIES. 
 
 The most frequent defects in the development of the mouth 
 are cleft palate and harelip. In the former of these the entire 
 hard palate may be divided, generally to one side of the middle 
 line ; and there may be associated harelip and fissure of the soft 
 palate. Anteriorly the division occurs between the superior 
 maxillary bone and the intermaxillary bone, the fissure of the lip 
 being also to one side and often extending into the nostril. The 
 soft palate is divided along the middle line, and the uvula may be 
 separated into lateral halves. The lip may be cleft on both sides, 
 so that there is a small central portion connected with the septum 
 of the nose and separated from the lateral portions of the lip. 
 Harelip is more frequently unassociated with cleft palate. 
 
 Complete absence of the lips ; or unusual shortness, especially 
 of the upper lip ; excessive largeness of the mouth by extension 
 of the fissure outward toward the ear ; and imperfect development 
 of the lower jaw-bone, are rare congenital conditions. 
 
 CIRCULATORY DISTURBANCES. 
 
 Anemia of the mucous membranes of the mouth is seen in 
 cases of general anemia, and is often one of the most striking evi- 
 dences of that condition. It is particularly noticeable in the lips. 
 
 Hyperemia. — Active hyperemia occurs in the early period of 
 various inflammations, while passive congestion is met with as the 
 result of obstruction of the circulation in pulmonary and cardiac 
 diseases. 
 
468 TEXT-BOOK OF PATHOLOGY. 
 
 Hemorrhages in the form of small petechia? occur in pur- 
 pura and other hemorrhagic diseases, and sometimes in infectious 
 fevers. 
 
 INFLAMMATION. 
 
 Inflammation of the mucous membrane of the mouth is termed 
 stomatitis; inflammation of the tongue is designated by the name 
 glossitis. 
 
 Stomatitis may be of varying character and intensity. 
 
 Catarrhal stomatitis may result from direct irritation by hot 
 liquids or chemical substances, or may occur in depressed condi- 
 tions of the general system, possibly as a consequence of infection. 
 It is more common in children than in adults. The mucous 
 membrane of the mouth is red and usually covered with con- 
 siderable liquid exudation. When the inflammation is intense 
 small vesicular cysts may form from distention of the mucous 
 glands, and even localized erosions may appear. When the 
 inflammation has continued for a long time, or has been repeated, 
 there may form upon the surface silvery-white, slightly elevated 
 spots, which result from a hyperplasia of the epithelium, a form 
 of keratosis. This condition has been designated by the name 
 of leukoplakia. 
 
 Mild catarrhal conditions of the mucous membrane of the 
 mouth are especially common on the tongue, the epithelium of 
 which constantly desquamates. In the course of gastro-intestinal 
 and other diseases the desquamation may be more active, the 
 cells, however, being retained upon the surface. Portions of 7 
 food and bacteria cling to the masses of desquamated cells, and in 
 this manner the whitish or brownish furring of the tongue so 
 commonly met with in various diseases is formed. Sometimes 
 the heaping of epithelial cells takes place in localized areas, and 
 extends in peculiarly irregular patches, which, from their resem- 
 blance to maps, have given rise to the term "geographical tongue." 
 In chronic cases the whitish spots of leukoplakia alluded to above 
 are formed. Psoriasis of the tongue presents lesions analogous 
 to those of the skin. 
 
 Aphthous stomatitis occurs in children under conditions of 
 malhygiene and debility, or as a result of gastro-intestinal and 
 other diseases. Local irritation often plays an important part. 
 There appear in the mucous membrane, especially of the lower 
 lip and gums, small whitish spots lying upon an inflamed base. 
 Usually these are separated, but sometimes confluence occurs, 
 though there is rarely extensive spreading. The whitish mem- 
 brane covering or constituting the spots is composed of degener- 
 ated epithelium ; and sometimes of fibrin, so that the term croup- 
 ous stomatitis may in some cases be applied. The lesions are 
 superficial and rarely lead to actual ulceration. It has been held 
 
DISEASES OF THE G ASTRO-INTESTINAL TRACT. 469 
 
 that the preliminary lesion is a vesicle ; this, however, does not 
 appear to be frequent, and is certainly not essential. 
 
 Foot-and-mouth Disease. — A similar affection occurs in ani- 
 mals, particularly in cows, sheep, and goats, and is designated 
 foot-ancl-mouth disease. This condition is contagious, and con- 
 siderable epidemics have occurred among persons drinking the 
 milk of infected animals. The specific cause is unknown, though 
 several micro-organisms have been described. 
 
 Bednar's aphthae are small ulcers found in the mouths of suck- 
 ing infants and situated at the lateral portions of the palate over 
 the ends of the pterygoid processes, on other parts of the hard 
 palate, or occasionally on the soft palate. They are probably 
 caused by traumatism occurring in the act of sucking. 
 
 Ulcerative stomatitis may be met with in various parts of 
 the mouth, especially in the gums. In young children it is fre- 
 quently the result of malnutrition and lack of cleanliness of the 
 mouth. In various cachectic diseases, particularly in scurvy, the 
 gums become soft and spongy and tend to ulcerate. Mercuric 
 and other forms of poisoning may lead to extensive ulcerations. 
 Deeper ulcerations are found upon the sides of the tongue or the 
 inner part of the lip in cases of injury due to the sharp edges of 
 broken or carious teeth. Ulcerative stomatitis may be secondary 
 to necrotic conditions of the bones or suppurative inflammations 
 about the roots of teeth. Ulceration beneath the tongue is met 
 with in many cases of whooping-cough, and is due to the irritation 
 of the teeth in the paroxysms of coughing. 
 
 In ordinary cases of ulcerative stomatitis the gums at the junc- 
 tion with the teeth become reddened and soft, and may present 
 hemorrhagic infiltration. Later the epithelium of the surface is 
 destroyed and open ulcers result. Considerable suppuration may 
 occur, and the teeth may be loosened and dislodged. 
 
 Pseudomembranous stomatitis is most frequently due to the 
 action of the bacillus of diphtheria, and is therefore, strictly 
 speaking, diphtheria of the mouth. It is usually secondary to 
 pharyngeal diphtheria, but may occur primarily upon the lips or 
 other parts of the mouth. In some cases of aphthous stomatitis 
 the lesion is in reality a pseudomembranous one. 
 
 Phlegmonous stomatitis is more common in the lips than 
 in other parts of the mouth, and may be the result of trau- 
 matic injuries with intense infection, or a secondary condition after 
 facial erysipelas or other cellular inflammations of the face. The 
 lips and cheeks may be greatly swollen, and suppuration may 
 occur, forming abscesses which tend to rupture into the mouth. A 
 chronic form of inflammation of the deeper tissues of the lips may 
 lead to hypertrophy. This is especially common in the upper lip 
 as the result of long-standing coryza or eczema. 
 
 Gangrenous stomatitis, or noma, affects the mucous membrane 
 
470 TEXT-BOOK OF PATHOLOGY. 
 
 of the cheeks, and occurs in ill-nourished children, especially after 
 measles and other infectious fevers. There is formed a sloughing 
 ulcer on the inner side of the cheek, and inflammatory induration 
 involving the entire thickness of the cheek. The skin at first 
 presents a dark-red or bluish discoloration, and later extensive 
 destruction (gangrene) may occur (Fig. 220). The pathologic 
 
 
 
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 Mr 
 
 mm / ^- sgm 
 
 -^ "' iMs 
 
 1 , 
 
 
 ^■m 
 
 tej 
 
 
 
 mk 
 
 
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 IX 
 
 h 
 
 ■ 
 
 Fig. 220.— Case of noma (Children's Hospital). 
 
 changes are those of a rapid necrosis of all the tissues, and micro- 
 organisms of suppuration or other saprophytes are usually present. 
 Putrefactive changes cause a fetid odor. Intense septic infection 
 and intoxication generally attend. 
 
 Associated Conditions in Stomatitis. — In many cases the 
 inflammation may extend from the mucous membrane of the mouth 
 posteriorly to the pharynx. Very commonly the lymphatic glands 
 of the neighborhood are involved, and enlargement of the sub- 
 maxillary or even the cervical glands is commonly observed. In 
 some cases, especially in mercurial stomatitis, the salivary glands 
 are coincidently or consecutively swollen and inflamed. Increased 
 flow of saliva (ptyalism or sialorrhea) is a frequent symptom. In 
 intense cases, especially in gangrenous stomatitis, parenchymatous 
 degenerations of other organs may result from general toxemia. 
 
 Glossitis. — Superficial catarrhal inflammations have been 
 referred to. More extensive inflammations of the tongue, leading 
 
DISEASES OF THE G ASTRO-INTESTINAL TRACT. 471 
 
 to parenchymatous glossitis, may result from injuries, especially 
 when accompanied by infection. The entire organ may in these 
 cases be swollen, and there is round-cell infiltration with a ten- 
 dency to suppuration. Localized parenchymatous glossitis with 
 ulceration may occur from injury by carious teeth. 
 
 Hemilateral glossitis, sometimes attended with the formation of 
 herpetic vesicles, is occasionally observed, and is probably depend- 
 ent upon diseases of the chorda tympani nerve. 
 
 ATROPHY AND DEGENERATIONS. 
 
 Atrophy of the muscles of the tongue and cheeks may occur 
 in association with nervous diseases (bulbar palsy). Physiologic 
 atrophy of the gums follows loss of the teeth in old age. 
 
 Degenerations of the mucous membrane usually accompany 
 inflammations. 
 
 Under the name of nigrities, or black-tongue, is described a 
 form of hypertrophy of the papillae of the tongue with pigmen- 
 tation. The dorsum of the tongue may be covered with a hair- 
 like coating of dark-brown or blackish color. The cause of this 
 affection is obscure. 
 
 INFECTIOUS DISEASES. 
 
 Thrush, or parasitic stomatitis, is met with in young 
 children, and is due to the action of a micro-organism now 
 generally known as Saccharomyces albicans. There are formed 
 upon the mucous membrane white patches resembling curdled 
 milk, and varying in size from mere points to large areas. These 
 tend to coalesce and to spread. The mucous membrane is reddish 
 and inflamed. The back and sides of the tongue and the inner 
 parts of the cheeks are favorite seats. Microscopically the white 
 coating is composed largely of mycelial threads of the parasite, 
 with which are mingled degenerated epithelial cells and generally 
 also other micro-organisms, notably micrococci. The process may 
 extend to the pharynx, and sometimes as far as the bronchi or the 
 stomach, through the larynx and esophagus. 
 
 Tuberculosis of the mouth may be primary or secondary. 
 The latter is especially frequent on the root of the tongue, and is 
 secondary to tuberculosis of the larynx or pharynx (Fig. 221). 
 Small nodular masses of tubercle are formed, and tend to undergo 
 cheesy desquamation, forming ulcerated areas. Primary tubercu- 
 losis leading to ulceration may occur upon the lips or upon the 
 tongue as a result of direct inoculation, as in the kissing of a 
 tuberculous person. Nodular masses are formed, which at first 
 present themselves as papillary elevations, but subsequently 
 undergo characteristic necrosis. The injury of the tongue by the 
 
472 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 teeth, and the favorable soil offered for the retention and multipli- 
 cation of the micro-organisms in carious teeth, may play a part in 
 the causation. 
 
 Syphilis is most frequently secondary, occurring in the form 
 
 Fig. 221.— Tubercle of the tongue (Karg and Schmorl). 
 
 of mucous patches upon the lips or tongue. Gummatous infiltra- 
 tion may appear in a localized form, or as an irregular involvement. 
 Fissuration and deformity of the tongue may result. The primary 
 
 Fig. 222.— Actinomycosis of the cheek (Illick) 
 
 syphilitic lesion (chancre) resulting from direct inoculation is rarely 
 observed. 
 
DISEASES OF THE GASTRO-INTESTINAL TRACT. 473 
 
 Actinomycosis affects the tongue, gums, and jaw-bone, and 
 is characterized by a slowly infiltrating process with a tendency to 
 necrosis and suppuration, in which the alveolar processes of the 
 jaw-bone are generally attacked. The lesion in the mouth may be 
 insignificant, while the secondary involvement of the cheeks, or of 
 the lvmphatic glands below the jaw and in the neck may be exten- 
 sive (Fig. 222). • 
 
 TUMORS. 
 
 Cystic formations, due to agglutination of the mouths of the 
 mucous glands, are met with upon the tongue and lips. Papillom- 
 atous growths of the mucous membrane are also occasionally 
 observed. Fibroma, lipoma, myxoma, and even chondroma are 
 rare forms of tumors of the submucous tissue of the tongue or 
 other parts of the mouth. Not rarely they are congenital. 
 Lymphadenoma or lymphosarcoma may occur at the root of the 
 tongue, where it takes origin from the lymphatic follicles or the 
 lingual tonsil. Sarcoma of other parts of the mouth is rare, ex- 
 cepting as an extension from sarcoma of the jaw-bone and other 
 parts. 
 
 Carcinoma is the most important new growth of the mouth, 
 and in nearly all cases is of the squamous-celled variety. The 
 favorite seats are the lower lip, usually toward one side of the 
 mouth, and the tongue. It appears as an irregular nodular eleva- 
 tion which tends to ulcerate upon the surface and spreads to adja- 
 cent structures. Metastasis usually occurs to the submaxillary 
 and cervical lymphatic glands. 
 
 Nodular masses having the structure of the normal thyroid 
 gland may be found at the base of the tongue. 
 
 Cysts are especially frequent beneath the tongue, at the sides 
 of the frenum. These have been termed ranula, and are formed 
 by the dilatation of the ducts of the small mucous glands. At 
 times ranula may be a cystic dilatation of a duct of the sublingual 
 salivary gland or that of a submaxillary gland. Ranula is usu- 
 ally found as a rounded or elliptical tumor which may fill the 
 floor of the mouth and displace the tongue backward and up- 
 ward. The contents consist of somewhat gelatinous albuminous 
 liquid. 
 
 Hemangioma, both of the telangiectatic and cavernous varie- 
 ties, is occasionally seen, but a more important tumor is lymph- 
 angioma affecting the tongue and lips, and giving rise to the 
 conditions known as macroglossia and macrocheleia. In these 
 conditions there is a uniform enlargement of the tongue or lips, 
 and on section distended lymphatic spaces more or less filled 
 with liquid and round cells are detected. Such enlargements 
 are usually congenital, and are especially met with in cretins. 
 
474 TEXT-BOOK OF PATHOLOGY. 
 
 THE TEETH. 
 
 Anomalous Development. — Unnatural largeness, or, on 
 the contrary, lack of development, is frequently observed. Com- 
 plete absence of the teeth has been noted. Numerical increase or 
 decrease is frequent. Delay in the eruption of the teeth and 
 irregularity in their formation occur in rachitis ; and a form of 
 maldevelopment of the upper central incisor teeth of the perma- 
 nent set is observed in cases of congenital syphilis (Hutchinson's 
 teeth). The characteristics of this condition are the wedge-shape 
 of the teeth, the cutting-edge being smaller than the crown, and 
 the concave notching of the cutting-edge (see Fig. 106). Hutch- 
 inson's teeth are not entirely peculiar to congenital syphilis. 
 
 Caries of the teeth results from malnutrition, digestive 
 disturbances, and lack of cleanliness. Micro-organisms which 
 lead to acid fermentation contribute in the causation by forming 
 acids which soften the enamel and occasion fissures through which 
 other bacteria (bacilli and micrococci) may gain entrance into the 
 channels of the dentin. The Leptothrix buccalis is commonly 
 found in the deposit upon the teeth, but is probably non-specific. 
 
 The carious process consists in a gradual disintegration of the 
 enamel and dentin, with the formation of more or less granular 
 detritus in which bacteria are abundant. The process may pene- 
 trate to the pulp of the teeth and set up a secondary inflammation, 
 or pulpitis. Occasionally caries of the teeth begins within. 
 
 Inflammation of the pulp of the teeth may occur in 
 association with caries, or sometimes independently. The pulp 
 becomes reddened and swollen, and may present hemorrhages and, 
 later, suppuration. The inflammatory process tends to spread 
 through the roots of the teeth to the tissues surrounding the roots 
 and to the alveolar periosteum. Abscesses may thus be formed 
 about the teeth, and may spread to the tissue of the gums (alveolar 
 abscesses), eventually rupturing upon the surface. 
 
 Tumors composed of tissue resembling the normal dentin are 
 spoken of as odontomata. They arise from the pulp during the 
 process of development and form irregular outgrowths of the 
 crown or roots. Similar outgrowths, resembling the enamel or 
 dentin, or cement-substance, are more frequent in later life, and 
 have been designated as odontinoids. 
 
 Sarcomata and fibromata may spring from the pulp during the 
 development of teeth or from the connective tissue about the 
 roots ; and polypoid outgrowths (hypertrophied granulations) from 
 the pulp may be met with in association with caries of the teeth 
 and pulpitis. 
 
 The most important tumor is the giant-celled sarcoma of the 
 alveolar process of the jaw. This is known by the name of 
 epulis, though strictly speaking the term is applied rather to the 
 
DISEASES OF THE GASTRO-INTESTINAL TRACT. 475 
 
 situation than to the kind of tumor. Extensive enlargements of 
 the jaw-bone and destruction of the surrounding tissues may ensue. 
 Cysts are met with in the alveolar processes, and arise from the 
 primary follicles in which the teeth are developed. 
 
 THE PHARYNX AND TONSILS. 
 
 CIRCULATORY DISTURBANCES. 
 
 Anemia of the soft palate and other portions of the pharynx 
 occurs in general anemia and in cases of phthisis or other wasting 
 diseases. The mucous membrane may be decidedly pallid. 
 
 Active hyperemia or congestion occurs in the beginning 
 stages of inflammation and when irritants have been in direct 
 contact with the mucous membranes. 
 
 Passive hyperemia is seen in heart-disease, emphysema, 
 phthisis, and other chronic pulmonary affections. In these cases 
 the mucous membrane is dark red, and not rarely becomes some- 
 what edematous. 
 
 IJdema of the pharyngeal tissues is found in association with 
 inflammatory affections, and may occasion considerable stenosis. 
 
 Hemorrhages may be the result of direct injury, as in the 
 swallowing of fish-bones and the like, or may occur in the form 
 of petechia? in purpura and other hemorrhagic diseases and in 
 intense infections (small-pox, septicemia). 
 
 INFLAMMATIONS. 
 
 Catarrhal pharyngitis, or angina, may affect the entire 
 lining membrane of the pharynx, or may be limited to the tonsils 
 or other parts. It results from direct irritation by hot liquids or 
 chemical substances, from exposure to cold, and particularly from 
 infections. Angina, or sore-throat, is met with in many of the 
 infectious fevers, or may appear as an independent infection. 
 
 The mucous membrane presents a bright-red color, is some- 
 what swollen, and covered with tenacious exudation composed of 
 mucus and desquamated cells. Small vesicular elevations may 
 form, and after the rupture of these erosions or even superficial 
 ulcers are sometimes seen. Occasionally there are hemorrhagic 
 extravasations. 
 
 A form of catarrhal pharyngitis, known as herpetic angina, is 
 analogous to herpes of the skin, and may accompany facial or 
 labial herpes. 
 
 Chronic catarrhal pharyngitis is met with in persons who 
 use the voice excessively, especially in the open air. It may also 
 result from the abuse of tobacco or alcohol. The posterior wall 
 of the pharynx and the pillars of the soft palate are particularly 
 involved. The mucous membrane is swollen in the earlier stages, 
 
476 TEXT-BOOK OF PATHOLOGY. 
 
 but later becomes atrophic, and is marked by slight granular ele- 
 vations, which are either hyperplastic lymph-follicles or distended 
 mucous glands. The veins in the submucous tissue are enlarged, 
 and are visible through the atrophic mucous membrane as tortuous 
 channels. Chronic hyperplasia of the tonsils and chronic laryn- 
 gitis are frequently associated. 
 
 Phlegmonous pharyngitis may result from wounds of the 
 pharynx, or may be associated with intense infections, such as 
 pseudomembranous tonsillitis and pharyngitis, particularly the 
 forms due to streptococci. It may result from pustular pharyn- 
 gitis in smallpox, or from glanders of the pharynx. Phlegmonous 
 tonsillitis sometimes extends to the peritonsillar tissues as far as 
 the retropharyngeal wall. 
 
 The soft palate, uvula, arches, or other parts affected are swollen 
 and tensely distended. There may be congestion or deep cyanosis 
 and edematous exudation. The usual termination is suppuration, 
 but sometimes gangrenous necrosis ensues. General septicemia is 
 frequently the result. 
 
 Retropharyngeal Abscess. — Phlegmonous pharyngitis primarily 
 affecting the retropharyngeal tissues may be due to caries of the 
 cervical vertebras ; occasionally it occurs in the infectious fevers 
 in consequence of embolism. 
 
 Pseudomembranous pharyngitis may be caused by the 
 Bacillus diphtheric? and be truly diphtheritic, or it may be due to 
 a variety of other micro-organisms, or to irritating gases, steam, 
 and like causes. Non-diphtheritic pseudomembranous pharyngitis 
 is especially common as a complication of scarlatina, measles, and 
 other infectious diseases, and seems in these cases to be caused by 
 the Streptococcus pyogenes. The appearance of the throat may 
 be identical with that observed in diphtheria, but extensive 
 necrosis is more common, while typical pseudomembranes are less 
 frequent. 
 
 The mucous membrane and the underlying parts, especially the 
 tonsils, become greatly swollen and edematous ; and subsequently 
 suffer necrotic changes. 
 
 There is formed upon the surface of the throat a whitish or 
 yellowish patch, or several patches, which tend to coalesce and 
 extend from the region of the tonsils to the pillars of the fauces 
 and the uvula, or to the mouth, nose, or larynx. The pseudo- 
 membrane is quite firmly attached to the mucous membrane, and 
 cannot be removed without tearing away part of the underlying 
 tissues. Microscopically the deposit is found to consist of gran- 
 ular or fibrillar fibrin entangling more or less degenerated leuko- 
 cytes and epithelial cells. In the deeper layers intense congestion 
 and round-cell infiltration are observed ; in the superficial strata 
 degenerated cells and detritus, together with masses of bacteria, 
 are conspicuous. 
 
DISEASES OF THE GASTBO-INTESTINAL TRACT. 477 
 
 The neighboring lymphatic glands, notably those below the 
 angle of the jaw, enlarge and may suppurate, and sometimes ex- 
 tensive cellulitis and suppuration of the floor of the mouth (Lud- 
 wig's angina) occur. There are intense systemic intoxication and 
 infection, and secondary lesions are frequently developed in various 
 organs (nephritis, myocarditis, etc.). The non-diphtheritic forms 
 of pseudomembranous pharyngitis may be distinguished from the 
 diphtheritic forms, in typical cases, by the greater intensity of the 
 local (necrotic) processes, the earlier and more marked involve- 
 ment of the local lymphatic glands, and by the greater tendency 
 to nephritis ; but unfortunately atypical cases are very common, 
 and an absolute diagnosis can be made by bacteriologic study alone. 
 
 Tonsillitis may be a part of a general pharyngitis, or it may 
 occur as an independent affection. Several varieties are described. 
 
 Catarrhal tonsillitis results from the same causes as catarrhal 
 pharyngitis in general, and presents similar appearances. The 
 tonsils are usually somewhat enlarged. 
 
 Lacunar or follicular tonsillitis occurs from similar causes, and 
 may involve the normal tonsil or one affected by chronic hyper- 
 trophy. The surface of the tonsil is marked with small white 
 or yellowish spots, into which the end of a probe may be 
 inserted. These are the lacuna? or crypts distended with epithelial 
 cells more or less degenerated. Bacteria of various kinds may be 
 found in the contents of the lacuna?, and doubtless play an im- 
 portant part in the etiology. Staphylococci, streptococci, pneumo- 
 cocci, tubercle-bacilli, and the bacillus of diphtheria have all been 
 observed. The latter two forms may be present merely as acci- 
 dental associations, but may possibly play an etiologic part, 
 
 Fig. 223.— Crypts in cases of tonsillitis : a, acute lacunar; b, chronic hypertrophic ; a, 
 surface-epithelium ; b, accumulated contents of crypt ; c, lymphoid follicles surrounding 
 crypt (Kaufmann). 
 
 especially the Bacillus diphtheria?. Ulceration may occur in the 
 walls of the lacuna?, and the surface of the tonsil may be consid- 
 erably broken down. In other cases the bacteria may penetrate 
 the tonsil at the bottom of the lacuna?, and phlegmonous tonsillitis, 
 or quinsy, may result (see below). The contents of the lacuna? may 
 be discharged upon the surface, and may adhere for a time as a 
 yellowish-white caseous pellicle, resembling diphtheritic pseudo- 
 
478 TEXT-BOOK OF PATHOLOGY. 
 
 membranes in appearance. In other cases the contents of the 
 crypts are retained, undergo inspissation, and may even calcify. 
 A certain amount of catarrhal pharyngitis may be associated, but 
 the follicular ulcers are rarely seen beyond the tonsils. 
 
 Enlargement of the submaxillary and cervical lymphatic glands 
 is commonly observed. General septicemia of mild type is not 
 infrequent ; myocarditis, endocarditis, and nephritis may result. 
 The association of tonsillitis and rheumatism has occasioned much 
 discussion. It is very probable that rheumatism frequently results 
 from tonsillitis, the latter being the first effect of micro-organ- 
 ismal invasion, which eventually causes rheumatism. 
 
 Chronic tonsillar hypertrophy may result from repeated attacks 
 of simple catarrhal or of follicular tonsillitis. The tonsils are 
 enlarged, usually irregularly so, and are harder than normal. On 
 section the connective-tissue reticulum and septa are found 
 increased, and the lymphoid follicles are likewise hyperplastic. 
 Pressure upon the orifices of the lacunae not rarely causes obstruc- 
 tion and repeated attacks of lacunar tonsillitis. Retention and 
 calcification of the contents of the crypts are particularly common 
 in the lacunar tonsillitis of hypertrophic tonsils. Chronic hyper- 
 trophy of the tonsils very often occurs in rachitic or badly nour- 
 ished children in association with hyperplasia of the lingual tonsil 
 and nasopharyngeal adenoid tissues. Distinct evidences of inflam- 
 mation are wanting in such cases, and the condition seems rather 
 a form of simple hyperplasia of the lymphoid structures. 
 
 Phlegmonous tonsillitis, abscess of the tonsil, or quinsy, may be 
 the result of simple catarrhal or of follicular tonsillitis, or may be 
 associated with phlegmonous inflammation of other parts of the 
 pharynx. One or both of the tonsils may be affected. Redness 
 and swelling are noted in the earlier stages, but later the mucous 
 membrane is pallid or even yellowish. Microscopically diffuse 
 round-cell infiltration and eventually focal collections leading 
 to abscess-formation are detected. The peritonsillar tissues may 
 be involved, and spreading phlegmonous inflammation results. 
 Rupture may take place into the pharynx, or the ulceration may 
 extend outward, causing discharge upon the neck at the angle of 
 the jaw. The internal carotid artery may be perforated. 
 
 PRESSURE=NECROSIS. 
 
 This condition occurs upon the anterior and posterior walls of 
 the pharynx, opposite the cricoid cartilage. It is met with in 
 marantic persons occupying a dorsal decubitus, and is caused by 
 the backward pressure of the cricoid cartilage against the opposite 
 vertebra. The mucosa becomes necrotic, and more or less exten- 
 sive ulcerations are formed. Complete perforation of the pharyn- 
 geal wall sometimes occurs. 
 
DISEASES OF THE GASTRO-INTESTINAL TRACT. 479 
 
 INFECTIOUS DISEASES. 
 
 Diphtheria of the pharynx usually begins in the mucous 
 membrane covering the tonsils, and spreads to the pillars of the 
 fauces, to the uvula, the posterior wall of the pharynx, the cheeks 
 and tongue, the posterior nares, or to the larynx. It rarely in- 
 vades the esophagus, but may sometimes extend along this struct- 
 ure as far as the stomach. 
 
 The specific cause is the Bacillus diphtheria? (see Diphtheria, 
 Part I.). The characteristic lesion is a pseudomembrane, which is 
 formed on the surface and within the mucous membrane. This 
 first appears as a grayish or yellowish-white pellicle, more or less 
 firmly attached to the mucosa ; it spreads rapidly, and may cover 
 the whole of the pharynx in a day or two. In other cases the 
 disease progresses slowly, or remains quite limited. The under- 
 lying tissues become swollen by inflammatory infiltration (cellular 
 and edematous), and swallowing and breathing may then be 
 greatly obstructed. When the pseudomembrane is removed from 
 the surface a raw and more or less necrotic base is exposed. Mi- 
 croscopically the surface of the pseudomembrane is found to con- 
 sist of a mass of debris, often containing micrococci and other 
 bacteria, as well as the specific organisms, in great numbers. 
 Somewhat more deeply the membrane is composed of a fibrinous 
 reticulum or masses of fibrin entangling degenerated epithelial 
 cells and leukocytes. Still more deeply the tissues of the pharynx 
 
 Fig. 224.— Pseudomembranous inflammation of the uvula : a, masses of micrococci ; 
 . b, necrotic cells ; c, round-cell infiltration ; d, fibrin network (Ziegler). 
 
 are found intensely congested and infiltrated with round cells (Fig. 
 224). In the late stages of the disease extensive necrosis of the 
 mucosa and submucosa may occur. 
 
480 TEXT-BOOK OF PATHOLOGY. 
 
 In some cases diphtheria may undoubtedly present the lesions 
 of an ordinary lacunar tonsillitis, and the clinician may be unable 
 to determine the nature of the disease. 
 
 Associated Conditions. — Some enlargement of the lymphatic 
 glands at the angle of the jaw is usual, and exceptionally this may 
 terminate in suppuration. Lesions of the internal organs, espe- 
 cially the heart and kidneys, are not infrequent, and disease of the 
 peripheral nerves is a common sequel (see Diphtheria, Part I.). 
 
 Pharyngomycosis I,eptothricia. — This condition is met 
 with on the tonsils, and less frequently the pillars of the fauces, 
 uvula, and other parts of the pharynx. It occurs in persons of 
 lowered vitality, and seems to be caused by the Leptothrix buccalis, 
 a form of bacterium very commonly met with in the collections 
 around the necks of the teeth. The lesions present themselves as 
 milky-white and somewhat chalk-like outgrowths arising from the 
 tonsillar crypts and the mucous glands. These are often tightly 
 adherent, but occasion very little inflammation of the surrounding 
 tissues. Microscopically the thread-like parasite is found in 
 abundance. 
 
 Tuberculosis may occur in the pharynx in the form of sub- 
 epithelial tubercles, which break down and occasion more or less 
 extensive ulcerations. 
 
 Tuberculosis of the tonsils may be primary or secondary. In 
 the former case infection probably occurs from the invasion of 
 the crypts by tubercle-bacilli ; this condition is doubtless more 
 common than has generally been supposed. Secondary tonsillar 
 tuberculosis usually follows tuberculosis of the lungs or larynx. 
 In either case there are formed in the tonsils small tubercles which 
 rapidly increase in size, fuse, and subsequently undergo caseous 
 change. Discharge of the caseous matter upon the mucous sur- 
 face is not unusual, and occasions ulcer-like formations. Second- 
 ary infection of the cervical and submaxillar lymphatic glands 
 is not infrequent. 
 
 Syphilis may occur in the pharynx in the form of the primary 
 lesion or chancre, as mucous patches, or as gummata. The last 
 are prone to undergo ulceration with secondary cicatrization. 
 Extensive distortion of the pharyngeal structures may be the 
 result of the scar-formation. 
 
 Glanders and lepra sometimes invade the pharynx. 
 
 Typhoid ulcers are occasionally met with. 
 
 TUMORS. 
 
 Among the tumors of the pharynx, fibroma, lipoma, chondroma, 
 and papillomata are occasionally found on the soft palate, uvula, 
 or tonsils. Of the malignant tumors, sarcoma of the tonsils is 
 most important. It is usually of the lymphosarcomatous variety, 
 
DISEASES OF THE O ASTRO-INTESTINAL TRACT. 481 
 
 and is rapid in growth and highly destructive. Epithelioma may 
 occur at the base of the tongue, in the soft palate, or tonsils. 
 Other varieties of cancer are rare. 
 
 Polypoid tumors of the nasopharynx and hyperplastic adenoid 
 growths of the same situation frequently extend downward into 
 the pharynx proper. 
 
 THE SALIVARY GLANDS. 
 
 Inflammation of the salivary glands affects the parotid most 
 frequently. 
 
 Parotitis may be the expression of an independent infection 
 (mumps) ; or may be secondary to various infectious diseases, 
 such as typhoid fever, typhus fever, or pyemia. 
 
 The specific cause of mumps has not been isolated (see Part I.). 
 The infection probably occurs through the parotid duct, and in 
 some instances inflammations of the mucous membrane of this 
 duct have been found to precede the parotitis. The gland is 
 swollen and tensely distends its capsule. The inflammatory exu- 
 date is probably largely serous, as it may be absorbed and removed 
 in the course of a very short time. The disease scarcely ever 
 terminates in suppuration. Orchitis is an occasional complication. 
 
 The secondary parotitis occurring in the course of various infec- 
 tious diseases is characterized by a marked tendency to abscess- 
 formation, and at all stages of the affection round-cell infiltration 
 is conspicuous. After the formation of an abscess perforation may 
 take place upon the cheek or into the mouth, and sometimes sali- 
 vary fistulse (see below) are established. Chronic induration of 
 the gland may remain after attacks of inflammation. 
 
 The submaxillary gland is occasionally affected with the 
 parotid, or independently, in, mumps. The sublingual gland 
 rarely becomes inflamed. 
 
 Angina I,udovici, or I^udwig'S angina, is a septic inflam- 
 mation of the tissues of the floor of the mouth surrounding the 
 submaxillary gland. It may result from carious processes at the 
 roots of the teeth, or from infection of the submaxillary lymphatic 
 glands in the course of various infectious diseases, particularly 
 scarlet fever. The most frequent termination is abscess-formation, 
 with perforation externally or into the mouth. Occasionally rapid 
 necrosis or gangrene results. 
 
 Tumors. — The parotid gland is more frequently the seat of 
 tumors than the other salivary glands. Benign tumors, such as 
 fibroma, lipoma, or chondroma, are rare. The most common new 
 growth is the so-called " mixed tumor," which is essentially sarT 
 comatous, with the addition of fibroma, chondroma, or myxoma, 
 and at times of all these. Epithelioma is rare. 
 
 Diseases of the Salivary Ducts. — Salivary fistulce may 
 
482 TEXT-BOOK OF PATHOLOGY. 
 
 result from traumatic injuries or from the perforation of abscesses. 
 They most frequently affect the duct of the parotid. 
 
 Concretions composed of phosphate and carbonate of calcium 
 are occasionally observed, and may lead to obstruction of the ducts. 
 
 Cystic dilatation of Steno's or Wharton's duct, or of those of 
 the sublingual glands, may be due to concretions or to inflam- 
 matory processes at the mouths of the ducts. Oval or elliptical 
 tumors are formed, and contain transparent, viscid liquid. Such 
 cysts belong to the group of conditions designated as ranula, but 
 more frequently this is due to obstruction of the small mucous 
 glands beneath the tongue. 
 
 THE ESOPHAGUS. 
 
 CONGENITAL DEFECTS. 
 
 Occasionally the esophagus is double, being divided into two 
 parts by a septum. Complete absence of the esophagus may occur 
 in certain monstrosities ; more frequently there is partial absence 
 of the lumen about the middle of the tube. The lower end of the 
 esophagus in such cases communicates with the trachea, while the 
 upper end terminates as a blind pouch. The intermediate defec- 
 tive portion may be represented by a fibromuscular cord, or may 
 be entirely wanting. Fistulous communications may pass from the 
 side of the neck to the upper end of the esophagus or pharynx. 
 They are due to incomplete closure of the branchial clefts. 
 
 CIRCULATORY DISTURBANCES. 
 
 Anemia may be due to general anemia, and active hyper- 
 emia, to the irritation of hot liquids or chemicals. 
 
 Passive congestion results from diseases of the heart or 
 lungs, or from cirrhosis of the liver. In the latter condition 
 large varicosities may be established in the lower end of the 
 esophagus, due to the communications between the left coronary 
 vein of the stomach and the esophageal veins. 
 
 INFLAMMATIONS. 
 
 Catarrhal esophagitis is characterized by hyperemia and 
 desquamation of epithelium, with very little liquid secretion. It 
 may be due to the ingestion of irritating acid or alkaline liquids, 
 to scalding, or occasionally to direct traumatic irritation. Super- 
 ficial erosions are sometimes met with. 
 
 Chronic catarrhal esophagitis is found in cases of passive 
 congestion continued for a long time, and particularly in alcoholics. 
 The mucous membrane is thickened and dark in color. Occasion- 
 ally erosions are met with, and more commonly areas of hyper- 
 trophy of the mucosa. 
 
 Pseudomembranous esophagitis may result from exten- 
 
DISEASES OF THE GASTRO-INTESTINAL TRACT. 483 
 
 sion of pharyngeal diphtheria or pseudomembranous pharyngitis, 
 or it may be primary in rare instances. 
 
 Ulcerative esophagitis may occur as the result of pustular 
 eruption in small-pox, or in consequence of irritation of foreign 
 bodies. It is not unusual to find small or even large ulcers in 
 the mucosa of esophageal diverticula. These are occasioned by 
 the retention of food. Peptic ulcers similar to those occurring in 
 the stomach are occasionally found in the lower end of the esophagus. 
 
 Phlegmonous esophagitis is rare. It may result from the 
 extension of intense inflammation of the mucous membrane into 
 the submucous tissue, or to penetration of the mucosa by sharp 
 points of fish-bones and the like. 
 
 STENOSIS. 
 
 Stenosis of the esophagus may be due to the pressure of 
 tumors or aneurysms upon the esophagus, to the lodgement of 
 foreign bodies, to the growth of tumors in the esophageal walls, 
 or to stricture of the esophagus. The last most frequently results 
 from the healing of ulcerations caused by the swallowing of cor- 
 rosive liquids. Syphilitic strictures are rare. Carcinoma of the 
 esophagus may obstruct by the growth within or by the attendant 
 contraction of the walls. 
 
 DILATATION. 
 
 Dilatation of the esophagus may occur in the form of a 
 simple dilatation or ectasia, or in the form of diverticula. The 
 former variety is common at the lower 
 end of the esophagus, and is occasioned 
 by obstructions at the cardiac end of 
 the stomach, or at the point where the 
 esophagus passes through the diaphragm. 
 The dilatation may reach considerable 
 size. The mucous membrane is usually 
 thin and often ulcerated. 
 
 Diverticula may be of two kinds, 
 those due to pressure from within (pul- 
 sion-diverticula) and those due to trac- 
 tion from without (traction-diverticida) 
 (Fig. 225). The former are more com- 
 monly found in the upper portion of the 
 esophagus or the lower part of the phar- 
 ynx, and arise from the posterior wall 
 of the esophagus. They are due to thin- 
 ning of the muscular coat and to her- fig. 225.— Traction-diverticu- 
 nious protrusion of the mucous mem- ^om Birch e -mSflid). (m0difled 
 brane. They may reach considerable 
 size by gradual distention. The traction-diverticula are most fre- 
 
484 TEXT-BOOK OF PATHOLOGY. 
 
 quently found near the lower end, opposite the bifurcation of the 
 trachea. They are caused by adhesion of diseased bronchial 
 glands and subsequent contraction of the attachments. They 
 occupy the anterior wall of the esophagus and have a somewhat 
 funnel-shape. Perforation may occur, with the development of 
 septic infection of the pleura, pericardium, or lungs. Perforation 
 of the pulmonary arteries may lead to fatal hemorrhage. 
 
 PERFORATION AND RUPTURE. 
 
 The esophagus may be perforated by necrotic or suppurative 
 processes surrounding it, or as the result of ulcers proceeding from 
 within. Aneurysms of the thoracic aorta occasionally rupture 
 into the esophagus. Retropharyngeal abscesses and phlegmonous 
 inflammations of the deep cervical tissues may likewise discharge 
 into the esophagus. Perforation by ulcers beginning within may 
 be due to the lodgement of foreign bodies, or to the pressure of the 
 cricoid cartilage in cases of great asthenia (see Pharynx). Per- 
 foration of the lower end of the esophagus may result from pep- 
 tic ulcers or esophagomalacia due to regurgitation of gastric liquid 
 either before or after death. Spontaneous rupture of the esoph- 
 agus occasionally takes place. In these cases there is doubtless 
 always some antecedent weakness of the walls. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis of the esophagus is extremely rare, and most 
 frequently results from extension of tuberculous adenitis of the 
 bronchial glands. 
 
 Syphilis occasionally occurs in the form of ulceration and 
 cicatrization, leading to stenosis. 
 
 Thrash may extend from the mucous membrane of the mouth 
 and pharynx. 
 
 TUMORS. 
 
 Fibroma, myoma, lipoma, or even sarcoma may occur as some- 
 what polypoid submucous tumors, but are rare. PapiUomaba, in 
 the form of outgrowths of the mucous membrane, are more com- 
 mon. 
 
 The most important tumor is carcinoma, which is usually found 
 in the lower third, generally at the position where the left bronchus 
 crosses the esophagus. It may, however, be found at any part. 
 The squamous variety is the most common, though a few instances 
 of glandular carcinoma are recorded. The tumor usually involves 
 the entire lumen of the esophagus, projecting inward and forming 
 irregular elevations of the mucous membrane. Later, the growth 
 extends outward through the muscular coat to the fibrous outer 
 layer, and even to the surrounding tissues. Dilatation occurs 
 
DISEASES OF THE GASTRO-INTESTINAL TRACT. 485 
 
 above the tumor, and occasionally perforation results from ulcer- 
 ations caused by retained food. Local or more distant metastasis 
 may take place. 
 
 THE STOMACH. 
 
 CONGENITAL DEFECTS. 
 
 Complete absence of the stomach has been found in certain 
 monstrosities ; but stenosis or atresia of the pylorus, division by 
 the formation of septa, and hour-glass contractions have been more 
 frequently observed. In cases of transposition of the viscera the 
 stomach may be reversed in its position, the pylorus being on the 
 left side, the cardiac end to the right. 
 
 CIRCULATORY DISTURBANCES. 
 
 Anemia of the mucous membrane is found in cases of general 
 anemia, particularly in pernicious anemia. The mucosa has an 
 extremely pallid appearance, and is prone to undergo fatty degen- 
 eration and atrophy. 
 
 Hyperemia. — Active congestion occurs in the beginning stages 
 of inflammation of the mucous membrane of the stomach, and 
 results from irritating mechanical or chemical agents. The mu- 
 cosa is bright-red in color and may present minute hemorrhages. 
 Moderate hyperemia is functional during the period of digestion. 
 
 Passive hyperemia occurs as a result of obstructive heart-dis- 
 ease, or more particularly from obstruction of the portal circulation 
 by cirrhosis or other diseases of the liver. Pulmonary affections, 
 by interfering with the outflow of blood from the right side of the 
 heart, may also occasion congestion of the stomach. The mucosa 
 is dark-red in color, swollen, and often edematous. Minute 
 hemorrhages may occur, and small erosions may appear upon the 
 surface. The changes are more marked near the pyloric end of 
 the stomach. When the congestion has persisted for some time 
 dark-reddish or bluish pigmentation, usually occurring in punctate 
 form, is developed and chronic gastritis results. 
 
 Hemorrhage in the mucous membrane or from the mucous 
 membrane of the stomach results from a variety of causes. Small 
 petechias are met with in active or passive congestion and in acute 
 inflammations. They are also present in various infectious or 
 hemorrhagic diseases, such as purpura, scurvy, septicemia, and the 
 like, and in anemic affections like pernicious anemia. In many 
 cases punctiform hemorrhages are developed just before death. 
 
 Larger hemorrhages, and particularly hemorrhages into the 
 cavity of the stomach, result from intense passive congestion in 
 cardiac disease or cirrhosis of the liver, and from gastric ulcera- 
 tion or carcinoma. When large vessels have not been eroded the 
 
486 TEXT-BOOK OF PATHOLOGY. 
 
 blood escapes gradually, and may be vomited in a semidigested 
 and disorganized condition (coffee-ground vomit). This is pecu- 
 liarly significant of carcinoma. When one of the larger vessels 
 has been eroded large quantities of fresh blood may be vomited 
 and rapid death may occur. 
 
 Melcena neonatorum, the vomiting of blood by the new-born, 
 results from disturbances of circulation due to insufficient respira- 
 tion, and possibly in other cases is a variety of infectious hemor- 
 rhagic disease. 
 
 INFLAMMATION. 
 
 Acute inflammation of the mucosa, or acute gastritis, 
 
 results from irritation by chemical, mechanical, or thermal agents. 
 Some cases are doubtless due to infection. The mucous membrane 
 is bright-red and covered with more or less viscid mucous exu- 
 date. Punctate hemorrhages may occur. Microscopically there 
 are found : marked mucous degeneration of the cylindrical cells of 
 the tubules, and desquamation and granular degeneration of the 
 cuboidal cells in the fundus of the glands. The mucous mem- 
 brane between the tubules is infiltrated with round cells, and not 
 rarely the same process occurs in the submucosa. The collections 
 of lymphatic tissue (follicles) in the mucous membrane are often 
 hyperplastic. Acute gastritis is more frequently found near the 
 pyloric end than elsewhere. 
 
 Pseudomembranous gastritis may result from the inges- 
 tion of corrosive poisons, and is occasionally seen in small-pox, 
 typhus fever, and various forms of septicemia. It may be met 
 with in diphtheria, and may be due to direct extension of the 
 process along the esophagus. The surface of the mucosa is cov- 
 ered with an irregular membrane, and necrosis and ulceration 
 are not rarely observed, especially in cases due to corrosive 
 poisons. 
 
 Ulcerative Gastritis. — Small erosions may be found in 
 cases of extreme congestion or petechial hemorrhage, as well as 
 in acute gastritis. Actual ulceration is seen in pseudomembranous 
 gastritis, and occasionally as a result of septic embolism in the 
 mucosa in cases of malignant endocarditis. Infectious ulcerations 
 occur in gastro-intestinal tuberculosis and anthrax, and in typhoid 
 fever, but are very rare. 
 
 Chronic gastritis may result from repeated attacks of acute 
 gastritis, and is especially prone to occur from improper habits 
 of eating, or from the abuse of alcohol. Chronic congestion, such 
 as occurs in heart-disease, strongly predisposes. 
 
 Pathologic Anatomy. — The appearance of the mucous mem- 
 brane varies greatly. In the milder cases the surface is more or 
 less irregular and granular, and is covered with mucous exudate. 
 The color may be grayish, but in cases in which passive congestion 
 
DISEASES OF THE O ASTRO-INTESTINAL TRACT. 
 
 487 
 
 has preceded the development of gastritis it is often slate-colored 
 from pigmentation. 
 
 Microscopically there may be found mucous degeneration of 
 the cylindrical epithelium of the tubules, and desquamation and 
 not rarely proliferation of the secretory epithelium in the fundus 
 of the glands. The glands may be considerably dilated and filled 
 with mucous exudate and desquamated cells. The interglandular 
 tissues are infiltrated, and may be thickened by the formation of 
 new connective tissue ; the same process may involve the sub- 
 mucous coat. The blood-vessels of the latter are often greatly 
 dilated and their walls may be thickened. In the later stages 
 the glands may undergo progressive atrophy, the epithelium dis- 
 appearing almost entirely and the lumen of the gland becoming 
 less and less distinct. Coincidently with these changes, and 
 to some extent causing them, there is fibrous overgrowth of the 
 interglandular tissues. 
 
 In some instances the contraction of the new-formed connec- 
 tive tissue causes protrusions of the mucous membrane or polypoid 
 
 Fig. 226. — Chronic gastritis, showing polypoid projections of the mucosa. 
 
 elevations (Fig. 226). These may still further enlarge by pro- 
 liferation and cystic distention of their glandular elements. In 
 other cases the proliferative changes in the interglandular tissues 
 may be more diffuse and the mucous membrane more regularly 
 thickened. To both of these forms the name hypertrophic gas- 
 tritis may be applied. In still other cases the formation of fibrous 
 tissue causes pressure-atrophy of the glands ; the surface in these 
 cases becomes smooth and the mucosa greatly thinned 
 
 The sclerotic process may involve not only the mucous mem- 
 brane, but also the submucous and even the muscular coat. In 
 
488 TEXT-BOOK OF PATHOLOGY. 
 
 such cases the thickness of the wall of the stomach may increase 
 greatly, and the size of the organ greatly diminish by contraction. 
 The term interstitial gastritis, or gastrophthisis, may be applied to 
 such cases. 
 
 Pathologic Physiology in Gastritis. — All forms of gas- 
 tritis cause disturbances of the functions of the stomach, desig- 
 nated by the terms dyspepsia and indigestion. These disturbances 
 are due to abnormal secretion of the gastric glands, reduced motor 
 power of the walls of the stomach, and altered conditions of the 
 nervous mechanism. The most important alteration of secretion is 
 reduction of the amount of hydrochloric acid. This is almost 
 constant in uncomplicated gastritis ; in some cases there is practi- 
 cally no hydrochloric-acid secretion. The ferments, pepsin and 
 curdling ferment, may be produced in insufficient amount, but are 
 very rarely absent. In cases in which certain general conditions or 
 nervous affections coexist with moderate gastritis, excess of hydro- 
 chloric-acid secretion occurs. Reduction in the amount of hydro- 
 chloric acid causes delay and inadequacy of digestion of proteids. 
 When the acid is wholly wanting decomposition of the proteids 
 may occur, and sulphuretted hydrogen and other products of 
 decomposition result. Excess of hydrochloric acid interferes with 
 salivary digestion in the stomach, and in consequence fermentation 
 of carbohydrates, with production of lactic, butyric, or acetic acid 
 and of various gases, takes place. Such fermentation, however, is 
 not, as a rule, observed unless the motor power of the stomach is defi- 
 cient and the food is retained in the stomach beyond the usual time. 
 It is not improbable that toxic substances are produced in some cases 
 by proteid decomposition, but accurate observations are wanting. 
 
 The motor power is usually deficient in proportion to the inten- 
 sity of the gastric disease. In some cases the food is retained 
 many hours longer than the usual periods, and fermentation 
 and decomposition are thus greatly favored. Dilatation of the 
 stomach may be brought about by the retention of food and the 
 accumulation of gases of decomposition, and the dilatation in turn 
 increases the motor insufficiency of the stomach. 
 
 Altered conditions of the nervous mechanism of the stomach 
 manifest themselves in a variety of ways. Sometimes there is 
 excessive irritability of the mucosa, causing vomiting ; in other 
 cases a feeling of heaviness, or pain. Alterations of appetite and 
 of gastric motility are other results probably brought about, in 
 part at least, through nervous disturbances. 
 
 The general metabolism suffers profoundly in gastric disease — 
 mainly in consequence of the insufficient food eaten or digested. 
 Emaciation and systemic depression are the clinical consequences. 
 It is probable that toxic substances produced in the stomach 
 contribute to the metabolic disturbances, but this remains to be 
 proved. 
 
DISEASES OF THE OASTRO-INTESTINAL TRACT. 489 
 
 PEPTIC ULCER. 
 
 Peptic or round ulcers of the stomach are most frequently 
 found in anemic young women, and are probably due to the 
 digestive action of the gastric juice. Similar lesions may occur 
 in the upper end of the duodenum and in the lower end of the 
 esophagus. 
 
 Etiology. — The great majority of the cases occur in young 
 women, and particularly in those suffering with chlorosis or 
 anemia and general malnutrition. The pathogenesis of these 
 ulcers has occasioned much. dispute. It is admitted that they are 
 due to the action of the gastric juice upon parts of lowered vitality, 
 and the term ulcus ex digestione is therefore appropriate. The 
 increased acidity of the gastric juice in chlorosis is an important 
 factor. The lowered vitality which localizes the ulceration has 
 been ascribed to many causes. Embolism or thrombosis with 
 infarction was suggested by the shape of the ulcers, and may be 
 the explanation for some cases. Spasm of the blood-vessels in 
 
 
 
 Fig. 227.— Peptic ulcer, showing erosion into a blood-vessel in the floor of the ulcer 
 (Bollinger). 
 
 localized areas, and thickening of the walls of the vessels, leading 
 to anemia, have been suggested, as have also direct traumatic 
 injuries of the mucous membrane and external traumatism, causing 
 rents of the mucous surface. Circulatory disturbances due to 
 tight lacing are supposed by some to be important. 
 
 Pathologic Anatomy. — Peptic ulcers may be single, but are 
 more often multiple. They are commonly situated in the lesser 
 curvature and the posterior wall of the stomach, near the pylorus ; 
 occasionally they are found at the fundus or at the cardiac 
 end. They vary in diameter from a few millimeters to three or 
 
490 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 five centimeters. Their shape is characteristic in that they have 
 sloping edges, giving them a funnel-form, with the apex toward 
 the muscular coat. The edges may be irregular and rough but 
 are often, especially in older ulcers, quite smooth and rounded. 
 
 w 
 
 rith perforation (Bollinger). 
 
 Two dangers are always imminent, hemorrhage and perfora- 
 tion. Constant oozing of blood may be due to erosion of the surface, 
 and laro-er hemorrhages may result from ulceration of one of tne 
 larger arterial branches of the stomach (Fig. 227). Perforation 
 
 Fig. 229— Stellate scar of a healed ulcer of the stomach (Bollinger). 
 
 is less common than hemorrhage. When the ulcer is situated 
 posteriorly perforation is prevented by adhesions attaching the 
 stomach to the head of the pancreas or other structures. A\ hen 
 the ulcer is in the anterior wall perforation is more liable to take 
 
DISEASES OF THE GASTRO-INTESTINAL TRACT. 491 
 
 place (Fig. 228). The rupture may occur into the peritoneal cav- 
 ity or into any of the surrounding structures, and fistulous com- 
 munications may be established with the pleural or pericardial 
 cavities, or even with the exterior through the abdominal walls. 
 Abscesses of the liver, spleen, or pancreas may result from per- 
 foration into these organs. 
 
 In the healing of the ulcers scars are formed in the wall of 
 the stomach. These have usually a rather characteristic stellate 
 shape (Fig. 229). In case of large ulcers extensive scars and 
 considerable contraction of portions of the walls of the stomach 
 result. Hour-glass contraction of the organ, or pyloric stenosis, 
 may follow, and secondary changes, such as gastric dilatation, may 
 ensue. Carcinomatous transformation is a not infrequent result 
 of long-standing ulceration. 
 
 ATROPHY AND DEGENERATIONS. 
 
 Atrophy of the glands or gastric tubules is frequently seen in 
 chronic gastritis. The same condition occurs as a senile change 
 and in association with various chronic diseases, especially perni- 
 cious anemia. A certain amount of atrophy of the entire mucous 
 membrane results in a purely mechanical way from gastric dila- 
 tation. 
 
 Decrease in the size of the stomach as a whole may be the re- 
 sult of chronic gastritis, when the new-formed connective tissue 
 contracts. In such cases the stomach may become quite small, 
 the walls, however, increasing in thickness. Somewhat similar 
 shrinkage in the size of the stomach occurs in some instances of 
 infiltrating cancer of the stomach. The tumor may involve all 
 parts of the organ equally, and cause more or less thickening of 
 its walls, but the size of the organ is diminished by contraction of 
 the connective tissues. 
 
 A form of true atrophy is sometimes caused by obstruction of 
 the cardiac orifice ; it is probably due, in part at least, to the in- 
 sufficiency of food admitted to the stomach. 
 
 Degenerations of the mucous membrane of the stomach are 
 met with in association with inflammation or as independent affec- 
 tions. 
 
 Fatty degeneration of the epithelial cells of the glands may be 
 the result of intoxications (phosphorus, arsenic), or of conditions 
 such as those which lead to simple atrophy. The occurrence of 
 atrophy and fatty degeneration of the gastric tubules in cases of 
 pernicious anemia is of great importance, though it remains un- 
 settled whether these conditions are the cause or result of the 
 anemia. Recent investigations would indicate that frequently 
 they are the cause. 
 
 Pigmentation is met with as a result of chronic congestion or 
 
492 TEXT-BOOK OF PATHOLOGY. 
 
 hemorrhage into the mucous membrane. The mucosa has a dark- 
 red or often a slaty discoloration, which is prone to be distributed 
 in lines or in circumscribed patches. Bluish pigmentation of the 
 stomach sometimes occurs from the ingestion of silver. 
 
 Amyloid degeneration may be found around the blood-vessels 
 of the submucosa, or more rarely of the mucosa itself, in cases of 
 general amyloid disease. Amyloid ulcerations may occur. 
 
 Calcification has been met with in cases of bone-disease with 
 surcharge of the blood with earthy salts. It appears in the form 
 of scales or plates of calcification upon the mucosa. 
 
 Gastromalacia, or simple softening of the walls of the stomach, 
 is usually a post-mortem condition, and is due to the action of the 
 gastric juice. The nature of this process has occasioned much 
 discussion, but it is now recognized as a post-mortem condition, or 
 as a condition occurring during life only in the agonal period. It 
 affects the fundus or posterior part of the stomach. The mucous 
 membrane becomes soft and more or less gelatinous, and is grayish 
 or yellowish in color if the mucosa Mas anemic, or brownish in 
 cases in which there was congestion before death. Rupture and 
 discharge of the contents of the stomach into the peritoneal cavity, 
 spleen, or other adjacent organs may occur. The walls of the 
 stomach in the affected area show granular degeneration of the 
 component cells, but no evidences of inflammatory reaction, and 
 when rupture has occurred there are no reactive inflammatory 
 lesions of the peritoneum, showing that the perforation occurred 
 after death. 
 
 ALTERATIONS IN POSITION AND SIZE. 
 
 Alterations in Position. — The stomach may be displaced 
 into the thoracic cavity in cases of perforation or rupture of the 
 diaphragm (diaphragmatic hernia). It may be displaced ante- 
 riorly as a congenital malposition in consequence of defects of the 
 anterior abdominal walls, and may in such cases be quite exposed. 
 Downward dislocation, or gastroptosis, is either congenital or ac- 
 quired. The acquired form may be due to diseases of the stomach, 
 particularly dilatation, to the traction of inflammatory adhesions, 
 to enlargement of the spleen, and possibly to tight lacing. Occa- 
 sionally in anemic and relaxed women all of the abdominal viscera 
 tend to descend (splanchnoptosis). 
 
 Dilatation, or gastrectasia, most frequently results from 
 obstruction of the pylorus. The latter may be due to cicatri- 
 zation the result of the healing of ulcers, to fibroid overgrowth 
 and contraction the result of chronic gastritis, or to pyloric carci- 
 noma. The pressure of tumors, of a movable kidney, or of aneur- 
 ysms may act similarly. At first, pyloric stenosis may be com- 
 pensated by hypertrophy of the muscular layer of the stomach, 
 
DISEASES OF THE GASTRO-INTESTINAL TRACT. 493 
 
 but soon dilatation occurs ; food stagnates, fermentation takes 
 place, and the dilatation is increased. The mucosa becomes thin 
 and ofttimes degenerated and atrophic. 
 
 A second group of cases (atonic dilatation) is independent of 
 stenosis of the pylorus, but due to weakness of the walls of the 
 stomach. The latter may be the result of chronic gastritis, or 
 of a general atonic state. Constant overeating may play an im- 
 portant part in some cases. Finally, dilatation may result 
 mechanically from abnormal adhesions of the stomach. 
 
 Dilatation of the stomach occasions great stagnation of food, 
 and in consequence imperfect digestion and decomposition of the 
 food. When hydrochloric acid is absent (as in cancerous stenosis 
 of the pylorus and marked atonic dilatation) lactic-acid fermenta- 
 tion is pronounced ; when hydrochloric acid is present lactic acid 
 is less abundant. Sulphuretted hydrogen and inflammable gases are 
 occasionally formed, especially in cases in which hydrochloric acid 
 is present. The mucous membrane of dilated stomachs loses its 
 absorptive power to a large degree. This, together with the reten- 
 tion of ingested liquid in the stomach and the consequent cessation 
 of intestinal absorption, leads to great emaciation, and especially 
 to desiccation of the tissues. 
 
 Among the micro-organisms met with in the gastric contents 
 the Sarcinas ventriculi are of interest. These occur in bundles of 
 peculiar square form. The sarcina is more frequent in non- 
 cancerous than in cancerous dilatation. 
 
 INFECTIOUS DISEASES. 
 
 A few cases of tuberculous ulceration have been recorded, and 
 syphilitic gummata may occur. Diffuse cirrhosis and ordinary 
 gastritis may be dependent upon syphilis, but the etiologic con- 
 nection is uncertain. Anthrax may lead to necrotic and hemor- 
 rhagic ulcers of the mucosa. Thrush is rarely met with, though 
 the spores of saccharomyces are frequently present in the stomach 
 when the mouth is affected. 
 
 TUMORS. 
 
 Connective-tissue Tumors. — Fibroma, myoma, and lipoma 
 are occasionally met with as submucous or subserous polypoidal 
 tumors. Sarcoma is rare. It atfects the lymphoid tissues of the 
 deeper parts of the mucosa, and rapidly spreads to the submucosa 
 (Fig. 230). Most cases are of the round-cell variety. Lympho- 
 sarcoma of the adenoid tissues of the stomach may be one of the 
 lesions of leukemia or Hodgkin's disease. 
 
 Epithelial Tumors. — Polypoid elevations, sometimes with 
 cystic enlargement of the glands, occur as a result of chronic 
 inflammation, and may be large enough to be regarded as tumors 
 
494 
 
 TEXT-BOOK OF TATHOLOGY. 
 
 in a clinical sense. Adenomatous proliferation of the glands is 
 met with in the form of irregular, flat tumors, but these so rap- 
 idly become carcinomatous that pure adenoma scarcely exists. 
 
 $ i f 
 
 it 
 
 •'/*w*i» 
 
 Fig. 230.— Sarcoma of the stomach, involving all of the coats; the original growth prob- 
 ably occurred in the mucosa and submucosa. 
 
 Carcinoma is the most frequent tumor of the stomach. It 
 occurs in advanced years, and more often in the male sex than in 
 
 0& 
 
 
 IP ** ! ^ 
 
 Fig. 231.— Fragment of carcinomatous tissue found in stomach-washings (Reinevoth). 
 
 the female. The pyloric end of the organ and the lesser curva- 
 ture are the favorite sites, but other parts may be affected and the 
 entire organ may be involved. Cancer of the stomach may appear 
 
DISEASES OF THE OASTRO-INTESTINAL TRACT. 
 
 495 
 
 as a ring-like swelling of the mucous membrane and submucous 
 tissue, surrounding the pylorus and causing stenosis ; as more or 
 less circular, flat elevations in the lesser curvature or elsewhere ; 
 and, finally, as a diffuse infiltration of the mucosa, submucosa, or 
 all of the coats of the entire organ. The mucous surface is 
 generally irregularly elevated, and tends to become ulcerated, 
 especially in the soft variety of cancer and in the cases in 
 which there are localized flat elevations. Sometimes portions 
 of the cancerous tissue may be found in the vomita, and the 
 diagnosis of the disease may be thus established (Fig. 231). 
 
 Fig. 232.— Carcinoma of the cardiac end of the stomach ; extension into duodenum : S, 
 dilated esophagus; K, ulcerated carcinoma; G, a perforating ulceration; M, stomach 
 (Orth). 
 
 Perforation of the wall of the stomach may result from necrotic 
 and ulcerative processes (Fig. 232). The neighboring lymphatic 
 glands, especially those in the lesser curvature of the stomach, 
 are usually implicated through the lymphatic vessels. Direct 
 extension to the peritoneum may occur, especially in cases of col- 
 loid cancer ; and metastasis through the blood-vessels is extremely 
 common. Cancerous emboli are frequently found in the portal 
 radicles within the liver, and multiple cancer-nodes of the liver 
 are usually found in cases which have existed for some length of 
 time. Hematogenous metastasis is most common in soft, ulcer- 
 ating cancers. 
 
 Varieties. — There may be distinguished hard or scirrhous 
 cancers, soft or medullary cancers, adenocarcinomata or malignant 
 adenomata, cylindrical-celled, and squamous-celled carcinomata. 
 All forms begin in the mucous membrane and spread rapidly to 
 the submucosa. The muscularis may be penetrated and infil- 
 tration of the serosa, or even of surrounding tissues, may be 
 observed. 
 
496 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 Scirrhous cancer may appear as a circular constricting new 
 growth at the pylorus (Fig. 233). In other cases the disease is 
 extensive, and the entire organ may be involved by uniform infil- 
 tration, and macroscopically the appearance of a simple cirrhosis 
 
 
 Fig. 233.— Scirrhus of the pylorus, causing pyloric stenosis: D, duodenum ; P, pylorus; 
 A', carcinomatous projections on the mucosa (Orth). 
 
 of the stomach is presented. The mucous surface in scirrhus 
 rarely ulcerates. 
 
 Encephaloid or soft cancer usually appears as a localized 
 tumor at the pylorus or in the lesser curvature. The mucous 
 
 Fig. 234.— Cauliflower carcinoma of pylorus : M, stomach : P, pylorus; D, duodenum 
 (Orth). 
 
 membrane is irregularly elevated, ofttimes in a cauliflower man- 
 ner (Fig. 234). Ulceration on the surface is common, and hem- 
 orrhagic extravasation into the stomach is therefore frequent. 
 Metastasis through the blood is liable to occur. Complete per- 
 foration of the stomach may take place. 
 
DISEASES OF THE QASTRO-INTESTINAL TRACT. 497 
 
 Malignant adenoma, or adenocarcinoma, begins as a prolifera- 
 tion of gastric tubules. The new-formed acini are, however, 
 atypical in arrangement and number, and there is a tendency to 
 conversion of the normal cylindrical cells into cuboidal cells, 
 and to extensive cancerous infiltration by destruction of the 
 basement-membrane of the acini. The appearance of the tumor 
 and its tendencies are the same as those of soft cancer. 
 
 Cylindrical cancer, or cylindrical epithelioma, probably springs 
 from the cylindrical lining cells of the stomach, or from the cells 
 in the upper parts of the tubules. Atypical tubular aggregations 
 of cylindrical cells with a tendency to conversion into cuboidal 
 cells are observed. The pylorus is the common seat. 
 
 Squamous cancer occurs at the cardiac end, and generally in 
 association with carcinoma of the lower end of the esophagus. It 
 is rare. 
 
 Colloid cancer of the stomach appears as a localized, or more 
 frequently, diffuse infiltrating, gelatinous new growth of the mucosa 
 and submucosa. Rapid extension through the walls of the stom- 
 ach and to the peritoneum is frequent. The degeneration may 
 affect different forms of cancer, but especially the cylindrical 
 variety. The cells and the stroma of the tumor show myxomatous 
 degeneration ; and the epithelial elements may in the later stages 
 entirely disappear. Extensive invasion of the peritoneum is not 
 infrequent. 
 
 Pathologic Physiology and Results. — Carcinoma of the 
 stomach is most frequently situated at or near the pylorus, and 
 therefore interferes with the propulsion of food. Stagnation of 
 the stomach-contents and fermentation result. The latter is 
 favored by the absence of hydrochloric-acid secretion so habitually 
 observed. In consequence of the stagnation the stomach dilates 
 and may reach enormous size, not rarely filling a large part of the 
 abdominal cavity. Lactic-acid fermentation is frequently pro- 
 nounced. Among the micro-organisms present in the stomach- 
 contents a long, thread-like bacillus has attracted much attention, 
 and has been supposed by some to occur only in cancer of the 
 stomach. It is certainly frequent, but just as certainly not peculiar 
 to the disease. Disturbances of metabolism, with loss of flesh and 
 strength, are marked. 
 
 THE INTESTINES. 
 CONGENITAL AND ACQUIRED ABNORMALITIES. 
 
 Occasionally total absence of large parts of the intestinal tract 
 is found in monstrosities. Lesser defects, leading to narrowing or 
 distortion of the intestines, are more frequent. Marked develop- 
 mental defects most frequently occur in the rectum, which may 
 
 32 
 
498 TEXT-BOOK OF PATHOLOGY. 
 
 be completely absent, or may be obliterated at the lower end. In 
 such cases there may be fistulous communications with the uro- 
 genital tract, or there may be a persistent cloaca, as in fetal life. 
 
 Congenital Enlargement of the Intestines. — The colon 
 is most apt to be affected, and may be greatly enlarged. 
 
 Diverticula. — Localized dilatations, constituting diverticula, 
 are frequent, the most common form being the Meckel's diverticu- 
 lum. This usually arises from the ileum, about a meter above the 
 ileocecal valve, and is attached to the intestine opposite the mesen- 
 tery. It represents the remains of the omphalomesenteric duct 
 of fetal life. Occasionally it has been found patulous to the um- 
 bilicus. More commonly there is merely a short diverticulum of 
 the intestines, varying from a few to several centimeters in length, 
 and having a closed extremity which may be somewhat dilated. 
 The extremity may be connected with the umbilicus by a cord, 
 but is usually free. 
 
 Diverticula are also formed in later life. Very commonly, in 
 cases of constipation, small pouchings or dilatations occur in the 
 large intestine, particularly in the descending colon and rectum. 
 Another form affects the small intestine more commonly than the 
 large bowel. In this there are found small pouches lying near the 
 mesenteric attachment, and owing their origin to localized weak- 
 ness or separation of the muscle-fibers of the bowel. Protrusion 
 of the mucosa takes place, probably, as a result of pressure from 
 within; and the pouch is therefore a hernious projection of the 
 mucosa and serosa. Such diverticula may be multiple or single. 
 
 Congenital Abnormalities in Position. — The position of 
 the several parts of the intestinal tract may vary widely from the 
 normal. Not rarely the ascending colon and cecum are situated 
 on the left side ; the sigmoid flexure and descending colon being 
 on the right side. Other abnormalities of position, of less practi- 
 cal importance, are frequent. 
 
 Enterocystoma. — A congenital cystic condition found at 
 the umbilicus has been described as cystic dilatation of parts of 
 the original omphalomesenteric system of the fetus, and has been 
 named enter* (cystoma. 
 
 Dilatation. — More or less uniform enlargement of the intes- 
 tines may result from long-standing constipation. Enormous 
 dilatation of the colon is sometimes seen. In this the wall of the 
 intestine undergoes compensatory hypertrophy, and small pouch- 
 ings or diverticula are commonly observed, especially in the rectum. 
 
 Narrowing, or stenosis, of the intestine at any part may be 
 due to pressure of new growths or displaced viscera, to cicatricial 
 constrictions following ulcerations, or to neoplasms. Cicatricial 
 stenosis is particularly common in the rectum following dysenteric 
 ulcer. Narrowing of the lumen may be due to an ingrowth of car- 
 cinoma or the presence of papillomatous or polypoid tumors within. 
 
DISEASES OF THE GASTBO-INTESTINAL TRACT. 499 
 
 Hernia. — This term is applied to malposition of any of the 
 viscera, with displacement of the organ from the cavity in which 
 it normally lies ; but it has been more particularly applied to such 
 displacements of the intestines ; and the single term hernia is 
 significant of intestinal hernia. 
 
 Occasionally hernise are congenital ; more often they are 
 acquired. Hernia occurs at the points where the abdominal walls 
 or the peritoneum is naturally weak from the emergence of vessels 
 or the existence of natural outlets. 
 
 Etiology. — The predisposition to hernia may consist in un- 
 natural weakness of the abdominal wall, especially at the points 
 where hernia is likely to occur, resulting from imperfect 
 closure of such portions or from general muscular weakness. 
 Abnormal movability of the intestines, resulting from natural or 
 acquired elongation of the mesenteric attachments and increased 
 weight of the abdominal contents from the deposit of peritoneal 
 fat, contributes largely to the formation of hernia?. The imme- 
 diate exciting cause in many cases is strain, and probably in all 
 cases repeated strain helps in the development of the protrusion. 
 The most frequent form of ventral hernia is the umbilical, which 
 occurs especially in infants as the result of imperfect closure of 
 the abdominal walls at the umbilicus. 
 
 There may be distinguished two groups or varieties — the inter- 
 nal and the external hernise. 
 
 Internal Hernia. — By this term are designated hernious dis- 
 placements of the intestines into other cavities within the body, 
 the most important being upward displacement into the thorax 
 through congenital or acquired clefts of the diaphragm {diaphrag- 
 matic hernia); and backward displacement through the peri- 
 toneum into the retroperitoneal space (retroperitoneal hernia). 
 
 External hernia may be inguinal, femoral, ventral, vaginal, 
 rectal, perineal, ischiatic, or obturator. The most frequent of these 
 are the inguinal and the femoral. In the former the protrusion may 
 occur through the external inguinal ring, the intestine descending 
 through the inguinal canal, sometimes as far as the scrotum (in- 
 direct inguinal hernia). In another group of cases the intestine 
 pushes directly forward through the internal inguinal ring, and 
 may present anteriorly under the skin, or may descend through 
 the lower part of the inguinal canal to the scrotum (direct inguinal 
 hernia). The indirect inguinal hernise are sometimes congenital, 
 and are due to the failure of closure of the peritoneal reflection 
 which passes downward through the inguinal canal. 
 
 Femoral hernia? are especially common in women, and are 
 formed by the protrusion of the intestine through the femoral 
 ring, the hernia presenting on the inner side of the thigh, at the 
 position of the saphenous opening. 
 
 Pathologic Anatomy. — The hernia consists of a sac or wall 
 
500 TEXT-BOOK OF PATHOLOGY. 
 
 and of the contents of the hernia. The sac is usually constricted 
 at its junction with the general peritoneal cavity (neck), and dis- 
 tended and dilated outside of or below this point (fundus or body 
 of sac). The sac of the hernia is always lined with the protruded 
 portion of the peritoneum. The contents of the hernia may be 
 coils of intestine or portions of omentum, or both. Most fre- 
 quently some part of the small intestine occupies the hernia, and 
 sometimes simply a Meckel's diverticulum has been discovered. 
 In rare cases the sigmoid flexure or other parts of the great bowel 
 may be found. 
 
 Secondary changes often ensue. Inflammation of the lining 
 membrane of the sac and of the intestinal coils may lead to fibrous 
 adhesions constricting the neck of the sac and binding the intes- 
 tines firmly in place. If the contents of the hernia have receded, 
 such inflammation may obliterate the sac completely or merely at 
 its neck, the body of the sac in the latter case becoming distended 
 with serous liquid. In cases in which portions of omentum are 
 included in the hernia hypertrophic overgrowth of the adipose tis- 
 sue may occur, and may lead to appearances not unlike those of a 
 lipoma. 
 
 Hernia? are described as being reducible and irreducible, accord- 
 ing to the ability of replacing the contents into the peritoneal 
 cavity or not. Hernise become irreducible when the coils of 
 intestine are distended by the accumulation of fecal matter, when 
 fibrous adhesions have narrowed the neck of the sac or bound the 
 coils firmly in place, or when additional coils of intestine or por- 
 tions of the omentum have descended into the hernia. 
 
 Strangulated Hernia. — This term is applied to hernise in which 
 pressure at the neck by inflammatory exudation or constriction, or 
 inveterate obstruction by accumulating contents of the bowel, has 
 led to obstruction of the circulation in the intestinal coils of the 
 hernia. Intense passive congestion, inflammation of the peritoneal 
 covering of the intestines within the hernia, and, finally, gangre- 
 nous necrosis are the frequent results. 
 
 INTESTINAL OBSTRUCTION. 
 
 Complete obstruction of the intestines, or ileus, may be due to 
 internal strangulation by bands of adhesions, to a twist or volvulus, 
 or to intussusception or invagination. 
 
 Internal strangulation may be due to the obstruction of a 
 coil of intestine by fibrous peritoneal adhesions, or by a coil slip- 
 ping through abnormal openings or perforations in the mesentery 
 or omentum. The persistence of the cord passing from the end 
 of a Meckel's diverticulum to the umbilicus is an unusual cause. 
 
 The results of internal strangulation are generally serious. 
 Great dilatation occurs above the point of obstruction, the intes- 
 
DISEASES OF THE G ASTRO-INTESTINAL TRACT. 
 
 501 
 
 tine below becoming collapsed. Great congestion and subse- 
 quently peritonitis occur at , the point of stricture, and necrosis 
 with perforation may ensue. 
 
 Volvulus is the term applied to a twist of some part of the 
 intestinal canal. Occasionally there is simple rotation of the 
 bowel about its own axis, but more commonly a loop of intestine 
 twists about its mesenteric attachment. Abnormal laxity of the 
 mesentery is an important predisposing cause, and may be a con- 
 genital condition, or may result from the absorption of fatty 
 deposit between the mesenteric layers. The immediate cause is 
 generally strain or abdominal compression. 
 
 The most frequent seat of volvulus is the sigmoid flexure. 
 The bowel above the point of obstruction becomes distended, as in 
 internal strangulation, while the coil included in the twist itself is 
 engorged with blood and frequently presents hemorrhagic infarc- 
 tions in consequence of the obstruction of the vessels in the mesen- 
 tery. Complete knots are occasionally observed in volvulus. 
 
 Intussusception, or invagination, is a condition in which 
 one part of intestine slips into an adjoining part, as one may in- 
 vert the finger of a glove (Fig. 235). The 
 upper part of the intestine is usually indupli- 
 cated and pushed into the lower part. Ir- 
 regular peristalsis, resulting from intestinal 
 disorders, and particularly from atony of one 
 part with increased activity of adjoining 
 parts, is the most frequent cause. Occa- 
 sionally polypoid tumors within the bowel 
 are dragged forward by the peristalsis, and 
 carry the higher part of the intestine to 
 which they are attached into the lower part. 
 Intussusception is more common in children 
 than in adults, and aifects the ileocecal region 
 most commonly. Not infrequently multiple 
 invaginations are found in the small intes- 
 tine of children ; these probably occur during 
 the death-agony or post-mortem. 
 
 The appearance of intussusception is sim- 
 ply that of one part of intestine pushed into 
 the adjoining part, with secondary inflam- 
 matory and congestive changes. Most fre- 
 quently invagination begins at the ileocecal 
 region, the valve and ileum being carried 
 forward into the ascending colon. Very 
 
 rarely the ileum itself invaginates through the valve. The 
 attachment of the mesentery leads to a sharp angulation of the 
 area of invagination, and the extent to which the protrusion may 
 occur will depend upon the length of the mesentery. Occasionally 
 
 Fig. 235.— Intussuscep- 
 tion (from a specimen in 
 the Museum of the Phila- 
 delphia Hospital). 
 
502 TEXT-BOOK OF PATHOLOGY. 
 
 the ileocecal valve may be carried through the colon and rectum 
 and present externally. The adjoining serous surfaces of the in- 
 vagination tend to unite by peritonitis, and the intussuscepted 
 portion may become gangrenous and be discharged. If peritonitis 
 has established union between the ensheathed and the ensheathing 
 section of the gut, recovery may ensue. Otherwise the perforation 
 leads to fatal peritonitis. 
 
 PROLAPSE OF THE RECTUM. 
 
 Prolapse of the rectum in consequence of weakness of the 
 sphincter and other parts of the wall, together with repeated 
 straining, is a common condition in infants, and is occasionally 
 met with in adults. In children any form of diarrhea may be 
 complicated by prolapse ; in adults chronic proctitis is the most 
 frequent cause. The weakened condition of the sphincter in 
 proctitis furnishes the predisposition, and the characteristic tenes- 
 mus of the disease is the immediate cause. Prolapse may be only 
 an occasional condition, or may be constant. Secondary inflam- 
 mation, ulceration, and even necrosis of the prolapsed portion 
 may occur. 
 
 ATROPHY AND DEGENERATIONS. 
 
 Atrophy of the mucosa is frequently met with as a part of 
 chronic enteritis in its later stages. This is especially marked in 
 young children suffering from chronic intestinal catarrh and 
 marasmus. Occasionally atrophy of the mucosa or of all of the 
 coats of the intestines may occur as an independent affection, as 
 the result of marantic or cachectic conditions. 
 
 Pigmentation. — Pigmentation may be due to hemorrhages 
 in the mucosa or submucosa, and not infrequently after intense 
 hemorrhagic inflammation the bowel may be quite black from the 
 deposit of hematogenous pigment. Brownish pigment deposited 
 in the muscle-cells, analogous to that of brown atrophy of the 
 heart, is occasionally observed in old and cachectic individuals. 
 Similar pigmentation of the muscle-cells and also of the submucosa 
 or mucosa, of even more decided character, occurs in youthful 
 persons addicted to alcohol. The intestines alone may be thus 
 affected, or the liver, spleen, and lymphatic glands are simulta- 
 neously involved. The term hematochromatosis has been pro- 
 posed for this condition. 
 
 Amyloid degeneration is met with in association with amy- 
 loid disease of the liver, kidneys, or spleen, and particularly in 
 cases in which there is tuberculous ulceration of the intestines. 
 The mucous membrane is principally involved, and becomes some- 
 what hardened and presents a peculiar grayish luster. Superficial 
 erosions and even considerable ulcers may result. The process 
 begins, as elsewhere, in and around the small blood-vessels. 
 
DISEASES OF THE G ASTRO-INTESTINAL TRACT. 503 
 
 CIRCULATORY DISTURBANCES. 
 
 Active hyperemia may occur from acute irritation, and 
 forms a part of inflammation. 
 
 Passive hyperemia results from causes similar to those 
 producing congestion of the stomach. Among these, obstructive 
 diseases of the liver, notably cirrhosis, and cardiac and pulmonary 
 affections are most prominent. The intestinal mucosa becomes 
 somewhat swollen, ofttim.es edematous, dark bluish-red in color, 
 and occasionally marked by punctate hemorrhages. The mesen- 
 teric veins are widely dilated. Occasionally hemorrhagic liquid 
 is found within the intestines, the points of hemorrhage remaining 
 undiscovered. 
 
 Hemorrhage. — Petechias are found in many cases of violent 
 septic or infectious diseases, in intense anemias, and as the result, 
 of marked passive hyperemia. Embolism in cases of ulcerative 
 or malignant endocarditis may lead to petechial hemorrhages, and 
 the same are observed as a part of the morbid anatomy of intes- 
 tinal anthrax. Large intestinal hemorrhages may occur from 
 typhoid, tuberculous, dysenteric, or syphilitic ulcerations, or from 
 the perforation of a large arterial branch by a peptic ulcer in the 
 duodenum. Hemorrhoids may occasion considerable hemorrhages 
 from the rectum. 
 
 Edema of the mucosa may result from passive congestion, and 
 attends acute or chronic inflammations, especially the more intense 
 forms. 
 
 Embolism and thrombosis of the mesenteric arteries are 
 rare conditions. Embolism may lead to hemorrhagic infarction. 
 
 Hemorrhoids result from varicose enlargement of the veins 
 of the rectum. They are usually found in the lower part of the 
 rectum, inside or outside the sphincter, and a distinction is made 
 between internal and external hemorrhoids. 
 
 Etiology. — Obstruction of the venous circulation is the import- 
 ant etiologic factor. It may be due to chronic diseases of the liver 
 (cirrhosis), repeated pregnancies, pelvic tumors, or chronic consti- 
 pation with frequent retention of feces in the rectum. The last- 
 named condition acts in a twofold manner. On the one hand, it 
 causes venous obstruction, and, on the other hand, chronic proctitis, 
 which in turn occasions disease of the veins of the rectum, and thus 
 predisposes them to dilatation. In all cases of hemorrhoids, con- 
 stipation and the resulting proctitis are important as auxiliary 
 causes. Hemorrhoids are rarely met with before adult age. 
 
 Pathologic Anatomy. — The hemorrhoid presents itself as a small 
 polypoid elevation of more or less congested appearance. On 
 section it is found to be highly vascular, and to consist of dilated 
 veins. There may be a congeries of slightly enlarged veins or 
 cavities of considerable size. Between the veins there is more or 
 
504 TEXT-BOOK OF PATHOLOGY. 
 
 less abundant inflammatory connective tissue. Thrombosis often 
 occurs within the cavities ; and occasionally the fibrous tissue 
 around them undergoes active proliferation, when a structure 
 resembling fibro-angiomata results. Hemorrhagic extravasations 
 may occur from the veins, and free hemorrhage from the surface 
 is a common symptom. Infective inflammation and phlebitis of 
 the veins sometimes occur. In these cases the hemorrhoid en- 
 larges and becomes inflamed and edematous. Inflammation of 
 the adjoining tissues may occur (proctitis, periproctitis). 
 
 Hemorrhoids may cause marked anemia by the repeated hem- 
 orrhages, and sometimes occasion septic infections when they have 
 themselves become infected and inflamed. 
 
 INFLAMMATIONS. 
 
 Inflammation of the intestines, or enteritis, may affect 
 any part of the intestinal canal, and involve the mucosa and sub- 
 mucosa more particularly. It is more frequently present in chil- 
 dren and in the aged than at other periods of life. 
 
 Etiology. — The causes of enteritis are similar to those of gas- 
 tritis, and among them may be reckoned all forms of irritating 
 foods or foreign matter taken with the food. Poisons of various 
 kinds operate in a similar manner. In many cases the irritant 
 poisons which occasion enteritis are developed within the body in 
 consequence of improper digestion and fermentation. Bacteria 
 play an important role in this process, and sometimes are them- 
 selves the direct cause of enteritis in instances in which impro- 
 prieties of diet or digestive disturbances have furnished favorable 
 conditions for their growth and multiplication. The normal colon- 
 bacillus is perhaps the most frequent and important micro-organ- 
 ism of ordinary non-specific enteritis, but other organisms doubt- 
 less frequently play a part. The colon-bacillus probably increases 
 in virulence under certain conditions and then occasions irritation. 
 
 Pathologic Anatomy. — There are a number of varieties of ente- 
 ritis, and different types may be described, though individual cases 
 rarely conform to a single variety. Of the acute forms of enteritis, 
 the important are the catarrhal, suppurative, and the pseudomem- 
 branous. 
 
 Catarrhal enteritis may affect any part of the intestinal tract. 
 The mucosa is swollen and usually light-red in color ; the arteries 
 are visibly distended, and not rarely there are petechial hemor- 
 rhages. The surface is covered with mucous exudate containing 
 desquamated and degenerated epithelial cells and emigrated leuko- 
 cytes ; while the intestinal contents are rendered liquid by serous 
 exudation. The solitary follicles or agminated collections of 
 lymphoid tissue may be particularly swollen and cause projections 
 above the surrounding mucosa. The term follicular enteritis is 
 
DISEASES OF THE GASTRO-INTESTINAL TRACT. 505 
 
 applied to such cases. In other instances the desquamation of epi- 
 thelium is more prominent than the mucous exudation, and con- 
 siderable shreds of mucosa may be loosened and discharged. The 
 term croupous enteritis is suggested by such conditions. 
 
 Suppurative enteritis differs from the catarrhal form in the 
 greater degree of emigration of leukocytes. The exudate upon 
 the surface may be largely composed of white corpuscles, and in 
 intense cases the surface may be covered with almost pure pus. 
 Round-cell infiltration of the mucosa and the submucosa is 
 present, and focal collections leading to submucous abscesses or 
 to ulcers upon the mucous surface are occasionally seen. The 
 solitary follicles are enlarged and tend to break down, forming 
 follicular ulcers. 
 
 Ulceration of the intestines occurs in a variety of conditions. Peptic 
 ulcers, similar to those met with in the stomach, are occasionally found in 
 the duodenum. They have the same characters and tendencies as those of 
 the stomach ; they may occasion sudden death from hemorrhage. Ulcers 
 in the duodenum are also an occasional result of extensive burns of the 
 skin ; and recently attention has been called to the frequency of duodenal 
 ulceration in cases of chronic Bright's disease. Ulcerations of the ileum 
 are habitual in typhoid fever and tuberculous enteritis, and are occasion- 
 ally due to anthrax or actinomycosis. Sarcomata and carcinomata are rare 
 causes. Ulcerations of the large bowel are met with in chronic enteritis 
 and dysentery. A form of peculiar clinical interest is anal fissure. This is 
 a linear ulceration of the rectum in the region of the sphincter. It may be 
 associated with hemorrhoids or be independent. 
 
 Pseudomembranous enteritis is characterized by the forma- 
 tion of a grayish membrane upon the surface of the intestine. 
 The large intestine is more frequently involved, and the process 
 is especially met with in dysentery (see p. 510). True diphtheria 
 of the bowel with pseudomembranous deposit may sometimes occur. 
 
 Chronic enteritis results from acute attacks or from repeated 
 irritation. Chronic congestion in consequence of hepatic or car- 
 diac affections is a predisposing cause of importance. 
 
 In the early stages the mucous membrane is usually more or 
 less swollen, and sometimes proliferative changes in the glandular 
 elements may lead to distinct polypoid elevations. These are 
 especially pronounced in cases in which the healing of ulcers of 
 acute enteritis has occasioned cicatricial constrictions and thus 
 elevated adjoining parts of the mucosa. The elevated portions 
 may undergo proliferative inflammation, and polypoid formations 
 result. In the later stages of chronic enteritis atrophy may ensue, 
 in part as the result of the overgrowth of the stroma of the mucosa 
 and the degeneration of the glandular elements, in part also as the 
 result of the overdistension or tympany resulting from fermentation 
 of the intestinal contents. This atrophy may affect the mucous 
 membrane alone, but more commonly also involves the muscularis. 
 Hyperplastic processes in the lymphoid elements may be a promi- 
 
506 TEXT-BOOK OF PATHOLOGY. 
 
 A, 
 
 nent feature in the hypertrophic stage of chronic enteritis, and may 
 give place to atrophy in the later stages. On the other hand, the 
 enlargement of the solitary follicles and Peyer's patches may per- 
 sist for a long time after atrophy has led to great thinning of the 
 remaining portions of the mucosa. 
 
 Pathologic Physiology. — Enteritis may occasion profound dis- 
 turbances in a variety of ways. In cases of infective character 
 general systemic intoxication may result from the absorption of 
 bacterial products or substances resulting from decomposition 
 of the intestinal contents. In other cases the intensity of the 
 local irritation may, through the nervous system, occasion great 
 depression or shock ; and subsequently the exudations into the 
 intestines may cause depletion of the vascular system and failure 
 of the circulation. The local effects and the resulting behavior of 
 the bowels differ in different cases. Sometimes the peristaltic 
 movements are arrested by the intensity of irritation and obstinate 
 constipation results ; more frequently hurried peristalsis and the 
 abnormal exudation (serous or mucous) occasion diarrhea. The 
 digestive processes fail from the diseased condition of the bowel, 
 as well as from the rapid peristalsis and premature discharge of 
 the intestinal contents ; more or less profound disturbance of 
 health results. 
 
 INFLAMMATIONS OF SPECIAL PARTS. 
 
 Duodenitis. — Duodenitis occurs in association with gastritis 
 from irritating food and the like. The appearances are the same 
 as in gastritis. Duodenitis is prone to occasion obstruction of the 
 terminal portion of the common bile-duct by the inflammatory 
 thickening of the mucosa and the accumulation of mucus in the 
 mouth of the duct ; and in this way gives rise to obstructive 
 jaundice (catarrhal jaundice). 
 
 Inflammation of the ileum presents no special charac- 
 teristics, excepting that enlargement of the follicles (follicular 
 enteritis) is frequently conspicuous. Follicular ileitis is particu- 
 larly common in children suffering from infectious fevers, such as 
 diphtheria and scarlatina, Peyer's patches may be considerably 
 enlarged and even ulcerated. The ulcers are generally small, and 
 several may occur in a single Peyer's patch instead of single ulcers, 
 such as occur in typhoid or tuberculous enteritis. 
 
 Typhlitis or cecitis (inflammation of the cecum) may be 
 due to the irritation of the intestinal contents in consequence of 
 constipation (stercoral typhlitis). This affection is probably very 
 frequent, though it leads to no severe consequences and occasions 
 no urgent symptoms. Typhlitis is probably generally of the 
 simple catarrhal variety, but in obstinate constipation or obstruc- 
 tion of the colon ulceration may occur. Perforation or extension 
 
DISEASES OF THE GASTRO-INTESTINAL TRACT. 507 
 
 to the surrounding tissues {perityphlitis) is the rarest of all conse- 
 quences. More frequently the latter is secondary to inflamma- 
 tions of the appendix vermiformis. 
 
 Appendicitis may be a primary condition, or it may result 
 from primary typhlitis or cecitis. The inflammation of the 
 mucosa of the cecum may extend directly to that of the appendix ; 
 or may cause obstruction of the mouth of the appendix in the 
 same manner as duodenitis causes obstruction of the common bile- 
 duct. There results a retention of the contents of the appendix 
 and multiplication with increased virulence of the contained 
 bacteria (Bacillus coli communis, staphylococcus, streptococcus, 
 and others). The mucosa of the appendix, rendered less resistant 
 in consequence of the overdistention and associated congestion, 
 may be penetrated by the micro-organisms and appendicitis 
 results. In many cases fecal concretions are found within the 
 appendix, and less commonly foreign bodies of various sorts have 
 been found. These have been assumed to be the direct cause of 
 the disease, and doubtless may play a part by irritating the mucosa, 
 or injuring it in such manner that micro-organisms easily pene- 
 trate it. On the other hand, there is much reason to believe that 
 the fecal concretions are often formed in consequence of the 
 accumulation of mucous and desquamated epithelial cells and the 
 stagnation of the contents of the appendix, after the disease has 
 begun. Obstruction of the arterial supply of the appendix was 
 formerly regarded as an important element in the etiology, but 
 probably is only of secondary importance. 
 
 Pathologic Anatomy. — The pathologic anatomy of appendi- 
 citis varies in different cases, and we may, for convenience, dis- 
 tinguish a catarrhal, a necrotic or gangrenous, and an interstitial 
 form. 
 
 In the mildest or catarrhal form there is merely retention of 
 the contents of the appendix and slight disease (swelling and 
 erosion) of the mucosa. The muscularis and serous coat may be 
 congested and edematous, but are not extensively involved. The 
 contents of the appendix are more or less mucopurulent in char- 
 acter. 
 
 In the necrotic or gangrenous form the mucous membrane suf- 
 fers rapid destruction and the muscular and serous coats are quickly 
 invaded. Fibrinous peritonitis soon develops in the serous coat 
 and over the adjacent intestines, either as a result of penetration 
 of bacteria through the walls of the appendix, or in consequence 
 of perforation of the walls. The local peritonitis serves the pur- 
 pose of restraining the infective disease and prevents diffuse peri- 
 tonitis. In cases of rapid gangrene, with early rupture or escape 
 of abundant bacteria, general peritonitis may result before a re- 
 straining wall can be formed. 
 
 The term interstitial appendicitis may be used to designate 
 
508 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 
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 cases in which all of the coats of the appendix are involved and 
 in which there is a special tendency to productive changes in the 
 connective tissues. In reality all cases of appendicitis show more 
 
 or less interstitial change of 
 this character (Fig. 236) ; but 
 in some it is the conspicuous 
 feature. These cases fre- 
 quently terminate in chronic 
 thickening of the appendix. 
 
 Results. — Mild cases of ca- 
 tarrhal appendicitis may sub- 
 side after free purgation, with 
 relief of the obstruction at the 
 mouth of the appendix. In 
 more serious inflammations 
 and in cases in which the 
 obstruction remains, the dis- 
 ease spreads through the walls 
 of the appendix to the perito- 
 neum and occasions local peri- 
 tonitis ; or rupture of the ap- 
 pendix occurs, and more in- 
 tense local or general perito- 
 nitis follows (Fig. 237). In 
 either case fibrinous deposits 
 are formed upon the perito- 
 neum, and not rarely a local- 
 ized abscess (perityphlitic ab- 
 scess) results. The appendix 
 itself may be separated from 
 the cecum, and may lie free in 
 the abscess, or it may be firmly 
 embedded in the fibrinous wall 
 of the abscess. The latter may 
 subsequently undergo inspissa- 
 tion, but more commonly rup- 
 tures into the general perito- 
 neal cavity, into some part of 
 the intestines, into the ureter, 
 bladder, or externally. In 
 cases with favorable outcome the appendix is usually bound down 
 by adhesions, attaching itself to neighboring coils of intestine or 
 to other structures. The appendix in such cases is usually dis- 
 torted and greatly thickened, and repeated attacks of inflammation 
 (relapsing or recurring appendicitis) are not unusual. 
 
 There is generally more or less systemic intoxication and infec- 
 tion, and secondary lesions may be found in distant organs. Not 
 
 » 
 
 
 Fig. 236.— Acute appendicitis, with round- 
 cell infiltration and hyperplasia of connective 
 tissue in all of the coats. In large part the 
 round cells of the mucosa and submucosa be- 
 long to the normal lymphoid tissue of these 
 parts. 
 
DISEASES OF THE G ASTRO-INTESTINAL TRACT. 
 
 509 
 
 rarely pylephlebitis and metastatic abscesses of the liver are 
 encountered. 
 
 Colitis, aside from the specific form, dysentery, is most fre- 
 quently due to irritation by fecal accumulations, and the sig- 
 moid flexure is the common seat. The entire colon may, how- 
 ever, be involved. Thickening of the mucous membrane and 
 
 Pig. 237. — Ulcerative and perforative appendicitis, showing perforations ; two fecal con- 
 cretions from other cases of appendicitis (modified from Bollinger). 
 
 abundant exudation of mucus are the prominent features of the 
 earlier stages ; while in the later stages atrophy and thinning are 
 observed. Ulcerations are not uncommon. When the mucous 
 exudation and the desquamated cells accumulate upon the surface 
 the appearance of a pseudomembrane is simulated, and casts of the 
 bowel or masses of mucus may be discharged from time to time 
 {mucous colitis). 
 
 Proctitis, or inflammation of the rectum, may be due to 
 direct irritation by retention of fecal matter, by parasites, or by 
 toxic agents ; or it may occur secondarily after various other 
 diseases of the rectum, such as tumors, hemorrhoids, and the 
 like. The inflammation tends to become chronic. The rectum 
 is generally involved with the colon in cases of mucous colitis. 
 
 The mucous membrane is considerably swollen, often edema- 
 tous, and usually presents petechial hemorrhages. Ulceration 
 may occur secondarily, and extension of the ulcerative process to 
 the surrounding tissues (periproctitis) is not unusual. In the 
 latter cases fistulous communication may be established between a 
 
510 TEXT-BOOK OF PATHOLOGY. 
 
 perirectal abscess and the rectum (incomplete fistula), or a fistulous 
 communication may form between the rectum and the exterior 
 {complete fistula in ano). Sometimes proctitis is secondary to peri- 
 proctitis occurring in diseases such as typhoid fever, pyemia, and 
 the like. 
 
 INFECTIOUS DISEASES. 
 
 Dysentery is a specific, endemic or epidemic inflammation 
 of the large intestine. The term probably includes a variety of 
 affections due to different causes. 
 
 In the milder cases of endemic dysentery tainted food and 
 products of fermentation, with perhaps specific bacteria, are the 
 causative agents. Occasionally certain poisons, like mercury, pro- 
 duce similar lesions. In cases of ulcerative dysentery, especially 
 the tropical forms, the Amoeba coli is usually regarded as the 
 specific cause (see Part I.). This organism probably enters the 
 intestinal tract through drinking-water and multiplies in the large 
 intestine, where it invades the mucosa and occasions widespread 
 ulceration. 
 
 The etiology of the most severe forms of dysentery remains 
 obscure, but the association of certain cases with violent septic 
 diseases suggests the causal factors. 
 
 Pathologic Anatomy. — Several varieties may be distinguished, 
 though one of these merges gradually into the other. 
 
 Catarrhal dysentery is the mildest form. It is characterized 
 by congestion, swelling, and edema of the mucous membrane. 
 Petechial hemorrhages and follicular enlargements or ulcers are 
 not unusual. 
 
 Ulcerative dysentery is marked by swelling of the mucosa and 
 scattered ulcers having a more or less irregular and ragged outline 
 and undermining the mucosa. The ulcers are often surrounded 
 by hemorrhagic infiltration. The ulcerative form tends to be- 
 come chronic, causing great thickening of the bowel and indolent 
 ulcers. 
 
 Diphtheritic dysentery is distinguished by the presence of a 
 pseudomembranous deposit in and upon the mucous membrane. 
 The entire wall of the colon and rectum may be covered with a 
 grayish or brownish, more or less necrotic, membrane ; or smaller 
 areas of like character may be scattered here and there upon a 
 thickened and catarrhal surface. In the mildest cases the process 
 is entirely superficial, in the severest it extends deeply, and the 
 muscularis mucosae and even the submucosa may be destroyed. 
 To the most violent of all forms the term gangrenous dysentery is 
 applicable. Microscopically, the epithelial cells show granular 
 degeneration and become more and more necrotic. They are 
 embedded in a fibrinous or mucofibrinous matrix, and round cells 
 invade the membrane as well as the subjacent tissues. 
 
DISEASES OF THE GASTEO-INTESTINAL TRACT. 511 
 
 Eesults of Dysentery*— In all cases there is a tendency to 
 chronic thickening or inflammation of the large bowel ; and 
 mucous colitis or merely a tendency to repeated acute colitis may 
 remain. Occasionally perforation occurs, and peritonitis or peri- 
 proctitis results. The most frequent complication is abscess of 
 the liver resulting from embolism or from ascending thrombosis 
 of the portal vein. In amebic dysentery the Amoeba coli is 
 carried to the liver in emboli and occasions secondary changes. 
 
 Cholera. — Cholera epidemica, or Asiatica, is an acute specific 
 inflammation of the small and large intestines, due to the comma- 
 bacillus or vibrion of Koch. This micro-organism is found in the 
 great majority of cases. Occasionally it is not discovered, while 
 other micro-organisms, Bacillus coli communis and streptococci, 
 are present. It is probable that in these instances errors of obser- 
 vation cause the failure of detection. 
 
 Pathologic Anatomy. — Cholera is characterized by redness and 
 swelling, and not rarely by petechial ecchymosis of the mucous 
 membrane, particularly of the small intestine. The superficial 
 epithelium suffers early and extensive degeneration, perhaps a 
 form of coagulation-necrosis. The solitary follicles and the 
 agminated glands may enlarge and may suffer ulceration. The 
 intestines contain and discharge a serous exudation, often in large 
 quantities, and containing grayish or whitish particles, which are 
 flakes of desquamated and degenerated epithelium. The term 
 "rice-water" discharges is applied to the evacuations. Exten- 
 sive areas of the mucous membrane may be laid bare by the 
 desquamation of the epithelium. When cholera has passed to 
 its later stages secondary pseudomembranous inflammation of the 
 mucous membrane is not unusual, and is probably the result of 
 secondary infection. 
 
 Associated Conditions. — The blood is thickened and dark-red in 
 color ; thrombosis in the heart or venous sinuses is frequent. The 
 kidneys present marked congestion and degeneration, which are 
 dependent upon the action of the toxins of the disease. Lobular 
 pneumonia is a common complication. 
 
 Typhoid fever is distinguished by an acute, specific inflam- 
 mation of the lymphoid elements of the intestines, particularly of 
 the ileum and upper portion of the colon. The specific cause is 
 the Bacillus typhi abdominalis, described by Eberth and Gaffky. 
 This organism enters the gastro-intestinal tract with drinking- 
 water, milk, or other food, and multiplies in the small intestine 
 (see Part I.). 
 
 Pathologic Anatomy. — The specific lesions of typhoid fever oc- 
 cur in the lymphatic structures, notably in the solitary follicles, 
 Peyer's patches, mesenteric glands, and spleen. 
 
 The solitary follicles and Peyer's patches of. the lower end of 
 the ileum are first affected, but later, or exceptionally in the be- 
 
512 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 filming, the lymphoid collections of the upper part of the ileum 
 
 and jejunum, or of the cecum and 
 colon, may be involved. At first 
 the follicles and patches are swol- 
 len and somewhat reddened by 
 congestion. Within a few days 
 of the onset, however, they lose 
 their congested appearance and 
 present themselves as grayish or 
 white elevations projecting from 
 one to several millimeters above 
 the surface (Fig. 238). Micro- 
 scopically the lymphoid elements 
 are found in a state of active pro- 
 liferation, and in addition large 
 round cells (endothelial or epithe- 
 lioid) are more or less abundant. 
 These large cells are actively 
 phagocytic, and have been dis- 
 covered in the lymphatic chan- 
 nels at some distance from the 
 local lesions, as well as in the 
 mesenteric glands, and in distant 
 parts. The surrounding mucosa 
 may be normal in appearance, or 
 may be somewhat inflamed. The 
 conditions of the lymphoid struct- 
 ures at this stage, to which the term medullar if infiltration has been 
 applied, remain unchanged for some days or a week. After the 
 
 Fig. 238.— Typhoid fever, showing stage 
 of medullary infiltration; enlargement 
 of lymphoid follicles and Peyer's patches 
 (modified from Kastand Rumpel). 
 
 Fig. 239.— Typhoid fever, showing necrosis of Peyer's patches and intense congestion of 
 the bowel (modified from Kast and Rumpel). 
 
 first week necrosis is prone to occur. The center of the solitary 
 follicles or part of the Peyer's patch becomes more and more soft 
 
DISEASES OF THE QASTBO-INTESTINAL TRACT. 513 
 
 and yellow, or sometimes reddish from absorption of blood-pigment. 
 The necrotic portions are discharged after a few days, leaving an 
 ulcerated surface of regular or irregular outline, and presenting 
 necrotic edges with hemorrhagic infiltration (Fig. 239). The ul- 
 cers resulting from destruction of the solitary follicles are small 
 and rounded, while those involving the Peyer's patches are elon- 
 gated, the long axis being parallel with the axis of the intestine. 
 The ulcers are usually found in an acute stage at the end of the 
 second or at the beginning of the third week of the disease. Reso- 
 lution may occur without necrosis and ulceration, but more com- 
 monly ulcers are formed and healing proceeds more slowly. The 
 lymphoid elements of the follicles and patches are usually perma- 
 nently destroyed, and healing takes place by proliferation of the 
 fibrous stroma. Occasionally, however, complete restitution of 
 the normal tissues occurs. When the lymphoid follicles of the 
 patches have become necrotic and have been infiltrated with blood 
 dark pigmented spots are formed, and give rise to the condition 
 designated as the " shaven-beard " appearance. 
 
 Complications. — Extensive necrosis may lead to erosion of a 
 blood-vessel and hemorrhage ; or the wall of the intestine may be 
 completely perforated by the necrotic process, and fatal peritonitis 
 may result. In other instances peritonitis occurs without perfora- 
 tion by direct extension of the inflammatory process through the 
 intestinal wall. Very commonly slight reactive peritonitis is 
 found on the serous surface opposite the ulcers. Extensive peri- 
 tonitis rarely occurs in this way. Peritonitis in rare instances re- 
 sults from necrosis of the mesentery glands, or from rupture of 
 the spleen. 
 
 The mesenteric glands are characteristically enlarged, those 
 nearest the points of ulceration being first and most prominently 
 involved. In the first stage they are soft and dark-red in color, 
 exuding a small amount of liquid on section. Later they become 
 larger, harder, and of whitish appearance ; they may finally suffer 
 necrosis and rupture. Usually, however, resolution takes place 
 after the first stage. 
 
 The spleen is enlarged in most cases, and presents the charac- 
 teristics of acute splenic tumor. Very rarely perisplenitis or 
 abscess may occur. 
 
 Lesions in Other Parts. — The muscles, particularly those of the 
 abdominal walls, frequently show spots of degeneration of a waxy 
 or hyaline character, as described by Zenker. Very rarely pete- 
 chial or considerable hemorrhages may be found in the muscles ; 
 and abscesses are sometimes met with as sequela?. 
 
 The heart-muscle is involved in perhaps a majority of the 
 cases. The muscle-fibers suffer parenchymatous and hyaline 
 degeneration ; and less commonly the intermuscular tissues pre- 
 sent the characteristics of acute myocarditis. Acute endocarditis 
 33 
 
514 TEXT-BOOK OF PATHOLOGY. 
 
 and inflammations of other serous surfaces are rare in typhoid 
 fever as compared with some other infectious diseases. 
 
 Acute degeneration of the kidney and acute nephritis are quite 
 common, and the kidney-substance may present small necrotic or 
 lymphomatous foci. Similar lymphomata occur in the liver and 
 throughout the peritoneum. 
 
 Acute lobular pneumonia and croupous pneumonia are frequent 
 complications. Osteomyelitis is rare. 
 
 The blood in typhoid fever, unlike other infections, presents no 
 leukocytosis, but, on the contrary, may be characterized by leu- 
 kopenia, the mononuclear leukocytes predominating. 
 
 Tuberculosis. — Tuberculosis of the intestines is very com- 
 mon. It may occur primarily from the drinking of infected milk 
 or consumption of the meat of tuberculous animals. Primary 
 tuberculosis of this character is especially frequent in young in- 
 fants. More commonly tuberculosis of the intestines is secondary 
 to pulmonary or laryngeal tuberculosis, and is due to the swallow- 
 ing of sputa. 
 
 The usual situation of the lesions is the lower end of the ileum, 
 and it is the lymphoid tissues that are prone to be attacked. At 
 first the follicles or Peyer's patches become enlarged and project 
 above the surface. Soon they undergo necrosis and discharge 
 their contents, leaving more or less irregular caseous ulcers. The 
 follicular ulcers are small and rounded, but the more characteristic 
 lesion is an irregular ulcer extending transversely to the long axis 
 of the bowel and often involving a half or more of the entire cir- 
 cumference. These ulcers usually begin as follicular ulcers ; later 
 
 
 
 
 
 
 
 A'- , ^ 
 
 
 
 
 ■^. ^^^ 
 
 ^& 
 
 
 
 
 Fig. 240.— Tubercular ulceration of the intestine. 
 
 the submucosa is invaded and the tuberculous process extends in 
 a lateral direction along the lymphatic channels running toward 
 the mesentery (Fig. 240). 
 
DISEASES OF THE QASTRO-INTESTINAL TRACT. 515 
 
 Microscopically the changes are found to involve the mucous 
 membrane and the adjacent submucous coat. Early caseation is 
 characteristic. On the serous coat may often be seen granular 
 elevations in clusters opposite the ulcers in the mucosa, and ex- 
 tending in lines from the region of ulceration around the bowel 
 toward the mesentery (Fig. 241). These represent tuberculous 
 
 I 
 
 Fig. 241.— Miliary tubercles in clusters and disseminated over the serosa (peritoneum) 
 of the intestine ; the clusters are situated opposite ulcerations of the mucous membrane 
 (modified from Bollinger). 
 
 lymphangitis and small miliary tubercles in the course of the 
 subserous lymphatic vessels. 
 
 Tuberculous ulceration rarely causes perforation of the bowel, 
 excepting in the rectum, where periproctitis and fistula in ano may 
 result. The ulcers may heal, causing cicatricial distortion or 
 stenosis. Very commonly there is associated tuberculous enlarge- 
 ment of the mesenteric glands, and sometimes the latter are 
 extensively diseased, though the primary intestinal involvement is 
 insignificant. Generalized enteritis of catarrhal character may 
 accompany the specific ulcerative disease. 
 
 Syphilis is most frequent in the rectum, though cases of 
 syphilitic disease of the small intestine or colon, in the form of 
 localized or diffuse gummatous involvement, sometimes with 
 secondary ulceration, have been observed, particularly in cases 
 of congenital syphilis. 
 
 In the rectum syphilis may appear in the form of warty eleva- 
 tions or as a chancre ; also as mucous patches, gummatous nodules 
 or infiltrations. Considerable thickening of the mucosa and sub- 
 mucosa, with ulceration and secondary cicatrization and stenosis 
 (syphilitic stricture), may result. 
 
 Anthrax occasionally aifects the small intestine in persons 
 exposed to infection by their occupations. It is met with among 
 wool-sorters, brushmakers, tanners, and the like. More or less 
 
516 TEXT-BOOK OF PATHOLOGY. 
 
 extensive ulceration is seen in the small intestine, and sometimes 
 in the large intestine. The ulcers are dark-colored and necrotic 
 in appearance, and are commonly surrounded by a hemorrhagic 
 zone. Considerable edema and hemorrhagic infiltration of the 
 neighboring parts of the intestine may accompany the ulceration. 
 The neighboring lymph-glands and the spleen are enlarged. The 
 bacilli of anthrax are found in considerable numbers in the ulcers 
 and in the surrounding tissues. 
 
 Actinomycosis of the intestines is very rare. It most com- 
 monly affects the region of the cecum, causing first infiltrations 
 and then ulcerations of the mucosa and submucosa. 
 
 Enteromycosis is a term applied to intestinal affections 
 resulting from the ingestion of putrid meat, fish, sausages, and the 
 like. Occasionally considerable epidemics may occur. The intes- 
 tines may present the lesions of catarrhal enteritis or of intense 
 croupous or pseudomembranous inflammation, and there may be 
 erosions or ulceration. Micro-organisms of various sorts have 
 been discovered, but no specific form is recognized. The acute 
 general symptoms, and even the local lesions, may be caused by 
 poisons elaborated by bacteria in tainted foods, rather than by the 
 micro-organisms themselves. 
 
 TUMORS. 
 
 Connective-tissue Tumors. — Among the benign tumors of 
 the intestines fibroma, myxoma, and lipoma are occasionally met 
 with in the submucosa as small nodular tumors or as pendulous 
 polyps. They may occasion intestinal obstruction and even invag- 
 ination. 
 
 Sarcoma of the intestine is rare. Lymphosarcomatous or lym- 
 phadenomatous enlargement of the solitary follicles or Peyer's 
 patches may be met with in leukemia or pseudoleukemia. Round- 
 celled sarcoma springing from the submucosa and deeper layers 
 of the mucosa, and sometimes infiltrating the mesentery, may also 
 occur as an independent and primary affection. Nodules of 
 secondary sarcoma are not rarely met with in the mucosa and 
 submucosa of the intestines (Fig. 242), and the serous covering 
 may be studded with miliary nodules in sarcomatosis. 
 
 Epithelial Tumors.— Among the epithelial tumors may be 
 included inflammatory papilloma, adenoma, and carcinoma. 
 
 Inflammatory hyperplasia of the mucous membrane may occur 
 in association with chronic inflammations, especially in the large 
 intestine, and may lead to the formation of papillomatous or poly- 
 poid elevations of considerable magnitude. 
 
 Adenomata are more strictly of the nature of tumors, being 
 independent of inflammatory processes, although no sharp dividing- 
 line can be drawn between the inflammatory proliferations and the 
 
DISEASES OF THE GASTBO-INTESTINAL TRACT. 
 
 517 
 
 adenomata proper. The latter may occur in the form of flat ele- 
 vations having a more or less uneven surface and a tendency to 
 
 Fig. 242.— Nodule of secondary sarcoma in the mucosa of the intestine (Kast and Rumpel). 
 
 hemorrhage and ulceration; or in the form of papillomatous 
 elevations of a cauliflower character. Adenomata arise by 
 
 Fig. 243.— Carcinoma of the duodenal papilla (modified from Kast and Rumpel). 
 
 hyperplasia of the crypts of Lieberkuhn in the duodenum or of 
 Muller's glands, and in their structure they present typical gland- 
 
518 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 ular acini, the tubules having a basement-membrane lined with 
 cylindrical epithelium. Adenomata are most frequent in the rec- 
 tum, but may occur in other parts of the large intestine and in 
 the duodenum. 
 
 Carcinoma is the most frequent tumor of the intestines. It 
 occurs in the duodenum, especially at the papilla of the common 
 bile-duct (Fig. 243) ; at the ileocecal valve, at the flexures of the 
 colon, and in the upper or lower part of the rectum. The appear- 
 ance is that of a soft, irregular, often ulcerated and bleeding ele- 
 vation, projecting into the lumen of the gut and causing considerable 
 narrowing, or surrounding the bowel by circular involvement of the 
 entire circumference. The carcinomata of the bowel are, for the 
 most part, cylindrical epitheliomata (Fig. 244) or glandular can- 
 
 Fig. 244.— Cylindrical epithelioma of the intestine (Perls). 
 
 cers, consisting of atypical acini and tubules, with irregular prolif- 
 eration and infiltration of the neighboring tissues with masses of 
 epithelial cells. Cases are met with, especially in the rectum, in 
 which there is a clear transition of adenoma into carcinoma (adeno- 
 carcinoma), and in general adenomata of the bowel have a tendency 
 to such transformation (Fig. 24-5). At the lower end of the rectum 
 squamous epithelioma may occur. 
 
 The results of carcinoma of the bowel are the same as those of 
 stenosis due to other causes, together with the consequences of the 
 cancerous cachexia and of metastasis. Ulceration of the tumor 
 may lead to perforation. 
 
 Myoma of the intestines and multiple cysts are occasionally met 
 with. 
 
DISEASES OF THE GASTBO-INTESTINAL TRACT. 
 
 519 
 
 Fig. 245.— Adenocarcinoma of the rectum (adenoma destruens) (Karg and Schmorl). 
 
 PARASITES. 
 
 Vegetable Parasites. — Various forms of bacteria are found 
 with such frequency in the intestinal contents that it is difficult to 
 estimate their pathologic significance. Tubercle-bacilli, the bacil- 
 lus of glanders and of typhoid fever, and the actinomyces produce 
 the specific lesions of these diseases. The Bacillus coli communis 
 is a constant inhabitant, but probably assumes pathogenic proper- 
 ties and leads to inflammatory lesions when the conditions (such as 
 irritation by coarse food, congestion, obstruction) favor its activity 
 and multiplication. Under the same circumstances other micro- 
 organisms likewise become active in the production of enteritis. 
 
 Animal Parasites. — The animal parasites are discussed in 
 detail elsewhere, but may be briefly mentioned here with reference 
 to pathologic results occasioned by their presence. Various forms 
 of protozoa have been found, and may occasion inflammations 
 when in considerable numbers. Coccidial psorospermia occur in 
 the epithelium of the villi of the small intestine, and the Megalos- 
 toma entericum may be found attached to the epithelium. The 
 Amoeba coli may lie free in the contents, or may penetrate through 
 ulcerations. It inhabits the large intestine, and is the probable 
 cause of certain kinds of dysentery. 
 
520 TEXT-BOOK OF PATHOLOGY. 
 
 The larger intestinal parasites are, for the most part, species of 
 vermes. Among the tape-worms Taenia saginata, Tsenia solium, 
 and Bothriocephalus latus are the most frequent. Occasionally 
 these may lead to intestinal obstruction by forming thick knots or 
 coils, and sometimes the head of the worm may be attached in the 
 mouth of the bile-duct, causing obstruction and jaundice. Inflam- 
 matory changes are rarely met with as a result of these worms. 
 
 Among the nematodes, or round worms, the Ascaris lumbri- 
 coides, or ordinary round worm, is the most frequent. It is usu- 
 ally multiple, and may occasion obstruction of the intestine or 
 inflammation. Sometimes they perforate the intestinal wall, but 
 it is improbable that the perforation is due entirely to the action 
 of the worm. Previous intestinal ulceration is the more import- 
 ant condition. Obstruction of the bile-duets or of the appendix 
 may occasionally be due to lumbricoids. The Ankylostoma du- 
 odenalis may cause petechial hemorrhages and inflammatory dis- 
 turbances in the duodenum or jejunum. The worms attach them- 
 selves firmly to the mucous surface and may be present in large 
 numbers. The Oxyuris vermicularis, or thread-worm, occupies 
 the large bowel, multiplying in the cecum and descending in the 
 mature state to the rectum ; it may occasion considerable proctitis. 
 In female children vaginitis sometimes results from migration 
 of the worms. The Trichina spiralis when ingested in large 
 numbers occasions violent gastro-enteritis, and its embryos per- 
 forate the wall of the intestine and migrate to the muscles. 
 
 Larva? of various forms of flies occasionally occupy the intes- 
 tinal tract, and owe their presence to the ingestion of the eggs 
 with food. They may occasion enteritis, and may be found in 
 immense numbers in the bowel or the stools. 
 
 INTESTINAL RUPTURE AND FOREIGN BODIES. 
 
 Rupture may be due directly to traumatism or penetrating 
 wounds ; but more frequently results from ulcerations within. 
 Duodenal (peptic) ulcers not infrequently perforate, and typhoid 
 ulcers occasionally cause rupture. Tubercular, dysenteric, and 
 other ulcers are less prone to penetrate completely. The appen- 
 dix may rupture from obstruction at its mouth and secondary 
 catarrhal, necrotic, or gangrenous inflammation of its walls. Rec- 
 tal ulcers frequently cause painful diarrhea, proctitis, periproctitis, 
 and fistulas. 
 
 Intestinal rupture usually leads to rapid peritonitis, but occa- 
 sionally recovery ensues. A localized peritonitis, by walling off 
 the infected area, may prevent general infection. The rupture 
 may take place between contiguous coils, causing spontaneous in- 
 testinal anastomosis. 
 
 Foreign-bodies. — Various bodies that have been swallowed 
 
DISEASES OF THE O ASTRO-INTESTINAL TRACT. 521 
 
 may lodge in the intestines. Occasionally fecal concretions or 
 enteroliths are found, especially in the appendix. These con- 
 sist of a nucleus of epithelial cells, mucus, hair, and the like, sur- 
 rounded by inspissated fecal matter and earthy salts, phosphate of 
 lime and carbonate of calcium. They may cause considerable 
 irritation, especially in the appendix, and even perforation. 
 
 THE LIVER. 
 
 Anatomic Considerations. — The liver is peculiar in hav- 
 ing a double circulation ; one system of vessels, the portal 
 vein and its ultimate subdivision, receiving the blood from the 
 digestive tract for functional purposes ; the other system, the 
 hepatic artery and its branches, supplying the nutritive blood 
 for the walls of the blood-vessels and for the interlobular con- 
 nective tissues, as well as to a certain extent the proper hepatic 
 structure itself. The portal capillaries ramify through the acini 
 and empty into small branches of the hepatic vein lying in the 
 center of the acini. The capillaries of the hepatic artery traverse 
 the interlobular tissue and ultimately empty into the interlobular 
 branches of the hepatic vein. The primary biliary capillaries are 
 merely spaces between the hepatic cells, the larger formed capil- 
 laries occupying the interlobular tissues. 
 
 MALFORMATIONS AND CHANGES OF POSITION. 
 
 Congenital malformations are uncommon. There may be 
 complete absence of the organ, especially in certain monstrosities ; 
 more frequently adventitious hepatic tissue is found in the suspen- 
 sory ligament or elsewhere. Minor abnormalities in the lobes or 
 fissures are more frequent. Absence of the gall-bladder and con- 
 genital stenosis or occlusion of the hepatic ducts are occasionally met 
 with. 
 
 Congenital Alterations of Position. — The liver may 
 occupy the left side in transposition of the viscera. More rarely 
 it is displaced downward, or occupies other abnormal positions. 
 
 Acquired Changes of Form. — The most important of 
 these is contraction and lengthening of the organ by lacing. 
 This gives rise to compression along the line of the lower mar- 
 gin of the ribs ; the right lobe of the liver may thus be divided 
 into an upper and a lower portion by a deep fissure. The capsule 
 is frequently thickened and the superficial acini atrophic at the 
 line of constriction. Similar indentation by the ribs posteriorly, 
 or by the right crus of the diaphragm, results from pulmonary 
 affections and enlargements of the liver. Other changes of form, 
 due to special diseases of the liver, will be discussed below. 
 
 Acquired Changes of Position. — Downward displacement 
 
522 TEXT-BOOK OF PATHOLOGY. 
 
 may result from pleural effusion or emphysema ; or it may be clue 
 to relaxation and Lengthening of the suspensory ligaments. The 
 latter form is more common in women than in men, and is often 
 part of a general enteroptosis. Tight lacing may be a cause of 
 importance. Displacement to the right or left, or tilting upward 
 of the lower edge, may occur in association with various abdominal 
 and thoracic affections. 
 
 CIRCULATORY DISTURBANCES. 
 
 Anemia of the liver may be part of a general anemia, or it 
 may be due to pressure upon the organ, to various diseases of the 
 liver-substance, or to compression of the blood-vessels. The sub- 
 stance becomes pale and, if the anemia persists, undergoes degen- 
 eration. 
 
 Active hyperemia is physiologic during digestion, and 
 occurs in association with various inflammatory abdominal dis- 
 eases. It is rarely extensive, and does not lead to marked 
 pathologic changes. 
 
 Passive hyperemia results from obstruction to the circula- 
 tion due to cardiac or pulmonary diseases, to pleural effusion or 
 adhesions, or to thrombosis or compression of the upper part of 
 the inferior vena cava. It is especially characteristie of cardiac 
 affections, the sluggish venous circulation of the liver accounting 
 for the fact that this organ first evidences failing cardiac power. 
 
 The liver increases in size, often considerably ; the edges are 
 rounded, and the color on the surface is darker than normal. On 
 section there may be seen deeply congested central veins sur- 
 rounded by lighter areas, representing the substance of the acini. 
 If the process has persisted, secondary fatty degeneration of the 
 peripheral zones of the acini or atrophy of these takes place, and 
 the light color of such portions, contrasting strongly with the dark, 
 congested central vein, suggests the name nutmeg-liver (Fig. 246). 
 In some instances of intense congestion small hemorrhages may 
 occur, especially in the portions lying beneath the capsule. In 
 the later stages degeneration and reduction of size may take 
 place and the organ may become dark-red from deposit of hema- 
 togenous pigment. To this form the term red-atrophy is some- 
 times given. In other instances hyperplasia of the connective 
 tissues between the lobules and acini occurs, while at the same 
 time the organ is darkly pigmented. The term cyanotic indu- 
 raiion may appropriately be given to such. Cases of this sort 
 are in reality instances of secondary cirrhosis. 
 
 Passive congestion of the liver may occasion considerable dis- 
 turbance of the hepatic function. The most striking evidence of 
 this is jaundice. This is probably due to the compression of the 
 smaller biliary ducts and capillaries, and in part to swelling of 
 
DISEASES OF THE GASTBO-INTESTINAL TRACT. 
 
 523 
 
 the lining cells of these channels. The bile at the same time is 
 probably thicker than normal, and does not therefore as readily- 
 escape through the ducts as in health. 
 
 !» 
 
 mm 
 
 ■'■;.-. ■■■■:<>■■■':.■:■: 
 ■ 
 
 :S 
 
 gSH 
 
 Fig. 246.— Nutmeg liver : chronic congestion due to cardiac < 
 
 (Bollinger). 
 
 Embolism and thrombosis of the portal vein may occur in 
 consequence of various diseases of the gastro-intestinal tract, par- 
 ticularly in cases of ulcerative enteritis. Embolic occlusion of 
 one of the larger branches of the portal vein may occasion no 
 serious circulatory disturbances, on account of the free collateral 
 circulation and from the fact that the hepatic artery is capable of 
 supplying the entire hepatic circulation. Embolic or thrombotic 
 occlusion of the branches of the hepatic artery is similarly devoid 
 of serious disturbance of the circulation. 
 
 Obstruction of the interlobular branches of the portal vein, 
 and particularly when several are coincidently occluded, may 
 occasion decided nutritive disturbances in the hepatic acini. 
 Small areas of necrosis having a grayish or yellowish and some- 
 what granular appearance, or in other cases foci of necrosis with 
 hemorrhagic infiltration, are the striking lesions. Such conditions 
 are observed in most instances of death from puerperal eclampsia 
 
524 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 in consequence of embolism of decidual cells (Fig. 247); and in 
 consequence of various intoxications or infections having their 
 origin in the distribution of the portal circulation. The imme- 
 
 Fig. 247.— Coagulation-necrosis of the hepatic cells in 
 (Karg and Schmorl). 
 
 of puerperal eclampsia 
 
 diate cause of the lesions in the latter conditions is hyaline 
 thrombosis of the interlobular portal vessels. 
 
 Thrombosis of the portal vein is most frequently the result of 
 infective inflammation of the vein (pylephlebitis), resulting from 
 ulcerative enteritis, appendicitis, or similar processes involving 
 the parts from which the portal blood is received. There may 
 be a gradual ascending inflammation and thrombosis extending 
 from the primary focus of disease to the portal vein ; or the 
 latter may be involved in a more direct manner by infectious 
 embolism. The portal vein and its branches in the liver become 
 more or less obstructed, and serious disease of the liver may 
 occur (multiple abscesses). At the same time the obstruction of 
 the vein occasions intense passive hyperemia of the peritoneum, 
 and ascites results. 
 
 ATROPHY AND DEGENERATIONS. 
 
 Atrophy of the liver occurs in cases of death from inanition 
 or from various organic diseases. (Pressure-atrophy has been 
 referred to above. Acute yellow atrophy is described below.) 
 
 The greater part of the liver-structure may be aifected, or the 
 atrophy may be limited to the edges or other limited portions. 
 The liver is more or less uneven, and may at the same time be 
 somewhat pigmented. 
 
 Microscopically the liver-cells are decreased in size, granular, 
 and dark-colored. At times the acini may disappear entirely, 
 and reactive hyperplasia of the stroma and even proliferation of 
 biliary ducts may ensue. 
 
DISEASES OF THE GASTBO-INTESTINAL TRACT. 525 
 
 Localized atrophy occurs in the vicinity of tumors, in the acini 
 surrounded by hyperplastic connective tissue in cirrhosis, and in 
 parts of the liver otherwise subjected to pressure. The liver-cells 
 of the affected part become distorted and decreased in size, and 
 are deeply pigmented (see Fig. 258). In the later stages they 
 break down completely, and are removed. Red atrophy (see 
 Congestion of the Liver) is a form of pressure-atrophy with 
 pigmentation, the compression of the hepatic cells being due to 
 overdistention of the hepatic veins and capillaries. 
 
 Pigmentation of the liver is prone to occur on account of the 
 sluggish circulation through that organ, and may be of various 
 kinds : 
 
 1. Hematogenous pigmentation in the portal areas. Particles 
 of altered blood-pigment are often deposited in the interlobular 
 tissues or in the peripheral zones of the acini in cases of abnormal 
 blood-obstruction in the portal circulation. This is particularly 
 common in pernicious anemia. In this disease the peripheral 
 zones of the acini are habitually infiltrated with pigment-matter, 
 which responds to tests for iron, such as with ammonium sulphid 
 or ferrocyanid of potassium and hydrochloric acid. Somewhat 
 similar pigmentation of the liver may occur in cases of absorp- 
 tion of hemorrhagic effusions in the peritoneum, or in consequence 
 of other forms of blood-destruction. Analogous pigmentation is 
 often met with in the livers and other abdominal organs of 
 drunkards (hematochromatosis). 
 
 2. Hematogenous pigmentation of the central portions of the 
 acini has been noted in connection with a red atrophy of the liver 
 consequent upon congestion. 
 
 3. Biliary pigmentation results from obstruction of the biliary 
 ducts, and is constantly met with in certain forms of cirrhosis and 
 in the vicinity of new growths which compress the biliary passages. 
 
 4. Very rarely anthracotic pigmentation has been observed. 
 In one case, at least, there was associated cirrhosis. 
 
 Patty infiltration is more or less physiologic, especially in 
 children and in overfed individuals. Pathologically there may be 
 diffuse infiltration or deposit in the liver-cells of all parts of the 
 organ. Such pathologic fatty-liver may result from overeating 
 and general obesity, or may be due to pulmonary disease or anemic 
 and cachectic conditions. It has generally been held that the im- 
 mediate cause is retarded oxidation, in consequence of which fat 
 accumulates. It is probable, however, that there is some disease 
 of the hepatic cells, rendering them more active in the storing up, 
 or less active in disposing of fats. This seems especially true in 
 certain cases due to poisons which cause a deposit of fat in the 
 liver, as in geese pampered by antimonial poisoning. 
 
 The liver increases in size, often considerably ; its edges are 
 rounded, its consistency is doughy, and the color is rather yellow- 
 
526 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 ish and glistening. On section there may be visible exudation of 
 oil-drops and the knife may be covered with droplets. 
 
 Microscopically the process is found to begin in the peripheral 
 portions of the acini in the form of droplets within the hepatic 
 cells. Soon these increase in size by confluence, adjacent cells are 
 involved, and the entire acinus eventually becomes affected (Fig. 
 248). In extreme cases the hepatic cell is filled with a single 
 
 Fig. 248.— Fatty infiltration of the liver. 
 
 large oil-drop, which compresses the protoplasm and nucleus. 
 The blood-vessels and other structures may be completely hidden 
 from view ; and the pressure of the fatty deposit may be sufficient 
 to produce a certain degree of anemia, though not enough to occa- 
 sion serious circulatory disturbances. The functional activity of 
 the liver is diminished. 
 
 Parenchymatous degeneration, or cloudy swelling, occurs 
 in various infectious fevers and in consequence of intoxications, 
 notably by phosphorus, arsenic, and antimony. The liver is some- 
 what enlarged, and of an opaque, grayish-yellow appearance, the 
 outlines of the lobules being extinguished. Microscopically, the 
 liver-cells are found filled with fine albuminous granules more or 
 less obscuring the nucleus. In most instances cloudy swelling 
 terminates by return to the normal state ; but if the intoxication 
 or infection is continued, fatty degeneration may result. 
 
 Fatty degeneration may occur as the result of severe 
 anemia, particularly" pernicious anemia, or, following cloudy 
 swelling, as the result of infectious diseases or of intoxications. 
 Among the infections, pyemia, yellow fever, relapsing fever, 
 and erysipelas are notable examples. The liver may be greatly 
 decreased in size and softer than normal ; the substance not rarely 
 is friable. The color is yellowish, and oil-drops may exude from 
 
DISEASES OF THE O ASTRO-INTESTINAL TRACT. 
 
 527 
 
 the surface. Microscopically the hepatic cells are filled with 
 small granular particles or droplets of fat, and in the advanced 
 stages they break down completely into granular detritus. Fatty 
 degeneration of localized areas of the liver or of individual acini 
 or cells occurs in association with chronic hepatitis or other dis- 
 eases causing pressure upon the acini. 
 
 Actlte Yellow Atrophy. — The most advanced fatty degen- 
 eration of the liver occurs in the affection of the organ termed 
 acute yellow atrophy. This condition is most frequent in young 
 women, and especially in those addicted to the excessive use 
 of alcohol. Occasionally syphilis seems the etiologic factor, and 
 in some instances of phosphorus-poisoning the appearance of the 
 liver is the same as that which is recognized as acute yellow 
 atrophy. Finally, some cases are idiopathic, arising without 
 recognizable cause. Parturition seems a determining cause in 
 some cases. Micro-organisms of various kinds have been found, 
 and it is likely that all cases are toxic or infectious. 
 
 Pathologic Anatomy. — The liver is decreased in size and be- 
 comes remarkably soft and friable. On section there is found a 
 variegated appearance, the prevailing color being a brownish or 
 grayish-yellow, in which are scattered bright or dark-red areas. 
 The yellowish areas represent the degenerated and pigmented 
 hepatic cells ; the reddish areas foci of hemorrhagic infiltration or 
 
 Fig. 249.— Acute yellow atrophy of the liver, showing extensive fatty degeneration and in 
 places complete destruction of the liver-cells (Kast and Rumpel). 
 
 pigmentation. The process usually begins in the left lobe, but 
 rapidly involves the entire organ. Sometimes the liver is in- 
 creased in size during the initial stages, and occasionally a liver 
 enlarged by previous disease suffers terminal acute atrophy. 
 
 Microscopically the hepatic cells are found to have undergone 
 rapid fatty degeneration or necrosis, and are filled with or replaced 
 by yellowish pigment-particles. As the process advances, the cells 
 are completely destroyed (Fig. 249). In the red areas referred to, 
 
528 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 infiltration with blood-cells and hematogenous pigmentation are 
 observed. 
 
 Associated Conditions. — Acute yellow atrophy leads to intense 
 cholemia, in consequence of which biliary pigmentation of the 
 various structures of the body may develop. Petechial hemor- 
 rhages may occur in the mucous or serous membranes, or in the 
 skin. The urine contains leucin and tyrosin. More or less pro- 
 found acid intoxication may occur (see Acid Intoxication, Part I.). 
 
 Amyloid degeneration occurs in consequence of syphilis, 
 tuberculosis, and suppurative diseases of the bones, or as a re- 
 sult of long-standing cachexia. It is habitually associated with 
 amyloid disease of the spleen, and often of the kidneys and other 
 structures. 
 
 Amyloid degeneration begins in the smallest blood-vessels 
 between and within the acini, causing a more or less pronounced 
 thickening of their walls. The liver-cells themselves may be 
 
 Fig. 250.— Amyloid liver (from a photograph by Dr. Wm. M. Gray). 
 
 secondarily involved, but more frequently undergo atrophy and 
 fatty degeneration in consequence of the pressure and of dimin- 
 ished nutrition due to compression of the blood-vessels (Fig. 250). 
 
 The liver is enlarged and denser than normal. Not rarely it 
 presents a striking translucency, and on section the color is gray- 
 ish-white or yellow. The peripheral and central zones of the 
 acini are sometimes readily distinguished by their light color from 
 the innermost portions, which are least affected. 
 
 Dropsical infiltration of the liver-cells occurs in cases of 
 intense infection and intoxication, especially such as originate in 
 some part of the portal circulation. It is found particularly in 
 the vicinity of necrotic areas due to embolic occlusion of the inter- 
 lobular portal veins. The liver-substance is swollen, and micro- 
 scopically the cells are cloudy and ofttimes vacuolated. 
 
DISEASES OF THE G ASTRO-INTESTINAL TRACT. 529 
 
 INFLAMMATIONS. 
 
 Hepatitis, or inflammation of the liver, may be of several 
 forms : a parenchymatous, an acute interstitial, or a chronic inter- 
 stitial. 
 
 Parenchymatous Hepatitis. — In the course of various 
 infections and intoxications a certain amount of parenchymatous 
 degeneration of the liver-cells may take place. This was for- 
 merly described under the name parenchymatous hepatitis. The 
 term is generally inappropriate, though in some instances there is 
 associated with the degeneration of the hepatic cells a certain 
 .amount of cellular infiltration and reactive inflammation. To 
 such cases the term parenchymatous inflammation might be ap- 
 plied, though in reality even these are more degenerative than 
 inflammatory in nature. 
 
 Acute Interstitial Hepatitis, or Abscess of the I/iver. 
 — In practically all, if not all, cases abscess of the liver is due to 
 the action of micro-organisms. The bacteria may gain access in 
 several ways. In some cases penetrating wounds, or perforation 
 of gastric or duodenal ulcers or of other pathologic lesions into 
 the liver, occasion direct infection. In other cases the micro- 
 organisms are carried in the circulation and enter the liver with 
 the portal or hepatic blood, or by retrograde embolism through 
 the hepatic veins from the vena cava. Finally, infection may 
 occur by invasion of the bacteria along the bile-ducts. 
 
 Most frequently hepatic abscess is secondary to ulcerative dis- 
 ease of the intestines, notably dysentery. In this disease the 
 specific amebae are carried to the liver in the portal circulation, 
 and occasion necrotic foci in which the bacteria carried within the 
 amebse multiply and give rise to the further changes constituting 
 an abscess. Similar embolic abscesses occasionally follow appen- 
 dicitis and perityphlitis, or various forms of intestinal ulceration. 
 Thrombophlebitis of the portal vein not rarely extends to the 
 smaller branches within the liver, and occasions multiple suppu- 
 rative foci. 
 
 In cases of general pyemia multiple abscesses of the liver may 
 •occur, especially when the primary infection occurs within the 
 abdomen. Infection by invasion along the biliary tract is espe- 
 cially prone to occur when there is obstruction of the bile-ducts 
 by calculi or otherwise. In tropical countries traumatism without 
 visible contusion may lead to abscesses, and it is not unlikely that 
 micro-organisms from the biliary passages penetrate the hepatic 
 structure in the injured portions. 
 
 Among the micro-organisms that have been discovered are 
 the streptococci and staphylococci, the Bacillus coli communis, 
 and others less frequently. 
 
 Pathologic Anatomy. — Dysenteric and traumatic abscesses are 
 
530 TEXT-BOOK OF PATHOLOGY. 
 
 usually solitary, and generally occupy the right lobe. In the 
 early stages they appear as spots of grayish or yellowish color, in 
 which the division of the lobules is lost and which assume a more 
 and more granular appearance. Subsequently softening takes- 
 place, and a cavity is formed. This increases in size until in ad- 
 vanced cases it may reach enormous proportions. The contents 
 consist of curdy or creamy pus having a yellowish, brownish, or 
 often (piite reddish appearance, and the wall is composed of an ill- 
 formed pyogenic membrane. The abscess may consist of a single 
 cavity, or may be partially lobulated. Sometimes there are mul- 
 tiple abscesses. If the cavity is small, resorption of the pus may 
 take place and a cicatrix may result. In other cases inspissation 
 and encapsulation ensue. Large abscesses may rupture into the 
 pleura, into the stomach or intestines, into the peritoneal cavity, 
 or externally. Not rarely the diaphragm and lungs are penetrated, 
 and the pus is evacuated through the bronchi. 
 
 Metastatic abscesses, and those due to infection from the biliary 
 ducts or to suppurative pylephlebitis, are multiple and usually of 
 small size. 
 
 Chronic interstitial hepatitis, or cirrhosis of the liver r 
 is a form of diffuse hyperplasia of the connective tissue, beginning 
 in the interlobular tissues and sometimes extending into the acini, 
 or causing secondary changes in the liver-cells. Hyperplasia of 
 the interlobular bile-ducts, and less frequently of the hepatic cells, 
 may be observed. 
 
 Etiology. — Cirrhosis of the liver is essentially the result of 
 hematogenous irritation. The most frequent cause is alcohol, 
 and it is particularly frequent in persons who consume raw spirits. 
 Overeating, with a sedentary life and a gouty diathesis, may also 
 contribute. Other cases are secondary to infectious diseases, 
 notably to syphilis, malaria, or tuberculosis. 
 
 Occasionally cirrhosis is due to the absorption of irritants 
 by the portal radicles and their transference to the liver in cases 
 of chronic peritonitis. Certain cases are due to chronic con- 
 gestion of the hepatic circulation in consequence of cardiac or pul- 
 monary disease ; and, finally, obstruction of the bile-ducts may 
 lead to another group of cases. 
 
 Morbid Anatomy. — Several varieties having rather marked dif- 
 ferences in their macroscopic and even microscopic appearances 
 may be distinguished. The process is essentially the same in 
 the different forms and the causes are similar. The most promi- 
 nent varieties are atrophic cirrhosis, hypertrophic cirrhosis, and 
 biliary cirrhosis. 
 
 Atrophic cirrhosis (Laennec's cirrhosis) is the ordinary form, 
 which is also known by the name "Gin-drinker's liver." In the 
 earliest stages the liver is often enlarged, but in the typical ad- 
 vanced form it is contracted, extremely hard, granular, or irregu- 
 
DISEASES OF THE G ASTRO-INTESTINAL TRACT. 531 
 
 larly uneven on the surface, and on section resistant to the knife 
 (Fig. 251). The size of the liver, even in advanced stages, is by 
 no means always small. A study of statistics obtained at the post- 
 mortem table shows that the liver in perhaps a majority of the 
 cases of otherwise typical Laennec's cirrhosis is larger than the 
 
 Pig, 251. — Atrophic cirrhosis of the liver of a boy aged sixteen years, showing also thick- 
 ening of the capsule and ligaments (perihepatitis). 
 
 normal organ. The surface of section presents bands of connec- 
 tive tissue surrounding groups of acini, and compressing them so 
 that they rise above the surface. The connective-tissue bands are 
 dull gray or white in appearance, the enclosed acini yellowish or 
 brownish. 
 
 Microscopically the process is found to begin as a proliferation 
 of the connective tissues around the interlobular branches of the 
 portal vein. In the earlier stage there are found round-cell infil- 
 tration and proliferation of fibroblastic cells, causing moderate 
 obstruction to the portal circulation. Later the connective tissue 
 becomes sclerotic, greater compression of the portal veins en- 
 sues, and considerable obstruction of the circulation results. At 
 the same time the acini are compressed and may suffer degenera- 
 tion. This, however, is rarely pronounced. There is little ten- 
 dency to extensive invasion of the acini themselves by the inflam- 
 matory process. New-formed biliary ducts may be present in 
 considerable numbers in the hyperplastic interlobular tissue. 
 
 Associated Changes. — The marked result of atrophic cirrhosis 
 is obstruction to the portal circulation. This occasions congestion 
 of the spleen and gastro-intestinal mucosa, and eventually ascites. 
 When the obstruction becomes extreme collateral circulation may 
 
532 TEXT-BOOK OF PATHOLOGY. 
 
 relieve the congestion of the portal system. The most prominent 
 anastomoses are those between the gastric and esophageal veins, 
 and between the hemorrhoidal veins and the veins of Retzius with 
 the retroperitoneal veins. The veins of the round ligament 
 increase in size and communicate with the superficial veins at the 
 umbilicus. 
 
 Gastro-intestinal catarrh and enlargement of the spleen are 
 usually prominent in cirrhosis. Jaundice is rare, because the bile- 
 ducts are rarely compressed. 
 
 In some instances the liver is large and smoother, softer and 
 lighter in color, from the fact that considerable fatty infiltration 
 of the acini is associated with the cirrhosis (Fig. 252). In the 
 
 Fig. 252.— Cirrhosis of the liver, showing new-formed connective tissue, proliferated bile- 
 ducts, and fatty infiltration of some of the hepatic cells. 
 
 later stages such cases may become converted into the typical 
 form by absorption of the fat. 
 
 Hypertrophic cirrhosis is perhaps more frequent in warm 
 climates than elsewhere. The liver is uniformly enlarged, smooth, 
 or moderately granular on the surface, and indurated. On section 
 the color is seen to be more or less yellowish or greenish, and either 
 uniform or mottled. 
 
 Microscopically proliferation in the interlobular connective 
 tissues is found, as in the atrophic form, but it does not bear the 
 same relation to the portal veins and is less prone to cicatricial 
 contraction. Unlike the atrophic form, there is decided extension 
 into the peripheral zones of the acini, and everywhere between the 
 columns of hepatic cells there maybe seen proliferated fibroblastic 
 cells. Within the new-formed connective tissue may be seen 
 columns of low cylindrical cells surrounding a narrow canal. 
 These are proliferated bile-ducts. Proliferation of the liver-cells 
 
DISEASES OF THE G ASTRO-INTESTINAL TRACT. 533 
 
 themselves is also frequent, and throughout the organ the cells are 
 found more or less deeply stained with biliary pigment. 
 
 Associated Changes. — The most prominent is jaundice. Ob- 
 struction of the portal circulation rarely becomes marked. 
 
 Biliary cirrhosis is a form of chronic hepatitis consequent 
 upon obstruction of the biliary ducts. The first eifect of such 
 obstruction is a swelling of the liver, due to the retention of bile, 
 and perhaps also to congestion. Eventually the stagnation of the 
 bile, with production of irritant substances, leads to reactive in- 
 flammation. 
 
 The appearance of the liver is much the same as that seen in 
 hypertrophic cirrhosis of the ordinary type. The organ is uni- 
 formly enlarged, and may be somewhat granular upon the surface 
 or entirely smooth. On section the substance is found to be 
 deeply bile-stained, and has a yellowish or greenish color. The 
 substance is firm, and the overgrowth of connective tissue may be 
 visible on the surface. 
 
 Microscopically the first discoverable changes are spots of in- 
 sular necrosis in the peripheral zones of the acini. Subsequently 
 
 Fig. 253.— Perihepatitis associated with cirrhosis of the liver. 
 
 proliferation of connective tissue replaces these and spreads to the 
 interlobular tissues. Proliferation around the interlobular biliary 
 capillaries (periangiocholitis) may be a striking characteristic from 
 the first, and multiplication of new bile-ducts and of hepatic cells 
 is frequently observed. In cases of absolute obstruction of the 
 gall-ducts, and in cases in which active fermentative changes in 
 the bile have occurred, rapid fatty degeneration and acute atrophy 
 of the liver may be the terminal change. 
 
 Perihepatitis. — Inflammation of the capsule of the liver and 
 
534 TEXT-BOOK OF PATHOLOGY. 
 
 of the superficial portions of the hepatic structure may be asso- 
 ciated with cirrhosis (Fig. 253), and not rarely occurs in conse- 
 quence of chronic peritonitis. It may lead to considerable thick- 
 ening of the capsule. The pressure of the contracting fibrous 
 tissue may occasion atrophy of the underlying hepatic substance, 
 &nd a more or less uneven and atrophic organ results. Primary 
 inflammation of the capsule may be an expression of syphilitic- 
 infection, and may occur alone or in association with thickening 
 of the peritoneum. Reference will be made, in the discussion of 
 diseases of the peritoneum, to a special form of hyperplastic peri- 
 hepatitis — that known as the Zuckergussleber of Curschmann. 
 
 HYPERTROPHY. 
 
 The regeneration after injuries of the liver shows the power of 
 the liver-cells to undergo active multiplication. Not rarely active 
 hyperplasia of liver-cells throughout the entire organ may occur 
 in association with other diseases, notably hypertrophic cirrhosis. 
 A simple hypertrophy of the liver also occurs in certain well- 
 developed, robust individuals. Enlargements of the liver for- 
 merly regarded as hypertrophies are, for the most part, due to 
 pathologic conditions. 
 
 RUPTURE OF THE LIVER. 
 
 Rupture may occur from direct traumatic injury, and is par- 
 ticularly common in the new-born when forcible delivery has been 
 necessary. In the latter cases small injuries with secondary hem- 
 orrhagic infiltration are observed near the surface of the organ. 
 Portions of liver-cells may be loosened and may be carried as 
 emboli to the lungs. The injury is repaired by active hyperplasia 
 of the liver-cells and of the biliary capillaries, and in this manner 
 the affected part may be restored without the development of scar- 
 tissue. Large injuries, however, occasion the formation of cica- 
 tricial tissue. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis may occur in the form of minute, translucent, 
 miliary tubercles, which may be scarcely visible to the naked eye 
 (Fig. 254), or in the form of larger foci. Tuberculosis of the liver 
 is always a secondary disease. The tubercles arise in the inter- 
 lobular tissue or from the acini themselves. The larger caseous 
 tubercles are rare ; they may be associated with diffuse cirrhotic 
 contraction of the organ. Miliary tuberculosis of the capsule of 
 the liver not rarely occurs in tuberculous peritonitis. 
 
 Syphilis is met with in the form of diffuse infiltration and 
 cirrhosis, or in the form of gummata. Either of these varieties 
 may be found as a result of acquired or of hereditary syphilis. 
 
DISEASES OF THE GASTRO-INTESTINAL TRACT. 
 
 535 
 
 In the diffuse form the liver presents much the same appear- 
 ances as in atrophic cirrhosis, but the connective-tissue bands 
 are much more pronounced and the liver is prone to be irregu- 
 
 Fig. 254.— Miliary tubercles in the liver. 
 
 larly contracted and lobulated (Fig. 255). Gummata may oc- 
 cur in any part of the organ, and may be single or multiple, 
 presenting themselves as rounded, yellowish, or grayish masses, 
 
 Fig. 255.— Syphilitic cirrhosis of the liver : lobulated liver (Kast and Rumpel). 
 
 ofttimes showing central necrosis and surrounded by connective- 
 tissue hyperplasia (Fig. 104). Complete cicatrization may lead to 
 decided scar-formation. In addition to these forms, congenital 
 
536 TEXT-BOOK OF PATHOLOGY. 
 
 syphilis may manifest itself in the form of a uniform, diffuse con- 
 nective-tissue hyperplasia and round-cell infiltration. The liver- 
 cells are pushed apart and are ill-developed or atrophic (Fig. 256). 
 
 . '£W «*• • • .- -■■■■ f- -> «'• V 
 
 il W9A 
 
 
 
 Fig. 256.- Diffuse congenital syphilis of the liver. 
 
 I/eprosy occasionally affects the liver, causing the formation 
 of nodular masses. 
 
 TUMORS. 
 
 Fibromata, lipomata, and myomata are occasionally 
 observed as nodular masses, but have little significance. 
 
 Angioma is a more important form. This tumor occurs upon 
 the surface of the organ, and is usually of small size, rarely 
 exceeding that of a walnut. It is more commonly found in 
 persons who have died at advanced years than in young persons. 
 Angiomata appear as dark-red or bluish, slightly elevated areas, 
 either sharply outlined and encapsulated, or merging gradually 
 into the surrounding tissue. Microscopically they are found to be 
 cavernous angiomata, and doubtless owe their origin to dilatation 
 of the capillaries, with coincident atrophy of the liver-cells. 
 
 Sarcoma of the liver may occasionally be primary, but is ex- 
 ceedingly rare. Secondary sarcoma, on the other hand, is very 
 common, especially the melanotic form following primary sarcoma 
 of the eye. 
 
 I/ymphadenomata are frequent in the liver in the course of 
 the generalization of leukemic lymphadenoma ; but it has not as yet 
 been fully determined to what extent these are to be considered 
 as true tumors, and to what extent as mere infiltrations of leuko- 
 cytes consequent upon the enormous leukocytosis of this disease. 
 Similar lymphomatous nodules, though much less marked and 
 numerous, occur in typhoid fever and other infectious diseases. 
 
DISEASES OF THE G ASTRO-INTESTINAL TRACT. 537 
 
 Adenoma of the liver is met with in several forms. There 
 may be either nodular masses, more or less encapsulated and of 
 grayish-white or pinkish color, or a form of diffuse infiltration of 
 the liver-substance by encapsulated nodules of similar character. 
 Considerable cirrhosis of the liver may be associated with the 
 latter cases, and they cannot be clearly distinguished from cir- 
 rhotic cancer (see below). 
 
 Carcinoma of the liver is rather rare as a primary tumor, but, 
 like adenoma, may be nodular or diffuse. The nodular or massive 
 cancer appears as a single mass of varying size, ofttimes sur- 
 rounded by local metastatic nodules. On section the color is 
 grayish or pinkish, and there may be central necrosis and soften- 
 
 Fig. 257.— Cirrhotic cancer of the liver (Hanot and Gilbert). 
 
 ing. Diffuse hepatic cancer occurs as a widespread and more or 
 less uniformly distributed infiltrating growth. Not rarely in such 
 cases there is associated cirrhosis, and the macroscopic appearance 
 of the liver may be strikingly like that of an ordinary cirrhosis, 
 though the liver is sometimes much enlarged (Fig. 257). The 
 terms cirrhotic cancer and cancer with cirrhosis have been applied 
 to this form. Finally, the diffuse form may surround and spring 
 from the periportal structures, and may ramify in the form of an 
 interlobular infiltration. 
 
 Formation and Structure of Adenomata and Carcinomata. — 
 Microscopically there is no sharp dividing-line between these 
 growths. The adenomata present tubular formations of a more or 
 
538 TEXT-ROOK OF PATHOLOGY. 
 
 less elongated and tortuous character, composed of cylindrical or 
 of more irregular-shaped epithelial cells. In some instances these 
 are strikingly like new-formed biliary capillaries, and perhaps 
 they occasionally originate from these structures. More com- 
 monly, however, the origin would seem to be from the hepatic 
 cells themselves. The columns of hepatic cells undergo prolifera- 
 tive change, and at the same time become somewhat transformed, 
 assuming the tubular arrangement of adenoma. Occasion- 
 ally adenoma and cystic adenoma originate from the mucous 
 glands of the larger biliary ducts. When cirrhosis is associated 
 with adenomatous infiltration it is probable that the primary 
 change is a cirrhotic overgrowth which induces secondary hyper- 
 plasia of the epithelial cells, instead of degenerative changes, such 
 as usually result from the pressure of new-formed fibrous tissue. 
 
 Carcinoma of the liver is similar in origin and structure to 
 adenoma. The cellular acini and tubules are more irregular, and 
 there is an evident tendency to diffuse infiltration and atypical 
 formation of acini. 
 
 Secondary carcinoma of the liver is very common as a 
 result of carcinoma of the stomach or of other parts of the portal 
 
 Pig. 258.— Secondary cancer of the liver : a, columns of liver-cells filled with bile-pig- 
 ment; b, endothelial walls of capillaries; c, carcinomatous emboli in the capillaries 
 (Hanoi and Gilbert). 
 
 distribution. It is usually due to cancerous embolism in the por- 
 tal capillaries, with subsequent development of the emboli (Fig. 
 258). The liver becomes enlarged, and presents nodular masses 
 
DISEASES OF THE GASTROINTESTINAL TRACT 
 
 539 
 
 upon its surface or within its substance. These nodules vary 
 from the size of a pea to that of an apple, and are frequently 
 sharply delimited by capsule-formation, especially those which 
 have reached considerable size. Not rarely the nodules are in- 
 dented upon the surface (umbilicated) from central softening or 
 from contraction of fibrous tissue within (Fig. 259). Secondary 
 
 Fig. 259.— Metastatic nodules of carcinoma on the surface of the liver (Hanot and Gilbert). 
 
 cancer of the liver may also result from direct extension of cancer 
 of the stomach or of the gall-bladder and biliary ducts. In all 
 cases the new growths tend to compress the bile-ducts and lead 
 to biliary pigmentation of the liver-substance, as well as to gen- 
 eral icterus. 
 
 Cysts of the liver are rare. They may spring from the biliary 
 ducts which have suffered simple dilatation, or from the mucous 
 glands of the larger bile-ducts (cystic adenoma). Occasionally 
 small cysts are seen which suggest origin from dilatation of the 
 lymphatic channels. 
 
 PARASITES. 
 
 Of the protozoa, coccidial Psorospermice (Fig. 260) have been 
 occasionally demonstrated in the human liver in small nodular 
 tumors ; but a more important parasite is the Amoeba coli, occur- 
 ring in abscess of the liver secondary to amebic dysentery. The 
 pus of the abscess may contain immense numbers of the amebse, 
 and doubtless these organisms bear an important relation to the 
 lesion, perhaps causing necrosis by their own activity and then 
 liberating pyogenic organisms which they have carried from the 
 intestines, and which complete the pathologic process. The larval 
 Pentastoma denticulatum is occasionally met with. 
 
540 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 The Distoma hepaticum and the Distoma lanceolatum occasion- 
 all} 7 infest the biliary ducts, and the Distoma hematobium the portal 
 vein. Asearides sometimes creep upward in the biliary ducts as 
 far as the branches within the liver. The Oysticercus cellulosce is 
 a rare parasitic formation. 
 
 Echinococcus cyst. — The most important parasitic disease of 
 
 m Mm 
 
 .<-,; 
 
 <&&«* Q - Q> ' «3 er ©0 € jM 
 
 l^fS 
 
 '-- 
 
 Fig. 260.— Coccidia in the wall of a bile-duct and the adjacent hepatic structure of a 
 
 rabbit. 
 
 the liver is the echinococcus-cyst, caused by the presence of the 
 larvae of the Taenia echinococcus (see Part I.). This parasite 
 occasions cystic formations of various kinds within the liver. The 
 cyst has a double wall : the outer, of connective tissue ; the inner, 
 
 Fig. 261.— Echinococcus niultilocularis (Luschka). 
 
 a parenchymatous membrane, from which buds (brood-capsules) 
 and secondary cysts are prone to originate. There may be a 
 single cyst containing clear liquid of low specific gravity, or a 
 mother-cyst containing daughter-cysts, either upon the inner wall 
 or floating free within the liquid after their separation. Some- 
 
DISEASES OF THE G ASTRO-INTESTINAL TRACT 541 
 
 times even granddaughter-cysts are formed. Occasionally the 
 daughter-cysts are found outside of the mother-cyst, extrusion in 
 such cases having taken place. A form of multilocular cyst is 
 more rarely observed in which there are numerous small cysts 
 embedded in more or less firm connective tissue (Fig. 261). 
 Echinococcus-cysts may rupture into the abdomen or into sur- 
 rounding viscera. The most serious condition is rupture into the 
 
 Fig. 262.— Echinococcus-cyst of the liver (from a specimen in the Museum of the Phila- 
 delphia Hospital). 
 
 vena cava, as the result of which hydatid disease of the heart, the 
 brain, or other organs may ensue. Bacterial invasion occasionally 
 takes place, and abscess may result. Finally, the liquid contents 
 may be absorbed, and the cyst may be reduced to a small cavity 
 having a shrivelled wall and containing granular or caseous 
 detritus (Fig. 262). Echinococcus-cysts may press upon the gall- 
 duct, producing jaundice, or upon the portal veins, causing ascites. 
 
 THE BILIARY DUCTS AND GALL-BLADDER. 
 INFLAMMATIONS. 
 
 Cholangitis, or inflammation of the biliary ducts, is 
 
 most frequently secondary to duodenal catarrh, though it may be 
 the result of direct irritation by gall-stones, by foreign bodies 
 which have entered from the intestine, or by parasites or bacteria. 
 In the cases secondary to duodenitis the inflammation usually 
 extends but a short distance upward from the mouth of the com- 
 mon bile-duct, but there may sometimes be more extensive in- 
 volvement of the ducts, and the mucous membrane of the gall- 
 bladder may be affected at the same time. The mucosa is swollen, 
 more or less edematous, and secretes abundant mucus. The 
 
542 TEXT-BOOK OF PATHOLOGY. 
 
 result is obstruction of the duct with retention of bile and jaun- 
 dice. 
 
 Suppurative cholangitis may result from bacterial in- 
 vasion and fermentation of retained bile, or, in a localized form, 
 from the impaction of a gall-stone. More rarely it is due to 
 rupture of suppurative foci in the liver into the gall-ducts ; and 
 occasionally it has been found as an independent affection asso- 
 ciated with pyemia or other infectious diseases. Among the 
 micro-organisms discovered in suppurative cholangitis the pyo- 
 genic micrococci and the Bacillus coli communis are most fre- 
 quent. The bile-ducts are filled with more or less decomposed 
 bile, or with puriform liquid, and the walls of the ducts, espe- 
 cially the larger ones, may present an ulcerated or necrotic ap- 
 pearance. Small dilatations may occur in places where the duct 
 has become deeply ulcerated, and later hepatic abscesses of con- 
 siderable size may form. 
 
 Chronic cholangitis may be the outcome of an intense 
 acute or repeated acute attacks, but is more commonly met with 
 as a consequence of chronic obstruction of the ducts and retention 
 of bile. A localized form, causing cicatricial stenosis, results from 
 intense inflammatory lesions following the passage of stones. The 
 gall-ducts in chronic cholangitis are more or less thickened, and 
 in the cases due to obstruction may be considerably dilated. 
 
 Results of Cholangitis. — In the acute form extension may take 
 place to the ducts within the liver, and in case of bacterial in- 
 vasion pericholangitis and abscesses may form. More commonly 
 acute cholangitis leads to but a temporary overfilling of the biliary 
 capillaries with bile, and in consequence to obstructive jaundice. 
 When the obstruction is continued for a considerable length of 
 time reactive changes occur in the liver, constituting the form of 
 cirrhosis called biliary cirrhosis (see page 533). 
 
 Cholecystitis, or inflammation of the gall-bladder, 
 may result from extension of cholangitis, or may be due to the 
 irritation of retained bile or of gall-stones. It is prone to assume 
 a purulent character ; and the gall-bladder may become filled 
 with pus [empyema of the (/all-bladder). This may rupture, dis- 
 charging into the abdominal cavity, into adjacent viscera, or ex- 
 ternally. The wall of the gall-bladder is usually much thickened, 
 and the mucous membrane is swollen and ulcerated. 
 
 STENOSIS AND DILATATION. 
 
 Stenosis of the bile-ducts is most commonly the result of 
 acute inflammation, causing thickening of the mucosa and ac- 
 cumulation of mucus. It may result from chronic cholangitis 
 with cicatricial overgrowth of connective tissue ; from the impac- 
 tion of gall-stones, or the presence of various foreign bodies, such 
 
DISEASES OF THE GASTRO-INTESTINAL TRACT. 543 
 
 as particles of food, mucus, round-worms or other parasites within 
 the duct ; from pressure by aneurysms, by tumors of the head of 
 the pancreas, pylorus, duodenum, lymphatic glands, or of the 
 liver ; and from tumors of the gall-ducts themselves. Sometimes 
 it is due to the constriction of adhesions resulting from peritonitis. 
 Obstruction of the ducts leads to the retention of bile and dilata- 
 tion of the ducts above, with consequent enlargement of the liver 
 and jaundice. Obstruction of the cystic duct, which is most fre- 
 quently due to the impaction of a stone, may occasion dilatation 
 of the gall-bladder with dropsical liquid, in consequence of the 
 passive hyperemia produced by compression of the veins at the 
 neck of the gall-bladder. This condition is spoken of as dropsy 
 of the gall-bladder. Sometimes suppurative inflammation occurs, 
 and empyema of the gall-bladder results. 
 
 Contraction of the gall-bladder, or even complete shrink- 
 age or atrophy, may result from obstruction at the mouth of the 
 cystic duct, or from inflammatory processes within its walls or 
 surrounding it. 
 
 Dilatation of the ducts or of the gall-bladder most frequently 
 results from stenosis of the ducts below. 
 
 GALL=STONES ; CHOLELITHIASIS. 
 
 Gall-stones are concretions resulting from inspissation of bile, 
 or from the deposit of various substances from the bile. Most 
 frequently they are formed in the gall-bladder ; occasionally they 
 originate in the bile-ducts. 
 
 Etiology. — The causes are imperfectly understood. Ad- 
 vanced years, the female sex, sedentary life, and high living seem 
 to be factors of importance. Inflammatory conditions leading to 
 obstruction and retardation of the outflow of bile, and also to des- 
 quamation of epithelium, which, with mucus, serves to form the 
 nuclei of the stones, seem to be among the causes. Besides these 
 conditions there are probably indefinite alterations of the bile 
 which permit of precipitation of some of its constituents, notably 
 cholesterin. Bacterial decomposition of the bile and inflammation 
 of the ducts, causing epithelial desquamation, are regarded as im- 
 portant factors by some authorities. 
 
 Structure and Pathologic Anatomy.— Gall-stones may 
 be single or multiple, and may vary in size from minute granular 
 particles of biliary sand to calculi several centimeters in diameter. 
 When single they occur as rounded or oval masses ; when multiple 
 they are prone to be marked with facets ; when formed within the 
 bile-ducts they are elongated. Biliary sand is, for the most part, 
 composed of biliary pigments in combination with calcium salts. 
 The larger stones on section usually show a central nucleus com- 
 posed of epithelium or mucus mingled with inspissated bile, sur- 
 
544 TEXT-BOOK OF PATHOLOGY. 
 
 rounded by a zone of somewhat radiating and crystalline structure, 
 composed of cholesterin. Around this may be a coat of bile-pig- 
 ment. In other cases the entire stone is formed of biliary pig- 
 ments in combination with calcium salts, or more rarely the 
 calculus consists entirely of carbonate of lime. 
 
 Gall-stones may lie in the gall-bladder or ducts without caus- 
 ing serious disturbances, or from time to time attacks of biliary 
 colic denote their passage through the ducts to the bowel. They 
 may pass through the ducts into the intestine when of small size, 
 but often become impacted in the lower part of the common duct, 
 generally just above the duodenal papillae or in the mouth of the 
 cystic duct. Secondary changes in the gall-bladder (dilatation and 
 inflammation) and in the liver (enlargement, cirrhosis) may result ; 
 and the stone may cause local ulceration, and may Anally escape 
 into the bowel or into other parts by ulceration. Occasionally 
 gall-stones remain impacted for long periods without causing 
 serious disturbances, enough space remaining to permit the es- 
 cape of bile. 
 
 TUMORS. 
 
 Tumors of the gall-ducts and gall-bladder are rare. Primary 
 carcinoma arising from the mucous glands is the most important. 
 This appears as an irregular elevation of the mucous surface, and 
 rapidly infiltrates the adjoining parts. In cases of primary cancer 
 of the gall-bladder the liver is soon involved. Gall-stones are 
 present in a great majority of the cases and probably play an im- 
 portant etiologic part by their continuous irritation. On the other 
 hand, the gall-stones may form in consequence of the stagnation of 
 bile and other local conditions caused by the tumor. Secondary 
 carcinoma of the gall-bladder or ducts most frequently results 
 from cancer of the liver. The lower end of the duct may be in- 
 volved in cases of carcinoma of the papilla of Vater. Sarcoma, 
 fibroma, and other tumors are rare. 
 
 JAUNDICE. 
 
 Jaundice, or icterus, is a discoloration of the skin and other 
 parts, resulting from the presence in the blood of biliary pigments. 
 
 Etiology. — Jaundice has been described as being of two forms, 
 the obstructive, mechanical, or hepatogenous, and the non-obstructive 
 or hematogenous variety. This distinction, however, has been to 
 a large extent abandoned, and it is now admitted that the abnor- 
 mal coloring-matter in all cases originates in the liver, and is in- 
 variably a hepatic pigment. 
 
 Among the distinctly mechanical causes of jaundice the most 
 frequent is occlusion of the ducts by catarrhal duodenitis and 
 cholangitis. To this form the term catarrhal jaundice is generally 
 
DISEASES OF THE G ASTRO-INTESTINAL TRACT. 545 
 
 applied. Less commonly obstruction may be occasioned by 
 foreign bodies, gall-stones, or parasites within the ducts ; by the 
 pressure of tumors of the duodenum, pancreas, and the lymphatic 
 glands of the liver or of the gall-ducts themselves ; by the press- 
 ure of aneurysms upon the ducts ; or by occlusion of the biliary 
 passages within the liver by abscess, hydatid cysts, hypertrophic 
 cirrhosis, carcinoma, or other tumors. Congestion of the liver 
 may lead to jaundice by the swelling of the organ consequent upon 
 the overfilling of the vessels with blood, or by reason of the re- 
 sorption of bile due to the alterations of pressure of the blood in 
 the different vascular channels. Hematogenous jaundice was for- 
 merly regarded as due to disintegration of the blood in the gen- 
 eral circulation, but it is now recognized that formation of the pig- 
 ments can take place only in the liver. There are, however, in- 
 stances of jaundice in which active hemolysis is an element of 
 importance. Jaundice of this character occurs in various severe 
 infections, such as yellow fever, acute yellow atrophy of the liver, 
 the jaundice of the new-born, and in consequence of certain in- 
 toxications (phosphorus, toadstools, the venom of snakes). Several 
 explanations may be applied to cases of this kind. Sometimes 
 excessive blood-destruction leads to formation of abnormally large 
 quantities of bile (polycholia), and in consequence to absorption 
 of biliary pigment by the lymphatics in the liver. In other cases 
 toxic degeneration of the hepatic cells may lead to stimulation of 
 the hepatic function, or to swelling of the cells and compression 
 of the biliary capillaries, and in consequence to absorption of the 
 bile. Finally, in the jaundice of the new-born, as well as in some 
 instances of sudden emotional jaundice, disturbance of the circula- 
 tion within the liver may be a potent cause. 
 
 Pathologic Anatomy. — Microscopic examination of the liver 
 may show the biliary capillaries distended with bile and the 
 hepatic cells themselves more or less pigmented. The bile is 
 absorbed by the lymphatics, and ultimately reaches the general 
 circulation and pigments the tissues. The earliest evidence is 
 seen in the intima of the vessels ; later, all the tissues and organs 
 of the body may be involved, and visible discoloration appears in 
 the skin and external mucous membranes. The urine is dark 
 brownish or greenish in color, and all of the secretions and liquid 
 exudates may be pigmented. In cases caused by obstruction of 
 the bile-ducts the bile cannot reach the intestines and the stools 
 have a quite characteristic putty color. In " hematogenous " 
 jaundice the color of the stools is to a certain extent maintained. 
 Intense disturbances, especially of the nervouc system, result from 
 excessive cholemia, but are due to the cholic acid salts, rather than 
 to the biliary pigments. 
 
546 TEXT-BOOK OF PATHOLOGY. 
 
 THE PANCREAS. 
 
 CONGENITAL ABNORMALITIES. 
 
 Complete absence lias been met with in monstrosities. More 
 frequently an adventitious pancreas or heterotopic pancreatic 
 tissue is observed. Small nodules of pancreatic tissue may be 
 found in the omentum, the wall of the intestines, or elsewhere. 
 
 CIRCULATORY DISTURBANCES. 
 
 Active hyperemia occurs during digestion and in association 
 with acute inflammation. 
 
 Passive hyperemia occurs in cases of obstruction to the 
 portal circulation, but rarely leads to notable changes. 
 
 Hemorrhage may occur in the pancreas, in the form of 
 minute petechias or diffuse hemorrhagic infiltration, as the result 
 of passive congestion or of various hemorrhagic and infectious 
 diseases, such as purpura, scurvy, septicemia, or the extreme 
 anemias. 
 
 More extensive hemorrhage in the pancreas and in the tissues 
 surrounding it sometimes occurs as an " idiopathic " affection, the 
 causes being obscure. It is more common in the young than the 
 old, and in the male than the female sex, and at times appears to 
 be dependent upon traumatism. Doubtless in some cases the hem- 
 orrhage is the result of necrosis or other pre-existing affections of 
 the pancreas or of its blood-vessels. The changes are most marked 
 in the head of the organ, although any part may be affected. There 
 may be diffuse infiltration, or the hemorrhage occurs in isolated 
 foci. Occasionally considerable collections of blood may be met 
 with, and secondary reactive inflammation and necrosis are fre- 
 quently observed. The peritoneum, the wall of the duodenum, 
 and other surrounding tissues may be coincidently involved. 
 
 Sudden death may occur in this condition from shock or com- 
 pression of the solar plexus, or the case may terminate in other 
 pancreatic affections. Doubtless chronic indurative pancreatitis 
 originates in this way in some cases. More commonly progressive 
 necrosis and suppurative inflammation terminate the disease. 
 
 ATROPHY AND DEGENERATIONS. 
 
 Atrophy of the pancreas occurs in old age and as the 
 result of marasmic conditions. The entire organ is involved in 
 such cases. Localized atrophy may be associated with various 
 degenerations or other diseases of the organ. Thus, in carcinoma 
 or in cirrhosis pressure-atrophies are extremely frequent. 
 
 The association of atrophy of the pancreas with diabetes is a 
 most important one, and it may be assumed that certain cases of 
 diabetes are wholly dependent upon disease or atrophy of this 
 
DISEASES OF THE GASTRO-INTESTINAL TRACT. 547 
 
 organ. Though atrophy is the most common pancreatic condition 
 in diabetes, cirrhosis, carcinoma, and calculous obstruction of the 
 ducts have been observed. It is believed by some that the pan- 
 creas elaborates sugar-destroying ferments whose presence in the 
 blood is necessary to prevent hyperglycemia. In diseases of the 
 pancreas this ferment is lacking and glycosuria results. 
 
 Parenchymatous degeneration may occur in consequence 
 of acute infections, and resembles the cloudy swelling of the liver, 
 kidneys, and heart occurring in the same diseases. The organ 
 becomes somewhat enlarged ; is softer than normal ; and may at 
 the same time be congested. 
 
 Microscopically the cells are found to have undergone granular 
 degeneration. 
 
 Amyloid degeneration is a rare condition occurring in 
 association with amyloid disease of other organs. 
 
 Pigmentation may be met with in the atrophic organ of old 
 persons, or in consequence of hemorrhagic infiltration and subse- 
 quent disorganization of the extravasated blood. Of particular 
 interest are the cases of hematochromatosis affecting the pancreas, 
 together with the intestines, liver, and other abdominal organs in 
 drunkards. The affected organs in this condition present more or 
 less extensive hematogenous pigmentation. 
 
 Necrosis of small areas of the pancreas may occur in conse- 
 quence of hemorrhage or of inflammatory conditions. Sometimes 
 the entire organ is disorganized by a form of gangrenous necrosis, 
 especially in case of pancreatitis resulting from perforation of a 
 gastric ulcer or from extension of other severe inflammatory 
 lesions. 
 
 Pat-necrosis is a form of degeneration or necrosis peculiar 
 to the fatty tissue of the pancreas and of the omentum. Most 
 frequently it is found in association with acute or chronic pancrea- 
 titis, with tumors of the pancreas, or obstruction of its duct ; but 
 it may occur independently, and it may appear in the fatty tissue 
 of the omentum without involving the pancreas. Minute foci, 
 having a gray or white, opaque appearance, or more rarely larger 
 areas due to confluence of small foci of necrosis, are found 
 in the adipose tissues. Hemorrhagic infiltration may be asso- 
 ciated, and sometimes extensive hemorrhage may ensue. Inflam- 
 mation of the pancreatic tissues around the foci of necrosis is com- 
 mon, and in some instances extensive disorganization (necrosis) of 
 the pancreas occurs. 
 
 Microscopically the changes consist of, first, the formation of 
 fat-crystals within the adipose cells, and subsequently the dis- 
 organization of these and the formation of calcium salts of the fat- 
 acids, the microscopic appearance at this stage being that of indefi- 
 nite granular or translucent masses. The nature of fat-necrosis 
 has been previously discussed (see page 94). 
 
548 TEXT-BOOK OF PATHOLOGY. 
 
 INFLAMMATIONS. 
 
 Pancreatitis may be acute or chronic. The acute variety 
 presents itself in different forms, the most frequent being the 
 hemorrhagic and the suppurative or necrotic. Chronic pancrea- 
 titis is analogous to chronic hepatitis, and leads to similar indura- 
 tion or cirrhosis. 
 
 Acute hemorrhagic pancreatitis occurs most commonly in young 
 persons, and is probably in most, if not all, cases dependent upon 
 infection of the pancreas through its ducts. It is likely that some 
 cases are not in reality inflammatory, but simply instances of 
 degenerations of the pancreas, with hemorrhage and round-cell 
 infiltration as consequences. The pancreas is swollen, especially 
 at its head ; the lobules are enlarged and the interlobular tissues 
 compressed. Hemorrhagic infiltration is a constant condition, but 
 variable in extent. Microscopically the cells of the pancreas are 
 swollen, and usually present the appearances of parenchymatous 
 degeneration. The interlobular tissues are infiltrated with round 
 cells. Localized necrosis and fat-necrosis may be associated. 
 Rapid death is the usual consequence, but it is probable that 
 some of the cases terminate in chronic pancreatitis. 
 
 Acute suppurative or necrotic pancreatitis may result from 
 direct extension of septic processes in the neighborhood, as in gas- 
 tric or duodenal ulceration, purulent collections in the peritoneum, 
 and the like. It may also occur as an independent affection, most 
 frequently in consequence of infection from the intestinal tract 
 through the ducts. Occasionally metastatic abscesses are observed 
 in the pancreas. Hemorrhagic pancreatitis may be converted into 
 the necrotic form in consequence of extensive extravasation of 
 blood and secondary infection. 
 
 The organ presents a variable appearance, according to the 
 cause and extent of the process. There is generally marked 
 swelling with more or less softening, and not rarely necrotic foci. 
 Complete gangrene or necrosis is an occasional termination. In 
 other cases parts of the pancreas may slough, and may be dis- 
 charged through the intestines or into the peritoneum, setting up 
 fatal peritonitis. 
 
 Chronic indurative pancreatitis, or cirrhosis of the pancreas, may 
 be hematogenous in origin, resulting from syphilis and alcoholism, 
 or it may be caused by prolonged irritation exercised through the 
 pancreatic ducts. In the latter case it may be secondary to duod- 
 enal catarrhs or obstructions of the pancreatic duct. In some 
 cases it is doubtless the outcome of acute attacks. 
 
 The pancreas in the earlier stages is enlarged and hard. On 
 section it may present a homogeneous structure and may be of 
 cartilaginous consistence. Macroscopically the tissues between 
 the acini are visibly infiltrated and hyperplastic, the amount 
 
DISEASES OF THE OASTRO-INTESTINAL TRACT. 549 
 
 of connective tissue being greatly in excess of the normal. In the 
 later stages the organ becomes contracted, and may be consider- 
 ably reduced in size and of stony hardness. 
 
 Microscopically the parenchyma of the organ is found to be 
 atrophied or degenerated in consequence of contraction of the 
 hyperplastic fibrous tissue. Fat-necrosis and fatty degeneration 
 of the pancreatic cells are frequently associated. 
 
 INFECTIOUS DISEASES. 
 
 Syphilis may occur in the pancreas in the form of indurative 
 pancreatitis or of gummata. The former may occur in adults, but 
 is more common in the new-born, in association with indurative 
 changes in the liver, lungs, and other organs. 
 
 Tuberculosis of the pancreas, in the form of miliary 
 tubercles, may occur in cases of generalized tuberculosis. 
 
 TUMORS. 
 
 Primary benign tumors have occasionally been met with, but 
 are unimportant. 
 
 Carcinoma. — Primary cancer may affect the head or other 
 parts of the pancreas, and is of the glandular (scirrhous), or, more 
 rarely, of the cylindrical-celled, variety. Compression with sec- 
 ondary cystic distention of the pancreatic duct and obstruction of 
 the common bile-duct or of the veins (portal, superior mesenteric, 
 and splenic) behind the head of the organ may result. Metastasis 
 to the neighboring lymphatic glands and to the liver is frequent. 
 Secondary cancer may affect the pancreas by extension of cancer 
 of the stomach or of the duodenum. 
 
 Pathologic Physiology. — Pancreatic carcinoma, and other chronic 
 diseases of the pancreas, often occasion rapid emaciation, and some- 
 times fatty diarrhea, lipemia, and lipuria. Keference has already 
 been made to the occurrence of diabetes (glycosuria) in pancreatic 
 diseases. In a mechanical way cancer of the head of the pancreas 
 may cause jaundice by obstruction of the bile-ducts ; splenic en- 
 largement, intestinal congestion, diarrhea, and ascites by obstruc- 
 tion of the adjacent veins ; repeated vomiting and sometimes 
 intestinal obstruction by compression of the duodenum. 
 
 Sarcoma is rarely primary. Secondary nodules are occasion- 
 ally observed. 
 
 Cysts of the pancreas may be of several kinds. Dilatation of 
 the pancreatic duct or its branches may occasion a single cyst or 
 multiple cysts filled with serous or gelatinous liquid. Hemorrhagic 
 cysts are sometimes the result of necrosis of portions of the organ, 
 or a primary hemorrhage (hematoma) may be converted into a 
 serous cyst. The latter is the mode of formation of some of the 
 large cysts occurring, for the most part, near the tail of the pan- 
 
550 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 creas. In other cases, it has been held, these cysts result from 
 primary necrosis and subsequent digestion of the necrotic area by 
 the pancreatic secretions. In rare instances cysts of the pancreas 
 have a glandular structure somewhat resembling that of ovarian 
 cystomata. 
 
 Cystic accumulations in the lesser omental cavity, resulting from 
 localized peritonitis, may be difficult to distinguish from true pan- 
 creatic cysts, as some of the latter lie more outside than within the 
 pancreas. In some instances such localized peritonitis seems to 
 be the result of extension of pancreatic inflammations. 
 
 The fluid of pancreatic cysts often contains a proteolytic and 
 an emulsifying ferment, but the contents of other abdominal cysts 
 mav have similar constituents. 
 
 The Pancreatic Duct. 
 
 Obstruction of the pancreatic duct may be due to tumors of 
 the papilla in the duodenum or of the head of the pancreas, to 
 calculi, to inflammatory thickening of the duct itself, or to the 
 pressure of contracting fibrous tissue in chronic pancreatitis. 
 Most commonly it leads to dilatation of the duct, this sometimes 
 becoming so great as to occasion actual cystic formations (Fig. 
 263). The dilated ducts are filled with clear liquid, but some- 
 
 Fig. 263.— Dilatation of the pancreatic duct and atrophy of the pancreas, due to calculi 
 (Orth). 
 
 times through bacterial infection this is rendered turbid, or is 
 actually converted into pus. Occasionally small cysts, caused 
 by distention of the finer divisions of the duct, are scattered 
 through the organ (pancreatic acne). These are supposed to 
 result from catarrhal processes in the ducts themselves. These 
 small cysts are filled with clear or puriform liquid. Some cases 
 so described are doubtless instances of fat-necrosis. 
 
 Pancreatic calculi are composed of carbonate or phosphate 
 of lime, and usually have an irregular shape. They may occasion 
 cystic distention of the ducts and abscess-formation. 
 
DISEASES OF THE OASTRO-INTESTINAL TRACT. 551 
 
 THE PERITONEUM. 
 
 CONGENITAL ABNORMALITIES. 
 
 Absence of the peritoneum has been described ; but more 
 frequently minor defects, such as absence of the omentum or 
 unnatural length of the omentum or mesentery, localized defects, 
 fenestrations, and the like, have been observed. The peritoneal 
 extension into the inguinal canal normally becomes occluded, but 
 may remain patulous and may lead to congenital hernia. 
 
 CIRCULATORY DISTURBANCES. 
 
 Active hyperemia may occur in association with inflam- 
 mation, or in the vicinity of lesions within the intestine which 
 have not yet occasioned actual inflammation of the peritoneum 
 itself. The affected part is bright red, the arterioles being dis- 
 tended and the endothelium somewhat swollen and elevated. 
 
 Passive hyperemia is more frequent. It may be part of a 
 general venous congestion, or may result from obstruction of the 
 portal vein by thrombosis, cirrhosis of the liver, and similar con- 
 ditions. The venules may be widely dilated, the deeper layers of 
 the peritoneum somewhat edematous, and the lining endothelium 
 swollen and loosened. Intense passive congestion may lead to 
 ascites or to hemorrhage. 
 
 Hemorrhage may occur in the form of punctate extravasa- 
 tions in various septic and hemorrhagic diseases, and in parts 
 adjacent to intense inflammatory lesions, as in the peritoneum 
 covering the bowel near anthrax-ulcerations. Hemorrhagic 
 extravasations may likewise be due to intense passive congestion, 
 as in death from suffocation or in obstructions of the portal circu- 
 lation. Certain forms of intoxication, like phosphorus-poisoning, 
 snake-venom, or the like, may occasion petechial ecchymosis or 
 large suffusions ; and occasionally hemorrhagic extravasations are 
 due to embolic occlusion of the mesenteric arteries. Large 
 hemorrhagic effusions may occur in the retroperitoneal tissues, 
 especially at the root of the mesentery, between the folds of the 
 omentum, or elsewhere into the subperitoneal cellular tissues. 
 These, as well as hemorrhages into the peritoneal cavity itself, are 
 frequently traumatic in origin. Rupture of the spleen, of the 
 liver, of the uterus or Fallopian tubes, or of aneurysms or 
 superficial blood-vessels may be the immediate source of large 
 hemorrhages. 
 
 The extravasated blood within the cellular tissues undergoes 
 gradual absorption, as elsewhere, and may leave pigmented areas 
 and fibrous thickening. The blood within the cavity of the peri- 
 toneum may be directly absorbed, or may be gradually removed 
 
552 TEXT-BOOK OF PATHOLOGY. 
 
 after clotting by degenerative processes and absorption through the 
 lymphatic channels. Inflammatory reaction is wanting unless the 
 blood-mass is infected. 
 
 Dropsy of the peritoneum, or ascites, may occur as a 
 part of a general anasarca in cardiac or renal disease, or may be 
 due to obstruction of the portal circulation, notably by cirrhosis 
 of the liver. In these cases ascites may be absent at first from 
 the freedom of the collateral circulation established between the 
 branches of the inferior and superior vena cava and the peripheral 
 radicles of the portal circulation. Eventually, however, ascites 
 ensues. In the earliest stages of certain cases of intense acute 
 peritonitis and in chronic peritonitis, especially the tuberculous 
 form, when the absorption of liquid from the peritoneum is dis- 
 turbed by occlusion of the lymphatics, the liquid effusion may have 
 a serous and not the ordinary inflammatory character. Chronic 
 peritonitis plays a part in the etiology of many cases of ascites 
 ordinarily regarded as the result of obstruction of the circulation 
 alone, as in cases of cirrhosis of the liver. In such cases the 
 venous stasis may occasion no dropsical exudation until a low- 
 grade chronic peritonitis has developed, when the membrane 
 becomes more permeable and effusion results. 
 
 An occasional cause of ascites is obstruction of the thoracic 
 duct by new-growths of its walls, thrombosis within, or pressure 
 from the outside. The ascitic liquid in such cases frequently has 
 a chylous character. 
 
 The abdomen in ascites is filled with clear watery or yellowish 
 liquid. Gelatinous masses often form in the dependent parts, as 
 in the pelvis and iliac fossae. Occasionally the liquid is quite 
 hemorrhagic ; in other cases it is milky from admixture of chyle 
 or lymph (chylous ascites). The latter cases are dependent upon 
 obstruction and rupture of the lymphatic channels. In other 
 cases, especially in instances of endothelioma or carcinoma of the 
 peritoneum, the liquid has a milky character from admixture of 
 degenerated cells and fatty matter. The term chylifoi-m ascites is 
 sometimes applied to such cases. Microscopically the liquid of 
 ordinary ascites shows red and white blood-corpuscles and occa- 
 sionally a few endothelial cells. In the hemorrhagic cases the 
 number of blood-corpuscles is notably increased, while in chylous 
 ascites there are fat-droplets and granular cells. 
 
 Occasionally collections of dropsical liquid occur between the 
 layers of the omentum (Jiydrops omenti). 
 
 Ascites causes more or less serious compression and displace- 
 ment of the abdominal organs. The respirations may be greatly 
 embarrassed by upward displacement of the diaphragm, and the 
 circulation may be obstructed by the pressure of the liquid upon 
 the veins. Secondary changes in the peritoneum are not unusual. 
 Long-standing ascites nearly always gives rise to a certain amount 
 
DISEASES OF THE OASTBO-INTESTINAL TRACT. 553 
 
 of chronic inflammation (fibrous thickening of the membrane), and 
 termination in tuberculous peritonitis is not infrequent. 
 
 INFLAMMATIONS. 
 
 Inflammation of the peritoneum, or peritonitis, is the 
 
 most important condition of this structure. Acute and chronic 
 eases may be distinguished. The latter, in most instances, merely 
 represent terminal conditions following acute forms of the disease. 
 Exceptionally, peritonitis may be a chronic affection from the 
 beginning. 
 
 Etiology. — Acute peritonitis is probably always caused by 
 bacteria or bacterial products. It is possible to produce it in 
 animals by injections of chemical poisons into the peritoneum, but 
 it is doubtful if spontaneous peritonitis ever occurs, excepting as 
 a result of infection. 
 
 The bacteria gain access to the peritoneum through the blood, 
 by direct migration from the Fallopian tubes, by invasion through 
 the walls of the abdominal viscera, or by perforation of the viscera 
 or external abdominal walls. Hematogenic peritonitis is some- 
 times met with in cases of general septicemia and pyemia, as in 
 osteomyelitis or malignant endocarditis, but such cases are rare. 
 In these instances the bacteria may be discharged into the peri- 
 toneal cavity from the blood, and may thus occasion a direct or 
 primary peritonitis ; more frequently a localized lesion, such as a 
 suppurating infarction, is first produced and the peritonitis results 
 secondarily from this. Undoubtedly bacteria are often set free in 
 the peritoneum in the course of infections, but this structure seems 
 to have a high degree of resistance, and seems to be possessed of 
 special means of defence. The experiments of Pfeiffer with re- 
 gard to the mechanism of immunity (see page 198) may be cited 
 in this connection. Idiopathic peritonitis was a term used by 
 older authors to designate forms of seemingly causeless peritonitis, 
 or such as follow exposure to cold and the like. At the present 
 time we must regard these as exceptional instances of primary 
 hematogenic peritonitis, or more commonly as cases of secondary 
 peritonitis resulting from abdominal infections that have been 
 overlooked. 
 
 Peritonitis resulting from direct extension of infective pro- 
 cesses is very common. A certain amount of irritation of the 
 serous coat (the peritoneum) of the abdominal organs occurs in 
 most of the diseases of these organs, and in the case of certain 
 infectious diseases this may attain considerable intensity. For 
 example, in cases of ulcers of the intestines or strangulation of 
 a coil of intestine with secondary necrosis, considerable peritonitis, 
 local and eventually general, may occur without perforation of the 
 gut. In such cases the bacteria penetrate the walls of the intes- 
 
554 TEXT-BOOK OF PATHOLOGY. 
 
 tines along the lymphatic channels, and thus reach the serous 
 covering. Similar extensions are found in diseases of the tubes 
 and ovaries, or of the uterus in puerperal sepsis. 
 
 Perforative peritonitis is the most important of the forms. It 
 may result from perforation of gastric ulcers or cancer, from trau- 
 matic or ulcerative perforations of other parts of the intestinal 
 tract, from perforation of the appendix in acute appendicitis, or 
 from rupture of diseased Fallopian tubes ; less commonly perfora- 
 tion of the other abdominal viscera, or rupture of infective foci, 
 such as abscesses of the spleen, liver, pancreas, ovaries, or other 
 structures, or penetration of the abdomen from without by stab- 
 woimds or disease, may lead to peritoneal infection. 
 
 Among the micro-organisms that have been detected, the 
 Streptococcus ■pyogenes is most important, and is the cause of the 
 severest forms of peritonitis, such as those occurring in puerperal 
 sepsis. Occasionally the disease is due to the Staphylococcus 
 pyogenes, the Bacillus coll communis, the Diplococcus pneumoniae 
 the bacillus of Friedldnder, the gonococcus, or other organisms. 
 The Bacillus coli is mainly operative in peritonitis secondary to 
 intestinal diseases, such as appendicitis. Very often, no doubt, 
 peritonitis is the consequence of mixed infection. 
 
 Pathologic Anatomy. — Localized and general peritonitis may be 
 distinguished. 
 
 Acute localized peritonitis is seen in cases in which 
 bacteria escape gradually and in small numbers through the 
 walls of the viscera, or in instances in which perforation takes 
 place after the production of some exudate which serves the 
 purpose of limiting the extension of the infection. Localized 
 peritonitis is most frequent in the pelvis in association with 
 diseases of the tubes or uterus, and in the region of the appen- 
 dix. The peritoneum of the area of disease first becomes in- 
 tensely injected (congested) and the normal luster disappears in 
 consequence of the beginning exudation and disease of the lining 
 endothelium. Subsequently the amount of exudate increases. It 
 may, first, be of serous character, but usually is largely fibrinous, 
 and the amount may be considerable. Thus the appendix is not 
 rarely surrounded by masses of fibrinous exudate a centimeter or 
 two in thickness. The exudate may remain fibrinous, but more 
 frequently becomes fibrinopurulent in the later stages; and in 
 cases of perforative peritonitis localized abscesses are commonly 
 met with. In such cases, if the disease remains well encapsulated, 
 and the patient survives, the exudate may be removed in several 
 ways. Very rarely the pus burrows toward the exterior and dis- 
 charges ; more frequently it empties into the intestine or some 
 other hollow viscus. It may decrease by gradual inspissation, 
 leaving a dry, cheesy mass, which in rare instances finally be- 
 comes calcareous. Fibrinous exudates in localized peritonitis 
 
DISEASES OF THE G ASTRO-INTESTINAL TRACT. 555 
 
 are frequently absorbed, and give place to fibrous-tissue adhe- 
 sions. 
 
 Acute general peritonitis may be the immediate result of the 
 discharge of large quantities of infective matter from a perforated 
 bowel or other organ ; or it may occur secondarily to a localized 
 peritonitis when the limiting-wall of exudation is broken down. 
 In these cases the peritoneal covering of the intestines, and to a less 
 extent the parietal peritoneum, become congested and lusterless, 
 as in the localized form. Serous exudation takes place, and may 
 be considerable in amount in some of the most violent forms of 
 the disease. Acute inflammatory ascites is thus produced. Usu- 
 ally, however, the serous exudation is scanty, and very soon the 
 intestines are covered with flakes or thin coatings of fibrinous 
 exudate and are matted together. Subsequently the exudate 
 grows more yellowish from the emigration of leukocytes or pus- 
 cells. When adjacent coils of intestine are agglutinated by the 
 exudate pockets containing serous or seropurulent liquid may be 
 formed between them. 
 
 In the most violent forms of peritonitis, local or general, such 
 as those due to strangulation and gangrene of a part of the bowel, 
 or to puerperal sepsis, the exudates may rapidly assume a putrid 
 character, and the deposit upon the serous surface, as well as the 
 serosa itself, may undergo necrotic change. In these cases the 
 cavity of the peritoneum contains more or less ill-smelling brown- 
 ish, grayish, or blood-tinged liquid exudate, and the affected areas 
 of the peritoneum are covered with greenish or brownish deposits. 
 
 Hemorrhagic peritonitis is sometimes observed. It represents 
 no special form, but merely indicates systemic or local conditions, 
 as a result of which hemorrhagic extravasation has taken place 
 into the exudate. This is found in the peritonitis of scorbutic 
 individuals or of persons reduced in vitality by other diseases. It 
 also occurs when passive congestion is associated with peritonitis, 
 as in cases of cirrhosis of the liver. The peritonitis accompany- 
 ing tuberculosis, and especially carcinoma of the peritoneum, may 
 present hemorrhagic exudate. 
 
 Effects of Acute Peritonitis. — The disease of the peritoneum has 
 an immediate and profound effect upon the intestines, and reflexly 
 or in other ways upon the general system. The peristalsis of 
 the bowel in the earlier stages is arrested by spasmodic contrac- 
 tion. Very soon the musculature is paralyzed and more obstinate 
 constipation results. The systemic effects are most strikingly 
 evidenced by the intense shock of the early stages. General 
 septicemia may be the consequence of the infective conditions of 
 the peritoneum. 
 
 Chronic peritonitis may be the termination of an acute 
 peritonitis, especially the localized form. In other cases chronic 
 inflammatory thickening occurs in the peritoneum adjacent to or 
 
556 TEXT-BOOK OF PATHOLOGY. 
 
 covering organs the seat of various diseases. Thus in cirrhosis of 
 the liver the peritoneal covering and the reflexions forming the 
 ligaments may be greatly thickened, and similarly the peritoneum 
 covering the spleen may be involved in consequence of chronic 
 congestion or inflammation of this organ. 
 
 Chronic peritonitis following local acute peritonitis usually pre- 
 sents itself in the form of fibrous thickenings or adhesions, such as 
 are so often encountered in the pelvis after uterine, tubal, or ovarian 
 disease complicated by peritonitis, and about the appendix after 
 inflammations of this structure. Less commonly chronic perito- 
 nitis is met with in the form of sacculated effusions. In such in- 
 stances the effusion formed during the acute stage is only partially 
 absorbed, and remains as an inspissated liquid. 
 
 In other cases dense adhesions are formed, and occasionally cal- 
 careous plates are found in the thickened peritoneal covering of the 
 bowels or other parts. 
 
 Chronic diffuse peritonitis may result from diffuse acute peri- 
 tonitis. In such cases there are widespread adhesions, and the peri- 
 toneum is more or less diffusely thickened. More or less liquid 
 effusion may be present. In other instances diffuse peritonitis arises 
 in an insidious manner as a chronic process from the beginning. 
 Some of these cases are entirely obscure in etiology ; in a few it has 
 seemed probable that syphilis was an etiologic factor. The perito- 
 neum is often uniformly thickened, but in some cases presents small 
 nodular lesions, suggesting miliary tubercles. In several instances 
 these nodules, together with the abundant serous effusion occasion- 
 ally met with, have led to the diagnosis of tuberculous peritonitis. 
 Microscopic examination of the nodules, however, shows a fibrous 
 structure, and neither giant-cells nor tubercle-bacilli. Tuberculous 
 and malignant peritonitis will be considered below. 
 
 Hyperplastic Perihepatitis. — A few cases have been observed of a re- 
 markable disease in which the upper part of the parietal peritoneum and 
 the reflexions covering the liver and spleen are greatly thickened and of 
 dense sclerotic character. The peritoneum is sometimes several millimeters 
 in thickness, gray or white, and suggests the appearance of the " icing " of 
 confectioners. This has led to the term proposed by Curschmann — Zucker- 
 gussleber. The liver and spleen undergo more or less pressure-atrophy, and 
 ascites is a frequent symptom. The etiology is obscure. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis may in rare instances affect the peritoneum 
 primarily, as in cases in which tubercle-bacilli penetrate the 
 mucosa of the intestines and enter the lymphatics without causing 
 an intestinal lesion ; or in cases of infection through the Fallopian 
 tubes. Usually tuberculosis of the peritoneum is secondary to 
 tuberculosis of some abdominal viscus or of more distant organs. 
 Thus among the more frequent causes are tuberculosis of the mes- 
 
DISEASES OF THE OASTRO-INTESTINAL TRACT. 557 
 
 enteric or retroperitoneal glands and tuberculous disease of the 
 tubes and ovaries in women. Intestinal tuberculosis rarely leads 
 to more than localized lesions of the serous coat opposite the ulcera- 
 tions of the mucosa. Pulmonary tuberculosis may occasion hema- 
 togenic infection of the peritoneum. Simultaneous tuberculosis of 
 various serous membranes, especially the pleura and peritoneum, 
 is occasionally observed. The source of infection is often hidden ; 
 sometimes the pleura is first involved and the peritoneum becomes 
 affected by extension ; less commonly the reverse occurs. 
 
 Pathologic Anatomy. — Miliary tuberculosis without marked in- 
 flammatory changes may occur as a generalized peritoneal affection 
 in acute or subacute general miliary tuberculosis. Local eruptions 
 of similar character are seen in the pelvic peritoneum in cases of 
 tubal or ovarian tuberculosis and upon the serosa of the intestines 
 adjacent to tuberculous ulcers of the bowel. 
 
 More important, from a clinical point of view, are the cases in 
 which inflammatory changes are associated with the specific tuber- 
 cle. In some instances extensive adhesions by fibrinous or fibrous 
 productions are met with, while the tubercles tend to agglutinate, 
 forming masses of considerable size and of cheesy character. The 
 mesenteric lymph-glands may be coincidently involved, being en- 
 larged and caseous. Sacculated collections of serous or seropuru- 
 lent liquid are sometimes observed. In another variety there is 
 abundant serous exudation. Occasionally the exudate is hemor- 
 rhagic. 
 
 Tuberculosis of the peritoneum sometimes terminates in com- 
 plete resolution, the peritoneum being left somewhat thickened, 
 but showing no other evidences of the previous disease. 
 
 TUMORS. 
 
 Fibromata and lipomata are sometimes met with as small 
 nodular or pedunculated outgrowths from the subperitoneal tissues. 
 
 Sarcoma may occur in the form of diffuse gelatinous tumors 
 of angiosarcomatous structure, or in the form of endotheliomata. 
 The latter variety occasions diffuse thickening, sometimes of con- 
 siderable areas, of the peritoneum. Secondary sarcoma is some- 
 times observed as nodules of considerable size or as numerous mil- 
 iary nodules. 
 
 Carcinoma of the peritoneum is usually secondary. Gelati- 
 nous or colloid cancers of the stomach and bowel (rectum) fre- 
 quently extend widely through the peritoneum, causing great 
 thickening and a remarkably gelatinous growth. Not rarely 
 rounded masses of pearly appearance are observed (Fig. 74). In 
 rare instances tumors of the peritoneum of the same general char- 
 acter seem to be primary, and the reasonable explanation has been 
 suggested that parts of intestinal tissue, pinched off in fetal de- 
 
558 TEXT-BOOK OF PATHOLOGY. 
 
 velopment, are the starting-points of the growths. Secondary 
 cancer frequently appears in the form of nodular tumors in asso- 
 ciation with ovarian cystomata that have become carcinomatous, 
 or with primary cancers of the ovaries and other pelvic organs. 
 Occasionally widespread eruption of miliary nodules is met with 
 as a part of acute carcinomatosis. 
 
 In all forms of carcinoma of the peritoneum inflammatory 
 changes with intestinal agglutination and adhesion are frequent. 
 Hemorrhagic exudation is not unusual. In rare cases the bowels 
 are so firmly fused by the spreading tumor and the inflammatory 
 exudates that they form a solid mass, which on section shows the 
 cavities of adjacent coils of intestines separated by more or less 
 uniform tumor-tissue. 
 
 PARASITES. 
 
 BchinocOCCUS-cysts occasionally occupy the peritoneal 
 cavity, and may fill it almost completely. Filarial have been 
 found in a few instances ; and the Pentastomum denticulatum and 
 Oysticercus cellulosce have been reported. Recently an ameboid 
 organism (Leydenia gemmipard) has been discovered in the liquid 
 exudate of cases of ascites. 
 
 CHAPTER Y. 
 DISEASES OF THE DUCTLESS GLANDS. 
 
 THE THYROID GLAND. 
 
 Anatomic Considerations. — The thyroid gland is a com- 
 pound tubular gland, which in fetal life communicates with the 
 pharynx at the base of the tongue by a duct. Later the duct is 
 obliterated, and the gland becomes ductless. Microscopically 
 there are found acini lined with polyhedral or cylindrical epi- 
 thelium, usually in a single layer. The lumen of the acinus 
 contains more or less gelatinous, or, as it is usually called, colloid 
 material, which seems to be a secretion of the epithelium. It is 
 an albuminate rich in sodium chlorid. The vascular supply of 
 the gland is very abundant, the blood-vessels being numerous and 
 the anastomoses very free. The lymphatic network is equally 
 abundant, and mainly situated in the stroma of the gland around 
 the acini. The larger lymphatics are supplied with valves like 
 those of the veins. Occasionally colloid material has been found 
 in the stroma and in the lymphatics. The capsule of the gland is 
 a fibrous covering from which trabecule extend into the substance 
 of the organ. 
 
DISEASES OF THE DUCTLESS GLANDS. 559 
 
 CONGENITAL DEFECTS. 
 
 Occasionally one or another part of the gland is wanting, or in 
 rare instances the entire organ. 
 
 Accessory thyroid glands have been found in various situations. 
 Sometimes small masses of thyroid tissue occur alongside of a nor- 
 mal gland, either above it, in the neck ; or below it, behind the 
 sternum and in the anterior mediastinum. In other cases the nor- 
 mal thyroid is absent, but is represented by small masses in the 
 situations named, or in other parts. In a few instances tumors at 
 the base of the tongue and within the larynx and trachea have 
 been found to be composed of thyroid tissue. 
 
 DISTURBANCES OF CIRCULATION. 
 
 Hyperemia of the thyroid gland is met with very frequently. 
 It occurs in cases of cardiac failure, and in consequence of obstruc- 
 tion of the large veins by mediastinal tumors, and the like. In 
 these instances the thyroid may be considerably enlarged, and has 
 a soft, doughy feel. Slight enlargement of the thyroid of con- 
 gestive character is found in perhaps a majority of the cases of 
 chlorosis, and may be present in any form of anemia. In Graves' 
 disease the thyroid is usually very vascular, and the enlargement 
 of the gland is in large part due to dilatation of the blood-vessels 
 (see page 561). 
 
 INFLAMMATIONS. 
 
 Acute inflammation, or acute strumitis, may occur in 
 the course of various infectious diseases, notably typhoid fever. 
 Occasionally it arises without definite preceding disease. The 
 gland enlarges and becomes rather tense. The termination is usu- 
 ally in resolution, and this may occur very rapidly, suggesting 
 that the enlargement of the gland is due largely to congestion and 
 liquid exudation, rather than to cellular (inflammatory) infiltration. 
 
 Acute suppurative strumitis, or abscess, occurs in con- 
 sequence of embolism, in cases of infected wounds, endocarditis, 
 or general pyemia. Sometimes the inflammation extends directly 
 from local diseases, such as diphtheria. The abscess may rupture, 
 or may undergo secondary changes — inspissation, calcification. 
 
 STRUMA OR GOITER. 
 
 Definition. — Goiter is the name applied to various enlarge- 
 ments of the thyroid gland. It is a clinical rather than a patho- 
 logic term. Sometimes a distinction is made between benign and 
 malignant struma, the latter term including definite tumors of the 
 thyroid gland. At the present time the term goiter is restricted 
 to enlargements of a hyperplastic character, which, though often 
 
560 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 resembling tumors, cannot be definitely classified among the tu- 
 mors of the gland. 
 
 Btiology. — Goiter occurs endemically in certain situations, as 
 in Switzerland and other parts of Europe, and in parts of Michi- 
 gan in this country. Sporadically it is met with in all parts of 
 the world. Local conditions of some kind are doubtless among 
 the fundamental causes, but the nature of these conditions is but 
 little known. The drinking-water has always been suspected, and 
 it seems likely that it has some influence, though it is certain that 
 the magnesium and calcium salts have not the importance for- 
 merly ascribed to them. Infectious causes have been suspected 
 and micro-organisms have actually been described, but no satis- 
 factory demonstrations have been made. 
 
 Pathologic Anatomy. — Two principal varieties may be dis- 
 tinguished : the parenchymatous and the vascular. 
 
 Parenchymatous Goiter. — Parenchymatous goiter is a variety in 
 which the glandular tissues or acini undergo more or less active 
 hyperplasia. The gland is generally uniformly enlarged, but 
 sometimes presents lobular or nodular elevations. The tissue is 
 ordinarily somewhat elastic, like that of the normal thyroid, but 
 may in other instances be very firm. Occasionally cystic forms 
 occur, and a subvariety is sometimes distinguished by the term 
 cystic goiter. 
 
 Microscopically there may be found merely a uniform hyper- 
 
 Fig. 264.— Colloid goiter, showing colloid material in the dilated acini (Karg and Schmorl). 
 
 plasia of the glandular acini, without any notable change in the 
 structure of the tissue. In other cases the acini are larger and 
 more irregular than in the normal thyroid, suggesting the struct- 
 
DISEASES OF THE DUCTLESS GLANDS. 561 
 
 ure of an adenoma, and the term struma adenomatosa is applied. 
 In most instances the acini contain but small quantities of colloid 
 material, as is the case in the normal gland. Sometimes, however, 
 there is abundant production of colloid, and the acini are greatly 
 distended ; the term colloid goiter may be applied in such instances 
 (Fig. 264). In certain cases the walls of the acini are destroyed 
 and the colloid of adjacent acini runs together, forming considerable 
 cysts. In these instances the thyroid consists of numerous cystic 
 excavations. Changes in the interstitial connective tissue of the 
 gland may be comparatively slight, but may in other cases become 
 conspicuous. The capsule of the gland may be thickened, and the 
 stroma may predominate over the glandular elements. The term 
 fibrous goiter has been suggested for such cases. 
 
 Vascular Goiter. — This term is applied to enlargements of the 
 thyroid gland characterized by marked dilatation of blood-vessels 
 within the gland. The glandular tissues themselves may play no 
 part in the process, or they may present changes similar to those 
 described under parenchymatous goiter. The gland undergoes 
 considerable and sometimes enormous enlargement, and may pul- 
 sate actively. This form of goiter is met with as the important 
 pathologic condition of Graves's disease (see page 564). 
 
 Secondary Changes. — The thyroid frequently suffers second- 
 ary changes in goiter. The hyperplasia of connective tissue 
 between the acini has been referred to. Sometimes this becomes 
 so considerable that the term fibrous goiter is warranted. Cystic 
 formations have also been mentioned, the cysts referred to result- 
 ing from the confluence of the dilated acini. The contents in such 
 cases consist of colloid material or of more or less serous or hemor- 
 rhagic liquid. Occasionally cysts result from hemorrhage in de- 
 generated parts of the gland, with subsequent absorption of the 
 blood, and exudation of serous liquid. The contents in such cases 
 may be purely serous or may consist of brownish grumous matter 
 containing abundant cholesterin. Very rarely secondary prolif- 
 erative changes occur in the walls of the cyst, causing papilloma- 
 tous projections. Calcification is a very common terminal change 
 in degenerated goiters. It may occur in isolated areas, or may 
 ■cause a uniform hardening of the gland. Actual ossification has 
 been observed. 
 
 Mechanical Effects of Goiter. — The enlarged gland presses 
 upon the adjacent structures more or less seriously. The trachea 
 is most frequently compressed or dislocated from its median posi- 
 tion. Pressure upon the large veins may occasion passive conges- 
 tions and edema ; and less commonly pressure on the carotid 
 artery may interfere with the circulation of blood in the brain. 
 The nerves in the vicinity (vagus, recurrent laryngeal, and sym- 
 pathetic) are likewise exposed to compression. 
 
562 TEXT-BOOK OF PATHOLOGY. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis may occur in the form of miliary tubercles or 
 as small caseous nodules. 
 
 Syphilis is met with in the form of gummata. 
 Actinomycosis is a very rare disease of the thyroid gland. 
 
 TUMORS AND PARASITES. 
 
 Tumors. — The term malignant struma is sometimes applied to 
 tumors, and it is difficult in certain cases to draw a sharp line be- 
 tween certain goiters and distinct new-growths (adenomata). 
 
 The term adenoma, however, should be restricted to cases in 
 which the proliferation of acini is more or less atypical, and in 
 which the tumor is circumscribed, nodular, or otherwise distin- 
 guishable from the pre-existing gland-tissue. Sometimes tumors 
 of the thyroid having typically adenomatous characters give 
 metastasis. 
 
 Carcinoma may occur in the form of a nodular, or more diffuse 
 tumor. Metastasis is frequent in cases of carcinoma, but also 
 occurs in cases that present the appearances of an ordinary 
 adenoma. The bones are frequently involved by metastatic de- 
 posits. Extension from the thyroid to the adjacent organs is not 
 infrequent. 
 
 Sarcoma occurs in several varieties. Round-celled sarcoma 
 and angiosarcoma are particularly malignant. 
 
 Secondary tumors in the thyroid are rare. 
 
 Parasites. — Echinococcus-cysts have been met with, but are 
 very rare. 
 
 GENERAL RESULTS OF THYROID DISEASE. 
 
 The physiology of the gland has not as yet been fully deter- 
 mined, though certain facts have become established. The old 
 authors believed the gland to be active as a blood-making organ, 
 and this is still maintained by some. It is, however, unlikely that 
 this function is an important one. The frequent association of 
 thyroid disease with certain general conditions (cretinism and 
 myxedema) has led to experiments upon animals that have estab- 
 lished certain important facts. 
 
 The immediate removal;, by operation, of the entire thyroid 
 gland causes severe nervous manifestations resembling those of 
 tetany followed by rapid death.- Partial removal of the gland 
 causes comparatively trivial consequences, but in cases in which 
 total ablation has been practised, and in which a certain amount 
 of thyroid influence has been kept up by injections of thyroid ex- 
 tract or the feeding of thyroid gland, marked symptoms have been 
 found to develop after a period of some months. Among these 
 
DISEASES OF THE DUCTLESS GLANDS. 
 
 563 
 
 symptoms are pallor, edema of the skin, general weakness, dis- 
 turbances of growth, and alteration of the cerebral functions 
 (intellection, sensation, and motor power). This condition has 
 been termed cachexia strumipriva, and its resemblance to cretin- 
 ism and myxedema will be apparent from a reference to the symp- 
 toms of those diseases. 
 
 Cretinism. — Cretinism is a peculiar disease, occurring with 
 great frequency in certain parts of central Europe, especially in 
 Switzerland, and not infrequently in 
 other parts of the world. The thy- 
 roid gland is sometimes atrophic, 
 and sometimes goiterous, but in all 
 cases diseased. The disease is not, 
 as a rule, present at birth, but usu- 
 ally develops soon after birth ; and 
 the parents may be cretinoid or 
 goiterous. Sometimes healthy par- 
 ents have cretin children. The 
 cretin remains physically and men- 
 tally undeveloped ; the subcutane- 
 ous tissue is flabby, abundant, and 
 sometimes distinctly myxedematous 
 (Fig. 265) ; the head is large ; the 
 lips and tongue enormously thick- 
 ened, and the latter usually pro- 
 trudes from the mouth ; the hairs 
 of the body are little developed. 
 
 Myxedema. — Myxedema is a 
 disease that develops in later life; 
 sometimes after distinct diseases of 
 the thyroid (goiter, gumma, tumors, 
 etc.), but often without any mani- 
 fest disease of thyroid, though 
 atrophy and degenerations (calcifi- 
 cation) may be disclosed by the 
 post-mortem examination. There 
 is a peculiar swelling of the eyelids and of the subcutaneous tissue 
 of the face and neck, and subsequently the same change occurs 
 elsewhere, involving the limbs and the entire body. The appear- 
 ances at first suggest edema, but there is not the usual pitting on 
 pressure, and the feeling conveyed to the hand is that of* an infil- 
 tration with some form of gelatinous tissue. This has been found 
 to consist of a mucin-like substance, often associated with increase 
 of the adipose tissue itself. The skin of the patient is pallid and 
 exceedingly dry ; the hair falls out, and nervous symptoms are 
 developed. Eventually intellection may be almost destroyed. 
 
 The resemblance of these diseases to the symptoms produced 
 
 Fig. 265. — Cretin, agea seven 
 months ; showing facial features and 
 myxedematous condition of hands 
 arid feet (author's case at the Chil- 
 dren's Hospital). 
 
564 TEXT-BOOK OF PATHOLOGY. 
 
 by operative removal of the thyroid gland makes it certain that 
 disease of the thyroid is the fundamental condition in cretinism 
 and myxedema. This fact is still more clearly demonstrated by 
 the numerous cures of these diseases following implantation of 
 sheeps' thyroids in the peritoneal cavity, and especially the feed- 
 ing of thyroid-gland tissue or extracts. 
 
 Graves' disease has been referred to in connection with 
 vascular goiters. The cardinal symptoms of this disease are 
 enlargement of lhe gland, palpitation of the heart, exophthalmos, 
 and muscular tremor. The pathology of the disease has not as 
 yet been fully determined. It seems likely, however, from recent 
 investigations that the thyroid disease, from whatever cause it may 
 result, is the primary disorder. Removal of large parts of the 
 gland has been found to control the symptoms of Graves' disease 
 in a large number of cases, and the feeding of thyroid extract for 
 a long period of time produces symptoms like those of Graves' 
 disease : rapid action and palpitation of the heart, exophthalmos, 
 and tremor. According to the view here expressed, the symptoms 
 which together constitute Graves' disease are probably due to 
 overproduction of thyroid secretion ; they are, in fact, the result 
 of hyperthyroidism. The opinion, however, is held by others that 
 Graves' disease is primarily an affection of the nervous system. 
 
 THE SUPRARENAL BODIES. 
 
 Anatomic Considerations. — The suprarenal bodies are 
 composed of a cortical and a medullary portion, and are enclosed 
 in a fibrous capsule from which septa extend into the substance. 
 The cortical portion is composed of aggregations of polygonal 
 cells which frequently contain fat-droplets. Three layers are 
 distinguishable in the cortex : an outer zone, in which the cells 
 are arranged in oval masses ; a middle zone, in which they form 
 cylindrical columns extending toward the medullary ; and an inner 
 zone, composed of irregularly anastomosing columns of cells. The 
 cells of the middle zone are deeply pigmented and contain abun- 
 dant, granular and globular fat. The medulla of the gland consists 
 of similar polygonal cells arranged in cords or irregularly anasto- 
 mosing columns. Between these are found large venous channels 
 and numerous non-medullated nerve-fibers, together with ganglion- 
 cells. The fibrous septa of the gland contain blood-vessels and 
 lymphatics. 
 
 CONGENITAL ANOMALIES. 
 
 Accessory suprarenal bodies may be found in the vicinity 
 of the main body. Of peculiar interest are the portions of supra- 
 renal tissue found in the capsule or cortex of the kidney. These 
 "rests" may subsequently proliferate and form tumors of the 
 kidney (see Tumors of the Kidney). 
 
DISEASES OF THE DUCTLESS GLANDS. 
 
 565 
 
 Occasionally the suprarenal bodies are found in unusual situ- 
 ations. 
 
 DEGENERATIONS. 
 
 Fatty degeneration is normal in adults. It affects the 
 cortex, giving this layer a yellowish color. The substance of 
 the cortex may separate through the middle zone, forming a 
 cavity suggesting a cyst. This is probably in part a post-mortem 
 production. 
 
 Pigmentation is observed in the cells of the medullary por- 
 tion in persons of advanced age. 
 
 Amyloid degeneration occurs in connection with amyloid 
 disease of other organs. The suprarenal body becomes hard and 
 of a grayish, translucent appearance. The degeneration affects 
 the walls of the blood-vessels, from which it extends to the con- 
 nective tissue. The glandular portions suffer pressure-atrophy. 
 The cortex is more frequently involved than the medulla. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis of the suprarenal body is the most important 
 of its diseases. Miliary tubercles may be met with in cases of 
 general tuberculosis, but a fibrocaseous 
 form of the disease is more frequent and 
 of much greater significance. The gland 
 is enlarged, sometimes reaching the size 
 of an egg ; it is hard and usually rather 
 nodular, or irregular in outline. The 
 capsule is thickened, and the substance 
 of the gland is composed of dry, yellow- 
 ish cheesy matter, or of a puriform mate- 
 rial (Fig. 266). In the later stages the 
 caseous or puriform matter may be ab- 
 sorbed, and fibrous-tissue growth may 
 convert the entire body into a shrivelled, 
 hard mass of connective tissue. Some- 
 times one gland alone is involved ; more 
 frequently the disease occurs bilaterally. 
 Tuberculosis of this form may be pri- 
 mary, but usually is secondary to tuber- 
 culosis of the lungs, intestines, or other 
 organs. The general effects of this dis- 
 ease will be discussed below (see Addi- 
 son's Disease). 
 
 Syphilis occurs in the form of 
 gummata. Uniform fatty degeneration 
 of the suprarenal body has been met with in congenital syphilis. 
 
 Fig. 266.— Caseous tuberculo- 
 sis of the suprarenal body (Kast 
 and Rumpel). 
 
566 TEXT-BOOK OF PATHOLOGY. 
 
 CIRCULATORY DISTURBANCES. 
 
 Hemorrhage is comparatively rare. It may occur in asso- 
 ciation with hemorrhagic diseases, or severe anemias, especially 
 leukemia. Sometimes it is caused by traumatism, or by obstruc- 
 tion of the venous circulation. The hemorrhage may be incon- 
 siderable, or may be quite large. In the latter instances second- 
 ary rupture of the hematoma may cause death by intraperitoneal 
 hemorrhage, or a hemorrhagic cyst may result. 
 
 INFLAMMATION. 
 
 Inflammation of the suprarenal body is very rare. A simple 
 and a hemorrhagic form have, however, been described. Abscess 
 may occur in consequence of pyemia, or as a secondary condition 
 following other forms of suprarenal disease. 
 
 TUMORS. 
 
 Sarcoma is the most frequent form of tumor. Melanotic, as 
 well as unpigmented, varieties are met with. The tumor may 
 reach considerable size, and may destroy the gland completely. 
 
 Adenoma and carcinoma may arise from the cells of the 
 acini. Histologically these tumors resemble the normal gland in 
 their structure, and the term adenoma is perhaps more suitable 
 than carcinoma. The tumor occurs as a nodular, irregular growth, 
 often of a yellowish or brownish color ; it most frequently arises 
 from the cortical portion of the gland. 
 
 Gliomata of the suprarenal bodies have been described, but 
 it is doubtful whether these tumors are true gliomata. Neuroma 
 is a rare form of suprarenal disease. 
 
 Secondary sarcoma and carcinoma are not infrequent. 
 
 Tumors of the cortex of the kidney, having the structure of 
 suprarenal tissue, are described under Tumors of the Kidneys. 
 
 GENERAL EFFECTS OF SUPRARENAL DISEASES. 
 
 The physiology of the suprarenal body is still obscure. It is 
 quite generally believed, however, that this gland holds some rela- 
 tion to pigment-formation, as well as to the circulation, either 
 through the action of substances elaborated within the gland or 
 through the nervous system. The last is suggested by the abun- 
 dance of nervous tissue in the gland. 
 
 Addison's disease, in which fibrocaseous tuberculosis of the 
 suprarenal bodies is commonly present, is an affection character- 
 ized by brownish pigmentation of the skin of exposed parts of the 
 body (face, neck, and hands), and of the skin in the flexures of 
 the joints, or in other parts subjected to pressure. The pigmenta- 
 
DISEASES OF THE URINARY ORGANS. 567 
 
 tion usually occurs in a mottled form at first, but soon becomes 
 uniform. Brownish or purplish spots upon the mucous mem- 
 branes (mouth) are not unusual. Besides pigmentation the char- 
 acteristic symptoms are great weakness, disturbances of the stom- 
 ach (vomiting), and cardiovascular asthenia. 
 
 Though fibrocaseous tuberculosis of the suprarenal gland is 
 discovered in many cases, Addison's disease may occur in associa- 
 tion with other affections of the suprarenal, such as tumors ; and 
 it may be absent despite the existence of tuberculosis or of other 
 diseases of both of the glands. The absence of Addison's dis- 
 ease in the latter cases has been explained by some writers by the 
 assumption that the suprarenal disease had not existed long enough 
 for the development of the symptoms of Addison's disease. Occa- 
 sionally alterations in the sympathetic nervous system (semilunar 
 ganglia and solar plexus) have been discovered when the supra- 
 renal glands were apparently normal. No explanation of such 
 cases can be made. It must be accepted at the present time that 
 the suprarenal bodies are in some way concerned in the etiology 
 of the disease. The disease of the gland need not, however, be 
 of any special sort. 
 
 CHAPTEE VII. 
 DISEASES OF THE URINARY ORGANS. 
 
 THE KIDNEYS. 
 CONGENITAL ANOMALIES. 
 
 Absence of one of the kidneys is frequently observed. Occa- 
 sionally one kidney, instead of being completely absent, is atrophic 
 or hypoplastic. The opposite kidney may undergo compensatory 
 hypertrophy. Both kidneys may be wanting in certain monstros- 
 ities. 
 
 Congenital lobulation is quite common, and is usually bilateral. 
 The kidney is divided into separate lobes by furrows of variable 
 depth. Occasionally there is almost complete separation into 
 numerous lobules. 
 
 A few instances have been observed in which there was a 
 third kidney, and usually in these cases two of the kidneys lying 
 to one side of the spinal column were agglutinated. 
 
 Fusion of the two kidneys may occur, and there may result a 
 single large organ, with a double pelvis and ureter lying to one or 
 the other side, or a horseshoe-lddney may be formed. In the latter 
 
568 TEXT-BOOK OF PATHOLOGY. 
 
 the two organs, which are generally displaced far downward, are 
 united at their lower ends by a commissure passing across the 
 spine just above the lumbosacral junction. The commissure may 
 consist of normal kidney-tissue, or may be fibrous ; more com- 
 monly the former. 
 
 Congenital cysts and other congenital diseases will be referred 
 to below. 
 
 CHANGES OF POSITION. 
 
 Congenital Malposition. — Not rarely one of the kidneys is 
 displaced downward. It may even occupy the pelvis. In other 
 cases it is displaced laterally or forward, and may be found imme- 
 diately beneath the anterior abdominal walls. 
 
 Acquired malpositions may result from pressure upon the 
 organ, or from elongation of the peritoneal reflections covering the 
 kidney and absorption of the perirenal fat. The right kidney is 
 more frequently displaced than the left, and the condition is espe- 
 cially common in women. Repeated pregnancies, the effects of 
 tight lacing, and diseases or displacement of the liver are prom- 
 inent causes. Movability or displacement of the kidney may be 
 but a part of a general visceral descent (enteroptosis). 
 
 Several grades of movability or displacement may be dis- 
 tinguished. In the first, the perirenal fat is wanting, and the 
 kidney is more movable beneath its peritoneal covering than is 
 normal. This occurs in a large proportion of women, and usu- 
 ally affects the right kidney. In more advanced grades the 
 peritoneal reflection covering the kidney is elongated and con- 
 siderable movability of the organ within the abdomen results. 
 The kidney may be moved from side to side, downward as far as 
 the pelvis in some cases, or upward to the normal position or under 
 the ribs. In a third group of cases the kidney, lying within an 
 elongated peritoneal pouch, is retained in an abnormal position 
 by adhesions. 
 
 Results. — Twisting of the pedicle may lead to serious circula- 
 tory disturbances, and twisting of the ureter to retention of urine, 
 sometimes causing hydronephrosis.. Pressure of the displaced 
 right kidney upon the duodenum may lead to dilatation of the 
 stomach. 
 
 CIRCULATORY DISTURBANCES. 
 
 Anemia of the kidney may occur as a part of general anemia. 
 The kidney is light in color and rather hard in the earlier stages ; 
 but if the anemia persists degenerative softening and enlargement 
 may ensue. 
 
 Complete arrest of the blood-supply, produced experimentally, 
 leads to rapid necrosis of the kidney, the organ becoming ashen- 
 
DISEASES OF THE URINARY ORGANS. 569 
 
 gray in color and of a homogeneous structure, so that the separate 
 parts (cortex, medulla, pyramids) are indistinguishable. Near the 
 cortex, where some circulation is maintained by the capsular ves- 
 sels, fatty degeneration is observed. Somewhat similar changes 
 are met with in circumscribed areas in diseases in which the circu- 
 lation in branches of the renal artery is obstructed (see Embolism). 
 
 Active hyperemia of the kidney is generally a part of acute 
 inflammation. It may result from irritant chemical poisons or 
 from the toxic action of infectious poisons. The kidney is en- 
 larged, dark red in color, and on section the cortical substance is 
 found to be swollen and marked by dark-red points— the Mal- 
 pighian bodies. Sometimes punctate or linear hemorrhages may 
 be observed. The urine is somewhat albuminous, and hyaline 
 casts occur. It is difficult to draw a sharp line between this 
 condition and acute nephritis. 
 
 Passive hyperemia occurs in cardiac and pulmonary dis- 
 eases which impede the circulation, or as a consequence of throm- 
 bosis of the inferior vena cava or renal veins, or of other local 
 causes obstructing the circulation in the renal veins. The kidney 
 is enlarged and on section the cortex is found to be swollen, the 
 substance of the kidney dark red in color, particularly in the 
 pyramids in the vicinity of the large veins. The Malpighian 
 bodies may be distinctly enlarged and dark red. 
 
 Long-standing passive congestion leads to reactive hyperplasia 
 of the interstitial connective tissue of the organ, and thus to a 
 form of secondary interstitial nephritis. In these cases the kidney 
 becomes contracted, the surface somewhat irregular, and the cap- 
 sule ofttimes adherent. The organ may be intensely hard and pig- 
 mented, and the term cyanotic induration is appropriate. 
 
 The urine in passive hyperemia is, as a rule, deficient in 
 quantity, and contains variable quantities of albumin and hyaline 
 or granular tube-casts. 
 
 Hemorrhage. — Punctate hemorrhages may occur in cases of 
 intense active or passive hyperemia, the extravasation of blood 
 occurring in the interstitial tissues, in the uriniferous tubules, or 
 within the capsule of Bowman. Similar hemorrhages may be ob- 
 served in acute or chronic nephritis. In these cases the extrava- 
 sation of blood may occur by diapedesis or by actual rupture of 
 the capillaries. Small hemorrhages may occur in the perirenal 
 tissues in certain of the hemorrhagic diseases. Large hemorrhages 
 occur within the kidney-substance only in cases of traumatism. 
 
 3$dema of the kidney results from obstruction of its venous 
 circulation. The kidney becomes enlarged and soft, and the spaces 
 between the convoluted tubules (the primary lymphatic spaces) are 
 distinctly enlarged. There is associated congestion in these cases. 
 Simple edema of the kidney may result from obstruction of the 
 urinary outflow. 
 
-<> 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 Thrombosis of the renal veins or their branches is rare. It 
 causes intense hyperemia, hemorrhages, and edema, and later 
 necrosis and degenerations. 
 
 Kmbolism is very common in the branches of the renal 
 arteries, especially in cases of disease of the aortic valves or 
 
 atheroma of the aorta, with fibrin- 
 ous deposits upon the atheroma- 
 tous areas. The blood-vessels of 
 the kidney correspond closely to 
 the conception of terminal arteries, 
 and infarction is therefore the usual 
 result. In most cases the infarcts 
 are light-colored areas having a 
 wedge-shape, the base of the wedge 
 being directed toward the capsule 
 of the organ. A zone of reactive 
 hyperemia or hemorrhage usually 
 separates the infarct from the sur- 
 rounding structures (Fig. 267). 
 Less frequently the infarcts are 
 purely hemorrhagic, the entire area 
 being dark red in color. Minute 
 emboli may lead merely to punc- 
 tate hemorrhages within the kid- 
 ney, or to ecchymotic extravasa- 
 tions on the surface. 
 
 The white or anemic infarcts 
 undergo gradual necrosis and ab- 
 sorption, with cicatrization or encapsulation, the contents in the 
 latter case remaining as a dry detritus. The hemorrhagic infarcts 
 more commonly soften, and finally terminate in cicatrization or in 
 the formation of small cysts. In cases of infective embolism the 
 anemic or hemorrhagic infarct may rapidly break down and form 
 a metastatic abscess. 
 
 Fig. 267.— Anemic infarcts of the 
 kidney surrounded by a zone of hemor- 
 rhagic infiltration (Kaufmann). 
 
 INFLAMMATIONS. 
 
 Inflammation of the kidneys may affect the substance [nephri- 
 tis), the mucous membrane of the pelvis {pyelitis), or the capsule 
 and peripheral portions (perinephritis). 
 
 NEPHRITIS. 
 
 Nephritis is the term given to a number of forms of degen- 
 eration and inflammation of the substance of the kidney. The 
 term Bright' s disease is a clinical rather than pathologic one, being 
 applied to various kinds of kidney-disease attended with albumin- 
 
DISEASES OF THE URINARY ORGANS. 571 
 
 uria and dropsy. As a rule, however, the names Bright's disease 
 and nephritis are used synonymously. 
 
 Nephritis may be acute or chronic ; and parenchymatous, dif- 
 fuse, or interstitial. The term parenchymatous is applied to cases 
 in which degenerative changes in the epithelium of the tubules or 
 glomeruli are the most conspicuous feature ; the term diffuse is 
 applied when exudative or proliferative changes affecting the con- 
 nective tissues between the tubules and around the glomeruli and 
 blood-vessels are associated in more or less equal proportions with 
 the parenchymatous changes ; and the term interstitial nephritis is 
 used in cases in which exudative and especially proliferative changes 
 are alone conspicuous. 
 
 Etiology. — Nephritis is due in the majority of cases to irritants 
 which reach the kidney through the circulation. Intense acute 
 nephritis may result from various poisons, particularly such as 
 attack the parenchyma of organs, and are, therefore, known as 
 parenchyma-poisons. Among these arsenic, mercury, phosphorus, 
 cantharides, and turpentine are conspicuous. A second group of 
 cases, and perhaps the largest of all, owe their origin to infections 
 of various kinds. Nephritis is a common complication or sequel 
 of scarlet fever, cholera, septicemia, diphtheria, and many other 
 infectious diseases. In these cases the micro-organisms them- 
 selves may reach the kidney through the circulation, as in typhoid 
 fever, anthrax, or pneumonia, or the renal irritation may be caused 
 by the toxins, as in cholera and diphtheria. Sometimes infectious 
 nephritis is cryptogenetic, the portal of entrance of the micro- 
 organisms being entirely obscure. In such cases streptococci, 
 particularly, are operative. Certain chronic infections lead to 
 nephritis by the action of the toxins or by slow nutritive disturb- 
 ances. Such is the case in syphilis, tuberculosis, and malaria. 
 Autointoxication occasions certain cases, as in the nephritis of 
 gout and lithemia. 
 
 In a small proportion of the cases nephritis results from irri- 
 tants reaching the kidney through other channels than the circu- 
 lation, as in pyelonephritis, a condition consequent upon inflam- 
 matory processes ascending from the bladder and ureters, or as in 
 nephritis secondary to extrarenal disease (psoas abscess). 
 
 Low-grade renal inflammation may result from chronic conges- 
 tion of the kidneys in consequence of cardiac and pulmonary dis- 
 ease. In certain cases also it is likely that arterial disease affect- 
 ing the renal arteries in common with other arteries of the body 
 may initiate renal changes eventuating in a chronic interstitial form 
 of nephritis. 
 
 Pathologic Anatomy. — In considering the morbid anatomy the 
 terms parenchymatous and interstitial are preserved, with the 
 understanding that they are not strictly applicable to any given 
 •case. Pure parenchymatous inflammation does not exist, nor does 
 
572 TEXT-BOOK OF PATHOLOGY. 
 
 interstitial nephritis occur without any parenchymatous change. 
 Diffuse nephritis is considered under the heading parenchymatous 
 nephritis. 
 
 Acute Parenchymatous Nephritis ; Acute Bright's Disease. 
 
 This results most frequently from infectious fevers and from 
 toxic agents. It is more common in young persons than in the 
 old. 
 
 Acute Degenerative Nephritis. — The process in this 
 condition may be almost purely parenchymatous in nature, and 
 more nearly allied to pure degeneration than to inflamma- 
 tion. The epithelium of the tubules, especially in the convo- 
 luted portions, and to a certain extent also that covering 
 the glomeruli, is swollen, cloudy, and considerably desqua- 
 mated. Emigrated leukocytes, and occasionally red corpuscles, 
 are found within the tubules and the capsule of the Malpighian 
 bodies. The term acute catarrhal or desquamative nephritis is 
 more or less appropriate in such cases. The kidney is enlarged, 
 somewhat swollen, and generally rather pale in color. The 
 changes are most marked in the cortex, which is thicker than 
 normal, and by its light color contrasts strongly with the pyra- 
 mids. The capsule strips easily. In most cases the affection is 
 one of slight severity. 
 
 Acute Glomerulonephritis. — In another group of cases, 
 occurring most commonly in scarlet fever, the glomeruli are 
 primarily attacked and most severely affected throughout the 
 disease. Such cases are designated glomerulonephritis. The 
 
 Fig. 268.— Acute glomerulonephritis in diphtheria : a, alhuminous exudate in Mal- 
 pighian body; b, convoluted tubule; c, vascular tuft or glomerulus covered with prolif- 
 erated epithelium (Kaufmann). 
 
 capillaries of the Malpighian tuft are distended, and the glom- 
 erulus is filled with albuminous exudate, red and white blood- 
 corpuscles and with proliferated and desquamated epithelial cells 
 
DISEASES OF THE URINARY ORGANS. 573 
 
 derived from the epithelium lining the capsule or that covering 
 the Malpighian tuft (Fig. 268). Occasionally thrombosis occurs 
 within the vessels, and hyaline degeneration may affect the cap- 
 illary walls ; in other cases marked necrotic changes may occur 
 in the epithelium covering the tufts of vessels and lining the sac. 
 
 Acute diffuse nephritis is the ordinary form of acute 
 Bright' s disease, and is the form in which either of the two pre- 
 ceding are prone to terminate. The kidney is enlarged, and some- 
 times congested and red in color ; at other times it is light-colored 
 or even yellowish in consequence of the epithelial degeneration and 
 the anemia caused by the epithelial swelling. On section the cor- 
 tex is much increased in width, and when congestion exists it is 
 more or less mottled, showing spots or streaks of reddish color, the 
 intervening portions of the substance being grayish or yellowish in 
 hue. In other cases the entire cortical substance is uniformly gray 
 or yellow. The latter appearance is prone to occur in cases of con- 
 siderable duration. In intense acute cases there may be punctate 
 or linear hemorrhages, especially toward the surface of the organ, 
 and the entire organ may be of a dark-red color. In all cases the 
 capsule strips easily from the underlying substance. 
 
 Microscopically the changes are most varied. In all cases 
 there is more or less degeneration of the epithelium of the convo- 
 luted tubules and of that in the Malpighian bodies. In the earlier 
 stages the cells become swollen and granular (cloudy swelling), 
 while in advanced stages they may be filled with dark granules 
 or droplets of fat (fatty degeneration). On the other hand, 
 cases of great intensity may be marked from the very first by 
 complete necrosis of the epithelial cells. Similar changes may 
 be met with in the epithelium of the Malpighian bodies, and the 
 latter may be converted into granular masses in which the capil- 
 lary tufts are more or less obscured. Associated with these purely 
 parenchymatous changes are found evidences of interstitial involve- 
 ment in the presence of masses of round cells between the tubules 
 and in the vicinity of the Malpighian bodies. Active proliferation 
 of the connective tissues is also observed, though less markedly, in 
 the same situations. Certain cases are distinguished by their spe- 
 cial tendency to hemorrhagic extravasations into and around the 
 tubules and into the Malpighian bodies. To such the name acute 
 hemorrhagic nephritis is sometimes applied. This variety is espe- 
 cially common in intense septic or infectious cases, particularly 
 such as are attended with minute embolism of the renal arterioles. 
 
 Acute Interstitial Nephritis ; Suppurative Nephritis. 
 
 Acute interstitial nephritis occurs in practically only one form, 
 namely, in that which is characterized by the formation of purulent 
 foci in the kidney. Acute interstitial changes, non-suppurative in 
 
574 TEXT-BOOK OF PATHOLOGY. 
 
 character, occur, as has been described, in association with paren- 
 chymatous nephritis, but not as an independent affection. 
 
 Suppurative nephritis may result from metastatic involve- 
 ment of the kidneys in cases of general septicopyemia, from ascend- 
 ing inflammation in association with pyelitis, or from involvement 
 of the kidney in cases of suppurative disease in the vicinity. 
 
 Embolic suppurative nephritis leads to the formation of small 
 foci of suppuration in the substance of the organ, especially toward 
 the periphery. These may occur as mere points of yellowish color, 
 or they may be surrounded by a considerable zone of hemorrhagic 
 infiltration. The surface of the organ may be studded with small 
 elevated points, and as the process advances larger foci may form 
 by confluence. Microscopically the changes are found especially 
 in the vicinity of the Malpighian bodies, in the small capillaries 
 of which the micro-organisms primarily locate themselves. 
 Hemorrhagic extravasation is usually marked, and the accumula- 
 tions of leukocytes leading to suppuration are the characteristic 
 feature. Degenerative changes may be seen in the epithelium of 
 the vicinity, and, if the case has persisted for a certain length of 
 time, parenchymatous changes may be quite extensive. 
 
 In certain infectious fevers micro-organisms escape from the 
 blood through the kidneys (pneumonia, typhoid fever, anthrax). 
 
 Fig. '269.— Pyelonephritis, showing lines of ascending suppuration (Kauftnann). 
 
 In such cases it is possible that the bacteria which have been ex- 
 creted may cause infection in the lower parts of the uriniferous 
 tubules. The occurrence of such nephritis is uncertain. 
 
 Suppurative pyelonephritis occurs in cases of suppurative pye- 
 litis, especially in consequence of impaction of calculi in the pelvis. 
 In the earlier stages small linear areas of light color are seen in 
 the pyramids and medulla, and microscopically these are found to 
 be uriniferous tubules infiltrated with pus-cells (Fig. 269). In the 
 later stages these may run together, forming purulent collections 
 of considerable size. The superficial portions of the medulla and 
 cortex are only secondarily involved, and the suppurative areas 
 
DISEASES OF THE URINARY ORGANS. 575 
 
 here assume a more rounded shape. Pyelonephritis may terminate 
 by rupture of the abscesses into the pelvis of the kidney and the 
 discharge of the pus with the urine ; by rupture on the surface of 
 the kidney, causing perinephritic abscess ; or by inspissation and 
 calcareous infiltration of the contents of the abscess. When dis- 
 charge has taken place, or when inspissation occurs, induration and 
 cicatrization of the diseased areas result. A considerable portion 
 of the kidney may be thus converted into scar-tissue. 
 
 Suppurative nephritis, following suppuration around the kidney, 
 leads to the formation of superficial abscesses and erosions. 
 
 CHRONIC NEPHRITIS. 
 
 Chronic nephritis presents itself in varieties allied to the acute 
 forms, and we may distinguish chronic parenchymatous and 
 chronic interstitial nephritis. The former is practically always a 
 diffuse process, presenting no such limitations to the epithelium 
 of the tubules or to the glomeruli as are witnessed in the acute 
 disease. Chronic interstitial nephritis is characterized mainly by 
 hyperplasia of the connective tissue. 
 
 CHRONIC PARENCHYMATOUS NEPHRITIS. 
 
 Chronic parenchymatous nephritis in most cases results from 
 acute attacks which have become chronic by continuation or repe- 
 tition. It occurs after various infectious diseases, in consequence 
 of alcoholism, or in an obscure manner, autointoxication probably 
 accounting for some of the latter group of cases. 
 
 Pathologic Anatomy. — The kidney is usually enlarged, and 
 on section the cortical substance is often increased in width. The 
 color is most frequently grayish or yellowish in consequence of the 
 disease of the epithelium and of the anemia caused by the swell- 
 ing of the cells. The pyramids may be quite red and swollen, 
 or may be compressed and light in color. The capsule strips 
 easily, and the substance of the organ is only moderately firm ; 
 sometimes, indeed, it is quite soft. To this form of chronic 
 parenchymatous nephritis the term large white kidney is often 
 applied. In other cases the substance of the organ may be quite 
 red in color, or may be mottled, light areas of yellowish or gray 
 color alternating with congested portions. In such cases careful 
 examination may show punctate or linear extravasations of blood, 
 and the term chronic hemorrhagic nephritis is not inappropriate. 
 The kidney is enlarged, as in the first variety, the cortex thick, 
 and the capsule easily removed. In either case small cysts may 
 form in the substance of the organ or upon the surface by disten- 
 tion of the convoluted tubules or capsules of Bowman. 
 
 In the later stages of chronic parenchymatous nephritis the 
 
576 TEXT-BOOK OF PATHOLOGY. 
 
 degenerative processes in the epithelium become pronounced, and 
 the organ may grow progressively lighter in color and more fatty 
 in appearance. At the same time interstitial processes associate 
 themselves, and the substance of the organ becomes more firm and 
 the kidney is reduced in size. Attachments are formed between 
 the substance and the capsule, which is no longer removable 
 without laceration of the underlying substance. This terminal 
 form of chronic parenchymatous nephritis has been designated as 
 fatty contracting kidney, or as secondary interstitial nephritis, ac- 
 cording to the amount of fatty parenchymatous change or of inter- 
 stitial overgrowth present in the individual case (see page 577). 
 
 Microscopically chronic parenchymatous nephritis is marked 
 by striking degenerative changes in the epithelial cells of the con- 
 voluted tubules, and to a less extent in those lining the capsule of 
 Bowman and covering the Malpighian tufts (Fig. 270). The 
 
 
 Fig. 270.— Chronic parenchymatous nephritis, showing marked involvement of the 
 Malpighian body and considerable interstitial change. 
 
 epithelium of the tubules is at first swollen and finely granular, 
 the nucleus being obscured and the cells oftentimes becoming 
 fused (cloudy swelling). In the more advanced stages of the pro- 
 cess marked fatty degeneration of the cells is discovered, and they 
 may break down completely, so that the lumen of the tubule is 
 filled with fatty and granular detritus (Fig. 271). Extravasations of 
 leukocytes or of red blood-corpuscles may take place, especially in 
 the form known as hemorrhagic nephritis. Many of the tubules may 
 be filled with tube-casts of hyaline or more frequently of granular 
 appearance. The Malpighian bodies are usually simultaneously, 
 though perhaps less markedly, affected. The epithelium in the 
 latter is proliferated and degenerated, and the vascular tuft may 
 
DISEASES OF THE URINARY ORGANS. 
 
 577 
 
 present considerable hyaline degeneration. In the hemorrhagic 
 variety the Malpighian body may be completely filled with extra v- 
 asated blood. Side by side with these parenchymatous changes 
 may be seen changes in the interstitial tissues. Notably, there 
 are proliferation and thickening of the capsule of Bowman and of 
 
 Fig. 271.— Chronic parenchymatous nephritis : a, convoluted tubules with cloudy swell- 
 ing of the epithelium ; &, glomeruli, more or less degenerated ; c, atrophic tubules ; d, 
 sclerotic interstitial tissue ; e, round-cell infiltration ; /, blood-vessel ; g, tube-casts in 
 tubules (Kaufmann). 
 
 the connective tissues between the tubules. In advanced stages 
 these interstitial changes are always present, and in those cases 
 known as secondary interstitial nephritis the connective-tissue 
 hyperplasia is the predominating condition. The walls of the 
 small blood-vessels of the kidney are usually thickened by hyper- 
 plasia. 
 
 CHRONIC INTERSTITIAL NEPHRITIS. 
 
 Chronic interstitial nephritis leads to the formation of a con- 
 tracted kidney. This may be a secondary form of nephritis fol- 
 lowing chronic parenchymatous nephritis, or it may be primary, 
 when it is often associated with diffuse arteriosclerosis. 
 
 Secondary chronic interstitial nephritis is the terminal 
 stage of certain cases of chronic parenchymatous nephritis, and 
 results from a continuous hyperplasia of the interstitial tissues, 
 with degeneration and atrophy of the parenchyma. The organ is 
 reduced in size, and may be quite irregular upon the surface, the 
 irregularity taking the form of large depressions or of fine granu- 
 lations. The capsule strips with difficulty, portions of the kidney- 
 
578 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 substance remaining attached. On section the kidney is found 
 to be firmer than normal, and is of light color, often yellowish 
 (fatty) in hue. The cortex may be nearly the normal thickness, 
 or may be considerably reduced. The small blood-vessels of the 
 substance of the organ may be patulous and evidently sclerotic. 
 
 Microscopically the epithelium of the tubules is granular, fatty, 
 or atrophic, and the cells are found detached in great numbers and 
 occupying the lumen of the tubules. The tubules themselves may 
 be compressed by surrounding interstitial overgrowth, or may be 
 distended even to the formation of cystic dilatations. The capsule 
 of Bowman is greatly thickened, and the Malpighian bodies may 
 be much distorted and compressed. 
 
 Primary Chronic Interstitial Nephritis ; Red Granu- 
 lar Kidney ; Arteriosclerotic Nephritis ; Gouty Nephri- 
 tis. — All of these terms have been applied to a form of inter- 
 stitial nephritis probably produced by irritants conveyed through 
 the circulation. It occurs in consequence of alcoholism, syphilis, 
 gout, chronic plumbism, and chronic cachexias of other kinds. It 
 is not rarely associated with diffuse arteriosclerosis. A certain 
 amount of interstitial nephritis of this variety is a natural lesion 
 of old age. 
 
 Pathologic Anatomy. — The kidney is usually decreased in size, 
 
 w 
 
 Fig. 272.— Chronic interstitial nephritis ; granular kidney (Orth). 
 
 and sometimes may be very much contracted. In other cases 
 the reduction in the dimensions is inconsiderable, and the size 
 may even be increased. The surface is irregular, and, on removal 
 
DISEASES OF THE URINARY ORGANS. 
 
 579 
 
 of the capsule, is found to be finely granular or irregularly tabu- 
 lated (Fig. 272). The capsule itself strips with difficulty. Small 
 
 Fig. 273.— Chronic interstitial nephritis : great increase of connective tissue around the 
 glomeruli, renal tubules, and blood-vessels. 
 
 cysts may be seen upon the surface. On section the substance is 
 firm, and may sometimes be almost cartilaginous in consistence. 
 
 ilpii^ '/ w " .-' 
 
 V'dT# £f^ 
 
 
 s n 
 
 i* "'/Vv . , ' 
 
 
 _ . 
 
 ■ * Va? 
 
 
 i,y 
 
 %■: :■■ ■fiv'iv" ■ 
 
 •'■J^t^ 
 
 
 4 gil: 1 
 
 
 **>«%.<«<< 
 
 
 "*^L . 
 
 Fig. 274.— Chronic intersti 
 
 :phritis (from a photograph by Dr. Wm. M. Gray). 
 
 The cortex is narrow, often being reduced to a quarter or one-sixth 
 its normal width ; while the pyramids may be increased in size or 
 contracted like the cortex, and not rarely show dense white sclero- 
 tic tissue radiating from the apices. In gouty cases deposits of 
 urates may be observed in the same situation. The color of the 
 kidney varies, but is usually grayish-brown or gray. The blood- 
 
580 TEXT-BOOK OF PATHOLOGY. 
 
 vessels in the substance of the organ are usually patulous and 
 their walls visibly thickened. 
 
 Microscopically, chronic interstitial nephritis .is characterized 
 by great hyperplasia of the connective tissue surrounding the Mal- 
 pighian bodies and the convoluted tubules, and by hyperplasia of 
 the walls of the blood-vessels (Fig. 273). The overgrowth of 
 connective tissue may be irregular in its distribution, and may 
 vary greatly in amount. In beginning cases there is only moder- 
 ate thickening of the capsules of Bowman and of the intertubular 
 tissues and walls of the blood-vessels. In the most pronounced 
 cases the kidney-substance is almost wholly transformed into 
 fibrous tissue of dense sclerotic character (Fig. 274). The epithe- 
 lium undergoes progressive atrophy, the cells shrinking in size and 
 becoming granular and loosened from the basement-membrane. 
 Hyaline or granular tube-casts may be found within the tubules, 
 and the latter are compressed by contraction of the new-formed 
 connective tissue, or in other cases dilated by the disappearance of 
 the epithelium. 
 
 Pathologic Physiology of Nephritis. — The effect of acute 
 or chronic nephritis varies greatly in individual cases. Profound 
 systemic disturbances in acute cases are doubtless often the result 
 of the action of toxic substances, which caused the nephritis, rather 
 than of the disease of the kidneys itself. In uncomplicated cases 
 of acute or chronic nephritis the influence upon the general metabo- 
 lism is seemingly slight. Investigations have not as yet shown 
 any decided increase in the metabolic consumption of the tissues, 
 and no specific disturbances of metabolism of any sort have been 
 discovered. It is very likely, however, that extensive disease of 
 the kidneys does exercise some influence, since these organs un- 
 doubtedly have actual glandular functions and are not merely 
 passive agents for the filtration of the blood and the excretion of 
 urine. The peculiar intoxication which occurs in nephritis, and to 
 which the name uremia (q. v.) is applied, has received no satis- 
 factory explanation. It is probable that substances normally 
 excreted in the urine are retained in the blood and accumulate to 
 such an extent that intoxication results. It is also likely that sub- 
 stances which are normally elaborated by the kidneys and excreted 
 in altered forms remain in the blood and occasion disturbances. 
 During the progress of uremia there seems undoubtedly to be 
 active tissue-consumption, but accurate studies are wanting. 
 
 Gastro-intestinal symptoms are frequent in renal disease. In 
 a notable proportion of cases the gastric secretion has been found 
 deficient, and this may account for some of the disturbances. 
 Putrefactive processes in the intestines have also been demon- 
 strated in some cases, being evidenced by the increased quantity 
 of ethereal sulphates in the urine. In the later stages of nephri- 
 tis, and especially in uremia, severe gastro-intestinal disorders 
 
DISEASES OF THE URINARY ORGANS. 581 
 
 sometimes develop. These have been explained by the assump- 
 tion that urea is excreted through the gastro-intestinal mucous 
 membrane, and undergoes ammoniacal decomposition within the 
 digestive tract. The ammonia formed by this decomposition is 
 supposed to be the immediate cause of the gastro-intestinal dis- 
 turbance. 
 
 The urine in nephritis is of the greatest interest. In acute 
 cases, and sometimes in chronic forms it suffers notable change of 
 appearance by admixture of blood. In other instances the color 
 and physical properties are to a large extent dependent upon its 
 amount. As a rule, the quantity of urine is decreased. The 
 nitrogenous elimination is of particular interest. In acute cases, in 
 which the quantity of urine is greatly deficient, there is undoubt- 
 edly an insufficient excretion of nitrogen from the urine. ; subse- 
 quently the nitrogenous element may be excreted in increased 
 quantities. In acute nephritis without marked diminution in the 
 quantity of urine, the nitrogenous elimination may remain satis- 
 factory. In chronic nephritis the elimination of nitrogen in the 
 urine may be reduced, both in the parenchymatous and interstitial 
 forms of nephritis. The amount of urea is very commonly de- 
 creased ; in part this may be compensated for by increased elimi- 
 nation through the skin and intestines. Nitrogen retention is 
 not invariable, and from time to time periods of increased elimi- 
 nation may occur. The uric acid is usually decreased in quantity, 
 but may be entirely normal in any form of nephritis, and may in 
 some instances be temporarily increased. Ammonia is present in 
 normal quantities. During uremia it may be increased. Xanthin 
 may be present in increased quantities, and creatinin is reduced in 
 quantity. 
 
 The urine in nephritis presents two striking peculiarities : the 
 presence of albumin, discoverable by chemical examination, and 
 the presence of tube-casts. Albuminuria is an almost constant 
 symptom, though occasionally, in chronic interstitial nephritis, the 
 amount may be so small that it is not detected by the cruder tests. 
 The more delicate methods will probably detect albumin in every 
 case. Serum-albumin is the more important form, but globulin 
 occurs in small amounts in every case. In hemorrhagic forms of 
 acute or chronic nephritis and in cases complicated by amyloid 
 degeneration globulin may be found in considerable quantity. 
 
 The tube-casts met with in nephritis are casts formed within 
 the convoluted tubules, or more rarely in other parts, and are com- 
 posed of albuminoid substances and possibly sometimes of fibrin. 
 They are formed partly of materials which have accumulated in 
 the tubules by exudation, partly of the granular detritus of the 
 degenerated epithelium, or of red and white blood-corpuscles. 
 We may distinguish a number of varieties, viz., hyaline, cellular, 
 crystalline, and granular casts and cylindroids. 
 
582 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 Hyaline casts are clear, rounded bodies having a diameter of 
 from 0.01 to 0.03 mm. and a variable length. Sometimes they 
 are quite short ; at other times they extend across several fields 
 of the microscope. They may be straight, or spiral or contorted. 
 Sometimes they are so transparent and light colored that they are 
 scarcely visible, or, on the other hand, they may be of a denser 
 structure and less transparent. Hyaline casts are frequently met 
 with in simple congestion of the kidney and in icterus unassociated 
 with discoverable nephritis. They are most abundant in acute 
 parenchymatous nephritis, but are met with also in chronic 
 parenchymatous and interstitial nephritis. A form of hyaline 
 cast known as the waxy cast is met with, sometimes in acute, but 
 more commonly in chronic nephritis (Fig. 275). It is distin- 
 
 M CQ 
 
 >M 
 
 \---< ■ 
 
 Fig. 275.— Waxy hyaline casts. 
 
 Fig. 276.— Blood-casts, composed wholly 
 of red or white corpuscles, or hyaline sub- 
 stance covered with blood-corpuscle. 
 
 guished by the moulded, wax-like appearance and by its apparent 
 rigidity. 
 
 Cellular Casts. — The most frequent form is that in which the 
 surface of a hyaline or granular cast is covered with epithelial 
 cells that have detached themselves from the tubules. The 
 entire surface may be covered, or there may be but a few cells 
 here and there. This form is found especially in acute parenchy- 
 matous nephritis. Leucocytic casts are moulds of the tubules com- 
 posed of masses of leukocytes. They are found especially in 
 purulent pyelonephritis. Occasionally leukocytes are found upon 
 the surface of other casts. Blood-casts, composed of red blood- 
 corpuscles, or of blood-pigment formed by disintegrated red cor- 
 puscles, are frequently observed in acute and chronic hemorrhagic 
 nephritis (Fig. 276). 
 
 Crystalline Casts. — Moulds of the tubules, composed of uric 
 acid or oxalate of lime, are sometimes observed in chronic nephri- 
 
DISEASES OF THE URINARY ORGANS. 
 
 583 
 
 tis, when there is a tendency to the deposition of the crystals 
 
 named (Fig. 277). Similar formations may be met with in the 
 
 urine of the new-born independently of nephritis (see page 589). 
 
 Granular casts may be light or dark, according to the amount 
 
 Fig. 277.— Tube-casts, composed of uric-acid Fig. 278.— Granular and fatty casts and 
 crystals. two compound granular cells. 
 
 and character of the granular material. They are composed of 
 substances derived from broken-down epithelial cells, and are 
 especially common in chronic nephritis, though they may occur in 
 
 Fig. 279.— Cylindroids : a and b, cast-like forms ; c, filamentous forms. 
 
 quite acute cases. Sometimes, instead of granular matter, the 
 debris of the epithelial cells occurs as oil-drops, and the term 
 fatty casts is appropriately applied (Fig. 278). The diameter and 
 length of granular casts vary considerably. As a rule, the diam- 
 eter is about the same as that of the hyaline casts, but the length 
 is rarely as great. 
 
584 TEXT-BOOK OF PATHOLOGY. 
 
 Cylindroids are formations resembling casts more or less 
 closely. Sometimes they appear as thread-like formations, rounded 
 or flat, and occurring singly or in twisted bunches. In other 
 cases they may be quite similar to hyaline casts, though distin- 
 guished by a long, tapering end or tail (Fig. 279). Cylindroids 
 occur in conditions of renal irritation not sufficient to constitute 
 nephritis, as well as in cases of genuine nephritis. They are also 
 supposed to be produced in the tubular glands of other parts of the 
 geni to-urinary tract, as in the glands of Cowper. 
 
 Other Constituents of the Urine. — Various cellular constituents 
 are found in nephritis. In acute and in chronic hemorrhagic 
 nephritis white and red blood-corpuscles are frequently observed ; 
 and epithelial cells are more or less abundant in all forms of 
 parenchymatous nephritis. In the acuter varieties swollen and 
 granular rounded cells are observed ; in the more chronic forms, 
 particularly when fatty degeneration is pronounced, epithelial 
 cells or leukocytes densely filled with dark granular or globular 
 fat are conspicuous. The term compound granule-cell has been 
 applied to these cells. 
 
 Results of Nephritis. — Nephritis leads to notable changes 
 in the entire organism, and particularly in the vascular system. 
 
 Cardiac Changes. — In acute nephritis there may be associated 
 acute degenerative or inflammatory lesions of the heart-muscle, and 
 cardiac dilatation may occur. These, however, are usually results 
 of the infectious or toxic cause underlying the nephritis, rather 
 than results of the nephritis itself. When parenchymatous nephri- 
 tis becomes subacute or chronic, hypertrophy of the heart (notably 
 of the left ventricle) takes place, and this reaches extreme propor- 
 tions in chronic interstitial nephritis. The cause of the hyper- 
 trophy of the heart has occasioned much controversy. It seems 
 likely that it is in large part the result of irritation and over-stimu- 
 lation of the heart-muscle by substances retained in the blood, 
 instead of being excreted. The obstruction to the circulation 
 occasioned by thickening of the walls of the renal vessels is of 
 little moment ; and the theory that the cardiac hypertrophy is 
 due to a hydremic condition and increased quantity of blood, 
 in consequence of retention of water in the system, is nega- 
 tived by the fact that such hydremic excess of blood is certainly 
 absent in many cases. Associated arteriosclerosis is undoubtedly 
 one of the important factors in the production of cardiac hyper- 
 trophy. 
 
 Arteriosclerosis. — The arteries are frequently sclerotic in cases 
 of chronic nephritis. In part this is due to the direct action of 
 toxic products of improper metabolism occurring in Bright's 
 disease ; in part it is coincidental or an antecedent condition. 
 
 Acute inflammatory lesions of the serous membranes, and to a 
 less extent of the mucous membranes, sometimes occur in Bright's 
 
DISEASES OF THE URINARY ORGANS. 585 
 
 disease. Acute endocarditis, acute pericarditis, and pleurisy are 
 the most frequent conditions. Of the inflammatory conditions of 
 the mucous membranes tonsillitis and pharyngitis are not infre- 
 quent. Enteritis, even of ulcerative type, may occur, especially 
 in chronic nephritis. This, in part, seems to result from vicarious 
 excretion of irritant matters from the intestinal mucosa. 
 
 Edema, or dropsy, is a frequent manifestation of nephritis. It 
 is most frequent in the parenchymatous forms, particularly in such 
 as occasion changes in the glomeruli and other vascular portions 
 of the kidney. The important etiologic factor is doubtless disease 
 of the blood-vessels. In chronic interstitial nephritis dropsy is 
 rarely observed until the late stages, when manifest arterial dis- 
 ease and failing circulation from cardiac weakness have super- 
 vened. The edema usually begins in the loose subcutaneous tissues 
 of the eyelids and hands, but extends to all parts of the body, 
 causing anasarca. Internal edema, and especially edema of the 
 lungs, may be met with. 
 
 Uremia is the name applied to certain clinical manifestations 
 probably caused by the retention of toxic substances in the blood 
 which ordinarily are excreted with the urine. The nature of the 
 substance or substances in question remains obscure. Neither 
 urea, potassium nor ammonium salts, uric acid, nor various other 
 constituents of the urine alone produce ursemic manifestations ; 
 though the injection into animals of some of these may cause toxic 
 symptoms, such as convulsions or coma. It may be that uremia is 
 caused by the conjoined action of a number of such toxic bodies, 
 but it is not improbable that the poisons are substances as yet un- 
 discovered. The theory that uremia is due to edema or anemia 
 of the brain may be definitely abandoned. 
 
 ATROPHY AND HYPERTROPHY. 
 
 Atrophy of the kidney may be congenital (hypoplasia), or may 
 occur in old age (senile atrophy). In the latter case the kidney is 
 small, hard, and usually darker in color than normal. The irreg- 
 ular atrophy of the parenchyma leads to irregularities upon the sur- 
 face of the organ. The capsule may be thickened, and not rarely 
 the perirenal fat is abundant, and considerable fatty deposit occurs 
 beneath the mucous membrane of the pelvis. 
 
 Microscopically the renal cells are small in size, somewhat 
 dark, and granular. They may disappear entirely from the 
 tubules in places, and the intertubular tissue and the basement- 
 membrane are correspondingly thickened. The Malpighian bodies 
 may be converted into contracted fibrous areas. In some cases 
 the interstitial processes become so pronounced that the changes 
 in the kidney become those of interstitial nephritis. These cases 
 
586 TEXT-BOOK OF PATHOLOGY. 
 
 are particularly met with in persons of advanced years having 
 arteriosclerosis (see Chronic Interstitial Nephritis). 
 
 Hypertrophy may affect one kidney when its fellow is eon- 
 genitally wanting, has become diseased, or has been removed. 
 Under these circumstances the remaining or healthy organ some- 
 times undergoes considerable hypertrophy. The appearance is 
 that of a much enlarged but otherwise normal kidney. 
 
 Microscopically there may be simply increase of the size of the 
 tubules, or in cases in which the compensatory hypertrophy has 
 begun before the completion of development there may be actual 
 increase in the number of tubules and Malpighian bodies. 
 
 DEGENERATIONS. 
 
 Parenchymatous degeneration, or cloudy swelling, 
 
 occurs in the kidneys in consequence of the action of various 
 poisons, infectious or chemical. It is met with in practically all 
 cases of diphtheria, scarlet fever, and cholera, and less commonly 
 in many other infectious diseases. Among the poisons the various 
 parenchyma-poisons (q. v., Part I) are all capable of attacking the 
 kidney and producing cloudy swelling. In case of either toxic or 
 infectious degenerations, however, the process is prone to become 
 more serious, and to terminate in acute parenchymatous nephritis. 
 No sharp dividing-line can be drawn between the two conditions. 
 The kidney is somewhat increased in size, is softer than nor- 
 mal, and on section the cortex is yellowish or of light-grayish 
 color (Fig. 280). The Malpighian bodies may be prominent as 
 
 Fig. 280. — Parenchymatous degeneration of the kidney, from a case of cholera (modified 
 from Kast and Rumpel). 
 
 red spots lying in the light-colored renal tissue. The pyramids 
 are often congested, and contrast strongly with the cortical sub- 
 stance. 
 
 Microscopically, fine granulation of the cells of the convoluted 
 
DISEASES OF THE URINARY ORGANS. 587 
 
 or other tubules is the striking feature. The nuclei of the cells 
 are obscured, and at times all of the cells of the tubule apparently 
 become fused. Exudative changes and hyperplasia of the inter- 
 stitial tissues are wanting in a purely degenerative condition. Fre- 
 quently the kidney is restored to the normal condition, but, on 
 the other hand, acute Bright's disease or fatty degeneration may 
 ensue. 
 
 Fatty Degeneration. — This occurs in consequence of the 
 last-described condition, or independently in consequence of gen- 
 eral anemia and systemic disorders, as in progressive pernicious 
 anemia and tuberculosis. Fatty degeneration of the kidney fre- 
 quently occurs in the course of pregnancy, when it is due to dis- 
 turbance of the circulation in the kidneys or possibly to obstruc- 
 tion of the ureters. In these cases the process usually advances 
 to the condition of diffuse nephritis. 
 
 In pure fatty degeneration the kidney is about the normal size, 
 or often smaller than normal ; is soft ; and on section the cortex 
 has about the normal width. The color is uniformly yellowish or 
 mottled, certain areas being yellowish in color and others normal 
 or perhaps hyperemia. Usually the surface of the kidney is 
 smooth, but sometimes localized spots of degeneration may become 
 depressed and give rise to irregularities. 
 
 Microscopically the epithelial cells are granular, or filled with 
 oil-drops (Fig. 281). Not rarely the cells are loosened and lie 
 
 
 V >**•.. 
 
 .••*• 
 
 Mi 
 
 -- !••••• 
 
 
 
 ' «.'.* *•• 
 
 .?#'"** v ^-- 
 
 • ° ' 
 
 
 
 ,;^, ♦• ' MS* 
 
 
 1 V 
 
 
 Fig. 281.— Fatty degeneration of the epithelium of the tubules : stained with osmic acid 
 (Simmonds). 
 
 free within the lumen of the tubules. The basement-membrane 
 and interstitial tissues may be somewhat thickened, either appar- 
 ently or actually. 
 
588 TEXT-BOOK OF PATHOLOGY. 
 
 Fatty infiltration is an unimportant condition. In the 
 atrophic kidney of old age and in the contracted kidneys of 
 chronic nephritis fatty infiltration of the areolar tissue beneath the 
 mucosa of the pelvis is frequently observed. Fatty infiltration of 
 the epithelial cells may occur under normal conditions, or in -cases 
 in which the blood is surcharged with fat (lipemia) and in which 
 the kidneys are actively engaged in its excretion. Fatty infiltra- 
 tion of the perirenal cellular tissues occurs in general obesity, and 
 sometimes as a localized affection in cases of advanced renal dis- 
 ease, particularly atrophy. 
 
 Calcification may occur in diseased areas of the kidneys, as 
 in sclerotic Malpighian bodies, in old infarcts and the like. Occa- 
 sionally calcification occurs in the epithelial cells themselves, 
 particularly in such as have undergone necrosis. 
 
 Glycogenic infiltration of the kidneys occurs in diabetes. 
 It affects the epithelial cells, particularly those in the portions of 
 the organ lying between the medulla and the cortex. The kidney 
 is usually increased in size, the cortex broader than normal, and 
 the consistency increased. The substance may be lighter colored 
 and of homogeneous appearance. Microscopically the epithelial 
 cells, particularly those of the tubes of Henle, are found to be 
 altered in character, the normal granular condition of the proto- 
 plasm having disappeared. The glycogenic nature of the infil- 
 trating substance is recognized by the dark-brown color obtained 
 by staining fresh sections with iodin. 
 
 Amyloid degeneration occurs in the kidneys under the same 
 conditions as in the liver and spleen. It is most frequent in cases 
 of chronic tuberculosis of the lungs, and occurs in cases of long- 
 standing suppuration connected with bone, in syphilis, and as a 
 result of other cachexias. The kidney is enlarged, sometimes to 
 twice its normal bulk, is harder than normal, and on section the 
 substance is found light grayish in color. It may be uniformly 
 grayish or waxy ; or, on the other hand, it may be mottled, gray- 
 ish areas alternating with portions of yellow color, the latter being 
 due to fatty degeneration. Amyloid degeneration begins in the 
 small blood-vessels, particularly those of the Malpighian tufts, and 
 spreads to the connective tissues of the organ, but does not involve 
 the epithelium. 
 
 Microscopically the glomeruli may present spots of hyaline or 
 homogeneous appearance in which the capillaries seem completely 
 disorganized, and the entire glomerulus may be transformed into 
 a transparent or translucent mass (Fig. 282). The capsule is 
 thickened and ofttimes simultaneously diseased. The tubules 
 habitually contain hyaline casts. The organ becomes more or 
 less anemic from obstruction of the capillaries, and sooner or later 
 fatty degeneration of the epithelial cells takes place. Inflamma- 
 tory processes are usually wanting, but nephritis may become 
 
DISEASES OF THE URINARY ORGANS. 
 
 589 
 
 associated with amyloid degeneration, and the latter process may 
 occur in kidneys primarily the seat of nephritis. The urine in 
 amyloid disease is albuminous and scanty ; the proportion of 
 serum-globulin is excessive. Not rarely it contains hyaline 
 casts which respond more or less distinctly to the color-tests for 
 
 Fig. 282.— Contracted and amyloid kidney (from a photograph by Dr. Wm. M. Gray). 
 
 amyloid substance, but these are not diagnostic, and it is doubtful 
 whether they are in reality composed of amyloid material. 
 
 CONCRETIONS IN THE URINIFEROUS TUBULES. 
 
 Various calcareous concretions, or " infarcts," occur in the uri- 
 niferous tubules, particularly in the large collecting tubules near 
 their termination at the apex of the pyramids. Collections of 
 urates, particularly urate of ammonium, are frequently seen in 
 the form of radiating lines of light-grayish, yellowish, or reddish 
 color, marking the pyramids near the apices in new-born infants. 
 These consist of crystalline concretions filling the large uriniferous 
 tubules, and have been considered as a valuable medicolegal indi- 
 cation that the infant had breathed. They are not, however, suf- 
 ficient proof. Sometimes the concretions are passed with the urine, 
 and are discovered as large casts of conglomerated crystals. Less 
 frequently other forms of crystals are met with in the infarcts of 
 the new-born. Similar concretions occur in gouty individuals, par- 
 ticularly in aged persons, and calcium salts may be deposited when 
 the blood is surcharged with them in consequence of diseases of 
 
590 TEXT-BOOK OF PATHOLOGY. 
 
 the bones. Triple phosphates may be found as a consequence of 
 obstruction of the urinary passages and stagnation of urine. 
 
 Concretions composed of bilirubin may be formed in extreme 
 jaundice, and particularly in the jaundice of the new-born. In- 
 farcts composed of hemoglobin may be seen in cases of hemo- 
 globinuria due to infectious and toxic causes. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis. — Tuberculosis may occur in the kidney in the 
 form of minute, grayish-white miliary tubercles as part of a 
 general hematogeneous tuberculosis. A second form, which is 
 also hematogenic, is known as chronic heal tuberculosis. In this 
 form the substance of the kidney near the cortex, or sometimes 
 that adjacent to the pelvis, is occupied by masses of cheesy tuber- 
 culous tissue, and there may be secondary miliary tuberculosis 
 near by. Softening is prone to occur, and the tuberculous focus 
 may discharge into the pelvis of the kidney, leaving a necrotic 
 cavity. The entire organ may be transformed in this manner. 
 Tuberculosis of the kidney may also result from ascending infec- 
 tion, being secondary to tuberculosis of the seminal vesicles of the 
 1 (ladder, of the ureters, and of the pelvis of the kidney. The pro- 
 cess first involves the discharging tubules at the apices of the 
 pyramids and spreads outward toward the cortex. Cheesy foci are 
 formed, which may soften and discharge into the pelvis, as in the 
 case of chronic local tuberculosis of the kidney. It is difficult to 
 determine whether tuberculosis of the kidneys is more frequently 
 the result of urogenital tuberculosis primarily affecting the parts 
 below, or the cause of the latter. Primary affection of the kid- 
 ney is certainly more common than many have been disposed to 
 admit. 
 
 Syphilis. — In the earlier stages of syphilis there may possibly 
 be acute nephritis similar to that of other infectious diseases. Syph- 
 ilis of long duration may lead to amyloid degeneration of the kid- 
 ney, or to chronic interstitial nephritis. In the latter case con- 
 tractions of fibrous tissue leading to marked lobulation are rather 
 characteristic. Syphilitic gummata are rare, but have been met 
 with, and in their healing lead to marked scar-formation. 
 
 TUMORS. 
 
 Fibromata and lipomata may occasionally be met with in 
 the kidney in the form of small rounded nodules. In association 
 with calculous pyelitis and other conditions of the kidney leading 
 to atrophy, the fatty tissue surrounding the kidney may be in- 
 creased to such an extent as to constitute practically a fatty tumor. 
 
 leiomyoma is an occasional growth of the kidney. 
 
DISEASES OF THE URINARY ORGANS. 591 
 
 Congenital Adenoma. — Under the name of struma aberrata 
 suprarenalis has been described a form of tumor of the kidney 
 which results from splitting off of a remnant of the suprarenal 
 capsule and its incorporation in the kidney, where it subsequently 
 grows. The tumor presents the appearance of a small lipomatous 
 growth beneath the capsule of the kidney, or, more rarely, it may 
 attain considerable size. Histologically it consists of epithelial 
 cells arranged in tubules similar to those of the cortical portion 
 of the suprarenal capsule. These undergo considerable fatty 
 infiltration, and almost the entire tumor may be fatty. Occasion- 
 ally active proliferative changes occur in the epithelium, and a 
 malignant character is assumed. 
 
 Sarcoma of the kidney is the most frequent malignant tumor. 
 It may occur congenitally, or in later life. The size and general 
 appearance vary considerably, but for the most part the structure 
 is soft and grayish or sometimes quite red. Extravasations of 
 blood or hemorrhages into the tumor are not uncommon. There 
 may be a distinct capsule, or the growth may be an infiltrating 
 one. Cystic softening is not infrequent. 
 
 Microscopically the appearance varies considerably, and the 
 growth may be composed of round cells, spindle cells, or cells of 
 various shapes. Not rarely a certain number of striped muscle- 
 fibers are found, and to such growths the term rhabdomyosarcoma 
 has been applied. In other cases there may be embedded in the 
 sarcomatous tissue glandular acini composed of cylindrical or irreg- 
 ular epithelium, and to such the name adenosarcoma is applicable 
 
 Fig. 283.— Adenosarcoma of the kidney (modified from Kast and Rumpel). 
 
 (Fig. 283). Occasionally myxomatous tissue, smooth muscle-fibers, 
 or even islets of cartilage are found. The multiform character of 
 sarcoma of the kidney suggests an embryonal origin, and it is not 
 unlikely that inclusions of the primitive Wolffian body are the 
 starting-point of the disease. 
 
 Adenoma of the kidney is rare. It originates in the convo- 
 luted tubules, and presents itself in the form of more or less 
 
592 TEXT-BOOK OF PATHOLOGY. 
 
 nodular masses. Microscopically the appearance is that of a 
 tubular adenoma. Proliferative changes occasionally affect the 
 uriniferous tubules in interstitial nephritis, and give rise to small 
 areas of adenomatous appearance. In such cases, however, the 
 appearances are not those of a tumor in the strict sense. 
 
 Papuliferous cystic adenoma is sometimes observed. It 
 occasions tumors of small or large size with fibrous capsules and 
 cystic excavations in which the lining epithelium is elevated in 
 a papillomatous manner. 
 
 Carcinoma is a rare primary tumor of the kidney, and occurs 
 in persons of advanced years. The growth begins in the cortical 
 substance or in the medulla, and presents itself as a soft white or, 
 in case of hemorrhage into it, red tumor. 
 
 Microscopically it is found to be a glandular carcinoma pre- 
 senting acini composed of epithelial cells of various shapes. 
 Metastasis is rare. 
 
 Secondary Tumors. — Among the secondary tumors of the 
 kidney are both sarcoma and carcinoma. 
 
 In the same group may be included the lymphomatous infiltra- 
 
 
 v -„ ; ir.. 
 
 ' ; - — . , 
 
 Fig. 284.— Lymphoid infiltrations between the renal tubules ; from a case of leukemia. 
 
 turns of leukemia (Fig. 284). In this disease the kidney is often 
 enlarged, and on section is found to be uniformly white or mottled 
 in color, the light-colored areas representing masses of lymphoid 
 cells. Most of these have doubtless been deposited from the cir- 
 culation, but there is also evidence of local multiplication. 
 
 Cysts of the kidney are of various forms. In the course of 
 chronic nephritis, especially the interstitial form, cystic dilatations 
 of the convoluted tubules and Malpighian bodies are observed. 
 These appear as small or large rounded bodies lying immediately 
 beneath the capsule, and on section are found to contain serous liquid, 
 
DISEASES OF THE URINARY ORGANS. 593 
 
 or colloid material, the result of degeneration of the epithelial lining 
 of the cyst. Sometimes very large cysts of this character are met 
 with in cases of nephritis, or even in otherwise healthy kidneys (Fig. 
 285). Cysts observed in kidneys which show no other disease 
 
 Fig. 285.— Large retention-cyst of kidney (from a specimen in the Museum of the Phila- 
 delphia Hospital). 
 
 are probably due to undiscovered obstructions of the uriniferous 
 tubules. 
 
 Congenital cystic kidneys are of striking appearance. Usually 
 both kidneys are affected, and are transformed into masses com- 
 posed of innumerable cysts varying in size from microscopic points 
 to cavities as large as a walnut (Fig. 286). On section the cysts 
 are found to be filled with clear urinous liquid, or with colloid 
 material, and between them is a stroma of more or less firm 
 
594 TEXT-BOOK OF PATHOLOGY. 
 
 fibrous tissue. The pelvis of the kidney is usually preserved. 
 These cysts are formed by dilatation of the uriniferous tubules 
 and Malpighian bodies, probably as the result of some fetal disease 
 
 
 
 
 
 " a flr 
 
 
 
 v .M 
 
 iVi:fev 
 
 
 
 
 «1 "A ** 
 
 
 
 
 ftBji ..:'' »V£ 
 
 
 
 
 ;I'lP V- 
 
 
 
 m 
 
 
 
 
 
 
 *^i 
 
 m 
 
 m ] t: -'$teM 
 
 Fig. 286.— Congenital cystic kidney (Specimen 2816, Museum N. Y. Hosp.).' 
 
 which causes obstruction of the tubules at their outlet at the apex 
 of the pyramids, or in consequence of faulty union between the upper 
 and the lower segments of the uriniferous tubules in the develop- 
 ment of the organ. Similar cystic degeneration, with enlargement 
 of one or both kidneys, may occur in later life. Finally, cystic 
 adenoma may again be alluded to. 
 
 PARASITES. 
 
 Bacteria occur in the kidney in various affections : thus 
 pneumococci, typhoid bacilli, the bacilli of glanders and anthrax, 
 
DISEASES OF THE URINARY ORGANS. 595 
 
 have been repeatedly demonstrated. In pyelonephritis the Bacil- 
 lus coli communis is probably the usual active etiologic agent. 
 Streptococci occur in the nephritis of septic conditions and 
 in primary infectious nephritis of cryptogenic origin. Bacte- 
 ria are occasionally found in the uriniferous tubules without 
 gross lesions of the kidney, and are probably excreted with the 
 urine. 
 
 Streptococci occur in the urine in the nephritis of septic con- 
 ditions, and in primary infectious nephritis of cryptogenic origin. 
 Various other bacteria may be met with in the urine (see Bac- 
 teriuria). 
 
 Animal parasites are occasionally observed, such as echino- 
 coccus-cysts, filarise, the eggs of Distoma hematobium, amebse, 
 and infusoria. Round worms aud the oxyuris sometimes migrate 
 into the bladder or enter through fistulse. 
 
 The echinococcus-cyst occurs in the form of hydatids, which 
 may perforate into the pelvis of the kidney and discharge with 
 the urine, or become inspissated and calcify. The Cysticercus 
 cellulosse and Pentastomum denticulatum are extremely rare. 
 The Filaria sanguinis hominis occurs in the lymphatic spaces and 
 in the blood-vessels of the kidney in cases of filariasis with chyl- 
 uria. The kidneys in these cases show a waxy appearance on 
 section, especially toward the apices of the pyramids, and the 
 surface of the kidney may be abnormally lobulated. Microscopi- 
 cally the lymphatic spaces about the uriniferous tubules are greatly 
 distended. 
 
 The Distoma hematobium occasionally produces pyelitis and 
 pyelonephritis, with enlargement of the pelvis of the kidney. 
 
 THE PELVIS OF THE KIDNEY AND URETER. 
 CONGENITAL AND ACQUIRED MALFORMATIONS. 
 
 Occasionally the pelvis or ureters, or both, may be absent or 
 imperfectly developed. Complete obliteration of the ureter may 
 be observed. More frequently there are two pelves or ureters, 
 and when this is the case the malformation is, as a rule, bilateral. 
 
 Obstructions of the ureter may be due to twists, to con- 
 genital atresia, or to other diseases of the ureter, particularly at 
 its entrance into the bladder. It may be brought about by the 
 lodgement of renal calculi, by tumors of the ureter, or by pressure 
 upon it from without. The outflow of the urine may be obstructed 
 by diseases of the bladder, and particularly by stricture of the 
 ureter. 
 
 Dilatation of the ureter results from the conditions just 
 named, and may reach considerable dimensions (Fig. 287). When 
 
596 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 the obstruction is continued the dilatation may affect the pelvis 
 of the kidney as well, and eventually the latter may be enor- 
 mously enlarged. The pyramids become 
 flattened, and the renal substance may 
 undergo progressive atrophy, so that the 
 kidney is converted into a sac-like for- 
 mation filled with clear liquid, partly 
 urine secreted in the earlier stages and 
 partly transudate formed after the com- 
 pression has stopped the renal function. 
 To this condition the term hydronephro- 
 sis is applied. 
 
 CALCULUS. 
 
 Calculi are of frequent occurrence 
 in the pelvis of the kidney, and are 
 formed by the precipitation of various 
 normal or abnormal constituents of the 
 urine. There may be merely small 
 gritty particles lying in the calices or in 
 the pelvis, to which the term renal sand, 
 or gravel, is given ; or there may be 
 large stones, almost filling the pelvis 
 and calices, and forming more or less 
 accurate moulds of these. The most fre- 
 quent forms are those composed of uric 
 acid and oxalate of lime, but phosphate 
 and carbonate of calcium and triple phosphate calculi are occa- 
 sionally found. Stones composed of cystin and xanthin are rare. 
 Uric-acid calculi are composed of the acid itself, or of urates, and 
 present themselves as yellowish, brownish, or red, smooth or some- 
 what irregular formations. Those composed of oxalate of lime 
 are irregular in shape and of brownish or red color. 
 
 The results of renal calculi may be trivial or serious. Small 
 particles of renal sand are frequently passed without serious dis- 
 turbance. Large calculi tend to set up inflammation of the pelvis 
 of the kidney, and may obstruct the outflow of the urine, causing 
 hydronephrosis (Fig. 288). In some cases cancer seems dependent 
 upon the continued irritation of a retained calculus. 
 
 Fig. 287.— Dilatation of the 
 ureter due to calculous obstruc- 
 tion. 
 
 INFLAMMATION. 
 
 Inflammation of the pelvis, or pyelitis, may result from 
 the irritation of poisons ingested, such as cantharides, turpentine, 
 and the like, or it may occur in the course of infectious diseases of 
 various kinds. More frequently it results from the irritation of a 
 calculus, or from ascending inflammation consequent upon cystitis 
 
DISEASES OF THE URINARY ORGANS. 
 
 597 
 
 and ureteritis. The mucous membrane becomes reddened and 
 swollen, and not rarely is marked with hemorrhagic ecchymoses. 
 The surface is covered with more or less desquamated epithelium 
 and pus-cells. The inflammation may extend to the substance of 
 the kidney (pyelonephritis). Considerable purulent exudate may 
 take place, particularly when there is a calculus partially obstruct- 
 ing the ureter. When there is complete obstruction the pelvis may 
 become dilated with pus, and the calices or the entire kidney may 
 be converted into a large pus-sac (pyonephrosis). Deposits of tri- 
 ple phosphate may occur in pyelitis, and may occasion incrusta- 
 tions upon the mucous surface. 
 
 Inflammation of the ureter, or ureteritis, may occur 
 under the same conditions as pyelitis. The mucous membrane 
 of the ureter becomes swollen and reddened, as in catarrhal in- 
 flammations elsewhere, and 
 there may be erosions or 
 superficial ulcerations. The 
 other coats are thickened 
 by inflammatory infiltration 
 and, in chronic cases, by 
 fibrous-tissue overgrowth. J ' 
 
 Fig. 288.— Calculus in the pelvis 
 of the kidney and upper part of 
 the ureter. 
 
 Fig. 289.— Tuberculous pyelonephritis (modified 
 from Bollinger). 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis of the pelvis of the kidney may occur as a 
 miliary tuberculosis, or in the form of caseous nodules or masses. 
 The latter may be primary and hematogenous in origin, or may 
 
598 TEXT-BOOK OF PATHOLOGY. 
 
 result from ascending infection (Fig. 289). In such instances 
 the mucosa becomes more or less extensively infiltrated, and later 
 caseous and ulcerated. The process extends to the calices, and 
 subsequently to the pyramids and other parts of the substance of 
 the kidneys. The pelvis may contain considerable quantities of 
 caseous or puriform matter, and the kidney-substance may be 
 extensively involved. The urine contains pus-corpuscles and 
 often tubercle bacilli in great numbers. Tuberculosis of the 
 ureters leads to nodular or diffuse thickening, and commonly to 
 more or less obstruction (Fig. 290). 
 
 Fig. 290.— Tuberculous nodule in the wall of the ureter, with beginning hydronephrosis 
 (from a specimen in the Museum of the Philadelphia Hospital). 
 
 TUMORS. 
 
 Primary cancer is extremely rare. Secondary cancer may affect 
 the pelvis in association with the kidney, or the ureters in asso- 
 ciation with the bladder. Small cystic formations are not uncom- 
 monly seen in the mucous membranes of the ureters, and may be 
 due to inflammatory obstruction of the crypts, to proliferation 
 and softening of the lymphoid follicles, or to parasitic invasion 
 {psorospermice). 
 
 PARASITES. 
 
 Round worms have occasionally been found in the ureters. 
 The eggs of Distomum haematobium are frequently deposited in 
 the mucous membrane, and occasion inflammation and papillom- 
 atous excrescences. 
 
DISEASES OF THE URINARY ORGANS. 599 
 
 THE URINARY BLADDER. 
 MALFORMATIONS. 
 
 Congenital malformations of the bladder are compara- 
 tively common. Among the more important is exstrophy. The 
 anterior wall of the abdomen and of the bladder being wanting, 
 the mucous membrane, with the openings of the ureters, is ex- 
 posed to view. Not uncommonly this condition is associated 
 with epispadias, or division of the clitoris. Sometimes the small 
 intestine discharges through the exstrophic bladder, the large in- 
 testine being contracted or completely absent. 
 
 Occasionally the urachus remains patulous in consequence of 
 atresia of the neck of the bladder or urethra, and the urine is dis- 
 charged from the umbilical end. In other cases the urachus is 
 closed at either end and the intervening portion is dilated, with 
 the formation of a cyst. Again, there may be only partial oblit- 
 eration of the urachus, the remaining portion in connection with 
 the bladder being patulous and greatly dilated, forming a congenital 
 adventitious sac. In one case under my observation this consti- 
 tuted a cavity of considerable size, and when filled distended the 
 abdomen as far as the umbilicus. Congenital diverticula may 
 occur in the anterior wall, and less commonly at the sides of the 
 bladder. Complete absence of the bladder, division into lateral 
 portions by a septum {vesica bipartitis), and other congenital 
 defects are rare. 
 
 Acquired Malformations. — Dilatation of the bladder may 
 result from congenital or acquired stenosis of its neck, or of the 
 urethra ; or from paralysis of its walls, in consequence of disease 
 of the spinal cord or nerves. The organ may be greatly increased 
 in size, often reaching the umbilicus. When the dilatation is 
 acute the walls are greatly thinned, but when it has been gradu- 
 ally developed compensatory hypertrophy of the muscularis and 
 of the submucous fibrous tissues leads to thickening of the walls. 
 In these cases the mucous surface presents a ribbed appearance, 
 fibrous-tissue bands standing out prominently and the mucosa 
 being pouched between the bands. Diverticula of considerable 
 size may form in this way, and the walls of the bladder sometimes 
 present a considerable number of pouches. 
 
 CHANGES OF POSITION. 
 
 The position of the bladder, or of portions of it, is sometimes 
 abnormal. Thus it may enter into a hernia, or a part of the wall 
 of the bladder may prolapse with the wall of the vagina, forming 
 vaginal cystocele. The latter is due to the traction of the pro- 
 lapsing uterus, or to repeated overdistention of the bladder, with 
 
600 TEXT-BOOK OF PATHOLOGY. 
 
 weakness of the anterior vaginal wall. Complete inversion of 
 the bladder through the urethra is occasionally observed in 
 
 RUPTURE. 
 
 Rupture of the bladder may be due to traumatism, and particu- 
 larly to perforation by fractured pelvic bones. Rupture from 
 overdistention is rare. Occasionally it may result from abdominal 
 compression when the bladder is distended with urine, and ulcera- 
 tive processes beginning in the mucous membrane may perforate 
 the wall, or phlegmonous inflammations or degenerating new- 
 growths surrounding the bladder may lead to perforation. In 
 women perforations are frequently established between the blad- 
 der and vagina in consequence of pressure of the fetal head or of 
 forceps, and vesicovaginal fistula results. Perforation into the 
 peritoneal cavity is usually followed by fatal acute peritonitis. 
 Rupture into the tissues below the peritoneal reflections gives 
 rise to widespread infiltration of urine and phlegmonous or gan- 
 grenous inflammation. 
 
 CIRCULATORY DISTURBANCES. 
 
 Active hyperemia may result from irritant poisons, such as 
 cantharides, or may occur in persons suffering from paraplegia, in 
 consequence of disturbances of innervation. 
 
 Passive hyperemia occurs when there is pressure upon the 
 inferior vena cava or thrombosis of that vein. The mucous mem- 
 brane becomes dark-red and is often marked with punctate hem- 
 orrhages. Considerable varicosity of the veins at the neck of the 
 organ may occur, and may give rise to copious hemorrhages, or to 
 obstruction and retention of the urine. 
 
 Hemorrhages in the mucous membrane occur in severe con- 
 gestion or inflammation, and in various hemorrhagic diseases. 
 Large hemorrhages into the cavity itself may result from trauma- 
 tism from without, or from calculi. The varicosities before men- 
 tioned may occasion considerable hemorrhage, as may also papil- 
 lomatous or other new-growths. Large quantities of blood with 
 little admixture of urine may lead to the formation of dense clots 
 within the organ, but when the quantity is small the blood is 
 mingled with the urine. 
 
 INFLAMMATION. 
 
 Inflammation of the bladder, or cystitis, varies in ex- 
 tent, duration, and character. Acute cystitis may result from irri- 
 tant poisons excreted with the urine, and frequently attends acute 
 infectious diseases. In these cases, however, the disease is gener- 
 
DISEASES OF THE URINARY ORGANS. 601 
 
 ally mild. More intense forms occur from extension of inflamma- 
 tion to the bladder in cases of urethritis, or when septic material 
 is introduced in catheterization. Retention and decomposition of 
 the urine from strictures or prostatic hypertrophy are frequent 
 causes of chronic cystitis. 
 
 Cystitis may present itself as a mucopurulent catarrh, acute or 
 chronic in course ; as phlegmonous inflammation ; or as a pseudo- 
 membranous process. 
 
 Mucopurulent cystitis in the acute stages causes swelling of the 
 mucous membrane, with injection of blood-vessels and sometimes 
 punctate hemorrhages. The surface, especially at the base, is 
 covered with mucopurulent exudate of a tenacious character, in 
 which pus-cells and desquamated epithelium are abundant. The 
 urine tends to undergo ammoniacal fermentation. 
 
 In chronic cases thickening of the submucosa and hypertro- 
 phy of the muscularis cause great thickening of the organ, and 
 the surface within is usually ribbed from the prominence of the 
 fibrous-tissue bands and the pouching of the mucous membrane 
 between the bands (Fig. 291). Erosions and ulceration may oc- 
 
 Fig. 291.-Dilated ribbed bladder. 
 
 cur upon the surface, and occasionally perforation of the walls 
 takes place. Incrustations of triple phosphate and of other 
 common salts frequently cover the surface. 
 
 Phlegmonous cystitis results from intense infections, or from the 
 retention of urine in paraplegia. The submucous tissue is consid- 
 erably swollen and infiltrated, and complete perforation of the 
 walls and paracystitis or phlegmonous inflammation of the tissues 
 surrounding the bladder may ensue. 
 
602 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 Pseudomembranous cystitis occurs in certain severe infectious 
 diseases, and may present itself in the form of a typical pseudo- 
 membrane, or as a combination of phlegmonous and pseudomem- 
 branous inflammation. Occasionally pseudomembranes are formed 
 without any inflammatory process, in nervous individuals, and in 
 the course of or after pneumonia I have seen a cast of the entire 
 bladder of this nature. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis of the bladder is usually secondary to tubercu- 
 losis of the kidney, or to that of the prostate, seminal vesicles, or 
 epididymis. Tubercular ulcers independent of tuberculosis else- 
 where in the urogenital tract may occur in phthisis or intestinal 
 
 Fig. 292.— Tuberculosis of the bladder (Orth). 
 
 tuberculosis, but such cases are rare. The lesions observed in 
 tuberculosis of the bladder are ulcerations, for the most part occu- 
 pying the base and surrounding the orifices of the ureters, and 
 there may be distinct or clustered tubercles. Numerous small 
 ulcers, or a single large ulcerated surface may be observed (Fig. 
 292). Deposits of triple phosphate frequently form incrustations 
 on the surface. 
 
 Syphilitic ulcers have been observed in the bladder, but are 
 extremely rare. 
 
DISEASES OF THE URINARY ORGANS. 603 
 
 CALCULI AND FOREIGN BODIES. 
 
 The bladder is the commonest seat of urinary calculi. They 
 may occur in the form of fine particles or gravel, or as stones of 
 considerable size. Usually there is but one ; sometimes a consid- 
 erable number may be present. The shape and general appear- 
 ance depend upon the composition of the stone. 
 
 The formation of calculi is due to precipitation from the urine 
 of its various earthy or other constituents as the result of stagna- 
 tion and fermentative change. Foreign bodies often form the 
 nuclei of stones, and thus a calculus in the bladder may form 
 around broken portions of catheters, hairpins, or other foreign 
 bodies inserted into the urethra. Similarly, parasites may be the 
 nucleus, and in ordinary cases of stone the mucous or degenerated 
 epithelial cells constitute the focus about which the deposit occurs. 
 There is practically never a simple sediment of saline or earthy 
 material, but a combination of the latter with some albuminous 
 matrix. Catarrhal conditions of the bladder, especially when 
 combined with stagnation of the urine as the result of hypertrophy 
 of the prostate, urethral stricture, and the like, are the most com- 
 mon antecedent causes. 
 
 Calculi in the bladder may be composed of uric acid or urates, 
 of oxalate of lime, of various phosphates, of carbonate of lime, or 
 of certain organic compounds. 
 
 Uric acid and urate calculi are less common in the bladder 
 than in the kidney. They result from surcharge of the urine 
 with uric acid in lithemic or gouty individuals, and from acid 
 decomposition rendering the uric acid and urates insoluble. They 
 are yellowish or red in color, rounded, slightly granular or smooth 
 upon the surface, and, as a rule, quite hard. The calculi com- 
 posed of urates are usually more irregular and softer, and are 
 generally lighter in color. Frequently phosphates are combined 
 with them. 
 
 Phosphatic calculi may be of several kinds ; they may be com- 
 posed of phosphate of lime, triple phosphate, or mixed phosphates. 
 They form the most frequent variety of calculi and concretions in 
 the bladder, and are generally due to alkaline decomposition 
 causing a deposit of the simple phosphate of lime or of the 
 combination of phosphate of magnesium with ammonium phos- 
 phate, known as triple phosphate. These deposits may occur in 
 the form of incrustations upon the surface of the bladder in 
 various diseases, or in the form of irregular, soft, and more or 
 less white calculi. 
 
 Oxalate of lime occasions rounded, hard calculi, of brownish 
 color and of irregular, granular surface, from which they derive 
 the name mulberry calculi. They occur in conditions similar to 
 those causing uric-acid stones. 
 
604 TEXT-BOOK OF PATHOLOGY. 
 
 Calculi composed of carbonate of calcium, sulphate of calcium, 
 cystin, xanthin, and indigo are extremely rare. 
 
 Results of Urinary Calculi. — While cystitis and retention 
 of urine frequently cause stone, the latter is prone to occasion in- 
 creased irritation and inflammation, and may cause serious obstruc- 
 tion to the outflow of urine, and thus retention in the bladder. 
 Ulceration may take place, and perforation of the bladder-walls 
 may ensue. Hypertrophy of the walls occurs when the stone only 
 partially obstructs the outflow, and under the same conditions the 
 ureters may become distended and hydronephrosis may occur. 
 
 
 ■ 
 
 Fig. 293.— Tuft of papilloma of the bladder (thionin ; X 90) (Martin and Taylor). 
 
 Not rarely the stone lies in a pouched dilatation of the wall of 
 the bladder, either from having been formed in that situation in 
 consequence of stagnation of the urine, or from having caused a 
 dilatation by weakening the walls at a certain point. Complete 
 encapsulation of the stone has been observed in such cases. 
 
 TUMORS. 
 
 Polypoid outgrowths from the mucosa may be observed in 
 chronic cystitis. 
 
 Papiilomata occur either as the result of chronic irritation, 
 
DISEASES OF THE URINARY ORGANS. 
 
 605 
 
 or as apparently causeless tumors. The papilloma presents itself 
 as a somewhat cauliflower-like elevation affecting the base, and 
 sometimes considerable portions of the mucosa, and has a whitish 
 or grayish color. It is usually vascular, and therefore frequently 
 occasions hemorrhages. 
 
 Microscopically it is composed of a delicate connective-tissue 
 stroma containing large, thin- walled blood-vessels, and covered 
 with cylindrical epithelium (Fig. 293). Occasionally papillomata 
 become transformed into malignant epitheliomatous growths. 
 
 Carcinoma is a rare form of primary tumor. It occurs as a 
 somewhat papillomatous thickening of the mucosa, or as a more 
 considerable infiltration of the wall of the bladder (Fig. 294). 
 
 Fig. 294.— A, epitheliomatous tumor ; B, wart-like growths ; C, villous growths (Clado). 
 
 Microscopically it is composed of large polymorphous epithelial 
 cells infiltrating the walls more or less deeply and irregularly, or 
 arranged in acini or alveolar formations. 
 
 Secondary carcinoma of the bladder may result from ex- 
 tension of prostatic or uterine cancer. Very rarely the bladder is 
 involved by metastasis. 
 
 Fibroma, fibro-adenoma, myoma, and myxoma are occa- 
 
606 TEXT-BOOK OF PATHOLOGY. 
 
 sionally observed, and cysts may be formed by closure of pouched 
 diverticuli or by distention of the patulous urachus. Cysts of 
 obscure origin are sometimes met with ; dermoid cysts are rare. 
 Sarcoma is very rare. 
 
 ABNORMAL CONDITIONS OF THE URINE. 
 
 Quantity. — The normal quantity in the adult is from 1500 to 
 2000 cc. Conditions which check the perspiration or action of 
 the bowels increase the amount of urine ; excessive sweating and 
 diarrhea have the reverse effect. In the latter case the excretion 
 may be almost suppressed (anuria). The same may occur in acute 
 nephritis, or chronic nephritis with uremia, in extreme anemia, 
 and in acute or chronic obstructive conditions in the gastrointes- 
 tinal tract interfering with absorption of water. Occasionally 
 anuria is reflex, resulting from obstruction of the urinary passages 
 by calculi. The quantity of urine is increased (polyuria) in cases 
 of excessive consumption of water, and habitually in diabetes 
 mellitus and insipidus and in chronic interstitial nephritis. 
 
 Specific Gravity. — Normally the specific gravity is 1015 to 
 1020. It becomes increased when the amount of urine is de- 
 creased, and vice versa. The specific gravity is especially high in 
 diabetes mellitus, despite the polyuria, sometimes reaching 1040 
 or 1050. It is low in most forms of chronic nephritis, in diabetes 
 insipidus or simple polyuria, and in anemia and hysteria, or other 
 nervous diseases. 
 
 Color. — The normal amber color is due to the presence of 
 various pigments, especially urobilin and uroerythrin. These are 
 derivatives of hemoglobin or bilirubin. 
 
 In pathologic conditions other pigments, such as hematopor- 
 phyrin, pathologic urobilin, melanin, etc., are met with. Indican 
 is present in the urine in the form of a chromogen, which may 
 sometimes become oxidized, with the formation of dark-colored 
 pigment-animal indigo. Certain drugs eliminated with the urine 
 cause discolorations. Bilirubin occurs in jaundice and other con- 
 ditions, and blood or hemoglobin may cause discoloration. 
 
 Reaction. — The normal reaction is acid, but frequently after 
 meals it becomes neutral or even alkaline. The ingestion of cer- 
 tain foods rich in alkalies or acids, which become converted into 
 alkaline carbonates (citrates, acetates, etc.), may occasion an alka- 
 line reaction, while other acids lead to the opposite result. De- 
 composition of the urine usually causes an intense alkaline reaction, 
 by conversion of the urea into ammonia. Occasionally the reac- 
 tion of the urine is amphoteric, both red and blue litmus-paper 
 being acted upon. 
 
 Glycosuria is a term applied to the presence of glucose or 
 grape-sugar in the urine. This may be a transient condition in 
 
DISEASES OF THE URINARY ORGANS. 607 
 
 various diseases, such as chorea, cerebrospinal fever, whooping- 
 cough, and epilepsy, and is not uncommon in gouty persons 
 indulging in a free diet. Sometimes it results from the effects 
 of poisons, such as morphin, chloroform, or carbonic oxid ; but 
 in some of these cases the reactions of glucose are simulated 
 by other and quite different reducing-substances present in the 
 urine. Permanent and decided glycosuria is characteristic of dia- 
 betes mellitus only. 
 
 I,evillosiiria, the presence of fruit-sugar, lactosuria, that 
 of milk-sugar, and dextrinuria, that of dextrin in the urine, 
 have been discovered. 
 
 Cholttria is the name indicating the presence of biliary pig- 
 ments and acids in the urine. It is most frequently observed 
 in cases of jaundice due to hepatic disease, but may also occur in 
 so-called hematogenous jaundice, the formation of the pigment in 
 some of the latter cases probably taking place in the kidneys them- 
 selves. The urine presents a dark color, varying from brownish 
 to greenish. Oxidizing substances, such as fuming nitric acid, 
 produce a play of colors. 
 
 Microscopically the cellular constituents of the urine are found 
 stained, and granular concretions of bilirubin or rhombic crystals 
 may be observed. Hyaline casts, more or less deeply stained by 
 the pigment, are frequently seen. 
 
 Urobilinuria. — Urobilin occurs in the normal urine mainly as 
 a chromogen, or is converted into urobilin on the addition of acid. 
 Sometimes, urobilin is present in large quantities in the fresh urine. 
 This has been particularly observed in fevers, in jaundice, and in 
 certain anemic diseases, especially in pernicious anemia. 
 
 Indicanuria. — Indigo-blue occurs in the urine as a chromo- 
 gen which gives rise to the formation of indigo on decomposition. 
 This indican, or indoxyl sulphate, is a product of indol derived 
 from the intestine, and an excess of indican in the urine is sig- 
 nificant of intestinal decomposition. 
 
 Other forms of the ether-sulphuric acid series occur in the 
 urine, but are less significant. 
 
 Acetonuria occurs to a slight extent in health, but more par- 
 ticularly in conditions of inanition, in gastro-intestinal disturbances, 
 and in fever. It is especially significant in diabetes mellitus, and 
 may become very pronounced toward the latter end of this affec- 
 tion. 
 
 Diacettiria, or the condition in which diacetic acid appears in 
 the urine, is also met with in fevers and inanition, but particularly 
 in diabetes. 
 
 Iyipaciduria refers to the presence of fatty acids in the urine, 
 but has no special significance. 
 
 Hydrothionuria refers to the presence of sulphuretted hydro- 
 gen in the urine. This is noted occasionally in autointoxications, 
 
608 TEXT-BOOK OF PATHOLOGY. 
 
 or as the result of fermentative changes in the urine. The urine 
 may have a foamy appearance, to which the term pneumaturia is 
 sometimes applied. Other gases may be present, but only in 
 small proportion and rarely. 
 
 Melanuria is a term applied to the dark discoloration of the 
 urine occasionally seen in persons suffering from pigmented tumors. 
 It also occurs in phthisis and other wasting diseases. As a rule, the 
 urine becomes darker after addition of oxidizing substances, but it 
 may be quite dark when passed. It contains iron and sulphur. 
 
 Albuminuria. — Minute traces of serum-albumin probably 
 occur in the normal urine. The term albuminuria, however, is 
 applied to cases in which albumin is readily detected. It may be 
 accidental — that is, dependent upon the admixture of albuminous 
 substances from the mucous membrane lining the urinary passages, 
 — or essentially renal in character. In the former instances the 
 presence of abundant blood or pus-cells indicates the nature of the 
 case. True renal albuminuria consists of the excretion with the 
 urine of serum-albumin and serum-globulin, the former being con- 
 siderably more abundant than the latter. Pure serumuria is ex- 
 tremely rare, and pure globulinuria perhaps even more so. 
 
 Albuminuria is more frequently the product of actual renal dis- 
 ease or nephritis, and is then due to the disease of the epithelium 
 of the glomeruli and tubides. A certain amount of albumin occurs 
 in degenerative or congested conditions of the kidneys ; in various 
 general diseases affecting the blood and without manifest disease 
 of the kidney, such as anemias, diabetes, and the like ; in certain 
 nervous affections probably influencing the circulation ; and in dis- 
 orders of the digestive tract. 
 
 At times albuminuria is periodic or cyclic, this periodicity 
 depending upon general conditions, such as diet, exposure, and exer- 
 cise, which in turn affect the blood or renal circulation. Consid- 
 erable amounts of albumin in the urine are never physiologic. 
 
 Large proportions of globulin occur in amyloid disease of the 
 kidneys. 
 
 Albumosuria. — Various albuminous substances derived from 
 serum-albumin or serum-globulin, and not coagulable by heat, 
 occur in the urine. These are hydration-products designated 
 albumoses or propepton. True pepton has never been found in 
 the urine. Albumosuria occurs in cases in w T hich pus-cells or 
 large exudates are undergoing absorption, as in septic processes, 
 pneumonia, and the like (pyogenic albumosuria). In another 
 group of cases intestinal malassimilation or decomposition comes 
 into play (enterogenic albumosuria). In the third group diseases 
 of the blood, such as leukemia and various intoxications, are 
 active (hematogenic albumosuria). A fourth, or puerperal, form 
 occurs after labor. It has also been observed repeatedly in malig- 
 nant tumors of the skeleton. 
 
DISEASES OF THE URINARY ORGANS. 609 
 
 Nucleo-albuminuria. — Nucleo-albumin, formerly supposed 
 to be mucin, is derived from the protoplasm of the surface-epithe- 
 lium of the urinary tract, and occurs in the urine in small quantity 
 in nearly all persons, and in large quantity when there is irritation 
 of the lining mucosa, particularly in pyelitis and cystitis. 
 
 Fibrinuria occurs in conditions in which lymph or blood gains 
 access to the urinary passages. Fibrinous casts or shreds may be 
 passed, or small flocculent particles are observed. Fibrinuria is 
 usually associated with hematuria or chyluria. 
 
 Hematuria is a term applied to the presence of blood in the 
 urine. This may be accidental from admixture of menstrual 
 blood and the like, or may be a pathologic condition, in which the 
 blood originates from the kidneys, ureters, bladder, urethra, or 
 other parts of the urinary system. Renal hematuria may result 
 from intense congestion or from hemorrhagic nephritis. Trauma- 
 tism, either from without or from calculi in the pelvis, is a fre- 
 quent cause. Tumors and specific inflammatory processes are occa- 
 sional causes. Sometimes hematuria is due to intense anemia, 
 hemorrhagic diseases, or severe intoxications. Hematuria which 
 is due to admixture of blood with the urine below the kidney 
 results from traumatism, injury by calculi or catheterization, from 
 vascular tumors, and occasionally from inflammatory or other dis- 
 ease-processes. 
 
 Renal hematuria is distinguished from that originating in the 
 bladder by the intimate admixture of urine and blood, and by the 
 associated evidences of renal disease — renal epithelium, tube-casts, 
 etc. Fragmentation of the red corpuscles is said to indicate renal 
 hematuria. In hematuria originating in the bladder larger clots 
 may pass, in association with bladder-epithelium and mucin (nu- 
 cleo-albumin). In cases of sudden renal hemorrhage large clots, 
 sometimes forming casts of the pelvis, may be formed and dis- 
 charged. 
 
 Hemoglobinuria indicates the presence of free hemoglobin 
 or of methemoglobin in the urine, without the presence of blood- 
 corpuscles. Hemoglobinuria results from causes which lead to 
 disorganization of blood and elimination of the coloring-matter 
 through the kidneys. It is met with in various infectious dis- 
 eases, such as malaria, and in intoxications, as in poisoning with 
 potassium chlorate, carbolic acid, arsenic, and other drugs, or with 
 toadstools. It occasionally results from snakebite or poisoning by 
 other venomous animals. 
 
 Paroxysmal hemoglobinuria is a form of intermittent disease 
 especially frequent in subtropical countries. The attacks some- 
 times seem to be determined by exposure to cold and other ex- 
 ternal influences, whilst the predisposition may be dependent 
 upon syphilis or other general disorders. The urine presents a 
 dark-red or brownish color, and when tested with the spectro- 
 
610 TEXT-BOOK OF PATHOLOGY. 
 
 scope shows the bands indicative of hemoglobin or methemo- 
 g-lobin. 
 
 Microscopically the hemoglobin may present itself in the form 
 of granules or cast-like formations, or sometimes as crystals. 
 Blood-corpuscles are absent, or at most present in extremely 
 small numbers. 
 
 I/ipuria. — A small amount of fat may appear in the urine in 
 cast's of advanced diifuse nephritis with fatty degeneration, and in 
 certain cases of pyelitis. In other cases lipuria results from dis- 
 orders in which there is excess of fat in the blood (lipemia). This 
 occurs in cases of excessive consumption of oil or fatty food and 
 in cases of intoxication, notably by arsenic. It is sometimes pres- 
 ent in diabetes, phthisis, chronic alcoholism, and obesity, and fract- 
 ures injuring the marrow, or serious traumatism of the subcuta- 
 neous fatty tissues may cause fat-embolism and lipuria. 
 
 The appearance of the urine varies with the amount of fat, 
 but, as a rule, there is a solid scum upon the surface, and there 
 may be large oil-drops. Occasionally the urine is quite milky 
 when recently passed. Microscopically, oil-drops are more or less 
 abundant ; and fat-crystals may be discovered. 
 
 Chyluria is the name applied to a milky condition of the 
 urine which probably results from admixture of lymph or chyle. 
 The urine is light colored, and more or less milky in appearance. 
 Often there is a reddish discoloration from associated hematuria 
 (henuitoehylurict). The urine contains albumin and sometimes 
 albumoses. 
 
 Microscopically, numerous oil-drops of varying size and, usu- 
 ally, blood-corpuscles are detected. The most frequent cause is 
 the obstruction of the lymphatic channels and their subsequent 
 rupture in the kidney or bladder in consequence of the lodgement 
 of the Filaria sanguinis hominis. In these cases the embryos of the 
 filarial are usually detected in the urine. Sometimes a chyluria is 
 non-parasitic, but the causes are obscure. 
 
 Bacteriuria. — Normally the urine contains no bacteria. In 
 cases of cystitis or other inflammatory diseases, however, and par- 
 ticularly when catheterization has been practised, bacteria of de- 
 composition may be present, such as the Micrococcus urece, Bac- 
 terivm termo, the Bacillus proteus, yeast-fungi, and other forms. 
 Not rarely the Bacillus coli communis is met with, particularly in 
 ascending infections of the urinary tract. In cases of certain in- 
 fectious diseases, such as typhoid fever, pneumonia, and erysipelas, 
 the specific micro-organisms may be found in the urine, having 
 escaped from the blood through the capillaries of the glomeruli. 
 Streptococci are also met with in primary and secondary infectious 
 nephritis. The Bacillus tuberculosis may be discovered in cases 
 of tuberculosis of the kidney, ureters, bladder, or other parts of 
 the urinary tract (Fig. 295). It is frequently present in clusters, 
 

 DISEASES OF THE URINARY ORGANS. 611 
 
 this constituting a marked point of distinction from the smegma- 
 bacillus, which is often found in urine, especially that of women, 
 and is easily mistaken for the tubercle-bacillus. Another point 
 
 Fig. 295.— Tubercle bacilli in the urine ; from a case of tuberculous cystitis (Jakob). 
 
 of distinction is the greater ease with which the smegma-bacillus, 
 stained with carbol-fuchsin, may be decolorized by alcohol. Posi- 
 tive differentiation in doubtful cases is made by injection of the 
 urine into guinea-pigs. 
 
 CHEMICAL CHANGES AND SEDIMENTS. 
 
 The various inorganic and organic constituents of the urine 
 may be present in excessive quantities, and may form deposits, or 
 abnormal chemical substances may be detected. 
 
 Uric acid is deposited in the form of yellowish, brownish, or 
 reddish crystals of whetstone shape, or as irregular angular forma- 
 tions superimposed or clustering together (Fig. 296). The color 
 is due to uroerythrin, taken up from the urine. Excess of uric 
 acid occurs in lithemic and gouty conditions, and the crystals may 
 deposit from a highly acid urine, even though there be no excess. 
 
 Oxalate of lime occurs in the form of highly refracting octa- 
 hedral corpuscles, their appearance being likened to that of an 
 envelope (Fig. 297). Certain foods rich in oxalates may cause 
 excessive excretion, and oxaluria occurs as an independent con- 
 dition of obscure nature allied to gout and lithemia. Oxalates 
 deposit from highly acid urine, even though no excess be present. 
 This must be distinguished from oxaluria proper. 
 
 Phosphates. — Various forms of phosphates are found in 
 crystalline form in urinary sediments. Basic phosphate of mag- 
 nesium and neutral phosphate of lime are found in urine becoming 
 alkaline, while the phosphate of ammonium and magnesium, or 
 
612 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 triple phosphate, is met with when alkaline decomposition takes 
 place. It presents itself in different forms, the most characteristic 
 being the large coffin-lid crystals and certain star-shaped forma- 
 tions (Fig. 298). Triple phosphate is especially abundant in 
 cystitis with alkaline decomposition of the urine in the bladder. 
 
 3 w**^' 
 
 - J> -t 
 
 =*o 
 
 ^ 
 
 
 Fig. 296.— Various forms of uric-acid 
 crystals. 
 
 Fig. 297.— Various forms of crystals of 
 oxalate of calcium. 
 
 Urates. — Urates are deposited from acid urines as a whitish 
 or reddish sediment of amorphous character. The reddish color 
 sometimes observed is due to admixture of urinary pigment. In 
 decomposing urine, of somewhat alkaline reaction, urate of ammo- 
 nium is deposited as hedgehog crystals or masses (Fig. 299). 
 
 Fig. 298.— Crystals of triple phosphate 
 (ammonium-magnesium phosphate). 
 
 Fig. 299.— Urate of ammonium crystals. 
 
 Hipptiric acid is rarely met with, excepting after the inges- 
 tion of benzoic acid or of certain fruits. It forms long, prismatic 
 crystals, which occur in groups. 
 
DISEASES OF THE URINARY ORGANS. 
 
 613 
 
 Carbonates and sulphates are rarely observed in urinary 
 sediments. 
 
 Fat-crystals occur in the form of fine needles, or of aggre- 
 gations arranged in a star-like manner and resembling tyrosin 
 groups (Fig. 300). They are found in cases of chronic nephritis, 
 pyelitis, and cystitis. 
 
 Tyrosin. — This substance usually occurs in the urine in solu- 
 tion, or rarely in the form of sheaves composed of fine needles 
 arranged in star-like clusters (Fig. 300). 
 
 I/eucin occurs as small spheres, often having a somewhat 
 radiated structure within. These are most readily discovered 
 when the urine has been partially evaporated. 
 
 Leucin and tyrosin are observed in acute yellow atrophy of the 
 
 300.— Leucin-spheres and tyrosin- 
 needles. 
 
 Fig. 301.— Cholesterin-plates and fat-crystals 
 (needles). 
 
 liver, in phosphorus-poisoning, and occasionally in severe infec- 
 tious fevers. I 
 
 Cystin occurs in the form of hexagonal plates often super- 
 imposed. They are most frequently associated with cystin calculi 
 in the kidney. 
 
 Xanthin is extremely rare, but may be associated with xan- 
 thin calculus. 
 
 Cholesterin appears in the form of flat, quadrilateral plates, 
 with a re-entering angle at one of the corners (Fig. 301). They 
 are met with in old cystitis or pyelitis, but are rare. 
 
 Indigo. — Amorphous particles or crystals of indigo may be 
 found in urine containing great excess of indoxyl sulphate. They 
 present a characteristic bluish color. 
 
 Bilirubin, hemoglobin, methemoglobin, and hetna- 
 toidin are occasionally seen as brownish granular concretions or 
 in the form of rhombic crystals (see Choluria, Hemoglobin- 
 uria). 
 
614 TEXT-BOOK OF PATHOLOGY. 
 
 THE URETHRA. 
 CONGENITAL ABNORMALITIES. 
 
 Absence of the urethra is sometimes met with in association 
 with other defects of development. Partial deficiencies and ab- 
 normal structure of the urethra are more frequent. Thus in the 
 female it may be reduced in length and open in the anterior wall 
 of the vagina, and in the male may terminate at the base of the 
 scrotum. Obliteration of part of the urethra (atresia) may occur 
 in cases of defective development of the corpus spongiosum ; more 
 commonly there is obliteration of the meatus. Other abnormal 
 conditions will be considered in connection with defective develop- 
 ment of the penis. 
 
 INFLAMMATIONS. 
 
 Inflammation of the nrethra, or urethritis, is most fre- 
 quently due to a specific micro-organism — the gonococcus of 
 Neisser. Some cases, however, are non-specific, resulting from 
 irritation by chemical or mechanical agents with associated infec- 
 tion (staphylococci, streptococci, or other organisms). Some of 
 these cases are caused by direct traumatism, as by blows, injuries 
 caused by catheterization, and the like ; in other cases foreign 
 bodies, as calculi, become lodged in the urethra and occasion in- 
 flammation, or injure the urethra in passing. Urethritis, like in- 
 flammations of other mucous membranes, may occur in various 
 infectious diseases, such as typhoid fever, scarlet fever, small-pox, 
 etc. In the female, inflammations of the vagina and vulva fre- 
 quently extend to the urethra. A form of pseudomembranous 
 urethritis of obscure origin has been observed in a few cases. 
 
 Specific urethritis, or gonorrhea, is always due to direct infec- 
 tion with the gonococcus (for description of the organism, see 
 Part I.). Certain conditions of the urethra favor infection ; thus 
 an adherent prepuce, by causing greater retention of the infective 
 matters, increases the liability, and probably congested and irri- 
 tated states of the urethral mucosa heighten the susceptibility. 
 The vulnerability of different individuals probably varies ;• and 
 doubtless the micro-organism has greater virulence in some in- 
 stances than in others. 
 
 Pathologic Anatomy. — Urethritis usually first affects the mucosa 
 at or near the meatus, but tends to spread rapidly to the posterior 
 parts. The mucosa is at first intensely congested, red, and swollen. 
 Soon a purulent exudate, of yellowish or greenish color, makes its 
 appearance. The small crypts or lacunae swell and become dis- 
 tended with purulent exudate. 
 
 Microscopically, urethritis presents the features of an intense 
 purulent catarrh. Within a few days of the onset the super- 
 ficial epithelium becomes loosened and begins to desquamate ; 
 
DISEASES OF THE URINARY ORGANS. 
 
 615 
 
 and at the same time polymorphonuclear leukocytes make their 
 way to the surface between the epithelial cells. The pus-cells 
 and epithelium of the surface-exudate contain gonococci in abun- 
 dance, and the organisms are discovered in the cells and to a less 
 extent between the cells of the deeper layers of the mucosa (Fig. 
 302). The process extends most deeply in those parts of the 
 
 Fig. 302.— Acute urethritis, showing purulent infiltration and gonococci in the cells and 
 between the cells (Birch-Hirschfeld). 
 
 urethra (penile portion) in which the lining epithelium is of the 
 columnar variety. 
 
 Associated Lesions. — In simple cases the disease proceeds no 
 further than has been described, but after a period of several 
 weeks gradually subsides. Very frequently, however, the inflam- 
 mation extends in various directions, and complicating conditions 
 arise. Sometimes the infective agents penetrate the membrana 
 propria of the small glands (Littre's glands), or enter the sub- 
 mucosa by direct invasion through the interglandular parts of the 
 mucosa. Leukocytic collections in the submucosa or periurethral 
 abscesses may result. In these cases the gonococcus alone may be 
 the infective cause, or other pyogenic organisms may be associated ; 
 sometimes periurethral lesions are caused by staphylococci inde- 
 pendently of gonococci. Occasionally accumulations of pus in 
 Tyson's glands may simulate periurethral abscesses. In the fe- 
 male similar purulent distention of the glands of Bartholin is a 
 frequent lesion. The inflammation of the urethra is often confined 
 to the anterior portion (anterior urethritis), but may extend to the 
 
616 TEXT-BOOK OF PATHOLOGY. 
 
 posterior portion (posterior urethritis). In the male, secondary in- 
 volvement of the prostate gland is likely to occur with posterior 
 urethritis ; and, more rarely, the organisms invade the vas deferens 
 and find their way to the epididymis, causing acute epididymitis. 
 The bladder is rarely involved, the mucosa apparently offering 
 considerable resistance to the infection. In the female, acute vag- 
 initis, and especially inflammation of the cervix uteri, are com- 
 monly associated. Secondary extension to the uterus may occa- 
 sion gonorrheal endometritis ; more frequently the uterus is but 
 little affected, while the Fallopian tubes suffer intense inflamma- 
 tion. Catarrhal or purulent salpingitis, often complicated with 
 local peritonitis, is one of the most important of the complications. 
 When pus from a gonorrheal urethritis is brought in contact with 
 the conjunctiva a severe form of purulent conjunctivitis results. 
 
 Metastatic lesions are not infrequent. Among these, gonorrheal 
 arthritis is the most familiar. It usually occurs late in the disease, 
 sometimes after an interval of weeks or months from the onset, and 
 involves the larger joints (knee, elbow, wrist). Purulent exuda- 
 tion and fibrous anchylosis may result. A similar lesion is gonor- 
 rheal tenosynovitis. Sometimes the pericardium, endocardium, and 
 myocardium are involved ; and, more rarely, the pleura and the 
 membranes of the cord. 
 
 Enlargement of the lymphatic glands of the inguinal (bubo) 
 region is frequent ; sometimes it terminates in suppuration. 
 
 Chronic urethritis is usually the result of continuation of the 
 acute form. It may present itself in the form of a chronic catar- 
 rhal process, as a hyperplastic inflammation, or as a productive or 
 cicatrizing form. 
 
 In the catarrhal form of chronic urethritis the lesion is practi- 
 cally the same as in the acute disease. The epithelium is loosened 
 and more or less desquamated, and sometimes distinct erosions are 
 observed. Definite ulcerations may occur in parts back of strict- 
 ures. The columnar epithelium may be converted into the squa- 
 mous form in localized areas or diffusely. The crypts and glands 
 of the mucosa may be distended with desquamated cells and 
 more or less periglandular inflammation may be observed. 
 
 In the hyperplastic variety the mucosa is thickened in a papil- 
 lomatous manner, and diffuse catarrhal inflammation is associated. 
 
 The productive or cicatrizing form is the most important. It 
 may be diffuse in character, but is usually localized and leads to 
 strict ure-formation . 
 
 Stricture of the urethra is most frequent in the membranous 
 portion, but may occur in the anterior parts. Not rarely there 
 are several strictures in the course of the canal. Histologically 
 the stricture is the result of productive inflammation of the mucosa 
 and submucosa. It is therefore a lesion of slow development, and 
 may not become obstructive for months or years after the acute 
 
DISEASES OF THE URINARY ORGANS. 617 
 
 attack of gonorrhea, to which it owes its origin, has subsided. 
 The lumen of the urethra is encroached upon in limited area or 
 for a considerable distance, and on section the stricture is found to 
 be hard and resisting. When the lumen of the urethra is greatly 
 narrowed the outflow of urine is impeded, and hypertrophy of the 
 walls of the bladder results. Later, dilatation of the bladder, and 
 even of the ureters and pelvis of the kidneys, may result. The 
 urethra back of the stricture frequently presents the lesions of 
 chronic catarrhal or hyperplastic urethritis, the obstruction serving 
 to prolong the original inflammation of these parts. Rupture of 
 the urethra and extravasation of urine into the cellular tissues, 
 with subsequent necrosis and gangrene, may occur. 
 
 In chronic urethritis there is usually a constant but slight dis- 
 charge of mucous exudate (gleet). Examination of this may dis- 
 cover no gonococci, or only an occasional group. The urine 
 contains flocculent shreds (clap-threads), which on microscopic 
 examination are found to be granular or homogeneous structures 
 resembling cylindroids, and often covered with pus-cells that have 
 adhered to the surface. The amount of discharge may be quite 
 copious at times, especially in the hyperplastic and catarrhal forms 
 of chronic urethritis. 
 
 INJURIES OF THE URETHRA. 
 
 The urethra may be injured by traumatism from without or 
 within. In cases of falls with injury of the perineum the mem- 
 branous portion of the urethra may be seriously lacerated, and in 
 women injuries sustained during labor may cause immediate 
 rupture of the urethra, or may first occasion inflammatory and 
 necrotic changes in the anterior wall of the vagina and secondary 
 perforation of the urethra. Injuries from within the urethra may 
 be due to forced attempts at catheterization when some form of 
 obstruction opposes the passage of the instrument. " False pas- 
 sages " are thus occasioned, and may result in fistulse and extrava- 
 sations of urine. Concretions or calculi from the kidney or bladder 
 may lodge in the urethra, and may cause immediate perforation or 
 primary inflammation, with secondary rupture of the walls. 
 
 Rupture of the urethra causes extravasation of urine into the 
 periurethral cellular tissues. If the skin is intact and the urine 
 cannot escape, widespread inflammation, necrosis, and gangrene 
 are liable to occur. Fistulous communications may be established 
 with the exterior, or, in women, with the vagina. 
 
 INFECTIOUS DISEASES. 
 
 Gonorrheal urethritis is the important infectious disease 
 of the urethra. For convenience, it has been described under 
 Inflammations. 
 
618 TEXT- BOOK OF PATHOLOGY. 
 
 Tuberculosis of the vesical end of the urethra may be asso- 
 ciated with tuberculosis of the bladder. Lupus sometimes in- 
 volves the meatus and anterior end of the urethra in cases of lupus 
 of the external genitalia of women. Very rarely tuberculosis of 
 papillary form is met with in the urethral mucosa. 
 
 Syphilis. — The chancre may occur in anterior parts of the 
 urethra in either sex. It usually undergoes rapid ulceration. 
 
 TUMORS. 
 
 The urethra of women is more often the seat of tumors than is 
 that of men. 
 
 Small polypoid tumors are occasionally seen hanging from 
 the meatus ; they may be of cystic character, like the polyps of 
 other mucous membranes. 
 
 Carcinoma is usually secondary to cancer of the external 
 genitalia (vulva, vagina, glaus penis). Primary carcinoma origi- 
 nating from Cowper's gland has been described, and a few cases 
 of carcinoma of other parts of the urethra have been observed. 
 
 Cysts of the mucous membrane, due to retention of the con- 
 tents of the small glands, are occasionally met with, especially in 
 the posterior portion of the urethra. The inner lining of the cyst 
 is elevated in the form of papillae covered with squamous epi- 
 thelium. 
 
 Sarcoma of the urethra has been described, but is very rare. 
 
 CHAPTER VIII. 
 DISEASES OF THE REPRODUCTIVE ORGANS. 
 
 THE UTERUS. 
 
 Development and Anatomy. — The uterus is formed by the 
 fusion of the middle portions of Midler's ducts, the fusion first oc- 
 curring below where the cervix uteri is developed. The epithelial 
 lining of the ducts gives rise to the mucosa of the uterus, and its 
 outer layers to the muscularis. The utricular glands are devel- 
 oped by ingrowths from the lining cells, and first appear and reach 
 their most complex development in the cervical portion. The outer 
 surface of the cervix (portio vaginalis) is lined with stratified squa- 
 mous epithelium ; the cavity of the uterus and cervical canal with 
 cylindrical ciliated cells. In the cervical portion are found nu- 
 merous racemose glands and between them simple tubular glands ; 
 in the corpus uteri the glands are simple tubules. 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 
 
 619 
 
 CONGENITAL ABNORMALITIES. 
 
 Absence of the uterus is very rare. The organ, however, may- 
 be represented only by a mass of rudimentary tissue. Hypoplasia 
 of the uterus may be a congenital condition, or may be the result 
 of arrested development and the consequent failure to increase in 
 size at the age of functional activity. The term uterus foetalis seu 
 infantilis is applied. Stenosis and atresia of the uterus and vagina 
 may be the result of disease or maldevelopments, due to partial 
 obliteration of Muller's ducts. 
 
 Among the more striking malformations of the uterus are those 
 which result from incomplete fusion of Miiller's ducts. In nor- 
 
 Fig. 303.— Uterus bicornis unicollis (Winekel). 
 
 mal development these ducts unite and fuse in the lower portion 
 to form the uterus and vagina, but remain separated above, where 
 they form Fallopian tubes. Among the anomalous conditions of 
 the uterus are uterus bicornis, in which the cervical portion of the 
 
 Fig. 304.— Uterus septus (Cruveilhier). 
 
 uterus is single, or two entirely distinct uterine cornua are present 
 {Fig. 303) ; uterus septus, in which the external appearance may 
 be that of a single uterus, but on section a septum is discovered, 
 which divides the organ into lateral halves (Fig. 304). The term 
 
620 TEXT-BOOK OF PATHOLOGY. 
 
 uterus unicornis is used to designate cases in which but one of 
 Miiller's ducts has developed, the other remaining rudimentary. 
 Malformations of the vagina may be associated with those of the 
 uterus already named, though this is rarely the case. A number 
 of subdivisions have been distinguished for each of these malforma- 
 tions, but they are unimportant. 
 
 ALTERATIONS OF POSITION. 
 
 The normal position of the uterus is one of slight anteversion 
 with anteflexion ; that is, the fundus lies a little farther to the 
 front than the cervix, and there is a slight band or flexure in the 
 middle portion. 
 
 Anteflexion is a condition in which there is marked angula- 
 tion of the uterus, the fundus falling forward. Relaxation of the 
 ligaments predisposes to this condition ; and it may be caused by 
 the pressure of tumors situated posteriorly, by distention of the 
 rectum with gas, by the traction of adhesions and by abnormal 
 conditions of the uterus itself, causing a loss of tone in the walls. 
 The grade of anteflexion varies greatly. Among the effects of 
 this condition is interference with the discharge of menstrual 
 blood, with consequent accumulation and intense dysmenorrhea. 
 
 Anteversion, or the tilting forward of the uterus without 
 abnormal angulation, occurs under similar conditions, but is less 
 important. 
 
 Retroflexion of the uterus occurs in cases in which the walls 
 of the uterus are abnormally soft and have lost their tone. It 
 may be caused by the pressure of tumors or the traction of adhe- 
 sions. Sometimes it is due to habitual constipation, causing pressure 
 of masses in the rectum upon the lower part of the uterus (cervix) ; 
 retroversion and subsequently retroflexion are produced. Laxness 
 of the vaginal walls and rupture of the perineum may cause this 
 or other abnormal positions of the uterus by depriving the organ 
 of its support from below and subjecting it to the unresisted press- 
 ure of the abdominal viscera. The degree of retroflexion varies 
 from slight angulation to a complete backward doubling of the 
 organ. The fundus may undergo considerable congestion from 
 the interference with circulation, and it is not rarely enlarged. 
 Adhesions between the uterus and rectum are frequent. 
 
 Lateral displacements of the uterus are rare. 
 
 Upward dislocation may be caused by pressure of tumors 
 in the pelvis ; it may be due to the traction of adhesions between 
 the uterus and large tumors of the ovary. In such cases the 
 uterus may be greatly stretched and the vagina may be similarly 
 affected. 
 
 Prolapse of the uterns is a term applied to descent or 
 downward displacement. It is possible to distinguish any num- 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 
 
 621 
 
 ber of degrees of prolapse, but it is sufficient to speak of two only : 
 incomplete prolapse, in which the os uteri is still within the vagina, 
 and complete prolapse, in which it projects through the vulva. 
 The causes of prolapse of the uterus are numerous. Injuries to 
 the perineal floor and unusual laxity of the vaginal walls or the 
 ligaments of the uterus are very important. Traumatism and ex- 
 cessive pressure upon the uterus from the abdomen may cause de- 
 scent of the organ, especially if laxity of the ligaments was present 
 before. Enlargement of the uterus itself may be the cause of pro- 
 lapse, and in any case the organ usually becomes enlarged after 
 the prolapse, in consequence of passive congestion. The cervix is 
 generally directed somewhat backward, and the mucous membrane 
 frequently presents catarrhal inflammation and contains enlarged 
 veins. The cavity may be filled with considerable mucous secretion. 
 
 In some instances of apparent complete prolapse the fundus of 
 the uterus may be but little displaced, the great descent of the os 
 uteri in such instances being due to hypertrophic elongation of the 
 vaginal portion of the cervix. 
 
 In all cases of prolapse the anterior and posterior walls of the 
 
 Fig. 305.— Complete prolapse of the uterus (Penrose). 
 
 vagina are displaced downward more or less, and sometimes may 
 be completely everted. The anterior vaginal prolapse may draw 
 with it the posterior wall of the bladder, and cystocele results. 
 Similarly the posterior vaginal wall may drag down the anterior 
 wall of the rectum, and rectocele is produced (Fig. 305). 
 
622 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 Inversion of the nterus is a condition in which the organ 
 is turned inside out to a greater or less extent. This condition is 
 caused by traction upon the placenta during labor, when it is 
 acutely developed ; or by the similar traction of polypoid sub- 
 mucous tumors, when it is more slowly formed (Fig. 306). There 
 
 Fig. 806.— Fibroid polyp, producing partial inversion of the uterus (Penrose). 
 
 may be only a slight inversion of the fundus, or the organ may be 
 completely inverted and may present itself through the vagina and 
 vulva. Secondary changes are apt to occur in such cases. The 
 mucous membrane suffers catarrhal inflammation with ulceration ; 
 and the entire uterus, though at first perhaps enlarged by conges- 
 tion, subsequently atrophies. 
 
 STENOSIS, DILATATION, AND RUPTURE. 
 
 Stenosis of the uterine cavity may occur as a congenital con- 
 dition, or may be acquired in cases in which inflammation has 
 led to cicatricial stricture. There may be almost complete obliter- 
 ation of the external or internal os uteri. 
 
 Dilatation of the cavity of the uterus is a not infrequent 
 result of stenosis. The dilated cavity may be filled with mucus 
 or seromucous secretion from the mucous membrane (hydrometra), 
 or with accumulations of menstrual blood (hematometra). 
 Occasionally in cases of hydrometra secondary decomposition of 
 the liquid causes gas-formation, and physometra results. In cases 
 of hematometra the amount of blood in the uterine cavity may be 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 623 
 
 very considerable, and in some instances rupture of the wall of the 
 uterus is the result. This may be simply due to the increasing 
 pressure, or it may result from inflammation or ulceration at the 
 point of stenosis. 
 
 Rupture of the uterus may occur during pregnancy or labor ; 
 and occasionally at other times in consequence of inflammations, 
 abscess, softened tumors, and the like. The most frequent and 
 serious consequence of rupture is peritonitis. Occasionally, when 
 rupture has occurred during pregnancy, the fetus may be enclosed 
 in a sac formed by circumscribed peritonitis ; the rupture may at 
 the same time heal. Subsequently the fetus may be disorganized 
 and discharge through the abdominal wall. This is a very unusual 
 termination. 
 
 Laceration of the cervix uteri is a very common accident of labor. 
 
 CIRCULATORY DISTURBANCES. 
 
 Hyperemia of the uterus is a physiologic condition during 
 menstruation, and occurs in all forms of acute inflammation of the 
 organ. There is no essential difference between menstrual hyper- 
 emia and that of pathologic conditions. 
 
 Menstruation. — Examination of the mucous membrane during 
 the period shows swelling of the membrane, with multiplication 
 of the interglandular cells and dilatation of the lymphatic chan- 
 nels. The uterine glands are elongated and the cells more or less 
 swollen. Congestion is always conspicuous, and the superficial 
 epithelial cells are desquamated more or less considerably. In 
 the interval between the periods regeneration of the mucous 
 membrane takes place. The term dys- 
 menorrhea membranaeea is applied to Mts^Mlt 
 abnormal menstruation in which mem- j** Aftfl ' 
 branous formations are discharged from /{ , ,,' '"'■' 
 the uterus (Fig. 307) and in which there V \ s • '<£ 
 is severe pain. The membranes consist \ 
 of intact portions of desquamated cells 
 more or less degenerated. Cases of this t ^ ,i 
 character are particularly prone to occur t ) " ' ;'- 
 when chronic inflammations of the mu- 
 cosa have existed, and the affection is Vm^^^^W 
 then termed endometritis exfoliativa. W^^^^^m 
 
 Passive hyperemia of the uterus M*'- 
 
 occurs in conditions of general venous W { t^Kw 
 
 stasis, but especially when dislocations Xs|F r 
 
 of the uterus cause pressure upon the cha ^ ed ff- JjEgSE, $* 
 
 VenOUS plexuses. The organ is enlarged, menorrhea (Penrose). 
 
 the veins in the serous surface are 
 
 prominent, the mucous membrane is dark red, and when the con- 
 gestion is long continued chronic endometritis may result. 
 
624 TEXT-BOOK OF PATHOLOGY. 
 
 Hemorrhages may occur into the uterine cavity, into the wall 
 of the uterus, or into the peritoneum outside the uterus. Hemor- 
 rhages during menstruation and in labor are physiologic forms. 
 Pathologic increase of menstrual hemorrhage is spoken of as 
 menorrhagia, which may occur in certain general diseases, such as 
 anemia, or in consequence of local conditions, notably tumors. 
 Intense congestion of the organ from cardiac disease or from mal- 
 positions of the uterus may also lead to hemorrhages during the 
 menstrual period. Hemorrhages between the menstrual periods 
 are spoken of as metrorrhagia. This may be caused by general 
 conditions, such as the hemorrhagic diseases, and infections (small- 
 pox, etc.) ; but it is especially frequent as a result of local diseases, 
 of which fibroid tumors are the most important. 
 
 Hemorrhages into the substance of the uterus are rare, and are 
 generally due to traumatism. 
 
 Hemorrhages into the peritoneal cavities or into the cellular 
 tissues in the vicinity of the uterus are more frequent. Of the 
 intraperitoneal hemorrhages the most frequent is accumulation of 
 blood in Douglas's pouch {retro-uterine hematocele). The blood in 
 this case may come from various sources, such as ruptured ovarian 
 follicles, ruptured tubes in tubal pregnancy, hematosalpinx, or 
 rupture of varicose veins in the broad ligament. The blood may 
 become absorbed without causing other pathologic results, or it 
 may set up inflammation and result in adhesions between the 
 uterus and rectum. Not rarely perforation with discharge of 
 the blood through the rectum or vagina occurs. 
 
 Hemorrhages into the vesico-uterine pouch and hematoma 
 between the layers of the broad ligament are rare. 
 
 INFLAMMATIONS. 
 
 Inflammation may affect the mucous membrane of the uterus, 
 when the term endometritis is applied, or the wall of the uterus, 
 when it is termed metritis. The names perimetritis, indicating 
 inflammation of the peritoneal covering of the uterus, and para- 
 metritis, inflammation of the cellular tissues in the vicinity of the 
 uterus, are unnecessary, as these conditions are simply forms of 
 local peritonitis. For purposes of convenience the inflammations 
 of the uterus occurring during the puerperium will be separately 
 considered. Some of the conditions here described as inflamma- 
 tory are not positively of such nature, though no sharp line of 
 division can be drawn between the inflammatory and the hyper- 
 plastic forms. 
 
 Acute catarrhal endometritis may result from trauma- 
 tism, or from infection with pyogenic organisms or gonococci. 
 Occasionally it occurs as a complication of general infectious 
 diseases, such as typhoid fever and cholera. The mucous mem- 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 
 
 625 
 
 brane is swollen and intensely hyperemic ; very often small hemor- 
 rhages are observed. Desquamation of the epithelial cells, with 
 mucopurulent secretion, causes considerable discharge. In most 
 cases the body of the uterus is affected, but in the gonorrheal form 
 the cervical portion is the most frequent seat. Very intense forms 
 may occasion necrosis of the epithelial cells and the formation of 
 pseudomembranous deposits. This is particularly frequent in the 
 infectious diseases. 
 
 Chronic endometritis may be the continuation of acute 
 endometritis, and is especially apt to occur in persons of reduced 
 vitality, such as scrofulous or chlorotic women, or in those in 
 whom the circulation is sluggish. The influence of passive con- 
 gestion has already been referred to. Very often the etiology is 
 entirely obscure. 
 
 The mucous membrane in the earlier stages is simply swollen, 
 and produces abundant mucopurulent secretion. Later, hyper- 
 plastic changes occur, the hyperplasia affecting either the uterine 
 glands or the interstitial tissue. The terms endometritis glandu- 
 laris and endometritis inter stitialis have been applied to distinguish 
 these varieties. In the former, microscopic examination shows an 
 abundance of proliferated glandular acini extending through the 
 depth of the mucous membrane (Fig. 308). In the latter the 
 
 glands are less conspicuous, but round-cell infiltration and abun- 
 dant connective-tissue hyperplasia between the glands are con- 
 spicuous features (Fig. 309). In some of the cases, particularly 
 in those of the glandular form, the process seems more closely 
 allied to tumor-formation than to inflammation ; and it is very 
 
626 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 difficult to draw a sharp line between some forms of adenoma 
 and sarcoma of the mucous membrane on the one hand, or chronic 
 inflammations on the other hand. The mucous membrane may in 
 
 Vt-, i»j$t 
 
 
 Fig. 309.— Interstitial endometritis. 
 
 the advanced stages be considerably swollen and project in a poly- 
 poid form (Fig. 310). Later, atrophy may take the place of hyper- 
 trophy, and in some instances the lining epithelial cells change 
 
 fill 
 
 # 
 
 
 
 
 t/ 
 
 their character from the typical columnar cells to a distinct 
 squamous type. The small glands of the membrane may be 
 obstructed at their mouths and cystic distention may result. This 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 
 
 627 
 
 
 is particularly conspicuous in the case of the Nabothian glands of 
 the cervix, and retention-cysts of these glands may reach the size 
 of a pea or a small cherry. Occasionally erosions or slight ulcer- 
 ations are met with in cases of chronic endometritis. 
 
 Chronic endometritis of the cervix is frequently secondary to 
 inflammations of the vagina, and may be due to gonorrheal infec- 
 tion or other causes. The mucous membrane of the cervical canal 
 is greatly thickened, and may project from the os uteri (ectro- 
 pium). Retention-cysts of the Nabothian glands are sometimes a 
 conspicuous feature ; and cystic mucous polyps are not unusual. 
 
 Chronic endometritis may lead to chronic metritis, or by exten- 
 sion may occasion tubal disease. Clinically it is characterized by 
 more or less constant mucopurulent discharge. 
 
 Erosions of the uterus are especially frequent in the cervix ; 
 they result from endometritis. The mucosa within the cervical 
 canal undergoes hyperplastic changes and projects from the os 
 uteri in a polypoid form. Between the papillomatous projections 
 cystic formations may develop, and these may rupture, leaving 
 exposed ulcerations. Granulation-tissue is developed from the 
 submucosa, and sometimes this becomes exuberant in character. 
 
 Fig. 311.— Left lateral laceration of the cervix, with erosion (Penrose). 
 
 Other erosions are due to laceration of the cervix (Fig. 311) ; and 
 occasionally congenital erosion has been observed. 
 
 Phagedenic ulceration of the cervix has been described as an 
 independent disease. Some of the cases are undoubtedly instances 
 of ulcerating carcinoma ; in other cases ulcerations in this situa- 
 tion have been met with in which microscopic examination showed 
 no evidence of carcinomatous tissue. 
 
 Acute metritis is rarely met with, except during the puer- 
 perium, but may be the result of acute endometritis. The wall 
 
628 TEXT-BOOK OF PATHOLOGY. 
 
 of the uterus becomes thickened, soft, and edematous. Occasionally 
 purulent infiltration is observed. 
 
 Chronic metritis frequently occurs in the puerperium as a 
 result of retarded involution of the uterus. It may be occasioned 
 by chronic congestion of the uterus, or may be secondary to chronic 
 endometritis. The uterine -wall is infiltrated with round cells, 
 and the connective tissues undergo active hyperplasia, which in 
 the later stages leads to great thickening and induration. Coinci- 
 dently there is usually some hypertrophy of the muscular elements 
 themselves. It is by no means certain that all of the cases 
 grouped under this term are inflammatory in nature. Some are 
 certainly more closely allied with diffuse tumor-formation. The 
 mucous membrane is usually thickened, and becomes secondarily 
 involved if it was not primarily diseased. The peritoneal cover- 
 ing may be similarly affected, and chronic perimetritis with adhe- 
 sions of the uterus results. 
 
 INFECTIOUS DISEASES. 
 
 Puerperal Infections. — This term may be applied to vari- 
 ous forms of infection occurring during the puerperium, but in 
 the majority of instances the streptococcus is the specific organ- 
 ism. 
 
 Etiology. — Two important factors are concerned : (a) injuries 
 to the surface of the uterus, vagina, or vulva ; and (6) some form 
 of infection. The more or less denuded surface of the uterus of- 
 fers a ready entrance to micro-organisms, as well as an absorptive 
 surface for soluble poisons produced by micro-organismal decom- 
 position within the uterus ; and infection may take place without 
 any further injury than that occasioned by the normal processes 
 of labor. In most instances, however, there is actual injury either 
 of the surface of the uterus, cervix, vagina, or vulva, and the 
 micro-organisms or poisons are admitted through these wounds. 
 There may be primarily, however, more than a simple injury of 
 the mucous surface. In consequence of prolonged pressure ne- 
 crotic lesions terminating in gangrene may first be established, 
 and from this secondary infections may take place. In cases in 
 which infection occurs without injury to the walls, as well as in 
 cases in which injury has been sustained, the pathogenic organisms 
 may first find a lodgement and multiply within the blood-clots or 
 retained secundines within the uterus ; and the organisms or their 
 toxic products are secondarily admitted to the uterine tissues. 
 
 Puerperal infection is probably in most cases the result of the 
 entrance of micro-organisms from without, and may be traced to 
 want of cleanliness on the part of the accoucheur or the surround- 
 ings. Sometimes widespread epidemics have been caused by the 
 carelessness of a single obstetrician, whose hands perhaps had be- 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 629 
 
 come infected from operating upon or examining cases of erysipelas, 
 general pyemia, or the like. 
 
 Among the micro-organisms, as has already been stated, the 
 Streptococcus pyogenes is most important. Staphylococci of vari- 
 ous sorts, bacilli resembling the Bacillus coli communis, the bacil- 
 lus of tetanus, gonococci, and other organisms occasionally infect 
 the puerperal uterus, but in these instances the pathologic condi- 
 tions are different from those met with in ordinary puerperal infec- 
 tion, which may be considered as practically always a streptococcic 
 infection. 
 
 Pathologic Anatomy. — In most instances there is primarily a 
 lesion upon the mucous surface of either the uterus, the vagina, or 
 the vulva. The nature and extent of this depend upon the amount 
 of injury occasioned during labor. In some instances the lesion is 
 trivial in extent, and remains so, though widespread infection re- 
 sults from it. In most cases, however, there is a rapidly spread- 
 ing inflammation of the endometrium or mucosa of the vagina, and 
 pseudomembranous deposits are very frequently met with upon 
 the surface. Necrotic and gangrenous changes in the mucous 
 membrane are most pronounced in cases in which prolonged press- 
 ure has been exerted by the head in its descent or by instruments. 
 
 The extension of the infection may occur in two ways, either 
 through the blood-vessels or through the lymphatic channels ; and 
 the local and general lesions vary correspondingly. 
 
 In cases in which the infection spreads along the blood-vessels 
 there may be primarily septic softening of the thrombi within the 
 uterus and purulent phlebitis of the venous channels at the pla- 
 cental site. Thrombosis extends from this situation through the 
 veins to the various plexuses in the vicinity, and infected emboli 
 are carried through the circulation to distant organs, such as the 
 lungs, the kidneys, and the spleen. Metastatic abscesses and in- 
 flammatory swelling of the affected organs result. The kidneys 
 in particular are often the seat of numerous punctate or miliary 
 abscesses. 
 
 In the cases in which extension occurs along the lymphatic 
 channels the uterus is enlarged, soft, and often pultaceous. Streaks 
 or lines of light color may be observed running from the mucous 
 surface toward the periphery. These represent the lymphatic 
 vessels filled with purulent exudate. The walls of the lymphatics 
 may be penetrated, and perilymphangitic abscesses are thus occa- 
 sioned. When the process has extended to the lymphatics in the 
 outer layers of the uterus phlegmonous inflammation of the sub- 
 peritoneal tissues (parametritis) results, and finally the peritoneum 
 itself may be involved. 
 
 The spleen is enlarged, though less decidedly than in the form 
 in which infection occurs through the blood-vessels. 
 
 Extension along the mucous membrane itself may lead to asso- 
 
630 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 ciated disease of the tubes ; more frequently the tubes are invaded 
 
 at their abdominal end after 
 peritonitis has developed. 
 
 Puerperal sepsis is pecu- 
 liarly virulent and rapid in 
 its course, and may occasion 
 widespread changes in all of 
 the tissues of the body. 
 
 Tuberculosis.— Tuber- 
 culosis of the uterus is most 
 frequently met with in the 
 mucous membrane, and is 
 usually secondary to disease 
 of the tubes. Direct infec- 
 tion may possibly occur 
 through coitus ; but is cer- 
 tainly rare. The disease 
 occurs in the form of a 
 nodular or diffuse infiltra- 
 tion with a tendency to rapid 
 ulceration or caseous necrosis 
 involving the mucous mem- 
 brane and to some extent the submucosa. The entire cavity of 
 the uterus may be covered with caseous and necrotic deposits 
 
 Fig. 312.— Diffuse tuberculosis (ulcerative and 
 caseous) of the endometrium (Kaufmann). 
 
 MM" 
 
 ^^^ffl^^ fin . . -M 
 
 <■■ 
 
 : m <&m 
 
 o 
 
 
 Fig. 313.— Miliary tuberculosis of the endometrium and glandular endometritis (Beyea). 
 
 (Fig. 312). In the later stages the process may extend deeply, 
 even involving the muscular layer of the organ. The cervix 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 631 
 
 is rarely attacked. Sometimes miliary tubercles are found in the 
 uterine mucosa without marked degeneration (Fig. 313). 
 
 Syphilis of the cervix uteri may occur in the form of a chan- 
 cer, or as tertiary infiltration. 
 
 ATROPHY AND DEGENERATIONS. 
 
 Puerperal Atrophy. — The uterus suifers a most remarkable 
 atrophy following labor. This proceeds very rapidly at first, and 
 then more slowly ; and under favorable conditions the organ re- 
 sumes its previous condition in the course of a few months. The 
 muscular fibers decrease progressively, from their previous hyper- 
 trophied condition, in which they frequently attain a length and 
 diameter three times the normal, until, at the end of involution, 
 the usual size and appearances are attained. Many muscle-fibers 
 undoubtedly are destroyed. The process of involution is really 
 one of fatty degeneration. 
 
 Senile Atrophy. — The uterus undergoes progressive atrophy 
 at and after the period of the menopause, and finally becomes 
 greatly reduced in size. The substance of the organ may undergo 
 a progressive sclerosis, or in other instances becomes softer than 
 normal. Catarrhal endometritis is often associated, and the co- 
 lumnar cells are sometimes converted into squamous epithelium. 
 
 Fatty degeneration, independent of that which occurs dur- 
 ing puerperal involution, is a rare condition, but may occur in the 
 course of certain infectious diseases, such as typhoid fever, or may 
 result from the action of the parenchyma-poisons. 
 
 Amyloid degeneration is rare and unimportant. 
 
 HYPERTROPHY AND HYPERPLASIA. 
 
 Hypertrophy of the entire uterus may occur in association 
 with inflammation or metritis, or may result from chronic conges- 
 tion of the organ. The enlargement in cases usually designated as 
 hypertrophied is, for the most part, due to new-formed connective 
 tissue. True hypertrophy occurs as a physiologic process during 
 pregnancy. In this variety the muscle-fibers increase enormously 
 in size, and doubtless also multiply their number. The blood-ves- 
 sels and connective tissues undergo corresponding hypertrophy. 
 
 Hypertrophy of the cervix uteri is occasionally met with 
 independent of hypertrophy of the uterus as a whole. It may be 
 caused by chronic irritations of the cervix, as in cervical endome- 
 tritis, or may result from obscure causes. Frequently it is met 
 with in prolapse of the uterus, and sometimes it may cause a 
 simulation of prolapse. 
 
 Hyperplasia of the mucous membrane of the uterus has 
 been referred to in the discussion of chronic endometritis. In 
 
632 TEXT-BOOK OF PATHOLOGY. 
 
 some instances that are designated as endometritis the pathologic 
 process seems to be rather of a purely hyperplastic character, and 
 more closely allied to tumor-formation than to ordinary inflam- 
 mation. In these cases the mucous membrane in all parts of the 
 uterus may be greatly thickened, and may suffer more or less 
 papillomatous transformation. Sometimes limited portions are 
 affected, and polypoid formations result. 
 
 Polyps of the uterus may be of various sorts. Very com- 
 monly they present themselves as simple mucous polyps, due to 
 projection of parts of the mucous membrane ; in other cases sec- 
 ondary changes, such as cavernous dilatation of the blood-vessels 
 or cystic transformation of the small glands contained in the polyp, 
 occasion marked variations from the original appearances. Myo- 
 fibromata, sarcomata, and other forms of tumors originating in the 
 mucous membrane or just beneath it may assume a polypoid 
 appearance. 
 
 TUMORS. 
 
 leiomyoma ; Myofibroma ; Fibroid. — The tumors of the 
 uterus designated by these terms are in nearly all cases composed 
 of smooth muscle-fibers and fibrous tissue ; and from the patho- 
 logic standpoint the term myofibroma is therefore most applicable. 
 They present themselves in the form of rounded and usually well- 
 circumscribed masses, from the size of a grape-seed to that of 
 tumors weighing forty or fifty pounds. They are generally mul- 
 tiple ; are very hard ; and on section have the appearance of con- 
 centric or irregular lamellae. Microscopically the tumor is com- 
 posed of smooth muscle-fibers and of fibrous tissue arranged in 
 bundles or layers running in various directions. The muscle- 
 fibers are frequently found arranged concentrically about small 
 blood-vessels, and in some instances the vessels are telangiectatic. 
 
 Secondary changes are very common, the most frequent being 
 calcification. This may begin either in the center or at the 
 periphery, but more commonly it is diffuse. Edema of the tumor 
 may cause it to become quite soft, and cystic transformations due 
 to softening or to distention of the lymphatic spaces are sometimes 
 observed. 
 
 Several varieties have been distinguished, according to the seat 
 of the tumors. In some instances they are embedded in the wall 
 of the uterus, when the term interstitial or mural fibroids is applied 
 (Fig. 314). In other cases they arise in the uterine walls just beneath 
 the mucous membrane, when they are called submucous fibroids. 
 These may gradually project into the cavity of the uterus as fibroid 
 polyps. In the third group of cases the tumors have a subperito- 
 neal location, and may project from the outer surface of the uterus 
 as knobbed masses (Fig. 315), which may become pedunculated. 
 In rare instances they extend between the layers of the broad liga- 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 
 
 633 
 
 ment. Fibroid tumors are benign in a pathologic sense, but occa- 
 sion serious disturbances either by pressure or by the metrorrhagia 
 
 Fig. 314.— Interstitial fibroid tumor of the uterus : a small submucous fibroid appears in 
 the uterine cavity (Penrose). 
 
 and endometritis to which they frequently give rise. Subperitoneal 
 fibroids may become free bodies in the peritoneal cavity, and the 
 
 Fig. 315.— Subperitoneal fibroids and an intraligamentous fibroid of the uterus (Penrose). 
 
 submucous form is sometimes discharged from the uterus after a 
 spurious labor. 
 
634 TEXT-BOOK OF PATHOLOGY. 
 
 Sarcoma of the uterus may arise from the muscular layer or 
 from the endometrium. That arising from the myometrium is 
 usually associated with myoma and fibroma. In some cases the 
 sarcomatous elements of the tumor are developed in a pre-existing 
 myofibroma. In other cases the sarcoma and fibroma are coinci- 
 dentally formed. These tumors differ from typical fibroids in 
 being more rapid in growth, less well circumscribed, softer, and 
 more homogeneous in appearance. Sometimes they are situated 
 just beneath the endometrium, and become converted into sarcom- 
 atous polyps. 
 
 Sarcoma of the endometrium may occur in a circumscribed or 
 papillomatous and in a diffuse form, the latter involving the entire 
 mucous membrane of the organ. The papillomatous variety is 
 soft and villous and highly vascular. In some cases the structure 
 is that of angiosarcoma. In the diffuse form the entire cavity of 
 the uterus may be filled with soft villous projections from the 
 mucous membrane. 
 
 A special form of sarcoma has been described as occurring in 
 the vaginal portion and cervix. In this the tumor has a grape- 
 like structure, and microscopically consists of myxomatous tissue 
 with areas of sarcomatous character. It occurs in young persons, 
 even in childhood. 
 
 Adenoma. — Adenoma may occur in the form of polypoid out- 
 growths from the mucous membrane, or as a diffuse process not 
 readily distinguishable from that commonly designated as endo- 
 metritis glandularis. Both of these forms are benign. 
 
 Malignant adenoma usually arises from the corpus uteri, 
 and presents itself as a soft, irregular elevation of the mucous 
 membrane in a localized area, or diffusely involving a large part 
 of the endometrium. It tends to spread through the walls of the 
 uterus, invading the myometrium (Fig. 316) and finally penetrating 
 to the peritoneal covering, where secondary nodules may develop. 
 Histologically it is characterized by the production of atypical 
 branched gland-acini with comparatively little stroma, the latter 
 being of soft fibrous character. The tumor is malignant in its 
 tendency to invade the wall of the uterus and neighboring struct- 
 ures, and it may become converted into actual carcinoma in the 
 later stages. In such instances the acini in places show a heaping 
 of epithelial cells and a tendency to destruction of the basement- 
 membrane, with proliferation of the cells in the stroma. 
 
 Carcinoma. — Carcinoma is the most frequent of the malig- 
 nant diseases of the uterus, and usually invades the cervical 
 portion ; more rarely it arises from the corpus uteri. Carcino- 
 mata starting on the vaginal surface of the cervix are squa- 
 mous-celled epitheliomata ; those originating in the cervical canal 
 and in the corpus uteri are tubular or glandular carcinomata. 
 
 Carcinoma of the portio vaginalis usually begins from the 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 
 
 635 
 
 inner surface of one of the lips of the os uteri, and causes a firm 
 infiltration of the affected portion, the disease penetrating into the 
 
 Fig. 316.— Malignant adenoma : the section is taken from the deeper parts of the tumor, 
 and shows the invasion of the myometrium. 
 
 submucosa and muscularis. Subsequently ulceration takes place, 
 and the diseased area becomes converted into an elevated and 
 
 Fig. 317.— Diffuse cancer of the endometrium (Penrose). 
 
 irregularly ulcerated surface. Extension may take place to the 
 vaginal walls and to the tissues surrounding the cervix uteri. 
 
636 TEXT-BOOK OF PATHOLOGY. 
 
 Ulceration may establish communications between the vagina and 
 bladder or rectum. Extension upward into the supravaginal 
 portions of the cervix and to the corpus uteri may occur through 
 the lymphatic channels, or by direct invasion. Secondary involve- 
 ment of the lymphatic glands of the iliac, lumbar, and inguinal 
 groups is frequent. 
 
 Instead of the usual indurated and ulcerating form, cervical 
 epithelioma may present itself as a cauliflower-growth — that is, as 
 a destructive or malignant papilloma. In such cases it is likely 
 that the growth often begins as a papilloma, causing irregular 
 elevations, and that the penetration into the tissue at the base of 
 the growth is a secondary development. In the later stages this 
 form, like the preceding, undergoes ulceration. Both varieties, 
 but particularly the latter, frequently cause uterine hemorrhages. 
 
 Carcinoma of the corpus uteri and of the cervical canal 
 develops from the tubular and acinous glands of the mucous 
 membrane. It may begin as an adenomatous growth, subse- 
 quently becoming transformed into carcinoma. Macroscopically 
 the growth presents itself as a villous or papillomatous thickening 
 of the mucosa, either localized or diffuse (Figs. 317 and 318). In 
 
 Fig. 318.— Cancer of the body of the uterus : a large, single cancerous nodule in the 
 anterior wall has been divided (Penrose). 
 
 the later stages considerable involvement of the wall of the uterus 
 occurs, and even perforation may take place. Microscopically the 
 usual appearances of glandular cancer or adenocarcinoma are 
 discovered (Fig. 319). 
 
 Squamous epithelioma is met with in rare instances in the 
 corpus uteri, especially in women of advanced years. The ex- 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 
 
 637 
 
 planation of this growth is that it arises from epithelium that has 
 undergone a change from the customary columnar to the squamous 
 form, in consequence of chronic endometritis. 
 
 Fig. 319.— Glandular cancer of the cervix uteri. 
 
 Cysts. — Small cysts of the wall of the uterus may be asso- 
 ciated with various forms of tumors, such as myofibromata ; and 
 a form of adenocystoma, probably originating from remnants of 
 the Wolffian duct, has been described. Dermoid cysts have been 
 occasionally observed. 
 
 PARASITES. 
 
 Echinococcus-cysts are sometimes met with, and a few cases of 
 supposed Cysticercus cellulosse have been described, though the 
 nature of the formations was uncertain. 
 
 THE OVARIES. 
 
 Development and Anatomic Considerations. — The 
 
 ovary and testis are developed from a primary indifferent sexual 
 gland, which is indistinguishable in the two sexes. This indiffer- 
 ent gland is formed on the ventro-mesial surface of the Wolffian 
 body by a localized thickening of the mesothelial elements. The 
 ovarian stroma is subsequently formed by ingrowths of the sur- 
 rounding mesoderm. The ovary consists of a stroma of peculiar 
 spindle-shaped connective-tissue cells. In the central or medullary 
 portion the tissue is highly vascular ; the peripheral or cortical 
 part contains abundant Graafian follicles in which the ova are de- 
 
638 TEXT-BOOK OF PATHOLOGY. 
 
 veloped. These follicles are formed from primary tubular inden- 
 tations of the cuboidal or columnar epithelium that covers the 
 organ. These indentations are the tubes of Pfliiger. After full 
 development of the ovary they are wanting, the greater part by 
 constriction of the deeper portions having formed Graafian folli- 
 cles. The paroophoron a vestigial structure, is the part of the 
 ovary at the hilum. It consists of connective tissue and blood- 
 vessels with a number of parallel tubes which are remnants of 
 the Wolffian body. The same tubules surrounded by connective 
 tissue extend outward between the layers of the broad ligament, 
 constituting the parovarium. Sometimes part of the Wolffian 
 duct remains patulous and constitutes the duct of Gartner. This 
 is the homologue of the vas deferens. 
 
 CONGENITAL ABNORMALITIES. 
 
 Occasional absence of one or both ovaries has been discovered 
 with other developmental defects, or independently. Hypoplasia 
 occurs in chlorosis, and occasionally in association with other con- 
 ditions. Sometimes supernumerary ovaries have been found. 
 The additional ovaries may be formed by division or by separa- 
 tion from one of the normal glands. 
 
 CHANGES IN POSITION. 
 
 More or less extensive dislocations of the ovaries may occur, 
 the most notable being that in which one of these organs descends 
 into a hernial sac, occupying either the inguinal or crural canal. 
 Dislocations resulting from pressure, adhesions, and the like are 
 frequent. 
 
 CIRCULATORY DISTURBANCES. 
 
 Active hyperemia, or congestion, may be either a physi- 
 ologic or pathologic condition. The former occurs during the 
 menstrual period, the latter in association with inflammation of 
 the neighboring structures or in the earlier periods of inflamma- 
 tion of the ovaries themselves. 
 
 Passive congestion is met with in chronic cardiac diseases, 
 and as a result of local obstructions to the circulation by tumors, 
 inflammatory adhesions, and the like. 
 
 Hemorrhage. — Small hemorrhages into the ovarian tissue are 
 very frequent. Their occurrence is usually sufficiently accounted 
 for when the functional activity of the organ is considered. At 
 each periodical ovulation a small follicle ruptures, to discharge the 
 contents containing the ovum. Generally there is a slight extrav- 
 asation of blood at such times, which is subsequently absorbed. 
 At the same time that the extravasation and absorption are taking 
 place the inner lining of the follicle proliferates somewhat, and 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 639 
 
 the cells then undergo fatty degeneration. The whole process 
 gives rise to a yellowish nodular formation, termed the corpus 
 luteum. Subsequently this is removed by absorption of the blood 
 and by degeneration and absorption of the proliferated cells 
 of the lining membrane, and a small scar alone remains. The 
 latter, especially when more than usually fibrous, is known as the 
 corpus fibrosum. This is commonly a little pigmented, in conse- 
 quence of the pre-existing extravasation of blood. The corpus 
 luteum, which is developed from a follicle formed at the time of 
 impregnation (corpus luteum of pregnancy), differs somewhat in 
 character. The epithelial proliferation is much more active, and 
 the wall of the follicle is intensely congested. Rapid involution 
 does not take place, the follicle often persisting for considerable 
 periods after the termination of pregnancy. 
 
 Exceptionally, considerable hemorrhages may take place into 
 the follicles, and small hemorrhagic cysts or cysts containing 
 blood-stained liquid may be formed. 
 
 INFLAMMATION. 
 
 Inflammation of the ovaries, or oophoritis, is generally 
 a secondary condition resulting from an extension of inflammation 
 from the neighboring reflections of the peritoneum, or from exten- 
 sion of infective processes along the Fallopian tube. The exten- 
 sion from the neighboring peritoneum, as well as from the uterus, 
 may be direct — that is, along the planes of tissue or through the 
 lymphatic or vascular channels. Primary oophoritis is probably 
 very rare. 
 
 The ovary becomes enlarged, and in the earlier stages is more 
 or less congested. Later the tissues become yellowish, either 
 uniformly or in scattered areas. Finally the process may termi- 
 nate in necrosis or abscess-formation. Such ovarian abscesses 
 may reach a considerable size, and break into any of the hollow 
 viscera near by or into the peritoneal cavity. In more favorable 
 cases there are only small collections of pus, and these may subse- 
 quently become inspissated. The most satisfactory of all termi- 
 nations is in complete resolution, or in induration {chronic 
 oophoritis). 
 
 Localized inflammations may sometimes occur about the folli- 
 cles. These may terminate in follicular abscesses, which either 
 discharge and lead to scar-formation, or become inspissated. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis. — Among the infectious diseases tuberculosis 
 alone is of importance. It may arise as a primary disease of the 
 ovaries, but much more frequently is secondary to inflammation 
 
640 TEXT-BOOK OF PATHOLOGY. 
 
 of the tubes or other parts of the genital tract. It may give rise 
 to the formation of small or large cheesy masses, showing a ten- 
 dency to softening with formation of tuberculous abscesses. The 
 ovaries may occasionally be the seat of miliary tuberculosis. 
 
 TUMORS. 
 
 The ovaries are frequent seats of tumors, both benign and 
 malignant. By far the largest proportion are cystic. 
 
 Connective-tissue Tumors. — Fibroma may occur as small 
 nodular growths, either single or multiple. In some cases the 
 tumors are of considerable size. Combinations of fibroma with 
 leiomyoma may also be met with ; these myofibromata resemble 
 those of the uterus. Occasionally fibrosarcoma is encountered. 
 
 Chondroma is a rare form of benign tumor. 
 
 Sarcoma may occur in the form of spindle-celled sarcoma, 
 fibrosarcoma, or more rarely as round-cell sarcoma. It appears 
 as rounded tumors with more or less pronounced encapsulation. 
 Degenerations, such as myxomatous, are not infrequent, and cystic 
 change may be occasioned by dilatation of the follicles. In some 
 cases proliferations of the Avails of the follicles constitute an im- 
 portant part of the growth. To such cases the name adenosarcoma 
 may be applied. Angiosarcomata and endotheliomata have 
 occasionally been described. 
 
 Cystic Tumors. — Of the cystic conditions of the ovary we 
 must distinguish the simple follicular cysts and the more important 
 myxoid or colloid cystomata and dermoid cysts. Of the cystomata 
 there are two varieties — the papillary and the glandular. 
 
 Follicular cysts are developed by distention of the Graafian 
 follicles with dropsical liquid. The ovary may be considerably 
 enlarged by cystic cavities, lined with epithelium and containing 
 clear watery liquid, or occasionally blood-tinged contents. Cysts 
 of this character are very common in cases of induration of the 
 ovary following oophoritis. 
 
 Colloid or Myxoid Cystomata. — Colloid or myxoid cystomata 
 present themselves as tumors of small or large size, having a 
 tendency to a multilocular cystic character. The cavities are filled 
 with a more or less gelatinous or mucoid liquid. Sometimes 
 hemorrhage takes place, and the contents are correspondingly 
 altered. Two subvarieties may be distinguished : the glandular 
 and the papillary. 
 
 Glandular cystomata are distinguished by the constant prolif- 
 eration of the epithelial elements in the form of acini. This occa- 
 sions a multilocular character, new cysts springing from the walls 
 of the original cavity or appearing within the substance of the pri- 
 mary tumor. The terms adenocystoma and cysto-adenoma are 
 appropriate. The tumor may present itself as a large, single, 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 641 
 
 rounded, cyst with insignificant projections of small cysts upon the 
 inner lining ; while in other cases there is found on section a uni- 
 form multilocular character. Microscopically the characteristic 
 feature of these tumors is the formation of regular gland-acini, 
 showing a single layer of epithelial cells, or at most a few layers 
 resting upon a basement-membrane. The stroma of the tumor is 
 composed of fibrous connective tissue, with some unstriped muscle- 
 fibers. The contents of the cysts have the mucoid or colloid char- 
 acter referred to, and chemically a substance is discovered that is 
 absent from simple follicular cysts of the ovary and is less abun- 
 dant in papillary cystomata. This substance is termed pseudo- 
 mucin or paralbumin, and is somewhat related to mucin. 
 Occasionally, when the cysts are old the contents may be quite 
 watery. 
 
 Cystomata soon destroy the ovary, the unaffected ovarian tissue 
 being spread out within the wall of the cyst. The tumor is 
 attached in the pelvis by a pedicle consisting of the broad liga- 
 ment and Fallopian tube, and often forms secondary inflammatory 
 adhesions to adjacent parts. 
 
 Glandular cystomata arise either from embryonal rests (Pfluger's 
 tubes), or from ingrowths of the surface-epithelium of the organ. 
 It is generally considered unlikely that they arise from Graafian 
 follicles. 
 
 Papillary Cystomata. — Papillary cysts occur in two forms, 
 the one closely resembling glandular cystoma in its general appear- 
 ance, the other presenting itself as a papillomatous condition of the 
 surface of the ovary. In the former, or papillary myxoid cysto- 
 mata, large cystic tumors are developed. On section through these 
 there is found a papillomatous or cystic proliferation of the lining 
 membrane, but the tendency to the formation of secondary cysts 
 is much less pronounced than in the glandular varieties, and the 
 fibrous stroma is less abundant. The secondary cysts in this 
 variety may be formed by fusion of the free ends of proliferat- 
 ing papilla?, or by myxomatous degenerations within the stroma 
 of the papillae. The liquid of the cysts resembles that of the 
 glandular form, but contains less pseudomucin, and is more fre- 
 quently hemorrhagic. On microscopic examination it is found 
 that the inner lining of the cyst and the papillary projections con- 
 sist of stratified ciliated epithelium. Calcareous bodies arranged 
 in a concentric fashion (psammoma-bodies) are frequently met 
 with in the stroma, as well as in the epithelium. The same 
 calcareous bodies are occasionally found in glandular cystomata. 
 
 The papillomatous ovarian tumors differ from the glandular in 
 being almost invariably bilateral (Fig. 320). Their origin has not 
 as yet been certainly determined, but it is probable that they origi- 
 nate from the paroophoron, a vestigial remnant of the parovarium. 
 Some have held that they may originate from the Graafian follicles, 
 
642 TEXT-BOOK OF PATHOLOGY. 
 
 or from ingrowths of the surface-epithelium. This is assuredly 
 not a frequent origin. 
 
 The surface-papillomata of the ovary present themselves as ir- 
 regular masses of a cauliflower appearance. The papillae of pro- 
 jections are covered with ciliated epithelium, as in the cystic form. 
 There is no essential difference in structure, and it is probable 
 
 Fig. 320.— Double papillomatous cyst of the ovary : the right cyst has ruyitured and is 
 turned inside out, showing a mass of papillomata ; papillomata have penetrated the wall 
 of thecyst ; the peritoneum has been infected, and a papillomatous growth appears on 
 the fundus uteri (Penrose). 
 
 that in most instances the superficial forms result from a rupture 
 of the cystic variety and the subsequent external proliferation. 
 
 The papillomatous cystomata and the surface-papillomata have 
 a marked tendency to carcinomatous transformation, and tend to 
 spread to the peritoneum, causing metastatic nodules in the 
 vicinity or throughout the entire abdomen. 
 
 Dermoid Cysts. — Dermoid cysts are frequently met with in the 
 ovary. They may occur as small nodules or as very large tumors, 
 and are usually unilateral. The larger ones substitute the ovarian 
 tissue completely ; less commonly they may be pedunculated, the 
 ovary in part remaining intact. Combinations with glandular 
 cystomata are not infrequent. 
 
 The dermoid cyst is a smooth-walled sac, the inner surface pre- 
 senting somewhat irregular projections and having more or less 
 pronounced characteristics of epidermal tissue. The cystic con- 
 tents are a putty-like material of grayish color, containing long, 
 blonde hairs and teeth, and sometimes ill-developed bone. The 
 grayish material consists of fatty detritus containing degenerated 
 epithelial cells, and usually abundant cholesterin-crystals. The 
 wall of the dermoid cyst, though usually in the main composed 
 of epidermal structure, may contain elements of the three blasto- 
 dermic layers. The dermoid cyst may occur in childhood, or even 
 in fetal life, but usually does not present itself till adult years. 
 
 The nature of the tumor has not been certainly determined, 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 
 
 643 
 
 but it is quite evident that it represents an attempt at the for- 
 mation of an organism. It has, therefore, been designated by- 
 some as a foetus infoetu. Others have looked upon it as the result 
 of a form of parthogenesis. 
 
 Secondary changes not infrequently occur. Inflammatory con- 
 ditions of the walls may occasion abscess. Sometimes the epithe- 
 lium proliferates actively, and the dermoid, in part or as a whole, 
 is converted into a carcinoma. 
 
 Carcinoma. — Carcinoma of the ovary may be a primary 
 growth of glandular character developing from the follicles, or it 
 may be of a mucous or colloid variety, when the ovarian tissue 
 becomes converted into a gelatinous mass. In the latter case the 
 tumor tends to spread to the adjacent peritoneum, and widespread 
 metastasis along this membrane may occur. 
 
 CYSTS OF THE PAROVARIUM. 
 
 Cysts of the parovarium may be considered in this place on 
 account of their clinical resemblance to ovarian cystomata (Fig. 
 321). They are distinguished, however, by their intraligamentous 
 
 Fig. 321.— Cyst of the parovarium : there is no distortion of the ovary ; the Fallopian tube 
 has been much elongated. 
 
 situation, by their almost invariably unilocular character, and 
 usually by their clearer and more serous liquid contents. The 
 
644 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 ovary is usually uninjured. The inner lining consists of ciliated 
 epithelium. 
 
 CYSTS OF KOBELT. 
 
 These are thin-walled, pedunculated cysts about the size of a 
 pea (Fig. 322). They are frequently met with, and are seated at 
 
 Fig. 322.— Fallopian tube, ovary, and parovarium : a, hydatid of Morgagni ; b, cyst of 
 Kobelt's tube ; c, Gartner's duct. 
 
 the side of the ovary. The wall is fibrous, the lining membrane 
 composed of cubical epithelium, and the contents a clear serous 
 liquid. The cyst results from distention of one of Kobelt's tubes 
 in the parovarium. 
 
 THE FALLOPIAN TUBES. 
 
 Development and Anatomy. — The tubes are formed from 
 the upper ends of Miiller's ducts. The lower ends of the ducts 
 fuse to form the uterus and vagina. Each tube is covered by a 
 peritoneal coat, and its walls consist mainly of longitudinal and 
 circular muscle-fibers. The mucosa is thrown into well-marked 
 longitudinal plications, which at the uterine end are further com- 
 plicated by secondary elevations. The epithelial lining consists 
 of columnar ciliated cells. 
 
 CONGENITAL ABNORMALITIES. 
 
 The tubes may be absent or may be defective. Congenital 
 atresia is occasionally observed. The tubes may be unusual in 
 length and may communicate with the uterus in abnormal situ- 
 ations. 
 
 CHANGES OF POSITION. 
 
 In dislocations of the ovaries the tubes are correspondingly dis- 
 located. Independent of displacements of the ovary, the tubes 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 645 
 
 may be distorted or pulled out of their usual position by inflam- 
 matory adhesions, and may thus be bent at sharp angles or bound 
 down in various malpositions. 
 
 STENOSIS. 
 
 Congenital stenosis of the tubes, or complete closure of the lu- 
 men, may affect the entire length of the tube or a limited portion, 
 principally near the middle. Acquired stenosis may result from 
 pre-existing disease of the tube itself, or from adhesions secondary 
 to localized peritonitis. The most frequent situation in these in- 
 stances is the abdominal or fimbriated end. A narrowing of the 
 lumen of the tube may be occasioned by angulation or by disloca- 
 tions. 
 
 DILATATION. 
 
 Dilatation on the proximal side of obstructions or stenosis is 
 frequent. The dilatation is more marked when inflammatory con- 
 ditions of the mucous membrane are present. The abdominal end 
 of the tube may enlarge so as to form a cyst of considerable size, 
 filled with serous or seromucous liquid, when the middle portion is 
 stenotic. When the lower end is obstructed the entire tube be- 
 comes dilated, and it frequently shows a tortuous and irregularly 
 pouched condition, due to its attachments to the broad ligament. 
 In such instances the mucous membrane is pushed inward at the 
 bends, and projects prominently into the lumen of the tube. 
 Secondary changes of the epithelial lining are not unusual in con- 
 sequence of the irritation of the retained secretions. The normal 
 epithelium may be wholly lost, and the lining may consist of squa- 
 mous epithelial cells. Purely inflammatory dilatations will be 
 referred to below. 
 
 CIRCULATORY DISTURBANCES. 
 
 Active hyperemia of the mucous membrane may be a part 
 of acute inflammations of the tubes, and is very frequently found 
 at the fimbriated extremity in association with peritonitis. The 
 mucous membrane is swollen and bright red in color. There may 
 be excess of mucous secretion. 
 
 Passive hyperemia occurs in conditions in which the gen- 
 eral venous circulation in the abdomen is impeded. 
 
 Hemorrhages into the tubes may occur physiologically during 
 the menstrual period, and sometimes considerable amounts of blood 
 are found under these circumstances. Small hemorrhages into 
 mucous membranes may occur in association with inflammations 
 of the tubes and in the course of some of the infectious diseases. 
 
 Hematoma of the tube, or the collection of blood in the 
 tube, results from stenosis of the lower end with accumulation 
 
646 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 of the menstrual discharges in the proximal portions. The blood 
 may remain in a more or less natural condition for a long time, 
 or may undergo secondary changes. Sometimes it discharges 
 through the abdominal end of the tube into the peritoneal 
 cavity, and leads to retro-uterine hematocele. 
 
 INFLAMMATIONS. 
 
 Inflammation of the tubes, or salpingitis, may be acute or 
 chronic. 
 
 Acute salpingitis presents itself in several forms, such as an 
 acute catarrhal and a suppurative form. In most cases the inflam- 
 
 I 
 
 X-: 
 
 
 Fig. 323.— Acute septic salpingitis : section about the middle of the tube (Beyea). 
 
 mation results from the entrance of irritants from the uterus, and 
 the tubal disease is secondary, therefore, to endometritis or to other 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 647 
 
 disease of the uterus. Among the micro-organisms discovered, 
 streptococci, staphylococci, the gonococcus, the Diplococcus pneu- 
 moniae, and the Bacillus coli communis may be mentioned. The 
 infective organisms may extend directly along the mucous mem- 
 brane, or more rarely may reach the tubes through the lymphatics. 
 In rare instances salpingitis may be secondary to local peritonitis. 
 Pathologic Anatomy. — In acute catarrhal salpingitis the mucous 
 membrane is swollen, hyperemic, infiltrated with round cells, and 
 covered with more or less abundant mucous secretion, which may 
 distend the tube considerably. In the later stages the secretion is 
 
 Fig. 324.— Chronic salpingitis : both Fallopian tubes are closed and adherent (Penrose). 
 
 apt to become mucopurulent. Interstitial inflammation, with 
 thickening of all of the layers of the tube-wall, is frequently a 
 secondary result. In acute suppurative salpingitis the walls of 
 the tube are infiltrated with round cells (Fig. 323), the mucous 
 surface may discharge abundant pus, and the tubes may become 
 distended with this exudate if the abdominal and uterine ends are 
 closed by the inflammatory process. This result, however, is less 
 frequent than in the case of chronic salpingitis. The mucous 
 membrane in these cases is intensely inflamed and often slightly 
 ulcerated upon the surface. Sometimes the distention is so great 
 that the tubes are converted into pus-sacs the size of an egg or a 
 small lemon. In case of acute suppurative or necrotic salpingitis 
 secondary to puerperal sepsis the mucous membrane may be covered 
 with a necrotic membrane ; the term diphtheritic salpingitis has 
 sometimes been applied to such a condition. 
 
 The exudates within the tube may remain for a long time with- 
 out change, or may undergo gradual inspissation, and sometimes 
 
648 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 even calcification occurs. When ulcers of the mucous membranes 
 have formed, rupture of the tube and consecutive peritonitis may 
 occur, especially during; straining efforts, as in labor. Acute local 
 or general peritonitis more frequently results from discharge of 
 infective matter from the abdominal end of the tube. 
 
 Microscopically, in all forms of salpingitis extensive round-cell 
 infiltration is observed in all of the layers of the tubes. 
 
 Chronic salpingitis, as a rule, results from the continuation 
 of an acute form. The wall of the tube becomes thickened and 
 the muscular layer is often hyperplastic. Proliferative changes in 
 the mucous membrane are not unusual, and may lead to actual 
 polypoid outgrowths. Occasionally small follicular formations 
 are seen in the mucosa ; but ulcerations of the mucous membrane 
 are infrequent. When the inflammation extends to the serous coat 
 inflammatory adhesions are frequently formed (Fig. 324), and may 
 bind the tube firmly to adjacent parts and occasion great conges- 
 
 Fig. 326.— Hydrosalpinx, showing complete inversion of the fimbriae (Penrose). 
 
 tion or distortion. Very often the abdominal end of the tube be- 
 comes occluded by inflammatory adhesions, or by inversion and 
 agglutination of the fimbria?. At the same time the swelling of 
 the mucosa obstructs the uterine end, and in consequence the tube 
 becomes a closed pouch which fills with pus (pyosalpinx), sero- 
 purulent liquid {hydrosalpinx) (Fig. 325), or hemorrhagic fluid 
 (hematosalpinx). Intercurrent acute salpingitis frequently takes 
 place in cases of chronic tubal disease. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis of the tubes may be either primary or second- 
 ary, and is probably much more frequent than has been supposed. 
 Secondary tuberculosis may occur in the miliary form in associa- 
 tion with tuberculosis of the peritoneum or with general tubercu- 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 649 
 
 losis. In other cases secondary tuberculosis leads to caseous and 
 fibrous changes in the walls of the tubes. The latter become 
 greatly thickened, and microscopically there is found a diffuse 
 cellular infiltration with scattered giant cells and here and there 
 definite tubercles. The fibrous changes progress more slowly, 
 and may eventually become the conspicuous feature. Primary 
 tuberculous salpingitis is similar in its appearance to the form 
 just described. The infection may occur through entrance of the 
 organisms at the uterine end of the tube, and certain observations 
 would indicate that pre-existing gonorrheal salpingitis predisposes 
 to secondary tuberculous infection. There are usually considerable 
 adhesions of the tubes to the neighboring organs, and particularly 
 to the ovary, and secondary miliary tuberculosis of the peritoneum 
 
 Fig. 326.— Tuberculosis of the Fallopian tubes. The disease has extended to the perito- 
 neum, which is covered with tubercles (Penrose). 
 
 is frequently observed (Fig. 326). The lumen of the tube is filled 
 with purulent liquid, and sometimes certain portions, particularly 
 the abdominal end, may be greatly distended, forming cysts con- 
 taining puriform liquid. 
 
 Syphilis has been observed in the form of gummata, and also 
 in the form of diffuse sclerosis, in cases of congenital origin. 
 
 TUMORS. 
 
 Fibromata and fibromyomata are met with in the external 
 walls of the tubes as nodular masses. They frequently undergo 
 secondary calcification. lipoma occurs in the external coat 
 lying between the layers of the broad ligament. 
 
 Papillomatous elevations of the mucous membrane are 
 quite frequent, and in some cases a transformation of papilloma 
 to carcinoma takes place. Probably most instances of primary 
 
650 TEXT-BOOK OF PATHOLOGY. 
 
 carcinoma of the Fallopian tubes have this origin. Secondary 
 carcinoma may result from extension of uterine cancer. 
 
 Sarcoma occurs in various forms, and syncytioma malig- 
 num may aifect the tubes after tubal pregnancy. 
 
 Cysts of the tubes are usually the result of localized distentions 
 of the lumen in consequence of obstructions. Small cystic for- 
 mations of obscure origin are sometimes found in the peritoneal 
 covering of the tubes and along the attachment of the broad liga- 
 ment. Their contents may be colloid or serous. 
 
 The hydatids of Morgagrni are small cystic formations about 
 the size of a pea, hanging by a long pedicle at the fimbriated end 
 of the tube. They are probably the result of distention of the 
 closed end of Midler's canal. 
 
 Tubo-ovarian cysts are formed by distention of the abdominal 
 end of the tubes when the fimbriated extremities are attached to 
 the ovary, or in other cases may be the result of rupture of fol- 
 licular cysts of the ovaries themselves into the abdominal eud of 
 the tubes. 
 
 EXTRAUTERINE PREGNANCY. 
 
 Htiology. — Any obstruction to the downward migration of the 
 ovum may lead to its retention and development in abnormal 
 situations. The actual cause is usually difficult to determine. 
 Impregnation possibly frequently takes place in the Fallopian 
 tube ; but unless some obstruction arrests the passage of the ovum 
 into the uterus, normal uterine gestation takes place. Swelling or 
 rapid decidua-formation of the mucosa of the tubes may be one 
 of the causes, and chronic salpingitis, by causing destruction of 
 the cilia of the epithelial cells, and thickening and adhesions of 
 the avails of the tubes, acts in a similar manner. Any other form 
 of obstruction, as by tumors or external compression, may be 
 included among the etiologic factors. 
 
 Varieties and Pathologic Anatomy. — All cases of extra- 
 uterine pregnancy are probably in the beginning tubal pregnancies. 
 This condition may occur in any part of the tube. It is rarely 
 found at the uterine end, but may occur there in that part of the 
 tube which is embedded in the wall of the uterus. The term in- 
 terstitial pregnancy is applied to this form. 
 
 Tubal Pregnancy. — The changes which occur in the tube are 
 analogous to those met with in the uterus. The same forms of 
 membranes and decidual are developed, and a placenta develops, 
 as in the uterus. The muscularis of the tube may hypertrophy 
 somewhat ; but in the end the increasing size of the contained 
 ovum leads to thinning and stretching of the walls of the tube. 
 It is an interesting fact that the mucous membrane of the uterus 
 forms a decidua of more or less complete development in cases of 
 extra-uterine pregnancy (Fig. 327). 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 651 
 
 Among the terminations of tubal pregnancy are the following : 
 
 1. The tube may rupture into the broad ligament, into the 
 
 peritoneal cavity, or, in cases of interstitial pregnancy, into the 
 
 uterus. As a result of these accidents hematoma of the broad 
 
 ligament, hematocele, and local or general peritonitis may occur, 
 
 .CHOMOflia VJLLI 
 
 Fig. 327.— Tubal pregnancy, removed before rupture. The opening that has been cut in 
 the tube shows the chorionic villi (Penrose). 
 
 or sudden death may take place as a direct result of the hemor- 
 rhage. Sudden death from collapse is more frequently due to 
 this cause than has generally been supposed. 
 
 2. The ovum may be destroyed in the tube and the gestation 
 cease. In this case the fetus subsequently undergoes various 
 changes. More or less degeneration usually occurs, and shapeless 
 masses or adipocere may result. In other cases calcification of the 
 remnants of the disorganized fetus leads to the formation of a 
 lithopedion. This may take place within the tube, or after rupture 
 of the tube and enclosure of the fetus in a sac formed by circum- 
 scribing peritonitis. 
 
 3. Premature discharge of the ovum (tubal abortion) may occur, 
 and the gestation may terminate without serious results. In other 
 cases, however, it leads to a discharge of the blood through the 
 unclosed abdominal ostium of the tube into the peritoneal cavity ; 
 and hematocele, peritonitis, or sudden death from hemorrhage may 
 occur. 
 
 4. In very exceptional cases tubal pregnancy goes on to full 
 term without rupture of the tube. Spurious labor may then 
 
652 TEXT-BOOK OF PATHOLOGY. 
 
 come on, the fetus, as a rule, perishing. The liquor amnii is 
 absorbed, and degenerative changes leading to mummification, or 
 the formation of adipocere or of a lithopedion, take place. The 
 mummified fetus may remain for many years. Very rarely after 
 spurious labor the fetus is discharged into the peritoneal cavity, 
 and may be delivered through the rectum or in other ways. 
 
 Abdominal Pregnancy. — This term is given to cases in which 
 the tube has ruptured and the ovum, enclosed in its membranes, 
 escapes into some part of the abdominal cavity, where it remains 
 free or surrounded by adhesions the result of peritonitis. The 
 placenta, as a rule, remains in the tube ; but it may also establish 
 secondary attachments to parts of the peritoneum. Primary 
 abdominal pregnancy — that is, impregnation and gestation in the 
 abdominal cavity — does not seem ever to occur. 
 
 THE VAGINA. 
 
 PROLAPSE OF THE VAGINAL WALLS. 
 
 Prolapse of the anterior or posterior wall of the vagina may be 
 due to abnormal relaxation of the tissues, or it may be secondary 
 to prolapse of the uterus and similar conditions that press the 
 vaginal walls downward. Not infrequently the posterior wall of 
 the bladder is dragged downward with the anterior wall of the 
 vagina, and vaginal ci/stoeele results. Similarly the anterior wall 
 of the rectum may be carried downward with the posterior wall 
 of the vagina ; this is termed vaginal rectoeele. 
 
 STENOSIS OF THE VAOINA. 
 
 Congenital stenosis is rare. More frequently the lumen of the 
 vagina is narrowed by contraction of cicatricial tissues formed in 
 inflammatory diseases of the walls, or by adhesion of the opposite 
 surfaces following ulcerations. Complete occlusion may occur in 
 the latter form of cases, especially in old women. 
 
 WOUNDS AND FISTUL/E. 
 
 Injuries to the vaginal walls may be caused by the insertion 
 of sharp bodies or instruments, or by coitus. Much more fre- 
 quently injuries are due to stretching or pressure during labor. 
 Superficial lacerations caused by overdistention are frequent, but 
 more extensive injuries may be caused by prolonged pressure of 
 the infant's head or by instruments used in delivery. In such 
 cases infection and phlegmonous inflammation are prone to occur, 
 and vesico-vaginal, urethro-vaginal, or recto-vaginal fistula? are 
 sometimes the result. The urine or feces may be discharged 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 653 
 
 through the vagina, and often cause secondary inflammations of 
 the entire vaginal mucosa. 
 
 Similar fistulse may be due to ulcerative processes of other 
 kinds, to necrosis of carcinomata of the vagina, or to diseases of 
 the bladder or rectum. 
 
 CIRCULATORY DISTURBANCES. 
 
 Active hyperemia occurs in the early stages of inflamma- 
 tion. The mucous membrane is light red in color and a little 
 swollen. 
 
 Passive hyperemia is frequent in pregnancy ; and occurs in 
 consequence of pressure due to other causes, such as uterine 
 tumors and the like. The mucosa becomes swollen and edema- 
 tous, and may be moist from increased secretions. 
 
 Hemorrhages into the vaginal walls are most frequently due 
 to traumatism. Inflammation and ulceration may result from the 
 hemorrhagic extravasation. 
 
 INFLAMMATIONS. 
 
 Acute Catarrhal Inflammation, Vaginitis, or Colpitis. 
 
 — This condition is frequently due to gonorrheal infection, but 
 may result from other causes, such as mechanical and chemical 
 irritants, or in young girls from the invasion of the Oxyuris 
 vermicularis from the rectum. The mucous membrane is usu- 
 ally deeply congested, and the surface is covered with muco- 
 purulent exudate. In gonorrheal cases the cervix uteri and 
 urethra are, as a rule, coincidently affected. 
 
 Exfoliative Vaginitis. — In rare cases of intense catarrhal 
 vaginitis, in which the deeper layers of the mucosa are principally 
 involved, membranous formations, consisting of parts of the super- 
 ficial epithelial layers, may be discharged. 
 
 Pseudomembranous vaginitis may occur in association 
 with various infectious diseases, such as pneumonia, pyemia, 
 cholera, etc. ; but it is more frequently the result of pressure- 
 necrosis and infection occurring during labor, and is one of the 
 lesions of puerperal sepsis. The surface of the vagina is more or 
 less extensively covered with a dirty and exfoliating pseudomem- 
 brane. After discharge of the latter ulcerations are often formed. 
 Extensive necrosis of the vaginal walls may occasion great de- 
 struction, and in some instances phlegmonous inflammations of 
 the perivaginal tissues may cause separation of the mucosa. 
 
 Chronic catarrhal vaginitis may be the continuation of an 
 acute inflammation, or may occur in a gradual manner in women 
 reduced in vitality. The mucosa usually presents appearances 
 somewhat like those of acute cases, though the congestion is less 
 
654 TEXT-BOOK OF PATHOLOGY. 
 
 marked. Abundant mucopurulent or mucous discharge (leucor- 
 rhea) may be present. Erosions of superficial epithelium and 
 enlargements of the lymphoid follicles are sometimes observed. 
 In long-standing cases the surface may be smooth and the entire 
 mucosa somewhat indurated. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis may occur in the form of ulcers associated with 
 uterine tuberculosis, or in the form of lupus from extension of 
 the latter from the vulva. 
 
 Syphilis. — Chancers may occur in any part of the vagina, 
 and circumscribed (gummatous) or diffuse infiltrations have been 
 described. 
 
 TUMORS. 
 
 Fibroma and myofibroma may arise in the muscular layer 
 of the vaginal wall, and may project as nodular masses or assume 
 a polypoid form. 
 
 Sarcoma may occur as a circumscribed mass, but more com- 
 monly as diffuse infiltration which tends to ulcerate. 
 
 Papillomata are not infrequent, in the form of small warts 
 or as considerably elevated condylomata. 
 
 Carcinoma of the vagina is most frequently secondary to 
 cervical cancer. Similarly it may follow cancer of the vulva. 
 Primary carcinoma of the vagina is rare. It occurs in the form 
 of a circumscribed villous projection. 
 
 Cysts of the vaginal walls vary in size and number. Fre- 
 quently they are multiple, and the size ranges from scarcely dis- 
 coverable cavities to those the size of an egg. The contents are 
 usually serous and colorless, or less frequently of brownish color. 
 In some instances a flat epithelial lining has been discovered. 
 The origin of these cysts is probably variable. Some seem to 
 arise from remnants of the lower end of the Wolffian duct; 
 others are probably lymphangiectatic. The multiple small cysts 
 sometimes occurring in pregnancy are due to follicular distentions, 
 or to small hemorrhages with subsequent cystic change. 
 
 THE DECIDUA, PLACENTA, AND FETAL MEMBRANES. 
 
 Anatomic Considerations. — The fetus is enclosed within 
 a delicate fibrous membrane, the amnion, and this is covered with 
 a second membrane, the chorion. After the deposit of the ovum 
 in the uterus the mucous membrane of the latter undergoes a form 
 of hyperplasia, in which the uterine glands and the blood-vesselfl 
 take part conspicuously, and thus the organ becomes lined with a 
 thickened mucosa. The latter is termed the decidua vera. A 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 655 
 
 reflection from this covers the fetus enclosed in its membranes, 
 the reflection being known as the decidua reflexa. At about the 
 fifth month of development the decidua reflexa and the decidua 
 vera unite and fuse. The portion of the decidua vera at which 
 the placenta is subsequently located is termed the decidua serotina. 
 In this portion the vascular system is particularly marked, and is 
 composed of large venous sinuses with thin walls. The fetal cho- 
 rion carries on its outer surface numerous small projections, or 
 villi. In the region of the decidua serotina these villi undergo 
 marked hyperplasia and bury themselves between the venous 
 sinuses of the decidua. At the junction of the villi and the 
 decidua two layers of cells are developed. The first, immediately 
 covering the villi, consists of cubical epithelial cells (Langhan's 
 cells). Outside of these, and uniting the villi with the maternal 
 tissue, is a layer of clear protoplasmic material containing large 
 nuclei. This has the appearance of nucleated protoplasm, rather 
 than that of collections of cells of definite outline. This proto- 
 plasmic layer, syncytium, is probably, like Langhan's cells, derived 
 from the covering of the chorionic villi though some authorities 
 contend that it is maternal in origin. 
 
 ABNORMALITIES OF DEVELOPMENT. 
 
 The Placenta. — Abnormal smallness of the placenta, or 
 hypoplasia, and abnormal largeness are occasionally observed. 
 More frequently an adventitious placenta (placenta succenturiata) 
 may be attached to the main placenta, or may lie near it. Abnor- 
 mal location of the placenta at or near the neck of the uterus 
 (placenta prcevia) is an important condition, from its liability to 
 cause hemorrhage and miscarriage. 
 
 The Umbilical Cord. — Occasionally the cord is divided near 
 its placental end into two or more branches. The placenta may 
 be correspondingly divided, or single. The attachment to the 
 placenta may be marginal instead of central, and sometimes the 
 blood-vessels spread out into a broad marginal attachment, with 
 absence of their gelatinous covering. The latter is termed vela- 
 mentous insertion. 
 
 Abnormalities of the blood-vessels, such as branching, a single 
 artery, two veins, etc., are unimportant. 
 
 Twists and knots of the cord are frequent, and may strangulate 
 the cord and stop the circulation, causing death of the fetus. 
 
 Thickening of the intima of the umbilical vein and of the ad- 
 ventitia of the arteries is probably syphilitic in nature. 
 
 CIRCULATORY DISTURBANCES. 
 
 Hydrorrhcea gravidarum is a condition in which abundant 
 serous or somewhat turbid liquid is secreted from the deciduse. 
 
656 TEXT-BOOK OF PATHOLOGY. 
 
 The condition occurs in women suffering from general anemia, but 
 is probably due to local conditions within the uterus. Abortion or 
 miscarriage is not unusual. 
 
 Hemorrhages from the decidua or into the decidua and pla- 
 centa are not infrequent. Hemorrhages from the surface may be 
 due to preceding decidual disease, or may be obscure in origin. 
 Large hemorrhages may cause rapid discharge of the uterine con- 
 tents. In cases of that abnormal position of the placenta called 
 placenta praevia hemorrhages are frequent. 
 
 Fleshy moles is the term used to designate formations in the 
 deciduse and placenta resulting from gradual hemorrhage and 
 destruction of the ovum. The hemorrhage takes place in the 
 decidua, and then extends between the chorionic villi into the fetal 
 membranes, which may be more or less extensively torn apart. 
 Irregular masses of clotted blood attached to the placental site and 
 to the chorion are discovered. The amniotic cavity contains vis- 
 cid fluid and the ovum is more or less completely disorganized. 
 Sometimes no recognizable remnants can be found. The moles 
 may be retained a long time, and may undergo secondary calca- 
 reous infiltration. Usually they are soon discharged. 
 
 Placental Infarcts.— This term is applied to light-colored, 
 more or less indurated areas met with in the placenta, deciduse, 
 and sometimes in the chorion. The nature of these formations is 
 still somewhat uncertain. They are composed of fibrin, of reticu- 
 lated or granular character, with occasional areas of softening and 
 hemorrhagic accumulations, and are not rarely surrounded by a zone 
 of cellular infiltration. Some of these " white infarcts " may be 
 only an exaggeration of the normal coagulation-necrosis occurring 
 toward the end of pregnancy. When they are extensive it is very 
 probable that they represent results of disturbances of circulation 
 caused by thickening of the walls of the blood-vessels. 
 
 INFLAMMATION. 
 
 Inflammations of the placenta {placentitis), of the chorion villi, 
 or of the decidua (endometritis decidualis) may occur in association 
 with preceding diseases of the uterus, and especially in cases of 
 syphilis of the mother or fetus. The inflammation takes the form 
 of cellular infiltration and induration. This may begin in the 
 decidua and extend to the placenta, and may be of a diffuse or 
 circumscribed character. The villi of the placenta may be greatly 
 compressed by the inflammatory tissue, and may suffer fatty de- 
 generation and atrophy. In other cases the inflammatory changes 
 are most pronounced in the walls of the blood-vessels and around 
 the vessels of the chorion and umbilical cord. Nodular thickening 
 or diffuse induration results, the latter especially in cases in which 
 coincident involvement of the chorionic villi has occurred. 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 657 
 
 Diffuse hyperplasia of the decidua is sometimes described as 
 endometritis decidualis. The inflammatory nature of sucli cases, 
 however, is uncertain. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis of the placenta was suspected as a possible con- 
 dition long before positive demonstrations were made. In recent 
 years, however, a number of undoubted cases have been described. 
 Microscopically there may be but little change in the appearance 
 of the affected parts. 
 
 Small tubercles, containing abundant giant cells and tubercle 
 bacilli, first appear in the decidua scrotina, and later invade the 
 placental and chorionic tissues between the villi. The epithelial 
 covering of the villi undergoes hyperplasia, forming collections of 
 large cells. In the later stages of the process caseous necrosis of 
 the tubercular structures takes place, and the villi themselves suf- 
 fer invasion and degeneration. Their blood-vessels are frequently 
 occluded by hyaline thrombosis and proliferation of the endothelial 
 lining. Tubercle bacilli have been demonstrated in the vessels of 
 the fetal side of the placenta, though less frequently and abund- 
 antly than in the maternal vessels. 
 
 Syphilis of the placenta may take the form of a diffuse hyper- 
 plasia, or of a nodular or gummatous process. The placenta is 
 enlarged, indurated, and heavy; it is light colored in localized 
 areas or diffusely. Microscopically, cellular proliferation spring- 
 ing from the adventitia of the blood-vessels is the characteristic 
 feature. The epithelial cells covering the villi may proliferate, 
 and fatty degeneration of the body of the villi is not infrequent. 
 The chorion and amnion may be diffusely thickened. The syphi- 
 litic nature of cases conforming with the above description is often 
 doubtful, as is also the nature of some of the cases of placentitis 
 that are often described as syphilitic. 
 
 HYPERPLASIA. 
 
 Occasionally diffuse or circumscribed thickening of the decidua? 
 occurs in association with chronic metritis ; the term endometritis 
 decidualis is applied to this condition (see Inflammation). 
 
 Placental Polyps. — Portions of the decidua, and especially 
 the placenta, retained in the uterus, may remain firmly attached 
 and may undergo subsequent proliferative change, forming poly- 
 poid tumors of adenomatous structure. These are particularly 
 frequent after abortion. 
 
 Destructive Placental Polyps. — Like the preceding, these 
 originate in retained portions of the placenta, but differ in the 
 more active proliferative changes that take place. On the uterine 
 surface they are covered with fibrin and blood-clots, and at their 
 
658 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 attachments are composed of variously formed cells, including 
 large epithelium-like cells enclosed in a vascular stroma. The 
 growth may involve the uterine tissues to a considerable extent. 
 Its nature is obscure in some particulars, but resembles that of the 
 syncytioma. 
 
 Hydatid moles present themselves as rounded, rather trans- 
 lucent bodies hanging by their pedicles to the outer surface of the 
 chorion, and often attached one to another in clusters, resembling 
 a bunch of grapes. Microscopically they are found to be composed 
 of myxomatous or more or less edematous fibrous tissue containing 
 few cells and free nuclei, and covered in the outer surface by epi- 
 thelial cells (Fig. 328). The nature of the hydatid mole has been 
 
 % fo v 'k?': r - 
 
 
 
 ^l'^,3^#SS;ffiS : 4f 
 
 Fig. 328.— Section of a hydatid mole. 
 
 the subject of some controversy. Yirchow taught that they are 
 simply myxomatous hypertrophied chorionic villi. More recent 
 investigators have found evidences of active hyperplasia of the 
 superficial epithelium of the chorion villi, with secondary degen- 
 eration, edema, and necrosis. This accounts for the fact that 
 sometimes the moles extend deeply into the decidua, and even 
 into or through the muscular wall of the uterus. 
 
 Hydatid moles are especially met with in women suffering from 
 chronic constitutional diseases (nephritis, anemia) and in those be- 
 coming pregnant late in life. Endometritis seems to bear some 
 relation, though the disease is evidently one of the fetal rather 
 than maternal tissues. This is shown by the limited extent of the 
 disease in some cases, and by the fact that in twin pregnancy the 
 membranes of only one of the fetuses may be affected. When the 
 disease is extensive death of the fetus usually results, and the 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 659 
 
 moles are discharged in the form above described, or enclosed in 
 clotted blood. 
 
 Syncytioma Malignum. — The nature and peculiarities of 
 this condition have been sufficiently described (see page 155). 
 
 THE VULVA. 
 
 WOUNDS. 
 
 Injuries of the vulva frequently occur during labor. Lacera- 
 tion of the fourchette is very common, and in a considerable pro- 
 portion of cases more extensive tears extending into the perineal 
 body, and sometimes through this into the rectum, are observed. 
 Prolonged pressure and contusion during labor may occasion 
 hemorrhages into the tissues of the vulva. 
 
 CIRCULATORY DISTURBANCES. 
 
 Active hyperemia is met with in acute inflammations. 
 
 Passive hyperemia and edema occur in conditions in which 
 there is general venous stasis, as in cardiac or pulmonary diseases. 
 They are also met with in pregnancy. The vulva is dark red in 
 color, sometimes cyanotic ; the subcutaneous and submucous tis- 
 sues become edematous, and in consequence the labia majora may 
 swell enormously. 
 
 Hematoma of the vulva is caused by compression and contu- 
 sion of the vulva during parturition, or less frequently at other 
 times. Varicosity of the veins is a predisposing cause of import- 
 ance. Considerable masses of blood (" thrombi ") accumulate in 
 the submucous tissues of the vulva and vagina. These may be 
 subsequently absorbed, or they may discharge through the skin in 
 consequence of superficial ulcerations and ruptures. Infection of 
 the thrombus may cause abscess of the labia or other affected 
 parts. 
 
 INFLAMMATION. 
 
 Acute catarrhal inflammation results from the same causes 
 as occasion acute vaginitis. The pathologic appearances are, in 
 general, the same, though edematous swelling is likely to be more 
 marked. Distention of the glands of Bartholin and secondary 
 abscess-formation in these glands are common conditions in 
 gonorrheal vulvitis. 
 
 Chronic inflammation sometimes follows acute vulvitis. 
 Considerable hyperplasia of the mucosa is sometimes the result. 
 Erosions and ulcerations are less frequent. 
 
 Phlegmonous inflammation, or abscess, of the sub- 
 mucous tissue of the labia majora sometimes results from exten- 
 
660 TEXT-BOOK OF PATHOLOGY. 
 
 sion of a similar process in the adjacent parts, or may be the 
 direct result of injuries and hematoma, with secondary infection. 
 
 INFECTIOUS DISEASES. 
 
 Diphtheria sometimes attacks the vulva, especially in puer- 
 peral women. The pathologic conditions are similar to those 
 observed in other mucous membranes. 
 
 Tuberculosis may occur in the form of lupus. The lesions 
 are irregular ulcers with elevated edges and more or less necrotic 
 bases. 
 
 Syphilis. — Chancers are met with on the sides of the labia 
 and elsewhere. 
 
 Chaucroids occur in the same situations as chancers. Very 
 often opposite sides of the vulva are involved by attrition. 
 
 Gangrene of the vulva may be the consequence of severe 
 contusions or inflammations occurring in the course of various 
 infectious diseases. 
 
 TUMORS. 
 
 Fibroma, fibromyxoma, and myofibroma are occasion- 
 ally met with as nodular tumors or polyps arising from the labia 
 majora. I^ipoma and sarcoma may present a similar macro- 
 scopic appearance. All of these growths are rare. 
 
 Elephantiasis vulvae is a not infrequent affection, especially 
 in eastern and tropical countries. It may be due to congenital 
 dilatations of the lymphatic channels, or to lymphangiomatous 
 tumor-growths. More frequently elephantiasis is caused by 
 inflammatory conditions that occasion obstruction to the flow of 
 the lymph. In some instances the etiology is very obscure. 
 
 Pathologically, elephantiasis consists of a thickening of the 
 subcutaneous connective tissue, with more or less involvement of 
 the skin as well. The disease may begin in the clitoris, or in one 
 or other of the labia, and may be confined to the part primarily 
 affected, or may extend to other parts. The affected portions are 
 tough and edematous ; the skin is tightly bound to the subcuta- 
 neous tissue. The surface may be irregularly elevated, but in 
 other cases is smooth. Superficial ulcers may occur, and some- 
 times the dilated lymph-channels communicate with the surface, 
 discharging lymph ( lymph orrhea). 
 
 Papillomatous tumors are not infrequent in syphilitic 
 women in the form of elevated condylomata. A somewhat 
 analogous condition of obscure etiology is that termed caruncle. 
 It presents itself as a papillomatous and highly vascular elevation 
 at the meatus of the urethra. t 
 
 Adenoma arising from the glands of Bartholin has been 
 described. 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 661 
 
 Carcinoma is uncommon. It most frequently arises from the 
 clitoris, but may affect any portion. Glandular cancer may begin 
 in Bartholin's glands. 
 
 Cysts are quite frequent. Small retention-cysts, containing 
 pultaceous (atheromatous) matter, are sometimes met with in the 
 labia majora. Larger cysts, containing serous or somewhat blood- 
 stained liquid, may result from hematomata, or may be lymphan- 
 giomatous in origin. Hydrocele of the canal of Nuck has the 
 superficial appearances of a cyst of the labia. Retention-cysts of 
 Bartholin's glands have been referred to above. 
 
 THE PENIS AND SCROTUM. 
 
 CONGENITAL ABNORMALITIES. 
 
 Absence of the penis is rarely observed ; more frequently it is 
 abnormally small, resembling the clitoris of the female. Occasion- 
 ally the organ is doubled, each half containing a duct, one for the 
 discharge of urine, the other for seminal fluid. 
 
 Hypospadias is the condition in which the urethra terminates 
 in an orifice on the under surface of the penis, in the pendulous 
 portion or at the bulb, or occasionally at the root of the scrotum 
 or in the perineum. Epispadias is a less frequent condition ; the 
 urethral orifice in this case is found upon the dorsal side of the 
 organ. Excessive length of the prepuce is a frequent abnormality ; 
 there may be associated with this stenosis of the preputial opening, 
 so that the glans penis cannot be exposed (phimosis). 
 
 INFLAMMATION. 
 
 Inflammation of the mucous membrane of the glans 
 penis (balanitis) and of the prepuce (posthitis) is not infrequent. 
 Among the more frequent causes are uncleanliness, with decompo- 
 sition of smegma retained beneath the prepuce, irritation by the 
 urine in cystitis or other inflammatory diseases, gonorrheal infec- 
 tion, and chancroids. The mucous membrane becomes swollen 
 and red, and considerable purulent exudate may be discharged. 
 Edematous swelling of the prepuce is frequent, and may cause 
 inability to retract the prepuce over the glans (phimosis). In other 
 cases the prepuce, previously drawn back, becomes so tensely 
 swollen that it cannot be pushed forward to its normal position 
 ( paraphimosis). 
 
 In catarrhal inflammation of the prepuce there may be associ- 
 ated retention-cysts of the mucous glands. The cysts may rupture, 
 causing small ulcerations. 
 
 Inflammation of the cavernous bodies may result from 
 traumatism, or from extension of gonorrheal urethritis, and may 
 sometimes occur in infectious diseases, such as small-pox, pyemia, 
 
662 TEXT-BOOK OF PATHOLOGY. 
 
 etc. The penis swells considerably, and abscesses or diffuse puru- 
 lent infiltration may result. In traumatic cases with hemorrhagic 
 exudation necrosis or gangrene may result. In case of favorable 
 termination after severe inflammations cicatrices may be formed. 
 
 INFECTIOUS DISEASES. 
 
 Syphilitic chancres and soft chancre or chancroid are 
 
 frequently located upon the prepuce or its frenum, or upon the 
 glans penis (the lesions are described in Part I.). 
 
 Tuberculosis is a rare condition in this situation. It has 
 been met with in the form of necrotic ulcerations. It is very 
 likely that direct infection of the penis may occur during coitus 
 with a woman Avho has genital tuberculosis. 
 
 TUMORS. 
 
 Papilloma, or condyloma acuminatum, is not infrequent 
 on the glans penis and prepuce. Sometimes it has a distinctly 
 inflammatory origin, occurring in association with gonorrhea, 
 syphilis, or other forms of local irritation ; in other cases it origi- 
 nates without discoverable cause. There are usually several or 
 many warty elevations, and occasionally a mass of warts is 
 aggregated in a cauliflower fashion. Microscopically, condy- 
 lomata are composed of a stroma of vascular connective tissue 
 covered with squamous epithelium. The cauliflower-form may be 
 distinguished from epithelioma by observing that the mucous mem- 
 brane is not infiltrated and is movable upon the underlying tissues. 
 
 Carcinoma (epithelioma) of the penis may arise from the 
 glans or from the prepuce. It may present itself as an infiltrating 
 growth with a tendency to ulceration, or as a papillomatous, cauli- 
 flower-like growth. In the latter case it is probable that the pri- 
 mary growth was papillomatous, with secondary carcinomatous 
 association, or that the original tumor was carcinomatous, followed 
 by papillomatous outgrowths. Considerable destruction of the 
 glans penis may occur, and metastatic nodules are frequently 
 formed in the inguinal glands. 
 
 Epithelioma of the scrotum is comparatively frequent in chim- 
 ney-sweeps and paraffin-workers. 
 
 Elephantiasis of the scrotum is a common disease of the 
 East. The scrotum may be enormously enlarged. Some cases 
 are due to filariasis ; in other cases filarise cannot be demonstrated. 
 Somewhat similar thickening of the prepuce is a rare condition. 
 
 Cysts. — Small cysts, due to occlusion of the glands of the 
 mucous membrane and of the skin, are occasionally met with un- 
 der the prepuce and in the scrotum. Dermoid cysts of the scrotum 
 are occasionally observed. 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 663 
 
 I,ipomata, angiomata, and fibromata are rare forms of 
 tumors of the penis. 
 
 Concretions beneath the prepuce result from phimosis with 
 retention of the smegma. Sometimes they increase by constant 
 additions until they reach considerable size (200 g.). In one case 
 under my observation gouty tophi in the prepuce grew to the size 
 of a small lemon. 
 
 INJURIES OF THE PENIS. 
 
 Direct traumatism may occasion serious laceration of the cor- 
 pora cavernosa, especially when the penis is erect at the time of 
 injury. Considerable hemorrhagic extravasation may occur, and 
 inflammation or even necrosis and gangrene may ensue. Fracture 
 of the penis is a term applied to rupture of the fibrous capsule of 
 the cavernous bodies. Both this and less extensive lacerations 
 occasion great hemorrhagic swelling, with subsequent inflamma- 
 tion or necrosis. Injuries to the penis may cause rupture of the 
 urethra, with extravasation of urine. 
 
 THE TESTICLES. 
 CONGENITAL ABNORMALITIES. 
 
 Absence of one or both testicles is a rare condition. More fre- 
 quently the organ is hypoplastic, remaining undeveloped through 
 life. 
 
 The most frequent congenital abnormality is cryptorchismus, 
 the condition in which one or both testicles remain in the abdomi- 
 nal cavity, in the inguinal canal, or elsewhere in the tract through 
 which normal descent occurs. The undescended testicle may de- 
 scend at or before puberty, or may remain fixed in its abnormal 
 position. In the latter case, especially if the testicle is in the 
 inguinal canal, secondary inflammation or atrophy may occur. 
 Slight defects in the development of the testicle are not infre- 
 quent, but are unimportant. 
 
 ATROPHY AND HYPERTROPHY. 
 
 Atrophy may follow any form of inflammation of the testicle 
 or epididymis, such as those occurring after gonorrhea, mumps, 
 and other infectious diseases or traumatism. In other instances 
 pressure upon the organ, as in hydrocele, tumors, etc., is the cause 
 of atrophy. The most frequent form is that which occurs as a 
 natural process of involution in old age (senile atrophy). 
 
 The testicle decreases in size, increases in hardness from over- 
 growth of connective tissue, and is usually more pigmented than 
 in health. Microscopically the seminal tubules are found to have 
 
664 TEXT-BOOK OF PATHOLOGY. 
 
 undergone fatty degeneration, and contain fatty debris and blood- 
 corpuscles. 
 
 Hypertrophy of one testicle may occur as a compensatory 
 process in cases of disease, atrophy, or removal of its fellow. 
 Hypertrophy of this sort has been produced experimentally in 
 animals. The seminal tubules increase in size, but are otherwise 
 normal. 
 
 DEGENERATIONS. 
 
 Fatty degeneration is frequently observed in testes sub- 
 jected to pressure through tumors or other pathologic conditions, 
 and in cases of atrophy of the testicle from any cause. The epi- 
 thelium of the tubules is attacked, and may be completely de- 
 stroyed, with production of fatty detritus. 
 
 Myxomatous degeneration occurs in various tumors of the 
 testis and in gummata. 
 
 Calcification may affect old inflammatory deposits, especially 
 those of the epididymis. 
 
 Caseation is a frequent condition in tuberculous and syphilitic 
 lesions ; and abscesses may undergo a process of inspissation, with 
 formation of dry, caseous material. 
 
 CIRCULATORY DISTURBANCES. 
 
 Active hyperemia of the testis, epididymis, and especially 
 of the membranes, occurs in association with acute inflammations. 
 
 Passive hyperemia is caused by pressure upon the veins or 
 disease of the veins (varicosity). The testis and epididymis be- 
 come swollen from edema, and, if the hyperemia persists, fatty 
 degeneration and atrophy may result. Serous effusion into the 
 tunica vaginalis (hydrocele) may occur, but this condition is more 
 frequently inflammatory (see page 666). 
 
 Kmbolism of the spermatic artery may occasion hemorrhagic 
 infarction, followed by necrosis or gangrene of the testis. This 
 sequence has been observed in a few cases, and has been proved 
 experimentally. Sometimes gangrene seems to be caused by 
 phlebitis of the pampiniform plexus. 
 
 INFLAMMATION. 
 
 Inflammation may involve the testis (orchitis), the epididymis 
 (epididymitis), or the tunica vaginalis (vaginitis testis). 
 
 Ktiology. — Traumatism is a frequent factor in the etiology, 
 and causes inflammation of the epididymis and membranes more 
 frequently than of the testicle itself. Blows, bruises, and contu- 
 sions are the usual conditions that cause this form of inflammation. 
 
 In another group of cases the irritants are micro-organisms 
 conveyed through the blood. Thus in typhoid fever, tuberculosis, 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 665 
 
 pneumonia, and various forms of septicopyemia the specific organ- 
 isms have been discovered in the areas of inflammation. Similar 
 inflammations occur in scarlet fever, syphilis, and small-pox, and 
 are doubtless caused in the same way, though the specific organ- 
 isms are unknown. In these cases the testis is more frequently 
 affected than the epididymis. 
 
 In a third group of cases infection occurs through the vas deferens, 
 and the epididymis is affected first and often alone. The most 
 frequent infectious agent in this group of cases is the gonococcus ; 
 but other micro-organisms may enter the vas deferens, reach the 
 epididymis and cause inflammation, in other diseases of the bladder 
 or urethra, or after operations upon these parts, such as crushing 
 vesical calculi, cutting urethral strictures, and the like. 
 
 Pathologic Anatomy. — Inflammations of the different parts 
 may be separately considered. 
 
 Acute Orchitis. — In acute orchitis the testis is swollen and more 
 or less edematous on account of inflammatory exudation. Micro- 
 scopically the striking feature is round-cell infiltration of the 
 intertubular tissues. This may be diffuse and uniform, or may 
 occur in circumscribed areas. The latter is especially common in 
 the orchitis of variola and pyemia. The round cells may infiltrate 
 the walls of the tubules, and may be discharged into the tubules 
 in great numbers. At the same time the epithelial cells may suffer 
 degeneration and desquamation. Intense orchitis may lead to the 
 formation of abscesses, single or multiple. These may subse- 
 quently undergo complete absorption, or may become inspissated 
 and encapsulated, the contents of such a focus consisting of fatty 
 detritus and cholesterin. In other cases the abscess may rupture 
 externally, and occasionally granulations springing from the tunica 
 albuginea or the testis may protrude through the opening. The 
 term benign fungus is applied to this condition. 
 
 Chronic orchitis usually results from the acute form. The 
 inflammatory changes of the intertubular tissues gradually lead to 
 induration, and the testis becomes hard and contracted, the con- 
 nective tissue and septa being increased in density, the tubules at 
 the same time suffering degeneration and atrophy. In cases fol- 
 lowing acute suppurative orchitis the tissues surrounding the 
 inspissated abscess become sclerotic, and the tubules are in large 
 part or wholly destroyed. Small nodular areas are discovered in 
 such cases, and on section these are found to consist of a dense 
 wall of fibrous tissue enclosing thickened pus containing fatty 
 detritus and cholesterin. The membranes surrounding the testis 
 are usually thickened and united by adhesions. 
 
 Chronic orchitis without a definite antecedent acute stage is a 
 frequent result of syphilis (see page 668). 
 
 Acute epididymitis occurs when infective agents have reached 
 the epididymis through the vas deferens. There is tense swelling 
 
666 TEXT-BOOK OF PATHOLOGY. 
 
 of the epididymis, and not rarely associated inflammation with 
 serous exudation in the tunica vaginalis. The testis is not, as a 
 rule, involved. The process begins as an acute catarrhal inflam- 
 mation of the tubules of the epididymis ; later, cellular infiltra- 
 tion and occasionally abscess-formation occur in the intertubular 
 connective tissues. The inflammation is sometimes completely re- 
 solved, but in other cases fibrous thickening, diffuse or nodular, 
 results. Inspissated abscesses surrounded by fibrous tissue are 
 sometimes seen, as in orchitis. The epithelium of the tubules 
 embedded in the new-formed fibrous tissue may undergo a cer- 
 tain amount of proliferation, suggesting the appearance of ade- 
 noma or cancer. The vas deferens may be permanently ob- 
 structed, and the tubules on the proximal side and in the testis 
 may undergo cystic distention. Extensive epididymitis very 
 commonly causes atrophy of the testis. 
 
 Vaginitis testis and periorchitis are terms applied to inflamma- 
 tion of the tunica vaginalis testis. This condition is usually the 
 result of orchitis or epididymitis, but may sometimes occur as a 
 primary inflammation resulting from traumatism or other forms of 
 irritation. 
 
 The tunica vaginalis is a reflection of the peritoneum, and in- 
 flammatory conditions arising in it resemble those of the abdomi- 
 nal peritoneum. 
 
 Serous or serofibrinous vaginitis testis is the most frequent 
 form. This may be acute or chronic, and is characterized by the 
 accumulation of small or large collections of serous liquid. In 
 slowly developed cases the quantity of liquid may be one or two 
 liters. It may be clear serum, but often contains flakes of fibrin, 
 or leukocytes, and is sometimes reddish from the presence of red 
 blood-corpuscles. Sometimes the liquid is milky or turbid, and 
 contains fat-droplets and cholesterin-crystals. A chylous variety 
 occurs in tropical countries, and is probably caused by the Filaria 
 sanguinis hominis. 
 
 Hydrocele is the term used to designate effusions of these sorts. 
 Sometimes the liquid contains spermatozoa, when the term hydro- 
 cele spermatica is applied. This condition is due to the escape of 
 spermatozoa from improperly developed spermatic tubules or from 
 ruptured cysts of the epididymis or testis. In certain cases it is 
 difficult to distinguish hydrocele spermatica and spermatocele (see 
 page 670). 
 
 When hydrocele persists the tunica vaginalis undergoes hyper- 
 plastic thickening, and small, wart-like elevations may be formed 
 (periorchitis prolifera). These nodules may become separated and 
 remain in the sac as free bodies, like those in the joints. Another 
 result of the secondary inflammatory changes in the membrane is 
 adhesion of the reflexions, causing a bilocular or multilocular 
 hydrocele. 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 667 
 
 When the canal connecting the sac with the peritoneal cavity 
 has remained patulous the fluid of hydrocele may be pressed into 
 the abdominal cavity. The term hydrocele processus vaginalis is 
 applied to such cases, and the term hydrocele funiculi spermatid to 
 cases in which only the upper part of the vaginal canal is patulous 
 and filled with liquid. Hydrocele funiculi cystica results from col- 
 lections of fluid in the middle portion of the canal, the upper and 
 lower ends being obliterated. 
 
 Purulent vaginitis testis occurs in association with epididy- 
 mitis and orchitis, and sometimes primarily after traumatism. An 
 ordinary hydrocele may be converted into a purulent collection by 
 puncture with infected instruments. The sac is more or less dis- 
 tended with purulent liquid, and the surface of the membrane is 
 covered with fibrinopurulent exudate. The pus may discharge 
 externally, or may become inspissated ; and extensive adhesions 
 may obliterate the sac. 
 
 Hemorrhagic Vaginitis Testis. — In severe acute inflammations 
 the exudation may be more or less hemorrhagic. More distinctly 
 hemorrhagic forms of inflammation result from traumatism ; in 
 these cases there is first extravasation of blood and then inflamma- 
 tion. The sac may be lined with fibrinous and hemorrhagic depos- 
 its, and the membrane becomes thickened. In the terminal stages 
 considerable thickening and sometimes calcification of the tunica 
 vaginalis are observed. 
 
 Inflammation of the vas deferens may be associated with 
 epididymitis or orchitis, or may occur independently in cases of 
 direct traumatism. In syphilitic disease of the testis, and less 
 commonly in other forms of orchitis, the vas deferens may be 
 greatly thickened. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis is most frequent in the epididymis, but may 
 involve the testicle as well. The infection occurs in one of two 
 ways : either through the vas deferens, in consequence of tuber- 
 culosis of the prostate, seminal vesicles, or bladder ; or through 
 the circulation in cases of pulmonary or other forms of tubercu- 
 losis. It has been shown that tubercle-bacilli are discharged from 
 the body in the seminal fluid in cases of pulmonary and other 
 forms of tuberculosis ; and when local conditions predispose tuber- 
 culous infection of the epididymis may occur. Gonorrheal epidid- 
 ymitis seems to constitute such a local predisposition. Primary 
 hematogenous infection of the epididymis seems to occur in rare 
 cases. 
 
 In cases of infection through the vas deferens there are formed 
 in the walls of the tubule of the epididymis small tubercular masses, 
 which rapidly increase in size and run together, forming caseous 
 
668 TEXT-BOOK OF PATHOLOGY. 
 
 areas of considerable size. Further invasion occurs along the 
 lymphatic channels and the tubule, and rapid involvement of a 
 considerable part of the epididymis results (Fig. 329). The tub- 
 ule surrounded by tuberculous tissue may become filled with des- 
 
 Fig. 329.— Tuberculosis of the epididymis and testicle (modified from Bollinger). 
 
 quamated epithelium and puriform or caseous matter, and may be 
 dilated in a cystic form. Extension to the testicle may occur, but 
 is unusual. 
 
 Associated serous or serofibrinous vaginitis testis is not infre- 
 quent ; and in some cases the tuberculous disease itself extends to 
 the testicular envelopes and causes nodular elevations, or ulcera- 
 tions and fistulous communications with the surface. 
 
 Hematogenous tuberculosis of the epididymis is, in the first 
 place, of the miliary form ; but the tubercles grow rapidly and 
 caseous nodules are rapidly formed. 
 
 Tuberculosis of the vas deferens may be secondary to tubercu- 
 losis of the seminal vesicles and bladder, or of the epididymis. 
 It is characterized by caseous swelling of the walls of the duct. 
 
 Syphilis is not infrequently seen in the testicle in the late 
 stages of acquired syphilis and in congenital syphilis. The epi- 
 didymis and the membranes are secondarily involved. Two 
 forms may be distinguished. The more frequent is that in which 
 diffuse induration of the testicle occurs; in the less frequent 
 variety there are circumscribed gummata. In the diffuse form 
 the organ is more or less uniformly indurated, and on section 
 dense bands of fibrous tissue are conspicuous. The tubules suffer 
 compression, degeneration, and atrophy, and sometimes become 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 669 
 
 converted into cheesy foci. The gummata have the usual translu- 
 cent or cheesy appearance. When the membranes are involved 
 diffuse thickening occurs ; and in rare cases the disease extends to 
 the skin, causing superficial granulations (syphilitic fungus). The 
 vas deferens is often greatly thickened, as are also the walls of 
 the blood-vessels of the testis and epididymis. 
 
 I^epra of the testis occasions nodular lesions and pressure- 
 atrophy of the tubules. Lepra-cells containing bacilli, as well as 
 free bacilli, occur in the tubules in abundance. This fact is im- 
 portant as indicating a possible mode of transmission of the disease. 
 
 TUMORS. 
 
 Fibroma is occasionally observed in the rete testis and tunica 
 albuginea as a small nodular tumor. 
 
 Chondroma is rare. It may occur in the epididymis or rete, 
 as a single node or as multiple small nodules. More frequently, 
 small cartilaginous areas are found in carcinomata or other tumors 
 of the testis. 
 
 Osteoma is very rare. 
 
 Myxoma is rare, except in association with other tumors. 
 
 Rhabdomyoma sometimes occurs in the form of flesh-like 
 growths of the testis. 
 
 Sarcoma may occur in any of its various forms in the testis, 
 and less commonly in the epididymis. It forms rapidly growing 
 whitish or reddish tumors. Secondary changes, such as fatty de- 
 generation, hemorrhage, cystic softening, and caseation, are not in- 
 frequent. Cystic dilatation of the seminal tubules may occasion 
 marked changes in the appearance of the tumor. The cysts are 
 small, and filled with turbid liquid containing fat, desquamated 
 cells, and cholesterin ; or large, and contain serous liquid, either 
 •clear, turbid, or blood-tinged. The lining epithelium of the cysts 
 is columnar, or, in case of cysts of the epididymis, often ciliated. 
 The walls of the tubules in some instances undergo active hyper- 
 plasia, giving rise to papillomatous elevations of the inner surface, 
 and a truly adenomatous proliferation may occur. In the latter 
 cases the tumor may be designated adenosarcoma. Growths of this 
 variety are sometimes met with in young adults or children, and 
 most frequently in the rete testis. They are more or less malig- 
 nant, causing frequent metastasis through the lymphatics or blood- 
 vessels. 
 
 Adenoma of the testicle is rare ; much more frequently cystic 
 tumors have a more or less adenomatous character (see Cysts). 
 
 Carcinoma may occur in the form of a scirrhus, but more fre- 
 quently as a soft or medullary variety (Fig. 330). Mucoid and col- 
 loid degenerations are rather frequent, and cystic softening may 
 occur. Cysts may also result from dilatation of the tubules. Carti- 
 
670 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 laginous areas are sometimes found in the stroma of the growth ; to 
 such the term chondrocarcinoma is applied. More or less com- 
 plete destruction of the testicle and epididymis is frequent, but the 
 tunica albuginea usually resists invasion for a considerable time. 
 Carcinoma of the testicle seems to originate from the epithelium 
 
 Fig. 330.— Carcinoma of the testicle (from a specimen in the Museum of the Philadelphia 
 Hospital). 
 
 of the convoluted tubules. Metastasis through the lymphatics 
 and blood-vessels is frequent, and extension through the testicular 
 envelopes to the skin may occur. 
 
 Cysts. — Retention-cysts of the tubules are frequent in cases 
 of inflammation and induration of the testis and epididymis. Some- 
 times they contain a simple milky liquid ; in other cases sperma- 
 tozoa are found in the fluid, and to these cysts the term xp< rma- 
 tocele is applied. The cysts may be numerous and small, or may 
 lie very large, containing a hundred or more cubic centimeters of 
 Liquid. The cysts arc found in the body of the organ ; but, when 
 large, project from the surface. Very large cysts push the testicle 
 and epididymis to one side. Occasionally cysts originate from the 
 hydatids or the paradidymis. These may be spermatoceles, when 
 one of the vasa aberrantia opens into them. 
 
 Secondary proliferations of the epithelium of the cysts may 
 convert a simple into a papuliferous cystoma; and occasionally 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 671 
 
 the primary process seems to be one of adenomatous character, the 
 cystic condition being the result of secondary distention or of the 
 peculiar character of the acini formed. 
 
 Small cystic cavities may contain mucous liquid or thick, curdy 
 material. In the latter case the term atheromatous cyst is appli- 
 cable. 
 
 Dermoid cysts are occasional tumors of the testis proper. 
 They may be simple sacs, lined with epidermal tissue and filled 
 with pultaceous matter ; or complicated dermoids, containing 
 teeth, bone, muscle-fibers, and nerve-tissue. 
 
 PARASITES. 
 Echinococcus-cysts are rarely met with. 
 
 THE PROSTATE GLAND. 
 INFLAMMATION. 
 
 Inflammation of the prostate, or prostatitis, is most 
 frequently secondary to posterior urethritis. Sometimes, however, 
 it results from other causes, such as metastatic involvement in 
 general pyemia or other forms of infection. Inflammations in the 
 vicinity and direct injuries of the prostate may likewise cause 
 acute inflammation. 
 
 Pathologic Anatomy. — A simple and a suppurative form may 
 be distinguished. 
 
 Simple Prostatitis. — In the ordinary prostatitis following 
 urethritis the disease takes the simple form, the gland being con- 
 gested and swollen, and causing by its enlargement more or less 
 obstruction of the urethra. Small suppurative foci may be formed 
 in and about the glandular pouches and tubules. 
 
 Suppurative or phlegmonous prostatitis, or abscess of the 
 prostate, may be a terminal condition of the previous form, or it 
 may be developed primarily. In cases of metastatic prostatitis 
 a number of foci of suppuration may occur and subsequently coa- 
 lesce, or a diffuse suppurative infiltration may take place. The 
 development of abscesses is usually acute, though in some cases it 
 may occur insidiously. If the abscesses are small they may sub- 
 sequently undergo encapsulation, inspissation, and even calcifica- 
 tion. Larger abscesses are prone to rupture into the urethra, 
 usually through a number of openings. Sometimes, however, the 
 inflammation extends to the tissues around the gland, causing 
 periprostatitis, and later rupture into the rectum may occur. Ex- 
 tensive phlegmonous inflammation of the pelvic tissues is an 
 unusual result. 
 
672 TEXT-BOOK OF PATHOLOGY. 
 
 ATROPHY AND DEGENERATION. 
 
 Atrophy of the gland is occasionally met with in youthful 
 individuals, and may be the result of disease or removal of the 
 testis. It also occurs in the aged, and in this case atrophy of the 
 tissues surrounding the prostatic ducts may be accompanied by dila- 
 tation of the ducts themselves. The gland then presents a cavern- 
 ous appearance. Atrophy of the gland sometimes leads to incon- 
 tinence of urine. 
 
 Fatty degeneration of the epithelium of the gland and of 
 the muscle-fibers is frequent in old age, and may occur as an in- 
 dependent condition or in association with hypertrophic enlarge- 
 ment of the gland. The gland becomes soft, and diffusely yellow 
 or mottled in color. 
 
 CONCRETIONS. 
 
 Prostatic concretions are not unusual in persons of advanced 
 age, and are frequently found in considerable numbers. They 
 vary in size from almost microscopic granules to bodies the size 
 of a millet-seed. On section through the gland these brownish- 
 colored bodies give the appearance of a surface sprinkled with 
 snuff. The granules are usually round or oval, and are character- 
 ized by concentric lamellations. They may be colorless at first, 
 but usually become brownish. The term amylaceous bodies has 
 been applied to them, and they have been supposed, though 
 erroneously, to be composed of amyloid material, such as occurs in 
 amyloid degeneration. When they reach considerable size calca- 
 reous salts may deposit around them and give them an irregular 
 form. Sometimes the concretions are discharged through the 
 prostatic ducts into the urethra ; in other cases the larger concre- 
 tions project prominently into the urethra beneath its mucous mem- 
 brane. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis of the prostate is usually found in association 
 with tuberculosis of the other genital organs, especially the vas 
 deferens and epididymis. It is also met with in association with 
 tuberculosis of the bladder or kidney. The prostate is usually 
 diffusely enlarged, and may be somewhat nodular upon the surface. 
 On section caseous areas are found, or the entire gland has a 
 caseous appearance. Recent tubercles are rarely visible, as .casea- 
 tion progresses with unusual rapidity in this organ. Primary 
 tuberculosis of the prostate is rare. 
 
 HYPERTROPHY AND TUMORS. 
 
 Hypertrophy of the prostate is a condition sometimes inflam- 
 matory in character, sometimes more probably of the nature of 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 
 
 673 
 
 tumor-formation. It occurs most frequently in the aged. The 
 causes are often quite obscure. In some cases chronic posterior 
 urethritis seems to be the important factor; in other instances 
 disturbances of the circulation, and especially varicose conditions 
 of the veins, are active in the causation. 
 
 
 Fig. 331.— Hypertrophy of the middle lobe of the prostate: A, middle lobe of prostate; 
 B, urethra (White and Wood). 
 
 The organ may enlarge in a uniform manner, or there may be 
 nodular or localized swelling. Of the localized form the most im- 
 portant, from a clinical aspect, is that in which the middle lobe or 
 the isthmus of the gland enlarges and projects under the posterior 
 wall of the urethra as a small or large rounded elevation, or as a 
 
674 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 transverse bar or obstruction (Fig. 331). According to the inves- 
 tigations of some authorities, the enlargement in such instances is 
 due to a hyperplasia of accessory prostatic tissue lying immediately 
 under the mucous membrane of the bladder and of the prostatic por- 
 tion of the urethra, with subsequent involvement of the isthmus of 
 the gland itself. 
 
 On section through the gland there may be a uniform indura- 
 tion, or in other cases, in consequence of associated changes in the 
 epithelial or glandular elements, there may be scattered through 
 the gland areas of softening or of proliferation of the glandular 
 elements, or of cystic distention of these. In such instances the 
 indurated gland presents more or less softened or cystic foci. 
 
 Microscopically, in the diffuse form, involving the stroma alone, 
 the gland presents merely the features of uniform fibromyomatous 
 
 Fig. 332.— Section of hypertrophies prostate of a man aged 74 years; natural size: a, 
 urethra; b, colliculus seminalis (Socin). 
 
 proliferation, and corresponds in structure with fibromatous or myo- 
 fibromatous tumors of the uterus (Fig. 332). In other cases the 
 glandular elements take an active part in the pathologic process, and 
 a distinctly adenomatous character is added. The glandular ele- 
 ments may undergo fatty degeneration, and the lumina of the acini 
 and tubules may be filled with milk-like, fatty material. In other 
 cases pronounced cystic distention of the gland occurs. 
 
 Results of Hypertrophy of the Prostate. — Enlargements of the 
 prostate usually interfere with the discharge of urine. This is 
 particularly marked in cases in which the middle lobe projects 
 into the urethra, though in some instances the opposite result may 
 be produced, viz., incontinence of urine due to interference with 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 675 
 
 the contractions of the sphincter of the neck of the bladder. In 
 cases of enlargement of one of the lateral lobes obstruction to the 
 flow of urine is caused by lateral deviation and compression of the 
 urethra. 
 
 The muscular walls of the bladder at first become hyper- 
 trophied and dilatation of the bladder subsequently occurs. 
 Cystitis, distention of the ureters and renal pelves, and ascend- 
 ing infection, causing ureteritis, pyelitis, and pyelonephritis, are 
 among the late results. 
 
 Sarcoma. — Sarcoma is a rare tumor of the prostate. It 
 generally has the characters of lymphosarcoma, and is a rapidly 
 growing, destructive tumor. In a few cases combination with 
 adenoma has been observed. 
 
 Carcinoma of the prostate is more frequent than sarcoma, 
 though it is not a common tumor. It occurs in relatively young 
 persons. The tumor arises from the epithelium of the tubules, 
 and takes the form of nodular, grayish or white masses which 
 cause irregular enlargements of the gland, and not rarely project 
 into the urethra or the base of the bladder. Superficial ulcera- 
 tion of the mucous membrane over these projections is not infre- 
 quent. The stroma of the gland usually proliferates actively. 
 Metastasis to the inguinal glands, or to distant parts, including 
 the bones, is not infrequent ; but direct extension to the bladder, 
 seminal vesicles, or rectum is more common. 
 
 Cysts of the prostate are usually the result of retention of exu- 
 dates within the glands or their ducts. Occasionally cystic forma- 
 tions seem to arise from remnants of Miiller's ducts. 
 
 COWPER'S GLANDS. 
 
 Inflammatory conditions are met with in these glands in asso- 
 ciation with similar affections of the prostate. Occasionally, inde- 
 pendent inflammation of Cowper's glands results from posterior 
 urethritis. The gland is enlarged and presents the usual appear- 
 ances of inflammation. The termination may be abscess-formation. 
 Obliteration of the mouths of the ducts may occasion cystic con- 
 ditions in the glands, and carcinoma has been described. 
 
 THE SEMINAL VESICLES. 
 
 Inflammation. — Acute inflammation of the seminal vesicles 
 may occur in association with gonorrheal urethritis. The vesi- 
 cles become distended with seminal secretion and mucopurulent 
 exudate. Their walls are swollen, and the mucous membrane 
 presents the appearance of catarrhal inflammation. 
 
 Chronic inflammation may result from the acute form, and 
 causes contraction and thickening: of the walls. 
 
676 TEXT-BOOK OF PATHOLOGY. 
 
 Tuberculosis of the seminal vesicles is common in cases of 
 urogenital tuberculosis. The vesicles are rarely independently 
 affected. The walls become thickened and may present nodular, 
 cheesy masses, and there may be ulcerations of the mucous surface. 
 The cavities of the vesicles contain caseous or puriform material. 
 
 Tumors. — Primary carcinoma has been described ; but second- 
 ary carcinoma, resulting from extension of cancer of the adjacent 
 structures, is more common. 
 
 Cystic distention and the formation of diverticula result from 
 obstructions of the ejaculatory duct. The contents of the vesicles 
 in such cases are seromucous in character. 
 
 Concretions frequently result from calcification of inflamma- 
 tory exudates. They are especially frequent in association with 
 tuberculosis. 
 
 THE MAMMARY GLANDS. 
 CONGENITAL ABNORMALITIES. 
 
 Absence of one or both breasts may occur in association with 
 other defects of development of the thoracic walls. Incomplete 
 development of the mammary glands, or hypoplasia, may be asso- 
 ciated with hypoplasia of the genital organs. 
 
 Supernumerary mammary glands are frequently observed ; 
 the term polymastia is given this condition. The supernumerary 
 gland or glands may be situated between the normal glands, below 
 these, or in distant parts, such as the back, shoulders, and arms. 
 They may occur in either sex, and may be structurally complete 
 and functionally active ; or may be merely rounded masses of 
 mammary tissue without excretory ducts or nipples. In the latter 
 instances the probable explanation of the condition is that in the 
 process of development parts of the normal glands have been split 
 off and have separately developed. 
 
 Early Development. — The mammary glands may be de- 
 veloped at an abnormally early period, in correspondence with 
 early development of the genital organs. 
 
 Abnormal functional activity (secretion) may be stimu- 
 lated by various diseases of the genital organs ; and in the new- 
 born of either sex during the first week of life slight secretion of 
 colostrum-like material is frequent. 
 
 Abnormal development of the male breast is occasion- 
 ally observed, especially about the age of puberty, and sometimes 
 copious secretion of milk takes place. Usually the organ subse- 
 quently atrophies, but exceptionally the enlargement and secretion 
 persist. 
 
 CIRCULATORY DISTURBANCES. 
 
 Hyperemia occurs during the menstrual period and at the 
 beginning of lactation, as a physiologic process, and causes slight 
 

 
 DISEASES OF THE REPRODUCTIVE ORGANS. 677 
 
 swelling and redness. Pathologic hyperemia plays a part in the 
 process of inflammation. 
 
 Hemorrhages are usually the result of traumatism. They 
 may occur into the gland itself, or into the connective tissue in 
 front of or behind the gland. Occasionally hemorrhages are due 
 to intense inflammation or to tumor-formation. The blood may 
 find its way into the lactiferous tubules, and may be in part dis- 
 charged from the nipple. In case of large hemorrhages the blood 
 may subsequently undergo absorption or inspissation, and hemor- 
 rhagic cysts may be formed. 
 
 INFLAMMATIONS. 
 
 Acute inflammation of the mammae, or acute mastitis, 
 
 is rarely met with, excepting during the puerperium. Exception- 
 ally it may occur in cases of general pyemia, or in the new-born 
 as a result of active secretion and obstruction to the outlets. 
 Sometimes inflammation of the glands results from direct exten- 
 sion of inflammatory processes of the skin, subcutaneous tissue, or 
 thoracic walls. Puerperal mastitis is infective in character, and 
 results from injury or disease of the nipple, from which the infec- 
 tive agents enter the glands. The actual portal of entrance may 
 be the discharging tubules, or may be fissures and erosions of the 
 nipple. Various micro-organisms have been discovered, including 
 staphylococci and streptococci. 
 
 Pathologic Anatomy. — The gland is swollen and distends its 
 capsule tensely, the skin is reddened, and a general hyperemia of 
 the gland is noted. During the earlier stages the inflammation 
 may be localized or may be diffuse. In the former case more or 
 less circumscribed induration is discovered, while in the latter the 
 organ is uniformly indurated. The tendency of mastitis is to a 
 termination in suppuration. On section through the gland areas 
 of light-yellowish color indicate the purulent infiltration, while in 
 the later stages more or less extensive abscesses are formed. The 
 latter may communicate with the lactiferous tubules, and pus and 
 milk may be discharged from the nipple. The abscesses tend to 
 extend in various directions, and may finally rupture upon the sur- 
 face through fistula?. After discharge of the pus granulation- 
 tissue is formed, and the cavities are obliterated by cicatricial 
 tissue. When the larger discharging tubules are opened by the 
 abscesses fistulas may be formed, which continuously discharge 
 milk. Small collections of pus may become encapsulated and 
 inspissated, being converted into cheesy or partly calcified matter. 
 
 The connective tissues around the mammary gland are some- 
 times involved by extension, and suppurative or necrotic perimas- 
 titis results. Extension to the thoracic walls and pleura is rare. 
 
 Chronic Mastitis. — Diffuse induration of the mammary 
 
678 TEXT-BOOK OF PATHOLOGY. 
 
 gland, resembling in its histologic features the indurative or 
 chronic interstitial inflammations of other organs, is occasionally 
 seen in middle-aged or old women. The causes are obscure, and 
 it is difficult to distinguish some of the cases from certain forms 
 of fibromatous tumors. The gland becomes hardened and some- 
 times slightly increased in size. In other cases retraction of the 
 connective tissue causes a reduction in the size. On section firm 
 bands of connective tissue are conspicuous, and the lactiferous 
 tubules may be distended, forming small or large retention-cysts. 
 This form of disease will be further discussed under Fibroma. 
 
 ATROPHY AND HYPERTROPHY. 
 
 Atrophy of the gland occurs as a physiologic process after the 
 menopause, or it may result from local causes, such as abscess or 
 tumor-formation. Artificial menopause, following oophorectomy 
 or diseases of the reproductive organs, may occasion atrophy simi- 
 lar to that normally present in old age. The gland may simply 
 decrease in size, without notable change of any other kind. Some- 
 times, however, connective-tissue hyperplasia accompanies the 
 atrophy of the glandular elements, and diffuse infiltration may 
 occur. 
 
 Hypertrophy of the gland is sometimes met with in girls at 
 the age of puberty, and leads to a uniform enlargement of the or- 
 gan. In some cases there is a true hypertrophy of all the con- 
 stituents of the gland ; in other instances dilatation of the lym- 
 phatic channels, or degenerative changes, may cause a simulation 
 of true hypertrophy. Both breasts, as a rule, are affected, and 
 there may be increased functional activity (galactorrhea). 
 
 DEGENERATIONS. 
 
 Fatty infiltration, or lipomatosis, of the gland may accom- 
 pany atrophy, or may occur as an independent condition. The 
 gland may be greatly enlarged. Accompanying this degeneration 
 there is usually diffuse hyperplasia of the connective tissue. 
 
 Myxomatous degeneration may be associated with fatty 
 infiltration. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis of the mammary gland may be associated with 
 tuberculosis of the axillary glands, or of other parts, or may be 
 primary. The tubercle-bacilli reach the gland either through the 
 lactiferous tubules or through the blood. The disease is charac- 
 terized by the formation of distinct tubercles, which tend to unite 
 and form caseous areas. There is rarely extensive disease. 
 
 Syphilis, in the form of gummata, is sometimes met with in 
 acquired or congenital syphilis. 
 
DISEASES OF THE REPRODUCTIVE ORGANS. 
 
 679 
 
 TUMORS. 
 
 Fibroma may be met with in the form of circumscribed nodu- 
 lar growths, or, according to the view of some pathologists, as a 
 diffuse process. Circumscribed fibroma presents itself as a hard, 
 nodular tumor, often having a distinct capsule, and on section 
 presenting a lamellar arrangement. The glandular elements of 
 the organ in the area of invasion may undergo secondary hyper- 
 plasia, and thus a form of fibro-adenoma may be developed. In 
 the cases termed diffuse fibroma the entire organ may be indurated, 
 or nodular areas of sclerosis may be found in various parts of the 
 gland. The acini and ducts may at the same time undergo pro- 
 liferation, forming adenomatous structures ; or compression of the 
 ducts may lead to retention-cysts. It is difficult to determine in 
 individual cases whether the process is one of tumor-formation or 
 one of inflammatory hyperplasia. 
 
 A form of particular interest is that known as intracanalicil- 
 lar fibroma. In this the proliferating fibrous tissue projects into 
 the normal or dilated tubules in the form of papillary elevations. 
 The mucosa lining the tubules is pushed forward by the ingrowths, 
 and covers these in the same manner as epithelium covers super- 
 ficial papillomata of the skin or mucous membranes. The gland 
 
 -Intracanalicular fibroma of the mammary gland (Kaufmann). 
 
 may be greatly enlarged, and on section presents an appearance 
 resembling that of a cut through a cauliflower (Fig. 333). 
 
 lipoma of the mammary glands occurs in the form of round, 
 
680 TEXT-BOOK OF PATHOLOGY. 
 
 encapsulated tumors of the interstitial or periglandular connective 
 tissues. 
 
 Myxoma may occur in a diffuse form, causing a transforma- 
 tion of the gland into myxomatous material, or as circumscribed 
 tumors. 
 
 Myomata containing smooth muscle-fibers, and mixed tumors 
 containing striated muscle-fibers, are rare. 
 
 Chondroma and osteoma have been observed. 
 
 Sarcoma is most frequently of the round-cell variety. It 
 occurs in a diffuse form or as circumscribed nodules ; association 
 with fibroma and myxoma is not infrequent. 
 
 In diffuse sarcoma the gland undergoes a uniform enlargement, 
 and the neoplasm extends rapidly, forming attachments to the 
 skin and sometimes causing superficial ulceration. In other cases 
 extension toward the chest-walls may occur, and may finally reach 
 the pleura. On section through the gland a lobular character of 
 the tumor may be recognized, and areas of fibrous or myxomatous 
 character are visible here and there. Cystic conditions, sometimes 
 met with, may be due to obstruction and consequent distention of 
 the lactiferous tubules. The term eystosarcoma is appropriately 
 applied to such cases. The sarcomatous tissue may project into 
 the dilated tubules in a polypoid form (intra<-<nia/irtdaf .sarcoma). 
 Section through the gland in such cases presents an appearance 
 not unlike the surface of section of a head of cabbage. Cysts may 
 also be formed in sarcomata by degenerative softening. 
 
 Localized sarcomata occur as nodular tumors arising from the 
 connective tissue surrounding the acini. On section through the 
 tumor the glandular acini may be seen within the nodules. 
 
 In any form of sarcoma the epithelium of the tubules and acini 
 may undergo secondary proliferation, when the term adenosarcoma 
 is applicable. 
 
 Adenoma of the mammary glands may be an independent 
 growth, or may be associated with fibroma, sarcoma, or other tu- 
 mors. The independent form presents itself as a circumscribed, 
 encapsulated, nodular tumor, somewhat firmer than the substance 
 of the normal gland. Microscopically it consists of more or less 
 typical glandular acini. These are usually somewhat dilated, and 
 the epithelial cells are larger than those of the normal gland (Fig. 
 64). Instead of a single layer of columnar cells, active hyperplasia 
 may cause a complete filling of the acinus with epithelial cells. 
 Fatty degeneration of the cells is not infrequent, and sometimes 
 there is a certain amount of milk-secretion, causing additional dis- 
 tention of the cavities. 
 
 Carcinoma. — Carcinoma may develop from the tubules or 
 from the acini of the glands. It may begin as an adenomatous 
 tumor, which subsequently undergoes carcinomatous transforma- 
 tion, or may be a typical glandular cancer from the beginning. 
 
DISEASES OF THE REPRODUCTIVE ORGANS, 
 
 681 
 
 In the cases primarily adenomatous the structure of the acini be- 
 comes atypical and the epithelial cells tend to penetrate the mem- 
 brana propria and form irregular collections or columns in the 
 interstitial tissue. Degenerative changes are often observed, 
 among which fatty degeneration is most frequent. Mucoid de- 
 generation and a form of caseation are sometimes met with, and 
 calcification may take place in the interstitial tissues. Occasion- 
 ally an attempt at formation of milk occurs in the cancer-acini. 
 
 Varieties. — Among the varieties of carcinoma are the medul- 
 lary, the simple, the scirrhous, and the myxomatous. 
 
 Medullary carcinoma, or soft cancer, is characterized by its 
 softness and the abundance of liquid (cancer-juice). It grows 
 rapidly and soon invades a large part of the gland, and attaches 
 
 Fig. 334.— Ulcerated carcinoma of the breast. 
 
 itself to the skin, which may finally be broken, exposing an 
 ulcerated surface (Fig. 334). Actual inflammatory changes ter- 
 minating in suppuration are not infrequent. 
 
 Scirrhous cancer is slower in growth, ^nd is usually very 
 hard ; the skin is firmly attached to the tumor, and the nipple is 
 usually retracted. On section the tumor is found to be of a firm, 
 fibrous, and somewhat translucent character ; extensions of the 
 growth are seen radiating in various directions from the body of 
 the tumor. Microscopically the growth consists of fasciculated 
 connective tissue, enclosing round or elongated collections of 
 cancer-cells (Fig. 72). 
 
682 TEXT-BOOK OF PATHOLOGY. 
 
 Simple carcinoma stands between the medullary and the 
 scirrhous forms in point of hardness, as well as in point of malig- 
 nancy. The three forms differ only in the relative amount of 
 epithelial elements and fibrous tissue. 
 
 Myxomatous, colloid, or gelatinous cancer is a rare form in 
 which the interstitial connective tissue suffers mucoid change, and 
 the epithelial cells of the cancer-acini undergo more or less fatty 
 or exceptionally mucoid degeneration (Fig. 73). 
 
 Results. — Cancer of the breast may extend directly to the sub- 
 cutaneous tissues and skin on the one hand, or to the walls of the 
 chest and pleura on the other hand. Metastasis frequently takes 
 place through the lymphatics, the axillary glands, as a rule, 
 presenting the first evidence of metastasis. Malignancy varies 
 with the softness or hardness of the tumors, the scirrhous form 
 frequently having a comparatively benign character. s Sometimes 
 the increasing growth of connective tissue in this variety leads to 
 practical cessation of the growth of the tumor. 
 
 Mammary cancers are much more frequent in the female than 
 in the male sex. They are commonly met with after the age of 
 forty, and traumatic influences seem to bear some relation to their 
 occurrence. 
 
 Cysts. — Repeated reference has been made to the retention- 
 cysts of the lactiferous tubules caused by compression or other 
 forms of obstruction. The gland may contain a few or many 
 cystic cavities about the size of a pea, containing whitish or 
 milky liquid. Occasionally the contents of the cysts are cheesy 
 (atheromatous). Distention of the acini of the glands in conse- 
 quence of obstructions to the outflow of milk may lead to large 
 cystic tumors containing milk (galadocele). In the later stages 
 the contents of such cysts may become thickened or caseous. 
 
 CHAPTER IX. 
 
 DISEASES OF THE B0NE5. 
 
 Anatomy and Development. — Bone is a dense form of 
 connective tissue, the cement-substance being impregnated with 
 lime-salts. It may be spongy or compact in character. On 
 transverse section one sees certain oval openings, surrounded by 
 concentric lamella? of a substance containing lime-salts. Each 
 opening is the end of a so-called Haversian canal, which with the 
 surrounding lamella? forms a Haversian system. The areas be- 
 tween the Haversian systems are filled with osseous tissue not 
 arranged concentrically. Between the lamella? of bony tissue are 
 
DISEASES OF THE BONES. 683 
 
 seen irregularly oval spaces — lacuna? — from which ran branching 
 canaliculi. In preparations of fresh bone the lacunae are found to 
 be occupied by the bone-cells, which are irregular and have branch- 
 ing projections extending some distance into the canaliculi. In 
 the center of the bones are found hollow spaces containing the 
 bone-marrow. This is a vascular tissue, in the meshes of which 
 are found large and small rounded cells resembling the lymphoid 
 cells, red corpuscles, ordinary leukocytes, and some nucleated red 
 corpuscles. A form of cell of particular interest is the large mul- 
 tinucleated giant-cell, or myeloplaque. The marrow extends in 
 the form of projections into the substance of the bone and com- 
 municates with the Haversian canals. 
 
 Surrounding the bone is the fibrous periosteum. This consists 
 of a dense outer layer and a more cellular inner one, which is osteo- 
 genetic in function. 
 
 Development. — The beginning of the change of the original car- 
 tilage into bone consists in the multiplication of the cartilage-cells 
 and their arrangement in longitudinal rows. They grow into car- 
 tilage-corpuscles of considerable size, calcification at the same time 
 occurring in the matrix between these cells. Simultaneously vas- 
 cular projections extend inward from the perichondrium ; the car- 
 tilage-cells and preliminary calcareous deposit are subsequently 
 removed, primary marrow-spaces being thus formed. Bone-cells 
 are deposited in the spaces between the original cartilaginous tra- 
 becular, and at once begin to cover themselves with bony deposits, 
 the cartilaginous trabecular gradually diminishing by absorption. 
 By these processes a spongy form of bone is developed. Subse- 
 quently the concentric calcareous lamella? of the Haversian sys- 
 tems are deposited within the spaces, and the spongy bone is thus 
 converted into the dense form. 
 
 DISORDERS OF DEVELOPMENT. 
 
 Many congenital defects of development are observed, such as 
 the appearance of supernumerary bones, the absence of certain 
 bones, the failure of union between epiphyses and diaphyses, etc. 
 These conditions are of little pathologic interest. The most im- 
 portant developmental disease is rickets. 
 
 RICKETS. 
 
 Definition. — Rickets or rachitis, is a constitutional disorder, 
 attended with abnormal developmental processes in the bones, of 
 which active proliferation of the cellular elements and lack of 
 normal calcification are the most important. 
 
 Etiology. — The causes of rickets are still very obscure. The 
 disease is in some way connected with improper nourishment, though 
 
684 TEXT-BOOK OF PATHOLOGY. 
 
 there is probably also an inherited disposition. It has been sought 
 to establish a connection between rickets and syphilis, but any such 
 relation is doubtful. Various chemical theories have been offered 
 in explanation. Formerly it was supposed that the presence in the 
 digestive tract of lactic acid in excess prevented the proper absorp- 
 tion of calcium ; this theory, however, is generally abandoned. 
 The disease occurs in infants during the first year of life, and 
 continues during the second and third years, after which the 
 active manifestations subside. 
 
 Pathologic Anatomy. — Rickets leads to various deformities, 
 principally situated in the long bones and skull. The epiphy- 
 ses, as those of the wrist, ankle, etc., are swollen, and in more 
 advanced stages the shafts of the long bones may be variously 
 distorted. 
 
 Sharp bends (infractions) may be observed in the long bones, 
 and complete fractures may occur. The alteration of the skull is 
 characteristic. The head is large and square in shape, the fore- 
 head prominent, and the fontanelles remain open a long time. 
 Osteophytes may form, and not rarely areas are found in the tem- 
 poral or other bones in which the mineral substance is deficient 
 or almost completely wanting (craniotabcs), the spaces being filled 
 by a parchment-like membrane. Deformities of the chest are 
 frequent, the chicken-breasted condition being the most marked. 
 In the beginning of the disease slight enlargement of the ends of 
 the ribs at the junction with the costal cartilages, causing the 
 
 Fig. 335.— Rachitic enlargement of the end of a rib (modified from Bollinger). 
 
 beaded appearance called the " rachitic rosary," is observed (Fig. 
 •335). Various distortions of the spinal column, flattening of the 
 pelvis, and other deformities may be met with in marked cases. 
 
 The minute changes of rickets consist in a form of abnormal 
 development, in which calcareous deposition does not progress in 
 the normal manner, but is replaced by proliferation of the cellular 
 elements. In consequence of this the bone presents irregular areas 
 of partial calcification lying between portions made up of greatly 
 proliferated and enlarged cartilage-cells. Projections from the 
 marrow and periosteum extend deeply and visibly into the body 
 of the bone, which is thus composed for the most part of osteoid 
 instead of osseous tissue. The marrow-spaces are irregular and 
 excessive in size. These changes in the bone are marked at 
 
DISEASES OF THE BONES. 685 
 
 the epiphyseal extremities, and thus lead to the visible enlarge- 
 ments. It is thus seen that the process in rickets is failure of 
 development of the normal structure, rather than absorption of 
 existing bone. The original calcareous deposit around the carti- 
 lage-cells is largely or completely absorbed, as in normal bone-for- 
 mation, and often even more rapidly. The subsequent deposit of 
 calcareous bone does not form, but in place of it there occurs a 
 rapid proliferation of cartilaginous and other cells. 
 
 Associated Conditions. — The changes in the bones do not 
 constitute the entire pathology of rickets. There are frequently 
 gastro-intestinal disorders, such as catarrhal inflammations of the 
 mucous membrane. Proliferative changes are met with in the 
 spleen and liver, leading to fibrous overgrowth and enlargement, 
 and the blood is more or less profoundly altered. Decrease in the 
 number of red corpuscles and leukocytosis are the conspicuous 
 features. Nucleated red corpuscles may be found in more or less 
 abundance, according to the grade of anemia, and the leukocytosis 
 involves a special increase of mononuclear elements, and myelo- 
 cytes may be present. 
 
 Congenital rickets differs in some respects from the dis- 
 ease met with after birth. The extremities are short and thick, 
 the ends of the bones enlarged, and the shafts bent. There is 
 increase of the original cartilage and of the periosteum, with an 
 arrest of development of the bones. 
 
 REGENERATION OF BONE. 
 
 Regeneration of bone occurs most typically in the healing of 
 fractures, and also as a part of various pathologic processes in 
 which a certain amount of destruction of bony tissue has taken 
 place. Hypertrophy may be included in the same group of affec- 
 tions. 
 
 Fractures. — Definition. — Fractures are breaches in the con- 
 tinuity of bone which occur in consequence of direct force or 
 of muscular contractions. The bone may be broken in vari- 
 ous directions, the line of fracture being straight or irregular, 
 directly transverse to the long axis of the bone, or oblique. The 
 bone may be broken into a number of splinters (comminuted fract- 
 ure), or the fracture may be a single one. There is always more 
 or less injury to the soft parts immediately surrounding the bone, 
 and sometimes extensive injury causes communication between the 
 outer surface and the seat of fracture through flesh wounds (com- 
 pound fracture). 
 
 Repair of Fractures. — The process of repair is much the same as 
 the process in the original formation of bone. Immediately after 
 the fracture there is more or less hemorrhagic extravasation with- 
 in the marrow and around the broken ends of the bone. Within 
 
686 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 a few days cellular infiltration, with congestion and edematous 
 swelling of the periosteum and marrow, as well as of the bones, 
 may be noted. Proliferative changes then take place in the same 
 situations and new blood-vessels are formed. The tissue soon 
 becomes somewhat hardened from deposit of calcareous matter and 
 cartilaginous formation. Its condition varies greatly in different 
 cases ; sometimes it is quite fibrous, in other cases almost purely 
 cartilaginous. Gradually it is converted into bone by the regular 
 processes of bone-formation. At this stage the seat of fracture is 
 occupied by a deposit of soft, bony material of considerable bulk, 
 which causes a local thickening of the bone. Finally the excess 
 
 Fig. 336.— Fracture of the femur, show- 
 ing malposition of the ends of the bone 
 and abundant callus (modified from Bol- 
 linger). 
 
 Fig. 337.— Fracture of humerus; sec- 
 tion through the bone, showing the repair 
 of the fracture (modified from Bollinger). 
 
 is removed by absorption, the parts in the direct line of the bone 
 upon which the strain naturally falls becoming thickened, while 
 other parts are absorbed. 
 
 The original deposit of osteoid or chondroid material at the seat 
 of fracture is termed callus (Fig. 336). Part of this is deposited on 
 the exterior ( 'periosteal callus), and is derived from the periosteum ; 
 part is within the marrow-cavity {myelogenous callus) ; and a third 
 
DISEASES OF THE BONES. 687 
 
 part is sometimes seen between the ends of the bone (intermediary 
 callus). The last is produced by the periosteum. 
 
 The healing of fractures under the most favorable circum- 
 stances — that is, in cases in which the fragments of bone are 
 restored to their proper position — is accomplished with but little 
 disturbance of the normal relations. The seat of fracture may 
 be permanently thickened, and there is always some shortening of 
 the aifected bone. When the fragments are not placed in proper 
 position, angular deformities, with considerable thickening from 
 deposit of bony material between the fragments, result (Fig. 337). 
 
 When the fragments are not kept in apposition, or when the 
 general condition of the patient is unsatisfactory, the union of the 
 fragments may be prevented and " ununited fractures " result. 
 The ends of the fragments in these cases become rounded by ab- 
 sorption of the sharp edges, forming false joints (pseudarthroses). 
 
 Hypertrophy. 
 
 Local or general hypertrophy of bone may be found. Local 
 hypertrophies may occur in consequence of increased strain upon 
 certain parts of a bone, either directly or through the muscles. 
 In muscular individuals hypertrophy of this kind is frequently 
 seen at points of attachment of the muscles. In cases of in- 
 jury or incapacity of one of the limbs the other may show 
 hypertrophy. 
 
 Giant growth of certain bones, or of the entire skeleton, may 
 be observed. Local hypertrophy of this kind, dating from child- 
 hood, is especially common in the upper extremities, and is fre- 
 quently unilateral. It may be observed as a bilateral condition in 
 the fingers. Complete giant growth usually begins about the age 
 of puberty. The individual, previously developed as others, begins 
 to grow abnormally until an excessive size is reached. The bones 
 are not only very large, but often markedly thickened and irregu- 
 lar. 
 
 Acromegaly is an allied condition in which giant growth of 
 the hands and feet, forearms and legs, and parts of the face, 
 notably the lower jaw and bridge of the nose, is observed. A 
 certain amount of hyperplasia of the soft tissues in the aifected 
 region accompanies this change. The etiology of this affection is 
 still unsettled. Hyperplastic conditions, tumors, and other diseases 
 of the hypophysis cerebri have been met with in a considerable 
 proportion of the cases. In some of the skeletons of giants 
 investigated with regard to this point enlargement of the sella 
 turcica has been found, and this evidences the occurrence of en- 
 largement of the pituitary body in some, at least, of such persons. 
 The exact relation between pituitary disease and bony hyper- 
 trophies remains obscure. 
 
688 TEXT-BOOK OF PATHOLOGY. 
 
 CIRCULATORY DISTURBANCES. 
 
 Hyperemia is normal during the development of bone, or 
 may accompany inflammatory disturbances of the neighboring 
 parts. The marrow becomes more or less light- or dark-red in 
 color, and the periosteal vessels may be injected. The entire bone 
 may have a pink or reddish color. 
 
 Thrombosis may occur in the blood-vessels of the marrow. 
 
 Hemorrhage beneath the periosteum and in the marrow is 
 comparatively common. It may result from traumatic causes or 
 from scorbutic or purpuric conditions, as well as from inflamma- 
 tory affections of the parts involved. Considerable subperiosteal 
 hemorrhages are found in cases of infantile scurvy. The sepa- 
 ration of the periosteum from the bone may lead to necrosis of the 
 superficial layers of the bone. A similar accumulation of blood 
 beneath the periosteum is that found over the bones of the skull 
 in the new-born — the cephalhematoma. This results from the 
 traumatism of labor. Large accumulations of blood of this nature 
 may be absorbed or may undergo suppuration. 
 
 Hemorrhage into the substance of bone may accompany other 
 diseases affecting it, such as caries, tumors, and the like. 
 
 INFLAMMATIONS. 
 Periostitis. 
 
 Definition. — Periostitis, or inflammation of the periosteum, 
 may be of various forms, and may lead to different results. Some- 
 times the evidences of inflammation are very apparent; in other 
 cases the disease appears in the form of a chronic productive pro- 
 cess, leading to overgrowth. 
 
 Btiology. — Periostitis may be the result of traumatism, with 
 or without the establishment of a communicating wound. In the 
 latter case the injury provides an area of lessened resistance, which 
 may subsequently become infected. In the former case the infec- 
 tion is direct, coming from the outside. Hematogenous infection 
 without local injury is frequently observed. Infective periostitis 
 may result from extension of an inflammation situated near the 
 bones or from osteomyelitis. In all forms of bone-disease more 
 or less local periostitis occurs as a complication. In some cases 
 the etiology is obscure, as in the periostitis which occurs during 
 pregnancy and leads to the formation of osteophytes. 
 
 Pathologic Anatomy. — We may distinguish simple, sup- 
 purative, and ossifying periostitis. 
 
 Simple Periostitis. — The membrane becomes swollen, red, 
 and sometimes infiltrated with blood. Microscopically there are 
 round-cell infiltration and proliferation of the periosteal tissue. 
 If the process has been extensive, and the irritation long con- 
 
DISEASES OF THE BONES. 689 
 
 tinued, a termination in fibroid thickening may be observed. This 
 is not unusual in cases of fractures. 
 
 Purulent Periostitis. — The disease may be circumscribed or 
 diffuse. There are marked swelling and cellular infiltration, 
 particularly in the deeper layers, and abscess-formation results. 
 Separation of the periosteum from the bone ensues, and may 
 lead to local interruption of the circulation between the peri- 
 osteum and the bone, and consequent superficial necrosis of the 
 bone with exfoliation results. In the diffuse form of periostitis 
 widespread areas of the periosteum may be quickly involved and 
 rapid destruction takes place. In these cases a considerable 
 inflammation of the surrounding tissues is customary. In all 
 instances there is a tendency to burrowing of pus toward the sur- 
 face, and its eventual discharge. The retention of necrotic portions 
 of the bone may lead to continued suppuration, but with removal 
 of the dead portions healing usually occurs. Ostitis and osteo- 
 myelitis are very frequent results of periostitis ; on the other hand, 
 they may be in certain cases the original cause. 
 
 Ossifying- periostitis leads to the formation of bony excres- 
 cences, exostoses, or osteophytes. There is first a proliferation 
 of the osteogenetic layer of the periosteum, then partial ossification, 
 and finally complete bone-formation with firm attachment to the 
 underlying bone. These changes may be circumscribed or diffuse, 
 and cause irregular elevations or general thickening of the bone. 
 Occasionally the surrounding connective tissues are implicated 
 [par ostitis). Ossifying periostitis may occur in the vicinity of 
 joints affected with chronic arthritis. It may occur as a result 
 of diseases of bones attended with considerable destruction, such 
 as tumors, tuberculosis, etc. Occasionally the causes are entirely 
 obscure. An interesting form is that Avhich occurs in the bones 
 of the hands and feet, forearms, and legs in tuberculosis of the 
 lungs and empyema, or more rarely in other diseases ; to this the 
 term hypertrophic, osteo-arthropathy has been applied. This is a 
 form of osteoperiostitis of ossifying type, and it seems to be due 
 to the action of circulating toxins developed in the diseases with 
 which it is associated. 
 
 Associated Conditions and Results. — The conditions met 
 with in the adjacent bones and other parts have been referred to. 
 General infection and intoxication may follow upon the suppurative 
 cases, and death may then occur from septicopyemia. Permanent 
 thickening of the bone may result in any case, or resolution may 
 be practically complete. 
 
 Osteomyelitis and Ostitis. 
 
 Definition. — Acute osteomyelitis and ostitis are usually com- 
 bined, and occur as an inflammatory condition affecting the mar- 
 
690 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 row and its extensions into the communicating canals of the 
 
 bone. The lamellar substance of the bone is only secondarily 
 
 involved. 
 
 Utiology. — Osteomyelitis is an infective disease resulting 
 
 from hematogenous infection in the course of various diseases, 
 from local infections in cases of trauma- 
 tism (fracture, amputation), or from peri- 
 ostitis. Various micro-organisms, includ- 
 ing staphylococci, streptococci, typhoid 
 bacilli, and the Bacillus coli communis, 
 have been discovered. 
 
 Pathologic Anatomy. — The mar- 
 row first becomes red and edematous, 
 then cellular infiltration and proliferation 
 are superadded, and finally collections of 
 pus or diffuse purulent transformation fol- 
 low. The surrounding bone is involved, 
 becoming more or less infiltrated, soften- 
 ing, and not rarely undergoing necrosis 
 (Fig. 338). Small or large sequestra may 
 be formed, or the bone may necrose com- 
 pletely. Periostitis is generally associated, 
 and the tissues around the bone are usu- 
 ally infiltrated and suffer suppurative or 
 necrotic changes. Hypertrophic changes 
 may occur in the periosteum and super- 
 ficial layers of bone, causing a bony en- 
 casement of central sequestra. In such 
 instances a suppurating sinus, extending 
 from the bone to the surface, usually 
 remains. 
 
 Associated Conditions. — Implica- 
 tion of the neighboring parts is habitual — 
 fig. 338,-Necrosis of femur, deep-seated abscesses, arthritis, etc. Gen- 
 
 inisT^rren)! 101116 osteomye ' eral infection is usually the final result, 
 and commonly leads to a fatal end. 
 
 Marked changes in the blood have been observed — leukocytosis, 
 
 large proportions of large mononuclear cells, myelocytes. 
 
 Chronic Ostitis. 
 
 Chronic inflammatory processes are more apt to involve the 
 bone than the marrow, though the beginning of the disease may 
 be frequently in the latter situation. It may be suppurative, de- 
 generative, or hypertrophic in character. 
 
 Btiology. — Chronic ostitis may follow osteomyelitis and ne- 
 crosis, necrotic sequestra keeping up a constant irritation. In 
 
DISEASES OF THE BONES. 691 
 
 these cases the disease is primarily infective. The chronic inflam- 
 mations of bone due to tuberculosis and syphilis have special char- 
 acters, which will be described below. In many cases the cause 
 of chronic ostitis is obscure, though probably circulating toxic 
 substances are the specific factors. Direct traumatism, periostitis, 
 or other inflammatory diseases surrounding the bone may be the 
 immediate causes. 
 
 Pathologic Anatomy. — In the necrotic and suppurative 
 form, following osteomyelitis, there is more or less softening of 
 the bony substance by absorption of the calcareous matter, and at 
 the same time proliferation, in the form of granulation-tissue, of 
 the cellular elements of the marrow and its prolongations within 
 the Haversian channels. Localized abscesses may be formed, or 
 infiltration of pus in various directions with increasing necrosis of 
 the intervening bone may occur. 
 
 The degenerative form of ostitis is a variety in which the cal- 
 careous matter is absorbed and the bone thus rendered more soft 
 and porous. The term inflammatory osteoporosis is applied to this. 
 In the process of absorption there are formed upon the outer and 
 inner surfaces of the bone, or within its substance, areas of erosion, 
 hollow spaces or indentations, showing bone-corpuscles and giant- 
 cells lying upon the eroded bony tissue. These depressions are 
 the so-called Howship's lacunae. The giant-cells, which are active 
 in the absorptive process, have been termed osteoclasts, and are 
 identical with the osteoblasts or osteoplaxes of developing bone. 
 Simultaneously with this absorption of the lamellse of bone there 
 is proliferation of the marrow-substance in the eroded areas, and 
 at the same time there may be increased vascularization of this in- 
 tervening tissue. Perforations are frequently established through 
 the lamellse by the penetration of new-formed blood-vessels, so that 
 neighboring excavated areas communicate. This form of inflam- 
 mation of the bone is frequent in the neighborhood of necrotic 
 areas or osteomyelitic collections of pus, and plays a part in the 
 pathologic processes of osteomalacia and other bone-diseases. It 
 is rarely an independent condition. 
 
 The hypertrophic form of chronic inflammation leads to in- 
 creased density of the bone, to which the term condensing ostitis, 
 or osteosclerosis, is applicable. It may occur as a reactive process 
 surrounding areas of osteoporosis or other local diseases of the 
 bone, or in association with ossifying periostitis. Occasionally it 
 occurs in certain bones or parts of bones without local or well- 
 ascertained general causes. Such cases are met with in syphilitic 
 persons. The anatomical changes consist in the deposition of in- 
 creased quantities of bony tissue by the same processes as are 
 operative in normal bone-formation. 
 
 The disease designated as leontiasis ossium is a form of osteo- 
 sclerosis affecting the bones of the head and face, and causing 
 
692 TEXT-BOOK OF PATHOLOGY. 
 
 irregular thickening and enlargement of these bones. The cause 
 of this condition is obscure. 
 
 HYPOPLASIA AND ATROPHY. 
 
 Hypoplasia, or the lack of development of bones, may occur 
 as a local or general condition. Local hypoplasia may be due to 
 injuries or diseases which render a part of the body useless. Gen- 
 eral hypoplasia is found in cretins and dwarfs. 
 
 True atrophy of the bones may involve an entire bone or 
 only portions of it. General atrophy of the whole or of parts of a 
 bone occurs as a result of inactivity or want of use, as in cases of 
 palsy, chronic rheumatism, and the like. The implication of cer- 
 tain parts of the nervous system (trophic centers) is particularly im- 
 portant, as the atrophy resulting in such cases is much more 
 extensive than that occurring in cases of similar inactivity from 
 other causes. 
 
 Partial atrophy of the bone may be due to pressure by 
 aneurysms, tumors, and the like. In these cases there is gradual 
 absorption of bony substance, and the process is really one of in- 
 flammatory osteoporosis. 
 
 General Atrophy. — Absorption of the bony substance, with 
 resulting osteoporosis, may occur in marasmic individuals, par- 
 ticularly in seniles. In these cases it is held by most author- 
 ities that the pathologic condition is dependent upon the fail- 
 ure of replacement of bone to make up for the normal absorp- 
 tion constantly taking place. In these cases the bone becomes 
 extremelv fragile from the increase of its marrow-spaces and its 
 general porosity. This condition of fragility is termed fragilitas 
 ossium, or ostt opsathyrosis. Occasionally this condition of fragility 
 is met with as an idiopathic disease, without definitely discover- 
 able causation and without evident disease of the bones. Such 
 cases have been found to occur in certain families through several 
 generations. 
 
 DEGENERATIVE CONDITIONS. 
 Caries. 
 
 Caries is a term applied to the molecular destruction of bone, 
 corresponding to ulceration of the soft parts. It may be asso- 
 ciated with osteomyelitis, or with necrosis due to traumatism or 
 various infective conditions. The changes consist in progressive 
 softening and crumbling of the bone, with eventual destruction of 
 more or less considerable areas. Caries is especially frequent as 
 a part of tuberculosis of the bones, and will be described in con- 
 nection with that disease. 
 
DISEASES OF THE BONES. 693 
 
 Necrosis. 
 
 Definition. — Necrosis is a term applied to the death of a 
 small or large portion of bone in mass. 
 
 Utiology. — Among the causes are the various acute or chronic 
 diseases of the periosteum, bone-marrow, and adjacent bone. In 
 cases of purulent periostitis the separation of the periosteum from 
 the underlying bone leads to interruption of blood-supply and 
 superficial necrosis. Similar results occur in cases of osteomye- 
 litis. Necrosis of the bone may also occur in consequence* of 
 embolic obstruction of the blood-vessels. 
 
 Pathologic Anatomy. — Necrosis may be partial or total, 
 and may occur in the center of the bone or at the periphery. The 
 dead portion of the bone, termed sequestrum, presents itself as an 
 irregular, more or less eroded fragment, almost completely or 
 completely separated from the remaining structure. The separa- 
 tion occurs by the process of demarcation, as in necrosis of the 
 soft parts. This line consists of an area of absorption of the cal- 
 careous matter and proliferation of the cellular elements. The 
 necrotic portion, or sequestrum, acts as a foreign body, and by its 
 continued irritation keeps up a suppurative inflammation of the 
 surrounding tissues. Fistulous communication with the exterior 
 is usually observed. If the sequestrum is peripheral and has 
 been discharged, the periosteum or the bone may replace the lost 
 tissue by regeneration. If the fragment is large or centrally 
 placed, discharge is impossible and suppurative inflammation con- 
 tinues, sometimes for years. In these cases considerable hyper- 
 plastic material may be deposited over and around the sequestrum, 
 and thus irregular thickening of the bone may be produced. 
 
 A peculiar form of necrosis is that occurring in consequence of 
 chronic phosphorus-poisoning. It is met with in persons engaged 
 in the manufacture of phosphorus-matches, and affects the maxil- 
 lary bone. The existence of carious teeth aids in the develop- 
 ment of this form of necrosis, probably by admitting micro-organ- 
 isms which infect the bone already altered by the poison. The 
 process begins in the periosteal and subperiosteal portions of the 
 bone, and ends in more or less complete necrosis. 
 
 Associated Conditions. — Long-standing necrosis causes 
 great deterioration of the general health, particularly in cases in 
 which suppurating sinuses are formed. Systemic infections may 
 follow and amyloid degeneration of various organs may occur. 
 
 Osteomalacia. 
 
 Definition.- — This is probably a general disease leading to 
 absorption of the bone-salts and to other changes in the bone, 
 which cause extreme flexibility. 
 
694 TEXT-BOOK OF PATHOLOGY. 
 
 Etiology. — The causes of osteomalacia are still obscure. It 
 is a disease occurring with especial frequency in puerperal women, 
 but it may occur in men and in non-puerperal women. A number 
 of theories have been offered to explain the disease, but none of 
 them has been established. In some respects it seems not unlikely 
 that it is a trophoneurosis. It is particularly frequent in certain 
 regions (endemic), while in others it occurs very rarely (sporadic). 
 
 Pathologic Anatomy. — The changes in the bone lead to 
 various deformities and changes of appearance. Distortions, 
 bends, and even fractures are observed in the long bones, and 
 deformities due to abnormal curvatures of the spine are not infre- 
 quent. The pelvis shows peculiar changes which may prove very 
 troublesome during labor. The characteristic change is a beaked 
 condition, due to displacement forward of the pubes and a lateral 
 indentation. This gives a triangular form to the outlet of the pel- 
 vis or superior strait. The bone-marrow is often quite red, and 
 the periosteum in the neighborhood of bends or fractures may be 
 thickened by cellular proliferation. The minute structure of the 
 bone in osteomalacia shows a more or less pronounced absorption 
 of calcareous matter, but the normal lamellar arrangement of 
 the bone may be preserved. In the region of bends and fractures 
 osteoid tissue of irregular structure, with bony corpuscles of con- 
 siderable size, may be observed ; while in other situations the 
 regular lamellar arrangement and the ordinary small-sized bone- 
 corpuscles are seen. Irregular areas of homogeneous or granular 
 appearance may be interspersed within the normal osseous tissues. 
 The line of demarcation between such abnormal non-calcareous 
 portions and the unaltered bone may be either sharply drawn or 
 diffuse. 
 
 Associated Conditions. — Patients suffering from osteo- 
 malacia are usually greatly reduced or cachectic, and frequently 
 perish with terminal pneumonia. Some cases end in recovery by 
 restitution of the bone. It has been claimed that there is evidence 
 in all eases of puerperal women of some bony absorption, and 
 osteomalacia, therefore, would seem to be but an exaggeration of 
 normal conditions. Normally the slight bony changes are cor- 
 rected after the puerperal period is passed. 
 
 INFECTIOUS DISEASES. 
 Tuberculosis. 
 
 Tuberculosis may occur in bones in several forms. Miliary 
 tubercles may be found in the bone-marrow in the course of 
 general miliary tuberculosis, and local tuberculous disease of the 
 periosteum may be met with. The most frequent and most im- 
 portant form of tuberculosis is tuberculous ostitis with caries. 
 
DISEASES OF THE BONES. 
 
 695 
 
 Etiology. — The involvement of the bones is nearly always 
 secondary, the first manifestations of tuberculosis occurring in 
 other structures, notably the lymphatic glands and the lungs. 
 The disease of the bones may be due to direct extension or to 
 hematogenous infection. Not rarely the joints are first involved 
 and the neighboring bones only secondarily. 
 
 Traumatic influences are of importance in determining the 
 situation of hematogenous tuberculosis. The traumatism causes 
 circulatory disturbances in the bone, and thus produces a suitable 
 soil for the bacilli to find lodgement. Bone-tuberculosis is most 
 frequent in early life ; it may actually begin in utero. 
 
 Pathologic Anatomy. — The tuberculous lesion of bone first 
 presents itself as an area of grayish color, with congestive redden- 
 ing of the parts around and intense injection of the bone-marrow 
 in its vicinity. Subsequently there are rapid cheesy change and 
 
 - ; * .• i 
 
 Fig. 339.— Tuberculous caries of one of the bones of the foot : a,} bony trabecula ; 5, 
 tubercle with caseous center; c, caseation in a focus of tuberculous tissue: d, giant-cells 
 in tubercles ; e, osteoclasts ; /, fatty marrow (Kaufmann). 
 
 more or less softening of the area of inflammation. Microscopically, 
 tubercles in various stages of degeneration are discovered, and in 
 addition areas of diffuse tuberculous granulation-tissue and caseous 
 degeneration (Fig. 339). At the same time extension occurs at 
 the periphery and new foci are established. The entire diseased 
 area may be separated from the uninvolved bone as a sequestrum, 
 but more frequently there is gradual carious softening, with forma- 
 tion of semifluid, cheesy material containing gritty particles of 
 bone or calcareous matter. Complete softening leads to the for- 
 
696 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 mation of a " tuberculous abscess " (Fig. 340). In these cases 
 a more or less irregular cavity is formed within the bone, 
 the wall of the cavity being covered with a pyogenic membrane 
 developed from the marrow and its extensions into the Haversian 
 canals. The contents of the abscess are 
 puriform or cheesy. The process tends to ex- 
 tend to neighboring parts, particularly to the 
 joints. When the abscess has penetrated the 
 encasing bone it may spread within the soft 
 parts, thus forming large tuberculous abscesses 
 (so-called cold abscesses). These may burrow 
 along the planes of the tissues to considerable 
 distances from the point of formation, present- 
 ing at the surface of the body in some favor- 
 able situation, as, for example, in the groin, in 
 psoas-abscesses. 
 
 Reactive changes may occur locally, and 
 more or less restitution may take place. Com- 
 plete encapsulation of a small focus may occur 
 by the formation of a surrounding zone of gran- 
 ulation-tissue and cicatrization, or by new-for- 
 mation of bone occurring after the activity 
 of the tuberculous process has been arrested. 
 "When adjacent portions of articulating bones 
 are involved the integrity of the articulation 
 is disturbed, and subsequently ankylosis may 
 be established by the formation of exostoses 
 and their union. 
 
 Seats and Associated Conditions. 
 
 Among the bones more frequently affected are 
 the vertebras, the long bones, particularly the 
 femur, and parts of the skull. In the vertebrae 
 the bodies are generally affected, and angula- 
 tion or distortion of the spine results (Pott's 
 disease). The cold abscesses formed in these 
 cases may burrow considerable distances, point- 
 ing far below the place of origin. Those spring- 
 ing from the cervical vertebra? may point be- 
 neath the mucous membrane of the pharynx or 
 esophagus, or anteriorly in the neck above the 
 clavicle or shoulder. The abscesses formed 
 in tuberculous caries of the dorsal vertebras may point under Pou- 
 part's ligament. Tuberculous disease of the petrous portion of 
 the temporal bone is not infrequent following tuberculous disease 
 of the ear ; it is important as a possible cause of tuberculous men- 
 ingitis. Tuberculosis of the head of the femur and of the hip- 
 joint is one of the most frequent forms of surgical disease in chil- 
 
 Fig. 340.— Tubercu- 
 lous "abscess" in the 
 lower end of the hume- 
 rus (modified from Bol- 
 linger). 
 
DISEASES OF THE BONES. 697 
 
 dren. The phalanges are sometimes involved in early childhood 
 by a curious form of tuberculosis, in which the shaft of the bone 
 increases in size by gradual absorption and tuberculous softening 
 within and deposition of new bone from the periosteum without. 
 
 Syphilis. 
 
 Syphilitic disease of bones may appear in various forms. Allu- 
 sion has already been made to the condensation of the bones, or 
 osteosclerosis, in this disease. Syphilis may also occur in the peri- 
 osteum as a nodular periostitis, or in the substance of the bone in 
 the form of degenerating gummata. Congenital syphilis gives rise 
 to certain peculiar alterations. 
 
 Etiology. — Syphilitic changes in bone are confined almost 
 exclusively to the tertiary period. They may occur without other 
 luetic disease, or as concomitants of hepatic, splenic, or other vis- 
 ceral disorders. The disease of the bones is frequently determined 
 by local injuries ; especially is this true of the periosteal forms. 
 
 Pathologic Anatomy. — Syphilitic periostitis is very common 
 upon the shin-bone, less frequent in the periosteum of other long 
 bones. There is, first, slight swelling of the periosteum, due to 
 multiplication of the cells. Subsequently this cellular mass 
 undergoes gummy or mucous degeneration, and the mass presents 
 the appearance of a small gumma. Superficial erosion, or even 
 necrosis, of the bone may take place, and discharge of the con- 
 tents may occur. Following this, hypertrophic processes in the 
 bone and adjacent periosteum lead to the formation of bony nodes. 
 These nodes may, however, be formed without the occurrence of 
 softening and discharge from the periosteal lesion, the process in 
 this case being one of simple ossifying periostitis. Gummata of 
 the bones generally begin in the deeper layers of the periosteum, 
 but tend to involve the bone more extensively than the form just 
 described. The gummatous infiltration and proliferation occur 
 along the blood-vessels of the periosteum and extend into the sub- 
 stance of the bone. Considerable areas may thus be implicated. 
 The bone itself is absorbed, or may -undergo rapid caries or 
 necrosis. Around the area of syphilitic change may occur a 
 zone of reactive hyperplasia of the bone and periosteum. The 
 gummata themselves become cheesy or undergo mucoid degenera- 
 tion, and eventually may discharge upon the surface. Syphilitic 
 gummata are most frequent in the bones of the head, tibia, and 
 sternum. 
 
 Occasionally gummata arise in the marrow of the bones instead 
 of the periosteum. 
 
 Congenital Syphilis. — The bony changes of congenital syphilis 
 are quite characteristic. The alterations occur at the junction of 
 the epiphyses with the diaphyses of the long bones. Longitudinal 
 
698 TEXT-BOOK OF PATHOLOGY. 
 
 section through these parts shows the line of junction as a bluish- 
 white or yellowish-white irregular zone about 2 or 3 mm. in thick- 
 ness (Plate 7). In more advanced stages this line becomes thicker 
 and more yellow. The minute changes consist in proliferation of 
 the cartilage-cells and subsequent fatty degeneration. Microscopi- 
 cally the proliferated cellular elements, fatty cells, and granular 
 detritus are conspicuous features. The epiphyses may be com- 
 pletely separated from the shaft. 
 
 Associated Conditions. — Involvement of the neighboring 
 parts is not infrequently seen in syphilitic diseases of the bones ; 
 thus there may be gummatous infiltration of the superficial tissues 
 with syphilis of the bones of the extremities, while in the case 
 of skull-bones extension inward may lead to involvement of the 
 dura and brain. When the process occurs about the foramina 
 of exit of nerves the sheaths of the latter may become involved. 
 Gummata of the sternum sometimes lead to the formation of retro- 
 sternal collections of puriform material. Amyloid degeneration 
 of various organs frequently follows bone-syphilis. 
 
 Lepra. 
 
 Changes may occur in the bones in cases of mutilating leprosy, 
 or more rarely in nervous lepra. Among these changes are ostitis 
 and osteomyelitis ; considerable destruction of the bones may be 
 produced. 
 
 TUMORS. 
 
 Exostoses are frequently met with in connection with defi- 
 nite disease of the bones and joints, or as more or less idiopathic 
 outgrowths (Fig. 44). They may be cartilaginous or fibrous in 
 character, but subsequently may become osseous. They present 
 themselves as flat, rounded elevations, or as more or less irreg- 
 ular outgrowths. Sometimes they are multiple and involve a 
 number of bones of the skeleton. In such cases, particularly, 
 heredity has been claimed as an important cause. 
 
 Fibroma, lipoma, myxoma, and angioma may be men- 
 tioned among the true tumors as benign growths occasionally met 
 with. They arise most frequently from the periosteum. 
 
 Chondroma and osteoma are more common than these, and 
 involve any part of the bone (Figs. 42 and 45). 
 
 Sarcoma. — The most important of the primary tumors of 
 bone is sarcoma. This may originate in the periosteum, bone- 
 marrow, or the bone itself. It may be spindle-celled, or less fre- 
 quently round-celled or alveolar. Sometimes it is melanotic. The 
 giant-cell sarcoma, or osteosarcoma, is particularly important. 
 It is most frequently met with in the lower jaw, beginning within 
 the bone and causing a more or less rapid swelling. The tumor 
 is surrounded by a shell of bone, which, however, sooner or later 
 
Plate 7. 
 
 
 .-A-V"^ 
 
 ;-v 
 
 Epiphyseal junction in congenital syphilis; specimen stained with hematoxylin. 
 
DISEASES OF THE BONES. 699 
 
 becomes perforated when the new growth spreads to the neighbor- 
 ing parts (Fig. 58). In all forms of sarcoma there is absorption of 
 the bone-substance in the vicinity. A form of sarcoma springing 
 from the periosteum is described under the name of osteoid sar- 
 coma. This tumor consists of fibromatous or round-celled sarcom- 
 atous tissue in which osteoid elements are irregularly embedded. 
 More or less calcification and bone-formation are observed. The 
 tumor may be quite soft or very hard ; it tends to spread to the 
 neighboring soft parts, and may give rise to metastasis. It is 
 particularly frequent at the ends of the long bones. 
 
 Secondary sarcoma of the bone-marrow is not rare in gen- 
 eral sarcomatosis. 
 
 Myeloma. — This term has been applied to a form of multiple 
 primary tumor of the bone-marrow allied to the lymphatic growths 
 of leukemia and Hodgkin's disease. The term lymphadenia ossea 
 has also been given to it. Probably a number of distinct condi- 
 tions (some of them secondary tumors) have been described under 
 these names. 
 
 Chloroma is a form of sarcoma, having a greenish or yellow- 
 ish color, that is met with in the periosteum, especially about the 
 orbits and other parts of the skull. 
 
 Primary carcinoma of the bones has been observed in a 
 few cases. It can only be explained upon the assumption that 
 islets of epithelial tissue have been deposited in the bone by faulty 
 development. Most cases, however, described as primary carci- 
 noma were probably in reality alveolar sarcomata. 
 
 Secondary carcinoma of the bones is not rarely met with, 
 especially in cases of cancer of the breast, thyroid gland, and 
 prostate. The secondary nodules may occupy the periosteum or 
 the bone-marrow. The bone becomes exceedingly fragile, and 
 fractures are not infrequent. 
 
 Cysts and Parasites. — Cystic transformation of myxomata 
 and of sarcomata may be met with. Occasionally dermoid cysts 
 are observed. Among the parasitic diseases Cysticercus cellulosse 
 has been described in a number of instances. 
 
700 TEXT-BOOK OF PATHOLOGY. 
 
 CHAPTER X. 
 
 DISEASES OF THE JOINTS. 
 
 I/Uxation. — The most frequent injury of joints is that known 
 as luxation, in which the relations of articulating bones are dis- 
 turbed. In these cases the ligaments and other soft tissues around 
 the joints are more or less torn, and in consequence become in- 
 flamed. If the luxation is reduced, this inflammation subsides 
 quickly, and frequently normal conditions are restored. If the 
 luxation persists, various secondary changes may occur. Anky- 
 losis in abnormal positions may take place by the formation of 
 fibrous adhesions, or in more favorable cases a false joint may be 
 established. In the latter cases local atrophy takes place in one 
 of the bones, forming a depression into which the end of the other 
 fits. Later, ossifying periostitis produces an elevation around the 
 depression of the socket, and thus a well-formed joint may be 
 produced. 
 
 Ankylosis is the term applied to the condition in which the 
 normal movability between articulating bones is prevented by in- 
 terosseous attachments. Pathologically, ankylosis may be fibrous, 
 cartilaginous, or bony. All of these forms are met with after 
 chronic inflammatory conditions of the joints. 
 
 DISTORTIONS OF JOINTS. 
 
 Distorted conditions of the joints may be due to contractions 
 of the muscles and tendons, or to cicatricial tissue in the neigh- 
 borhood of the articulation. Changes in the joints themselves 
 may be present as primary or as secondary conditions. Among 
 the more important of such deformities of joints are the various 
 sorts of club-foot : pes varus, the sole of the foot turned in ; 
 pes valgus, the sole of the foot turned out ; pes equinus, the foot 
 extended and supported upon the anterior ends of the metatarsal 
 bones ; pes calcaneus, the foot flexed and resting on the heel. 
 Combinations of these conditions are frequently met with. At 
 the knee-joint are found : genu valgum, in which the knees are 
 bent in (knock-knee), and genu varum, in which the knees are 
 bent out (bow-legs). 
 
 CIRCULATORY DISTURBANCES. 
 
 Hyperemia of the joints occurs as a part of acute inflamma- 
 tions, and involves the synovial membranes particularly. The 
 synovial fluid may be increased in quantity. 
 
 Hemorrhage into the joint may result from traumatic causes 
 or from inflammatory conditions, particularly in the course of hem- 
 
DISEASES OF THE JOINTS. 701 
 
 orrhagic diseases, notably scurvy and hemophilia. The blood may 
 remain fluid for a long time, and the joint not rarely has the ap- 
 pearance of chronic arthritis with effusion. Later, resorption of 
 the blood takes place. 
 
 Dropsy of the joints occurs in the course of acute and chronic 
 inflammations. 
 
 INFLAMMATIONS. 
 
 Acute arthritis may be traumatic or hematogenous, or in 
 other cases is secondary to disease in the vicinity. Hematogenous 
 arthritis may occur in the course of various infectious diseases, 
 such as scarlet fever, small-pox, pyemia, etc. In the same group 
 must be considered acute articular rheumatism, which is doubtless 
 an infection conveyed to the joint through the blood. 
 
 Pathologic Anatomy. — Various forms may be distinguished, 
 such as the dry or fibrinous, the serous, and the seropurulent. In 
 all cases there is, first, a deep congestion of the synovial mem- 
 brane. The ligaments and the cartilage are more or less impli- 
 cated at the same time. The terms synovitis, implying involve- 
 ment of the synovial membrane, and panarthritis, implying gen- 
 eral involvement, may be applied. In the dry or fibrinous form 
 there is a deposit of fibrin upon the surface, with or without serous 
 exudation. In the genuine serous form the exudation is purely ser- 
 ous, but more commonly seropurulent liquid is observed. Entirely 
 purulent exudate is sometimes formed (empyema of the joints). 
 
 Results. — In the milder cases complete resolution may take 
 place without destruction of the tissues of the joint. In the more 
 serious cases there is inflammation of the articulating cartilages, 
 with consequent ulceration or caries, or even considerable necro- 
 sis, of the cartilage. The underlying bone may be laid bare, and 
 ostitis or osteomyelitis may result. Sometimes discharge of 
 purulent material into the surrounding tissues occurs, and fistulous 
 communications with the exterior may be established. These 
 processes may lead to extensive disorganization of the joints, with 
 luxations and, in later stages, ankylosis. 
 
 Associated Conditions. — General systemic infection may follow 
 these acute inflammations of the joints. 
 
 Chronic arthritis may be due to a variety of causes. It 
 may follow the acute forms already described or may be primarily 
 chronic. Among the more important causes are traumatism and 
 certain infections. It occurs in the course of gout and in certain 
 nervous diseases, probably as the result of disturbance of the 
 trophic mechanism. Chronic arthritis of the aged has perhaps a 
 similar causation, and rheumatoid arthritis is nearly allied. 
 
 Pathologic Anatomy. — A variety of forms may be distinguished. 
 The same etiologic factors may, however, give rise to one or 
 another in individual cases. 
 
702 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 Chronic serous arthritis, or hydrops articulorum, is fre- 
 quently due to repeated acute arthritis. The joint is filled with thin 
 svnovia, and the synovial membrane is somewhat thickened. The 
 surface of the joint may be more or less covered with an injected 
 synovial membrane (synovitis pannosa). The knee-joint is most 
 frequently involved. 
 
 Chronic purulent arthritis is always infectious, and is usually 
 the outcome of an acute seropurulent or purulent arthritis. The 
 conditions met with have already 
 been described. It terminates in 
 more or less extensive disorganiza- 
 tion of the joint, and in favorable 
 cases in fibrous ankylosis (Fig. 341). 
 Arthritis deformans, or rheuma- 
 toid arthritis, occurs in persons past 
 middle age, but sometimes in young 
 persons, and even in childhood. Con- 
 stitutional depression and exposure 
 seem in some way to predispose. 
 There are, first, alterations in the 
 cartilages of the joints, consisting 
 of softening and ulceration or ero- 
 sion, which make the surface irreg- 
 ular and rough. At the same time 
 some hyperplasia of the cartilage- 
 cells takes place, but the hyperplas- 
 tic elements subsequently undergo 
 degeneration, and are absorbed. In 
 this way the cartilage is gradually 
 reduced and the ends of the bone 
 laid bare. The synovial membrane 
 and ligaments at the same time become thickened by hyperplasia. 
 Subsequently the articulating end of the bone is involved. There 
 is, first, absorption, and secondarily proliferative changes at the 
 periphery of the articulation, in the form of exostoses or osteo- 
 phytes. The joint is considerably deformed and thickened. Sub- 
 luxations are common, and the deformity leads to immobility of 
 the joint, or ankylosis. This form of arthritis is particularly 
 common in the metacarpophalangeal joints of the hand, and in 
 the other small joints of the hands and feet (Fig. 342). Later 
 the knee, elbow, and vertebral articulations may be involved. 
 
 Chronic dry arthritis with ulceration, or senile arthritis, is 
 particularly common in the hip-joint (malum coxaz senile). There 
 is gradual absorption of the cartilages and of the exposed surfaces 
 of the bone. Subsequently the surrounding parts of the bone 
 undergo selerosjs and hypoplasia. The changes are similar to 
 those of rheumatoid arthritis, but are more slowly developed. 
 
 Fig. 341.— Fibrous ankylosis, due to 
 chronic purulent arthritis. 
 
DISEASES OF THE JOINTS. 
 
 703 
 
 
 Fig. 342.— Rheumatoid arthritis, showing extensive deformity of the hands. 
 
 Neuropathic arthritis is met with in the course of spinal dis- 
 eases, such as locomotor ataxia and syringomyelia (Fig. 343). It re- 
 
 Fig. 343.— Neuropathic arthritis of the knee in a case of locomotor ataxia. 
 
 sembles the forms just described, is slowly developed, and is usually 
 quite painless, suggesting a purely degenerative or trophic disorder. 
 
704 TEXT-BOOK OF rATHOLOGY. 
 
 Gouty Arthritis. — Gout is a constitutional disease with a 
 tendency to a peculiar form of arthritis. The latter consists in 
 the deposit of crystals of urate of sodium and calcium in the carti- 
 lage-cells and intercellular substance of the articulations, and in 
 more advanced cases in the connective tissue of the joints and the 
 tissues round the joints (Fig. 344). These crystalline deposits occur 
 
 Fig. 344.— Deposit of crystals of urate of sodium in an articular cartilage (Lancereaux). 
 
 in definite attacks, as a rule, each attack (gouty paroxysm) being 
 marked by inflammatory processes in the joint. Hyperemia of the 
 synovial membrane, with serous effusions and with sometimes more 
 evident inflammatory manifestations (hyperplasia of the cartilage- 
 cells and round-cell infiltration), is observed during the parox- 
 ysms, and by their repetition chronic changes in the joint are 
 produced. The cartilages may become more or less eroded, and 
 even carious changes and suppuration may take place. The joints 
 most frequently involved are the small joints of the hands and 
 feet, notably the metatarso-phalangeal joint of the great toe. The 
 larger articulations are less commonly involved, and usually after 
 the smaller joints. 
 
 Associated Conditions. — The pathology of gout is by no means 
 confined to the changes in the joints. The disease is a general 
 one, and pathologic changes are found in various organs. There 
 is a tendency to thickening of the blood-vessels, to atheroma, and 
 to sclerotic changes in the kidney, liver, and heart ; and uratic 
 deposits may occur in the organs named or in the subcutaneous 
 tissue or superficial cartilages, such as those of the ear and nose 
 {gouty tophi). Concretions or calculi are frequently formed in the 
 kidney or bladder. 
 
 INFECTIOUS DISEASES. 
 Tuberculosis. 
 
 Tuberculosis, when primary in the joints, usually begins in the 
 synovial membrane. Frequently it is secondary to tuberculosis 
 of the adjacent bone. In such cases any part of the joint may be 
 first involved. 
 

 DISEASES OF THE JOINTS. 705 
 
 Etiology. — Tuberculous arthritis is most frequent in child- 
 hood, and occurs in those predisposed by heredity. The immedi- 
 ate determining cause may be traumatism, this serving to localize 
 the disease in a joint rendered peculiarly susceptible. Tubercu- 
 lous arthritis is frequently secondary to scrofulous disease of the 
 skin or glands, or to pulmonary tuberculosis, but is often primary. 
 
 Pathologic Anatomy. — The changes met with in the joints 
 vary somewhat in different cases. In instances beginning in the 
 synovial membrane there are formed more or less abundant, soft, 
 spongy granulations, which may eventually fill the entire joint- 
 cavity. These are pinkish or whitish in color, and may show 
 gray or yellow spots or tubercles quite plainly. Later this granu- 
 lation-tissue tends to degenerate, becoming mucoid or breaking 
 down by suppurative or cheesy change. In the early stages the 
 soft tissues of the joint are considerably inflamed and edematous ; 
 later they may show ulcerative or necrotic change, and similar 
 alteration may occur in the articular cartilages. Puriform soften- 
 ing of the granulations and the tissues of the joint may lead to the 
 development of cold abscesses within the joint, and the latter may 
 eventually burrow to the exterior. In cases progressing unfavor- 
 ably the joint is greatly disorganized by the advancing necrotic 
 changes. The abnormal productions are either discharged or in- 
 spissated, and ankylosis of the joint by fibrous adhesions takes place. 
 
 The external appearances of tuberculous joints are often quite 
 distinctive. The joint is swollen and boggy, or somewhat elastic 
 to the touch, and usually more or less distorted from subluxation. 
 There is little evidence of acute inflammation. In cases termi- 
 nating in ankylosis the bones are generally left in faulty position 
 in consequence of the formation of adhesions and the irregular 
 contractions of muscles. 
 
 Secondary Disorders. — Long-standing tuberculosis of the 
 joints occasions profound disturbances of the general health, and 
 sometimes causes definite disease, such as amyloid degeneration of 
 various organs. Disseminated tuberculosis rarely results. 
 
 Syphilis. 
 
 Syphilitic disease of the joints may occur in hereditary lues. 
 The cartilages of the joints are eroded, and thickening of the 
 ligaments with puriform exudation into the joint is observed. 
 The phalangeal articulations are most frequently involved. In 
 later life gummata in the neighborhood of the joints may invade 
 the latter by contiguity. 
 
 TUMORS. 
 
 Hyperplastic conditions are met with in the synovial fringes 
 of the joints in association with arthritis or independent of such. 
 
706 TEXT-BOOK OF PATHOLOGY. 
 
 These hyperplasias may take the form of fibrous growths, or they 
 may become lipomatous. An interesting form of new growth is 
 seen in the so-called rice-bodies. These are small fibrous or carti- 
 laginous bodies, up to the size of a small nut, which are entirely 
 free in the joint or attached by a fine pedicle to the synovial mem- 
 brane. They are formed from the synovial fringes, and probably 
 result from injury in most cases. The joints may be secondarily 
 involved in various forms of bony tumors. 
 
 THE TENDON=SHEATHS AND BURS/E. 
 
 Inflammations of the sheaths of tendons {tenosynovitis) and 
 of the bursa? (bursitis) occur under similar circumstances and in 
 similar forms as inflammations of the joints. A form of chronic 
 bursitis with dropsical effusion frequently occurs in the bursa 
 beneath the patella from chronic irritation (housemaid's knee), and 
 in the bursa at the joint of the elbow (miner's elbow). These 
 conditions are analogous to hydrops articulorum. 
 
 Ganglion is a condition of the tendon-sheaths of some clinical 
 interest. It presents itself as a rounded cystic nodule, most fre- 
 quently upon the back of the hands and wrists. Distinct fluctua- 
 tion may be discovered, or the cyst may be so dense that it feels 
 stony hard. The ganglion results from a localized dropsical con- 
 dition of the sheath of the tendons, with frequently a lateral 
 hernious projection. A similar condition is sometimes caused by 
 projection of the synovial membrane of the joints. 
 
 CHAPTER XI. 
 
 DISEASES OF THE VOLUNTARY MUSCLES. 
 
 Congenital malformations are occasionally met with, such 
 as absence of a part or of an entire muscle. 
 
 HYPERTROPHY. 
 
 Hypertrophy is frequently produced by athletic exercise or 
 laborious occupations. This affects the parts brought into play, 
 and is proportioned to the amount of work and the constitution or 
 condition of the individual. The muscle-fibers increase in thick- 
 ness and probably also in number. 
 
 Sometimes muscular hypertrophy is met with in cases in which 
 no adequate cause is discoverable. Thus in local or general giant 
 growths the muscles may be involved with other parts. 
 
 Pseudohypertrophy will be discussed among the degenerative 
 conditions. 
 
DISEASES OF THE VOLUNTARY MUSCLES. 707 
 
 CIRCULATORY DISTURBANCES. 
 
 Anemia of the muscles may be part of a local or general 
 anemia ; it is often quite insignificant in comparison with anemia 
 of other parts. In some of the general anemias the muscles may 
 present a dark appearance, clue to degenerative conditions. 
 
 Hyperemia is physiologic during and after exercise. It 
 occurs as an active process in association with inflammatory con- 
 ditions and as a passive congestion in cases of vascular stasis. 
 
 Hemorrhages may be traumatic, or may result from rupture 
 of the vessels in consequence of inordinate blood-pressure or local 
 degeneration of the vessel- walls and the surrounding muscle-fibers. 
 Among the conditions in which hemorrhage takes place are tetanus 
 and other convulsive disorders, fevers, and hemorrhagic diseases, 
 such as scurvy, hemophilia, and septic diseases. The hemorrhages 
 may occur in the form of small extravasations between the fibers, 
 or of more extensive infiltrations in the intermuscular planes. In 
 cases of traumatism, scurvy, or hemophilia, considerable blood- 
 tumors may be formed, the muscle-fibers being pushed aside or 
 torn apart. The blood is more or less rapidly absorbed. Pigmen- 
 tation and fibrous-tissue proliferation may result. 
 
 Bmbolism of the arteries or thrombosis of the veins does 
 not produce serious disturbances, as a rule. In cases of embolism, 
 secondary results may follow if the embolism is infective. 
 
 INFLAMMATIONS. 
 
 Inflammation of the muscles, or myositis, may be acute 
 or chronic, and may present itself in a variety of forms. Acute 
 myositis may be local or disseminated. 
 
 I/Ocalised Acute Myositis. — This form may be due to 
 injuries, such as contusions of the muscles or wounds communi- 
 cating with them, or may be infectious in character, resulting from 
 the direct extension of infectious diseases of the skin, subcutaneous 
 tissues, bones, and other adjacent parts, or from embolism. A 
 serous, a hemorrhagic, and a purulent form may be distinguished. 
 
 Serous myositis is characterized by an edematous condition of 
 the muscle, which gives it a peculiar gelatinous appearance on 
 section. Microscopically there is cellular infiltration of the mus- 
 cle-bundles, while the muscle-fibers themselves become swollen 
 and suffer granular degeneration or hyaline change, and some- 
 times vacuolation. 
 
 Hemorrhagic myositis is an intense form, and is met with in 
 muscles adjacent to gangrenous or phlegmonous lesions, malignant 
 pustules, and the like. Myositis occurring in scorbutic individuals 
 is frequently of the hemorrhagic form, as is also that which occurs 
 in consequence of the sting of venomous snakes or other animals. 
 
708 TEXT-BOOK OF PATHOLOGY. 
 
 The muscle becomes more or less tensely swollen, and on section 
 the hemorrhagic infiltration is plainly visible as a diffuse process 
 or as localized areas of hemorrhage. 
 
 Suppurative myositis may be circumscribed or diffuse. Circum- 
 scribed myositis, or abscess of the muscle, may result from entrance 
 of micro-organisms through the lymphatic or vascular circulation, 
 or it may be due to traumatism, with communications from the 
 surface. Occasionally suppurative inflammation occurs in an ob- 
 scure manner, when the term cryptogenetic myositis is applicable. 
 Distinctly metastatic abscesses may be occasioned by embolism. 
 
 In association with suppurative inflammations of the skin or sub- 
 cutaneous tissues and the mucous membranes there may be sero- 
 purulent or phlegmonous myositis, with the formation of irregular 
 abscesses. In these cases the lesion spreads by infiltration, and 
 the muscle-fibers undergo widespread degeneration (fatty degenera- 
 tion, hyaline change, and necrosis). Abscesses in the muscles ex- 
 tend and rupture in various directions, and may leave consider- 
 able areas of scar-formation. 
 
 Disseminated acute myositis or polymyositis may ap- 
 pear without any definite cause, sometimes in association with 
 tuberculosis of the lungs, or as a distinctly secondary affection in 
 association with infectious diseases, like typhoid fever, diphtheria, 
 etc. In the primary form there may be widespread muscular dis- 
 ease, with swelling and tenderness of the muscles and sometimes 
 redness and edema of the skin. The term pseud otrichinosis was 
 applied from the resemblance of the appearances to those of trichi- 
 nosis, and the name dermatomyositis has also been given this con- 
 dition. Some of the conditions included under the heading mus- 
 cular rheumatism by clinicians are doubtless instances of the kind 
 here referred to. Examination of the muscles shows pallor of the 
 tissue, and sometimes visible areas of degeneration. Microscopi- 
 cally there are cellular infiltration between the muscle-fibers and 
 swelling, with loss of striation of the fibers themselves. More 
 advanced degenerations of the fibers, such as granular change, 
 coagulation-necrosis, and vacuolation, may be observed. The 
 affected muscles lose their functional contractile power, and more 
 or less palsy results. When affecting the muscles of the pharynx 
 and respiration this becomes serious in predisposing to inspiration- 
 pneumonias. 
 
 The condition described as secondary acute polymyositis is 
 degenerative to a greater extent than inflammatory, and' will be 
 considered among the degenerations. 
 
 Chronic myositis may be suppurative in type or produc- 
 tive. 
 
 Chronic suppurative myositis may be the outcome of acute sup- 
 puration, and is particularly frequent in association with tubercu- 
 losis and actinomycosis. 
 
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DISEASES OF THE VOLUNTARY MUSCLES 709 
 
 Chronic productive myositis is characterized by the formation of 
 connective tissue between the muscle-fibers. The fibers them- 
 selves, as a rule, undergo degenerative changes, though occasion- 
 ally snowing regeneration to some extent. This condition may be 
 the termination of acute myositis, or it may occur in the vicinity 
 of various localized diseases of the muscles or of the neighbor- 
 ing parts. In some cases, if not all, the primary change is 
 degeneration of the muscle-fibers, and the interstitial or fibrous 
 tissue is reactive in character. Some of the cases will be con- 
 sidered under the head of muscular atrophies. The changes 
 that occur in the interstitial tissue of the muscles consist pri- 
 marily of proliferation and round-celled infiltration. Later there 
 is formation of firm connective tissue. Some multiplication of 
 the muscle-nuclei and actual increase in size of the muscle- 
 fibers may be observed. Degeneration of the muscle-fibers, 
 however, is more prominent, and is generally in proportion to 
 the degree of connective-tissue change. The fibers may show 
 cloudy swelling or hyaline changes, or more complete degenera- 
 tion, such as fatty degeneration, fragmentation, or vacuole-forma- 
 tion. 
 
 Ossifying' myositis is a variety of productive myositis. It may 
 occur in the form of bony nodules in parts subjected to constant 
 irritation or strain, as in the case of the deltoid muscle in soldiers 
 and the adductor muscles in horsemen. Similarly, in the vicinity 
 of disease of the bones and periosteum, nodules may develop in 
 the muscle. A form of more general disease, termed myositis 
 ossificans progressiva, has been observed in youthful persons, with- 
 out discoverable cause. It affects the muscles of the back and 
 neck, and sometimes those of all parts of the body. The muscles 
 are swollen, and first present inflammatory manifestations, termi- 
 nating in fibrous change which finally leads to bone-formation. 
 The osseous tissue is at first in the form of spicules or small 
 nodules, but gradually increases to considerable proportions. The 
 muscles themselves contract, and various deformities with pseudo- 
 ankyloses may result. The muscles of the face, diaphragm, and 
 heart are unaffected. 
 
 ATROPHY AND DEGENERATIONS. 
 
 Several forms of atrophy are recognized. Certain cases are 
 dependent upon disease of the spinal cord or nerves (neuropathic 
 form), others occur as primary diseases of muscles (myopathic 
 form), and in another group the change is due to simple nutritional 
 processes (simple and senile forms). 
 
 Neuropathic muscular atrophy may be the result of dis- 
 ease of the anterior horns of the gray matter of the cord. To the 
 cases in which this lesion is the underlying pathologic condition the 
 
710 
 
 TEXT-BOOK OF PATHOLOGY. 
 
 term progressive muscular atrophy has been applied. The causes 
 of this disease are obscure. 
 
 It leads to progressive atrophy of the muscles of the hands, 
 arms, and shoulders, and less frequently of those of the body and 
 buttocks. It usually begins in the small muscles of the hands, 
 but sometimes affects those of the shoulders first. The muscles 
 become pale and rather flabby. Microscopically the fibers show 
 various forms of degeneration. Fragmentation in a longitu- 
 dinal or in a transverse direction, coagulation-necrosis, and occa- 
 sionally fatty degeneration of the fibers may be seen. Sometimes 
 the fibers seem to grow smaller by a simple atrophic process (Fig. 
 345). Coincidently, reactive proliferation is seen in the connective 
 
 
 A; 
 
 
 Fig. 345.— Neuropathic muscular atrophy, showing atrophy of the muscle-fibers. 
 
 in the interfascicular fibrous tissue, and thickening of the blood-vessel walls 
 
 tissue between fibers, and doubtless this to some extent causes 
 further muscular degeneration. The muscle-cells themselves may 
 proliferate quite extensively. 
 
 Secondary neuropathic muscular atrophies may occur in various 
 spinal diseases, such as syringomyelia and in degenerations follow- 
 ing cerebral disease. These are essentially similar in character to 
 the primary neuropathic variety, though their clinical character is 
 different. Section, disease, or injury of motor nerves may lead to 
 local atrophies by separating the muscles from their trophic cen- 
 ters in the cord. 
 
 Myopathic muscular atrophy occurs in children and young 
 persons, and is frequently hereditary. It begins in the buttocks, 
 thighs, or calves, and sometimes in the shoulders. Two forms 
 have been distinguished : the simple atrophic form and the pseudo- 
 hypertrophic form. The anatomical changes in the former are 
 the same as in the neuropathic variety just described. 
 
DISEASES OF THE VOLUNTARY MUSCLES. 711 
 
 Pseudohypertrophic Muscular Atrophy. — In this condition the 
 muscles increase greatly in size, but are soft and flabby. The 
 child may present the appearance of an athlete, with enormous 
 calves and thighs, but is extremely weak and can scarcely stand. 
 Microscopically the causation of the enlargement is found to be a 
 considerable degree of intermuscular proliferation of connective 
 tissue, with marked fatty infiltration. Sometimes in this form, as 
 well as in other varieties, some actual enlargement of the muscle- 
 fibers is observed, but this is doubtless degenerative. 
 
 Simple muscular atrophy may be senile in origin or due to 
 lack of exercise. In these cases the muscle-fibers become smaller, 
 and some proliferation of the connective tissue is generally present. 
 In senile cases brown atrophy may occur, brownish pigment- 
 particles being deposited in the atrophic fibers, especially near the 
 nuclei. 
 
 Parenchymatous degeneration of the muscles may occur 
 in the vicinity of inflammatory lesions, tumors, or other areas of 
 disease. It may also occur in the course of infectious diseases in 
 association with coagulation-necrosis. The fibers become cloudy 
 and lose their striated appearance from the presence of minute 
 granules. In some instances inflammatory changes in the inter- 
 fascicular connective tissues are associated with the degeneration 
 of the fibers. Cases of this sort may be called secondary acute 
 polymyositis. 
 
 Patty degeneration is found under the same circumstances 
 as the above, and also in chronic cachectic diseases and in cases 
 of poisoning with phosphorus and other "parenchyma-poisons." 
 The muscle-fibers have a streaked or spotted, yellowish appear- 
 ance, and are more or less flabby. Microscopically the fibers are 
 seen to be filled with small oil-droplets, which obscure the stria- 
 tions. All parts of the fiber may become degenerated until the 
 sarcolemma-sheath contains only a mass of fat-droplets and 
 detritus. 
 
 Fatty infiltration may occur in association with atrophy in 
 the condition above described — pseudohypertrophic muscular 
 atrophy ; and in various nervous diseases in which the muscles 
 waste from disease or trophic change. A certain amount of 
 lipomatosis may occur in general obesity. 
 
 Amyloid degeneration is rare and unimportant. 
 
 Calcification may occur in the form of ossifying myositis, 
 and locally in scars following various local diseases — abscesses, 
 etc. 
 
 Coagulation-necrosis, or hyaline degeneration, is of 
 great clinical importance. It was first discovered by v. Zenker 
 as one of the lesions occurring in typhoid fever. The muscle- 
 fibers at first become granular and cloudy (parenchymatous degen- 
 eration), and later waxy or hyaline change occurs in streaks or 
 
712 TEXT-BOOK OF PATHOLOGY. 
 
 completely transforming the fibers. Transverse fragmentation is 
 common, and gross rupture of the muscle may be met with. In 
 the latter cases hemorrhagic infiltration, or even considerable 
 hemorrhage (hematoma), may be occasioned. Reactive inflam- 
 matory change in the interstitial connective tissue is generally 
 present. This disease occurs in the course of typhoid fever, but 
 also in various other febrile and infectious conditions. It is most 
 common in the abdominal muscles (rectus abdominis), in certain 
 muscles of the extremities, and in the heart. The latter situation 
 is, of course, of greatest significance (see Diseases of the Heart). 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis may occur in the form of cold abscesses in 
 association with tuberculous disease of bone, or less frequently of 
 the lymphatic glands or other parts. In these cases there is a 
 gradual extension of the caseous and liquefying tuberculous dis- 
 ease into the muscles, and sometimes the abscesses burrow to 
 great distances within the muscular sheath, as, for example, in 
 jysoas abscess. Less destructive tuberculous myositis may occur 
 in the muscles beneath the skin and mucous membranes by exten- 
 sion of tuberculous processes. In these cases cellular infiltration 
 and tubercle-formation, with some caseous change, may be observed. 
 Miliary tubercles, or larger tubercular nodules due to hematogenous 
 infection, are rare. 
 
 Syphilis may occur in the form of gummata, and it is likely 
 that some cases of diffuse productive myositis are syphilitic in 
 nature. As in other parts of the body, the blood-vessels in these 
 cases have been described as particularly thickened. 
 
 Glanders, actinomycosis, and anthrax may involve the 
 muscles in the vicinity of the specific lesions. Nodular and, later, 
 necrotic or suppurative foci are the lesions observed. 
 
 TUMORS AND PARASITES. 
 
 The tumors of muscles, for the most part, spring from the 
 interstitial connective tissue. Among the benign tumors fibromata, 
 myxomata, and lipomata are sometimes met with. Osteoma and 
 chondroma are found as localized lesions resulting from irritation 
 or as true tumors. Striped muscle-tumors, or rhabdomyomata, 
 are rarely found in the muscles, though occasionally seen as small 
 nodules. 
 
 More important than the above is sarcoma, which occurs as 
 a primary tumor comparatively frequently. The fibrous and 
 spindle-celled varieties are common, and round-celled sarcoma are 
 sometimes observed. The tumors originate from the connective 
 tissue, though it is held by some that the muscle-fibers themselves 
 may undergo sarcomatous transformation. 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 713 
 
 Carcinoma is a rare tumor, and is always secondary. The 
 secondary form is not rarely seen in the muscles in the vicinity of 
 carcinomata of other structures, such as the mammary gland. 
 
 Among the -parasitic diseases of muscles may be mentioned 
 trichinosis, cysticercus invasion, and hydatid disease. The first 
 occasions disseminated myositis, to which reference has already 
 been made. The other two conditions are rare and not important. 
 
 CHAPTER XII. 
 DISEASES OF THE BRAIN AND ITS MEMBRANES. 
 
 THE DURA MATER. 
 
 CIRCULATORY DISTURBANCES. 
 
 Active hyperemia occurs in the dura in association with 
 tumors, gummata, and other focal diseases. The vessels of the 
 dura surrounding the area of disease become distended and the 
 membrane may be diffusely reddened. 
 
 Passive hyperemia may occur under the same circumstances 
 as the above, and also in cases of thrombosis of the venous sinuses. 
 
 Hemorrhages are usually due to traumatism, and may occur 
 on the outer or inner surface of the dura. Extradural hemor- 
 rhages are more common than intradural, especially in cases in 
 which there is fracture of the skull. A collection of blood be- 
 tween the skull and the dura is sometimes designated internal 
 cephalhematoma. Small hemorrhages into the dura may occur in 
 infectious or hemorrhagic diseases and in cases of death from 
 asphyxia. 
 
 INFLAMMATIONS. 
 
 Inflammation of the dura, or pachymeningitis, may be 
 
 acute or chronic, and hemorrhagic, suppurative, or productive in 
 character. 
 
 Hemorrhagic pachymeningitis occurs more frequently in the aged 
 than in the young, and is a not uncommon condition in the insane. 
 Chronic alcoholism and traumatism seem to be factors of some im- 
 portance. In the early stages of the disease the inner surface of the 
 dura exhibits a superficial deposit or membrane of grayish color, 
 with brown or red spots, the latter being composed of altered blood- 
 pigment (hematoidin). Microscopically the membranous deposit 
 is found to consist of soft granulation-tissue containing numerous 
 thin-walled blood-vessels. Later, diapedesis of blood-corpuscles, 
 
714 TEXT-BOOK OF PATHOLOGY. 
 
 or actual hemorrhages, occur, and the diseased area may have the 
 appearances of a simple collection of blood or of a more or less 
 stratified hemorrhagic exudate. Sometimes the amount of exu- 
 date and of hemorrhage may be such as to cause considerable 
 cerebral compression, and in other cases death may occur from 
 the hemorrhage itself. Occasionally the blood is in part ab- 
 sorbed, and a serous collection [hygroma durce matris) results. 
 The seat of the disease is usually in the area of distribution of the 
 middle meningeal artery. 
 
 Suppurative pachymeningitis may occur in consequence of 
 injuries, caries, or other diseases of the skull. Sometimes it re- 
 sults from purulent softening of thrombi in the venous sinuses, 
 and very rarely it is secondary to leptomeningitis. Not rarely 
 localized suppurative pachymeningitis results from disease of the 
 middle or internal ear, with extension through the petrous bone. 
 The dura becomes thickened by cellular infiltration, is soft and 
 edematous, and not rarely undergoes necrotic change. The dis- 
 ease may be localized or diffuse, and may occasion secondary 
 thickening and adhesions of the dura in cases terminating favor- 
 ably. 
 
 Productive pachymeningitis may be of fibrous or ossify- 
 ing character. The etiology is often obscure. Some cases follow 
 hemorrhagic or suppurative pachymeningitis ; in some the process 
 seems to be primarily productive. Syphilis is probably a cause 
 of importance. The dura, in the fibrous variety, is simply thick- 
 ened and more or less attached to the pia-arachnoid and the inner 
 surface of the skull. When firm attachments with the skull are 
 formed osteophytes are frequently found upon the surface of the 
 bones and in the dura (ossifying pachymeningitis). Osseous 
 plates may be met with in the falx cerebri and tentorium cerebelli. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis may occur in the form of miliary tubercles in 
 association with tuberculous leptomeningitis. It may also be 
 associated with tuberculosis of the bones ; and, in rare instances, 
 has been met with as a primary disease of the dura. In the latter 
 cases the disease takes the form of a caseous nodular thickening 
 of the membrane. 
 
 Syphilis may occasion a form of diffuse productive pachy- 
 meningitis, or gummata. The latter may originate in the dura, 
 and extend to the pia or skull-bones, or they may originate in the 
 bones and invade the dura secondarily. Gummata in this situa- 
 tion present themselves as more or less flattened nodular growths 
 of grayish color, having a marked tendency to caseous change 
 and to resolution, with formation of circumscribed thickenings 
 and adhesions of the dura. 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 715 
 
 TUMORS. 
 
 Tumors of the dura mater occur with considerable fre- 
 quency. The most common is probably alveolar sarcoma. This 
 may occur in various situations, either as a flat swelling, or as a 
 somewhat pyramidal mass, with the apex toward the brain, into the 
 substance of which it projects ; it is often firmly attached to the skull. 
 Other forms of sarcoma are angiosarcoma, characterized by the pro- 
 liferation of the cells of the adventitia of the blood-vessels, and a 
 form in which the fibrous tissue so predominates as to make it really 
 a fibroma, although nests of endothelial cells are found scattered 
 throughout it. Other forms of sarcoma, however, also occur, par- 
 ticularly a small round-cell variety, which is usually multiple and 
 the result of metastasis from some other portion. The latter 
 tumors are usually flat, diffuse, and often extensive. They may 
 or may not cause bulging of the skull. In any of these forms, 
 but particularly in those in which the fibrous connective tissue is 
 in excess, calcareous infiltration is not uncommon. In nearly all 
 cases these tumors may produce erosion of the inner surface of the 
 skull. Hyaline degeneration of the intercellular substance is 
 very common. Among the other tumor-like growths are fibrous 
 changes that may or may not be inflammatory in nature, and lead 
 to circumscribed or diffuse thickening of the dura mater, and 
 usually cause it to adhere densely to the skull. These are most 
 apt to be found in old people. In addition to the round-cell sar- 
 coma, gliosarcoma of the brain and carcinoma of the scalp may 
 give rise to secondary growths in the dura mater, but these are 
 extremely rare. 
 
 THE PIA AND ARACHNOID. 
 
 CIRCULATORY DISTURBANCES. 
 
 Anemia of the pia may occur in cases of general anemia. 
 
 Active hyperemia is constantly present in the early stages 
 of meningitis. It is also met with in cases of death from alcohol- 
 ism, and in severe infectious fevers, though in most of these cases 
 microscopic examination discloses the fact that the process is really 
 one of beginning inflammation. The pia is red and the small 
 arterioles are injected. The fluid in the subarachnoid space is in 
 excess, and may be slightly turbid or sanguinolent. 
 
 Passive hyperemia occurs in cases of general venous stasis, 
 as in heart-disease, pulmonary diseases, and venous thrombosis. 
 The large veins are greatly swollen, and the subarachnoid fluid is 
 excessive. 
 
 Hemorrhages. — Small punctate hemorrhages may occur in 
 cases of meningitis, in scurvy, purpura, and the like. Larger 
 
716 TEXT- BOOK OF PATHOLOGY. 
 
 hemorrhages between the pia and arachnoid are most commonly 
 due to traumatism, and may sometimes be the result of rupture of 
 aneurysms. The blood in cases of large hemorrhages may cause 
 injurious cerebral compression, if rapid death does not follow the 
 hemorrhage itself. Occasionally the blood becomes inspissated 
 and absorbed, the membranes in these instances becoming thick- 
 ened and pigmented, or it may be encapsulated and the pigment 
 absorbed, giving rise to a clear cyst {hygroma). 
 
 Kdetna of the membranes themselves, or collections of edem- 
 atous liquid in the subarachnoid space (external hydrocephalus), 
 may be due to passive congestion. The membranes are thickened 
 and of translucent, gelatinous appearance ; the subarachnoid fluid 
 causes elevation of the arachnoid and more or less compression of 
 the cerebral convolutions. Hydrops ex vacuo is a form of dropsical 
 eifusion under the arachnoid, resulting from atrophy or hypoplasia 
 of the cerebral convolutions. The space normally occupied by 
 cerebral substance is in these cases filled with serous liquid. 
 
 INFLAMMATION. 
 
 Inflammation of the arachnoid and pia is called lepto- 
 meningitis. It is always an infectious process, and may be 
 either acute or chronic. 
 
 Etiology. — The commonest cause of acute leptomeningitis is the 
 pneumococcus. It is found in about 60 per cent, of all cases, and 
 in these pneumonia is often an associated or primary condition. 
 The pneumococcus may reach the meninges either by the blood- or 
 lymph-channels, or by creeping along the lymphatic spaces in the 
 areolar tissue between the esophagus and vertebral column ; occa- 
 sionally it enters directly from the ear or nasal cavity. Other 
 micro-organisms that have been found are the streptococcus, the 
 staphylococcus, Friedlander's bacillus, the Bacillus pyocyaneus, 
 the bacillus of glanders ; the actinomyces, the typhoid bacillus 
 (of which a number of cases have been reported), the Bacillus 
 coli communis, and the bacillus of bubonic plague. Meningitis 
 occasionally occurs in the course of gonorrhea, but no case has as 
 yet been reported in which the gonococcus was certainly demon- 
 strated. Mixed infection is not uncommon, consisting usually of 
 the pneumococcus and one or other of the more common pyogenic 
 micro-organisms, and the latter are also frequently found associated 
 with the tubercle-bacillus. The cause of epidemic cerebrospinal 
 meningitis is the Diplococcus intraceUularis meningitidis, discov- 
 ered in 1887 by Weiehselbaum in six cases that he examined, and 
 subsequently found in other cases by Goldschmidt, Guarnieri, 
 Xcttcr, Faber, and others. 
 
 Pathologic Anatomy. — The gross changes may vary from those 
 that are not recognizable macroscopically, to collections of green- 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. Ill 
 
 ish pus in the subarachnoidal space half an inch or more in thick- 
 ness and covering the entire surface of the brain. In the slight- 
 est forms the presence of the condition may be suspected by the 
 slight edema of the arachnoid, and perhaps a small collection of 
 fluid containing flakes along the fissures of the brain. In some 
 cases, however, even this does not occur, and it is impossible, with- 
 out a microscopic examination, to say that inflammatory processes 
 exist. Microscopically, sections in these cases usually show over- 
 filling of the small vessels with blood, and a greater or less num- 
 ber of round cells, usually polynuclear, immediately surrounding 
 it. Often this collection of round cells is most marked in the 
 recesses of the convolutions. Staining for bacteria usually reveals 
 the presence of a few, although in these cases they are rarely nu- 
 merous. If the process has been more severe, or of longer dura- 
 tion, the edema of the arachnoid becomes more pronounced ; its 
 glassy, moist appearance being very distinctive. The vessels are 
 usually injected; and this applies particularly to the veins, which 
 appear as dark-blue tortuous cords running through the mem- 
 branes. In the subarachnoidal space there is now a considerable 
 collection of fluid, and along the sides of the arteries usually a 
 distinct collection of lymph or pus. Sometimes, but not always, 
 the arterioles are also distinctly injected, and occasionally there is 
 a faint pinkish coloration, due to the injection of the capillaries. 
 
 This form may be localized or diffuse, and is usually secondary 
 to some local source of inflammation, which is most frequently 
 middle-ear disease. The process often shows distinct indications 
 of rapid extension. 
 
 The more extensive diffuse forms show considerable variation 
 in the part affected with greatest intensity, and have been divided 
 into leptomeningitis of the vertex and leptomeningitis of the base. 
 Ordinarily the purulent exudate is most pronounced along the 
 course of the middle cerebral artery, extending from either side 
 of the sella turcica outward and upward. 
 
 The changes observed consist of diffuse injection of the soft 
 membranes, edema of the arachnoid, and a perivascular sero- 
 fibrinous exudate along the course of the vessels coming from the 
 veins. Microscopically, sections show around these vessels a mass 
 of fibrin, in which are embedded a considerable number of poly- 
 nuclear leukocytes. Often cells undergoing fatty degeneration are 
 also found in these masses, lying close to the walls of the vessels 
 in the portions of the brain where the changes are most pro- 
 nounced. In this condition micro-organisms are usually found 
 quite readily, either within or without the cells, those within the 
 cells, in particular, frequently showing a partial loss of staining- 
 power, that has been taken to indicate phagocytic activity. 
 
 In the most severe cases the entire subarachnoidal space is dis- 
 tended with a purulent accumulation. The surface of the brain 
 
718 TEXT-BOOK OF PATHOLOGY. 
 
 can no longer be seen, the thick greenish exudate covering the 
 convolutions as a smooth mantle. In nearly all these cases there 
 is also pronounced edema, the arachnoid looking thick, shiny, and 
 moist. Microscopic sections show the ordinary picture of a puru- 
 lent accumulation ; pus-cells in a fibrinous meshwork, desquamated 
 endothelial cells, and micro-organisms. In all forms of acute 
 leptomeningitis petechial hemorrhages into the arachnoid are com- 
 mon. The substance of the brain and cord may also be involved, 
 and this involvement may vary from a slight increase of the neu- 
 roglia-elements just beneath the pia, to the presence of foci of 
 round cells. These foci are usually found about the small vessels 
 or lymphatics dipping in from the pia, the latter situation being 
 by far, the more frequent. Ordinarily they are microscopic and 
 surrounded by a narrow zone of partially degenerated nervous 
 substance, outside of which there is again a slight increase in the 
 neuroglia-tissue and cells. Occasionally, however, the cerebral 
 involvement may be more extensive, and large abscesses are 
 formed, leading to the destruction of considerable portions of the 
 nervous substance. The nerve-fibers, even those in the neighbor- 
 hood of the lesion, rarely show distinct alterations. The ganglion- 
 cells, however, exhibit slight diffuseness in taking the stain, or 
 irregularities in the arrangement of the chromophilic bodies. If 
 the abscesses are larger, either involving or close to the gray sub- 
 stance, the ganglion-cells may show extensive degeneration, with 
 entire loss of staining-power and fragmentation of the protoplasmic 
 processes, nothing being left to indicate the position of the cells 
 excepting an irregularly shaped vesicle containing some brownish 
 pigment. These larger foci, however, are usually found in the 
 white substance. 
 
 An attempt has been made to distinguish varieties of menin- 
 gitis according to the infective agents, and Netter has stated that 
 in pneumococcic infection the pus is viscid and greenish ; in strep- 
 tococcic infection, more serous and less adherent to the mem- 
 branes. Honl believes that only four forms can be differentiated — 
 the thick, viscid pus of the pyogenic micro-organism, the yellow- 
 ish exudate of tuberculosis, the bluish-green pus of the Bacillus 
 pyocvaneus, and the purulent exudate containing yellowish grains 
 of actinomyces. 
 
 Epidemic cerebrospinal meningitis does not differ essen- 
 tially from the ordinary septic form, excepting in its cause. 
 As a general rule the inflammatory process begins upon the 
 convexity of the frontal lobes, and proceeds backward and down- 
 ward, the basal meninges being involved late in the course of the 
 disease. Aside from those forms occurring as a complication of 
 other pathologic conditions that lead to death before the menin- 
 gitis has been fully developed, it is the one most likely to kill the 
 patient before distinct alterations have become evident. These 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 719 
 
 cases are spoken of as foudroyant or fulminant. , The disease is 
 often accompanied by lesions in other parts of the body, as pete- 
 chiae in the skin, suppuration in the joints, multiple abscesses, en- 
 docarditis, degenerations of the myocardium, and suppuration of 
 the labyrinth of the ear. 
 
 Associated Changes. — Besides the meninges of the brain, those 
 of the cord are almost always involved, even in cases of tuber- 
 cular meningitis. The peculiarities of these conditions are de- 
 scribed in the section on the spinal cord. Extension along the 
 fold of pia mater that covers the choroid plexus is also exceed- 
 ingly common. The cerebrospinal fluid may be turbid, there is a 
 moderate amount of lymph on the ependyma and over the surface 
 of the plexus, and the latter may even contain small abscesses. 
 Not infrequently, in prolonged cases, meningitic adhesions and 
 occlusion of the aqueduct of Sylvius give rise to an acute hydro- 
 cephalus. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculous meningitis is usually a secondary affection, 
 although in children it may occasionally appear in connection with 
 a few recent foci in other parts of the body. The bacilli reach the 
 meninges ordinarily by the blood-vessels, particularly, in all prob- 
 ability, by the left carotid, from which situation they may spread 
 along the base or to the vertex. Occasionally they seem to pass 
 up the vertebral arteries, and may then affect the cerebellum more 
 severely than the base of the cerebrum. Tuberculosis may also 
 extend directly from the tubercular lesions of the skull or of the 
 middle ear, and it has occasionally been observed to occur after 
 traumatism. Other routes of infection, however, have been sug- 
 gested, particularly, as in acute purulent meningitis, the organisms 
 have been supposed to pass up the posterior mediastinum, the retro- 
 pharyngeal areolar tissue, and thence into the cranial cavity. Mixed 
 infection not infrequently occurs, and has been supposed to account 
 for the purulent exudate. It is certain, however, that pure tuber- 
 culous meningitis may occasion the formation of pus. The organ- 
 ism that is most frequently found in connection with tubercle- 
 bacillus is the pneumococcus, and it may be found intimately 
 associated, although it has been stated that the tubercle-bacillus 
 appears to predominate at the base of the brain and the pneu- 
 mococcus in the exudate of the convexity. 
 
 Pathologic Anatomy. — In cases that die of pulmonary tubercu- 
 losis it is not uncommon to find, particularly upon the convexity 
 of the pia mater, a number of small grayish nodules. These are 
 not always apparent upon superficial inspection, but by cutting 
 through the cerebral hemisphere as far as the pia, and then strip- 
 ping it away from the under surface of the membrane and holding 
 the latter up to the light, they may readily be seen. In certain 
 
720 TEXT-BOOK OF PATHOLOGY. 
 
 cases tubercle-bacilli have been found when recognizable macro- 
 scopic lesions were entirely absent. Microscopic examination, 
 however, has usually revealed a few masses of epithelioid cells 
 and some slight perivascular round-cell infiltration. 
 
 When the infection is more severe the tubercles are usually 
 most numerous upon the base of the brain, particularly on either 
 side of the carotid canal and in that part of the base just poste- 
 rior to the dorsum sella?. Ordinarily the disease assumes the form 
 of disseminated miliary tuberculosis. The tubercles are situated 
 between the arachnoid and the pia, often in the depths of the sulci. 
 They vary in size up to 0.5 cm. in diameter, and often show slight 
 cheesy degeneration in the center. The meninges are congested, 
 and usually there is an exudate of inflammatory liquid that contains 
 flocculi of lymph, or is even seropurulent in character. Micro- 
 scopic examination shows that the tubercles are composed of epi- 
 thelioid cells, which occasionally present some evidence of division. 
 Giant-cells are also present, although perhaps not so frequently as 
 in lesions in other parts of the body. There is usually round-cell 
 infiltration about the vessels, and the latter are apt to be distended. 
 This round-cell infiltration may also extend into the cortex of the 
 brain, and the tubercles are often found in the latter situation. 
 Tubercles may also exist in the choroid plexus. Sometimes, if the 
 process has lasted for some time, and the tubercular masses have in- 
 creased in size, they may undergo cheesy degeneration and form ir- 
 regular masses ; these are usually found at the base of the brain, and 
 often cause serious pressure upon the cranial nerves that they involve. 
 
 Occasionally, when only a small number of bacilli have reached 
 the meninges and have been deposited in one point, a single cheesy 
 nodule may be found, particularly in one of the sulci, forming the 
 meningeal tyroma, that sometimes attains a considerable size. In 
 these less acute cases the exudate is considerable, and involves not 
 only the subarachnoidal space, but also the ventricles of the brain, 
 causing a condition that was formerly described as acute hydro- 
 cephalus. Numerous tubercles are found in the choroid plexus, 
 and the cpendyma is covered with slight elevations resembling 
 somewhat the appearance of cor villosum. These are usually 
 found to consist of proliferated endothelial cells and of the sub- 
 ependymal neuroglia and fibrous tissue. Tuberculous infiltration 
 of the brain-substance is, however, very common. This may 
 either be nothing more than an extension by continuity along the 
 lymph-spaces and blood-vessels dipping from the pia or ependyma 
 into the brain-substance, and giving rise to small foci composed of 
 epithelioid and giant-cells surrounded by leukocytes, and perhaps 
 exhibiting a slight degree of cheesy degeneration in the center ; or 
 else considerable areas of softening, which are perhaps caused by 
 the formation of thrombi. These are most frequent in the corpus 
 striatum and the crura, and appear as grayish-white or yellowish 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 721 
 
 areas of softened and degenerated nervous tissue. Not infre- 
 quently, punctiform hemorrhages are found in the cortex about 
 these areas of softening. The tubercle-bacillus is usually readily- 
 found, although this is exceedingly difficult if the tissue has been 
 hardened in Miiller's fluid. In general, extension of the tuber- 
 cular process to the meninges of the cord occurs if the duration 
 of the process is at all prolonged, but the vertebral canal is so 
 much longer than the spinal cord that pressure-symptoms rarely 
 occur, and, as the irritation is slight, the cranial symptoms domi- 
 nate the clinical course. 
 
 Syphilis may occur in the form of gummatous infiltration. 
 In these instances there are found flattened nodular thickenings 
 of the arachnoid and pia, of grayish or pinkish color, and tending 
 to undergo necrotic change. The process begins in the inner 
 surface of the arachnoid, or sometimes in the walls of the blood- 
 vessels, and extends to the pia and cerebral substance on the one 
 hand, and to the dura on the other. In another form of syphilis 
 there is diffuse infiltration or syphilitic leptomeningitis, causing 
 considerable thickening of the meninges. 
 
 Chronic syphilitic leptomeningitis and meningo-encephalitis are 
 
 Fig. 346.— Gummatous meningo-encephalitis (Ziegler). 
 
 occasionally met with. In these cases the membranes are thick- 
 ened and fibrous, and secondary extension of the infiltration into 
 the cerebral cortex occurs (Fig. 346). 
 
 TUMORS. 
 
 The Pacchionian Bodies. — The most common, and clini- 
 cally perhaps the least important, tumors of the arachnoid are the 
 
722 TEXT-BOOK OF PATHOLOGY. 
 
 Pacchionian bodies. These occur as small granular masses or 
 circumscribed nodules, chiefly along the upper edge of the superior 
 longitudinal sinus, often extending a short distance laterally over 
 the convex surface of the convolutions. Microscopically they 
 •consist of dense masses of fibrous tissue, covered by a layer of 
 proliferated endothelial cells, which give them a concentric struct- 
 ure. Occasionally some calcareous nodules may be found in them. 
 They usually grow only outwardly, and frequently erode the skull, 
 giving rise to little pits upon the inner surface. 
 
 Bndotheliomata are most frequently found in the pia mater. 
 They occur as irregular alveoli, lined with cuboidal or round endo- 
 thelial cells. These are not always arranged in a single layer, but 
 may occasionally fill the alveolus, although this is not common, and 
 more frequently some have broken loose and lie free in the cavity. 
 The cells often show karyokinetic changes, and occasionally alter- 
 ations in shape, due to mutual pressure. These tumors resemble 
 carcinomata closely, but the presence and proliferation of the 
 
 Fig. 347.— Endothelioma of the pia mater. 
 
 epithelium-like cells in the stroma, such as occur in carcinoma, 
 have not been observed (Fig. 347). 
 
 Cholesteatomata are of two kinds : those consisting exclu- 
 sively of squamous epithelial cells, and those containing, in addition, 
 various other epidermal structures, such as hairs or sebaceous 
 glands. They are usually situated in or about the median line, 
 along the base of the brain or on the upper surface of the corpus 
 callosum, or somewhere along the choroid plexuses. Those con- 
 taining hair are most frequently found near the cerebellum, grow- 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 723 
 
 ing either from the arachnoid, or, more rarely, from the outer sur- 
 face of the dura. The latter may occur upon the frontal or occip- 
 ital bones, and often show calcareous infiltration, or even true 
 osseous formation. 
 
 I/ipomata are rare. They are usually found in children, and 
 always in the soft membranes, especially the pia mater. The 
 most frequent seats are the upper surface of the corpus callosum 
 and the corpora candicantia. According to Bostroem, they are 
 probably epidermal in origin, nothing but the subcutaneous fatty 
 tissue being left. 
 
 Teratomata may be present. Chiari has described a case 
 that grew from the lining membrane of the third ventricle in an 
 infant that died at the age of seven weeks. It consisted of a 
 medullary white mass and a number of serous cysts. The solid 
 substance was composed of fetal brain-substance, in which were 
 fissures lined with epithelium similar to that of the central canal 
 of the cord, and ganglioh-cells, retinal cells, skin-glands, and jelly 
 of Wharton. Fibrous and cartilaginous tissues were also present. 
 
 THE BRAIN. 
 
 DEVELOPMENT AND ANATOMY. 
 
 Development. — (For convenience, the development of the cord is con- 
 sidered in this place with that of the brain.) The central nervous system 
 commences as a shallow depression, that appears in front of the primitive 
 streak in early embryologic existence. It is bounded on either side by ridges, 
 known as the medullary folds. The groove gradually becomes deeper, and 
 finally the two medullary folds unite, giving rise to the formation of the 
 medullary canal, which is soon separated from the dorsal surface of the em- 
 bryo by the interposition of mesoblastic tissue. The canal is first formed 
 in the portion that subsequently forms the cervical region of the spinal cord. 
 Just beneath the medullary canal there is a cylindrical collection of cells, 
 often with a small cavity in the center that forms anteriorly a shallow groove, 
 the so-called notochord. Its function is unknown, and it eventually disap- 
 pears during embryonic existence, although traces may still be found in the 
 intervertebral cartilages at birth. In some of the lower animals a small 
 sac-like dilatation is found anteriorly, from which a process extends down- 
 ward and apparently stops at the hypophysis cerebri ; but it is not certain 
 that it forms a portion of this organ. The anterior extremity of the embryo 
 continues to grow, and bends downward, forming the cephalic fold. In 
 this part of the neural canal three dilatations occur — the primary vesicles 
 of the brain; the posterior portion ultimately forms the spinal cord. 
 
 The Cord. — At first the wall of the embryonal cord is composed of a 
 single layer of cylindrical epithelial cells {spongioblasts), with nuclei at 
 various distances from the central canal; these ultimately become the 
 nuclei of the glia-cells. The central ends remain cylindrical; the periph- 
 eral ends become branched, forming the myelospongium, probably the 
 antecedent of the neuroglia-fibers, which, according to some recent investi- 
 gations, become separated from the cells. At the age of about five weeks 
 in the human embryo, certain cells, with a considerable amount of clear 
 protoplasm, are found near the inner limiting membrane, the so-called 
 germinal cells. Subsequently other cells appear, probably derived from the 
 
724 TEXT-BOOK OF PATHOLOGY. 
 
 germinal cells, as they are first found in the situations occupied by these, 
 the so-called neuroblasts. These are distinguished by the appearance of a 
 projection, pointing toward the periphery of the spinal cord, that grows 
 out from the protoplasm and ultimately pierces the external limiting 
 membrane to become an axis-cylinder. The central canal, at this period, 
 is usually elliptical in shape, with the long axis dorsoventral. The anterior 
 and posterior ends are very thin, and the former ultimately becomes invagi- 
 nated to form the anterior commissure. 
 
 Just outside of the cord, probably from masses of epiblastic cells derived 
 from its wall, the cells of the spinal ganglia appear. These are, at first, 
 bipolar, one process extending into the spinal cord, and the other peripher- 
 ally, but ultimately tbe two processes unite at their commencement. The 
 spinal cord at first completely fills the spinal canal, but after the fourth 
 month the vertebral column begins to grow somewhat more rapidly, and 
 at birth the conus terminalis is opposite the third, and in the adult extends 
 only to the lower end of the first, lumbar vertebra. The nerve-fibers are 
 at first non-medullated, but later myelin-sheaths appear, first in certain 
 parts of the posterior columns, and lastly in the pyramidal tracts, which 
 often, at birth, are not yet entirely medullated. The membranes are 
 derived from the mesoblast. 
 
 The Brain. — The three primary vesicles from which the brain is devel- 
 oped continue to grow, and the first is subdivided by a median constriction 
 into two secondary vesicles, the prosencephalon and the thalamencephalon. 
 From the former two lateral offshoots appear, which give rise to the 
 cavities of the lateral ventricle ; and from the walls of these are developed 
 the cerebral hemispheres, the olfactory lobes, and the corpus callosum. 
 The cavity of the second vesicle forms the third ventricle, and from its walls 
 grow the nervous part of the eye, the optic thalami. and the pituitary 
 and pineal bodies. The cavity of this vesicle (mesencephalon) forms the 
 aqueduct of Sylvius, and from its walls grow the corpora quadrigemina 
 and the crura. The posterior primary vesicle also becomes constricted, 
 forming the epencephalon and the metencephalon. The two cavities, 
 however, remain united and form the fourth ventricle. From the walls 
 of the anterior portion are developed the cerebellum and the pons. From 
 those of the posterior portion, the medulla oblongata. 
 
 The ultimate shape of the brain, however, is largely determined by certain 
 flexures and by the growth and extension of the axis-cylinders, which pass in 
 various directions and form the white matter, the greater bulk of the central 
 nervous system. The first flexure is beneath the mesencephalon and concave 
 from the ventral surface. The second flexure is concave dorsally, and is just 
 beneath the epencephalon. The third grows at the junction of the meten- 
 cephalon with the spinal cord, and is concave ventrally. Differing from 
 the cord, the growth of the brain exceeds that of its containing bony cap- 
 sule. As a result the surface of the hemispheres is usually thrown into 
 folds. The earliest of these appear during the third month, and are usually 
 transverse to the axis of the brain, although not invariably. The lateral 
 ventricles at this stage are very large, and the sulci project into their cavi- 
 ties as ridges. During the fourth month they disappear, with the exception 
 of three — the Sylvian, the calcarine, and the parieto-occipital fissures. The 
 hippocampal fissure also appears about this time. The other permanent 
 sulci appear about the end of the fifth month, the earliest being the fissure 
 of Rolando ; but many of the secondary fissures do not develop until after 
 birth. 
 
 The sympathetic nervous system is probably only an offshoot of the 
 central nervous system. The cells first appear upon the spinal nerves, from 
 which they wander, remaining connected with them by short branches, 
 the rami communicantes. Some authorities, however, believe that the 
 sympathetic system is developed from the mesoblast. 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 725 
 
 Anatomy. — The brain consists of the two cerebral hemispheres, the 
 basal ganglia, the pons, the medulla, and the cerebellum. Its weight varies 
 from 1200 to 1300 grams in the adult female, and from 1300 to 1400 grams 
 in the adult male. Its consistency at birth is very soft ; in the adult it 
 becomes somewhat firmer, but is always softer than the normal liver. Its 
 color varies from grayish-white in the parts composed of medullated fibers, 
 to reddish-gray in those composed chiefly of ganglion-cells. The cerebral 
 hemispheres are two large symmetrical masses occupying the greater por- 
 tion of the cranial cavity; they are separated by the superior longitudinal 
 fissure, and united by the corpus callosum and the anterior commissure. 
 They are joined to the pons by the crura. Their surfaces are rendered very 
 irregular by the presence of numerous fissures or sulci ; and are divided into 
 the frontal, parietal, occipital, and temporosphenoidal regions. The impor- 
 tant fissures are the Sylvian, the Eolandic, and the parieto-occipital on the 
 external surface; the calloso-marginal, the calcarine, and the parieto- 
 occipital on the medium surface. 
 
 The hemispheres are composed essentially of an outer layer of gray 
 matter, the cortex, containing ganglion-cells, and of fibers passing from 
 these in various directions and uniting them with other parts of the central 
 nervous system. These may be divided into three main classes : the pro- 
 jection-fibers, passing between the cortex and the basal ganglia, or into the 
 internal capsule ; the transverse or commissural fibers, passing between two 
 hemispheres ; and the association-fibers, passing between different areas in 
 the same hemisphere. The most important of the projection-fibers are 
 those which arise in the motor portion of the cortex, and pass first into 
 the internal capsule, where they are grouped about the knee, thence through 
 the crusta and the pons, to form ultimately the pyramids of the medulla. 
 They decussate in the first cervical segment of the cord and form the pyram- 
 idal columns of the cord. The fibers of the optic radiation commence 
 in the cortex about the calcarine fissure and in the cuneate lobe, and pass 
 forward to the pulvinar of the optic thalami. They are also associated 
 with the external geniculate body and the anterior corpus quadrigeminus. 
 From the pulvinar, the optic tracts pass around the crusta, then lie below 
 and to the inner side of the internal capsules, and unite in front of the 
 tuber cinereum to form the chiasm from which the optic nerves arise. 
 The transverse or commissure-fibers include those of the corpus callosum 
 and of the anterior commissure. The fibers in the corpus callosum appear 
 to correspond closely to those regions of the brain situated nearest to them. 
 The anterior commissure is composed of fibers uniting the temporosphe- 
 noidal lobes of the two hemispheres. The association-fibers either connect 
 adjacent lobes {fibroz propria}), or unite distant portions of the hemispheres 
 (the long association-fibers). The most important of the latter are the 
 superior, interior, and anterior association-bundles, the cingulum, and the 
 fornix ; the latter is a group of arching fibers connecting the hippocampal 
 region with the corpora albicantia. 
 
 In the substance of each hemisphere are found the lateral ventri- 
 cles : two long, narrow, branching cavities, joined to the third ventricle 
 by the foramen of Monro. Each contains a choroid plexus, and is nor- 
 mally lined with epithelium and contains clear cerebrospinal fluid. The 
 anterior portion of the two ventricles is separated by the septum. A small 
 double layer of epithelial cells line and almost fill the cavity of the fifth 
 ventricle. The basal ganglia of the brain are the lenticular nucleus, the 
 caudate nucleus, forming together the corpus striatum, and lying on either 
 side outside of the internal capsules, the optic thalamus, a large oval mass 
 lying beneath the caudate nucleus. The outer portion on the lenticular 
 nucleus is usually known as the putamen ; the two inner segments are 
 known together as the globus pallidus. To the outer side of the 
 putamen is a band of white fibers, known as the external capsule, that 
 
726 TEXT-BOOK OF rATHOLOGY. 
 
 is separated from the cortex by a thin layer of pigmented cells, the 
 claustrum. 
 
 The third ventricle communicates with the fourth by a narrow canal, 
 the aqueduct of Sylvius, which passes through the tegmentum of the crura. 
 It is surrounded by a zone of gray matter, in which are found the nuclei of 
 the oculomotor nerves. Above it are the four corpora quadrigemina; two 
 pairs of rounded eminences with a white cortex and a gray center. The 
 superior corpora, as has been already stated, are intimately connected with 
 the optic tract. Just anterior to these bodies is the small pineal gland, a 
 hypoplastic median eye situated above the posterior commissure. Exter- 
 nally to the crusta on either side, continuous with the posterior portion of 
 the thalamus, are the two geniculate bodies, separated by the optic tract, 
 with which the external geniculate body is closely connected. The optic 
 thalami lie on either side of the third ventricle, and just beneath the cau- 
 date nuclei ; they are oval bodies containing numerous groups of nerve- 
 cells, the anterior portion being called the anterior tubercle, and the pos- 
 terior portion the pulvinar. 
 
 The two great channels by which fibers pass to and from the cerebrum 
 are the crura cerebri. These are divided by a narrow layer of dark-gray 
 material, the substantia nigra, composed of pigmented ganglion-cells, into 
 the crusta, or inferior portion, and the tegmentum, or superior portion. 
 A part of the crusta is formed, as has already been stated, by the pyram- 
 idal tract. Sensory nerve-fibers are found in two groups in the tegmen- 
 tum toward the outer edge, comprising the inferior and superior fillets. 
 These fibers divide into three bands: one passes into the superior portion 
 of the tegmentum, and some of these enter the posterior portion of the 
 interior capsule; another band passes to the anterior corpora quadrigemina 
 and the thalamus ; and a third into the posterior corpora quadrigemina, 
 although it is not certain that all the fibers are thus distributed. 
 
 The two crura unite to form the pons, which is composed, ven- 
 trally, of bundles of motor fibers separated by the commissural fibers 
 of the cerebellum, and dorsally, partly of the fibers of the fillet and partly 
 of gray matter. Below the pons is found the medulla, which is really noth- 
 ing but the upper portion of the spinal cord. Anteriorly we find the two 
 well-defined bundles of motor fibers, the pyramids ; just back of these the 
 lower olives; and on the dorsal surface the nuclei of the tenth and twelfth 
 nerves, and externally to them the nucleus gracilis and nucleus cuneatus, 
 the terminations respectively of the columns of Goll and Burdach in the 
 cord. The axis-cylinders of the cells that compose these nuclei pass toward 
 the brain and form the fillets. On the outer surface of the medulla, near 
 the dorsal surface, are the two restiform bodies, the continuations of the 
 cerebellar peduncles. 
 
 The cerebellum is composed of two lobes and the vermiform process. 
 Upon cross-section it is seen to be composed of a great number of narrow 
 gyri separated by deep ramifying sulci, each convolution being lined 
 externally by medullated fibers, beneath which is a layer of ganglion-cells 
 enclosing a center of medullated fibers. It is united to the cerebrum by 
 the superior peduncles, which terminate in the nucleus ruber of the tegmen- 
 tum. The middle peduncles form the transverse fibers in the pons, and 
 the inferior peduncles pass into the restiform bodies of the medulla. Certain 
 nuclei are found in the interior of the white substance, of which the most 
 important is the dentate nucleus, analogous structurally to the olives of the 
 medulla. 
 
 The Neuron. — Histologically the essential element of the nervous sys- 
 tem is the neuron. This, in the sense of Waldeyer, comprises the nerve- 
 cell, its protoplasmic processes (which are branched), and the axis-cylinder, 
 which may be a single fiber giving off lateral collaterals, or is extensively 
 branched (Golgi cells). The cell-body consists of protoplasm without a dis- 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 727 
 
 tinct cell-wall, and containing or not containing chromophilic bodies. Ac- 
 cording to Nissl, two groups of cells are thus formed, the somatochromes 
 with, and the caryochromes without, these bodies. According to zoologists, 
 these are respectively motor and sensory in function, but the cells of the spinal 
 ganglia, which appear to be sensory, contain these granulations. Cells are 
 spoken of as multipolar or bipolar, according to the number of processes that 
 project from them. It is impossible to describe in this place all the varieties 
 of cells and their distribution in the nerve-substance. The neurons may be 
 divided into endogenic, wholly within the central nervous system, and 
 exogenic, partly in the peripheral nervous system. Each axis-cylinder 
 terminates in a tuft of fibers that surround, without touching, some other 
 ganglion-cell, or, if it extends to the periphery, terminates in a special sen- 
 sory corpuscle or a muscle-plate. 
 
 Preservation of the Brain and Cord.— After the brain has been 
 removed from the cranial cavity it is probably bqgt to place it at 
 once in a 10 per cent, solution of formalin. The formalin should be 
 changed at intervals of three or four days. If it is hardened in Miiller's 
 fluid, deep incisions should be made, preferably parallel to the upper sur- 
 face of the corpus callosum, after the removal of the frontal and occip- 
 ital lobes. The fluid should be changed at the end of the first hour, then 
 at the end of twelve hours, and then every day for one or two weeks. If it 
 is desired to examine the brain at once, it may still be preserved for micro- 
 scopic investigation by making two horizontal incisions through the cere- 
 bral hemispheres, parallel to the upper surface of the corpus callosum, then 
 cutting into the lateral ventricles. If a hemorrhage exist, it can usually be 
 detected by the presence of blood in one of the ventricles, or by discolora- 
 tions of the floor. The most important part of the brain, for the purpose of 
 tracing secondary degeneration, consists of the stem, so called — that is, the 
 basal ganglia, the crura, the pons, and medulla. It is usual to make serial 
 sections through this part, which may be removed by cutting off the frontal 
 lobes at the knee and the occipital lobes opposite the splenium, and then 
 removing the temporal portion of the brain by sagittal section just outside 
 of the lateral ventricles. As soon as the cord has been removed the dura 
 mater should be cut on both sides and laid back. It is usually desirable to 
 remove the cord first, as by this means a horizontal section can be made 
 through one of the upper cervical segments, and the remainder of the cord 
 then removed with the brain. In this manner the usual oblique incision, 
 that renders the upper portion useless for microscopic study, is avoided. It 
 is unnecessary, and for many reasons undesirable, to make transverse incis- 
 ions through the cord before hardening, even if Miiller's fluid be employed. 
 
 CONGENITAL ABNORMALITIES. 
 
 The deformities of the brain are numerous and complicated. 
 They may be divided roughly into those associated with altera- 
 tions in the skull and those occurring within the cranial cavity. 
 
 Acrarlia is a deformity characterized by absence of the skull. 
 The membranes are usually preserved, and form a sac filled with 
 serum, on the inner surface of which small particles of nervous 
 tissue may occasionally be found. More frequently the brain forms 
 only a small mass at the upper portion of the spinal canal, lying on 
 the basilar process of the occipital bone. Sometimes it appears as 
 if the sac had ruptured, or had never completely closed, for the 
 membranes are collapsed, and form upon the base of the skull 
 a mass consisting of fibrous connective tissue and blood-vessels. 
 
728 TEXT-BOOK OF PATHOLOGY. 
 
 Often in this case the encephalon is entirely absent, but the pons 
 and medulla may be almost completely developed. The cranial 
 nerves are usually present. 
 
 Hemicrania is a condition in which more or less of one of 
 the parietal bones, or of a portion of the frontal or temporal bone, 
 has failed to develop. The corresponding portions upon the oppo- 
 site side that have developed are usually hypoplastic. Ordinarily, 
 anencephaly, or only partial development of the brain, is associ- 
 ated with these changes. 
 
 Cranioschisis is the name applied to imperfect closure of the 
 skull along the middle line. This may be associated with rha- 
 chischisis, when both skull and spine are cleft. The commonest 
 situations for small fissures are in the frontal bone, in the region 
 of the posterior fontanelle, in the median line of the posterior por- 
 tion of the occipital bone, and, more rarely, in the region of 
 the anterior Jbntanelle or the sagittal suture, or in the sphenoid 
 bone. 
 
 Fissures or other small defects usually occasion hernia of the 
 brain, which is named encephalocele, and according to its situation 
 anterior or posterior, frontalis or occipitalis, superior, inferior, or 
 lateral. If, instead of brain-substance, only the membranes pro- 
 trude through the fissure, the condition is known as meningocele. 
 In these cases the cavity is filled with cerebrospinal fluid. Some- 
 times the under surface of the membrane is lined with nervous 
 tissue, showing that it represents a dilatation of one of the pri- 
 mary cavities of the brain, corresponding to the condition found in 
 spina bifida. These congenital hernise are probably the result of 
 fetal hydrocephalus, although it is possible that the chief cause is 
 the imperfect development of the cranium. In cases in which the 
 fissure is in the sphenoid bone, it is not uncommon to find, as an 
 associated condition, cleft palate. Life is, of course, incompatible 
 with extensive encephalocele. If it is small, the neck of the sac 
 is sometimes constricted, either spontaneously or as a result of 
 surgical interference, and recovery ensues. 
 
 Cyclencephaly is a peculiar deformity in which there is fail- 
 ure of the anterior cerebral vesicle to develop. The frontal lobes 
 remain fused, and a single rudimentary eye develops. 
 
 Abnormalities in Sise. — The size of the brain is subject to 
 considerable variation. 
 
 Macrocephaly is the condition in which the brain is excessively 
 large — that is, more than 1500 gm. This may be of two kinds. 
 In the first, and perhaps less common, form the brain is entirely 
 normal in structure, the proportion between the various parts being 
 maintained and the relation between the nervous tissue and the 
 neuroglia not altered. In some instances the subjects possess un- 
 usual intelligence ; in others this is not the case. The second 
 form is enlargement of the brain with hyperplasia of the neurog- 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 729 
 
 liar tissue. This is not infrequently found in the so-called hyper- 
 trophic nodular gliosis. In this condition the brain may be con- 
 siderably enlarged, and the convolutions may be increased in size, 
 although not abnormal in arrangement. Microscopically, the 
 changes described in the section on sclerosis are discovered. A 
 pseudo-enlargement of the brain is produced by hydrocephalus. 
 The weight of the brain, after the liquid has been removed from 
 the cavities, is usually less than normal, although this is not 
 always the case. 
 
 Hypertrophy of the brain may be limited to certain parts. 
 These are usually individual gyri, and are nearly always sclerotic. 
 Sometimes only a portion of a convolution is thus affected, and 
 produces a tumor-like swelling. Hypertrophy of individual 
 sections of the encephalon does not appear to have been observed ; 
 that is to say, simple enlargement of the cerebellum, or of one of 
 the cerebral hemispheres. 
 
 Microcephaly is a condition in which the brain is much smaller 
 than normal, as a result of defective growth, or else of disease, 
 either in early life or later. In some instances the brains, aside 
 from their small ness, appear perfectly normal, and this diminution 
 in size, within certain limits, is not incompatible with normal in- 
 telligence. Usually, however, there are sclerosis and decrease in 
 size of some of the gyri. There are, of course, the associated 
 changes usually found in sclerotic conditions. 
 
 Hypoplasia of individual portions of the brain has been observed, 
 particularly of the corpus callosum, the cerebral hemispheres, and 
 the cerebellum. 
 
 Hypoplasia of the cerebral hemispheres is usually due to some 
 pathologic change, and will be discussed under sclerosis and poren- 
 cephaly. 
 
 The congenital absence, either total or partial, of the corpus 
 callosum has been observed in a number of cases. It may occur 
 in brains otherwise normal, but is usually associated with micro- 
 cephaly or other profound structural changes. In the cases in 
 which no other lesions exist the intelligence may be normal, but 
 in the great majority of instances the patients are idiots. In all 
 cases, however, the following associated alterations have been 
 observed : absence of the calloso-marginal sulcus, division of the 
 gyrus fornicatus by perpendicular fissures, the splitting of the 
 fornix, and, in certain cases, secondary degenerations. The tape- 
 tum is usually intact. The absence of the transverse fibers in the 
 centrum ovale renders the superior longitudinal fasciculus very 
 distinct. The appearance of the brain is quite characteristic. As 
 soon as it is removed the hemispheres fall widely apart, showing 
 the third ventricle covered with a delicate layer of pia mater. 
 The inner surfaces of both hemispheres are divided by numerous 
 fissures, and appear atypical. When only a portion of the corpus 
 
730 TEXT-BOOK OF PATHOLOGY. 
 
 callosum is absent the splenium is nearly always preserved. Oc- 
 casionally, in eases of marked hydrocephalus, the corpus callosum 
 may be extremely thin, and be torn during' the removal of the 
 brain, and this may possibly be mistaken for congenital absence. 
 A little careful examination, however, will usually reveal the true 
 state of affairs. 
 
 Hypoplasia of the cerebellum, or even total absence of one or both 
 hemispheres, has been occasionally observed. It is nearly always 
 associated with sclerosis. A collection of cerebrospinal fluid in part 
 supplies the place of the absent organ. The cerebellum may be of 
 normal shape, and even microscopically show no changes other than 
 diminution in size. More commonly, however, the changes are 
 asymmetrical, one lobe being markedly smaller than the other, and 
 perhaps reduced even to a small papilla. There are often sclerotic 
 changes, with marked atrophy of the cortex and disappearance of 
 many of the medullated fibers. In these cases the cerebellum is 
 usually of somewhat firmer consistency. The associated changes 
 are diminution in size of the olivary bodies ; in the unilateral cases, 
 of that upon the opposite side ; the pons and medulla are usually 
 smaller than normal, and in the former the pyramidal tracts, on 
 account of the absence of the transverse fibers, are usually com- 
 pact and distinct. Sometimes the corpora quadrigemina are also 
 altered, but this is not invariably the case. 
 
 Other changes of unknown significance that have been described 
 are abnormal arrangement of the convolutions. Of these the most 
 important is the presence of anneetant gyri across the Rolandic 
 fissure, or the absence of anneetant gyri in the parieto-occipital 
 fissure. It does not appear, however, although the claim has been 
 frequently made, that these changes are in any way associated 
 with intellectual disturbances. Bundles of nerve-fibers, taking an 
 abnormal course, have occasionally been found in the pons and 
 medulla. These seem to be produced by premature decussation 
 of portions of the pyramidal tract, and are of no clinical sig- 
 nificance. 
 
 Anencephaly, or total absence of brain, is a congenital lesion 
 usually associated with acrania. Sometimes it is associated with 
 total absence of the spinal cord ; in other cases a portion of the 
 pons, medulla, and the cord are still present, although much 
 smaller than normal. The cranial nerves are usually present, and 
 the eyes, in particular, are nearly always perfectly developed. 
 The lesion is, of course, incompatible with life, although when 
 the medulla is present a few respirations may take place after 
 birth. The appearance of the monsters is very characteristic. 
 From the orbital ridge of the frontal bone the skull slopes in 
 almost a direct line to the neck, making the face and eyes un- 
 usually prominent — the so-called frog-face. Frequently other 
 deformities are also present. 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 731 
 
 POST=MORTEM DEGENERATIVE CONDITIONS. 
 
 It is important to be acquainted with the post-mortem altera- 
 tions that may take place in the nervous system, in order to avoid 
 the confusion of such changes with those that have occurred as 
 the result of disease. Little attention has been paid to the macro- 
 scopic changes, and they are not characteristic. Their degree 
 depends upon the temperature at which the body has been kept 
 after death, the nature of the disease that preceded death, and the 
 period that elapsed before the tissues are removed. Ordinarily no 
 changes will be noticed under thirty-six hours if the body is 
 kept on ice. If kept at a temperature of about 16° C. (59° F.), 
 the brain and cord will appear normal if removed within twenty- 
 four hours. There is first softening of the nervous tissue, that is 
 general and not associated with pigmentation ; the tissues may 
 become so soft that it is almost impossible to remove them with- 
 out injury. Later there is often a considerable extravasation of 
 blood-pigment around the vessels ; and, finally, if putrefaction is 
 advanced, the tissues become almost diffluent and light brown in 
 color. 
 
 Lately, Italian authors have studied methodically the micro- 
 scopic changes. The nerve-cells swell, their protoplasmic processes 
 break off, and there is a gradual loss of the staining-power of the 
 chromatin-bodies ; vacuoles appear in the protoplasm and the out- 
 line of the cell becomes irregular ; and finally the chromatin-sub- 
 stance completely disappears. The outlines of the nucleus become 
 indistinct, it swells, and then contracts, with irregularity of the 
 outline. It stains homogeneously, due to diffusion of the chro- 
 matin, and may contain small granules of hyaline material. It 
 is often placed excentrically in the cells. Later it loses its stain- 
 ing-power, and finally disappears completely. The nucleolus is 
 the last structure to show alteration ; it may swell slightly, be- 
 come filled with vacuoles, and then break up into granular mate- 
 rial and disappear. The protoplasmic processes do not exhibit 
 varicosities, but apparently become more fragile, and are very apt 
 to be broken off during staining. Changes may take place in the 
 myelin-sheaths that, when studied by Marchi's method, are not 
 greatly different from those seen in areas of softening — that is, 
 small fatty granules appear along the course of the nerve-fiber. 
 In post-mortem lesions, however, there is no perivascular round- 
 cell infiltration ; no compound granular cells can be found in the 
 tissue ; there are no signs of proliferation in the neuroglia ; and 
 the process is more general and uniform than is apt to be the 
 case in morbid conditions. 
 
732 TEXT-BOOK OF PATHOLOGY. 
 
 GENERAL PATHOLOGIC ANATOMY OF THE NERVOUS 
 SYSTEM. 
 
 The pathology of the nervous system differs from that of the 
 other organs of the body chiefly in the fact that the special struct- 
 ures of which the nervous tissue is composed have no close anal- 
 ogies to the epithelial cells and connective tissues. It is desirable, 
 therefore, to discuss, first, the general changes occurring in the 
 nerve-cells, nerve-fibers, and the neuroglia. 
 
 The Nerve=cell. 
 
 Of late years, considerable progress has been made in the 
 elucidation of the finer pathologic changes that occur in the nerve- 
 cell. On account of their characteristic appearance and sharply 
 differentiated structure, the cells of the anterior cornua of the 
 spinal cord have been most carefully studied, and it is necessary, 
 therefore, that we should give a brief description of their anatomy. 
 The appearance depends largely upon the method of staining em- 
 ployed. By the Golgi method the cell appears as an irregular 
 body, from which come a number of thick processes, that rapidly 
 divide and subdivide, until they appear as a maze of independent 
 delicate branches, upon either side of which can be seen minute 
 projections, the so-called gemmules ; from one portion of this cell 
 a fine process arises that is of uniform width. At regular inter- 
 vals this neuraxon gives off the so-called collaterals, delicate 
 branches that spring from it at right angles and have a differ- 
 ent course. By this method other ganglion-cells in the nervous 
 system have also been carefully studied, and show numerous 
 variations in type, the most important being the number and 
 complexity of the protoplasmic processes, and the division or 
 even excessive branching of the neuraxon. The morbid changes 
 that can be observed by the application of this stain are but few, 
 since it appears that the pathologic cells soon lose their power 
 of impregnation. Golgi and, in this country, Berkley have made 
 the most extensive investigations by this method. It must be 
 said, however, that in the majority of instances their studies were 
 made upon the pyramidal cells of the cerebral cortex, and not 
 those of the anterior cornua of the cord. 
 
 The alterations are essentially of two kinds : first, the appear- 
 ance of varicosities upon the protoplasmic processes in their thicker 
 branches ; second, the disappearance of the gemmules from the 
 terminal filaments. Such alterations Golgi has seen in chorea, 
 Nageotte in general paresis, and Berkley in alcoholism and other 
 forms of poisoning. Sailer has found very marked changes of 
 this character in the spinal cords of guinea-pigs killed with teta- 
 nus-toxin, and Steele has described a varicosity upon the axis- 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 733 
 
 cylinder in the cortical cell in an animal killed by diphtheria- 
 toxin. Lenhossek appears to regard the varicosities of the proto- 
 plasmic processes as the result of an accumulation of the chromo- 
 philic bodies, and Kolliker states that they are merely artefacts, a 
 view held by most zoologists. Sailer l has found very character- 
 istic changes of this type in the brain of a guinea-pig that was 
 apparently healthy and killed for histologic purposes. 
 
 In 1885, Nissl described a method for staining the nerve-cells 
 which, on account of its differentiation of the structures of the 
 protoplasm, and the possibility that by it cells in any stage of 
 degeneration may be stained, has yielded most valuable results. 
 It consists essentially of staining tissue, hardened in alcohol, by 
 one of the basic anilin-stains, such as thionin or methylene-blue. 
 The cells of the anterior cornua show the irregular outline and 
 the numerous protoplasmic processes as before. Throughout the 
 protoplasm are small, irregular bodies, sometimes vacuolated, that 
 take the basic stain intensely. They are arranged somewhat con- 
 centrically around the nucleus, but at the points where the pro- 
 toplasmic processes come off become spindle-shaped and turn 
 into them, and are also found in the processes as spindles. Be- 
 tween these bodies the cytoplasm refuses to take the stain, and 
 is called the aehromatie substance. Nissl and some others be- 
 lieve that it has a delicate fibrillar structure, but this has not 
 been positively determined. A cup-shaped portion of the proto- 
 plasm remains clear, and is usually rather sharply delimited from 
 the remainder of the cell. From this extends a long, faintly 
 staining, undifferentiated neuraxon. The nucleus does not stain, 
 but remains as a clear space near the center of the cell, contain- 
 
 'e~^ «, - • ~— - : 
 
 i- ... ■-..■ ■ " . ^ . • .a-.;, 
 
 k .. . ^ 7 ^"" 6 &g*'J* .i-< :'..%& 
 
 
 #• - . %%§■ ' WM 
 
 Fig. 348.— Normal and degenerated nerve-cells of the anterior cornua of the spinal 
 cord ; X 600. 
 
 ing a round, deeply staining, and usually vacuolated nucleolus, 
 
 surrounded by a membrane with irregular thickenings (Fig. 348). 
 
 It has been claimed (Kronthal) that these so-called chromophilic 
 
 1 Verbal communication. 
 
734 TEXT-BOOK OF PATHOLOGY. 
 
 bodies do not exist in the living cell, but are the products of dis- 
 integration. In 1893, De Quervain laid down the following cri- 
 teria by which he recognized pathologic changes : (a) modification 
 of the nucleus, (b) vacuolization of the nucleolus, (c) disappear- 
 ance of the nucleus, (d) diminished stain ing-capacity, (e) swelling 
 of the ganglion-cells, (/) fragmentation of the protoplasmic pro- 
 cesses, ( g) shrinking of the cell, (h) vacuolization of the proto- 
 plasm. He does no£ consider enlargement of pericellular space as 
 of pathologic significance, even when mononuclear leukocytes are 
 found in it. It must be confessed that these criteria are not 
 entirely adequate, nearly all of the changes described depending 
 in part upon the length of time between death and the fixa- 
 tion of the tissue and upon the methods of preparation. The 
 course of the pathologic changes appears to be somewhat as fol- 
 lows : The granules become first very irregular in distribution and 
 somewhat finer, so that the concentric arrangement is no longer 
 distinct. They may then diminish considerably in number, so 
 that the cell as a whole appears very much paler ; finally, the 
 protoplasm may become entirely clear, a small amount of baso- 
 philic substance only remaining that is collected in irregular 
 masses around the nucleus. This also may disappear, and the 
 cell remain as an irregular, faintly and diffusely stained mass in 
 the midst of the tissue. This series of changes is by no means 
 the only one that has been described. Occasionally the chromo- 
 philic granules seem to dissolve, although their capacity for stain- 
 ing is unimpaired, resulting in deeply and diffusely staining cells 
 without any apparent structure, excepting the vesicle in the situa- 
 tion of the nucleus (pyknomorphous state). Nissl regards these as 
 artefacts, and it is true that they are frequently found in tissues 
 supposed to be healthy. It must not be forgotten that they are 
 always far more numerous in diseased tissues or in the neighbor- 
 hood of focal lesions. I have observed some singularly beautiful 
 examples of this change in the brain of a guinea-pig killed by 
 anthrax, in which the micro-organisms were found in the nervous 
 tissue. The solution, with or without loss of stain ing-power, cor- 
 responds very closely to the changes observed in the chromatin in 
 karyolysis, and may be very properly described as a sort of chro- 
 molysis. In other cases chromophilic bodies may collect in diffuse, 
 irregular masses in one or more parts of the protoplasm, a change 
 which I have observed in the spinal cells of cases of tetanus. 
 
 Still another form is the coalescence of the chromophilic bod- 
 ies, so that each individual one appears larger; their number is 
 less, and they still maintain a rather regular arrangement in 
 the protoplasm. These masses may then further coalesce, giving 
 rise to the appearance just previously described, or may break up, 
 causing a uniform granulation of the cell, or they may disappear. 
 Berger has attempted to explain most of these phenomena by sup- 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 735 
 
 posing that the chromophilic bodies are really composed of small 
 granules that are adherent to the sides of the spaces formed by 
 the reticulum of the protoplasm of the cell. If these spaces 
 dilate, the granules will be more widely separated and the appear- 
 ance will be that of diffuse granulation. If they contract, as 
 occurs in cases of general cellular contraction, the so-called in- 
 spissation of the cell, they will appear darker and the neighboring 
 ones may seem to coalesce. The changes in the reticulum may 
 
 Pig. 349.— Degenerated nerve-cells in the neighborhood of a collection of pus ; the gran- 
 ular appearance is due to an excess of pigment; X 600 (case of Lloyd and Sailer). 
 
 be local, and give rise to local alteration in the arrangement 
 {Fig. 349). 
 
 Another change that frequently occurs in pathologic cells is 
 vacuolization. It is possible that a few vacuoles of small size 
 may be the result of the hardening processes. In some cases, 
 however, this alteration is very extensive, the vacuoles reaching 
 70 p. in diameter. They appear to be filled with a liquid, possi- 
 bly lymph, that may undergo slight coagulation-necrosis ; at least 
 fibrillse, that may be fibrin, have been observed. The cells often 
 acquire extraordinary appearances. Indeed, it looks as if the 
 pericellular space was enormously dilated, and that bands of pro- 
 toplasm extend from it to the surrounding neuroglia. The 
 arrangement of the vacuoles is always exceedingly irregular, and 
 if more than one is present, as is usually the case, the vacuoles 
 vary greatly in size. 
 
 Sometimes, instead of the vacuoles, there may be found in the 
 cells masses of some substance that differs from the protoplasm. 
 These are usually homogeneous irregular masses that take the acid 
 stain, and have been described as " colloid " in nature, using the word 
 in the sense given to it by von Recklinghausen. The true nature 
 of this change, however, is not very clearly understood. Some- 
 
736 TEXT-BOOK OF PATHOLOGY. 
 
 times the vacuoles appear to be replaced by clefts distributed irreg- 
 ularly in the protoplasm. 
 
 In nearly all degenerated cells there is accumulation of a 
 peculiar cellular pigment. This may be fatty in nature, as it 
 stains black with osmic acid. In some cases it seems to increase 
 •pari passu with the disappearance of the chromophilic bodies, so 
 that ultimately the cell appears as an irregular mass filled with 
 this yellowish-brown pigment. It occurs normally in old age, is 
 found in the cells of the substantia nigra of the crura, is an almost 
 invariable accompaniment of those diseases in which a sort of early 
 senility appears to occur, such as general paralysis, and is rarely 
 found in cells undergoing very acute degeneration. 
 
 The changes of the nuclei first appear in the nucleolus ; this, 
 as has been said, normally contains one or two vacuoles. In de- 
 generative processes it begins to swell, and more vacuoles develop, 
 so that finally it presents the appearance that has been likened by 
 Berger to the morula stage of the ovum. Ultimately, as the de- 
 generation progresses, it may grow 7 fainter and disappear entirely. 
 Clumps of chromatin are often observed at the periphery of the 
 nucleolus, and occasionally ray-like fibers project from them into 
 the nucleus. Two or more nucleoli have also been observed, but 
 it is doubtful if this is a morbid change. 
 
 The nucleus itself exhibits a variety of changes. Stained with 
 hematoxylin, it shows a delicate chromatin reticulum, and this may 
 exhibit, in the ordinary forms of degeneration, changes that are 
 found in other cells in the process of karyolysis ; occasionally the 
 chromatin collects in a diffuse, irregular mass about the nucleolus. 
 In various forms of degeneration the nucleus seems to be stimu- 
 lated, and shows karyokinetic figures, or may even divide com- 
 pletely, so that two nuclei are found in the same cell. This, how- 
 ever, is not necessarily a degenerative change, because similar ap- 
 pearances are found in embryonal and in lacerated nerve-tissue. 
 Perhaps the most important nuclear change, and one that is 
 most certainly pathologic in nature, is the dislocation of the 
 nucleus. It may be found at the periphery of the cell, or even 
 protruding from it, as if to be expelled. AVagner has even de- 
 scribed nuclei lying outside the cells without nuclei ; but Berger 
 suggests that in these cases the cells have become excessively 
 vacuolated, and that the nuclei lie among the vacuoles, whose 
 situation at the periphery of the cell causes it to appear smaller 
 than it really is. I have never seen nuclei more than slightly pro- 
 truding from degenerated cells. It has been said that the nucleus 
 can disappear from the cell when it does not present marked de- 
 generative changes ; it must be remembered, however, that the 
 large diameter of the multipolar cell renders it possible with a 
 good microtome to make a number of sections through a single 
 cell, and it is very likely that these conditions are due simply to 
 

 DISEASES OF THE BRAIN AND ITS MEMBRANES. 737 
 
 sections beyond the plane of the nucleus. In the most advanced 
 types of degeneration the nucleus certainly disappears completely. 
 
 Changes may also take place in the cell as a whole. In the 
 process of degeneration its outline usually becomes irregular and 
 angular. The cell appears to be smaller, and often the pericellular 
 space is very obvious. In many cases, however, this is an arte- 
 fact, produced by the hardening fluid, and although it may be also 
 the result of some morbid process, it is impossible to give it any 
 value as such. In the early stages of degeneration the proto- 
 plasmic processes may be unimpaired. Varicosities, such as 
 shown by the silver-impregnation, are rarely observed by the 
 Nissl method. I have, however, seen them in the nerve-cells of 
 the cord of a guinea-pig killed by tetanus. Tortuosity of the 
 protoplasmic processes is very common, particularly in chronic 
 conditions, such as sclerosis. It is impossible to stain the terminal 
 ends by the Nissl method, and the changes in the gemmules can- 
 not therefore be recognized. Sometimes the processes become 
 friable, break off, and disappear completely, leaving the cells 
 with a rounded outline. Finally, dislocation in the arrangement 
 of the pyramidal cells has been observed, particularly in cases 
 of sclerosis of the brain, and it is probable that it occurs in all 
 parts of the nervous system, although when the normal arrange- 
 ment is irregular, it is impossible to estimate its extent. Berger 
 lias recently called attention to a very peculiar appearance which 
 may occur in degenerated cells. Sometimes in the portion of the 
 nucleus opposite the nucleolus there is a small projection from the 
 wall which passes inward toward the nucleolus, but before it 
 reaches it, branches into three or four arms that have dilated ends. 
 These seem to encircle the nucleolus, but are not directly in con- 
 tact with it. He is unable to give a satisfactory explanation of 
 this appearance, but suggests that perhaps it represents some form 
 of duct conveying the secretion of the nucleus to the protoplasm 
 of the cell, ordinarily unstainable, but in degenerated conditions 
 filled with altered fluid. 
 
 The nerve-fibers are of two kinds, the medullated and the 
 non-medullated. Non-medullated nerve-fibers consist of the axis- 
 cylinder alone. They are found in the olfactory nerve and in the 
 sympathetic nervous system, and when they undergo degeneration 
 exhibit swelling and varicosities, and ultimately break down into a 
 granular detritus. Non-medullated nerve-fibers may also be pro- 
 vided with a sheath, the neurilemma ; such fibers are found in 
 some of the cerebrospinal nerves. Medullated nerve-fibers may 
 consist only of the myelin-substance and the axis- cylinder — that 
 is, the neurilemma is absent ; such fibers are found in the central 
 nervous system. Ordinarily, they consist of the neurilemma, the 
 myelin-substance, and the axis-cylinder ; such fibers are found in 
 the central nervous system and in the peripheral nerves. These 
 
738 TEXT-BOOK OF PATHOLOGY. 
 
 fibers may branch, either giving off collaterals in their course, or 
 forming more or less complex aborizations at their terminations. 
 The axis-cylinder usually exhibits a somewhat fibrillar structure. 
 The myelin-material resembles fat and has a high refractive in- 
 dex. It does not extend the whole length of the fibers, but, at 
 rather regular intervals, is absent (nodes of Ranvier). These 
 points are perhaps for the purpose of providing access for nutri- 
 ment to the nerve-fiber. Upon the inner surface of the neuri- 
 lemma are found a few oval nuclei surrounded by protoplasm. 
 The earliest symptom of degeneration in the nerve-fibers is the 
 appearance of granules in the myelin-sheath. These soon run 
 together and form droplets that give all the reactions typical of 
 fat. Such a fiber, examined microscopically in longitudinal sec- 
 tion, exhibits these droplets arranged irregularly along its course, 
 giving rise to a somewhat beaded appearance. (Such axis-cylin- 
 ders may be stained by osmic acid (Marchi's method), or by 
 Sudan III., providing the tissue has not been hardened in alcohol.) 
 The next change is usually found in the axis-cylinder. This may 
 swell and become extraordinarily varicose, so that indeed it loses 
 all resemblance to a nerve-fiber. Instead of being fibrillar, it has 
 an irregular granular appearance, and may contain here and there 
 minute droplets of fat, or the fiber may shrink and become granu- 
 lar, and ultimately disappear, nothing remaining to indicate its 
 previous existence excepting a mass of delicate granular detritus. 
 These changes may be brought about, either by the destruction of 
 the ganglion-cell from which the axis-cylinder forming the fiber 
 arises ; or by separation of the fiber from its ganglion-cell ; or by 
 injurious agencies acting locally upon the nerve-fiber. The second 
 form of degeneration — that is, taking place in the peripheral por- 
 tion of the cut nerve — is known as Wallerian. Changes in the 
 proximal end also occur, but rarely extend further than the first 
 node of Ranvier. When a nerve has been divided the earliest 
 change is found on either side of the point of division, and con- 
 sists in fragmentation of the myelin. About the third day fat- 
 droplets appear in the myelin ; there is some swelling of the axis- 
 cylinder ; and often proliferation of the nuclei in the neurilemma 
 may be observed. As the myelin breaks down into a fatty detri- 
 tus, it is gradually absorbed by the compound granular-cells, which 
 appear all along the course of the nerve-fiber, and at the end of 
 three or four months it has entirely disappeared. During this 
 period the neuroglia is undergoing proliferation ; at first there is a 
 slight increase in the number of neuroglia-cells ; later, the pro- 
 liferation of the fibers preponderates, and, finally, the degenerated 
 area is occupied by a thick mass of coarse fibers that usually 
 undergo slight contraction. The proliferation of the cells ceases 
 about the time that the fibers have become completely degen- 
 erated. The subsequent proliferation, if any, occurs only in the 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 739 
 
 neuroglia-fibers. The central portion of the separated fiber will, 
 after a long interval, also degenerate ; this is possibly due to 
 functional inactivity, and appears to be more of the nature of an 
 atrophy. Thus in amputations that have occurred in early life, 
 the anterior roots, forming the nerves that supply the amputated 
 limb, become smaller and contain fewer fibers, and there is ulti- 
 mately some degeneration in the ganglion-cells of the anterior 
 horns. Regeneration of nervous tissue occurs in the invertebrates 
 and possibly among fishes and reptiles, although this is very un- 
 certain. Regeneration of nerve-fibers in the peripheral nervous 
 system occurs in all the higher animals, including man. After the 
 nerve-trunk has been cut, the peripheral ends of the axis-cylinder 
 of the central portion of the nerve become swollen and split up 
 into very fine fibrillse. These grow in various directions, and, if 
 they unite with the distal portion of the nerve, will use it as a 
 skeleton, and one of them, at least, will grow toward the periphery, 
 ultimately forming new nerve-fibers. These changes occur in both 
 sensory and motor fibers. (See section upon the Regeneration of 
 the Peripheral Nerves.) 
 
 The neuroglia of the nervous system may proliferate or 
 undergo softening, the former change producing various forms of 
 sclerosis or gliosis. Sclerosis of the brain may be either diffuse or 
 circumscribed, and the latter is again subdivided into the hyper- 
 trophic and atrophic forms. 
 
 Diffuse sclerosis of the brain never involves all parts equally. 
 To a certain extent it is normal in old age, and is usually found to 
 be limited to the most superficial portion of the cortex beneath 
 the pia, or else to the layer of the gray substance adjacent to the 
 white matter. The neuroglia-tissue in either situation appears to 
 be composed of rather coarser fibers than common, either forming 
 wavy bands or a coarse network. Macroscopically the brains 
 exhibit only slight alteration. The consistency may, on account 
 of other senile changes, be even slightly reduced ; the gray matter 
 is usually narrower than normal ; the pia mater is generally firmly 
 adherent, but not invariably. This condition sometimes occurs in 
 connection with other diseases, as epilepsy, or may be congenital. 
 
 Disseminated selerosis is sometimes only slight in extent. It 
 may occur in the brains of epileptics, of criminals, of old persons, 
 and of idiots. The small sclerotic foci are usually found at the 
 junction of the gray and white matter, more particularly in the 
 former than in the latter. The neuroglia-tissue forms a coarse, 
 irregular network ; as a rule, it is unusually vascular and without 
 any or only a few true nervous elements. These areas may be 
 detected, when large enough, by the naked eye, by the fact that 
 they are paler than the surrounding tissue and often slightly 
 sunken. If the process is more extensive and involves the whole 
 thickness of one or more gyri, it gives rise either to the atrophic 
 
740 TEXT-BOOK OF PATHOLOGY. 
 
 or hypertrophic form, or both may coexist in the same brain. The 
 external appearance in these cases is characteristic, and cannot be 
 mistaken for any other process. 
 
 In the atrophic form the gyri are reduced perhaps to the thick- 
 ness of a lead-pencil, they are pale, firm, slightly granular upon the 
 surface and the pia mater may be slightly adherent ; but this is 
 not common. Section through one of these convolutions shows 
 that the cortex is considerably thinner and has an immediate ten- 
 dency to retract. The white substance is also involved, but 
 apparently less severely. The extent of the process is very 
 variable ; only one or two convolutions may be affected, perhaps, as 
 in several reported cases of epilepsy, only the cornua ammonis. 
 Sometimes a number of convolutions are affected, and in the 
 majority of these cases there is some tendency to an irregularly 
 symmetrical distribution. Microscopically these lesions show 
 marked hyperplasia of the neuroglia-tissue — that is, increased 
 number of neuroglia-cells and coarseness of the neuroglia-fibers, 
 which, however, form coarser meshes than usual. Many of the 
 neuroglia-cells are swollen, the nuclei are enlarged, pale, and the 
 outlines of the cells are irregular. In some cases a number of the 
 cells show a slight projection upon one side. The nervous elements 
 may appear to be more thickly placed and somewhat irregularly 
 distributed, and the protoplasmic processes of the ganglion-cells 
 are often tortuous. More frequently they are considerably dimin- 
 ished in number or else entirely absent. The myelinated fibers 
 are always decreased, particularly the tangential fibers of the cor- 
 tex. The vessels are more numerous than usual and often show 
 wide perivascular spaces filled with fibrous tissue. In the most 
 advanced areas, however, the vessels may be entirely absent. 
 Corpora amylacea or kindred products of nerve-degeneration are 
 sometimes found. Ordinarily the neuroglia-fibers are arranged 
 in bands just beneath the pia. Sometimes they form distinct 
 whorls. These changes are usually found in epilepsy and idiocy, 
 and when the lesions occur in the motor region are always asso- 
 ciated with motor disturbances. 
 
 In the hypertrophic nodular form, the brain, as a whole, is 
 usually somewhat enlarged, and nodules are found in the cerebral 
 cortex that project from the surface and are much harder than the 
 surrounding substance. The larger ones are often slightly umbili- 
 eated. The surface of these nodules is often granular. The micro- 
 scopic changes are similar to those found in atrophic sclerosis, with 
 the exception that the excess of neuroglia-tissue is much more 
 pronounced. In these brains there are often sclerotic areas 
 beneath the ependyma of the ventricles, the lateral ventricles 
 being more frequently affected than the third or fourth. These 
 nodules are small, round, and very hard. Microscopically they 
 are found to consist of neuroglia-fibers arranged in a somewhat 
 

 DISEASES OF THE BRAIN AND ITS MEMBRANES. 741 
 
 concentric manner. They may be vascular or entirely deprived 
 of blood-vessels, and sometimes contain chalky deposits or masses 
 of hyaloid material. As in all destructive lesions of the central 
 nervous system, secondary degenerations may occur, but they are 
 far less common than would be suspected from the apparent extent 
 of the degenerative processes. These forms of congenital sclerosis 
 probably commence after the seventh month of fetal life, because, 
 as Kundrat has pointed out, the arrangement of the convolutions 
 is rarely disturbed. They have been ascribed . to syphilis, to in- 
 flammatory change, to congestion of the lymphatic system, and as 
 akin to tumor-formation. The absence of round-cell infiltration, 
 and the fact that the pia is rarely adherent, even when the sclero- 
 sis takes place in the most superficial layers of the cortex, would 
 seem to exclude inflammatory causation. Neurogliar proliferation 
 occurs about gumma, but there is no ground for believing that 
 other forms are also due to syphilis. The dilatation of the peri- 
 vascular spaces is favorable to the theory of congestion of the 
 lymphatic system. This, however, is probably secondary. It is 
 no explanation for this process to say it belongs to the tumors, but 
 at present it appears impossible to give a more satisfactory eti- 
 ology. Softening of the neuroglia is a part of all processes of 
 softening in the brain, which are described in connection with 
 thrombosis and embolism. A condition that is possibly the result 
 of softening during fetal existence, but may be a congenital mal- 
 formation, and consists of the formation of cavities in the brain, 
 may be properly described here. 
 
 Porencephaly is a condition characterized by the absence of 
 a greater or less amount of the substance of one or both of the 
 cerebral hemispheres, leading to the formation of a cavity or cav- 
 ities filled with cerebrospinal fluid. 
 
 Etiology. — The cause of porencephaly is not definitely known. 
 As Von Kahden remarks, the similarity of the lesions in typical 
 cases is such that it seems reasonable to accept a uniform etiology. 
 Kundrat believed that the lesions were due to anemic infarction, 
 as a result of the occlusion of the Sylvian arteries. Freund also 
 accepts this as the cause in a certain number of cases. Von 
 Kahlden, however, believes that it is the result of some disturb- 
 ance in a development of the brain, and bases his opinion upon 
 the symmetry of the lesions and their peculiar situation. Other 
 authors have suggested an inflammatory origin of the process, 
 because of the adhesions between the membranes. A certain num- 
 ber of cases certainly develop after birth ; these may be due to 
 injury, such as might be produced by instrumental delivery, or by 
 blows upon the skull, or by embolic or inflammatory processes. It 
 can only be said, however, that the etiology is at present unknown. 
 
 Pathologic Anatomy. — Von Kahlden has divided the cases 
 hitherto reported into two classes : the typical and the atypical. 
 
742 TEXT-BOOK OF PATHOLOGY. 
 
 The former class comprises about two-thirds of all the cases, and 
 is characterized by the presence of a funnel-like cavity in the 
 motor region of the brain, usually bilateral, although unequal, that 
 extends from the subarachnoid space to the cavity of the ventricle 
 (Fig. 350). Frequently this condition is associated with imperfect 
 development or exposure of the island of Reil. In the atypical form 
 the lesions are exceedingly various ; they may be found in any part 
 of the cerebral hemispheres ; the shape of the cavity may be either 
 a shallow depression or a considerable loss of substance. Often — 
 
 Fig. 350.— Porencephaly (case of Dr. J. H. Lloyd). 
 
 in fact, usually — there is no communication between the cavity and 
 the ventricle. These varieties may even be found in the cerebel- 
 lum, but perhaps are most frequent in the lateral lobes at the point 
 where they unite with the vermiform process. Cases have also 
 been recorded with cavity-formation in the base of the brain, com- 
 municating sometimes with one of the horns of the lateral ventri- 
 cles. A sort of cystic formation has been described, in which 
 multiple cavities, not communicating with either the ventricle or 
 subarachnoid space, have been found in the substance of the brain. 
 The macroscopic changes observed in the typical form are as fol- 
 lows : ordinarily a distinct depression is noticed in the dura after 
 the skull has been removed. When this region is more carefully 
 examined it is found that the dura may or may not be adherent 
 to the arachnoid which covers the cavity. The pia usually dips 
 into and covers the wall, and may be continuous with the epen- 
 dyma of the ventricle. The adjacent convolutions of the brain 
 are arranged in a somewhat radiate manner and turn down into 
 the cavity, although this is not invariably the case, for they some- 
 times may appear as if simply cut off, being otherwise normally 
 arranged. Associated changes in the brain are microgyria ; pro- 
 liferation of the neuroglia-tissue, and perhaps also of the con- 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 743 
 
 nective tissue ; atrophy of the nerve-cells in the cortex, particu- 
 larly of the large pyramidal cells ; and more or less complete 
 destruction of the nerve-fibers in the region adjacent to the defect. 
 Rarely there is a sort of cystic degeneration of the walls of the 
 cavity. The spinal cord usually exhibits a secondary degen- 
 eration in the pyramidal columns ; this, however, is not always 
 the case, for sometimes it appears that one or both pyramidal 
 columns have failed entirely to develop, giving rise to a condition 
 of micromyelia. Other parts of the brain appear to be rarely 
 affected in the typical form of the condition. When the lesion 
 is situated in any other part than the central region, corresponding 
 secondary degenerations may, of course, occur. 
 
 THE BLOOD=VESSELS. 
 
 The arteries of the brain may be divided into two groups, 
 those nourishing the cortex and those nourishing the basal gan- 
 glia. The former are the ramifications of the terminal branches 
 of the circle of Willis ; the latter arise directly from the main ves- 
 sels of the base of the brain. 
 
 Atheroma. — The changes that occur in the arteries are those 
 ordinarily occurring in the vessels of the other parts of the body, 
 atheroma of the arteries of the base being perhaps more frequent 
 than of the arteries of the majority of other organs. These athe- 
 romatous changes usually lead to calcareous infiltration, and in old 
 age often the entire circle of Willis is composed of typical pipe- 
 stem arteries. When the process is less extensive, the calcareous 
 infiltration is most apt to affect the two internal carotids, the mid- 
 dle cerebrals, and the basilar artery. 
 
 Hyaline degeneration may also occur. It is of two kinds : 
 that which forms simply the early stage of arterial sclerosis, and 
 another process that is apparently independent of this, and occurs 
 as a diffuse degeneration of the intima and media. This latter 
 form is frequently found in the brains of chronic idiots even dur- 
 ing early life. Occasionally it is also found in senile brains, but 
 in these cases is not so certainly independent of arterial sclerosis. 
 Amyloid degeneration of the blood-vessels may occur as a part of 
 general amyloid disease, but is not especially common in the brain. 
 
 Colloid Degeneration. — A rare form of degeneration has 
 been spoken of as colloid, although the material discovered in the 
 blood-vessels seems more akin to that of hyaline degeneration. In 
 this process the adventitia and the media are greatly thickened as 
 a result of their infiltration with a homogeneous translucent mate- 
 rial, which may be deposited irregularly in masses, or else cause a 
 diffuse thickening of the wall. The masses project into the sur- 
 rounding nervous tissue, and may sometimes be detached, forming 
 then independent clumps that are not unlike the so-called amyla- 
 
744 TEXT-BOOK OF PATHOLOGY. 
 
 ceous bodies, although they fail to give all the characteristic amy- 
 loid reactions. This condition is usually associated with profound 
 disturbances of the intellect, and may give rise to clinical symp- 
 toms that resemble those of general paresis. A case of this nature 
 has been reported by Alzheimer. This colloid or hyaloid material 
 is soluble in boiling water and in alkaline solutions. It stains a 
 bright-red by Van Giessen's method, and usually blue by Wei- 
 gert's fibrin-method. Sometimes it stains brown with iodin, but 
 not invariably. There is usually extensive degeneration of the 
 nervous elements, which may be associated with secondary changes 
 in the spinal cord. 
 
 Syphilis frequently causes thickening of the intima or endarte- 
 ritis, which may be due either to the usual round-cell infiltration 
 or to the formation of fibrous tissue. Tuberculosis may also cause 
 endarteritis. This form is most frequently associated with tuber- 
 cular meningitis, and therefore the basilar artery is the one most 
 frequently affected. 
 
 Aneurysms may occur in any of the components of the circle 
 of Willis. The basilar artery is the one most frequently involved, 
 usually just at its posterior extremity. Large aneurysms of the 
 arteries of the brain proper, or of the arteries of the vertex, are 
 exceedingly rare. A saccular aneurysm, as large as a cherry, 
 springing from the anterior communicating artery, was observed 
 at the Philadelphia Hospital. Miliary aneurysms of the brain are, 
 on account of their etiologic relation to cerebral hemorrhage, the 
 most important form of vascular disease in the brain (see Fig. 182). 
 These aneurysms may be ectatic or saccular. The ectatic forms 
 are usually fusiform in shape, and often consist of but a single coat 
 of the vessel-wall ; that is to say, they are merely endothelium 
 surrounded by a thin layer of fibrous tissue. The saccular aneu- 
 rysms are usually somewhat larger ; they appear as bulbous swell- 
 ings on one side of the vessel, connecting with the lumen by nar- 
 row openings. They may consist of a single wall, as in the fusiform 
 type, the most common variety, or of the intima or adventitia, with 
 a considerable amount of fibrous thickening. Occasionally the 
 fusiform aneurysms may exhibit distinct atheromatous change, but 
 even in these instances the media is atrophic, and they are certainly 
 exceptional. It is doubtful whether arteriosclerosis is of much 
 importance in connection with the formation of these aneurysms, 
 and it is certain that in the majority of cases the first change in 
 the vessel is a fatty degeneration of the media. This leads to local 
 weakening of the wall and to consequent distention ; a change 
 that is favored by a considerable degree of pressure, to which the 
 arteries springing from the middle cerebral or from the beginning 
 of the basilar artery are subjected. According to some authors, 
 these aneurysms are to be regarded as hernise of the intima, really 
 the result of atrophy of the muscularis, nevertheless they are more 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 745 
 
 frequent in the old, and certainly in the majority of cases in which 
 they are found, the arteries of the base are distinctly atheromatous. 
 The formation of thrombi in miliary aneurysms is exceptional. 
 
 CIRCULATORY DISTURBANCES. 
 
 Circulatory disturbances in the brain differ from those in other 
 parts of the body on account of the presence of a rigid bony cap- 
 sule (the skull), which prevents any increase or decrease in the 
 size of the contained viscus. Variations in the quantity of blood, 
 however, do take place in adults, and are rendered possible, first, 
 by the elasticity of the nervous substance itself, which is capable 
 of undergoing a slight degree of compression or extension, and, 
 second, by the free communication of the subarachnoid spaces of 
 the brain and cord and the ventricular cavities, so that the cere- 
 brospinal fluid may be in greater or less quantity in the cavity 
 of the skull or in the spinal canal, and thus permit variation 
 in the amount of blood in either region. Local congestion or 
 anemia may occur as a result of local disturbances, but the free 
 anastomosis of the arteries of the circle of Willis provides such 
 facility in equallizing the amount of blood flowing to the different 
 parts of the brain, that neither is often found in general condi- 
 tions. In very young children these mechanical restrictions do 
 not obtain, because the fibrous union between the bones of the 
 skull permits of very considerable changes in the size of the 
 cranial cavity. 
 
 Acute anemia of the brain may occur as a result of severe 
 hemorrhage, or of hyperemia in other parts of the body, particu- 
 larly the pulmonary and abdominal organs, and it has been sup- 
 posed to exist in fainting, during hysterical crises, and in sleep. 
 It must be admitted, however, that certain proof of its existence 
 either as a cause or effect of the three latter conditions is lacking. 
 Microscopically the brain is usually pale and firm. There is little 
 or no tendency on the part of the small venules of the white sub- 
 stance to bleed upon cross-section, and the gray matter is dis- 
 tinctly paler, so that the distinction between it and the medullary 
 substance is not so distinct as is the case in normal tissue. Some- 
 times in these conditions there is overfilling of the veins of the 
 pia as a result of the shrinking of the brain. 
 
 Chronic anemia of the brain may occur in severe cachectic 
 conditions, such as progressive pernicious anemia, lead- or malarial 
 poisoning. It may also be the result, though less frequently, of 
 atheroma of the cerebral arteries, with a general narrowing of 
 their lumina. The brain is small, the consistency varies accord- 
 ing to the duration and nature of the process, being at first hard, 
 later, probably as a result of degenerative changes, slightly softer 
 than normal. The ventricles are not dilated at first, but the con- 
 
746 TEXT-BOOK OF PATHOLOGY. 
 
 volutions are shrunken and the sulci are wider as a result of the 
 diminution in size of the brain as a whole. The substance of the 
 brain is pale, and often seems slightly moister than normal. Local 
 anemia may occur as a result of thrombosis or embolism, and 
 usually leads to softening. 
 
 Active hyperemia of the brain is nearly always associated 
 with inflammatory or toxic conditions. It is perhaps most fre- 
 quent in association with meningitis or encephalitis. It is always 
 found after death from sunstroke, acute delirium, cholera, and 
 hydrophobia ; as well as, occasionally, after death from infectious 
 disease. It may be local or general. 
 
 Local hyperemia is usually associated with meningitis, and 
 may be limited to the superficial layer of the cortex beneath the 
 meningitic areas. The affected parts are darker than normal and 
 may even contain punctiform hemorrhages. Microscopically the 
 blood-vessels are found to be dilated, and there is more or less 
 degeneration of the adjacent nerve-substance, according to the 
 duration of the process. Local hyperemia may also occur after 
 thrombosis, and leads to red softening of the nerve-tissue. 
 
 General active hyperemia is supposed to be associated with un- 
 usual activity of the mind, particularly prolonged and intense 
 mental effort. Certain proof of this, however, has not yet been 
 furnished. The brain is darker and larger and its consistency is 
 softer. The blood-vessels of the pia are injected. The gray mat- 
 ter is darker and, as in the local form, may contain minute hemor- 
 rhagic foci. The white matter is moist; its color is rarely altered, 
 but as soon as the section is made it is covered with small red 
 spots, representing hemorrhages from the veins and capillaries. 
 These may be readily distinguished from interstitial hemorrhages by 
 allowing a little water to flow over the surface of the section, when 
 they will disappear. Microscopically, aside from the distention 
 of the vessels with blood, pronounced degenerative changes are 
 rarely found, excepting in those cases resulting from infectious 
 diseases. In these the alterations commonly associated with severe 
 toxemia are present, but are to be considered as complications, and 
 not as the result of the circulatory disturbances. 
 
 Passive hyperemia may be associated with valvular heart- 
 disease or chronic lung-disease, or it may be caused by tumors 
 in the neck pressing upon the jugular veins, or by intracranial 
 conditions. Of the latter, the most important are brain-tumors 
 compressing the veins, whilst the arteries still continue to con- 
 vey blood, and thus cause increase of the cranial contents. 
 When the tumors press upon the veins of Galen passive hyper- 
 emia and distention of the ventricles are particularly common. 
 Passive hyperemia may also be caused by thrombosis of the dura] 
 sinuses. In acute passive congestion the veins of the dura are 
 widely distended ; the subarachnoid space is moist ; the brain 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 747 
 
 seems to be slightly larger, softer and moister than normal. The 
 gray matter is of a slaty color. The white matter may have a 
 faint bluish tinge, and its capillaries and ventricles bleed freely 
 upon cross-section. The ventricles may not be larger, but appear 
 to contain fluid under pressure, that wells forth when they are 
 opened. 
 
 Edema of the brain nearly always occurs when passive hyper- 
 emia persists. This is characterized by the distention of the sub- 
 arachnoid space with liquid, so that the convolutions are no longer 
 distinct, and the surface of the brain has a clear or pearly appear- 
 ance. The arachnoid is usually thicker, particularly along the 
 sulci. The fluid is clear, or perhaps very slightly turbid ; it has a 
 higher specific gravity than the cerebrospinal liquid, coagulates 
 upon boiling, and is usually found to contain numerous cellular 
 elements. A microscopic examination of the brain and its 
 membranes shows marked distention of the subarachnoid space, 
 which is usually divided into irregular spaces by delicate fibrous 
 bands. The endothelial cells appear to have undergone some pro- 
 liferation, and in many places have desquamated and lie free in the 
 areolar spaces. Around the blood-vessels there is occasionally 
 slight extravasation of round cells, which are usually mononuclear 
 and resemble lymphocytes, and indicate an inflammatory reaction 
 to the long-continued pressure. The arachnoid is usually thicker, 
 the thickening being almost exclusively fibrous in nature. The 
 pia is slightly thicker, and sometimes may be seen to have coalesced 
 with the superficial layer of the cortex. In the brain-substance 
 the perivascular spaces are distended, the neurogliar meshwork is 
 coarser than normal, and there may be slight evidences of degen- 
 eration in the cells. 
 
 Local edema of the brain, the so-called apoplexia serosa, is 
 occasionally found in the neighborhood of areas of softening. In 
 cases of acute hydrocephalus this serous infiltration sometimes 
 occurs in the neighboring internal capsules, and may even lead 
 to transient hemiplegia. 
 
 Cerebral hemorrhage occurs in two varieties : the so-called 
 punctate form, and massive hemorrhage. 
 
 Punctate hemorrhages are due to some alteration of the vessel- 
 walls or of the degree of blood-pressure, causing extravasation 
 of blood into the surrounding tissues. The hemorrhages are 
 small, often microscopic, and are by far most common in the gray 
 matter, especially in the cortex. The principal causes are hy- 
 peremia, particularly if associated with inflammatory conditions 
 of the brain, or convulsions. The wall of the blood-vessel may 
 be diseased, but does not always show solution of continuity. The 
 blood-pigment is more or less altered, according to the length of 
 time that has elapsed between the occurrence of the hemorrhages 
 and the examination of the tissues. The nervous tissue immedi- 
 
748 TEXT-BOOK OF PATHOLOGY. 
 
 ately involved is edematous, and there is usually some prolifera- 
 tion of the neuroglia-cells in the immediate vicinity. Such hem- 
 orrhages, of course, may heal without leaving any trace, for the 
 secondary degenerations that may possibly be caused are too 
 slight to be detected. 
 
 Massive hemorrhages usually occur from the branches of the 
 middle cerebral artery — that is, from the vessels most frequently 
 the seat of miliary aneurysms. They may also, however, occur 
 in the centrum ovale or the pons, or, in fact, in almost any portion 
 of the central nervous system. The blood usually collects in the 
 form of an irregular dark-red mass that, in recent cases, rapidly 
 becomes bright red upon exposure to the air. The size of the 
 hemorrhagic area naturally varies with its location and the amount 
 of blood extravasated. Its outline is exceedingly irregular, and 
 almost always small separate hemorrhagic foci are found in the 
 surrounding tissue. According to the density of the tissue, the 
 blood is more or less dispersed. Thus, in the white matter the 
 extravasation is usually more diffuse than in the gray, where hem- 
 atomata are exceedingly apt to form. The substance of the brain 
 is soon converted into an area of softening. Its structure is usually 
 entirely lost, although it may be possible, in recent cases, to recog- 
 nize the presence of altered cells and nerve-fibers. The neuroglia 
 usually shares in this softening, but in case the hemorrhage is not 
 extensive it may remain and form a sort of skeleton ; the tissue 
 then is not nearly so soft, and the surface of section usually is- 
 smooth. If the hemorrhage occurs in the internal capsule, as is 
 usually the case, and is at all extensive, the blood may creep in- 
 ward toward the ventricle, into which it may rupture, filling the 
 lateral ventricle, and sometimes extending into the third ventricle 
 and into the lateral ventricle on the other side (Fig. 351). Oc- 
 casionally, in exceedingly severe cases, almost the whole of one 
 of the hemispheres may be destroyed ; this is usually associated 
 with sudden death, and is known as the foudroyant form of apo- 
 plexy. The softened brain-substance can usually be readily washed 
 away by a current of water, leaving the blood-vessels, which may 
 then readily be examined with a low power for the presence of 
 miliary aneurysms. If the patient survives his first attack, rapid 
 alterations begin to take place in the diseased tissue. The throm- 
 bus contracts, causing edema in the surrounding tissues. A cap- 
 sule of delicate fibrous tissue may even be formed about it. The 
 small hemorrhages in the surrounding tissue are absorbed. The 
 color of the .softened region becomes dark brown, and it may 
 either go on to complete liquefaction, with the subsequent absorp- 
 tion of the pigment and the formation of a cyst, or else be gradu- 
 ally entirely absorbed, leaving a pigmented scar. The walls of 
 the cysts are usually discolored by pigment, and in the neighbor- 
 In mm 1 pigment-granules and compound granular cells are found in 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 749 
 
 great numbers. These old hemorrhagic cysts are very difficult to 
 distinguish from those produced by other forms of softening. 
 Often the contents are slightly discolored, the walls are dense and 
 somewhat sclerotic in nature, and may contain crystals of hema- 
 toidin. It is somewhat doubtful whether the walls are composed 
 of neurogliar tissue or of true fibrous connective tissue derived 
 from the blood-vessels. It is certain, however, that shortly after 
 extravasation of the blood, hyperplasia of the neuroglia in the 
 immediate vicinity takes place. This may occur very rapidly, so 
 that in the course of a few days new neuroglia-fibers may be seen 
 pushing their way into the hemorrhagic area from the collection 
 of neuroglia-cells in the nearest healthy tissue. After healing has 
 
 Fig. 351.— Hemorrhage into the internal capsule and the caudate and lenticular nucleus 
 of the right cerebral hemisphere (from Bollinger). 
 
 taken place the hemisphere is usually reduced in size. This re- 
 duction is not merely equivalent to the amount of nerve-tissue 
 that has been destroyed, but represents also the secondary degen- 
 eration that occurs in the nerve-fibers whose course has been in- 
 terrupted by the lesion. These are both ascending and descend- 
 ing, and frequently cause sclerosis that involves not only the 
 brain, but extends throughout the pyramidal columns. 
 
 Secondary Degeneration after Hemorrhages. — As a result of hem- 
 orrhage into the brain-substance with destruction of tissue, second- 
 ary degenerations appear, which, of course, are systemic and fol- 
 low the direction in which the nerve-fibers convey impulses. Of 
 these the most important are the degenerations of the pyramidal 
 tract, of the optic tract, and of the projection-fibers from the 
 temporo-sphenoid lobes. A discussion of this subject involves 
 
750 TEXT-BOOK OF PATHOLOGY. 
 
 consideration of the anatomy of the brain more than of the pathol- 
 ogy, and only the most important details can be given here. De- 
 generation of the pyramidal tract may be sharply circumscribed if 
 the focal lesion is situated in the cortex or the centrum ovale. In 
 this case a slender band of degenerated fibers may be traced along 
 the pyramidal tract. This is only possible, however, if the lesion 
 is sufficiently recent to permit the employment of Marchi's stain- 
 ing-method, for it is otherwise impossible to recognize a small 
 number of degenerated fibers in the midst of a group of healthy 
 ones. As the hemorrhage usually takes place from the lenticulo- 
 caudate artery and involves the complete destruction of the pyram- 
 idal fibers in the internal capsule, it not unfrequently happens 
 that the entire pyramidal column of one side undergoes secondary 
 degeneration. Hoche, who has recently studied two cases of 
 cerebral hemorrhage, involving complete destruction of the motor 
 fibers on one side, by Marchi's method, has found a rather pe- 
 culiar distribution of the motor fibers in the crusta. Dividing 
 this region into five parts, he finds that the two median sections 
 are free from degenerated fibers. The middle section is almost 
 completely degenerated, and there is also an area of degeneration 
 in the median part of the fourth section, extending partly into the 
 fifth. Degenerated fibers can also be traced going to the nucleus 
 facialis of the opposite and the same sides, and to the nucleus 
 hypoglossus of both sides. There were also degenerated fibers in 
 the lateral pyramids of the same side. Interruption of the fibers 
 of the optic radiation, or destruction of the primary optic centers, 
 causes secondary degeneration which does not, however, appear as 
 promptly as in the motor fibers. There is degeneration in the 
 external geniculate body, in the pulvinar, and in the anterior cor- 
 pus quadrigeminus of the same side. Ultimately, after some years, 
 degeneration may also occur in the optic nerves. Destruction of 
 the second and third temporal lobes, or of the projection-fibers 
 arising from them, causes secondary degeneration in the posterior 
 limb of the internal capsule. The fibers appear to extend into 
 the thalamus, and also into the crusta. Destruction of other parts 
 of the brain-cortex causes degeneration, which seems to affect 
 chiefly the projection-fibers. Extensive hemorrhages into the 
 cerebellum usually cause death, as a result of pressure upon the 
 medulla. If, however, the patient survives, and if the nucleus 
 dentatus is particularly involved, there is degeneration of the 
 superior cerebellar peduncle, which may be traced as far as the red 
 nucleus in the tegmentum. Degenerations have been produced 
 experimentally in the other peduncles. All these secondary de- 
 generations are quite typical in character. They appear about the 
 ninth day, the first changes being the degeneration of the myelin- 
 sheath. This is followed by the appearance of compound gran- 
 ular cells and hyperplasia of the neuroglia, and later corpora 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 751 
 
 araylacea may sometimes be found. Ultimately nothing but the 
 neuroglia remains, and this is composed of coarser fibers than are 
 found in normal nervous tissue. Occasionally nerve-fibers without 
 myelin-sheaths are found traversing the sclerotic tissue. 
 
 Thrombosis and embolism of the vessels of the brain are 
 due to causes that produce the same processes in other parts of the 
 body. Thrombosis may occur anywhere. It is perhaps more fre- 
 quent in the basilar artery than in other situations, but this rule 
 is by no means certainly established. The causes are, of course, 
 chiefly atheroma of the vessels or syphilitic endarteritis. Embo- 
 lism, on the other hand, usually occurs in the artery of the Sylvian 
 fissure. Perhaps 80 per cent, of all cases occur in this situation. 
 Less frequently, an embolus will lodge in the anterior cerebral, 
 but it is probably extremely rare for an embolus to travel along 
 the posterior communicating artery and lodge in the posterior cere- 
 bral. A more frequent route of embolism into the latter artery is 
 along the vertebrals to the basilar. Embolism in the basilar artery 
 can, of course, never occur, as its lumen is greater than that of 
 either of the branches from which it receives blood. A saddle-embo- 
 lus may occasionally lodge at its bifurcation and give rise to local 
 thrombosis. Sometimes the two processes occur simultaneously — 
 that is, fragments of a parietal thrombus in one of the vessels may 
 be washed off into the blood-stream and be carried along the 
 artery until they occlude its lumen or that of one of its branches. 
 The results of embolism or thrombosis may be either infarction, or, 
 if the obstruction takes place slowly, as in thrombosis, and it is 
 possible for a collateral circulation to be established, there may be 
 no changes, or such only as are temporary. 
 
 Infarction of the brain usually leads very rapidly to cerebral 
 softening (encephalomalacia). It has been usual to describe three 
 forms of this — red, yellow, and white softenings. 
 
 Red softening corresponds very closely to the hemorrhagic 
 infarct. It consists of a serous infiltration of the tissue, the ex- 
 travasated liquid containing numerous red corpuscles. The same 
 theories that have been suggested for the explanation of a hemor- 
 rhagic infarct have been used to explain its occurrence. 
 
 Yellow softening is really only the red softening after more 
 complete liquefaction has taken place and most of the pigment 
 has been absorbed. 
 
 White softening is a term applied to two very different 
 conditions. The first corresponds to the anemic infarct, and 
 appears very shortly after the occlusions of the vessels. The 
 second is a late stage of any form of softening, and is character- 
 ized by the formation of an excessive amount of fat in the softened 
 area, producing an emulsion. The white color becomes even more 
 pronounced after the fat has been absorbed, and the lesion is rep- 
 resented only by coarse neuroglia-fibers. Microscopically the 
 
752 TEXT-BOOK OF PATHOLOGY. 
 
 earliest changes usually appear toward the end of the first twenty- 
 four hours. The brain-substance in the softened area is swollen, 
 softer, and somewhat mottled in appearance and may even exhibit 
 small punctiform hemorrhages. The lesion is not sharply delim- 
 ited, but fades gradually into the surrounding tissues. 
 
 If a large artery has been obstructed, a considerable portion of 
 the brain may be softened and there will be a large extravasation 
 of blood. In this case, the parts of the brain showing the great- 
 est alteration are those nearest the periphery of the distribution 
 of the obstructed vessel, and these changes may even occur with- 
 out complete obstruction if the general circulation is impaired, as 
 in valvular heart-disease, or as a result of profound general 
 anemia. As the process continues, more and more blood is ex- 
 travasated into the tissue, giving it a bright-red appearance. The 
 lesion by this time becomes more circumscribed, although the sur- 
 rounding tissue may be somewhat softened, and, as in the case of 
 hemorrhage, may contain punctiform hemorrhages. As soon as 
 the demarcation is complete, the brain-tissue becomes rapidly 
 softer, probably as a result of the obstruction of the lymph-chan- 
 nels by which the nutritive fluids enter. The nerve-cells undergo 
 almost complete degeneration ; they lose their axis-cylinders and 
 their tinctability, and may either disappear completely or be no 
 longer recognizable. The myelin-sheaths undergo a fatty degen- 
 eration, in which the nerve-fibers soon take part. The whole 
 tissue is filled with compound granular cells. The neuroglia- 
 fibers may also become softened and, to a large extent, liquefied, 
 although they persist longer than the other elements. The wall 
 of what has now become a cyst is composed of the surrounding 
 neuroglias tissue, newly formed capillaries, and nervous tissue in 
 an advanced stage of degeneration. The blood-vessels, however, 
 usually persist for some time, although they are filled with thrombi 
 and form an irregular spongy network in the lesion. 
 
 When organization commences the blood-pigment gradually 
 disappears, and the material changes from a brownish, turbid fluid 
 to a lighter yellow mass, often irregularly surrounded by deeply 
 pigmented cells. Later, complete contraction takes place, and a 
 scar, composed chiefly of neuroglia-tissue, but also containing some 
 fibrous connective tissue that has developed from the walls of the 
 blood-vessels, is left. It is, of course, clear, that red softening is 
 more frequent in the vascular parts of the brain, and white soften- 
 ing in those regions that are poorly supplied with blood, particu- 
 larly in the white substance of the cerebrum. The areas are rarely 
 as well circumscribed as those of red softening, and often do not 
 lead to complete destruction of the tissue, causing only numerous 
 adjacent minute focal lesions, the so-called etat crible. 
 
 A peculiar form of softening occurs in the cortex of the brain. 
 It is usuallv found as lesions that have existed for some time. 
 
 
DISEASES OF THE BBAIN AND ITS MEMBRANES. 753 
 
 The area is yellow, depressed, and somewhat circumscribed. The 
 pia mater over and around the lesion is somewhat thickened, and 
 often the surrounding blood-vessels show thickening of the lumen, 
 although this latter change is probably the cause and not the result 
 of the changes. These are the so-called plaques jaunes of French 
 writers, and if extensive they lead to considerable retraction of 
 the brain-substance and to the formation of collections of liquid 
 in the subarachnoid space (hydrops ex vacuo; external hydro- 
 cephalus). 
 
 Areas of softening, probably due to capillary thrombosis, are 
 frequently found in children suffering from tubercular meningitis. 
 They may also occur in other forms of meningitis, and also in 
 encephalitis, although in these latter conditions the presence of 
 pyogenic micro-organisms in the emboli lead to somewhat differ- 
 ent changes, which will be described in connection with enceph- 
 alitis. Traumatism may also cause softening, often multiple in 
 character, and not necessarily situated directly beneath the point of 
 injury. As a result of the destruction of tissue, secondary degen- 
 erations occur that differ in no respect from those following hem- 
 orrhage. 
 
 INFLAMMATION. 
 
 Encephalitis, or inflammation of the brain-substance, 
 
 is probably not essentially different from inflammation of the other 
 tissues in the body. The nature of nervous tissue, however, and 
 the peculiar reaction that it manifests to various injurious agencies, 
 render this subject one of the most doubtful and difficult in the 
 pathology of the central nervous system. The various forms may 
 be classified, first, as acute and chronic. The important forms of 
 acute encephalitis are the parenchymatous, the simple, the hemor- 
 rhagic, and the suppurative. Chronic encephalitis may take the 
 form either of sclerosis or of scar-formation, which is really only 
 a modification of the former. Acute encephalitis may be consid- 
 ered to be invariably disseminated or focal. JSTo case has been re- 
 corded in which there was extensive inflammatory change in the 
 brain, and it is inconceivable that such a condition should be com- 
 patible with life. 
 
 Acute parenchymatous encephalitis is rather a form of degen- 
 eration than a disease. Changes in the nerve-cells without associ- 
 ated vascular phenomena have, in the last few years, been observed 
 and described in a number of intoxications, either the result of 
 poisoning or infection ; thus Berkeley has carefully studied the 
 changes in the brain in alcoholic poisoning. More or less exten- 
 sive changes have also been recorded as a result of poisoning by 
 malon nitrite, arsenic, and other poisonous substances. Of the 
 infectious diseases that have been studied, the most important are 
 diphtheria, tetanus, leprosy, and hydrophobia. The changes differ 
 
754 TEXT-BOOK OF PATHOLOGY. 
 
 somewhat in nature, and, of course, in the different cases, consid- 
 erably in degree. The most important and typical have been 
 already described in the section upon degeneration of the nerve- 
 cells. These forms of encephalitis, if the name may properly be 
 applied to them, may lead to death, but recovery even from the 
 advanced stages is not impossible, as has been indisputably proved 
 by the experimental research of Goldscheider and Flatau. Neither 
 the brain nor the cord in these cases exhibits any macroscopic 
 changes, excepting, perhaps, passive congestion of the membranes 
 ■when death was preceded by violent convulsions, as in tetanus. 
 
 Simple acute focal encephalitis is characterized by the develop- 
 ment, in various parts of the brain, of areas of softening that may 
 range from a millimeter to several centimeters in diameter. They 
 are usually irregular in size, and very indistinctly separated from 
 the surrounding tissue. The most common situations are the region 
 of the third and fourth ventricles and the aqueduct of Sylvius. 
 The gray matter is more often involved than the white. 
 
 Etiology. — The cause is probably in all cases the presence of 
 infection in the body, such as influenza, typhoid fever, or septicemia. 
 Authors, whose opinions we must respect, have, however, described 
 encephalitis as the result of simple concussion of the brain, or of 
 various forms of poisoning, such as lead. The difficulty in the latter 
 group of cases is due to the close resemblance between encephalo- 
 malacia and encephalitis. Collections of round cells, with slight 
 degenerative changes in the nervous system, have been described 
 in chorea, and have been supposed to represent the subacute or 
 chronic form of encephalitis. The observations are, however, at 
 present insufficient to establish this point. References will be 
 made again to it under the heading of Chronic Encephalitis. Some 
 years ago, various observers reported the occurrence of acute 
 encephalitis in new-born children, but it has since been shown 
 that compound granular cells occur normally in the brain of the 
 fetus and persist for some days after birth. 
 
 Pathologic Anatomy. — The two most important changes are 
 those in the color and consistency. The former is usually slightly 
 darker than normal, but may, if, as is not unfrequently the case, 
 extensive hemorrhage has occurred, become a bright red, resem- 
 bling, upon inspection, an area of hemorrhage, or perhaps more 
 closely, an area of red softening. The consistency is always 
 decreased, probably as a result of serous infiltration. Often the 
 diseased area projects slightly from the surface of the section. 
 Microscopically the characteristic change is the perivascular 
 round-cell infiltration. This usually involves the majority of 
 vessels in the lesion, and may also be found in regions of the 
 brain in which softening has not already commenced. Usually 
 there is the characteristic inflammatory congestion, the blood-ves- 
 sels, and particularly the small capillaries, being sometimes greatly 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 755 
 
 distended and packed with red blood-cells. In some cases 
 thrombi have formed. Hemorrhages are exceedingly frequent ; 
 these are sometimes punctiform and sometimes diffuse extrav- 
 asations into the tissue. Often they appear to represent rupt- 
 ured capillaries, and produce a peculiar speckled appearance on 
 the surface of section. In the early stages the cellular exudate 
 is chiefly composed of polynuclear leukocytes. If the process is 
 more advanced, these may exhibit more or less degenerative 
 ■changes. Later they are replaced by mononuclear cells, probably 
 representing proliferation of the endothelial cells, and perhaps of 
 the neuroglia-cells. The ganglion-cells in the inflammatory re- 
 gion undergo rapid degeneration, usually passing through various 
 stages of chromatolysis, until they are reduced to little colorless 
 vesicles of irregular form. The nerve-fibers also degenerate ; the 
 myelin forms fatty droplets ; the axis-cylinders at first swell and 
 then share in the granular disintegration. In the midst of the 
 focus, the neuroglia ordinarily shares in the softening. At the 
 periphery there is usually a noticeable proliferation of the neu- 
 roglia-cells and the formation of a coarse, thick network of neu- 
 roglia-fibers. Of course, these changes are not found about very 
 early lesions. In the earliest stages compound granule-cells are 
 usually absent ; later they may appear in considerable numbers, 
 but their presence is by no means sufficient to indicate the existence 
 •of an acute or chronic inflammatory process. Disappearance of 
 the tangential fibers in the cortex, in lesions situated in this area, 
 have also been described. Ordinarily in these forms of encepha- 
 litis, the rest of the brain exhibits no macroscopic changes, and 
 often none can be detected by the microscope. The membranes 
 are smooth, the vessels of normal elasticity, and not surrounded 
 by a round-cell infiltration. Complete resolution may perhaps 
 occur ; of course, this can only be supposed from the clinical 
 isymptoms of the disease, there being no definite experimental or 
 pathologic evidence to support it. 
 
 The focal lesions may undergo softening and lead ultimately to 
 scar-formation ; and if they are extensive, there will be considera- 
 ble atrophy of the affected part of the brain. The great majority 
 of cases, however, in all probability terminate fatally. The nature 
 of the process is generally accepted to be primarily vascular ; the 
 secondary changes being the result of alteration in the nutrition 
 of the surrounding part. 
 
 Suppurative encephalitis has already been in part described in 
 connection with purulent meningitis. In that condition, the pyo- 
 genic emboli appear to enter the brain-substance along the lym- 
 phatics that dip into it from the pia. They are usually small, not 
 circumscribed, and more apt to be found in the gray matter of the 
 •cortex, particularly near the base of the brain and in the struct- 
 ures adjacent to the ventricles, than in the white substance. Oc- 
 
756 TEXT-BOOK OF PATHOLOGY. 
 
 casionally, larger collections, forming rather ill-defined abscesses, 
 are found. 
 
 Abscess of the brain is a condition characterized by the pres- 
 ence in the brain-substance of one or more cavities containing pus. 
 The usual cause is suppurative bone-disease, particularly that re- 
 sulting from otitis media. The condition may, however, occur in 
 general pyemia as a result of metastasis from some neighboring or 
 remote focus of suppuration. Suppuration may also occur in the 
 course of pneumonia, or in chronic suppurative diseases of the 
 lungs, such as fetid bronchitis. Direct infection of the brain, 
 either experimentally or as a result of wounds penetrating the 
 skull, has also been observed. In many of these cases the nature 
 of the transmission is clear ; thus the abscess resulting from dis- 
 ease' of the ethmoidal sinuses or from direct inoculation is usually 
 situated in the immediate neighborhood of the original focus. 
 Abscess secondary to pulmonary disease is usually found at the 
 base of the cerebral hemispheres, and is probably transmitted 
 along the retropharyngeal lymphatics. Abscess due to injury 
 without penetration of the skull has occasionally been recorded. 
 Sometimes it is found in the contused area, sometimes on the 
 opposite side of the brain. The micro-organisms that have been 
 found in the pus are practically all the pyogenic forms. The 
 most frequent are, perhaps, the staphylococcus, the streptococcus, 
 and the pneumococcus. Occasionally the actinomyces, the Bacillus 
 pyocyaneus and the Bacillus tuberculosis have been found, the 
 latter in cases that were apparently acute abscesses of the brain, 
 and not softened solitary tubercles. 
 
 Statistical studies of the literature show that in about two- 
 thirds of all cases the cerebrum is the seat of the lesion. In the 
 remaining third it is chiefly the cerebellum. Unusual seats are 
 the pons, crura, and medulla. This distribution does not, of 
 course, apply to the disseminated forms of purulent encephalitis. 
 Solitary abscesses are usually the result of embolism or extension 
 from the bones. They may be small or of considerable size, and 
 one is on record from which 400 c.c. of pus were removed. They 
 may be either surrounded by softened brain-substance or dis- 
 tinctly encapsulated. The latter condition usually occurs if they 
 have lasted any length of time — that is, three or four weeks ; 
 although cases are on record in which a distinct wall did not 
 develop about an abscess that had existed for several months. 
 The wall, when it exists, varies in thickness from a half to several 
 millimeters. The contents of the cavity are pus and detritus, and 
 in it may frequently be found thrombosed blood-vessels. The 
 surrounding brain-tissue is usually undergoing softening. It may 
 be either white, or, as a result of hemorrhagic extravasation, red 
 in color. The abscesses usually spread more or less gradually ; 
 that is to say, there is probably no tendency to heal spontaneously. 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 757 
 
 If large, they cause considerable intracranial pressure, which is 
 indicated by the flattening of the convolutions or bulging of the 
 brain after the skull has been trephined. Those due to punctured 
 wounds are usually associated with meningitis. Those due to 
 caries must also be associated with inflammatory changes in the 
 meninges, and not unfrequently there is thrombosis of the cerebral 
 sinuses. Microscopically, we find the ordinary characteristics of 
 pus. The wall or periphery is usually undergoing fatty degener- 
 ation, and there is a considerable accumulation of round cells in 
 the surrounding tissue. Multiple abscesses are usually metastatic. 
 A group may be found either in one situation in the brain or they 
 may be very widely distributed. Occasionally the course of the 
 case is so chronic that secondary degeneration may occur. In 
 such a case, examined by Sailer, with abscesses in the cerebellum, 
 cerebrum, and particularly the pons, there was degeneration of 
 both pyramidal tracts. This, of course, is a rare condition. 
 In cases of severe encephalitis, more or less pronounced changes 
 may be observed in the ganglion-cells in other parts of the cen- 
 tral nervous system. 
 
 Primary Acute Hemorrhagic Encephalitis. — Striimpell has de- 
 scribed under this name a form in which the dura was normal but 
 somewhat dry ; the pia injected, the centrum ovale softened, ede- 
 matous, slightly pinkish or gray, and marked by fine hemorrhagic 
 points. Microscopically there were no granular cells, but drops of 
 myelin and some detritus. There was some hyperemia and cel- 
 lular infiltration of the pia. The ganglion-cells of the cortex were 
 normal. In the white matter the vessels were distended with 
 blood and surrounded by a thick mass of round cells ; the peri- 
 vascular spaces were distended ; the neurogliar tissue coarser than 
 normal. In many situations there was bleeding from the capil- 
 laries. 
 
 General Progressive Paralysis. — There has been much 
 diversity of opinion concerning the true nature of general pro- 
 gressive paralysis. The lesions hitherto described have varied in 
 nature and situation. Nevertheless, there seems to be good reason 
 to accept an infectious origin of the disease, and unquestionably 
 the symptomatology and, to a certain extent, the morbid changes 
 indicate that the brain is the organ chiefly involved. The changes 
 found most frequently are as follows : the dura mater is adherent to 
 the skull ; it may be thickened, and often shows upon its under 
 surface the exudate of a hemorrhagic pachymeningitis. The 
 arachnoid is thickened and opaque, particularly along the course 
 of the veins ; and in the subarachnoid space there is often a con- 
 siderable effusion of liquid. The pia mater is thickened and 
 opaque, and may or may not be adherent to the cortex ; in the 
 latter case the subpial areolar tissue is distended with fluid. 
 Microscopically, there is often found a round-cell infiltration about 
 
758 TEXT-BOOK OF PATHOLOGY. 
 
 the blood-vessels ; their walls are thickened and show some 
 hyaline degeneration. The fluid in the areolar spaces mav be 
 clear, or, as is more commonly the case, it is viscid and even colloid 
 in nature. The gross appearance of the brain is frequently con- 
 siderably altered. The convolutions are flattened; the sulci 
 broader than normal ; the consistency of the brain is slightly in- 
 creased ; the cortex is usually pale and greatly reduced in thick- 
 ness. The white matter may appear to be slightly looser in text- 
 ure, but ordinarily presents no change. Microscopically, the 
 blood-vessels in the cortex have thickened walls, and occasionally 
 one is found with a completely obliterated lumen. There is 
 usually distention of the perivascular spaces, which may be filled 
 with round cells and various products of degeneration, such as 
 pigment-granules. The glia-cells are greatly increased in number, 
 although it is difficult to decide whether this is absolute or relative. 
 The neuroglia-fibers are usually slightly coarser than normal. The 
 tangential fibers of the cortex may be reduced in number or 
 entirely absent. The ganglion-cells exhibit a great variety of 
 alterations. The protoplasmic processes are varicose, and when suf- 
 ficiently well impregnated show the absence of the gemmules. 
 The axis-cylinder is usually distinct, due to the degeneration of 
 the myelin-sheath. The body of the cell may be irregular and 
 vacuolated, and there is often extensive chromatolysis. The ventri- 
 cles of the brain are usually slightly distended, probably the result 
 of simple atrophy, and the choroid plexus is often cystic. Changes 
 are frequently found in the spinal cord. The ganglion-cells in all 
 parts show pronounced degenerative characteristics. This is par- 
 ticularly interesting in view of the fact that the motor symptoms 
 progress so gradually. The posterior roots are often slightly 
 degenerated, and there is systemic degeneration of the posterior 
 columns not unlike that found in the early stages of tabes dor- 
 salis, excepting that ordinarily it is most pronounced in the cervi- 
 cal region. The pia and arachnoid of the cord, particularly those 
 portions covering the posterior columns, are thickened and more 
 or less adherent. The dura is often markedly thickened, and may 
 exhibit pachymeningitis. The etiology of progressive general 
 paralysis is not clear. The great majority of cases commence in 
 middle adult life, and have been preceded by an attack of syphilis. 
 Certain cases, however, fail to give any syphilitic history, and pre- 
 sent no signs of the disease. 
 
 Chronic encephalitis may take the form of sclerosis or of 
 scar-formation, which is really but a variety of sclerosis. 
 
 Lobar sclerosis is usually an extensive but sharply circum- 
 scribed process affecting the whole or part of one or more lobes of 
 the brain. The involved area is usually considerably diminished 
 in Bize. The convolutions are smaller, the sulci broader, but, of 
 course, not so deep ; the surface is often finely granular, and the 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 759 
 
 pia is adherent. The consistency is greatly increased, the tissue 
 being almost like cartilage. Microscopically there are the same 
 changes found in the other forms — that is, excessive proliferation 
 of the neuroglia, with partial or complete disappearance of the 
 nervous elements. The cause appears to be some vascular dis- 
 turbance occurring during fetal existence, as the localization nearly 
 always corresponds to the distribution of one of the arteries sup- 
 plying the brain. If the anterior cerebral artery is affected, the 
 frontal lobe is sclerotic. If the artery of the Sylvian fissure is 
 involved, there will be sclerosis of all the hemispheres, with the 
 exception of a part of the occipital lobe ; and if the lesion is situ- 
 ated on the proximal side of the lenticular striate artery, this part 
 will also be degenerated. If the posterior cerebral artery is oc- 
 cluded, the lesion will be found at the tip and in the lower half 
 of the occipital lobe. Extensive secondary degeneration always 
 occurs in this form. 
 
 Multiple sclerosis is a condition characterized by the formation 
 throughout the nervous system of various foci in which the neu- 
 roglia is somewhat hyperplastic, the myelin-sheaths more or less 
 degenerated, and the axis-cylinders, as a rule, slightly, if at all, 
 affected. The sclerotic areas are of very irregular size and dis- 
 tribution, and are much more frequently found in some situa- 
 tions than in others. When they affect the white matter of the 
 brain and cord they appear as grayish or grayish-pink areas, 
 which may even, if at the surface, be observed through the pia. 
 They resemble the gray matter of the cord too closely to be clearly 
 distinguished from it. Their edges are usually sharp. After hard- 
 ening in Miiller's fluid they appear of a bright-yellow color and 
 are exceedingly distinct. The smallest may be only a millimeter 
 in diameter, and the largest may occupy the whole transverse sec- 
 tion of the spinal cord or even entire convolutions of the brain. 
 Occasionally sclerotic areas may be found in the nerve-roots. The 
 most important change that is found upon microscopic examina- 
 tion is a thickening of the walls of the blood-vessels. This re- 
 sembles hyaline degeneration, and may be so extreme that the 
 lumen is almost obliterated. The perivascular lymphatic space 
 is often filled with cells containing droplets that stain black with 
 osmic acid. Occasionally the vessels appear to be increased in 
 number, although this is possibly due to contraction of the sur- 
 rounding tissue bringing them more closely together. Immedi- 
 ately around the diseased vessels the neuroglia is proliferated. 
 In the center of the foci the neuroglia-cells are not markedly 
 increased ; in the periphery, however, they seem to have under- 
 gone a distinct hyperplasia. The neuroglia-fibers throughout are 
 somewhat thicker and more irregular, and form a large-meshed net- 
 work. In the midst of the neuroglia compound granular cells 
 and amyloid bodies are often found. If stained by Weigert's 
 
760 TEXT-BOOK OF PATHOLOGY. 
 
 method, it is at once evident that the myelin-sheaths have disap- 
 peared almost entirely, all the sclerotic areas appearing bright 
 yellow. If the Marchi method be used, however, a certain 
 number of degenerated myelin-sheaths will be found, as a rule, 
 still present, The edge of the sclerotic area does not end as 
 sharply as appears macroscopically, but gradually fades into the 
 healthy tissue. The axis-cylinders, in spite of the destruction of 
 the myelin-sheaths, are nearly always present, and apparently 
 normal, a fact which explains the absence of secondary degenera- 
 tion beyond the lesions. In those situations where the hyperplasia 
 of the neuroglia-fibers is most pronounced, the axis-cylinders may 
 be swollen or show partial fatty degeneration, or be entirely ab- 
 sent, Popoff believes that these persistent axis-cylinders are not 
 those that originally pass through the lesion, but are regenerated 
 nerve-fibers ; a view, however, for which there is not sufficient 
 proof. The ganglion-cells are shrunken and pigmented, and may, 
 in rare cases, completely disappear. In advanced cases of the dis- 
 ease, the process resembles more closely a chronic myelitis ; the 
 axis-cylinders passing through the lesion may be totally destroyed 
 and secondary degeneration occur. In those cases that have been 
 studied in the early stages of the process perivascular inflamma- 
 tory changes have been present, and it is about these that the scle- 
 rotic areas have formed. In some cases thrombi have been also 
 detected in the vessels, and many of them showed the early stages 
 of hyaline degeneration. For this reason, and because dissemi- 
 nated sclerosis frequently develops after an infectious disease, it is 
 generally accepted that the process is due to infectious embolism, 
 a view particularly supported by Marie. Certain authors, how- 
 ever, particularly Taylor, hold that the vessels are not the primary 
 origin of the disease, as in many of the sclerotic foci they are 
 perfectly healthy. 
 
 INJURIES TO THE CENTRAL NERVOUS SYSTEM. 
 
 Injuries to the central nervous system produce a great 
 variety of lesions, according to their nature and severity. 
 
 Concussion, either from a single shock or from repeated blows, 
 may give rise to transient or permanent changes. In the latter 
 case autopsies have shown the existence sometimes of multiple 
 hemorrhages, sometimes of disseminated areas of sclerosis in the 
 white and the gray substances. Occasionally in the spinal cord, after 
 experimental repeated concussions, changes, somewhat systemic in 
 character and affecting chiefly the posterior columns, have been 
 observed. The hemorrhages may be punctate or, in some cases, 
 particularly if the injury is severe and the arteries diseased, mas- 
 sive. 
 
 Lacerated wounds of the brain are usually produced by fraet- 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 761 
 
 ure of the skull. There is extensive interstitial hemorrhage 
 and softening, and the surrounding tissue is edematous. If only 
 subdural hemorrhage occurs, it may produce compression with 
 secondary yellow softening. Any of these lesions may heal with 
 the formation of a scar and the production of more or less exten- 
 sive secondary degeneration. Extensive lacerations of the brain 
 are sometimes the result of injury during birth, giving rise to so- 
 called cerebral palsies of childhood. In these cases, as the central 
 nervous system is not fully developed when the injury occurs, there 
 is hypoplasia of the aifected parts. 
 
 Punctate wounds of the brain are due to fragments of bone, to 
 sharp instruments, or to bullets. In nearly all cases a certain 
 amount of infection occurs, giving rise to encephalitis. The in- 
 jured area usually undergoes complete necrosis, and this extends 
 for some distance into the surrounding tissues. The necrotic area 
 is composed of a granular detritus, in the midst of which are 
 found altered blood-pigment and broken-down nuclei. At the 
 periphery there is usually some granulation-tissue, proliferation 
 of the neuroglia, and more or less round-cell infiltration, accord- 
 ing to the intensity of the inflammatory process. Experimental 
 lesions may be produced in various ways ; the most interesting 
 results, perhaps, being those found after the introduction of for- 
 eign bodies, or after careful aseptic laceration. In either case, 
 shortly after the operation, necrotic changes will be found in the 
 enlarged area. There is marked proliferation of the neuroglia- 
 cells, even as early as the third day, and of the neuroglia-fibers. 
 New capillaries may be seen pushing into the area, the endothelial 
 cells of their walls exhibiting karyokinetic figures. The nervous 
 tissue in the immediate neighborhood is in various stages of de- 
 generation. The myelin-sheaths form balls of fat ; the ganglion- 
 cells become swollen, vacuolated, and lose their protoplasmic proc- 
 esses. If there has been much hemorrhage, the blood-pigment 
 will be found in irregular homogeneous masses or in the form of 
 hematoidin-crystals. Later, evidences of regeneration in the nerv- 
 ous tissue may be observed, particularly the appearance of karyo- 
 kinetic figures in the nuclei of the ganglion-cells. The enlarged 
 area is ultimately replaced by a mass of coarse neuroglia-fibers 
 containing, usually, fewer cells than normal. That true regen- 
 eration of the central nervous system ever occurs in the human 
 body is exceedingly doubtful ; indeed, it is not certain that it occurs 
 in any of the vertebrates, although after removal of the tail in liz- 
 ards a spongy mass of neuroglia may be found in the new organ. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis occurs in the brain in the form of miliary tu- 
 bercles or as large masses, the so-called solitary tubercle, or tyroma. 
 
762 TEXT-BOOK OF PATHOLOGY. 
 
 Miliary tubercles are met with in association with tuberculous 
 meningitis. They are most frequent at the base of the brain. 
 
 Solitary tubercles occur independently of tuberculosis of the 
 meninges. They are more frequent in children than in adults, 
 and usually occur in cases in which there is tuberculosis of other 
 parts of the body, notably the lymphatic glands. The infection 
 reaches the brain through the blood-vessels. The lesions are 
 rounded masses of grayish or yellowish color, sometimes showing 1 
 fresh gray tubercles at the periphery. The growth of the mass is 
 caused by increase in size of the original tubercles and by con- 
 glomeration of new-formed tubercles at the periphery. Early 
 caseation is usual. Secondary infection of the pia sometimes occurs. 
 
 Syphilis appears in the brain in the form of gummata or as a 
 diffuse vascular disease with secondary degenerative conditions. 
 
 Gummata usually begin in the subarachnoid space, originating 
 in the membranes and involving the brain-substance secondarily. 
 The dura may be simultaneously involved, and the three mem- 
 branes may be adherent to each other and firmly attached to the 
 brain. Primary gumma of the brain-substance is certainly very 
 rare. In the earlier stages the gumma is a grayish and rather 
 translucent growth, but secondary caseation occurs so rapidly that 
 the primary stage is rarely observed. As a rule, the lesion appears 
 in the form of an irregular, dry, caseous area occupying the cortical 
 portion of the brain and attached to the pia and arachnoid, and 
 even the dura. Microscopically the substance of the growth con- 
 sists of round and spindle or stellate cells in the earlier stages, 
 and of granular material in the later stages. The cerebral sub- 
 stance surrounding the growth is more or less softened and degen- 
 erated. The blood-vessels in the affected area or its vicinity are 
 the seat of endarteritis, which in some cases causes complete occlu- 
 sion of the lumen. In hereditary syphilis symmetric gummata of 
 the brain are occasionally found. 
 
 Syphilitic disease of the blood-vessels of the brain takes the 
 form of more or less diffuse endarteritis. Secondary degenerations 
 and softening, or sclerosis, of a diffuse or focal character, may re- 
 sult from the vascular disease ; but neither these changes nor the 
 vascular changes are peculiar and distinctive. 
 
 Actinomycosis of the brain is generally secondary to actino- 
 mycosis of the tissues of the neck, and results from extension up- 
 ward through the base of the skull. The membranes are first in- 
 volved ; the brain-substance secondarily. The lesion may take 
 the form of a chronic abscess or may be tumor-like in appearance. 
 
 TUMORS. 
 
 Tumors of the brain are important clinically on account 
 of their situation rather than on account of their nature. The 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 763 
 
 most common is probably glioma, but almost equally as com- 
 mon is sarcoma. Carcinoma, excepting the form springing from 
 the lateral ventricles, is almost never a primary growth, but 
 secondary nodules are frequently found in the brain. Cho- 
 lesteatoma, lipoma, endothelioma, and teratoid cysts also oc- 
 cur, but they spring from the membranes, and have been de- 
 scribed in connection with them. Gumma and tyroma also 
 occur very frequently in the brain, but as their etiology is in- 
 fectious they are described in connection with the infectious 
 conditions. 
 
 Glioma usually appears as an infiltrating mass, causing little 
 alteration in the structure of the brain, somewhat harder in con- 
 sistency than the brain-substance, and slightly darker. It is 
 rarely a multiple growth, and shows no marked predilection for 
 any particular portion of the brain, although it occurs more fre- 
 quently in the cerebral hemispheres than in the basal ganglia or 
 the cerebellum. It always springs from the neurogliar tissue of 
 the central nervous system, and is remarkable for its extreme 
 richness in cells, that by suitable staining-methods may be shown 
 to possess protoplasmic processes {astrocytes). These protoplasmic 
 processes, either wholly or in part, form the so-called matrix of 
 the tumor, which appears to be composed of numerous fine, inter- 
 lacing fibers, in the midst of which, by the ordinary staining-methods, 
 the cell appears to lie. Usually the tumor is exceedingly vascular, 
 the vessels consisting of small capillaries or larger spaces lined 
 with endothelium, and this vascularization may be so excessive 
 that the tumor in parts has a delicate pinkish or reddish color, giv- 
 ing to the cross-section a mottled appearance. Stroebe considers 
 as one of the characteristics of this tumor the fact that it does not 
 infiltrate the pia mater, and can invariably be shown not to spring 
 from it. In some cases the consistency of the tumor is quite hard, 
 and in these the cellular elements are increased in amount propor- 
 tionately to the fibrous tissue. Ordinarily true nervous tissue is 
 absent from the midst of the tumor, the mass in the center being 
 made up of the neuroglia-tissue. This gradually diminishes to- 
 ward the periphery, and ultimately fades into the true nervous 
 tissue, that may be somewhat edematous. In some cases, however, 
 as in ordinary sclerosis of the central nervous system, myelinated 
 nerve-fibers may be found in the midst of the tumor, and it fre- 
 quently happens that the secondary degeneration extending from a 
 glioma is much slighter than the apparent extent of the process 
 would lead one to expect. Occasionally, either glioma-cells, or 
 possibly ganglion-cells, that have undergone proliferative changes 
 in the midst of the growth, may be found. These are much larger 
 than the ordinary cells and contain numerous branched processes, 
 and often one or several large nuclei. This is the so-called gan- 
 glionar neuroglioma. 
 
764 TEXT-BOOK OF PATHOLOGY. 
 
 Some pathologists hold that the starting-point of glioma is always one 
 or more ependymal cells that have been displaced in embryonal existence 
 and have failed to assume the type of glia-cells, basing their theory in part 
 upon the atypical shape of many of the glioma-cells. 
 
 Sarcoma of the brain is probably the next most frequent 
 tumor. It usually occurs in middle adult life, although it is quite 
 frequent in children. The commonest seat is the cortex, which it 
 probably invades from a primary focus of proliferation in the 
 membranes. The tumors are ordinarily nodular growths, usually 
 distinctly circumscribed from the surrounding tissue, and in some 
 cases even surrounded by a fibrous capsule, from which they can 
 be readily removed. They are rather firmer than the brain-tissue, 
 and sometimes slightly umbilicated if at the surface. The surface 
 of section is pale and dry, but frequently mottled on account of the 
 presence of hemorrhages. If primary, the sarcomata are single ; if 
 secondary, more frequently multiple, and in these cases they are 
 very apt to be found upon the convex surface of the hemispheres, 
 forming, if large, irregular flattened masses. Histologically, almost 
 any type of sarcoma may be found, the most frequent, perhaps, 
 being the round-cell, non-pigmented form. Giant-cells are very 
 frequently found. In the midst of true sarcoma, proliferated 
 fibrous tissue is not found, but many of the tumors are traversed 
 by fibrous trabecular, and some of them contain considerable 
 masses of fibrous tissue, giving rise to the so-called fibrosarcoma. 
 Ordinarily the tumors are extremely vascular, and occasionally 
 contain interstitial hemorrhages. The surrounding brain-tissue 
 shows the symptoms of marked compression, is edematous, and 
 mav contain small interstitial hemorrhages. The true nervous 
 substance is ordinarily degenerated, and we find extensive second- 
 ary degeneration as a result of the presence of the tumor. Sar- 
 coma springs primarily from the brain, and nearly always grows 
 toward the surface and infiltrates the pia mater. 
 
 Certain forms of tumors have been described, probably sar- 
 comatous in nature, that appear to spring from the adventitia of 
 the blood-vessels. They consist of masses of cells usually sharply 
 circumscribed, somewhat cylindrical in shape, having in their 
 center a small lumen in which blood-cells may sometimes be 
 detected. The cases reported of this form of tumor, the so-called 
 perithelioma, are very few and somewhat uncertain. 
 
 Many authors believe that a combination of glioma and sarcoma may 
 occur, and gliosarcomata have been frequently described. As the neuroglia- 
 tissue has the functions of connective tissue, and in many respects resembles 
 it in its pathologic processes, it is natural that a glioma should be similar 
 to a sarcoma, and this has possibly caused an error of diagnosis in some 
 cases. As the two tumors arise from tissue of different natures, and develop 
 in different situations, their combination is theoretically unlikely. 
 
 Fibroma occurs as a hard, circumscribed tumor, sometimes 
 found in the hemispheres, but it is extremely rare. 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 765 
 
 lymphangioma appears to arise from the pia. 
 
 Osteoma is usually an extension inward from the skull or 
 membranes, but occasionally occurs as a tumor, apparently origi- 
 nating in the brain-substance, forming hard masses from the size 
 of a pea to that of a cherry, and somewhat irregular in shape. 
 
 Psammoma. — This special term has been given to tumors 
 containing calcareous granules. It has already been mentioned in 
 connection with the choroid plexus and the membranes. Occa- 
 sionally circumscribed fibrous tumors containing calcareous gran- 
 
 
 
 Fig. 352.— Psaninioina, showing calcareous spicules and whorls. 
 
 ules are found in the brain-substance, but these are extremely 
 rare (Fig. 352). 
 
 Carcinoma of the substance of the brain is invariably a 
 metastatic growth. It appears either as small, round, circum- 
 scribed nodules, of firm consistency and pale color; or as larger, 
 more or less infiltrating masses with softened interior. Histologi- 
 cally, the tumor may present any type of carcinoma, according to 
 the nature of the primary growth. It usually replaces entirely 
 the nervous tissue, either pushing it aside or destroying it, and 
 gives rise, therefore, to more or less pronounced secondary degen- 
 eration. Multiple metastatic carcinomatous growths, however, 
 may exist in the brain without causing clinical symptoms. 
 
 THE CHOROID PLEXUS. 
 
 The choroid plexus, as has been stated, consists of a plexus 
 of vessels derived from the mesoblast, that are everywhere cov- 
 
766 TEXT-BOOK OF PATHOLOGY. 
 
 ered by a layer of cuboidal or columnar epithelium. Histologi- 
 cally, therefore, it consists of an inner layer of endothelial cells 
 and an outer layer of epithelial cells, separated by a small amount 
 of areolar fibrous tissue. This condition is most distinct and 
 typical in the lower vertebrates, particularly in amphibians, in 
 which the choroid plexus consists, in some parts, of a single 
 vessel covered by epithelial cells. The structure of the choroid 
 plexus, therefore, bears a very close resemblance to the structure 
 of the glomeruli of the kidneys, and, as it is obvious that the 
 blood-vessels of which it is composed can have no nutritive func- 
 tion, excepting in so far as they supply the epithelium that covers 
 them, it has been supposed that the choroid plexus is a secretory 
 organ, its object being to secrete the cerebrospinal fluid. This 
 theory is sustained by the fact that the cerebrospinal fluid differs 
 in composition from the lymph, or from the fluid poured out in 
 serous exudations. It would naturally be supposed, therefore, 
 that in all conditions in which the alterations in the composition 
 of the cerebrospinal fluid have been detected, there is primarily 
 some disease of the plexus. 
 
 Inflammation. — In inflammatory conditions, particularly men- 
 ingitis, encephalomyelitis, and ependymitis, either separate or com- 
 bined, and associated with the presence of an abnormal quantity 
 of albumin in the cerebrospinal fluid, more or less inflammation 
 of the choroid plexus is usually found. This is indicated particu- 
 larly by round-cell infiltration about the vessels and beneath the 
 epithelium. Sometimes there is a slight amount of exudation 
 upon the epithelial surface, and occasionally small foci of suppura- 
 tion can be detected. 
 
 Infectious Diseases. — Among the infectious diseases the only 
 one of importance is tuberculosis. In this condition miliary 
 tubercles or large cheesy foci may be found. 
 
 Chronic inflammation appears to be exceedingly rare, or, what is 
 probably more accurate, has rarely been described, for there is 
 every reason to believe that the choroid plexus shares in all con- 
 ditions that involve the pia mater. Atheromatous conditions seem 
 to be very infrequent, but a certain amount of thickening of the 
 walls of the vessels may be observed in old age. A certain 
 amount of overgroAvth of connective tissue, sometimes associated 
 with slight round-cell infiltration, is also occasionally found in old 
 people. 
 
 Hemorrhage may take place into the choroid plexus, and is 
 usually an agonal phenomenon. 
 
 Degenerations. — Calcification is the most frequent of the infil- 
 trations. This may be recognized by the gritty sensation upon 
 cutting into the choroid plexus. Microscopically, the calcareous 
 nodules appear as minute dark granules that stain purplish with 
 hematoxylin. Masses of cholesterin are by no means uncommon ; 
 

 DISEASES OF THE BRAIN AND ITS MEMBRANES. 767 
 
 they rarely present the form of typical cholesterin-plates, but are 
 somewhat irregular in outline, of a faint yellowish color, and shine 
 brightly when examined by oblique light. Both conditions are 
 common in old people. 
 
 Pigmentary infiltration probably also occurs, certainly in mala- 
 ria, and perhaps in old age. 
 
 Amyloid degeneration occurs in cases of amyloid disease. 
 
 Tumors. — A great variety of tumors occur in the plexus. 
 Cysts may be either retention- or extravasation-cysts, or parasitic. 
 The retention-cysts may be lined with epithelium, and probably 
 represent adhesions at the edges of fissures with persistence of 
 secretory activity. More commonly they are lined with endothe- 
 lium and represent dilated lymph-spaces. They may be single or 
 multiple, and often are more numerous upon one side of the brain 
 than on the other. They appear as small translucent sacs, filled 
 with a clear, slightly yellowish liquid, or else a colloid-like, viscid 
 mass. Parasitic cysts are usually due to Taenia solium. They 
 may be either single, the Cysticercus cellulosse, which may be 
 attached to the plexus or lie free in the ventricular cavity, or 
 multiple, forming the so-called Cysticercus racemosa of the brain. 
 
 Among the benign tumors, fibromata, possibly but organized 
 thrombi, and lipomata have been described. The latter is ex- 
 ceedingly rare, and is usually associated with multiple lipomata in 
 other parts of the brain. A dermoid cyst has been reported by 
 Lebert. Endotheliomata may spring from the lymphatic space. 
 They are small, white, infiltrating growths, of firm consistency. 
 They possess, microscopically, the ordinary alveolar structure, the 
 cavities being lined by endothelial cells, which have proliferated 
 and may lie loose in or fill up the lumen. Epitheliomata may arise 
 from the epithelial covering. Two varieties have been described : 
 the papillomatous epithelioma is a small, often microscopic, tumor 
 that appears as a villous outgrowth upon the surface of the plexus, 
 and is composed of flat or polygonal epithelial cells, with dis- 
 tinct evidence of proliferation that may, in the lower layers, cause 
 a breaking through of the basement-membrane. These tumors, 
 however, are apparently non-malignant. The so-called cylindrical 
 carcinomata also occur. These grow very rapidly and usually 
 become attached to the wall of the ventricle, and from this situa- 
 tion invade the substance of the brain. They are alveolar in 
 structure and soft in consistency. There is some doubt as to 
 whether these tumors do not arise from the ependyma, and it has 
 also been suggested that they are sarcomatous in nature and spring 
 from the adventitia of the blood-vessels. They are usually single 
 growths and do not give metastases. The choroid plexus, as a 
 whole, may be altered, by the presence of cysts, into a mulberry- 
 like mass, or by a general fibrous change, into a pale, solid body 
 of cylindrical shape with a finely granular surface. 
 
768 TEXT-BOOK OF PATHOLOGY. 
 
 THE VENTRICLES. 
 
 The cerebrospinal fluid is a clear liquid with a specific 
 gravity of about 1008, a slightly alkaline reaction, and a faint salty 
 taste. The fluid obtained from a calf was carefully studied by 
 Nawratzki, and it was found to contain 1.093 per cent, of solid 
 material, of which about 0.8 per cent, was organic. The average 
 quantity of albumin was 0.02 per cent., just sufficient to cause a 
 slight opalescence upon boiling. The same author has also ex- 
 amined the cerebrospinal fluid in human beings, and finds that it 
 is very similar in composition, with the exception of the greater 
 proportion of albumin, which at times reaches 0.177 per cent. 
 Fresh cerebrospinal fluid from either man or the lower animals 
 contains a small proportion of grape-sugar, equivalent to between 
 0.17 and 0.27 per cent. According to Halliburton and Hammer- 
 sten^the reducing substance is not sugar, but brenzcatechin. This 
 reducing substance invariably disappears within a few hours after 
 death. 
 
 Pathologically the fluid may show the following changes. The 
 color may become yellowish from the admixture of blood, or turbid 
 from the admixture of pus. Micro-organisms are frequently found 
 in it in all forms of meningitis, but particularly in epidemic cerebro- 
 spinal meningitis. It must not be forgotten, however, that in the 
 late stages of this and in the early stages of meningitis due to the 
 tubercle-bacillus, the fluid may be clear. Nawratzki observed a 
 considerable increase in the amount of albumin as the only change 
 in a case of hemorrhagic pachymeningitis. Microscopic exam- 
 ination, even in normal cerebrospinal fluid, usually shows the 
 existence of some blood-discs and leukocytes. In pathologic 
 changes a greater or less number of pus-cells may be present, 
 and often there is a considerable amount of fibrin. 
 
 Hydrocephalus. — Excess in quantity of the cerebrospinal 
 fluid in the ventricles is known as hydrocephalus. This may be 
 produced by a great variety of causes. It may be congenital, and 
 perhaps due to a malformation, but is more often a result of dis- 
 ease. Congenital hydrocephalus frequently appears to be due to 
 some defect on the part of the parent, and is particularly common 
 in the children of drunkards. 
 
 Congenital hydrocephalus internus is characterized by a gradual 
 accumulation of cerebrospinal fluid in the lateral and third ven- 
 tricles of the brain, probably the result of excessive secretion 
 from the choroid plexus (Fig. 353). As a general rule, the fourth 
 ventricle is not involved. The aqueduct of Sylvius, however, 
 is often dilated. Sometimes the fifth ventricle is distended, or 
 the septum has atrophied and disappeared, allowing free commu- 
 nication between the two lateral ventricles. Less frequently, the 
 infundibulum is distended and forms a small sac at the base of 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 769 
 
 the brain. Usually the disease is manifest at the time of birth, 
 and the head may even at this period have attained the circum- 
 ference of more than 50 cm. Externally, the head is spherical 
 and large ; the face is small, and, with the bulging forehead, gives 
 to these patients a characteristic expression. The cranial bones 
 
 are usually more or less separated ; fre- 
 
 quently the edges of the sutures are an 
 inch or more apart. The anterior fon- 
 tanelle is large and usually bulging. If 
 the bones of such a skull be examined, 
 it will usually be found that they are 
 very thin, and that ossification is in- 
 complete. The dura mater is tense, 
 and beneath it may be found the 
 greatly flattened convolutions. The 
 brain-substance seems softer; often 
 there is distinct fluctuation, although 
 the brain collapses as soon as it is re- 
 moved from the cranial cavity. The 
 distance from the wall of the ventricle 
 to the surface is much less than nor- 
 mal, this atrophy seeming to affect the 
 white substance more than in the cor- 
 tex. The total weight of the brain, 
 however, is often normal or nearly so, 
 and it is impossible to say that an act- 
 ual atrophy has really taken place. 
 The substance of the brain is pale, 
 probably as a result of the pressure, 
 and often softened, particularly in the 
 neighborhood of the ventricles, al- 
 though this is probably only an unusually rapid post-mortem 
 change. The floor of the ventricles may be smooth or slightly 
 roughened, and occasionally distinct nodules may be observed. 
 In the latter case there is usually considerable proliferation of 
 the neuroglia in the cortex, and just beneath the floor of the 
 ventricle a sort of sclerosis of the brain-substance. The cere- 
 brospinal fluid is usually clear, and not abnormal in consistency. 
 Occasionally, however, it is somewhat turbid, particularly if 
 there are any signs of old inflammatory action. The choroid 
 plexus is often somewhat enlarged, pale, and may contain cysts. 
 As the patients increase in age there is usually considerable 
 increase in size of the head ; nevertheless, the convolutions grad- 
 ually become more rounded, and the white substance appears to 
 undergo a sort of redevelopment, for the layer of brain-tissue be- 
 tween the ventricle and the surface becomes thicker. Systemic 
 degenerations of the white fibers are uncommon. There may, 
 
 Fig. 353.— Congenital internal 
 hydrocephalus, with marked 
 atrophy of the white substance 
 (from Bollinger). 
 
770 TEXT-HOOK OF PATHOLOGY. 
 
 however, be marked thinning of the corpus callosum and the ante- 
 rior commissure. Cases have been described in which a descending 
 degeneration along the pyramidal columns was found in the cord. 
 
 Partial hydrocephalus has been described. It is probably, in 
 the great majority of cases, of congenital origin. It may affect 
 only one ventricle, or even only a part of a ventricle, as, for ex- 
 ample, the anterior or posterior horn of one of the lateral ventri- 
 cles. It appears to be the result of an obliteration of one of the 
 normal passages by which the ventricles communicate with one 
 another. 
 
 External hydrocephalus is the accumulation of fluid that oc- 
 curs in the subarachnoid space to replace brain-tissue that has un- 
 dergone atrophy, or to till the cavity of porencephaly. Occasionally 
 symmetrical collections of liquid are found, as in a brain reported 
 by Sailer that was removed from an idiot, in which both temporo- 
 sphenoidal lobes were excavated and replaced by large cysts. 
 
 Acquired hydrocephalus may be either acute or chronic. The 
 acute forms are usually secondary to inflammatory changes in the 
 meninges, extending to the choroid plexus and to the ependyma, 
 or are caused by some abnormal growth pressing upon the veins 
 of Galen. In the atrophic brains of the aged dilated ventricles 
 are frequently found. 
 
 Acute acquired internal hydrocephalus is usually the result 
 of acute basilar meningitis, either inflammatory or tuberculous. 
 The brain, in addition to the meningitic changes, presents all the 
 characteristics of intense intracranial pressure. The convolutions 
 are flattened and pale. The brain-tissue is usually soft, or at least 
 softens rapidly after death, particularly the part that surrounds 
 the distended ventricles. Upon opening the brain the fluid is 
 usually found under considerable pressure, and often almost gelat- 
 inous inconsistency. Frequently, microscopic examination of the 
 brain-substance will show the presence of acute, disseminated, 
 suppurative encephalitis. The ependyma of the ventricles is 
 injected and often covered with lymph. In the tubercular form 
 it may be roughened, as a result of the presence of numerous 
 miliary tubercles. The choroid plexus is injected. In the acute 
 forms it also has some lymph upon the surface, and in the tuber- 
 cular form may contain miliary tubercles. 
 
 Chronic hydrocephalus is usually a late result of meningitis, 
 particularly the epidemic form. Occasionally it is the result of 
 gradual compression of the veins of Galen, as, for example, by a 
 tumor of the cerebellum. Perhaps most frequently it is the result 
 of a chronic granular ependymitis. In these cases the distention 
 is more pronounced than in the acute form. The ependyma is 
 thickened and opaque, and often contains small hard nodules. 
 Occasionally bands of organized fibers may be found in the cavity 
 of the ventricle. 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 771 
 
 Upendymitis may be chronic or acute. The acute form is 
 always secondary to meningitis, and is characterized by prolif- 
 eration of the ependymal cells and the usual inflammatory changes. 
 
 Fig. 354.— Sclerotic nodule in the floor of the lateral ventricle, with wrinkling of the 
 ependyma ; X 100 (Sailer). 
 
 Chronic ependymitis is usually associated with sclerosis of the 
 brain. The surface is granular or even nodular. The ependyma 
 
 Fig. 355,— Sclerosis of the brain ; X 300. 
 
 is thrown into folds, and there is great proliferation of the sub- 
 ependymal neurogliar fibers (Figs. 354, 355). 
 
 THE PITUITARY BODY, OR HYPOPHYSIS CEREBRI. 
 
 The hypophysis is a small glandular organ, situated at the base 
 of the brain, lying upon the upper surface of the body of the 
 
772 TEXT-BOOK OF PATHOLOGY. 
 
 sphenoid bone, and further protected posteriorly by a wall, form- 
 ing a cavity which is known as the sella turcica. It varies slightly 
 in size, the average weight in the adult being from 0.59 gm. 
 (Schonemann) to 0.48 gm. (Comte). It reaches its maximum 
 between twenty-one and forty years of age. 
 
 The hypophysis is a double organ, developed from the central nervous 
 System and from the alimentary canal. The nervous part originates from 
 the middle primary cerebral vesicle as an evagination from the cavity. 
 This forms the infundibulum and the small posterior lobe. The larger 
 anterior lobe appears to arise from two sources, one, the primitive oral 
 tissue in early embryonal life, and the other the anterior portion of the 
 alimentary canal ; both portions become contracted at their origins, fuse, 
 and are ultimately separated from the alimentary canal, although this 
 separation is not complete in some of the lower vertebrata. Histologi- 
 cally, the organ may be divided into three parts : the anterior portion of 
 the anterior lobe is composed of somewhat polygonal epithelium-cells en- 
 closed in alveoli, whose walls are made up of fibrous connective tissue. These 
 groups of cells are very irregular, although sometimes they are arranged 
 about the periphery of the cavity, leaving in the center a small lumen, 
 which, more frequently than not, is filled with an oxyphilic homogeneous 
 mass that is supposed to be colloid. The amount of connective tissue is 
 usually relatively small, and it contains a considerable proportion of cells 
 as compared with connective tissues of other parts of the body, and is ex- 
 ceedingly vascular. The cells are of two kinds, the chromophilic and the 
 chromophobic. The former are further divided by Comte into the eosino- 
 philic, in which the protoplasm stains deeply and homogeneously with 
 eosin, and usually contains vacuoles ; and the cyanophilic cells, in which 
 the protoplasm colors dark blue with hematoxylin, and rarely contains 
 vacuoles. The protoplasm of the chromophobic cells does not stain. Some 
 authors consider that these distinctions are not morphologic, but only indi- 
 cate that the different cells are in different stages of secretory activity. 
 The posterior part of the anterior lobe usually contains, in man, a small 
 bilobed cavity lined with cylindrical ciliated epithelium. In addition, 
 there are also a few larger cavities lined by columnar or polygonal epi- 
 thelium, and usually filled with colloid material. The posterior or nervous 
 lobe consists of neuroglia-tissue, and, according to Berkeley, a few ganglion- 
 cells containing an excess of pigment, and some varicose fibers may be 
 found in it. Kolliker, however, denies that there is any nervous tissue at 
 all in the posterior lobe, and has been able to find nothing but neuroglia. 
 
 From its analogy in structure to the thyroid gland, it has been 
 supposed that the function of the pituitary body is to abstract 
 some material from the blood, to alter it, and then to return it to 
 the circulation — that is to say, it is one of the internal secretory 
 glands. Pronounced changes following its removal or destruction 
 cannot, however, be said to have been definitely established. If 
 we can believe the assertions of those who have systematically 
 examined large numbers of these bodies, a normal gland is the 
 exception ; thus, Schonemann found only 27 normal specimens in 
 110 cases, and Comte 33 in 108. 
 
 Hypertrophy of the hypophysis occurs in cretinism, myx- 
 edema, and acromegaly. In some of these cases the hypertrophy 
 is due to tumor-formation ; in others, particularly in those occur- 
 
DISEASES OF THE BRAIN AND ITS MEMBRANES. 773 
 
 ring as a result of removal of the thyroid gland, it appears to be 
 compensatory, or rather, as the functions of this gland and the 
 thyroid cannot be exactly identical, at least vicarious. This en- 
 largement, often apart from tumor-formation, may be very con- 
 siderable. De Conlon records a case in which the hypophysis 
 weighed 1.55 gm., and, aside from an apparent proliferation of 
 the epithelium-cells, was normal in structure. 
 
 Circulatory Disturbances. — The gland, as has been men- 
 tioned, is excessively vascular. It is possible that in some cases 
 this vascularity may increase and give rise to a true hyperemia, 
 although it is difficult to be certain of this. Changes such as 
 are found in the thyroid gland in exophthalmic goiter have 
 certainly not been described. In case of passive congestion re- 
 sulting from thrombosis of the cavernous sinuses intense edema 
 may be present. Hemorrhage in the gland is a frequent agonal 
 phenomenon. In these cases the blood-cells, usually normal in 
 appearance, are found infiltrating the connective-tissue stroma. 
 Hemorrhages during life may occasionally occur, and give rise 
 to small, deeply pigmented areas of softening, which ultimately 
 form scars. 
 
 Inflammation is usually secondary and suppurative. Sailer 
 has observed a case in which the anterior lobe was infected from 
 the parotid gland, probably as a result of ascending infection 
 along the retropharyngeal lymphatics. In this case the capsule 
 enclosing the gland was inflamed, and there were small collections 
 of round cells in the substance. 
 
 Degenerations. — Infiltrations with either calcareous mate- 
 rial or pigment have not been hitherto described. The degenera- 
 tions, however, are numerous. The most important and frequent 
 is colloid degeneration, the colloid material being found in the 
 cavities of the epithelial nests, or even as small masses in the con- 
 nective-tissue septa. This may be looked upon as almost physi- 
 ologic. It seems to be increased in those conditions in which we 
 have reason to suspect increased functional activity of the glands ; 
 but also is more pronounced in cases of partial atrophy. Amyloid 
 degeneration occurring in the blood-vessels has been observed in 
 cases of general amyloid disease. The walls of the blood-vessels 
 frequently undergo hyaline degeneration in old age. 
 
 A sort of cheesy or liquefactive necrosis is also observed in the 
 center of adenomatous formations, and is probably due to pressure- 
 necrosis, as a result of the limited space in which the hypophysis 
 is placed. 
 
 Infectious Diseases. — Of the infectious inflammations, the 
 only ones of importance are tuberculosis, in the form of miliary 
 tubercles, and syphilis, in the form of gummatous nodules. Occa- 
 sionally a large single gumma has been observed. 
 
 Tumors are perhaps the most interesting and important 
 
774 TEXT-BOOK OF PATHOLOGY. 
 
 changes that occur, and there is still considerable difference of 
 opinion regarding their nature. 
 
 Cysts are very common, particularly a form of cystic degenera- 
 tion with distention of the follicles by colloid substance. These 
 are almost normal in old age, the only interesting feature being the 
 atrophy and disappearance of the epithelial cells. Teratoid cysts 
 have been described, but are much less frequent than would be 
 expected from the complicated embryology of the gland. Of this 
 nature is the myoneuroma described by White. 
 
 Of the malignant tumors, the only one hitherto described is 
 the sarcoma. This is usually round-cell or spindle-cell in type, 
 and apparently springs from the capsule of the gland and replaces 
 its substance, but rarely infiltrates the surrounding tissues or gives 
 rise to metastasis. Cases have been reported as lymjthosarcoma in 
 which there were numerous collections of round cells in the alveoli 
 of the connective tissue and some hypertrophy of the latter ; appar- 
 ently, however, no other lymphatic organs were involved. 
 
 Adenoma of the hypophysis causes increase in the size ; the 
 organ remains soft or may be slightly indurated, and is of normal 
 color. The resistance of the bony structures that surround it may 
 cause the gland to assume extraordinary shapes. Microscopically 
 there is proliferation of the epithelium-cells, which form long tor- 
 tuous and sometimes branched tubes, and often complete atrophy 
 of the nervous lobe. These tumors have been described particu- 
 larly in connection with the disease known as acromegaly. 
 
 Pathologic Physiology. — The relation of disease of the 
 hypophysis to acromegaly is a much disputed question. In all 
 cases that have hitherto come to autopsy the hypophysis has been 
 found diseased and, in all but one, enlarged. In view of the 
 analogy of structure between the hypophysis and the thyroid gland, 
 and the certain etiologic relation of disease of the latter to myx- 
 edema and cretinism, it was at first assumed, almost without ques- 
 tion, that acromegaly was caused by disease of the pituitary body. 
 Many cases have been reported in which there was disease of this 
 gland without any symptoms of acromegaly, and a certain degree 
 of general splanchnomegaly has been observed in acromegaly. It 
 is, of course, possible that the enlargement of the pituitary is sim- 
 ply a part of the latter condition. The thyroid gland, however, 
 does not partake of this change, nor do, apparently, any of the 
 other secretory organs, the various enlargements being usually the 
 result of a hyperplasia of the lymphoid tissue. Neither are the 
 changes of other organs as constant as those of the hypophysis. 
 There is certainly no characteristic lesion in the latter organ, for 
 nearly all forms of disease have been described — adenoma, sar- 
 coma, cystic degeneration, and sclerotic change. In the absence 
 of definite knowledge of the results of experimental lesions, the 
 question must remain at present undecided. 
 
DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 775 
 
 THE PINEAL GLAND, OR EPIPHYSIS CEREBRI. 
 
 The pineal gland, or epiphysis cerebri, is an outgrowth from the 
 roof of the posterior portion of the anterior vesicle of the brain. 
 Its base is soon constricted, and it is finally completely separated 
 from the primary cerebral vesicle and enclosed in a sheath of con- 
 nective tissue which is surrounded by pia mater. Histologically, 
 it is found to consist of septa of connective tissue, dividing it into 
 numerous alveoli, in which are found epithelial cells, some of 
 which are branched. It is very vascular, and contains a plexus 
 of sympathetic nerve-fibers. The gland is in all probability 
 wholly without function. 
 
 At all ages it contains small calcareous concretions (acervulus, 
 brain-sand), which must therefore be looked upon as physiologic. 
 It is sometimes enlarged in acromegaly and cretinism, or as a 
 result of a hyperplasia of the epithelial structures, giving rise to 
 adenomatous or strumous formations. As a result of its position 
 it may in these conditions occlude the veins of Galen and produce 
 hydrocephalus. Pathologically, aside from the calcareous infiltra- 
 tion already mentioned, hyaline degeneration of the blood-vessels 
 may occur. There are usually signs of inflammation, more or less 
 marked, in cases of meningitis, which may even lead to pus-for- 
 mation. Of the tumors, the most important are probably sar- 
 comata springing from the connective-tissue septa. Adenomata 
 may also occur. Cystic conditions, associated with the presence of 
 hair, cartilage, and other tissues, have been described. 
 
 CHAPTER XIII. 
 
 DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 
 
 THE DURA MATER. 
 
 Diseases External to the Dura Mater.— Among the mi- 
 nor processes that may occur externally to the spinal dura mater is 
 fatty infiltration, sometimes associated with general obesity, but 
 occasionally found in patients that are moderately emaciated. 
 
 Hemorrhage may occur on the external surface of the dura, the 
 blood being found distributed in the extradural areolar tissue. 
 The usual cause is traumatism, but it may also occur in convulsive 
 conditions. Ordinarily the blood remains circumscribed and forms 
 a spinal hematoma ; rarely, a cyst results. 
 
 Diseases of the Dura Itself. — Most of the pathologic proc- 
 esses are secondary to some disease of the vertebral column. The 
 most important is tuberculosis ; this gives rise to external tubercu- 
 
776 TEXT-BOOK OF PATHOLOGY. 
 
 ious pachymeningitis, characterized by a collection of cheesy ma- 
 terial which may have undergone either softening or necrosis, or 
 else contains pus-cells. The dura in the affected region is usually 
 considerably thickened, and may have upon its inner surface a 
 slight amount of exudate. The character of the lesions is not 
 different from that of tuberculosis in other serous membranes 
 (Fig. 356). 
 
 Pachymeningitis cervicalis is a localized tuberculosis of the dura 
 mater occurring in the cervical region, and characterized by con- 
 
 Fig. 356.— Tuberculous pachymeningitis secondary to spinal caries. 
 
 siderable thickening, sometimes amounting to \ cm. or more. The 
 dura is usually adherent to the spinal canal and to the arachnoid 
 and pia, the latter showing more or less involvement. The serious 
 changes consist of compression of the roots and of the spinal cord, 
 the latter especially in the anteroposterior direction. The process 
 may extend into the substance of the cord and produce a myelitis 
 of the periphery, and occasionally extends deeper and causes more 
 or less extensive secondary degenerations. 
 
 Of the acute inflammations the most important is internal 
 hemorrhagic pachymeningitis, a process similar to that occurring 
 in the dura mater of the brain. It consists of a layer of granula- 
 tion-tissue in which many of the capillaries have ruptured, giving 
 it a uniform reddish appearance ; it is somewhat irregular in out- 
 line and of varied extent, and not infrequently adhesions form 
 between the dura and the arachnoid. 
 
 Syphilis occurs either in the form of discrete gummata or as a 
 regular and diffuse thickening of the inner membrane. 
 
 Tumors from the spinal canal frequently invade the dura. 
 The most common of these is sarcoma. This occasions consider- 
 able thickening of the dura, and it is often difficult to separate the 
 dura from the sarcomatous bone. In consequence of these condi- 
 tions there may be pressure and atrophy of the spinal cord. 
 
 Tumors of the dura itself may be either benign or malignant. 
 Of the former, Upomata, which also occur in the brain, are the 
 most frequent. Myxomata and fibromata are exceedingly rare. 
 Sarcoma may be of the round-cell, angiomatous or alveolar type. 
 It is usually irregular in outline, spreading like a fungous mass 
 over the surface of the membrane, which exhibits fibrous thicken- 
 ing. If small and occurring on the anterior aspect, it may pro- 
 
DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 777 
 
 duce no symptoms whatever. In this situation it is frequently 
 secondary. 
 
 Upon the inner surface a variety of tumors have been observed. 
 Horsley mentions myxomata, fibromata, carcinomata, and sar- 
 comata. In rare cases echinococcus-cysts have been observed, and 
 even the cvsticercus. 
 
 THE PIA AND ARACHNOID. 
 CIRCULATORY DISTURBANCES. 
 
 Active hyperemia precedes inflammatory changes, and of 
 itself is of little significance. It is rarely seen post-mortem, and 
 in the majority of cases its existence can only be inferred. 
 
 Passive hyperemia is very common — that is to say, in many 
 cases the veins of the pia mater are found to be tortuous and 
 greatly distended with blood. This is usually due to post- 
 mortem hypostasis. 
 
 DEGENERATIONS. 
 
 Calcareous infiltration sometimes occurs, appearing as 
 small, hard plates, rarely more than 0.5 cm. in diameter, scattered 
 along the whole length of the spinal cord. It is probably always 
 secondary to inflammatory processes, as spinal syphilis and tuber- 
 culosis. 
 
 Pigmentary infiltration may occur, but is rare. 
 
 INFLAMMATIONS. 
 
 Acute inflammation, or acute leptomeningitis, is often 
 secondary to cerebral meningitis. It may occur, however, inde- 
 pendently as a result of local suppurative processes, particularly 
 those of the spinal column. It may be serous or purulent in 
 character, and in the latter an exudate is found upon the inner 
 surface of the dura and in the subarachnoid space, often extending 
 the entire length of the spinal cord. The microscopic changes 
 are essentially similar to those found in the membranes of the 
 brain. Involvement of the cord is, however, much more common. 
 There is usually extensive round-cell infiltration in the anterior 
 commissure and small foci of round cells scattered throughout the 
 gray and the white matter, especially in the latter. Frequently 
 these can be seen to surround a blood-vessel, but this is not always 
 the case, and it is not unlikely that purulent material can enter 
 from the lymphatics of the pia. If death does not occur, adhe- 
 sions may form between the dura and arachnoid, but these are 
 certainly exceedingly uncommon in the cord. 
 
 Chronic leptomeningitis is usually associated with scle- 
 
778 TEXT-BOOK OF PATHOLOGY. 
 
 rosis of the spinal cord ; thus, in locomotor ataxia the pia mater 
 over the posterior column may be opaque and slightly thickened. 
 It may also be consecutive to some of the other inflammatory 
 processes, and in this form adhesions may be found between the 
 dura and arachnoid (pachymeningitis and arachnitis adhesiva). 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis may occur in the form of miliary nodules or as 
 small cheesy masses, usually extending a slight distance from the 
 pia mater into the substance of the cord. It is disputed whether an 
 acute leptomeningitis without miliary or cheesy nodules may be 
 caused by this organism alone, but this has not as yet been decis- 
 ively established. Solitary tubercles may occur in any part of 
 the spinal cord. They are rarely encapsulated. They usually 
 consist of an aggregation of round cells with vesicular nuclei, 
 and are often softened in the center. 
 
 Syphilis appears as a thickening of the membranes with mul- 
 tiple gummata, often projecting into the substance of the cord or 
 extending to and involving the dura mater. The vascular changes 
 are very characteristic ; nearly all the blood-vessels exhibit the 
 typical round-cell infiltration and thickening of the intima which 
 have been described in the section on endarteritis syphilitica. There 
 are also a perivascular round-cell infiltration and some prolifera- 
 tion of the adventitia. The veins may also be involved. The 
 lumen of both sets of vessels is usually contracted, and there is a 
 great tendency to the formation of thrombi. In these thrombi 
 organization may take place, with the formation of new blood- 
 vessels. The spinal cord may also exhibit various lesions, due 
 either to pressure or to direct extension inward from the pia. 
 
 In congenital syphilis the upper part of the spinal cord 
 appears to be more considerably involved than the lower part. 
 
 ANATOMY OF THE CORD. 
 
 The spinal cord is composed, as are the other parts of the central nervous 
 system, of gray and white matter ; the gray matter occupying the central 
 part, and the white matter being distributed around it. It is of varying size, 
 somewhat broader and flatter in the cervical region than elsewhere ; almost 
 circular in the dorsal region, and again thicker in the lumbar region. It 
 communicates with the rest of the body by means of the spinal nerves, 
 which arise anteriorly and posteriorly as roots ; eight from the cervical, 
 twelve from the dorsal, five from the lumbar, and five from the sacral re- 
 gion. It is surrounded by three membranes: the pia, adherent to it; the 
 arachnoid, adherent to the pia, but not dipping into the anterior fissure, 
 and the dura mater, which is adherent neither to the arachnoid nor to the 
 vertebral column. The gray matter is divided into two parts by the ante- 
 rior commissure and posterior septum, each part consisting of an anterior 
 horn, a thick, roundish mass, and a posterior horn, a slenderer projection. 
 The lateral halves are united by the gray commissure, in which is the central 
 canal lined with cuboidal epithelium and continuous with the fourth ventricle 
 
DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 779 
 
 above. In the anterior cornua are found the large multipolar ganglion- 
 cells, whose axis-cylinders pass out through the anterior roots and end in 
 the muscles ; commencing in the dorsal region, there is a group of cells in 
 the inner portion of the posterior horn, near the gray commissure, which 
 are bipolar and whose axis-cylinders pass outward to the cerebellar tract, 
 in which they ascend to the vermiform process of the cerebellum. The 
 posterior roots are composed of fibers that originate in the spinal ganglia 
 and pass into the cord. These spinal ganglion-cells have a single process, 
 which careful embryologic investigation has shown to be formed by the fusion 
 of two polar processes, that have been brought in contact by the shrinking 
 of one side of the cell. This process appears to divide into two fibers, one 
 passing outward into the peripheral nerves and usually terminating in the 
 sensory corpuscles of the skin, the other passing inward through the poste- 
 rior root to the spinal cord. Lenhossek believes that the peripheral fiber 
 represents the protoplasmic process of the cell which normally conveys im- 
 pulses cellipetally. The white substance of the spinal cord is composed of 
 bundles of nerve-fibers that have, for the most part, a common function, a 
 common mode of origin and of termination. 
 
 Anatomically the cord may be divided into three regions: anterior, lat- 
 eral, and posterior, although these do not correspond to regions embryo- 
 logically distinct. According to the manner of development, it should be 
 separated into the anterolateral and the posterior regions. 
 
 The most important bundles of fibers in the anterolateral columns are 
 those known as the pyramidal tracts, for the reason that they are continu- 
 ations of the pyramids of the medulla. They originate in the motor region 
 of the cerebral cortex and, in the first cervical segment, decussate through 
 the representatives of the anterior cornua to reach their situation in the 
 lateral columns. This decussation does not occur in all of the fibers, many 
 passing down in the direct pyramidal columns and some without decussation 
 in the lateral columns. These undecussated fibers subsequently cross to the 
 other side through the anterior or white commissure. The fibers of the 
 pyramidal columns terminate in arborizations which surround, but are not 
 in contact with, the ganglion-cells of the anterior cornua. 
 
 The cerebellar tract has already been described. Anterior to it and close 
 to the periphery of the cord is the so-called anterolateral column of Goivers. 
 The fibers which form this probably originate in the lateral groups or cells 
 in the anterior cornua and in the cells in the middle portion of the spinal 
 cord. The column increases in size upward and degenerates in the same 
 direction. Its termination is unknown. It also contains fibers that degen- 
 erate downward, of whose origin and termination we are ignorant. 
 
 The rest of the anterolateral column is composed of short fibers, uniting 
 different segments of the spinal cord. 
 
 The posterior columns are composed of the fibers that enter by the pos- 
 terior roots. These fibers divide into two branches, one ascending and the 
 other descending, the latter terminating in the gray matter of the posterior 
 horn. The ascending fibers may be divided into two groups, the lateral and 
 median bundles. The fibers of the lateral bundle are somewhat finer, and 
 evidently belong embryologically to a different period, because they acquire 
 their myelin-sheaths later. They pass directly into the zone of Lissauer, 
 and thence into the substantia gelatinosa of Rolando, and some of them 
 terminate in arborizations about the ganglion-cells in the column of Clarke. 
 The fibers of the median bundle are coarser. They pass inward, then up- 
 ward along the inner side of the posterior horns, and then become the 
 column ofBurdach. The median fibers from the lower part of the cord 
 bend inward and continue their course in the column of Goll, terminating 
 finally in the nucleus gracilis of the medulla oblongata. The fibers that 
 enter the cord in the cervical region pass upward in Burdach's column and 
 terminate in the nucleus cuneatus. Other fibers pass forward to the gan- 
 
780 TEXT-BOOK OF PATHOLOGY. 
 
 glion-cells of the anterior cornua, and have been supposed to be concerned 
 in reflex action. Others decussate in the posterior commissure and then 
 pass upward in the posterior columns of the opposite side. At somewhat 
 regular intervals they give off at right angles fine collateral branches, which 
 pass forward, and some of them, at any rate, end in arborizations about the 
 cells of the anterior cornua of the gray matter. These are known as the 
 reflex collaterals of Kolliker. A small portion of the posterior column just 
 back of the gray commissure appears to be composed of fibers uniting the 
 different segments. 
 
 [It is sometimes convenient to identify the nerve-roots in the spinal cord 
 for the sake of locating lesions or tracing the alteration in systemic degen- 
 erations. The most satisfactory method of doing this is to cut through the 
 dura along the anterior and posterior surfaces of the cord. The cord is then 
 stretched out at full length and the dura pulled downward as far as the 
 roots allow it to go. The root that pierces the dura opposite the conus ter- 
 minalis is the second lumbar. The lower cervical roots are all of large 
 size. The first dorsal is sometimes smaller, but the difference between it 
 and the second dorsal is still more considerable, and this serves as a check 
 upon the previous estimation. Familiarity with the appearance of the cord 
 at the different levels also enables one to locate sections with considerable 
 accuracy.] 
 
 CONGENITAL ABNORMALITIES. 
 
 Total absence of the cord, or amyelia, can only exist in 
 association with anencephalus. It is interesting to note that the 
 spinal ganglia are usually still present. Partial absence of the 
 upper portion occurs in cases of anencephalv. 
 
 Abnormal smallness is known as micromyelia. The 
 cord may be normal in structure, all the elements being propor- 
 tionately reduced, but more commonly only certain parts are 
 affected, particularly the pyramidal columns, as a result of fetal 
 lesions in the motor tract. 
 
 Double cord, or diastematomyelia, is usually localized to 
 one portion of the cord, particularly the lumbar region. Occa- 
 sionally the cord is completely divided by a bony septum. In 
 this case the gray matter in either half presents the normal 
 arrangement of the gray matter in the cord. 
 
 Unusual length of the cord may also occur, the conus ter- 
 minals being in these cases elongated and extending to the end 
 of the sacrum. 
 
 The spinal roots may be excessive or defective in number on one 
 or both sides. This usually occurs in the dorsal region, the com- 
 monest condition being the presence of eleven roots on one side. 
 
 The cord may be asymmetrical. This usually involves only 
 the pyramidal columns, and is due to incomplete decussation. 
 
 Heterotopia of the gray matter is not infrequent. This may 
 consist of doubling of one of the horns ; disorganization of one 
 or both horns, or fissures extending into the substance. Accord- 
 ing to van Giessen, the majority, if not all, of these cases are the 
 result of injury during removal, and are therefore to be regarded 
 as artefacts. This statement is, however, too sweeping. Abnor- 
 
DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 781 
 
 mal bundles, producing heterotopia? and due to alterations in the 
 medulla or even higher in the central nervous system, have been 
 found. These appearances may also be produced by tumors or 
 other conditions causing pressure. 
 
 Dilatation of the Central Canal. — The central canal may 
 be dilated, either locally or throughout its whole length. This 
 condition is known as hydromyelia, or hydrorrhaehus, and is akin 
 to hydrocephalus, with which it is sometimes associated. Hemor- 
 rhage may take place into these dilated canals and gives rise to 
 hematomyelia (vide infra). 
 
 Localized collections of liquid in the subarachnoid spaces are 
 sometimes spoken of as hydrorrhaehus externa. 
 
 Spina Bifida. — There may be imperfect closure of the poste- 
 rior processes of the vertebrae, giving rise to clefts, which are known 
 as rachischisis. If the membranes of the spinal cord protrude 
 through the cleft in an imperfectly closed canal in the form of a 
 sac or hernia, the condition is called spina bifida. In some cases the 
 skin is still present, and is often covered by an abnormally thick 
 growth of hair. In other cases the pia is the only membrane that 
 enters into the formation of the wall. It is usually thickened, 
 and may be covered with granulations. Sometimes the dilatation 
 evidently takes place in the central canal, for the substance of the 
 spinal cord may be recognized adhering to the inner layer of the 
 pia mater. This condition is called myelomeningocele. Spinse 
 bifidse usually appear in the sacral or lower lumbar region, and are 
 probably due to imperfect closure of the vertebral arches. 
 
 HYDROMYELIA AND SYRINGOMYELIA. 
 
 Hydromyelia is a condition in which the central canal of the 
 spinal cord is dilated. It frequently occurs in circumscribed 
 portions and is apparently without clinical significance. More 
 rarely the whole canal has a microscopic lumen throughout its 
 entire length, particularly in cases of hydrocephalus, although in 
 the majority of cases of this latter disease the spinal cord is not 
 involved. A patulous canal can be distinguished from a patho- 
 logic cavity by the fact that the cavity is lined by the normal 
 cuboidal epithelium of the ependyma. Usually there is a consid- 
 erable collection of ependymal cells in the neighborhood of the 
 central canal, and this is more apt to be the case if it is dilated or 
 otherwise altered than if it is normal. Occasionally the central 
 canal is doubled. This rarely happens throughout the whole 
 length of the cord, but is more frequently found in a limited 
 portion, especially the lumbar region. This doubling is due in 
 some instances to the obliteration of the central part of a dilated 
 canal with its long axis transversely placed. Sometimes a slit- 
 like canal shows a dilatation in only one part. Sometimes the 
 
782 TEXT-BOOK OF PATHOLOGY. 
 
 lumen of the canal is completely obliterated, leaving nothing but 
 a mass of cells in the gray commissure, in the midst of which 
 capillaries may be observed. More distinct pathologic changes 
 are the diverticula that occasionally spriug from the canal. These 
 seem to be most frequent in the cervical and dorsal regions. They 
 usually extend downward, and are situated posteriorly to the gray 
 commissure. It is possible that collections of epithelial cells from 
 the ependyma under similar circumstances may form masses in the 
 posterior column without distinct cavity-formation, although this 
 is doubtful. These changes are particularly significant on account 
 of their relation to the disease known as syringomyelia (Fig. 357). 
 
 / 
 
 m^— -—-^--^^ 
 
 1 4 
 
 Hydrornyelia (partly diagrammatic). 
 
 V 
 
 :--\ 
 
 Syringomyelia. — Pathologically this is essentially a cavity 
 in the spinal cord that is not lined throughout with the columnar 
 epithelium of the ependyma. This cavity may appear as a wide 
 dilatation or as a narrow slit. It usually occupies the posterior 
 part of the cord, is exceedingly asymmetrical, sometimes limited 
 entirely to one side, and in these cases is ordinarily found in the 
 posterior horn or on its inner side. The cord may be unaltered 
 externally. The dura mater is commonly normal. The pia 
 and arachnoid are either normal or else thickened slightly, the 
 change being not unlike that found in senility or in cases of 
 chronic edema of the membranes. The shape of the cord may be 
 entirely normal. This, however, is rare. Usually there is some 
 asymmetry, and frequently, particularly if the cavity is large, the 
 cord upon being removed and laid upon a flat surface seems to 
 collapse, giving rise to the so-called ribbon-appearance. Section 
 through the cord shows the existence of a larger or smaller cavity 
 filled with the products of liquefaction-necrosis, cerebrospinal 
 fluid, or else more rarely with blood. Sometimes it appears to 
 have been empty, in which case the cord probably was collapsed 
 
DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 783 
 
 in the spinal canal, and the space thus formed was filled with 
 cerebrospinal fluid. The solid portion of the cord is usually some- 
 what darker in color, and the distortion of the outline corresponds 
 to the extent of the process. The portions of spinal cord not 
 involved by the lesion, and below it, commonly show more or less 
 descending degeneration. In the portion above the cavity, if it 
 does not extend as far as the medulla, some degeneration in the 
 posterior columns is often found. In many cases, however, both 
 the ascending and descending tracts are intact ; at least they appear 
 so to the naked eye. Microscopic examination shows that the 
 cavity is bounded, as a rule, by a delicate reticulum of neuroglia. 
 Sometimes this is lined with what appears to be connective tissue, 
 and is supposed to be an inclusion of the pia mater. At other 
 times it is lined with ependymal epithelium ; occasionally, as has 
 been previously mentioned, it may contain blood. The tissue in 
 the neighborhood is usually hyperplastic neuroglia. The fibers are 
 coarse ; the cells are sometimes swollen, sometimes shrunken, and 
 show various signs of commencing degeneration. They may be 
 numerous or few. The cord in the immediate neighborhood may 
 show curiously few changes, the ganglion-cells being perfectly 
 normal and the fibers uninjured. If the cavity is extensive and 
 the proliferation of the neuroglia considerable, this is not usually 
 the case. An entire posterior root may be destroyed, or perhaps 
 half or more of the spinal cord, and the nerve-fibers in the neigh- 
 boring columns will be extensively degenerated ; in these cases 
 secondary degeneration always occurs. Not only the pyramidal 
 tracts, but also bundles in the posterior columns degenerate down- 
 ward. In a case that I have studied the coma-tract of Schultze 
 was beautifully outlined. The nerve-roots are also usually involved, 
 and there is descending degeneration along the anterior roots, 
 which may be detected also in the nerves. The posterior roots 
 may show some degeneration, but this is rare and the cells of the 
 spinal ganglia are usually intact. Sometimes there is considerable 
 vascular proliferation in these portions of the cords not unlike 
 cavernous change. Atypical forms frequently occur. There may 
 be extensive gliosis, with small or no cavity-formation ; or the 
 eavity may be extensive and the proliferation of the neuroglia 
 slight. Occasionally the cavity may communicate with the dilated 
 central canal, a condition that has given rise to the supposition 
 that it is originally due to some congenital malformation. 
 
 As the great majority of all the cases of syringomyelia are associated 
 with hyperplasia of the neurogliar tissue of the spinal cord, it is necessary, 
 in order to understand the various theories that have been suggested to 
 explain its origin, to briefly consider the more recent investigations in 
 regard to this tissue. It is now established that it is ectodermal in ori- 
 gin, and due to a proliferation of the ependymal cells lining the central 
 canal of the spinal cord and the ventricles of the brain. In the cord these 
 cells elongate radially, and the nuclei show active karyokinesis, continuing 
 
784 TEXT-BOOK OF PATHOLOGY. 
 
 to proliferate until the neuroglia-cells are found in all parts of the spinal 
 cord. The cells lining the central canal and, in the human cord, groups of 
 cells in its immediate neighborhood, remain cuboidal in shape, and are 
 spoken of as ependymal cells. Those cells forming the connective tissue 
 of the nervous system are called astrocytes. It was formerly supposed that 
 the fibrous portion of the neuroglia was due to the interlacing of the numer- 
 ous radiating protoplasmic processes of the latter; although Eanvier and 
 Chaslin had both suspected that the fibers were independent of the cells. 
 Since the introduction of the Weigert and Mallory staining-methods, it 
 appears certain that, in the human cord at least, the neuroglia-fibers form 
 a network independent of the neuroglia-cells. In regard to the origin of 
 these 'cells, it is not certain that they all develop directly from the ependyma ; 
 indeed, it is very likely that the astrocytes may themselves redivide, for ob- 
 servations have been made and reported in which they were seen to possess 
 karyokinetic figures. Moreover, the repeated proliferation of the neuroglia 
 in cases of injury to the central nervous system in situations far removed 
 from the primitive ependyma would be an argument in favor of this view. 
 Pathologically, various interesting theories have been suggested to account 
 for this apparently idiopathic proliferation of the neuroglia. Lenhossek 
 believes that besides the fully formed astrocytes other neuroglia-cells remain 
 throughout life in a sort of latent condition and represent superfluous ele- 
 ments formed during embryonal existence. These, he believes, may, under 
 certain circumstances, commence to proliferate and give rise to gliosis. A 
 certain amount of neurogliar proliferation appears to be normal in the neigh- 
 borhood of the central canal of the human spinal cord, and has already been 
 described in the discussion of hydromyelia ; in some cords it may reach 
 a very extreme degree, often causing obliteration of the central canal, whose 
 place is then taken by an irregular group of cells, in the midst of which 
 blood-vessels may be found. Of the various theories that have been sug- 
 gested, the most important is that of lymphatic or venous congestion, 
 based upon the general dilatation of the perivascular spaces in all instances 
 of gliosis. Cases, however, do occur in which this dilatation of the lymph- 
 spaces does not exist. A more widely supported theory is that of congenital 
 dislocation of some of the ependymal cells of the central canal, either in 
 the form of diverticula, or as solid plugs, or as wholly separated cavities. In 
 many of the cases of syringomyelia such ependymal cells are found lining 
 the abnormal cavity, and in some cases, as has been stated, the syringo- 
 myelic cavity communicates with that of the central canal. According to 
 this, syringomyelia is only a pronounced modification of hydromyelia. This 
 theory is particularly supported by Hoffmann, who draws a distinction in 
 the hyperplasia between gliosis and gliomatosis; the former representing 
 proliferation of the ependymal cells, and the latter being a neoplastic forma- 
 tion, giving rise to elongated tumors with increase in the size of the spinal 
 cord. 
 
 Schlesinger also believes that the hyperplasia commences in the epen- 
 dymal cells, and that congenital anomalies play a large part in their etiol- 
 ogy. Saxer suggests that the neuroglia-cells may have retained some of 
 their embryologic properties and be capable of proliferating. Weigert, who 
 disbelieves emphatically in the theory of softening of the gliosis, suggests 
 that the gliosis, if it exists at all, is possibly secondary. Among the other 
 theories are those of softening after traumatism or the result of angioma- 
 tous degeneration of the blood-vessels. Gerlach has reported a case in 
 which the cavity appeared to be lined with pia mater. It is certain that 
 in the great majority of cases there is true proliferation of the neuroglia- 
 tissues, the cells being increased in number, and the fibers coarser and forming 
 a wide-meshed network around the canal. A true gliomatous formation 
 may also occur, and it is not unlikely that syringomyelia is rather a syn- 
 drome than a pathologic, or at least an etiologic, entity. 
 
DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 785 
 CIRCULATORY DISTURBANCES. 
 
 Diseases of the walls of the blood-vessels are similar 
 to those occurring in the blood-vessels of the other parts of the 
 body. Extensive atheromatous changes are relatively rare. Per- 
 haps the most frequent disease is hyaline degeneration. Hyal- 
 ine degeneration is exceedingly common in cases of sclerosis, 
 and may occur in early life, even in childhood. It is almost 
 invariably present in the cords of persons dying after middle life. 
 Round-cell infiltration of the intima (endarteritis) occurs in syph- 
 ilis, and also, though less frequently, in tuberculosis. Fibrous 
 thickening of the intima and proliferation of the connective tissue 
 of the adventitia are common senile changes. 
 
 Attention has been recently directed more particularly to these 
 changes on account of the suggestion by Redlich that they are the 
 anatomic basis of paralysis agitans. According to him, the 
 characteristic changes are endarteritis and periarteritis, with exten- 
 sion of the latter process into the surrounding nerve-substance 
 and the formation of perivascular insular scleroses. In addition, 
 there is often some degeneration in the posterior columns, and 
 occasionally in the lateral columns in the cervical and lumbar 
 enlargements. The vascular changes, curiously enough, appear 
 to be more severe in the posterior horns than in the other parts 
 of the cord, and amyloid bodies are nearly always present in these 
 regions. However, in examining the cord of a typical case of 
 paralysis agitans Sailer failed to find these lesions ; while in 
 another case, equally characteristic clinically, they were quite pro- 
 nounced. Fiirstner has also reported a case of paralysis agitans 
 without spinal lesions. Redlich's views, therefore, are probably 
 incorrect. 
 
 Miliary aneurysms are very infrequent in the spinal cord. 
 Aneurysms of the vertebral arteries, however, sometimes involv- 
 ing the commencement of the spinal branches, have been reported, 
 but are rare. 
 
 Amyloid degeneration is found in cases of general amyloid 
 disease. 
 
 Active hyperemia of the spinal cord is rather a clinical 
 hypothesis than a pathologic entity. Occasionally, however, the 
 gray matter seems to be slightly darker than normal, and there is 
 rather free bleeding from the vessels cut transversely. In many 
 cases of myelitis the arteries and capillaries may be found dis- 
 tended with blood. 
 
 Passive hyperemia is more readily detected in the veins of 
 the membranes than in the cord itself. 
 
 Anemia is an important and easily recognized condition. 
 Experimentally it has frequently been produced by ligation of the 
 abdominal aorta. Cases have occasionally occurred in human 
 
786 TEXT-BOOK OF PATHOLOGY. 
 
 beings in which the same vessel was occluded by a thrombus, giv- 
 ing rise to similar changes. The cord, under these circumstances, 
 is somewhat swollen, pale, and soft ; not invariably, however, for 
 cases have been reported in which microscopically it was entirely 
 normal. The ganglion-cells, particularly those of the anterior 
 cornua, are most distinctly affected. They exhibit usually the 
 characteristic features of chromolytic degeneration. The proto- 
 plasmic processes become varicose and shortened, and the nucleus 
 may be situated at the periphery. Similar changes may occur in 
 other portions of the cord, but are exceedingly rare, partly on 
 account of the free anastomosis of the blood-vessels, partly be- 
 cause if, as sometimes happens, thrombi are formed in the verte- 
 bral arteries, death occurs before characteristic changes have had 
 time to develop. 
 
 Varicose Veins. — Occasionally a group of vessels in one 
 part of the spinal cord will be dilated and varicose, forming a 
 sort of plexiform angioma. A condition of this kind has been 
 described by Edinger. In this case the vascular plexus had 
 evidently developed some time after birth, for there was some 
 degeneration of the surrounding nerve-substance, and the patient 
 had presented distinct clinical symptoms of pressure in the upper 
 part of the cord. Similar angiomatous formations are frequently 
 observed in various forms of myelitis and sclerosis. 
 
 Hemorrhages may be of two kinds : punctate and mas- 
 sive. 
 
 Punctate hemorrhages are really nothing but pericapillary exu- 
 dations of blood-cells, which can readily be distinguished from 
 the drops of blood that form at the cross-section of blood-vessels 
 by the fact that they cannot be washed off. It is probable that, 
 if death does not occur at once, they are in great part absorbed, 
 leaving perhaps a minute scar that may be readily overlooked. 
 These minute hemorrhages are perhaps more common in the cer- 
 vical region than elsewhere. They are found in the course of in- 
 fectious diseases, particularly those affecting chiefly the nervous 
 system, such as tetanus, and especially hydrophobia. Small agonal 
 hemorrhages into the substance of the spinal cord, particularly in 
 the region of the central canal, are not uncommon. Occasionally 
 these may be visible to the naked eye ; they are, of course, to be 
 distinguished from ante-mortem changes by the regular form of 
 the blood-cells and the absence of blood-pigment. They are only 
 important on account of the possibility of their being mistaken 
 for pathologic changes. 
 
 Massive hemorrhages may be infiltrating or circumscribed. In 
 the former the blood is found between the nerve-fibers and in the 
 meshes of the neuroglia. The nerve-substance is usually more or 
 less degenerated, and the lesion corresponds anatomically to the 
 hemorrhagic infarct. Circumscribed hemorrhages are usually 
 
 
DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 787 
 
 small when compared to those in the brain, a circumstance due> 
 of course, to the restricted area in which they can occur. 
 
 The most common cause of this form of hemorrhage is trau- 
 matism, and it may sometimes occur as a result of concussion 
 without fracture of the spinal column. Hemorrhages may also 
 occur in persons with diseased arteries as a result of violent effort 
 or emotional disturbance. 
 
 The clots are usually irregularly oval in outline, and are often 
 surrounded by hyperplastic neuroglia, in the midst of which are 
 found compound granular cells, and more or less degenerated 
 nervous tissue. 
 
 In the later stages the formation of fibrous tissue is apparent ; 
 capillaries may also be found bending into the substance of the 
 clot, which eventually is absorbed, leaving a scar that nearly 
 always contains some pigment surrounded by coarse-meshed 
 neuroglia-tissue. Rarely the pigment is absorbed and a cyst re- 
 mains. Occasionally the hemorrhagic focus is restricted to the 
 gray substance, the blood being found in cylindrical masses. 
 This arrangement is due to the fact that in normal circumstances 
 the gray matter is softer than the white, and offers less resistance 
 to the extravasation of the blood. In this case the infiltrated area 
 soon becomes filled with granular cells, the nerve-fibers degener- 
 ate, and crystals of hematoidin appear. 
 
 Hematomyelia. — If the central canal is dilated and contains 
 blood, the condition is known as hematomyelia. This may occur 
 as the result of traumatism or as a result of some vascular de- 
 generation. The latter form is occasionally associated with 
 syringomyelia, and is found most frequently in the cervical por- 
 tion of the cord. If the hemorrhage occurred some time before 
 death, the only traces that persist will be discoloration of the 
 ependyma, and perhaps the adjacent tissue. Hemorrhage may 
 also occur during the death-agony, in which case the central 
 canal may either be filled with normal blood-cells, or, if it is 
 at all dilated, there will be a thin layer of blood-cells upon the 
 surface. The most common situation is at the point where the 
 central canal opens into the fourth ventricle. 
 
 INFLAMMATIONS. 
 
 Myelitis, in the strict sense, is a term signifying an inflam- 
 mation of the substance of the spinal cord. According to this 
 view, it should be limited exclusively to forms of spinal disease 
 secondary to hematogenous infection, extension from the pia, or 
 possibly extension from the central canal, although the latter can 
 be dismissed as an unknown variety. The name has been used, 
 however, to signify any form of softening that may occur, whether 
 it be produced by injury or disease of the spinal column, by 
 
788 TEXT-BOOK OF PATHOLOGY. 
 
 tumors, or by poisons circulating in the blood. It has also been 
 applied to secondary changes the result of meningitis and to 
 obscure lesions that either commence with a proliferation of the 
 neuroglia, or as a primary degeneration or atrophy of the nerve- 
 substance and secondary increase in the neuroglia-tissue. 
 
 According to the distribution of the lesions, myelitis is spoken 
 of as circumscribed, transverse, or disseminated. Older writers 
 were accustomed to distinguish between those forms which were 
 found only in the white matter, those found only in the gray mat- 
 ter, and the diffuse forms. The first were known as leukomyeli- 
 tis, the second as poliomyelitis, and the third as diffuse myelitis. 
 Several varieties may be distinguished by the pathologic character 
 of the lesions. 
 
 Hematogenous Purulent Myelitis. — As a rule, the membranes 
 of the brain are also infected, and show the characteristic ap- 
 pearances of acute leptomeningitis, with subarachnoid accumu- 
 lations of pus and injection of the vessels. Cross-section of 
 the cord shows here and there small reddish or yellowish 
 areas distributed irregularly throughout the cord ; in longi- 
 tudinal sections these usually appear as streaks following the 
 course of the blood-vessels. The cord often seems to be softer 
 and may be darker than normal. The microscopic changes con- 
 sist of accumulations of pus in the pia mater and distention of the 
 vessels, the presence of a perivascular round-cell infiltration, 
 slight degeneration of the nervous tissue in the neighborhood of 
 the lesions, and alteration of the neuroglia, which may show some 
 looseness of its fibers. Unless the process is advanced, with the 
 formation of abscesses of considerable size, or extensive vascular 
 change, the true nervous tissue not in the immediate neighbor- 
 hood of the foci is but slightly altered. Ordinarily, however, 
 alterations may be seen in the ganglion-cells, which consist chiefly 
 of irregularity in the arrangement of the chromophilic bodies and 
 perhaps somewhat diffuse staining. Should, however, ganglion- 
 cells lie in the midst of, or very close to, the purulent focus, they 
 show a severer type of degeneration, and often have lost their 
 protoplasmic processes. In these cases micro-organisms are not 
 infrequently found. In some rare instances the changes in the 
 substance may be very pronounced, whilst those in the meninges 
 are so slight as entirely to escape macroscopic observation, and to 
 be even readily overlooked with the microscope. 
 
 Myelitis secondary to purulent leptomeningitis is not greatly dis- 
 similar from this, excepting that there is generally a more marked 
 degeneration in the periphery of the cord. The neuroglia-eells 
 are increased in this region ; there are often minute hemorrhagic 
 foci, and occasionally small peripheral accumulations of pus. 
 These lesions have recently been observed, particularly by Coun- 
 cilmann, in epidemic cerebrospinal meningitis. 
 
DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 789 
 
 Transverse myelitis, without local foci, secondary to injury or 
 infectious disease — that is, the condition generally denominated 
 myelitis — presents three stages, the stage of red softening, of yel- 
 low softening, and of gray degeneration. In the first the mem- 
 branes of the cord are usually somewhat opaque. The substance 
 of the cord itself may be either swollen or shrunken, and is softer 
 than normal in consistency. Upon section of the cord the surface 
 is seen to be pink, and there may be minute hemorrhages ; the tis- 
 sue swells so that the surface of the cross-section is slightly convex. 
 Microscopically the most characteristic feature is the congestion 
 of the blood-vessels ; this is more marked in the veins than in the 
 arteries. There is usually a considerable amount of perivascular 
 cellular exudate, the majority of these cells being polynuclear leu- 
 kocytes. The myelin-sheaths show here and there degeneration ; 
 the axis-cylinders are swollen, granular, and somewhat shrunken. 
 The neuroglia-cells are sometimes swollen ; sometimes irregular in 
 outline and increased in number. The neuroglia-fibers in the 
 neighborhood of the vessels form a loose, irregular network. The 
 ganglion-cells show pronounced alterations, usually similar to 
 those already described as occurring in intoxication, such as 
 irregularity in staining, peripheral situation of the nucleus, and 
 varicosity or fragmentation of the protoplasmic processes. If the 
 process has lasted any considerable time, the most characteristic 
 feature of myelitis, namely, the accumulations of granular cells, 
 begins to take place. It is not certain what these cells are, but 
 in all probability they represent the wandering connective-tissue 
 corpuscles that have absorbed the granular fatty detritus of the 
 myelin-fibers. Occasionally hyaloid bodies are present, even in 
 considerable numbers. These are more irregular in outline than 
 those seen in more chronic conditions, and, according to Leyden 
 and Goldscheider, are probably due to coagulation of an inflam- 
 matory exudate. In the next stage a pressure-anemia begins to 
 be apparent. A cross-section through the freshly removed cord 
 shows that it is still somewhat swollen ; the color is yellow. The 
 distinction between the gray and the white matter is preserved, 
 but the gray matter is distinctly shrunken. Microscopically the 
 blood-vessels are shrunken ; the perivascular cellular exudate is 
 still present, but many of the cells contain fat-droplets. 
 Throughout the whole cord are found compound granular cells, 
 giving to it a peculiar and characteristic appearance. The nerve- 
 fibers are swollen, granular, or shrunken. The myelin-sheaths 
 are filled with droplets of fat, or have partially disappeared. 
 The neuroglia may be still looser in its texture. The neuroglia- 
 cells are more apt to show degenerative changes. In this stage 
 the alterations in the ganglion-cells are extreme. They may be 
 swollen and irregular ; often they form irregular, vacuolar-looking 
 masses ; some, however, are shrunken, stain dark, and exhibit no 
 
790 TEXT-BOOK OF PATHOLOGY. 
 
 trace of a nucleus. Others may perhaps be still recognized by the 
 presence of a small vesicle containing the peculiar brownish pigment, 
 and finally it is evident that some have wholly disappeared, because 
 the number is much less than normal. In the severest grades of this 
 condition the substance of the cord has undergone liquefaction and 
 is reduced to a puriform mass, which it is impossible to examine, 
 excepting upon films. It is then found to contain fat-droplets, 
 granular cells, and detritus. In the stage of gray degeneration 
 there is a secondary distention of the blood-vessels, giving it a 
 somewhat redder appearance. There is proliferation of the con- 
 nective tissue, which has a tendency to retract and cause concavity 
 of the surface of the section. The granular cells are found chiefly 
 in the neighborhood of the blood-vessels. The neuroglia-tissue is 
 looser and appears to inclose numerous vacuoles. The nerve- 
 fibers have in large part disappeared, although a few show degen- 
 erative changes, and the ganglion-cells are reduced to a few masses 
 of pigment or else have disappeared entirely. After the cord has 
 been hardened, as also occurs sometimes in various forms of 
 sclerosis, cracks may appear in its substance from the retraction 
 of the connective tissue. By this time secondary degenerations 
 usually begin to appear above and below the lesion, particularly 
 in the sections stained by Marchi's method. 
 
 Pressure-myelitis. — The alterations produced in the cord by 
 slowly-developing pressure, such as the growth of a tumor in the 
 membranes, or gradual bending of the spinal canal, as in Pott's 
 disease, produce somewhat characteristic changes. The cord at 
 first becomes anemic, due to the mechanical occlusion of blood- 
 vessels in the affected segment. As the pressure increases and the 
 anemia continues degenerations ensue in the white matter. These 
 are accompanied by the appearance of a moderate number of 
 granular cells and by slight proliferation of the neuroglia. It 
 appears that this degeneration affects first the myelin-sheaths, and 
 that the axis-cylinders may maintain their vitality for a consider- 
 able length of time ; for regeneration has occurred after the cord 
 has been considerably reduced in size by long-continued pressure. 
 The gray matter appears to persist for a longer time. This does 
 not mean that the ganglion-cells remain absolutely intact, for in 
 the early stages of the process they exhibit various degenerative 
 changes. As we already know, hoAvever, such degenerative 
 changes are not necessarily fatal to the vitality of the cell. Later, 
 they begin to shrink, usually becoming at first darker, then losing 
 their protoplasmic processes, and ultimately undergoing change 
 into small irregular vesicles that are frequently pigmented. The 
 neuroglia gradually proliferates, and ultimately the cord is con- 
 verted into a sclerotic mass at the point of pressure. This mass 
 is gray in color, seems dry, and often in the process of hardening 
 develops numerous irregular fissures. The central canal is van- 
 
DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 791 
 
 ously affected. It may be, at different levels, obliterated, dilated, 
 doubled, or even tripled. This appearance of doubling or trip- 
 ling, however, is due to the extrusion of diverticula, which pass 
 upward or downward more or less parallel to the axis of the cord. 
 The epithelium lining the central canal maintains its vitality to a 
 remarkable degree, and, even when all other nervous structures 
 have disappeared, stains distinctly and is of normal shape. Sec- 
 ondary degenerations, of course, occur as soon as the axis-cylin- 
 ders begin to swell, and are identical with those found in other 
 complete transverse lesions. 
 
 Acute Anterior Poliomyelitis. — In this disease, clinically 
 designated infantile palsy, the ganglion-cells of the anterior cornua 
 of the spinal cord, their neuraxons passing out through the anterior 
 roots, and the muscles over which they have trophic influence, are 
 the principal parts involved. The disease is undoubtedly due to 
 hematogenous intoxication or infection. It develops after expos- 
 ure to cold, subsequent to some other infectious disease, such as 
 scarlet fever or measles, and occasionally has appeared as an epi- 
 demic. Children are almost exclusively affected, usually about 
 the period of the second dentition. The nature of the poison that 
 causes it is unknown. 
 
 Microscopically the cord presents no characteristic external 
 alterations. If section is made through the diseased portion, it 
 can be seen that the tissues of the cord are somewhat redder than 
 normal, particularly the anterior cornua of the gray matter, and 
 minute hemorrhages may also be observed in this region. The 
 tissue is somewhat softer than normal, and the blood-vessels are 
 considerably distended. In old cases — that is, those with changes 
 consecutive to the cessation of the acute process — the cord may be 
 smaller and somewhat denser. Upon section it is readily observed 
 that one or both of the anterior cornua are considerably reduced 
 in size. The anterior roots from the diseased area may be con- 
 siderably shrunken and fibrous. Microscopically, in the early 
 stages the most striking appearance is that presented by the blood- 
 vessels. These are greatly distended and surrounded by a wall 
 of round cells. The vessels in the gray matter of the anterior 
 cornua, in the anterior commissure, and in the anterior septum 
 appear to be chiefly involved. The posterior half of the cord 
 presents few, if any, alterations. The neurogliar tissue seems to 
 be somewhat looser, and throughout all the affected tissue there is 
 more or less cellular infiltration, the majority of the cells being 
 mononuclear. The ganglion-cells are much altered. They 
 may be swollen and colorless, the chromatin-granules may be 
 arranged in irregular masses, the processes are irregular, the 
 nucleus may stain diffusely, and the nucleolus show vacuolar de- 
 generation. In the more advanced stages both nucleus and pro- 
 toplasmic processes have disappeared, leaving nothing but the 
 
792 TEXT-BOOK OF PATHOLOGY. 
 
 thickened axis-cylinder springing from the cell. The perivas- 
 cular spaces may be somewhat distended, and often contain round 
 cells. Even in cases examined a few days after the onset, it is 
 evident that some of the ganglion-cells have degenerated com- 
 pletely and have disappeared, as their number is markedly di- 
 minished. The fibers of the anterior roots show the ordinary 
 forms of degeneration, the presence of globules of fat in the 
 sheaths, and swelling or fragmentation of the axis-cylinders. The 
 affected muscles very early exhibit fatty degeneration and atrophy 
 of the fibers. In cases examined several months after onset 
 considerable atrophy has usually taken place in the anterior horns. 
 The perivascular round-cell infiltration is still very distinct, and 
 usually compound granular cells are found in considerable num- 
 bers in the lesions. The ganglion-cells are fewer, and those that 
 remain may be either normal or partially degenerated. Many 
 fibers have disappeared from the anterior roots, and the trophic 
 changes in the muscles are still more pronounced. In those cases 
 examined very late — that is, some years after the development of 
 the process — the anterior horns appear to be markedly diminished 
 in size, although this alteration is exceedingly unequal, often one 
 horn being involved whilst the other is perfectly normal or ex- 
 hibits only slight alterations. Occasionally the anterior horns 
 appear paler, but of almost normal size, apparently the result of 
 a colloid degeneration of the neuroglia-tissues. The blood-vessels 
 are dilated and their walls thickened, and they may contain some 
 cellular infiltration. In those parts where the process is most 
 severe all the ganglion-cells have disappeared. In others a few 
 may remain, and these are usually normal. The neuroglia has 
 undergone hyperplasia, and consists of a coarse meshwork con- 
 taining many nuclei. The medullated fibers of the anterior roots 
 are partially or completely destroyed. Degeneration of the me- 
 dullated fibers of the pyramidal tract may sometimes be traced 
 for a few segments above the affected region ; as a rule, it is 
 slight, and involves only a few of the fibers. The lesions usually 
 attack several segments of the cord, and are most frequent in the 
 lumbar region, although any part may be affected, even the cells 
 of the medulla. It has been disputed whether the primary 
 changes occur in the blood-vessels or in the ganglion-cells, but it 
 seems now to be conclusively established that the disease is of 
 hematogenous origin. In favor of this view are the pronounced 
 vascular changes, and the fact that the ganglion-cells in the neigh- 
 borhood of the vessels are usually more degenerated than those 
 somewhat remote, and that definite groups of ganglion-cells are 
 not affected, but rather those supplied by an individual vascular 
 system. 
 
DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 793 
 
 PRIMARY DEGENERATIONS OF THE CORD. 
 
 Primary degeneration of the spinal cord is characterized by 
 the more or less complete destruction of certain systems of fibers, 
 affecting their whole length, without solution of continuity in any 
 part of their course, or distinct degenerative changes in the gan- 
 glion-cells from which they arise. In other words, the distinguish- 
 ing characteristic of this condition is the absence of any lesion 
 that would serve to explain its occurrence. Certain groups of 
 fibers appear to be more frequently affected than others ; these are 
 particularly the columns concerned in the conduction of impulses 
 from or to the brain. They may be classified as follows : 1. The 
 sensory neurons of the cord, which are composed of the unipolar 
 cells of the spinal ganglia, and their neuraxons. They pass from 
 the posterior roots into the spinal cord, and enter first the column 
 of Burdach, subsequently bending into the column of Goll, 
 and ending in the nuclei of Goll and Burdach in the medulla. 2. 
 The central motor neurons, commencing in the pyramidal layer of 
 the motor cortex, passing down through the internal capsule, the 
 pyramids, and the pyramidal columns of the cord. 3. The periph- 
 eral motor neurons, commencing in the ganglion-cells of the 
 anterior cornua, passing out from the anterior groups, and termi- 
 nating in the muscles. 
 
 The most important primary degeneration is tabes dorsalis, or 
 posterior sclerosis; it involves almost exclusively the sensory 
 neuron. Involvement of the peripheral motor neuron gives rise 
 to the disease known as progressive spinal muscular atrophy ; de- 
 generation of both motor neurons, to amyotrophic lateral sclerosis. 
 
 Posterior Sclerosis. 
 
 Degeneration of the posterior columns, when occurring inde- 
 pendently of distinct lesions of the posterior roots or section of 
 the spinal cord — that is, as a definite form of disease — is known 
 as tabes dorsalis, and corresponds clinically to locomotor ataxia. 
 There has been considerable discussion of late years as to whether 
 this is due to systemic disease attacking primarily certain columns 
 or tracts of fibers in the spinal cord, or to a condition secondary 
 to disease of the posterior roots. The great majority of patholo- 
 gists have now come to accept the latter view, and the evidence 
 in its favor is so strong that it will be here adopted. The fibers 
 of the posterior roots appear to originate in the spinal ganglia. 
 Upon entering the cord they divide into the ascending and de- 
 scending branches, both of which give off collaterals. They may 
 be divided into two groups, the lateral and the median bundles. The 
 lateral fibers are somewhat finer, and evidently belong embryo- 
 logically to a different group, because they acquire their myelin- 
 
794 TEXT-BOOK OF PATHOLOGY. 
 
 sheaths later and pass directly into the zone of Lissauer, thence 
 into the substantia gelatinosa of Rolando, and some of them ter- 
 minate in arborization about the cells of the columns of Clarke. 
 The median bundles, which consist of coarser fibers, pass inward, 
 then upward to the inner side of the posterior roots, then bend in 
 and form the columns of Burdach, and, finally, those from the 
 lower regions of the cord enter the columns of Goll and terminate 
 in the nucleus and the medulla. Experimental degeneration 
 caused by section of the posterior roots in animals, or destruction 
 of the posterior roots as a result of pathologic processes in human 
 beings, causes ascending degeneration of the posterior columns 
 that corresponds very closely in many respects to the lesions of 
 tabes dorsalis (Fig. 358). 
 
 The macroscopic lesions of this disease are as follows : The 
 
 Fig. 358.— Sclerosis of the cord ; from a specimen stained by Weigert's method. 
 
 dura shows no changes ; the pia mater in the segment between the 
 posterior roots is somewhat thickened and opaque, a change 
 which cannot usually be observed in the lateral and anterior re- 
 gions. The posterior roots may be enlarged. In the advanced 
 cases, however, they seem to be somewhat thinner and more trans- 
 lucent. On section through the cord the gray matter, especially 
 that of the septum and anterior horns, appears to be normal. The 
 anterior and lateral regions of the white matter are similarly in- 
 tact. In the most advanced cases the white matter between the 
 posterior roots is darker than normal and seems to be shrunken. 
 Its consistency is somewhat softer than that of the normal cord, 
 and the fact that it becomes depressed after section shows that 
 there is some tendency to retraction. In early cases these changes 
 may be slight ; in fact, in cords removed from patients suffering 
 from general paresis, in which the earliest stages are usually ob- 
 served, there may be no macroscopic changes found. In these 
 
DISEASES OF THE SPINAL COED AND ITS MEMBRANES. 795 
 
 early stages sections stained by some myelin-method exhibit the 
 following changes : In the lumbar region the columns of Goll are 
 degenerated, excepting the anterior portion ; usually there is a 
 small oval region lying in the middle of the posterior septum ; in 
 the dorsal region there are usually two areas of degeneration in 
 the column of Burdach ; in the cervical region a portion of Goll's 
 column is involved, and there are usually two areas on either side 
 in the column of Burdach near the posterior horns. In nearly all 
 cases there is usually more or less degeneration of the posterior 
 roots. In the more advanced cases the portion of the posterior 
 columns immediately behind the posterior commissure contains 
 normal fibers, but all the rest of the posterior column and Lis- 
 sauer's zone are degenerated. In the cervical portion the degen- 
 eration of the column of Goll is most pronounced, and there is 
 only a small number of normal fibers anteriorly and on either 
 side lying close to the posterior roots. The degeneration extends 
 upward through the medulla as far as the nuclei of Goll and Bur- 
 dach. It occasionally happens that one portion of the cord seems 
 to be more severely affected than the others ; as a general rule, 
 
 ^Wm 
 
 Fig. 359.— Sclerotic and contracted posterior columns in posterior sclerosis (Karg and 
 Schmorl). 
 
 this is the lumbar region or the dorsal and lumbar regions, whilst 
 the cervical portion shows fewer changes. Occasionally, however, 
 the cervical portion of the cord will be particularly involved and 
 the other regions more or less intact. In these cases the columns 
 of Goll show only slight degeneration, whilst in the cervical por- 
 tion the column of Burdach is markedly degenerated. As the 
 fibers turn toward the center, healthy fibers from the posterior 
 
796 TEXT-BOOK OF PATHOLOGY. 
 
 roots of the cervical segments are usually less involved, so that 
 the degenerated area lies near the posterior median septum, in the 
 region usually called the middle root-zone. These degenerated 
 areas are characterized by destruction of the myelin-sheaths and 
 the axis-cylinders, their places being taken by proliferated neu- 
 roglia, which is characterized by the appearance of thicker and 
 somewhat wavy fibers. In the late stages this hyperplastic neu- 
 roglia may undergo considerable contraction (Fig. 359). Pro- 
 liferation of the neuroglia-cells may be observed in the earlier 
 stages, but in the later stages this has largely disappeared. The 
 degeneration of the fibers is in all respects similar to that of the 
 ordinary secondary degeneration. Accumulation of the peculiar 
 amyloid bodies is usually observed. The gray matter of the cord 
 is little affected, the cells in particular rarely showing distinct 
 traces of degeneration, although it is not unlikely that more 
 careful investigation with the Nissl method will exhibit various- 
 changes in their finer structure. The fibers that normally pass 
 through the gray matter often disappear completely. This is 
 true especially of the fine fibers of Lissauer's zone and those 
 that form the plexus around the cells of the column of Clarke. 
 The reflex collaterals also frequently disappear, and this is sup- 
 posed to explain the loss of the reflexes, which is a common 
 symptom of the disease. The vessels usually exhibit some thick- 
 ening of the adventitia, and occasionally an accumulation of 
 granular cells either in the adventitia or beneath the ependyma. 
 Hyaline degeneration is found occasionally. The pia mater, cor- 
 responding to its macroscopic appearance, shows some thickening- 
 of the fibers, although it is absent in the earlier cases. 
 
 The most interesting subject connected with this disease is the 
 condition of the peripheral nerves, the spinal ganglia, and the 
 posterior roots. Degeneration of the peripheral cutaneous nerves- 
 is frequently observed ; but it is impossible to say, for lack of 
 sufficient investigation, whether it occurs in every case. The 
 changes consist of thickening of the perineurium and the connec- 
 tive-tissue trabecule, more or less degeneration of the myelin- 
 sheaths, and occasionally swelling of the axis-cylinders. 
 
 The results of the examination of the spinal ganglia have been 
 very contradictory, and some authors find them intact, while 
 others describe contraction and irregularity in the outlines of the 
 cells. In no case, however, have the changes been sufficiently 
 pronounced to account for the extensive degeneration in the poste- 
 rior columns. The posterior roots are invariably degenerated. 
 Some of the fibers are completely destroyed, others show disap- 
 pearance of the myelin-sheaths and alteration of the axis-cylin- 
 ders. Nazeotte claims to have discovered a round-cell infiltration 
 in the membranes surrounding the roots that causes a pressure- 
 degeneration. Eedlich and Obersteiner believe that the changes 
 
DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 797 
 
 are most marked after the entrance of the fibers into the cord, and 
 explain this by supposing that there has been a slight constriction 
 at the point where they pierce the pia mater. In this region 
 there is certainly often considerable disappearance of the myelin- 
 sheaths, but it cannot be said positively whether the intramedul- 
 lary portion of the posterior roots is more degenerated than the 
 extramedullary. 
 
 Friedreich's Ataxia. 
 
 In Friedreich's ataxia the most constant change is hypoplasia 
 of the spinal cord. This hypoplasia may be regular, so that the 
 whole cord is three-fourths or even less of its normal diameter, 
 or it may seem irregular in the latter instance, being, perhaps, 
 more pronounced in the cervical and upper dorsal regions. Hypo- 
 plasia of the cerebellum is a frequent associated lesion. The two 
 conditions are, however, rarely equal, and, according as one or 
 the other preponderates, Marie has described spinal and cerebellar 
 forms of hereditary ataxia. The next most common lesion is 
 degeneration in the posterior columns. This is particularly 
 marked in the column of Goll, but, in severe cases, may also in- 
 volve the column of Burdach. No degeneration at all may be 
 found ; such a case has been reported by Nonne ; but in these 
 instances the larger fibers are usually absent. Degeneration in 
 Clarke's columns is not uncommon. The cells exhibit various 
 forms of chronic degeneration, and the fibers either disappear 
 completely, or at least lose their myelin-sheaths. As a result of 
 this latter condition there is also degeneration of the ascending 
 cerebellar column. In regard to the degenerative areas found in 
 the lateral columns, there is much difference of opinion. The 
 majority of authors believe that they represent degeneration of 
 the pyramidal columns, although it is certain that none of the 
 clinical symptoms associated with this lesion are present. The 
 degeneration is usually most pronounced in the lower part of the 
 cord, diminishes in intensity upward, and disappears near the nor- 
 mal decussation of the pyramidal columns. According to Marie, 
 the degenerated areas usually lie to the outer side of the normal 
 situation of the pyramidal columns. In all these degenerated 
 areas there is considerable proliferation of the neuroglia-tissue, 
 the fibers being especially increased, indicating the likelihood that 
 the change is secondary. Other secondary changes are the thick- 
 ening and partial adhesion of the pia mater, particularly that 
 part in contact with the posterior columns of the spinal cord, and 
 also the thickening of the walls of the blood-vessels, such as is 
 usually found in sclerotic nervous tissue. Degeneration is also 
 found in the posterior roots, which are smaller than normal. In 
 regard to the condition of the peripheral nerves there is some 
 difference of opinion, but it seems certain that, in some cases at 
 
798 TEXT-BOOK OF PATHOLOGY. 
 
 least, there is a degeneration of the sensory fibers. The disease 
 partakes, therefore, of the nature of a combined sclerosis. Some 
 authors hold that it is due primarily to a hypoplasia of the third 
 primary vesicle and of the neural canal — that is to say, the 
 medulla, cerebellum, and cord. The disease, however, appears to 
 be slowly progressive, and it is not evident in infancy. This may 
 be explained by assuming that the hypoplastic central nervous 
 system is sufficient for the needs of the child, and that, as the 
 organism develops, it becomes relatively insufficient. This, how- 
 ever, would not enable us to understand why such extensive 
 secondary degenerations are sometimes present. 
 
 Amyotrophic Lateral Sclerosis. 
 
 Amyotrophic lateral sclerosis is a disease which, theoretically, 
 should present the following pathologic changes : Degeneration in 
 the pyramidal columns, atrophy of the ganglion-cells of the 
 anterior cornua, degeneration of the nerve-fibers in the anterior 
 roots and of the motor fibers in the peripheral nerves, and degen- 
 erative atrophy of the muscles. The lesions that are actually 
 found, however, are very various. Common to almost all cases is 
 the atrophy of the motor cells of the spinal cord and degenera- 
 tion of their neuraxons, and the presence of compound granu- 
 lar cells, but there is no other sign of inflammatory reaction. The 
 degeneration of the ganglion-cells is usually extensive, and the 
 muscles exhibit the changes characteristic of progressive spinal 
 muscular atrophy — that is, swelling of the fibers, increase of the 
 number of the nuclei, indistinctness of the striation, and increase 
 in the amount of connective tissue, with, in the later stages, 
 extreme atrophy of the fibers. The degree to which the pyram- 
 idal columns are affected is not constant ; at times the degenera- 
 tion is pronounced and extends as far as the internal capsule. 
 Indeed, distinct alterations have been reported in the motor cortex 
 of the brain — that is to say, degeneration of the ganglion-cells 
 and the presence, in more or less considerable number, of com- 
 pound granular cells. In other cases the degeneration may cease 
 at a lower point, and in at least one case was not found at all. It 
 has been supposed that in such cases there is only a slight alter- 
 ation in the nutrition of the ganglion-cells, and that the degenera- 
 tive changes commence at the peripheral portion of the neuraxon 
 and advance cellipetally. The changes found in the pyramidal 
 columns are, of course, similar to those occurring in the other 
 primary degenerations. 
 
 Combined sclerosis has been described in a great number 
 of instances, and a characteristic symptomatology has been ascribed 
 to the condition. Usually the parts affected are the posterior 
 columns, the columns of Clarke, and, in part, the lateral pyram- 
 
DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 799 
 
 idal tracts. The lesions do not differ in appearance from those 
 of the other forms of primary degeneration. The areas are gray, 
 somewhat shrunken, and contain an excess of neuroglia, granular 
 cells, and amyloid bodies. The nature of the process is still un- 
 decided. The frequency with which a certain definite combination 
 occurs has led some neuropathologists to believe that it is a mor- 
 bid entity. Others, however, contend that the parts of the cord 
 affected are those least able, on account of their poor blood-supply, 
 to resist noxious influences, and that, therefore, the disease is only 
 the reaction of the weaker parts of the spinal cord to a general 
 morbific agent. 
 
 Chronic anterior poliomyelitis, or progressive spinal 
 muscular atrophy, is strictly a degeneration of the peripheral 
 motor neuron. It is characterized by gradual atrophy of the 
 ganglion-cells of the anterior cornua and by diminution of the 
 size of the cornua themselves. No lesions that distinctly indi- 
 cate the existence of an inflammatory process are present. The 
 cells gradually grow smaller, become pigmented, and may ulti- 
 mately disappear. There is degeneration of the fibers in the 
 anterior roots and degenerative atrophy of the muscles. The 
 clinical course is slowly but irregularly progressive. The con- 
 dition in many respects resembles amyotrophic lateral sclerosis, 
 and cases have been recorded in which other degenerations were 
 found, particularly in Clarke's column and in the posterior col- 
 umns. The lesions apparently commence in the cervical region, 
 and may later extend to other parts of the cord, and even to the 
 motor nuclei of the medulla. There is a form of chronic polio- 
 myelitis in which distinct lesions of the vessels are present, and 
 which is apparently only a slow form of the ordinary acute polio- 
 myelitis. 
 
 Degenerations in the white matter of the spinal cord 
 have been described in various forms of chronic anemia, especially 
 pernicious anemia. Two varieties can be distinguished, those in 
 which the areas of sclerosis are disseminated irregularly through 
 the cord, and those in which the degeneration is systemic in na- 
 ture and follows more or less closely the area of distribution of 
 the fibers of the posterior root. In the latter case the posterior 
 columns are affected most severely, and the lesions are most 
 pronounced in the cervical region. Degeneration, however, may 
 also be found in the lateral columns, either involving only a 
 small patch of fibers, or so extensive as to give rise to the 
 appearance of combined sclerosis. The degeneration appears to 
 occur primarily in the nerve-fibers, with secondary prolifera- 
 tion of the neuroglia. Vascular changes, particularly minute 
 hemorrhages and thickening of the vessel-cells, are also found, 
 and when present the nerve-fibers in the immediate vicinity of 
 the vessels are often degenerated. Lissauer's zone, the posterior 
 
800 TEXT-BOOK OF PATHOLOGY. 
 
 roots, the spinal ganglia, and the gray matter of the spinal cord 
 are rarely involved. These changes are not, however, found in 
 all cases of progressive pernicious anemia, a number of cases 
 being now on record in which the spinal cord showed no trace 
 of degeneration. No satisfactory explanation has hitherto been 
 given to account for them. It has been suggested that the anemias 
 with spinal lesions belong to a different group, but this is, of 
 course, a mere hypothesis. The absence of degeneration in the 
 posterior roots seems to exclude a peripheral neuritis, although it 
 is possible that in case of slight disease of a spinal ganglia the 
 terminations of their nerve-fibers in the medulla would exhibit 
 the first trace of degeneration, and this, in fact, corresponds with 
 the condition found in some of the cases. 
 
 Similar changes have also been found in other conditions, es- 
 pecially the chronic cachexias, such as tuberculosis, diabetes, and 
 carcinoma. Tuczek has described changes occurring in the spinal 
 cord in ergotism and pellagra. In the former the areas of degen- 
 eration were chiefly in the posterior columns, limited, excepting 
 in the cervical regions, to Burdach's column, and there were lesions 
 in the posterior roots. In the latter disease he found degeneration 
 in Goll's column, particularly in Burdach's column, and usually 
 in the lateral columns also. There was also partial disappearance 
 of the cells of the anterior cornua, and small degenerative foci in 
 the anterior columns. Marie believes that these lesions are due 
 to degeneration of the endogenous fibers of the spinal cord. 
 Changes limited to the posterior column have also been noted after 
 diphtheria and leprosy. In old age small, irregular areas of 
 degeneration, particularly in the posterior median column, and 
 sometimes at the periphery of the spinal cord, may be observed. 
 
 SECONDARY DEGENERATIONS OF THE CORD. 
 
 Secondary degenerations of the spinal cord occur after any 
 lesion interrupting the course of one or more of the columns 
 of fibers, and also after any disease of the ganglion-cells that 
 nourish these fibers. It has been divided into ascending and 
 descending degeneration, according to the direction in which the 
 degeneration proceeds. It will be clear, from the description 
 already given of the course of the columns of the cord, that the 
 chief variety of descending degeneration will be that of the pyram- 
 idal columns. This may occur as a result of injury to the 
 motor cortex, or of interruption of the motor fibers in any part 
 of their course from the cortex to the conus terminalis. If the 
 lesion is unilateral and above the decussation, ordinarily only one 
 pyramidal column is distinctly aifected — that is to say, the anterior 
 pyramidal tract of the same side and the lateral pyramidal tract 
 of the opposite side. Careful microscopic investigations, however, 
 
DISEASES OF THE SPINAL CORD AND ITS MEMBRANES. 801 
 
 have shown that certain fibers that do not decussate, pass down 
 the spinal cord in the lateral columns. In cases of long-standing 
 secondary degeneration of the pyramidal columns a certain amount 
 of simple atrophy of the ganglion-cells of the anterior cornua has 
 
 Sclerosis of the white substance of the cord. 
 
 been observed. Descending degeneration has also been observed 
 in the posterior columns. In the upper portion of the cord it 
 assumes the form of two small areas that project from a point 
 slightly posterior to the gray commissure and extend backward 
 and outward. This has been called the comma-degeneration of 
 Schultze. In the lower part of the cord these descending fibers 
 appear to approach the posterior commissure, and form the oval 
 field of Flechsig. Descending degeneration for a short distance 
 below a total transverse lesion may be found in all the columns. 
 Ascending degeneration occurs chiefly in the posterior columns, 
 and will be described in connection with tabes dorsalis. In case 
 of isolated injury to one of the posterior roots, there may be 
 traced upward a slender band of degeneration that gradually 
 approaches the posterior septum. Ascending degeneration also 
 occurs in the direct cerebellar tract, and may often be found to be 
 associated with disease of the ganglion-cells in Clarke's columns. 
 It extends as far as the restiform bodies in the medulla. Ascend- 
 ing degeneration also occurs in the anterolateral tract of Gowers. 
 
802 TEXT-BOOK OF PATHOLOGY. 
 
 After total transverse lesion secondary alterations may usually be 
 detected in the remote portions of the cord in the course of from 
 five to seven days. These alterations consist of a swelling of the 
 axis-cylinders and, within a very short time, fatty degeneration 
 of the myelin-sheaths. Granular cells appear early in the tissue. 
 In the course of a month the degenerative changes are quite pro- 
 nounced, and may readily be detected by Weigert's method. The 
 myelin-sheaths have disappeared wholly or in part ; the axis- 
 cylinders have also vanished, although some varicose fibers maybe 
 found here and there in the lesion. Compound granular cells 
 largely fill the field, but there is also a distinct hyperplasia of the 
 neuroglia-tissue, giving the area, microscopically, a somewhat 
 grayish appearance. Still later, contraction begins to occur, and 
 the appearances seen in the primary degenerations are found. 
 
 TUMORS. 
 
 Glioma. — Of the primary tumors of the spinal cord, the most 
 frequent and important is glioma. This is usually infiltrating in 
 type and elongated, extending for a distance of several segments 
 along the cord, and sometimes involving the nerve-roots, causing 
 them to swell and become harder. It may give rise to curious 
 distortions in shape, and an apparent hypertrophy ; this latter is 
 probably the result of the compression in a longitudinal direction 
 of some portion of the cord, so that in a given section more gan- 
 glion-cells are found than would normally be present. 
 
 Sarcoma alone, or containing gliomatous or mucoid tissue, or 
 of the type known as angiosarcoma, may also appear. 
 
 Carcinoma and sarcoma may also appear as metastatic 
 growths. 
 
 Cysts are exceedingly rare, but both the echinococcus and the 
 Cysticercus cellulosae have been reported. 
 
 CHAPTER XIV. 
 DISEASES OF THE PERIPHERAL NERVOUS SYSTEM. 
 
 THE GANGLIA OF THE CRANIAL AND SPINAL NERVES. 
 
 The ganglia of the cranial nerves may be diseased as a 
 result of extension of pathologic processes, usually tuberculosis, 
 from the surrounding bony structures. It is probable that they 
 are also subject to inflammatory changes. Spiller and Keen have 
 reported the results of the examination of a number of Gasserian 
 ganglia removed on account of persistent trifacial neuralgia, in 
 
DISEASES OF THE PERIPHERAL NERVOUS SYSTEM. 803 
 
 which they found degeneration — in some cases total — of the 
 myelin-sheaths and the nerve-fibers in the ganglia. In one case 
 the degenerated nerve- tissue was replaced by connective tissue, 
 giving rise to marked sclerosis. Occasionally the cells in the 
 ganglia had undergone atrophy, and in all instances the vessels 
 were distinctly sclerotic, the lumen being sometimes completely 
 obliterated. The authors believe that these changes are not pri- 
 mary, but secondary to lesions in the peripheral sensory nerves. 
 
 The spinal ganglia may also be diseased. Slight degenera- 
 tive changes have been noted in locomotor ataxia and as a result 
 of peripheral neuritis. In this case the walls of the ganglia show 
 swelling and granulation of the chromatin-bodies, and are often 
 somewhat shrunken. More frequently the ganglia are involved 
 as a result of disease of the surrounding bones ; particularly caries 
 or sarcoma of the spine may produce pressure, resulting in 
 atrophy, or, in the case of the former, areas of tubercular 
 softening. The ganglia of the spinal nerves are sometimes found 
 diseased in ca^es of herpes zoster, and are supposed to have an 
 etiologic relation to that disease. Zinno has reported a case in 
 which there appears to have been a chronic swelling of the ganglia, 
 some of which were as large as a pigeon's egg, as a result of a 
 hyperplasia of the neuroglia and the connective tissue. These 
 swollen ganglia pressed upon the cord and produced secondary 
 degenerations. Enlarged spinal ganglia have also been observed 
 in acromegaly. 
 
 THE NERVES. 
 CIRCULATORY DISTURBANCES. 
 
 Hyperemia of the nerve-trunks attends acute inflammations. 
 The vessels of the perineurium may be intensely injected. 
 
 Hemorrhages may result from acute congestion or from 
 traumatic injuries. They take the form of punctate ecchymoses 
 in the perineurium or endoneurium. 
 
 Kdema of the nerve-trunks may occur in the nerves travers- 
 ing areas of inflammation. 
 
 ATROPHY AND DEGENERATION. 
 
 Atrophy of the nerves occurs in consequence of pressure 
 upon the nerve or as a result of disease (neuritis) of the nerves. 
 It may also result from disease of the central nervous system, 
 causing disturbance or destruction of the nuclei of origin of the 
 peripheral nerves. Occasionally atrophy arises without definite 
 cause in old age. The changes in the nerve are similar to those 
 following section of the nerve, and are described under the head- 
 ing Degeneration. 
 
 Degeneration. — Injury of a nerve in its course produces 
 
804 TEXT-BOOK OF PATHOLOGY. 
 
 various manifestations in the nerve-fibers corresponding more or 
 less to the nature of the destructive agencies. It is obvious that, 
 if the nerve be divided by a clean incision, the degenerative 
 changes below the point of incision will be less extensive than if 
 the destructive agent is severe, such as in cauterization, the crush- 
 ing of the nerve-trunk with extensive disintegration, or the re- 
 moval of a section of some length. Still milder changes, how- 
 ever, may be produced by a ligature that is not drawn tightly 
 enough to destroy completely all the nerve-fibers. Degenerative 
 changes are less pronounced if there is prompt coaptation of the 
 injured ends, or if the continuity of the nerve is not entirely 
 destroyed. 
 
 If a nerve is examined immediately after injury, there will be 
 found only deformity of the nerve-fibers. This consists in 
 dislocation of the myelin and perhaps fibrillation of the axis- 
 cylinder, so that it seems to be crushed into and diffused through- 
 out the white substance of the nerve-fiber. Within a few hours 
 the cells in the myelin-sheath begin to exhibit signs of degenera- 
 tion, the chromatin swells, stains more feebly, and may undergo 
 fragmentation. At the end of eighteen hours the axis-cylinder is 
 usually slightly swollen and its outline becomes irregular. These 
 changes, however, are by no means uniform throughout the whole 
 nerve ; some parts perhaps being almost normal, and others ex- 
 tensively degenerated. Wieting states that the cones of Schmidt- 
 Lantermann become evident, and are the first indication of nutri- 
 tive disturbance. At the end of thirty-six hours the myelin-sub- 
 stance has undergone fatty degeneration, with the formation of 
 small globules. These changes are found on both sides of the 
 lesion ; on the proximal side extending to the first node of Ran- 
 vier, and on the peripheral side extending considerably beyond 
 this. At first the changes in both fragments are approximately 
 equal, but those in the peripheral end rapidly progress, and soon 
 dominate the field. The changes in the peripheral fragment, 
 however, are more pronounced near the lesion and diminish to- 
 ward the periphery. In the central end there are nearly always 
 a few fibers that degenerate as far as the spinal cord, but these are 
 the exception. 
 
 REGENERATION AFTER INJURY OF A NERVE. 
 
 The first sign of regeneration is proliferation of the cells 
 of the sheaths. Their nuclei exhibit karyokinetic figures, and 
 there appears to be an increase in their protoplasmic substance. 
 At the same time the cells of the connective tissue also under- 
 go multiplication and, to a certain extent, act as phagocytes, 
 absorbing the fatty detritus. The protoplasm of the cells of 
 the sheath gradually elongates and occupies the situation of the 
 
DISEASES OF THE PERIPHERAL NERVOUS SYSTEM. 805 
 
 myelin-substance and the old axis-cylinder. There appears to be 
 some doubt whether these changes are more pronounced in the 
 proximal or distal fragments ; at any rate, the protoplasm of 
 the cells of the sheaths on both sides of the lesion seem to 
 possess phagocytic properties and to absorb some of the fat and 
 detritus resulting from the degenerative changes. The proto- 
 plasmic mass usually closes the free ends of the nerve-fibers, 
 and assumes a somewhat conical form, not unlike a node of 
 Ranvier. This mass appears to be continuous with the partially 
 degenerated end of the axis-cylinder. Toward the end of the 
 first week the elongated protoplasmic masses in the end of the 
 nerve-fibers become somewhat differentiated. In the interior 
 may be seen a delicate fibrillated structure that appears to be con- 
 tinuous with the axis-cylinder of the nerve ; outside of this is a 
 delicate grayish membrane, but both of these structures lie within 
 the old myelin-sheath, in as far as it is preserved. There is con- 
 siderable dispute among pathologists as to whether the central 
 fibrillated mass arises from the pre-existing axis-cylinder or from 
 the protoplasm of the cells of the sheath. Stroebe maintains 
 the former view, and believes that the axis-cylinder, as soon as a 
 supporting and directing skeleton has been formed by the proto- 
 plasm of the cells, begins to grow, extending toward the lesion, 
 outward along the protoplasmic support. It is certain, at any 
 rate, that in the course of time the differentiation becomes so dis- 
 tinct that it can be seen that the fibrillated central portion is a 
 delicate axis-cylinder continuous with the old one, and that the 
 gray mass is becoming the myelin-sheath of the fiber. As 
 the new nerve-fibers increase in length they gradually pass 
 through the injured area and come in contact with the proximal 
 area of the peripheral fragment. In this a somewhat similar, but 
 certainly less active, process has been taking place — that is to say, 
 the cells of the sheath have undergone proliferation and have 
 formed protoplasmic masses at the ends of the fiber. Differentia- 
 tion in this protoplasmic mass does not, however, appear to occur 
 until the new axis-cylinder reaches it. Gradually the nerve 
 approximates more and more closely to the normal appearance, 
 the axis-cylinder becoming more distinct and the myelin-sheath 
 thicker till it can be said to be re-established. In the course 
 of the absorption of the fatty and other detritus, cells accu- 
 mulate in the connective tissue of the nerve and between the 
 fibers that are filled with fat-droplets, which are probably ordi- 
 nary compound granular cells. It is questionable, however, 
 whether they are derived from the endothelium of the lymph- 
 spaces or from the leukocytes, or whether they represent the 
 excess of the proliferated cells of the sheath. Somewhat later, 
 concentric masses may be found that resemble very closely the 
 amyloid or hyaloid bodies of the central nervous system. In the 
 
806 TEXT-BOOK OF PATHOLOGY. 
 
 study of these subjects, as in the study of the details of all the 
 finer structures of the nervous system, much depends upon the 
 freshness of the tissue, the method of fixation, and the stain em- 
 ployed. Stroebe used chiefly anilin-blue, which stains the axis- 
 cylinder distinctly. Von Biingner employed saffranin. Neither 
 method renders it absolutely certain whether the new axis-cylinder 
 is formed by the elongation of the pre-existing axis-cylinder or 
 from the protoplasm of the cells of the sheath. It seems, a priori, 
 reasonable to conclude that if the axis-cylinder does not directly 
 elongate and form the new axis-cylinder, at any rate it exercises 
 some peculiar trophic influence upon the protoplasm of the cells 
 in immediate contact with it, and is the cause of the peculiar 
 differentiation into fibrillar substance. It is certain, moreover, 
 that as this fibrillar mass grows downward it passes by the nuclei 
 of the cells of the sheath, and does not appear to grow by the 
 simple conversion of contiguous protoplasm. On the other hand, 
 if the lesion has caused destruction of an extensive portion of the 
 nerve, so that the new axis-cylinders do not come in contact with 
 the peripheral fragment, they cease to grow, forming first an 
 irregular mass of fibers with delicate myelin-sheaths, that are 
 soon surrounded and compressed by fibrous connective tissue. 
 It therefore seems plausible to believe that certain nutritive ele- 
 ments are contained in the peripheral segment, which, if they do 
 not form the axis-cylinder directly, are at least absolutely essen- 
 tial to its growth and vitality. 
 
 INFLAMMATIONS. 
 
 Neuritis may be either acute or chronic. It has also been 
 classified as parenchymatous and interstitial ; the former compris- 
 ing the degenerations of the nerve-fibers without involvement of 
 the connective tissue, and the latter comprising all those forms 
 associated with the characteristic signs of an inflammatory proc- 
 ess in the connective tissue of the nerve. 
 
 Acute interstitial inflammation, or neuritis proper, may be caused 
 by direct extension from an inflammatory focus in the surrounding 
 tissue or by trauma, or as the result of some as yet unknown 
 poison, which is generally supposed to be rheumatic in nature. It 
 may also occur in the course of acute infectious diseases, or as an 
 independent condition, as in beri-beri. The inflammatory changes 
 occur in the perineurium and the endoneurium. The nerve is 
 swollen, soft, and pinkish in color. Microscopically, both the 
 perineurium and the trabecular of connective tissue are increased 
 in size, the blood-vessels are distended, and there is extensive 
 round-cell infiltration. In the acute forms partially degenerated 
 fibers with fatty myelin-sheaths and swollen axis-cylinders are 
 found very early. The primary change unquestionably occurs in 
 
DISEASES OF THE PERIPHERAL NERVOUS SYSTEM. 807 
 
 the connective tissue, and the nerve-fibers are involved secondarily, 
 the myelin-sheaths being the parts first affected. 
 
 Chronic interstitial neuritis may follow the acute form or com- 
 mence as an independent condition. The nerve is harder than 
 
 Fig. 361.— Neuritis : longitudinal section, showing degenerated nerve-fibers (black) ; Azou- 
 lay's method ; X 300. 
 
 normal, the connective tissue is increased, the walls of the blood- 
 vessels are thickened and their lumina may be partially obliterated. 
 More or less round-cell infiltration is found in the hyperplastic 
 
 Fig. 362.— Chronic hypertrophic interstitial neuritis (case of Dejerine) ; X 100. 
 
 connective tissue, and the nerve-fibers show extensive degenera- 
 tion, many of them having disappeared, and the few that remain 
 presenting marked morbid changes. Often there is a distinct pro- 
 liferation of the cells in the neurilemma. This form of neuritis 
 
808 TEXT-BOOK OF PATHOLOGY. 
 
 in particular is associated with muscular degeneration, and appears 
 to give rise to the type known as the neural form of progressive 
 muscular atrophy. Associated changes are often found in the 
 spinal cord, and consist of an ascending degeneration in the pos- 
 terior columns and more or less alteration of the ganglion-cells. 
 In a variety of this disease, described by Dejerine under the name 
 <of chronic hypertrophic interstitial neuritis, there is an actual over- 
 growth of the connective tissue, the nerve-trunks forming huge, 
 firm cords, several times the normal thickness, that may readily 
 be felt beneath the skin. This disease is apparently due to some 
 hereditary influence ; two of the three cases, hitherto reported, 
 occurring in the same family. Microscopically, the changes con- 
 sist of an enormous proliferation of the connective tissue with 
 round-cell infiltration, partly about the sclerotic blood-vessels, 
 and pronounced degeneration of the nerve-fibers. The muscles 
 undergo degenerative atrophy, and there are secondary degenera- 
 tions in the spinal cord. 
 
 Suppurative neuritis is nearly always secondary to suppuration 
 in the tissue surrounding the nerve. It is characterized by the 
 presence of small foci of pus in the connective tissue and softening 
 of the nerve-trunk. The nerve-fibers degenerate very rapidly. 
 
 Parenchymatous neuritis is characterized by a primary degener- 
 ation of the nerve-fibers, the alterations in the connective tissue 
 being secondary. It is always due to some toxic or infectious 
 substance circulating in the fluids of the body. The most common 
 causes are lead, arsenic, alcohol, and diphtheria ; but it also occurs 
 as a result of other poisons and infectious diseases, and in the 
 course of tabes dorsalis. The nerve-trunk becomes slighter, 
 firmer, and graver. Inflammatory changes are slight or absent, 
 Avhile the degeneration of the nerve-fibers is pronounced. Changes 
 have frequently been found in the cells in the anterior cornua of 
 the spinal cord. 
 
 Polyneuritis does not differ from the isolated form, excepting 
 that a number of nerve-trunks in various parts of the body, 
 usually the limbs, are affected at the same time. It is most fre- 
 quently of the parenchymatous type. 
 
 INFECTIOUS DISEASES. 
 
 Tuberculosis of the nerve-trunks is due to direct extension. 
 It most commonly affects the roots of the nerves, and occurs in 
 the course of tubercular spinal or cerebral pachymeningitis. The 
 connective tissue is first affected, and may contain small cheesy 
 foci, in which epithelioid and giant-cells are found. The nerve- 
 fibers degenerate secondarily. 
 
 Syphilis also occurs, chiefly in the nerve-roots. It causes 
 overgrowth of the connective tissue, particularly in the perineu- 
 

 DISEASES OF THE PERIPHERAL NERVOUS SYSTEM. 809 
 
 rium, with pressure upon and degeneration of the nerve-fibers. 
 Oummata are sometimes observed upon the cranial nerves. 
 
 I^eprosy is characterized by the presence, in the connective 
 tissue of the nerve-fibers, of large epithelioid cells containing 
 vacuoles more or less filled with lepra-bacilli. The bacilli cause 
 a certain amount of hyperplasia of the connective tissue, which 
 presses upon and eventually destroys the nerve-fibers. The dis- 
 ease affects the small cutaneous nerves almost exclusively, and 
 causes anesthesia and trophic changes in the skin. 
 
 TUMORS. 
 
 Neuroma. — The tumors embraced by this term have been 
 sufficiently described under the heading Neuroma, in Part I. 
 
 Sarcoma is a rare tumor of nerve-trunks. It takes its origin 
 from the connective tissues of the nerve. 
 
 MtlSCle-fibers are sometimes found in intramuscular nerve- 
 trunks. They usually exhibit proliferation of the nuclei, but the 
 striations remain distinct. Their position has been ascribed to 
 errors of development, but it is not certain that they are without 
 function. 
 
INDEX. 
 
 Abdominal pregnancy, 652 
 Abnormal cell-division, 97 
 Abortion, tubal, 651 
 Abrin, poisoning by, 27 
 Abscess, 105 
 
 actinomycotic, 249 
 
 alveolar, 474 
 
 of brain, 756 
 
 of heart, 364 
 
 of liver, 589 
 
 of prostate, 671 
 
 of spleen, 330 
 
 of thyroid gland, 559 
 
 of tonsil 478 
 
 of vulva, 659 
 
 perityphlitic, 508 
 
 periurethral, 615 
 
 retropharyngeal, 476 
 
 submucous, of intestine, 505 
 Absolute immunity, 197 
 Accessory suprarenal bodies, 564 
 Acervuloma, 149 
 Acervulus cerebri, 775 
 Acetone, excess of, effects of, 40 
 Acetonuria, 607 
 
 Achromatic substance of nerve-cell, 733 
 Acid-intoxication, 33 
 
 cryptogenic, 34 
 
 etiology of, 34 
 
 experimental, 34 
 
 in man, 34 
 
 symptoms of, 35 
 Acid -stain, definition, 301 (note) 
 Acne, pancreatic, 550 
 Acquired immunity, 197 
 Acrania, 727 
 Acromegaly, 687 
 
 relation of pituitary body to, 774 
 Actinomyces bovis seu hominis, 247 
 Actinomycosis, 247 
 
 of brain, 768 
 
 of heart, 375 
 
 of intestines, 516 
 
 of lungs, 456 
 
 of mouth, 473 
 
 of muscles, 712 
 
 of pericardium, 380 
 
 of thyroid gland, 562 
 Actinomycotic abscesses, 249 
 Active hyperemia, 46 
 
 immunity, 197 
 Acute yellow atrophy of liver, 527 
 Addison's disease, 566 
 Adenia, 137 
 
 Adenin, 36 
 Adenocarcinoma, 161 
 
 of stomach, 497 
 Adenocystoma of ovaries, 640 
 Adenoma, 159 
 
 alveolar, 160 
 
 cystic, 162 
 
 destruens, 161 
 
 malignant, of stomach, 497 
 
 of intestines, 516 
 
 of kidney, 591 
 congenital, 591 
 papuliferous cystic, 592 
 
 of liver, 537 
 cystic, 539 
 
 of mammary gland, 680 
 
 of pituitary body, 774 
 
 of suprarenal bodies, 566 
 
 of testicle, 669 
 
 of thyroid gland, 562 
 
 of uterus, 634 
 malignant, 634 
 
 of vulva, 660 
 
 racemose, 160 
 
 tubular, 160 
 Adenomatous proliferation of glands of 
 
 stomach, 494 
 Adenosarcoma, 161 
 
 of kidney, 591 
 
 of testicle, 669 
 Adhesions, formation of, 109 
 Aerobic bacteria, 189 
 Afanassiew, bacillus of, 261 
 Affentuberculose, 334 
 Agar-agar, 190 
 
 Age in the etiology of carcinoma, 164 
 "Ague-cake," 330 
 a-granules, 300 
 Air-embolism, 52, 54 
 Albuminoid degenerations, 71 
 Albuminous infiltration, 64. See Cloudy 
 
 swelling. 
 Albuminuria, 608 
 Albumose, poisoning by, 28 
 Albumoses, formation of, 35 
 
 in blood, effect of, 35 
 Albumosuria, 608 
 
 enterogenic, 608 
 
 from extensive burns, 20 
 
 hematogenic, 608 
 
 pyogenic, 608 
 Alcohol, poisoning by, 29 
 Aleukemic lymphadenoma, 138 
 Alexins, 198 
 
 811 
 
812 
 
 INDEX. 
 
 Alimentary glycosuria, 37 
 Alkaloids, poisoning by, 29 
 Alloxin bases, 36 
 Alveolar abscess, 474 
 adenoma, 160 
 angiosarcoma, 144 
 sarcoma, 143 
 Ameboid movements of red blood-cor- 
 puscles, 304 
 Amido-bodies in urine, 35 
 Amnion, 654 
 Amoeba cacbexica, 272 
 coli, 265 
 
 in liver, 539 
 urinalis, 266 
 Ampbistoma bominis, 296 
 Ampbitrichous bacteria, 185 
 Amyelia, 780 
 Amyeliuic neuroma, 154 
 Amylaceous bodies of prostate, 672 
 Amyloid degeneration, 71. See Degen- 
 eration. 
 of arteries, 382 
 of choroid plexus, 763 
 of heart, 360 
 of intestines, 502 
 of kidney, 588 
 of liver, 528 
 
 of lympbatic glands, 334 
 of muscles, 711 
 of pancreas, 547 
 of pituitary body, 773 
 of spleen, 331 
 
 of submucosa of stomach, 492 
 of suprarenal bodies, 565 
 of uterus, 631 
 formations, local, 73 
 material, composition of, 71, 73 
 Amyotropbic lateral sclerosis, 798 
 Anaerobic bacteria, 189 
 
 cultures, 192 
 Anal fissure, 505 
 Anastomotic aneurysm, 391 
 Anemia, 313 
 collateral, 47 
 direct. IT 
 local. 47 
 lympbatic, 137 
 of brain, 745 
 of heart-muscle, 359 
 of kidney, 568 
 of liver, 522 
 of lungs, 415 
 
 of mucous membrane of mouth, 467 
 of muscles, 707 
 of pharynx, 475 
 of pia, 715 
 of spinal cord, 785 
 of spleen, 328 
 of stomach, 485 
 primary, 315 
 
 progressive pernicious, 317 
 secondary, 313 
 spleuic, 315 
 Anemias, classification of, 313 
 Anemic infarcts, 53 
 Anencephaly, 730 
 
 Anesthetic leprosy, 236 
 Aneurysm, 388 
 
 associated conditious in other parts 
 with, 393 
 
 cirsoid, 391 
 
 cylindrical, 391 
 
 definition of, 388 
 
 dissecting, 390, 393 
 
 ectatic, 390 
 
 etiology of, 388 
 
 false, 388, 395 
 
 fusiform, 390 
 
 miliary, 390 
 
 of arteries of brain, 744 
 
 of heart, 374 
 
 pathologic anatomy of, 390 
 
 saccular. 391 
 
 spindle-shaped, 390 
 
 spurious, 388, 395 
 
 true, 388 
 
 varicose, 395 
 Aneurvsma racemosum seu cirsoideum, 
 
 133 
 Aneurysmal varix, 395 
 Angina, 475 
 
 herpetic, 475 
 
 Ludovici, 477, 481 
 
 Ludwig's, 477, 481 
 Angiolipoma, 134 
 Angioma, 132. See also Hemangioma. 
 
 cavern osum, 133 
 
 of bone, 698 
 
 of liver. 536 
 
 of penis, 663 
 
 of spleen, 333 
 
 telangiectaticum, 132 
 Angioneurotic edema, 61 
 Angiosarcoma, 139, 144 
 
 alveolar, 144 
 
 myxomatodes, 146 
 
 of dura mater, 715 
 
 plexiform, 144 
 Angiosclerosis, 384 
 Anguillula intestiualis, 290 
 
 stercoralis, 290 
 Anhydremia, 307 
 Anilin, poisoning by, 28 
 Animal parasites. 265 
 
 in etiology of disease, 31 
 Ankylosis of joints, 700 
 Ankylostoma dnodenale, 289 
 
 duodenalis, 520 
 Annectant gvri, abnormalities of, 730 
 Annelides, 296 
 Anteflexion of uterus, 620 
 Anteversion of uterus, 620 
 Anthracosis, 83 
 
 of lungs. 439 
 
 of lvmphatic glands, 336 
 Anthrax, 242 
 
 antitoxin of, 244 
 
 bacillus of, 242 
 
 of intestines. 515 
 
 of muscles, 712 
 
 of stomach, 493 
 Antistreptococcic serum, 205 
 Antitoxin. 199 
 
INDEX. 
 
 813 
 
 Antitoxin, action of, 200 
 elimination of, 201 
 of anthrax, 244 
 of diphtheria, 214 
 of leprosy, 238 
 of tetanus, 247 
 of yellow fever, 261 
 Anuria, 606 
 Anus, fistula of, 510 
 Aorta, stenosis and atresia of, 347 
 Aphthous stomatitis, 468 
 Aplasia, definition of, 62 
 Apoplexia pulmonum vascularis, 415 
 
 serosa, 747 
 Appendicitis, 507 
 catarrhal, 507 
 gangrenous, 507 
 interstitial, 507 
 necrotic, 507 
 
 pathologic anatomy of, 507 
 recurring, 508 
 relapsing, 508 
 results of, 508 
 Aqueduct of Sylvius, 726 
 Arachnoid, cerebral, 715 
 cholesteatomata of, 722 
 edema of, 716 
 endothelioma of, 722 
 hemorrhages into, 715 
 inflammation of, 716 
 lipomata of, 723 
 syphilis of, 721 
 teratomata of, 723 
 tumors of, 721 
 spinal, 777 
 
 inflammation of. 777 
 syphilis of, 778 ' 
 tuberculosis of, 778 
 Argyria, 85 
 
 Arnold on diapedesis, 49 
 Arsenic, poisoning by, 26 
 Arseniuretted hydrogen, poisoning by, 
 
 28 
 Arterial disorders, effect of, on circula- 
 tion, 45 
 hemorrhage, 48 
 hyperemia, 45 
 Arteries, 381 
 amyloid degeneration of, 382 
 anatomic considerations of, 381 
 atrophy of, 381 
 calcareous infiltration of, 382 
 congenital defects of, 381 
 fatty degeneration of, 382 
 hyaline degeneration of, 382 
 hypertrophy of, 381 
 hypoplasia of, 381 
 inflammation of, 383 
 of brain, atheroma of, 743 
 colloid degeneration of, 743 
 hyaline degeneration of, 743 
 syphilis of, 744 
 syphilis of, 388 
 tuberculosis of, 388 
 Arteriocapillary fibrosis, 384 
 Arterioliths, 58 
 Arteriosclerosis, 384 
 
 Arteriosclerosis from nephritis, 584 
 Arteriosclerotic nephritis, 578 
 Arteritis, 383 
 
 acute, 383 
 
 productive, 383 
 suppurative, 383 
 Arthritis, 701 
 
 acute, 701 
 
 chronic, 701 
 dry, with ulceration, 702 
 purulent, 702 
 serous, 702 
 
 deformans, 702 
 
 gonorrheal, 616 
 
 gouty, 704 
 
 neuropathic, 703 
 
 rheumatoid, 702 
 
 senile, 702 
 Arthropodia, 296 
 Arthrospores, 184 
 Ascarides in liver, 540 
 Ascaris lumbricoides, 286, 520 
 
 maratiana, 287 
 
 mystax, 287 
 Ascites, 552 
 
 chyliform, 552 
 
 chylous, 552 
 Asphyxia, 22 
 
 Aspiration-pneumonia, 431, 434 
 Asporogenous races, 185 
 Association-fibers of brain, 725 
 Astrocytes, 769 
 Asymmetric karyokinesis, 97 
 Atavism, 18 
 
 Ataxia, Friedreich's, 797 
 Atelectasis, 423 
 
 congenital, 423 
 Atheroma of arteries of brain, 743 
 Atheromatous cyst of testicle, 671 
 
 plate, 385 
 
 ulcer, 385 
 Atmospheric pressure, decreased, in eti- 
 ology of disease, 22 
 increased, in etiology of disease, 21 
 Atonic dilatation of stomach, 493 
 Atrophic cirrhosis of liver, 530 
 
 sclerosis of brain, 740 
 Atrophy, 62 
 
 acute yellow, of liver, 527 
 
 brown, 63 
 of heart, 370 
 
 definition of, 62 
 
 etiology of, 62 
 
 muscular, myopathic, 700 
 
 neuropathic, 709 
 
 progressive, 700 
 
 pseudohypertrophic, 711 
 
 simple, 711 
 
 numerical, 62 
 
 of arteries, 38 
 
 of bone, 692 
 
 of bone-marrow, 344 
 
 of gastric glands, 491 
 
 of heart, 370 
 
 of kidney, 585 
 
 of liver, 524 
 
 of lungs, 419 
 
814 
 
 INDEX. 
 
 Atrophy of mucosa of intestines, 502 
 
 of lymphatic glands, 334 
 
 of mammary gland, 678 
 
 of muscles, 709 
 
 of nerves, 803 
 
 of pancreas, 546 
 
 of prostate, 672 
 
 of spleen, 331 
 
 of stomach, 491 
 
 of tongue and cheeks, 471 
 
 of uterus, senile, 631 
 puerperal, 631 
 
 of testicle, 663 
 
 pathologic anatomy of, 62 
 
 pathologic physiology of, 63 
 
 progressive spinal muscular, 799 
 
 simple, 62 
 Atropin, poisoning by, 29 
 Auricular septum of heart, defects of, 
 
 348 
 Auriculoventricular orifices, stenosis and 
 
 atresia of, 348 
 Auto-intoxication, definition of, 19 
 Autonomous new-growths, 115 
 Avian tuberculosis, 235 
 
 Bacillus, 182, 183 
 aerogenes capsulatus, 245 
 
 anthracis, 242 
 coli communis, 218 
 in urine, 610 
 in kidney. 595 
 oedematis maligni, 240 
 diphtherias, 211 
 
 cultivation of, 215 
 
 distribution of, 212 
 
 pathogenicity of, 212 
 icteroides, 260 
 influenzae, 252 
 leprae, 235 
 mallei, 239 
 neapolitanus, 218 
 of bubonic plague, 253 
 of Ducrey, 259 
 of malignant edema, 240 
 of syphilis, 254 
 of tetanus, 246 
 
 phlegmoues enipliyscniatosse, 245 
 pneumonia? of Friedlander, 210 
 proteus in urine, 610 
 pyocyaneus, 205 
 pyogenes foetid us, 205, 218 
 tuberculosis, 223 
 
 culture of, 224 
 
 demonstration of, 225 
 
 distribution" of, 226 
 
 in urine, 610 
 
 modes of infection by, 226 
 
 toxic properties of, 233 
 typhi abdominalis, 214 
 distribution of, 216 
 pathogenicity of, 215 
 cultivation of, 215 
 Bacteria, 181 
 
 artificial cultivation of, 190 
 etiology of, 188 
 cell-contents of, 183 
 
 Bacteria, cell-membrane of, 185 
 
 chemistry of, 186 
 
 classification of, 183 
 
 conditions of growth of, 189 
 
 definition of, 182 
 
 demonstration of, 186 
 
 diseases due to, 201 
 classification of, 30 
 
 embolism by, 52 
 
 entrance of, into the body, 31 
 
 functions and products of, 192 
 
 in etiology of disease, 29 
 
 in urine, 610 
 
 local effects of, 195 
 
 morphology of, 183 
 
 of kidney,* 594 
 
 of suppuration, entrance of, into body, 
 104 
 in suppurative inflammation, 104 
 
 spores of, 184 
 
 staining of, 186-188 
 
 toxic products of, effects of, 196 
 poisoning by, 27 
 Bacteriacese, 183 
 
 Bactericidal action of bodily fluids, 198 
 Bacterioprotein, 104 
 Bacterium, 183 
 
 coli commune, 218 
 
 termo in urine, 610 
 Bacterinuria, 610 
 Balanitis, 661 
 Balantidium coli, 276 
 Ball thrombi, 57, 351 
 Basic stain, definition of, 301 (note) 
 Bednar's aphthae, 469 
 Beggiatoacese, 183 
 Beri-beri, 265 
 
 Bichlorid of mercury, poisoning by, 24 
 Bile, pigmentations derived from, 87 
 Biliary cirrhosis of liver, 533 
 
 ducts, 541 
 
 dilatation of, 543 
 
 inflammation of, 541. See Cholan- 
 gitis. 
 stenosis of, 542 
 tumors of, 544 
 Bilirubin-infarcts in urinary tubules, 88 
 
 in urine, 613 
 
 pigmentation by, 87 
 Biliverdin pigmentation, 87 
 Bilocular heart, 347 
 Biology of bacteria, 188 
 Black-tongue, 471 
 Bladder, 599 
 
 calculi of, 603 
 
 carcinoma of, 605 
 
 changes of position of, 599 
 
 circulatorv disturbances of, 600 
 
 cvsts of, 606 
 
 dilatation of, 599 
 
 exstrophy of, 599 
 
 fibro-adenoma of, 605 
 
 fibroma of, 605 
 
 hemorrhages of, 600 
 
 hyperemia of, 600 
 
 inflammation of, 600. See Cystitis. 
 
 malformations of, 599 
 
INDEX. 
 
 815 
 
 Bladder, myoma of, 605 
 myxoma of, 605 
 papilloma of, 604 
 polypoid growths of, 604 
 rupture of, 600 
 syphilitic ulcers of, 602 
 tuberculosis of, 602 
 tumors of, 604 
 Blastomycetes as a cause of cancer, 
 
 272 
 "Bleeders," 50 
 Blood, anatomy of, 298 
 -casts, 582 
 changes in character of, effects of, on 
 
 circulation, 45 
 in chlorosis, 316 
 -corpuscles, red, 298 
 
 alterations of isotonicity of, 305 
 ameboid movements of, 354 
 formation of, 303 
 nucleated, 304 
 pathogenic changes in, 303 
 pigmentation of, 305 
 shape of, 303 
 size of, 303 
 vacuolation of, 305 
 white, 298. See also Leukocytes. 
 -crisis, 304 
 -current, alterations in, a cause of 
 
 thrombosis, 55 
 •decrease of quantity of, effect of, on 
 
 circulation, 45 
 -destruction, 95 
 •diseases of, 298 
 fixation of, 325 
 fixed, preparations of, examination of, 
 
 325 
 foreign bodies in, 324 
 -formation, 303 
 fresh, examination of, 324 
 increase of quantity of, effect of, on 
 
 circulation, 45 
 in leukemia, 321 
 
 in progressive pernicious anemia, 318 
 methods of examining, 324 
 parasites of, 324 
 -plaques, 302 
 -plasma, 302 
 
 pathologic changes in, 306 
 poisons, 28 
 
 -pressure, increased, a cause of edema, 
 59 
 increase of, hemorrhage from, 450 
 -serum as a culture-medium, 190 
 staining of, 325 
 
 -vessels, diseases of, hemorrhage from, 
 50 
 Bone, anatomy of, 682 
 angioma of, 798 
 atrophy of, 692 
 carcinoma of, 699 
 caries of, 692 
 cysts of, 699 
 development of, 683 
 diseases of, 682 
 
 disorders of, development of, 683 
 fibroma of, 698 
 
 Bone, giant growth of, 687 
 
 hemorrhage of, 688 
 
 hyperemia of, 688 
 
 hypertrophy of, 687 
 
 hypoplasia of, 692 
 
 inflammation of, 688 
 
 lepra of, 698 
 
 lipoma of, 698 
 
 -marrow, 343 
 atrophy of, 344 
 fatty infiltration of, 343 
 hypertrophy of, 344 
 inflammation of, 344 
 mucoid degeneration of, 343 
 pigmentation of, 343 
 
 myxoma of, 698 
 
 necrosis of, 693 
 
 parasites of, 699 
 
 regeneration of, 685 
 
 sarcoma of, 698 
 
 syphilis of, 697 
 
 thrombosis of, 688 
 
 tuberculosis of, 694 
 
 tumors of, 698 
 Bothriocephalus cordatus, 286 
 
 cristatus, 286 
 
 latus, 285 
 
 liguloides, 286 
 Bouillon as a culture-medium, 190 
 Bow-legs, 700 
 (3-oxybutyric acid, excessive formation 
 
 of, in body, 34, 39 
 Brain, abscess of, 756 
 
 actinomycosis of, 768 
 
 anatomy of, 725 
 
 anemia of, 745 
 
 arteries of. See Arteries of brain. 
 
 carcinoma of, 771 
 
 circulatory disturbances of, 745 
 
 congenital abnormalities of, 727 
 
 degeneration of, after hemorrhage, 749 
 
 development of, 723 
 
 diseases of, 713 
 
 edema of. 747 
 local, 747 
 
 embolism of, 751 
 
 examination of, 727 
 
 fibroma of, 770 
 
 glioma of, 769 
 
 gumniata of, 768 
 
 hyperemia of, 746 
 
 inflammation of, 753. See also Enceph- 
 alitis. 
 
 lacerated wounds of, 760 
 
 lymphangioma of, 771 
 
 method of hardening, for examination, 
 727 
 
 multiple sclerosis of, 759 
 
 osteoma of, 771 
 
 post-mortem degenerative conditions 
 of, 731 
 
 primary vesicles of, 723 
 
 punctate wounds of, 761 
 
 red softening of, 751 
 
 sand, 775 
 
 sarcoma of, 770 
 
 sclerosis of, atrophic, 740 
 
816 
 
 INDEX. 
 
 Brain, sclerosis of, diffuse, 739 
 disseminated, 739 
 hypertrophic, 740 
 lobar, 758 
 
 syphilis of, 768 
 
 thrombosis of, 751 
 
 total absence of, 730 
 
 tuberculosis of, 767 
 
 tumors of, 768 
 
 white softening of, 751 
 
 yellow softening of, 751 
 Bread-and-butter pleurisy, 463 
 Breast. See Mammary gland. 
 
 male, abnormal development of, 676 
 Bright's disease, acute, 572 
 Bromin, poisoning by, 24 
 Bronchi, anatomic considerations, 409 
 
 anemia of, 409 
 
 congenital malformations of, 409 
 
 dilatation of, 412 
 
 foreign bodies in, 414 
 
 hemorrhages of, 409 
 
 hyperemia of, 409 
 
 inflammations of, 409 
 
 parasites of, 403 
 
 stenosis and obstruction of, 412 
 
 syphilis of, 413 
 
 tuberculosis of, 413 
 
 tumors of, 413 
 
 ulcers of, 412 
 Bronchiectasis, 412 
 
 cylindrical, 413 
 
 fusiform, 413 
 
 saccular, 413 
 Bronchiolitis, 433 
 
 exudativa, 412 
 Bronchitis, 409 
 
 acute catarrhal, 410 
 
 capillary, 433 
 
 chronic catarrhal, 410 
 
 fetid, 410 
 
 fibrinous, 411 
 Bronchogenic pneumonia, complications 
 in. 450 
 
 purulent pneumonia, 440 
 
 tuberculosis of lungs, 443, 444 
 Bronchopneumonia, catarrhal, 430 
 etiology of, 430 
 pathogenesis of, 433 
 pathologic physiology of, 431 
 pseudolobar form of, 433 
 simple, 431 
 Bronchorrhea, 410 
 Brown atrophy, 63 
 of heart, 370 
 
 induration from hyperemia, 47 
 Bubo, 337 
 
 syphilitic, 255 
 Bubonic plague, 253 
 bacillus of, 253 
 Bullous emphysema of lungs, 421 
 Bursse, inflammation of, 706 
 Bursitis, 796 
 
 Cachectic leukocytosis, 311 
 Cachexia strumipriva, 563 
 Calcareous infiltration of arteries, 382 
 
 Calcareous infiltration of spinal pia, 777 
 Calcicosis, 83 
 Calcification, 81 
 
 differentiation of, from ossification, 83- 
 
 etiology of, 81 
 
 of choroid plexus, 762 
 
 of kidney, 588 
 
 of lymphatic glands, 335 
 
 of mucosa of stomach. 492 
 
 of muscles, 711 
 
 of spleen, 332 
 
 of testicle, 664 
 
 of thrombus, 58 
 
 of veins, 396 
 
 pathologic anatomy of, 81 
 
 physiology of, 83 
 
 seats of, 82 
 Calcium salts, poisoning by, 28 
 Calculi in bladder, 503 
 
 mulberry, 603 
 
 pancreatic, 550 
 
 phosphatic, 603 
 
 renal, 596 
 
 uric acid, 603 
 
 urinary, 603 
 Calculus in pelvis of kidney, 596 
 Callus, 596 
 
 intermediary, 687 
 
 myelogenous, 686 
 
 periosteal, 686 
 Calomel, poisoning by, 26 
 Canalization of a thrombus, 58 
 Cancer, 163. See Carcinoma. 
 
 cirrhotic, of liver, 537 
 
 colloid, 174 
 
 diffuse hepatic, 537 
 
 endothelial, 150 
 
 of stomach, 494 
 Cantharidin, poisoning by, 24 
 Capillary bronchitis, 433 
 
 hemorrhage, 48 
 Capsule of bacteria, 185 
 
 staining of, 188 
 Carbohydrates, disposition of, by the 
 body, 37 
 
 value of, in nutrition, 31, 32 
 Carbolic acid, poisoning by, 24 
 Carbolized thionin, 187 
 Carbon-monoxid poisoning, 28 
 Carbonates in urine, 613 
 Carbonic acid in blood, effect of, 45 
 
 gas, poisoning by, 28 
 Carcinoma, 163 
 
 animal parasite in, 270 
 
 appearance of, 165 
 
 definition of, 163 
 
 degenerative changes in, 168 
 
 etiology of, 163 
 
 glandular, 172 
 
 medullary, 172 
 
 nature of, 169 
 
 of bladder, 605 
 
 of bone, 699 
 
 of hair,771 
 
 of dura mater, 715 
 
 of esophagus, 484 
 
 of Fallopian tubes, 650 
 
INDEX. 
 
 817 
 
 Carcinoma of intestines, 518 
 
 of kidney, 592 
 
 of larynx, 407 
 
 of liver, 537 
 
 of lungs, 458 
 
 of lymphatic glands, 343 
 
 of mammary gland, 680 
 
 of mouth, 473 
 
 of muscle, 713 
 
 of ovary, 643 
 
 of pancreas, 549 
 
 of penis, 662 
 
 of peritoneum, 557 
 
 of prostate, 675 
 
 of spinal cord, 802 
 
 of spleen, 333 
 
 of stomach, 494 
 
 of suprarenal bodies, 566 
 
 of testicle, 669 
 
 of thyroid gland, 562 
 
 of urethra, 618 
 
 of uterus, 634 
 
 of vagina, 654 
 
 of vulva, 661 
 
 parasites of, 270 
 
 pathologic physiology of, 170 
 
 scirrhous, 172 
 
 seats of, 166 
 
 secondary, 538 
 
 simple, 172 
 
 structure of, 166 
 
 theories as to causes of, 163 
 
 varieties of, 170 
 Carcinomatosis, general, 166 
 Carcinomatous cylindroma, 175 
 Cardioliths, 58 
 Caries of bone, 692 
 
 of teeth, 474 
 Carnification of lung-tissue, 424 
 Caseation, 93 
 
 of testicle, 664 
 Casts, blood-, 582 
 
 cellular, 582 
 
 crystalline, 582 
 
 fatty, 583 
 
 granular, 583 
 
 hyaline, 582 
 
 in urine in nephritis, 581 
 
 leukocytic, 582 
 
 waxy, 582 
 Catarrh, acute nasal, 402 
 
 mucopurulent, 105 
 Catarrhal appendicitis, 507 
 
 bronchopneumonia, 430. See Broncho- 
 pneumonia. 
 
 dysentery, 510 
 
 enteritis, 504 
 
 esophagitis, 482 
 
 jaundice, 544 
 
 pharyngitis, 475 
 
 pneumonia, 530 
 bacteria of, 210 
 
 stomatitis, 468 
 
 tonsillitis, 477 
 Caustic ammonium, poisoning by, 24 
 
 potash, poisoning by, 24 
 
 soda, poisoning by, 24 
 52 
 
 Caustics, action of, 24 
 Cavernoma, 133 
 
 lymphaticum, 132 
 Cavernous bodies of penis, inflammation 
 
 of, 661 
 Cavities, tuberculous, 448 
 Cecitis, 506 
 
 Cecum, inflammation of, 506 
 Cell-contents of bacteria, 183 
 
 -division, abnormal, 97 
 
 -membrane of bacteria, 185 
 
 -multiplication, 110 
 
 -nuclei, degenerations of, 97 
 Cells, edema of, 80 
 
 Cellular and attraction theory of inflam- 
 mation, 98 
 
 casts, 582 
 
 necrosis, etiology of, 97 
 general pathology of, 97 
 Central nervous system, injuries of, 760 
 Cephalohematoma, 688 
 
 internal, 713 
 Cercomonas coli hominis, 275 
 
 intestinalis, 274 
 Cerebellum, anatomy of, 726 
 
 hyperplasia of, 730 
 Cerebral arteries. See Arteries of brain. 
 
 hemispheres, hypoplasia of, 729 
 
 hemorrhage, 747 
 
 degeneration after, 749 
 massive, 748 
 punctate, 747 
 
 vesicles, primary, 723 
 Cerebrospinal fluid, 764 
 disease of, 764 
 
 meningitis, epidemic, 718 
 Cervix uteri, chronic endometritis of, 
 627 
 hypertrophy of, 631 
 
 phagedenic ulceration of, 527 
 
 sarcoma of, 634 
 Cestodes, 277 
 Chalicosis, 439 
 Chalmydobacteriacese, 183 
 Chancre, 255, 257 
 
 soft, 259 
 Chancroid, 259 
 
 of vulva, 660 
 Charcot-Neumann crystals of the blood, 
 
 322 
 Chauveau's theory of toxin immunity, 
 
 200 
 Cheesy pneumonia, 435 
 Chemical conditions, 
 
 effect of, on growth of bacteria, 189 
 Chemotaxis, negative, 100 
 
 positive, 100 
 Chilblain, 21 
 Chlorin, poisoning by, 24 
 Chloroform, poisoning by, 29 
 Chloroma, 149, 699 
 Chlorosis, 315 
 Cholangitis, 541 
 
 chronic, 542 
 
 results of, 542 
 
 suppurative, 532 
 Cholecystitis, 542 
 
818 
 
 INDEX. 
 
 Cholelithiasis, 543 
 Cholera, 219, 511 
 bacillus of, 219. See Spirillum cholerse 
 
 Asiaticse. 
 etiology of, 219. 
 pathologic physiology of, 221 
 spirillum, 219. See Spirillum cholerse 
 Asiaticse. 
 Chuhsteatorna, 180 
 
 of pia and arachnoid, 722 
 Cholesterin in fatty degeneration, 70 
 in fatty infiltration, 67 
 in urine, 613 
 Choluria, 607 
 Chondroblasts, 111 
 Chondrocarcinonia of testicle, 670 
 Chondroma, 127 
 appearance of, 127 
 definition, 127 
 etiology, 127 
 nature of, 129 
 of lung, 457 
 
 of mammary gland, 680 
 of mouth, 473 
 of muscles, 712 
 of ovary, 640 
 of pleura, 465 
 of testicle, 669 
 seats of, 128 
 structure of, 128 
 Chorion, 654 
 Choroid plexus, 761 
 
 amyloid degeneration of, 763 
 calcification of, 762 
 cysts of, 763 
 endotheliomata of, 763 
 epithelioma of, 763 
 fibroma of 763 
 hemorrhage into, 762 
 inflammation of, 762 
 pigmentation of, 763 
 tuberculosis of, 762 
 tumors of, 763 
 Chromogenesis, 195 
 Chromophilic bodies of nerve-cell, 733 
 Chromophoric bacteria, 195 
 Chronic inflammation, 105 
 
 relapsing fever, 137 
 Chyliform ascites, 552 
 Chylous ascites, 552 
 
 hvdropericardium, 376 
 Chyluria, 132, 610 
 Cicatrices fistuleuse, 449 
 Circulation of blood, disturbances of, 43 
 Circulatory disturbances, 350 
 
 system, diseases of, 346 
 Circumscribed tumors, 118 
 Cirrhosis, atrophic, 530 
 biliary, 533 
 hypertrophic, 532 
 Laennec's, 530 
 of liver, 530 
 of pancreas, 548 
 Cirrhotic cancer of liver, 537 
 Cirsoid aneurvsm, 391 
 Cladothrix, 183 
 Clap-threads, 617 
 
 Claustrum, 726 
 Cleft palate, 467 
 Cloudy swelling, 64 
 definition of, 64 
 etiology of, 764 
 of heart, 359 
 of kidney, 586 
 of liver, 526 
 pathologic anatomy of, 64 
 
 physiology of, 65 
 seats of, 65 
 Clubbing of finger-ends, 349 
 Coagulating ferments, 193 
 Coagulation-necrosis, 91 
 definition of, 91 
 etiology of, 01 
 morbid physiology of, 92 
 of muscle, 711 
 pathologic anatomy of, 91 
 Coal-dust pigmentation, 83 
 
 -tar derivatives, poisoning by, 28 
 Coceacese, 183 
 Coccidiuni oviforme, 269 
 
 perforans, 270 
 Coccus, 182 
 
 Coffee-ground vomit, 486 
 Cohnheim's theory as to origin of carci- 
 noma, 163 
 of tumors, 116 
 Cold abscess of joints, 705 
 
 in etiology of disease, 21 
 Colitis, 509 
 
 mucous, 509 
 Collateral anemia, 47 
 hyperemia, 46 
 of lungs, 415 
 Colloid cancer, 174 
 of stomach, 497 
 cystomata of ovaries, 640 
 degeneration, 78. See Degeneration. 
 of arteries of brain, 743 
 of pituitary body, 773 
 goiter, 561 
 Colon, inflammation of, 509 
 Colpitis, 653 
 
 Combined sclerosis of spinal cord, 798 
 Comma-bacillus, 219 
 Comminuted fracture, 685 
 Commissural fibers of brain, 725 
 Compound fracture, 685 
 ! granule-cell, 584 
 Concentric hypertrophy of heart, 372 
 Concretions beneath prepuce, 663 
 in prostate, 672 
 in seminal vesicles, 676 
 in uriniferous tubules, 589 
 Concussion of dental nervous system, 76( 
 Condensing osteitis, 691 
 Condyloma acuminatum of penis, 662 
 
 latum. 255, 257 
 Congenital cyanosis, 348 
 cystic hygroma, 132 
 rickets, 685 
 syphilis, 258 
 
 theory of carcinoma, 163 
 Congestion, hypostatic, 44 
 Conglutination of blood-plaques, 56 
 
INDEX. 
 
 819 
 
 Connective tissue, fibrous, regeneration 
 of, 111 
 regeneration of, 112 
 Contagious disease, definition of, 30 
 Contagium vivum, 29 
 Cor bovinum, 372 
 
 villosum, 377 
 Cord, spinal. See Spinal cord. 
 
 umbilical. See Umbilical cord. 
 Cornutin, 27 
 Coronary artery, embolism of, 351 
 
 thrombosis of, 351 
 Corpora quadrigemina, 726 
 Corpus callosum, congenital absence of, 
 729 
 
 fibrosum, 639 
 
 luteum, 639 
 Corpuscles of Hassall, 345 
 Corrosive cblorid of mercury, poisoning 
 by, 26 
 
 poisons, 24 
 Coryza, 402 
 Cowper's glands, 675 
 Cranioschisis, 728 
 Craniotabes, 684 
 Crenothrix, 183 
 Cretinism, 563 
 Croton oil, poisoning by, 24 
 Croupous enteritis, 505 
 
 laryngitis, 406 
 
 pneumonia, 207, 425. See also Pneu- 
 monia. 
 Crura cerebri, 726 
 Crusta, 726 
 
 Cryptogenic acid-intoxication, 34 
 Cryptorchismus, 663 
 Crystalline casts, 582 
 Cultivation of bacteria, 190 
 Culture-media, 190 
 
 inoculation of, 191 
 Cultures, anaerobic, 192 
 Currant-jelly clots, 350 
 Curschmann's spirals, 412 
 Cutaneous absorption, pigmentation bv, 
 
 85 
 Cyanogen-poisoning, 28 
 Cyanosis, 46 
 
 congenital, 348 
 Cyanotic induration of liver, 522 
 of lungs, 417 
 of the spleen, 328 
 Cyclencephaly, 728 
 Cylindrical aneurysm, 391 
 
 bronchiectasis, 413 
 
 cancer of stomach, 497 
 
 epithelioma, 171 
 Cylindro-adenoma, 162 
 Cylindroids, 584 
 Cylindroma, 145, 162 
 
 carcinomatous, 175 
 Cyst-adenoma, 162 
 Cystic adenoma, 162 
 
 of liver, 539 
 Cysticerci of tape-worm, 278 
 
 racemose, 279 
 Cysticercus cellulosse, 540 
 Cystin in urine, 613 
 
 Cystitis, 600 
 
 mucopurulent, 601 
 
 phlegmonous, 601 
 
 pseudomembranous, 602 
 Cysto-adenoma of ovaries, 640 
 Cystocele, 624 
 
 vaginal, 652 
 Cystoids, 177 
 
 Cystoma of ovary, colloid, 340 
 glandular, 640 
 myxoid, 640 
 papillary, 641 
 Cystomata. Same as Epithelial cysts, 177 
 Cysts, 176 
 
 classification of, 177 
 
 dermoid, 180 
 
 due to foreign bodies, 177 
 
 epithelial, 177 
 
 of alveolar processes of jaw, 475 
 
 of bladder, 606 
 
 of bone, 699 
 
 of choroid plexus, 763 
 
 of Fallopian tubes, 650 
 
 of kidney, 592 
 
 of Kobelt, 644 
 
 of liver, 539 
 
 of lungs, 459 
 
 of mammary gland, 682 
 
 of mouth, 473 
 
 of pancreas, 549 
 
 of parovarium, 643 
 
 of penis, 662 
 
 of pituitary body, 774 
 
 of prostate, 675 
 
 of scrotum, 662 
 
 of spinal cord, 802 
 
 of spleen, 333 
 
 of testicle, 670 
 
 of urethra, 668 
 
 of uterus, 637 
 
 of vagina, 654 
 
 of vulva, 661 
 
 proliferation-, 177 
 
 retention-, 177 
 
 softening-, 177 
 
 tubo-ovarian, 650 
 Cytorcytes variolse seu vaccinae, 274 
 
 Daughter-stars, 111 
 Decidua, 654 
 hemorrhage from, 656 
 hyperplasia of, 657 
 inflammation of, 656 
 reflexa, 655 
 serotina, 655 
 vera, 654 
 Defensive proteids, 200 
 Degeneration, amyloid, 71 
 definition of, 71 
 etiology of, 71 
 local formations of, 73 
 of arteries, 382 
 of choroid plexus, 763 
 of heart, 360 
 of intestines, 502 
 of kidney, 588 
 of liver, 528 
 
820 
 
 INDEX. 
 
 Degeneration, amyloid, of muscles, 711 
 
 of pancreas, 547 
 
 of pituitary body, 773 
 
 of spleen, 331 
 
 of submucosa of stomach, 492 
 
 of suprarenal bodies, 565 
 
 of uterus, 631 
 
 microscopic appearances of, 72 
 
 pathologic anatomy of, 71 
 physiology of, 73 
 
 reactions for, 73 
 
 seats of, 73 
 colloid. 78 
 
 definition of, 78 
 
 etiology of, 78 
 
 of arteries of brain, 743 
 
 of pituitary body, 773 
 
 pathologic anatomy of, 78 . 
 
 ' physiology of. 79 
 defined, 64 
 fatty, 68 
 
 definition of, 68 
 
 etiology of, 68 
 
 microscopic appearances of, 70 
 
 of arteries, 382 
 
 of gastric glands, 491 
 
 of heart. 362 
 
 of kidney, 587 
 
 of liver, 526 
 
 of muscles. 711 
 
 of prostate, <i?2 
 
 of suprarenal bodies, 565 
 
 of testicle. 664 
 
 of uterus. 631 
 
 of veins. 396 
 
 pathologic anatomy of. 69 
 physiology of, 70 
 
 seats of. 70 
 hyaline, 74 
 
 definition of, 74 
 
 etiology of. 74 
 
 of arteries, 382 
 of brain, 743 
 
 of heart, 360 
 
 of muscles, 711 
 
 pathologic anatomy of. 74 
 physiology of, 75 
 
 seats of, 75 
 mucoid, 76 
 
 definition of, 76 
 
 etiology of, 76 
 
 microscopic appearances of, 77 
 
 pathologic anatomy of, 77 
 physiology of, 78 
 
 seats of, 78 
 mvxomatous, of mammarv gland, 678 
 
 of testicle, 664 
 parenchymatous, 64 
 
 of heart, 360 
 
 of kidney, 586 
 
 of liver, 526 
 
 of muscles, 711 
 
 of pancreas, 547 
 Degenerations, 64 
 Deglutition-pneumonia. 431 
 Dendritic tumors, 118 
 Denecke, spirillum tyrogenicum, 222 
 
 Dental osteoma, 131 
 Dermatomyositis, 708 
 Dermoid cyst, 180 
 
 of choroid plexus, 763 
 of ovary. 642 
 of testicle, 671 
 Destructive adenoma, 161 
 Determining causes of disease, 19 
 Dextrinuria, 607 
 Dextrocardia, 347 
 ^-granules, 301 
 Diabete bronze, 40, 88 
 Diabetes, 38 
 
 etiology of, 38 
 
 from puncture of medulla, 39 
 
 metabolism in. 39 
 
 pathogenesis of, 38 
 
 pathologic anatomy of, 40 
 
 phosphaticus, 41 
 Diacetic acid, excessive formation of, in 
 
 body, 34, 39 
 Diaceturia. 607 
 Diapedesis of red blood-corpuscles, 48 
 
 in inflammation, 101 
 Diaphragmatic hernia, 499 
 Diastatic ferments, 193 
 Diastematomyelia, 780 
 Dichotomy of bacteria, 186 
 Diffuse nephritis. 571 
 acute, 573 
 
 sclerosis of brain, 739 
 Diffusion, escape of fluid by, 59 
 Dilatation of bladder, 599 
 
 of Fallopian tubes, 645 
 
 of heart. 371 
 
 of intestines, 498 
 
 of stomach, 492 
 atonic. 493 
 
 of ureter, 595 
 
 of uterus, 622 
 Diphtheria, 211 
 
 antitoxin of. 214 
 
 bacillus of, 211 
 
 -bacilli, non-pathogenic, 212 
 
 of animals, 212 
 
 of pharvnx, 479 
 
 of vulva. 660 
 
 pathologic anatomy of, 213 
 phvsiologv of, 213 
 
 toxin of. 213 
 Diphtheritic dysentery, 510 
 
 endocarditis, 354 
 
 inflammation, 103 
 
 laryngitis, 406 
 
 membrane, structure of, 103 
 
 rhinitis. 403 
 
 salpingitis, 647 
 Diplococcus intercellularis meningitidis 
 in leptomeningitis, 716 
 
 pneumonia?, 207 
 
 in diseases other than pneumonia, 
 209 
 Direct heredity, 18 
 Disease, causes of, 18 
 determining, 19 
 predisposing, 18 
 
 definition of, 17 
 
INDEX. 
 
 821 
 
 Disease, etiology of, 18 
 
 Disorders of nutrition and metabolism, 
 
 31 
 Dissecting-aneurysm, 390, 393 
 Disseminated sclerosis of brain, 739 
 Distoma conjunctum, 296 
 crassum, 296 
 haematobium, 294, 540 
 
 in kidney, 595 
 hepaticum, 294, 540 
 heterophyes, 296 
 lanceolatum, 294, 540 
 ophthalmobium, 296 
 pulmonale, 296 
 sinense, 296 
 Disturbances of circulation of blood, 43 
 Diverticula of intestines, 498 
 Diverticulum, Meckel's, 498 
 Dochmius duodenalis, 289 
 Dracunculus medinensis, 291 
 Dropsical infiltration, 80. See Infiltration. 
 
 of liver, 528 
 Dropsy from nepbritis, 585 
 of gall-bladder, 543 
 of joints, 701 
 of peritoneum, 552 
 Dry gangrene, 95 
 pericarditis, 376 
 Ducrey, bacillus of, 259 
 Ductus Botalli, patulous, 348 
 Duodenitis, 506 
 
 Duodenum, inflammation of, 506 
 Dura mater, 713 
 
 angiosarcoma of, 715 
 carcinoma of, 715 
 fibroma of, 715 
 gliosarcoma of, 715 
 hemorrhages of, 713 
 hyperemia of, 713 
 inflammation of, 713 
 syphilis of, 714 
 tuberculosis of, 714 
 tumors of, 715 
 spinal, 775 
 
 fatty infiltration of, 775 
 fibroma of, 776 
 hemorrhage into, 775 
 lipoma of, 776 
 myxoma of, 776 
 sarcoma of, 776 
 syphilis of, 776 
 tuberculosis of, 775 
 tumors of, 776 
 Dust-cells, 437 
 -corpuscles, 304 
 -embolism, 54 
 Dwarf tape-worm, 281 
 Dysentery, 510 
 catarrhal, 510 
 diphtheritic, 510 
 gangrenous, 510 
 ulcerative, 510 
 Dysmenorrhcaa membranacea, 623 
 Dyspepsia, 488 
 
 Eccentric hypertrophy of heart, 372 
 Ecchondromata, 127 
 
 Ecchondroses, 128 
 Eccbymosis, definition of, 51 
 Echinococcus cyst, 283 
 of kidney, 595 
 of larynx, 408 
 of liver, 540 
 of peritoneum, 558 
 of testicle, 671 
 of thyroid gland, 562 
 
 endogenes, 284 
 
 hydatidosus, 284 
 
 multilocularis, 284 
 
 scolicipariens, 283 
 Echinorrhynchus gigas, 293 
 Ectatic aneurysm, 390 
 Ectogenous teratoma, 179 
 Ectoplasm of bacteria, 185 
 Edema, angioneurotic, 61 
 
 character of the liquid in, 61 
 
 definition of, 59 
 
 etiology of, 59 
 
 from nephritis, 584 
 
 inflammatory, 60 
 
 malignant, 240. See Malignant edema. 
 
 of brain, 747 
 local, 747 
 
 of cells, 80 
 
 of intestines, 503 
 
 of kidney, 569 
 
 of larynx, 404 
 
 of lungs, 417 
 
 of nasal cavities, 402 
 
 of nerves, 803 
 
 of pharynx, 475 
 
 of pia and arachnoid, 716 
 
 pathologic anatomy of, 61 
 
 results of, 61 
 Edematous inflammation, 103 
 
 laryngitis, 405 
 ^-granules, 301 
 Ehrlich's classification of leukocytes, 299 
 
 triple stain, 326 
 Electrical currents, effects of, on bacte- 
 ria, 189 
 
 influences in etiology of disease, 23 
 Elephantiasis congenita mollis, 132 
 
 Grsecorum, 235. See Leprosy. 
 
 of scrotum, 662 
 
 pblebectatic, 398 
 
 vulvae, 660 
 Emboli, 51 
 
 sources and nature of, 51 
 Embolism, 51 
 
 air-, 54 
 
 dust-, 54 
 
 fat-, 54 
 
 infective, 54 
 
 of brain, 751 
 
 of coronary artery, 351 
 
 of intestines, 503 
 
 of kidney, 570 
 
 of liver, 523 
 
 of lungs, 419 
 
 of muscles, 707 
 
 of spermatic artery, 664 
 
 of spleen, 328 
 
 paradoxic, 5& 
 
822 
 
 INDEX. 
 
 Embolism, results of, 52 
 retrograde, 52 
 seats of, 52 
 Embryonic rests, 116 
 Emigration of leukocytes of blood, 48 
 
 -theory of inflammation, 98 
 Emphysema, infectious, 244 
 of lungs, 419 
 bullous, 421 
 interstitial, 419 
 senile, 422 
 substantial, 420 
 vesicular, 420 
 vicarious, 420 
 Empyema, 403 
 
 of gall-bladder, 542 
 Emulsifying ferments, 193 
 Encephalitis, 753 
 acute parenchymatous, 753 
 chronic, 758 
 
 primary acute hemorrhagic, 757 
 simple acute focal, 754 
 suppurative, 755 
 Eucephalocele, 728 
 Encephalomalacia, 751 
 End-arteries of Cohnheim, thrombosis 
 
 of, 53 
 Endarteritis, 383 
 
 chronica deformans, 384 
 obliterans, 387 
 
 of cerebral blood-vessels, 785 
 Endemic disease, definition of, 30 
 Endocarditis, 352 
 acute, 352 
 
 etiology of, 352 
 lesions in other organs in, 356 
 pathologic anatomy of, 353 
 results of, 355 
 changes in other organs in, 358 
 chronic, 356 
 etiology of, 356 
 pathologic anatomy of, 356 
 diphtheritic, 354 
 malignant, 354 
 micro-organisms of, 352 
 mural, 352 
 mycotic, 354 
 
 pathologic physiology of, 358 
 septic, 354 
 ulcerative, 354 
 verrucose, 354 
 Endocardium, 346 
 diseases of, 352 
 inflammation of, 352 
 Endogenic neurons, 727 
 Endogenous teratoma, 179 
 Endometritis, 624 
 acute catarrhal, 624 
 chronic, 625 
 
 of cervix, 627 
 decidualis, 656 
 exfoliativa, 623 
 glandularis, 625 
 interstitialis, 625 
 Endoplasm of bacteria, 185 
 Endospores, 184 
 Endosporium, 184 
 
 Endothelial cancer, 150 
 Endothelioma, 150, 400 
 
 of arachnoid and pia, 722 
 
 of choroid plexus, 763 
 
 of lungs, 457 
 
 of pleura, 465 
 Enteritis, 504 
 
 catarrhal, 504 
 
 chronic, 505 
 
 croupous, 505 
 
 etiology of, 504 
 
 follicular, 504 
 
 pathologic anatomy of, 504 
 physiology of, 506 
 
 pseudomembranous, 505 
 
 suppurative, 505 
 Enterocystoma, 498 
 Enterogenic albumosuria, 608 
 Enteroliths, 521 
 Enteromycosis, 516 
 Enterorrhagia, 51 
 Enzymes, 193 
 Eosinophile granules, 300 
 Ependymitis, 766 
 Epidemic cerebrospinal meningitis, 718 
 
 disease, definition of, 30 
 Epididymis, inflammation of, 664 
 
 tuberculosis of, 667 
 Epididymitis, 616, 664 
 
 acute, 665 
 Epiphysis cerebri, 775 
 Epispadias, 661 
 Epistaxis, 50, 402 
 Epithelial cysts, 177 
 
 perles, 171 
 Epithelioma, 171 
 
 contagiosum, animal parasites in, 272 
 
 cylindrical, 171 
 
 of choroid plexus, 763 
 
 of penis, 662 
 
 of scrotum, 662 
 
 of thymus gland, 345 
 
 squamous, 171 
 Epulis, 149, 474 
 Equatorial spores, 184 
 Ergot, poisoning by, 26 
 Erythroblasts, 303* 
 Erythrocytes, 298 
 Erythrocytosis, 310 
 Escharotics, action of, 24 
 Esophagitis, catarrhal, 482 
 
 chronic catarrhal, 482 
 
 phlegmonous, 483 
 
 pseudomembranous, 482 
 
 ulcerative, 483 
 Esophagus, anemia of, 482 
 
 carcinoma of, 484 
 
 circulatory disturbances of, 482 
 
 congenital defects of, 482 
 
 dilatation of, 483 
 
 diverticula of, 483 
 
 inflammation of, 482 
 
 passive congestion of, 482 
 
 perforation and rupture of, 484 
 
 stenosis of, 483 
 
 syphilis of, 484 
 
 thrush of, 484 
 
INDEX. 
 
 823 
 
 Esophagus, tuberculosis of, 484 
 
 tumors of, 484 
 Estivo-autumnal fever, parasite of, 268 
 Etat crible, 752 
 
 segmentaire, 364 
 Ether, poisoning by, 29 
 Ethylendianiin, poisoning by, 29 
 Etiology, definition of, 17 
 
 of disease, 18 
 Eustrongylus gigas, 293 
 Exfoliative vaginitis, 653 
 Exogenic neurons, 727 
 Exosporium, 184 
 Exostoses, 130, 698 
 Experimental acid-intoxication, 34 
 
 glycosuria, 38 
 Exposure to general high temperature, 
 
 effects of, 20 
 Exstrophy of bladder, 599 
 External hernia, 499 
 Extra-uterine pregnancy, 650 
 
 Facultative aerobes, 189 
 
 saprophytes and parasites, 189 
 Fallopian tubes, 644 
 anatomy of, 644 
 carcinoma of, 650 
 congenital abnormalities, 644 
 cysts of, 650 
 dilatation of, 645 
 displacement of, 644 
 fibromata of, 649 
 fibromyomata of, 649 
 hematoma of, 645 
 hemorrhages of, 645 
 hyperemia of, 615 
 
 inflammation of, 646. See Salpingitis. 
 lipoma of, 649 
 
 papillomatous elevations of, 649 
 sarcoma of, 650 
 stenosis of, 645 
 
 syncytioma malignum of, 650 
 syphilis of, 649 
 tuberculosis of, 648 
 tumors of, 649 
 False croup, 405 
 neuroma, 154 
 Fat-crystals in urine, 613 
 -embolism, 54 
 
 in fatty infiltration, staining of, 67 
 -necrosis, 94 
 
 of pancreas, 547 
 of body, origin of, 32 
 •splitting ferments, 193 
 Fats, value of, in nutrition, 31, 32 
 Fatty acids, origin of, 34 
 casts, 583 
 
 contracting kidney, 576 
 degeneration, 68. See Degeneration. 
 of arteries, 382 
 of gastric glands, 491 
 of heart, 362 
 of kidney, 587 
 of liver, 526 
 of muscle, 711 
 of prostate, 672 
 of suprarenal bodies, 565 
 
 Fatty degeneration of testicle, 664 
 of uterus, 631 
 of veins, 396 
 infiltration, 66 
 definition of, 66 
 etiology of, 66 
 of bone-marrow, 343 
 of dura mater of cord, 775 
 of heart, 361 
 of kidney, 588 
 of liver, 525 
 of mammary gland, 678 
 of muscles, 711 
 pathologic anatomy of, 66 
 
 physiology of, 67 
 seats of, 67 
 Febris undulans, 264 
 Femoral hernia, 499 
 Fermentation, 193 
 
 thrombosis, 55 
 Ferments, coagulating, 193 
 diastatic, 193 
 effects of, 193 
 emulsifying, 193 
 fat-splitting, 193 
 hydrolytic, 193 
 inverting, 193 
 oxidizing, 193 
 produced by bacteria, 192 
 proteolytic, 193 
 Fetal membranes, 654 
 Fetid bronchitis, 410 
 Fetus in fetu, 180 
 Fever, blood-cbanges in, 42 
 conservative effects of, 43 
 definition of, 41 
 effects of, on bacteria, 43 
 etiology of, 42 
 nature of, 41 
 pathologic results of, 42 
 Fibrin-ferment, poisoning by, 28 
 Fibrinous bronchitis, 411 
 inflammation, 103 
 pericarditis, 376 
 pleuritis, 462 
 pneumonia, 425 
 Fibrinuria, 609 
 
 Fibro-adenoma of bladder, 605 
 Fibroblasts, 111 
 Fibroid of uterus, 632 
 interstitial, 632 
 mural, 632 
 submucous, 632 
 subperitoneal, 632 
 phthisis, 449 
 polyps of uterus, 632 
 Fibroma, 120 
 appearance of, 121 
 definition of, 120 
 etiology of, 120 
 irrtracanalicular, 123 
 mammse nodulum, 122 
 nature of, 123 
 of bladder, 605 
 of bone, 698 
 of brain, 770 
 of choroid plexus, 763 
 
824 
 
 INDEX. 
 
 Fibroma of dura mater, 715 
 of cord, 776 
 
 of Fallopian tubes, 649 
 
 of intestines, 516 
 
 of kidney, 590 
 
 of larynx, 407 
 
 of liver, 536 
 
 of lungs, 457 
 
 of mammary gland, 679 
 intracanalicular, 679 
 
 of mouth, 473 
 
 of muscles, 712 
 
 of ovaries, 640 
 
 of penis, 663 
 
 of peritoneum, 557 
 
 of pleura, 465 
 
 of spleen, 333 
 
 of stomach, 493 
 
 of testicle, 669 
 
 of tooth-pulp, 474 
 
 of vagina, 654 
 
 of vulva, 660 
 
 seats of, 122 
 
 structure of, 123 
 Fibromyonia of Fallopian tubes, 649 
 
 of vulva, 660 
 Fibrosarcoma of ovary, 640 
 Fibrosis, general, 108 
 Fibrous connective tissue, regeneration 
 of, 111 
 
 goiter, 561 
 
 pneumonia, 437 
 peribronchial, 439 
 perivascular, 439 
 pleurogenic, 439 
 secondary, 439 
 Filaria bronchialis, 293 
 
 diurna, 292 
 
 hominis oris, 293 
 
 immitis, 293 
 
 in peritoneum, 558 
 
 labialis, 293 
 
 lentis. 293 
 
 loa, 293 
 
 medinensis, 291 
 
 nocturna, 292 
 
 perstans, 292 
 
 sanguinis hominis, 291 
 in kidney, 595 
 Filariasis, 292 
 
 Filtration, escape of fluid by, 59 
 Fissure, anal, 505 
 Fistula in ano, 510 
 Fixation of blood, 325 
 Flagella of bacteria, 185 
 
 staining of, 188 
 Fleshy moles, 656 
 Fluke-worms, 293 
 Foetus in foetu, 643 
 Follicular cysts of ovary, 640 
 
 enteritis, 504 
 
 tonsillitis, 477 
 
 ulcers of intestine, 505 
 Food, diminished supply of, 31 
 
 increased supply of, effect of, 32 
 
 necessary constituents of, 31 
 Foot-and-mouth disease, 469 
 
 Foreign bodies, changes in tissues around, 
 108 
 in blood, 324 
 in intestine, 520 
 in. larynx, 408 
 in tissues, 19 
 Formative cells, 111 
 Fowl-tuberculosis, 235 
 Fracture, 685 
 comminuted, 685 
 compound, 685 
 repair of, 685 
 Fragilitas ossium, 692 
 Friedreich's ataxia, 797 
 Frog-face, 730 
 
 Fuchsin bodies of cancer, 272 
 Fuchsinopbile granules in fatty degen- 
 eration, 70 
 Fungiform tumors, 118 
 Fungoid tumors, 118 
 Fungus of testicle, benign, 665 
 
 syphilitic, 669 
 
 Furring of tongue, 468 
 
 Fusiform aneurysm, 390 
 
 bronchiectasis, 413 
 
 Galactocele, 682 
 Galactorrhea, 678 
 Gall-bladder, 541 
 
 contraction of, 543 
 
 dilatation of, 543 
 
 dropsy of, 543 
 
 empyema of, 542 
 
 inflammation of, 542 
 
 tumors of, 544 
 Gall-stones, 543 
 
 Ganglia of cranial nerves, disease of, 802 
 Ganglion, 706 
 
 Ganglionar neuroglioma, 769 
 Gangrene, 95 
 
 definition of, 95 
 
 dry, 95 
 
 gaseous, 240 
 
 moist, 96 
 
 of lungs, 442 
 
 of vulva, 660 
 
 primary, 95 
 
 secondary, 95 
 Gangrenous appendicitis, 507 
 
 dysentery, 510 
 
 inflammation, 109 
 
 stomatitis, 469 
 Gaseous gangrene, 240 
 Gastrectasia, 492 
 Gastric glands, atrophy of, 491 
 fatty degeneration of, 491 
 
 mucosa, pigmentation of, 491 
 Gastritis, acute, 486 
 
 chronic, 486 
 
 hypertrophic, 487 
 
 interstitial, 488 
 
 pathologic anatomy of, 486 
 physiology of, 488 
 
 pseudomembranous, 486 
 
 ulcerative, 486 
 Gastro-intestinal tract, diseases of, 467 
 Gastromalacia, 492 
 
INDEX. 
 
 825 
 
 Gastrophthisis, 488 
 Gastroptosis, 492 
 Gelatin as a culture-medium, 190 
 Gelatinous cancer, 174 
 General fibrosis, 108 
 
 pathology, definition of, 17 
 Genital pore of tapeworm, 278 
 Genu valgum, 700 
 
 varum, 700 
 Geographical tongue, 468 
 Germinal cells, 723 
 ^-granules, 301 
 Giant growth of bone, 687 
 Giant-cell sarcoma, 147 
 
 -cells of tuberculosis, 229 
 
 sarcoma of alveolar process of jaw, 474 
 Gibraltar fever, 264 
 Gin-drinker's liver, 530 
 Glanders, 239 
 
 bacillus of, 239. See Bacillus mallei. 
 
 effect on nasal cavities, 403 
 
 of larynx, 407 
 
 of lungs, 456 
 
 of muscles, 712 
 
 of pharynx, 480 
 Glandular carcinoma, 172 
 
 cystomata of ovaries, 640 
 Glans penis, inflammation of, 661 
 Gleet, 617 
 Glioma, 151 
 
 ganglionare. 153 
 
 of eyeball, 153 
 
 of hair, 769 
 
 of spinal cord, 802 
 
 of suprarenal bodies, 566 
 Gliosarcoma of dura mater, 715 
 Gliosis, hypertrophic nodular, 729 
 Globular thrombi, 351 
 Globulinuria, 608 
 Globus pallidus, 725 
 Glomerulonephritis, 572 
 Glossitis, 468, 470 
 
 hemilateral, 471 
 
 parenchymatous, 471 
 Glyceniia, 37 
 Glycogen, formation of, 37 
 
 staining of, 80 
 Glycogenic infiltration, 79. See Infiltra- 
 tion. 
 of kidney, 588 
 Glycosuria, 37, 606 
 
 alimentary, 37 
 
 clinical causes of, 38 
 
 experimental, 38 
 Goiter, 559 
 
 colloid, 561 
 
 definition of, 559 
 
 etiology of, 560 
 
 fibrous, 561 
 
 mechanical effects of, 561 
 
 parenchymatous, 560 
 
 pathologic anatomy of, 560 
 
 secondary changes in, 561 
 
 vascular,' 561 
 Golgi cells, 726 
 Gollasch's mixture, 325 
 Gonococcus of Neisser, 206 
 
 Gonorrhea, 614 
 
 bacteriology of, 206 
 Gonorrheal arthritis, 616 
 
 tenosynovitis, 616 
 
 urethritis, 617 
 Gout, 36 
 
 etiology of, 36 
 
 pathogenesis of, 36 
 
 pathogenic anatomy of, 36 
 Gouty arthritis, 704 
 
 nephritis, 578 
 
 tophi, 36, 704 
 Gram's method of staining bacteria, 187 
 Granular casts, 583 
 Granulations, 107 
 Granule-cell, compound, 584 
 Granules of the leukocytes, 300-302 
 Granuloma fungoides, 149 
 Grape-sugar in blood and urine, 37 
 Graves' disease, 564 
 Grawitz, slumbering cells of, 101 
 Gray hepatization of lung, 428 
 Guanin, 36 
 Gummata, 256 
 
 of bones, 697 
 
 of brain, 768 
 
 of lungs, 454 
 
 of lymphatic glands, 341 
 
 structure of, 227 
 Gymnobacteria, 185 
 
 Hairy polyp, 404 
 
 Hansen bacillus leprae, 235 
 
 Hard papilloma, 158 
 
 Harelip, 467 
 
 Healing by first intention, 107 
 
 by granulations, 107 
 
 by immediate union, 106 
 
 by second intention, 107 
 Heart, 346 
 
 abnormality of position of, 347 
 in size of, 347 
 
 abscess of, 364 
 
 actinomycosis of, 375 
 
 amyloid degeneration of, 360 
 
 anatomic considerations of, 346 
 
 aneurysm of, 374 
 
 atrophy of, 370 
 
 bilocular, 347 
 
 cloudy swelling of, 359 
 
 congenital diseases and deformities of, 
 346 
 
 defective development of, 347 
 
 degenerations of, 359 
 
 development of, 346 
 
 dilatation of, 371 
 
 -diseases, effect of, on circulation, 44 
 
 fatty degeneration of, 362 
 infiltration of, 361 
 
 hyaline degeneration of, 360 
 
 hypertrophy of, 371 
 
 hypoplasia of, 370 
 
 inflammation of, 364 
 
 -muscle, anemia of, 359 
 brown atrophy of, 63 
 hemorrhages in, 359 
 hyperemia of, 359 
 
826 
 
 INDEX. 
 
 Heart, parasites of, 375 
 
 parenchymatous degeneration of, 359 
 
 pathologic physiology of, 348 
 
 segmentation of fibres of, 363 
 
 syphilis of, 375 
 
 thrombi in, 57 
 
 thrombosis of cavities of, 350 
 
 trilocular, 347 
 
 tuberculosis of, 375 
 
 tumors of, 375 
 
 wounds and rupture of, 374 
 Heat-dissipation, 41 
 
 effect of, on growth of bacteria, 189 
 
 in etiology of disease, 20 
 
 local excess of, effect of, 20 
 
 -production, 41 
 Hemangioma, 132 
 
 appearance and seats of, 133 
 
 definition of, 132 
 
 etiology of, 133 
 
 nature of, 135 
 
 of mouth, 473 
 
 structure of, 133 
 Hematemesis, 51 
 Hematoblast, 302 
 Hematocele, retro-uterine, 624 
 Hematochromatosis, 502 
 
 of liver, 525 
 
 of pancreas, 547 
 Hematochyluria, 292, 610 
 Hematogenic albumosuria, 608 
 
 pneumonia, 425 
 purulent, 441 
 
 tuberculosis, 451 
 Hematogenous pigmentation, 85, 87 
 
 local, 86 
 Hematoidiu in urine, 613 
 
 pigmentation by, 85 
 Hematoma, definition of, 51 
 
 of Fallopian tube, 645 
 
 of vulva, 659 
 Hematomyelia, 787 
 Hematosalpinx, 648 
 Hematozoon malaria?, 267 
 Hematuria, 609 
 Hemicrania, 728 
 Hemilateral glossitis. 471 
 Hemispheres, cerebral, anatomy of, 725 
 Hemocytolysis, 309 
 Hemofuscin, pigmentation by, 85 
 Hemoglobin in urine, 613 
 
 -derivatives, pigmentation by, 85 
 Hemoglobinemia, 309 
 Hemoglobinuria, 609 
 
 from extensive burns, 20 
 
 paroxysmal, 609 
 Heinokonise, 304 
 Hemolysis, 95, 309 
 Hemopericardium, 376 
 Hemophilia, 50 
 Hemoptysis, 51 
 Hemorrhage, 48 
 
 arterial, 48 
 
 capillary, 48 
 
 causes of, 49, 262 
 
 cerebral, 747 
 ive, 748 
 
 Hemorrhage, cerebral, punctate, 747 
 
 classification of, 50 
 
 due to disease of blood-vessels, 50 
 
 from increase of blood-pressure, 50 
 
 neuropathic, 50 
 
 of bladder, 600 
 
 of bone, 688 
 
 of bronchi, 409 
 
 of choroid plexus, 762 
 
 c.f decidua, 656 
 
 of dura mater, 713 
 of cord, 775 
 
 of Fallopian tubes, 645 
 
 of heart-muscle, 359 
 
 of intestines, 503 
 
 of joints, 700 
 
 of kidney, 569 
 
 of larynx, 404 
 
 of lungs, 417 
 
 of mammarv gland, 677 
 
 of mouth, 468 
 
 of muscles, 707 
 
 of nerves, 808 
 
 of ovary, 638 
 
 of pancreas, 546 
 
 of pericardium, 376 
 
 of peritoneum, 551 
 
 of pharynx, 475 
 
 of pia, 715 
 
 of pituitary body, 773 
 
 of spinal cords, 786 
 
 of spleen, 328 
 
 of stomach, 485 
 
 of suprarenal bodies, 566 
 
 of uterus, 624 
 
 of vagina, 653 
 
 parenchymatous, 48 
 
 per diabrosin, 50 
 
 per diapedesim, 48 
 
 per rhexin, 48 
 
 results of, 51 
 
 ti'aumatie. 50 
 
 venous, 48 
 Hemorrhagic diathesis, 50 
 
 diseases, bacteriology of, 262 
 
 infarcts, 51, 53 
 of lungs. 417 
 
 inflammation, 109 
 
 myositis, 707 
 
 pachymeningitis, 713 
 
 pericarditis, 378 
 
 pleuritis, 464 
 
 vaginitis testis, 667 
 Hemorrhoids, 503 
 Hemosiderin, pigmentation by, 85 
 Hemothorax, 460 
 Hepatitis. 529 
 
 interstitial, acute, 529 
 chronic, 530 
 
 parenchymatous, 529 
 Hepatization of lung, 427 
 gray, 428 
 .red, 427 
 Heredity as a factor in etiology of carci- 
 noma, 165 
 
 as a predisposing factor in disease, 18 
 
 direct, 18 
 
INDEX. 
 
 827 
 
 
 Heredity, immediate, 18 
 
 polymorphous, 36 
 
 remote, 18 
 Jlernia, 499 
 
 diaphragmatic, 499 
 
 direct, 499 
 
 etiology of, 499 
 
 external, 499 
 
 femoral, 499 
 
 indirect, 499 
 
 inguinal, 499 
 
 internal, 499 
 
 irreducible, 500 
 
 pathologic anatomy of, 499 
 
 reducible, 500 
 
 retroperitoneal, 499 
 
 strangulated, 500 
 Herpetic angina, 475 
 
 laryngitis, 405 
 Heteroplastic osteoma, 131 
 Heterotopia of gray matter of spinal 
 
 cord, 780 
 Hexathyridium pinguicola, 296 
 
 venarum, 296 
 Hippuric acid in urine, 612 
 Hirudo ceylonica, 296 
 
 vorax, 296 
 Hodgkin's disease, 137, 323 
 Horseshoe kidney, 567 
 Housemaid's knee, 706 
 Hutchinson's teeth, 259, 474 
 Hyaline cast, 582 
 
 degeneration, 74. See Degeneration. 
 of arteries, 382 
 of brain, 743 
 of heart, 360 
 of lymphatic glands, 335 
 of muscles, 711 
 of spleen, 332 
 Hydatid moles, 658 
 Hydatids of Morgagni, 650 _ 
 Hydremia, 307 
 Hydrocele, 664, 666 
 
 funiculi cystica, 667 
 spermatid, 667 
 
 processus vaginalis, 667 
 
 spermatica, 666 
 Hydrocephalus, 764 
 
 acquired, 764 
 
 acute, 720 
 
 acquired internal, 766 
 
 chronic, 766 
 
 congenital, internal, 764 
 
 external, 766 
 
 partial, 766 
 Hydrofluoric acid, poisoning by, 24 
 Hydrogen-sulphid poisoning, 28 
 Hydrolytic ferments, 193 
 Hydrometra, 622 
 Hydronephrosis, 596 
 Hydrops articulorum, 702 
 
 ex vacuo, 716 
 
 omenti, 552 
 Hydromyelia, 781 
 Hydropericardium, 376 
 
 chylous, 376 
 -Hydrophobia, bacteriology of, 262 
 
 Hydrorrhachus, 781 
 Hydrorrhoea gravidarum, 655 
 Hydrosalpinx, 648 
 Hydrothionuria, 607 
 Hydrothorax, 461 
 Hygroma, congenital cystic, 132 
 
 durae matris, 714 
 
 of pia, 716 
 Hyperchromatosis, 97 
 Hyperemia, active, 46 
 
 arterial, 46 
 
 collateral, 46 
 
 local, 46 
 
 neuroparalytic, 46 
 
 neurotic, 46 
 
 of bladder, 600 
 
 of bone, 688 
 
 of brain, 746 
 
 of dura mater, 713 
 
 of Fallopian tubes, 645 
 
 of heart-muscle, 359 
 
 of joints, 700 
 
 of kidneys, 569 
 
 of liver, 522 
 
 of mammary gland, 676 
 
 of mouth, 468 
 
 of muscles, 707 
 
 of nerves, 803 
 
 of pericardium, 376 
 
 of pia, 715 
 
 and arachnoid of cord, 777 
 
 of pituitary body, 773 
 
 of pleura, 460 
 
 of spinal cord, 785 
 
 of spleen, 328 
 
 of testicle, 664 
 
 of uterus, 623 
 passive, 623 
 
 of vagina, 653 
 
 of vulva, 659 
 
 passive, 46 
 
 venous, 46 
 Hyperglycemia, 38 
 Hyperinosis, 306 
 Hyperplasia, 114 
 
 of deciduse, 657 
 
 of mucous membrane of uterus, 631 
 
 of spleen, 331 
 Hyperplastic perihepatitis, 556 
 Hyperthyroidism, 564 
 Hypertonicity of the blood-serum, 306 
 Hypertrophic cirrhosis of liver, 532 
 
 enlargement, 114 
 
 gastritis, 487 
 
 nodular gliosis, 729 
 
 sclerosis of brain, 740 
 Hypertrophy, 113 
 
 definition of, 113 
 
 etiology of, 114 
 
 numerical, 114 
 
 of arteries, 381 
 
 of bone, 687 
 
 of bone-marrow, 344 
 
 of cervix uteri, 631 
 
 of heart, 371 
 
 with dilatation, 372 
 
 of kidney, 586 
 
828 
 
 INDEX. 
 
 Hypertrophy of liver, 534 
 
 of lungs, 419 
 
 of lymphatic glands, 334 
 
 of mammary gland, 678 
 
 of muscles, 706 
 
 of pituitary body, 772 
 
 of prostate, 672 
 
 of testicle, 664 
 
 of uterus, 631 
 
 pathologic anatomy of, 114 
 physiology of, 114 
 
 simple, 114 
 
 true, 114 
 Hypiuosis, 306 
 Hypochromatosis, 97 
 Hypoleukocytosis, 312 
 Hypophysis cerebri, 771. See also Pitui- 
 tary body. 
 Hypoplasia, definition of, 62 
 
 of arteries, 381 
 
 of bone, 692 
 
 of cerebellum, 730 
 
 of cerebral hemispheres, 729 
 
 of heart, 347, 370 
 Hypospadias, 661 
 Hypostatic congestion, 44 
 of lungs, 416 
 
 pneumonia, 431, 434 
 Hypoxauthin, 36 
 
 Icterus, 544. See Jaundice. 
 
 seu febris amantium, 316 
 Ileitis, 506 
 
 Ileum, inflammation of, 506 
 Ileus, 500 
 
 Immediate heredity, 18 
 Immunity, 197 
 
 absolute, 197 
 
 acquired, 197 
 
 active, 197 
 
 mechanism of, 198 
 
 natural, 197 
 
 passive, 197 
 
 relative, 197 
 
 toxin-, 199 
 
 varieties of, 197 
 Inanition, 31 
 Indicanuria, 607 
 Indigestion, 488 
 Indigo in urine, 613 
 Indirect cell-division, 110 
 Indolent ulcer, 105 
 Infarction, 53, 684' 
 Infarcts, anemic, 53 
 
 formation of, 53 
 
 hemorrhagic, 53 
 
 placental, 656 
 
 pulmonary, 54 
 
 subsequent changes in, 54 
 
 white, 53 
 Infection, 196 
 Infectious disease, definition of, 30 
 
 embolism, 54 
 
 emphysema, 244 
 bacillus of, 245 
 
 leukocytosis, 310 
 Infiltrating tumors, 118 
 
 Infiltration, albuminous, 64 
 
 calcareous, of arteries, 382 
 
 defined, 64 
 
 dropsical, 80 
 
 fatty, 66. See Fatty infiltration. 
 
 glycogenic, 79 
 definition of, 79 
 etiology of, 80 
 pathologic anatomy of, 80 
 
 physiology of, 80 
 of kidney, 588 
 
 inflammatory, 101 
 
 lymphoid, 137 
 
 medullary, of lymphoid structures of 
 intestine, 512 
 
 uratic, 83 
 Inflammation, 98 
 
 as a cause of necrosis, 90 
 
 changes in the blood-vessels in, 99 
 
 chemotactic action in, 100 
 
 chronic, 105 
 
 definition of, 98 
 
 degenerative changes in tissues in, 101 
 
 diphtheritic, 103 
 
 edematous, 103 
 
 etiology of, 102 
 
 exudation in, 99 
 
 fibrinous, 103 
 
 gangrenous, 109 
 
 hemorrhagic, 109 
 
 historical views of, 98 
 
 interstitial, 106 
 
 necrotic, 109 
 
 of appendix vermiformis, 507. See 
 Appendicitis. 
 
 of arachnoid, 716 
 spinal, 777 
 
 of arteries, 383 
 
 of biliary ducts, 547. See Cholangitis. 
 
 of bladder, 600. See Cystitis. 
 
 of bone, 688 
 
 of bone-marrow, 344 
 
 of brain, 753. See, also, Encephalitis. 
 
 of bronchi, 409 
 
 of bursaj, 706 
 
 of cavernous bodies of penis, 661 
 
 of cecum, 506 
 
 of colon, 509 
 
 of decidua, 656 
 
 of duodenum, 506 
 
 of dura mater, 713 
 
 of epididymis, 664 
 
 of Fallopian tubes, 646. See Salpingitis. 
 
 of gall-bladder, 542 
 
 of ileum, 506 
 
 of intestines, 504 
 
 of joints, 701. See Arthritis. 
 
 of kidney, 570. See Nephritis. 
 
 of larynx, 405 
 
 of liver, 529. See Hepatitis. 
 
 of lungs. 425 
 I of lymphatic glands, 336 
 I of lymphatic vessels, 399 
 i of mammarv gland, 677 
 j of mouth, 468 
 I of muscles, 707. See Myositis. 
 ! of nasal cavities, 402 
 
INDEX. 
 
 829 
 
 ^Inflammation of nerve, 806. See Neuritis. 
 
 of ovaries, 639 
 
 of pancreas, 548 
 
 of pelvis of kidney, 596 
 
 of pericardium, 376 
 
 of peritoneum, 553. See Peritonitis. 
 
 of pharynx, 475 
 
 of pia, 716 
 of cord, 777 
 
 of pituitary body, 773 
 
 of placenta, 656 
 
 of pleura, 461 
 
 of prostate gland, 671 
 
 of pulp of teeth, 474 
 
 of rectum, 509 
 
 of salivary glands, 481 
 
 of seminal vesicles, 675 
 
 of spinal cord, 787. See Myelitis and 
 Poliomyelitis. 
 
 of spleen, 329 
 
 of suprarenal bodies, 566 
 
 of tendon-sheaths, 706 
 
 of testicle, 664. See Orchitis. 
 
 of thoracic duct, 401 
 
 of thymus gland, 345 
 
 of thyroid gland, 559 
 
 of thyroid plexus, 762 
 
 of trachea, 408 
 
 of ureter, 597 
 
 of urethra, 614 
 
 of uterus, 624 
 
 •of vagina, 653. See Vaginitis. 
 
 of vas deferens, 667 
 
 of veins, 396 
 
 of vulva, 659 
 
 parenchymatous, 106 
 
 phenomena in, 98 
 
 productive, 105 
 
 proliferative changes in, 101 
 
 resolution after, 109 
 
 round-cell, 101 
 
 serous, 103 
 
 special forms of, 102 
 
 suppurative, 104 
 
 theories of, 98 
 Inflammatory edema, 60 
 
 infiltration, 101 
 
 leukocytosis, 310 
 
 osteoporosis, 691 
 Influenza, 252 
 
 bacillus of, 252 
 Inguinal hernia, 499 
 Inhibitory action of bodily fluids, 198 
 Inoculation of culture-media, 191 
 Insects, venom of, poisonous effects of, 27 
 Insufficiency of heart-valves, 357 
 Intermediary callus, 687 
 Internal hernia, 499 
 Interstitial appendicitis, 507 
 
 emphysema of lungs, 419 
 
 gastritis, 488 
 
 hepatitis, acute, 529 
 chronic, 530 
 
 inflammation, 106 
 
 nephritis, 571 
 acute, 573 
 chronic, 577 
 
 Interstitial neuritis, acute, 806 
 chronic, 807 
 
 hypertrophic, 808 
 
 pregnancy, 650 
 
 uterine fibroids, 632 
 Intestinal obstruction, 500 
 Intestines, 497 
 
 abnormalities of, 497 
 
 absence of parts of, 497 
 
 actinomycosis of, 516 
 
 active hyperemia of, 503 
 
 adenoma of, 516 
 
 amyloid degeneration of, 502 
 
 anthrax of, 515 
 
 atrophy of mucosa of, 502 
 
 carcinoma of, 518 
 
 circulatory disturbances of, 503 
 
 congenital abnormalities of position of, 
 498 
 
 congenital enlargement of, 498 
 
 dilatation of, 498 
 
 distortion of, 497 
 
 diverticula of, 498 
 
 edema of. 503 
 
 embolism of, 503 
 
 fibroma of, 516 
 
 follicular ulcers of, 505 
 
 foreign bodies in, 520 
 
 hemorrhage of, 503 
 
 infectious diseases of, 510 
 
 inflammatory papilloma of, 516 
 
 internal strangulation of, 500 
 
 invagination of, 501 
 
 lipoma of, 516 
 
 myoma of, 518 
 
 myxoma of, 516 
 
 narrowing of, 497, 498 
 
 obstruction of, 500 
 
 parasites of, 519 
 
 passive hyperemia of, 503 
 
 peptic ulcer of, 505 
 
 pigmentation of, 502 
 
 rupture of, 520 
 
 sarcoma of, 516 
 
 stenosis of, 498 
 
 submucous abscess, 505 
 
 syphilis of, 515 
 
 thrombosis of, 503 
 
 tuberculosis of, 514 
 
 tumors of, 516 
 
 ulceration of, 505 
 Intoxication, 196 
 
 as a cause of necrosis, 90 
 Intracanalicular fibroma, 123 
 of mammary gland, 679 
 Intussusception, 501 
 Invagination of intestine, 501 
 Invasion diseases, definition of, 31 
 Inversion of uterus, 622 
 Inverting ferments, 193 
 Involution-forms of bacteria, 185 
 Iron-particles, pigmentation by, 83 
 Irreducible hernia, 500 
 Irregular pneumonias, 210 
 Ischemia, 47 
 
 Isotonicity of red blood-corpuscle, altera- 
 tions of, 305 
 
830 
 
 INDEX. 
 
 Jaundice, 544 
 
 catarrhal, 544 
 
 etiology of, 544 
 
 pathologic anatomy of, 545 
 Joints, ankylosis of, 700 
 
 cold abscess of, 705 
 
 diseases of, 700 
 
 distortion of, 700 
 
 dropsy of, 701 
 
 hemorrhage into. 700 
 
 hyperemia of, 700 
 
 inflammation of, 701. See Arthritis. 
 
 luxation of, 700 
 
 syphilis of, 705 
 
 tuberculosis of, 704 
 
 tumors of, 706 
 
 Kaeyokinesis, 110 
 
 abnormal, 97 
 
 asymmetric, 97 
 
 multipolar, 97 
 Karyokinetic figures in erythroblasts, 
 
 305 
 Karyomitosis, 110 
 Karyorrhexis, 97 
 Keloids, 120 
 Kidney, 567 
 
 adenoma of, 591 
 congenital, 591 
 papuliferous cystic, 592 
 
 amyloid degeneration of, 588 
 
 anemia of, 568 
 
 atrophy of, 585 
 
 bacteria in, 594 
 
 calcification of, 588 
 
 carcinoma of, 592 
 
 circulatory disturbances of, 568 
 
 cloudy swelling of, 586 
 
 congenital anomalies of, 5117 
 
 cyanotic induration of, 569 
 
 cysts of, 592 
 
 degenerations of, 586 
 
 echinococcus-cyst of, 595 
 
 edema of, 569 
 
 embolism in, 570 
 
 fatty contracting, 576 
 degeneration of, 587 
 infiltration of, 588 
 
 fibromata of, 590 
 
 glycogenic infiltration of, 588 
 
 hemorrhages in, 569 
 
 horseshoe-, 567 
 
 hyperemia of, 569 
 
 hypertrophy of, 586 
 
 inflammation of, 570. See Nephritis. 
 
 large white, 575 
 
 leiomyoma of, 590 
 
 lipomata of, 590 
 
 lymphomatous infiltrations of, 592 
 
 malpositions of, 568 
 
 parasites of, 594 
 
 parenchymatous degeneration of, 586 
 
 pelvis of. See Pelvis of kidney. 
 
 red granular, 578 
 
 rhabdomyosarcoma of, 591 
 
 sarcoma of, 591 
 
 syphilis of, 590 
 
 Kidney, thrombosis in 570 
 
 tuberculosis of, 590 
 
 tumors of, 590 
 Klebs-Lofller bacillus, 211 
 Knock-knee, 700 
 Kobelt, cysts of, 644 
 
 Koch's laws for etiologic importance of 
 bacteria, 30 
 
 stain for tubercle-bacillus, 225 
 
 tuberculin, 234 
 
 Lactic acid, excessive formation of, in 
 
 body, 34 
 Lactosuria, 607 
 Lacunar tonsillitis, 477 
 Laennec's cirrhosis of liver, 530 
 Langhan's cells, 176 
 Large white kidney, 575 
 Laryngitis, acute catarrhal, 405 
 
 chronic catarrbal, 405 
 
 croupous, 406 
 
 diphtheritic, 406 
 
 edematous, 405 
 
 herpetic, 405 
 Larynx, anatomic considerations of, 404 
 
 anemia of, 404 
 
 carcinoma of, 402 
 
 congenital abnormalities of, 404 
 
 echinococcus cysts of, 408 
 
 edema of, 404 
 
 fibroma of, 407 
 
 foreign bodies in, 408 
 
 glanders of, 407 
 
 hemorrhages in, 404 
 
 hyperemia of, 404 
 
 inflammation of, 405 
 
 lepra of, 407 
 
 lupus of, 406 
 
 mucous polyps of, 407 
 
 papilloma of, 407 
 
 parasites of, 408 
 
 syphilis of, 406 
 
 tuberculosis of, 406 
 
 tumors of, 407 
 Latent tuberculosis, 233 
 Lateral ventricles of brain, 725 
 
 thrombus, 56 
 Laveran's malarial parasite, 268 
 Lead, poisoning by, 26 
 Lecithin in fatty degeneration, 70 
 
 infiltration, 67 
 Leiomvoma, 154 
 
 of kidney, 590 
 
 of uterus, 632 
 Leontiasis leprosa, 236 
 
 ossium, 691 
 Lepra, 235. See also Leprosy. 
 
 affections of nasal cavities in, 403 
 
 -cell, 238 
 
 gangrenosa, 237 
 
 mutilans, 236 
 
 of bone, 698 
 
 of larynx, 407 
 
 of pharynx, 480 
 
 of testicle, 669 
 Leproma, 237 
 Leprosy, 235. See also Lepra. 
 
INDEX. 
 
 831 
 
 Leprosy, antitoxin of, 238 
 
 anesthetic, 236 
 
 bacillus of, 235 
 
 etiology of, 235 
 
 of liver, 536 
 
 of nerves, 809 
 
 pathologic anatomy of, 236 
 physiology of, 238 
 
 structure of lesions of, 237 
 
 tubercular, 236 
 Leptomeningitis, 716 
 
 spinal, 777 
 Leucin in urine, 35, 613 
 Leukemia, 319 
 
 acute, 323 
 
 blood in, 321 
 
 lienoniedullary, 322 
 
 lymphatic, 322 
 
 pathologic physiology of, 323 
 Leukemic lymphadenoma, 138 
 Leukocytes, 298 
 
 chemical composition of, 302 
 
 emigration of, in inflammation, 100 
 
 large mononuclear, 299 
 
 number of, 302 
 
 origin of, 303 
 
 pathologic changes in, 305 
 
 polynuclear, 300 
 
 proportion of different forms of, 302 
 
 small mononuclear, 299 
 
 transitional, 299 
 
 various forms of, 299 
 Leukocytic casts, 582 
 Leukocytosis, 310 
 
 cachectic, 311 
 
 infectious, 310 
 
 inflammatory, 310 
 
 medicinal, 311 
 Leukolysis, 312 
 Leukonuclein, 302 
 Leukopenia, 312 
 Leukoplakia, 468 
 Leydenia gemmipara, 558 
 Lienomedullary leukemia, 322 
 Light, effect of, on growth of bacteria, 
 
 189 
 Lipaciduria, 607 
 Lipemia, 308 
 Lipoma, 125 
 
 appearance of, 125 
 
 etiology of, 125 
 
 nature of, 126 
 
 of bone, 698 
 
 of choroid plexus, 763 
 
 of dura mater of cord, 776 
 
 of Fallopian tubes, 649 
 
 of intestines, 516 
 
 of kidney, 590 
 
 of liver, 536 
 
 of lungs, 457 
 
 of mammary gland, 679 
 
 of mouth, 473 
 
 of muscles, 712 
 
 of penis, 663 
 
 of peritoneum, 557 
 
 of pia and arachnoid, 723 
 
 of pleura, 465 
 
 Lipoma of stomach, 493 
 
 of vulva, 660 
 
 seats of, 126 
 
 structure of, 126 
 Lipomatosis, 125 
 
 of mammary gland, 678 
 Lipuria, 610 
 Liquefaction-necrosis, 92 
 
 definition of, 92 
 
 pathologic anatomy of, 93 
 Liquid blood-serum as a culture-medium, 
 
 190 
 Liquids of the tissues, alterations of, 
 
 cause edema, 60 
 Lithopedion, 651 
 Liver, 521 
 
 abscess of, 529 
 
 acute yellow atrophy of, 527 
 
 adenoma of, 537 
 
 amyloid degeneration of, 528 
 
 anatomic considerations, 521 
 
 anemia of, 522 
 
 angioma of, 536 
 
 atrophy of, 524 
 localized, 525 
 
 carcinoma of, 537 
 secondary, 538 
 
 changes of position of, 521 
 
 circulatory disturbances of, 522 
 
 cirrhosis of, 530 
 atrophic, 530 
 biliary, 533 
 hypertrophic, 532 
 Laennec's, 530 
 
 cloudy swelling of, 526 
 
 complete absence of, 521 
 
 cyanotic induration of, 522 
 
 cysts of, 539 
 
 dropsical infiltration of, 528 
 
 embolism of, 523 
 
 fatty degeneration of, 526 
 infiltration of, 525 
 
 fibromata of, 536 
 
 -fluke, 294 
 
 gin-drinkers', 530 
 
 hyperemia of, 522 
 
 hypertrophy of, 534 
 
 infectious diseases of, 534 
 
 inflammations of, 529 
 
 leprosy of, 536 
 
 lipomata of, 536 
 
 lymphadenoma of, 536 
 
 malformations of, 521 
 
 myomata of, 536 
 
 nutmeg-, 522 
 
 parasites of, 539 
 
 parenchymatous degeneration of, 526 
 
 pigmentation of, 525 
 
 red atrophy of, 522 
 
 relation of, to diabetes, 39 
 
 rupture of, 534 
 
 sarcoma of, 536 
 
 syphilis of, 534 
 
 thrombosis of, 523 
 
 tuberculosis of, 534 
 
 tumors of, 536 
 Lobar pneumonia, 425. See Pneumonia. 
 
832 
 
 INDEX. 
 
 Lobar sclerosis of brain, 758 
 Lobular pneumonia, 430 
 Local anemia, 47 
 
 hyperemia, 46 
 Locomotor ataxia, 793 
 Lofner's blood-serum, 191 
 
 methylene-blue, 187 
 Lopbotrichous bacteria, 185 
 Ludwig's angina, 477, 481 
 Lungs, actinomycosis of, 456 
 
 active hyperemia of, 415 
 
 anatomic considerations, 414 
 
 anemia of, 415 
 
 atrophy of, 419 
 
 carcinoma of, 458 
 
 collateral hyperemia of, 415 
 
 congenital defects of, 415 
 
 congestion of, 415 
 
 cyanotic induration of, 417 
 
 cysts of, 459 
 
 edema of, 417 
 
 embolism of, 419 
 
 emphysema of, 419 
 
 gangrene of, 1 12 
 
 glanders of, 456 
 
 hemorrhage of, 417 
 
 hemorrhagic infarcts of, 417 
 
 hypostatic congestion of, 416 
 
 hypertrophy of, 419 
 
 inflammation of, 425 
 
 parasites of, 459 
 
 passive hyperemia of, 416 
 
 sarcoma of, 457 
 
 syphilis of, 454 
 
 tuberculosis of, 443 
 
 tumors of, 457 
 Lupus vulgaris, 233 
 Lustgarten's bacillus, 254 
 Luxation of joints, 700 
 Lymphadenia ossea, 699 
 
 paniciosa, 320 
 Lymphadenitis, 336 
 
 "acute, 336 
 
 chronic, 337 
 
 suppurative, 336 
 Lymphadenoma, 135, 332, 341 
 
 aleukemic, 138 
 
 appearance and seats of, 135 
 
 etiology of, 135 
 
 leukemic, 138 
 
 nature of, 137 
 
 of liver, 536 
 
 of mouth, 473 
 
 structure of, 137 
 Lymphangiectasia, 399 
 
 acquired, 400 
 Lymphangioma, 132 
 
 cavern osum, 132 
 
 of brain, 771 
 
 of mouth, 473 
 
 of spleen, 333 
 Lymphangitis, 399 
 
 purulent, 442 
 Lymphatic anemia, 137 
 
 circulation, obstruction of, a cause of 
 edema, 61 
 
 glands, amyloid degeneration of, 334 
 
 | Lymphatic glands, anatomic considera- 
 tions, 334 
 anthracosis of, 336 
 atrophy of, 334 
 calcification of, 335 
 carcinoma of, 343 
 diseases of, 335 
 fatty infiltration of, 334 
 hyaline degeneration of, 335 
 hypertrophy of, 334 
 inflammation of, 336 
 necrosis of, 335 
 pigmentation of, 335 
 sarcoma of, 343 
 syphilis of, 341 
 tuberculosis of, 338 
 tumors of, 341 
 leukemia, 322 
 
 vessels, anatomic considerations, 399 
 dilatation of, :!!»!) 
 inflammation of, 399 
 parasites of, 401 
 syphilis of, 400 
 tuberculosis of, 400 
 tu mors of, 400 
 Lymphemia, 321 
 Lymph -formation, causes of, 59 
 Lymphocytes, 299 
 Lymphogenic tuberculosis, 453 
 Lymphoid infiltration, 137 
 
 'tubercle, 229 
 Lymphoma, 135 
 
 malignant, 135 
 Lymphomatous infiltration of kidney, 592 
 Lymphorrhea, 132 
 Lymphosarcoma, 135, 143, 332, 341 
 of mouth, 473 
 of pituitary body, 774 
 of stomach", 493 ' 
 of thymus gland, 345 
 
 Macrocephaly, 728 
 Macrochilia, 132, 400, 473 
 Macroglossia, 132, 400, 473 
 Madura-foot, 250 
 Malaria, hematozoon of, 267 
 irregular, parasite of, 268 
 Malarial hematozoa, 267 
 parasites, 267 
 staining of, 326 
 Male breast, abnormal development of, 
 
 676 
 Malignant edema, 240 
 bacillus of, 240 
 endocarditis, 354 
 lymphoma, 135 
 pustule, 242 
 Mallein, 240 
 Malta fever, 264 
 
 micrococcus of, 264 
 Malum coxae senilis, 702 
 Mamma. See Mammary gland. 
 Mammary gland, 676 
 adenoma of, 680 
 atrophy of, 678 
 carcinoma of, 680 
 chondroma of, 680 
 
INDEX. 
 
 833 
 
 Mammary gland, congenital abnormali- 
 ties of, 676 
 
 cysts of, 682 
 
 fatty infiltration of, 678 
 
 fibroma of, 679 
 
 hemorrhages of, 677 
 
 hyperemia of, 676 
 
 hypertrophy of, 678 
 
 inflammation of, 677 
 
 lipoma of, 679 
 
 lipomatosis of, 678 
 
 myoma of, 680 
 
 myxoma of, 680 
 
 myxomatous degeneration of, 678 
 
 osteoma of, 680 
 
 sarcoma of, 680 
 
 supernumerary, 676 
 
 syphilis of, 678 
 
 tuberculosis of, 678 
 
 tumors of, 679 
 Marantic thrombi, 55 
 Margarin-crystals in fatty infiltration, 67 
 Marrow-cells, 343 
 Massive cerebral hemorrhage, 748 
 Mast-cells, 300 
 Mast-cell granules, 301 
 Mastitis, acute, 677 
 
 chronic, 677 
 Measles, animal parasites of, 274 
 
 bacteriology of, 261 
 Mechanical agents as causes of necrosis, 
 
 90 
 Meckel's diverticulum, 498 
 Medicinal leukocytosis, 311 
 Mediterranean fever, 264 
 Medullary carcinoma, 172 
 
 infiltration of lymphoid structures of 
 intestine, 512 
 Megaloblasts, 304 
 Megalocytes, 303 
 Megastoma entericum, 276 
 Melsena neonatorum, 486 
 Melanemia, 308 
 Melanin, pigmentation by, 85 
 Melanosarcoma, 145 
 Melanuria, 608 
 Membranes of brain, diseases of, 713 
 
 of spinal cord, 775 
 Meningitis, epidemic cerebrospinal, 718 
 
 tuberculous, 719 
 Meningocele, 728 
 Menorrhagia, 51, 624 
 Menstruation, 623 
 Mercury, poisoning by, 26 
 Mesarteritis, 383 
 Mesencephalon, 724 
 Mesophilic bacteria, 189 
 Metabolic pigmentation, 88 
 Metabolism, disorders of, 31 
 
 in diabetes, 39 
 Metachromatic bodies, 184 
 Metaplasia, 113 
 
 Metastatic abscesses, production of, 54 
 Methemoglobin in urine, 613 
 Metritis, 624 
 acute, 627 
 chronic, 628 
 53 
 
 Metrorrhagia, 51, 624 
 
 Metschnikow's theory of phagocytosis, 
 
 198 
 Miasmatic disease, definition of, 30 
 Microblasts, 304 
 Microcephaly, 729 
 Micrococcus, 183 
 
 exanthematicus, 262 
 
 Maltensis, 264 
 
 tetragenus, 205 
 
 urese in urine, 610 
 Microcytes, 303 
 Micromyelia, 780 
 Microspira, 183 
 
 Migula's classification of bacteria, 183 
 Miliary aneurysm, 390 
 of brain, 744 
 of spinal cord, 785 
 
 tubercles, 227, 232 
 Milk as a culture-medium, 190 
 
 -spots, 378 
 Miner's elbow, 706 
 Mixed tumors, 129, 149 
 Moist gangrene, 96 
 Moles, fleshy, 656 
 
 hydatid, 658 
 Molluscum-bodies, 273 
 
 contagiosum, animal parasites of, 272 
 Mononuclear leukocytes, 299 
 Monostoma lentis, 296 
 Monotrichous bacteria, 185 
 Morbid anatomy, definition of, 17 
 Morbus cteruleus, 348 
 Morphin, poisoning by, 29 
 Mother-wreath, 111 
 Mouth, anemia of, 467 
 
 circulatory disturbances of, 467 
 
 congenital abnormalities of, 467 
 
 hemorrhages of, 468 
 
 hyperemia of, 467 
 
 inflammation of, 468 
 
 syphilis of, 472 
 
 tuberculosis of, 471 
 
 tumors of, 473 
 Movable spleen, 327 
 
 Mucin, hypersecretion of, distinguished 
 from mucoid degeneration, 76 
 
 nature of, 76 
 
 staining of, 77 
 Mucoid degeneration, 76. See Degenera- 
 tion. 
 of bone-marrow, 343 
 Mucopurulent catarrh, 105 
 
 cystitis, 601 
 Mucous colitis, 509 
 
 patch, 256, 257 
 
 polyps of larynx, 407 
 Mulberry calculi, 603 
 Multiple sclerosis of brain, 759 
 Multipolar karyokinesis, 97 
 Mumps, 481 
 
 bacteriology of, 261 
 Mural endocarditis, 352 
 
 fibroids, 632 
 Muscarin, poisoning by, 29 
 Muscles, actinomycosis of, 712 
 
 amyloid degeneration of, 711 
 
834 
 
 INDEX. 
 
 Muscles, anemia of, 707 
 anthrax of, 712 
 
 atrophy and degeneration of, 709 
 calcification of, 711 
 carcinoma of, 713 
 chondroma of, 712 
 coagulation-necrosis of, 711 
 congenital malformations, 706 
 diseases of, 706 
 emholism of, 707 
 fatty degeneration of, 711 
 
 infiltration of, 711 
 fibromata of, 712 
 glanders of, 712 
 hemorrhages of, 707 
 hyaline degeneration of, 711 
 hyperemia of, 707 
 hypertrophy of, 706 
 inflammation of, 707. See Myositis. 
 lipomata of, 712 
 myxomata of, 712 
 osteoma of, 712 
 parasitic diseases of, 713 
 parenchymatous degeneration of, 711 
 rhabdomyomata of, 712 
 sarcoma of, 712 
 syphilis of, 712 
 thrombosis of, 707 
 tuberculosis of, 712 
 tumors of, 712 
 Muscular atrophy, myopathic, 710 
 neuropathic, 709 
 progressive, 710 
 pseudohypertrophic, 711 
 simple, 711 
 Mycetoma, 250 
 Mycophylaxins, 201 
 Mycoprotein, 186 
 Mycosis aspergillina, 413 
 
 fungoides, 149 
 Mycosozins, 201 
 Mycotic endocarditis, 354 
 Mydalein, poisoning by, 29 
 Mydatoxin, poisoning by, 29 
 Myelinic neuroma, 154 
 Myelitis, 787 
 
 hematogenous purulent, 788 
 
 pressure-, 790 
 
 secondary to purulent leptomeningitis 
 
 788 
 transverse, secondary to injury or in- 
 fectious disease, 789 
 Myelocytes, 300 
 Myelogenous callus, 686 
 
 osteosarcoma, 148 
 Myeloid sarcoma, 147 
 Myeloma, 699 
 Myelomeningocele, 781 
 Myiasis, 296, 297 
 Myocardite segmentaire, 364 
 Myocarditis, 364 
 acute, 364 
 
 circumscribed, 364 
 diffuse, 365 
 chronic, 367 
 Myofibroma of ovary. 640 
 of uterus, 632 
 
 Myofibroma of vagina, 654 
 
 of vulva, 660 
 Myoma cavernosum, 155 
 cysticum, 155 
 laevicellulare, 154 
 of bladder, 605 
 of liver, 536 
 of mammary gland, 680 
 of stomach, 493 
 of uterus, 155 
 striocellulare, 157 
 Myomalacia, 374 
 
 cordis, 351 
 Myoneuroma of pituitary body, 774 
 Myopathic muscular atrophy, 710 
 Myositis, 707 
 chronic, 708 
 productive, 709 
 suppurative, 708 
 disseminated acute, 708 
 hemorrhagic, 707 
 localized acute, 707 
 ossificans progressiva, 709 
 ossifying, 709 
 serous, 707 
 suppurative, 708 
 Myxedema, 563 
 
 Myxoid cystomata of ovaries, 640 
 Myxoma, 124 
 
 appearance of, 124 
 definition of, 124 
 etiology, 124 
 nature of, 125 
 of bladder, 605 
 of bone, 698 
 
 of dura mater of cord, 776 
 of intestines, 516, 518 
 of mammary gland, 680 
 of mouth, 473 
 of muscles, 712 
 of testicle, 669 
 seats of, 124 
 structure of, 124 
 Myxomatous degeneration of mammary 
 gland, 678 
 of testicle, 664 
 
 N^vus lymphaticus, 132 
 
 prominens, 133 
 Nasal catarrh, acute, 402 
 cavities, active congestion of, 402 
 anatomic considerations, 402 
 congenital abnormalities of, 402 
 edema of, 402 
 hemorrhage of, 402 
 inflammations of, 402 
 parasites of, 404 
 passive congestion of, 402 
 syphilis of, 403 
 tuberculosis of, 403 
 tumors of, 403 
 Natural immunity, 197 
 Necrobiosis, 89 
 Necrosis, 89 
 cellular, general pathology of, 97 
 coagulation-, 91 
 definition of, 89 
 
INDEX. 
 
 835 
 
 Necrosis, etiology of, 89 
 fat-, 94 
 
 of pancreas, 547 
 liquefaction-, 92 
 of bone, 693 
 
 of lymphatic glands, 335 
 of pancreas, 547 
 Necrotic appendicitis, 507 
 
 inflammation, 109 
 Negative chemotaxis, 100 
 Neisser, gonococcus of, 206 
 Nematodes, 286 
 Neoplasms, 115. See Tumors. 
 Nephritis, 570, 573 
 acute catarrhal, 572 
 degenerative, 572 
 desquamative, 572 
 diffuse, 573 
 hemorrhagic, 573 
 inflammatory lesions from, 584 
 interstitial, 573 
 parenchymatous, 572 
 arteriosclerosis from, 584 
 arteriosclerotic, 578 
 cardiac changes from, 584 
 chronic, 575 
 
 hemorrhagic, 575 
 interstitial, 577 
 diffuse, 571 
 
 edema or dropsy from, 585 
 embolic suppurative, 574 
 etiology of, 571 
 gouty, 578 
 interstitial, 571 
 parenchymatous, 571 
 
 chronic, 575 
 pathologic anatomy of, 571 
 
 physiology of, 580 
 results of, 584 
 secondary interstitial, 576 
 suppurative, 574 
 tube-casts in, 581 
 uremia from, 585 
 urine in, 581 
 Nerve-cell, anatomy of, 732 
 changes in nuclei of, 736 
 degenerative changes in, as a whole, 
 737 
 processes of, 732 
 Nissl's method of staining, 733 
 pathologic changes in, 732 
 pigmentation of, 736 
 vacuolization of, 735 
 Nerve-fibers, anatomy of, 737 
 
 degeneration of, 738 
 Nerve-poisons, 29 
 Nerves, 803 
 atrophy of, 803 
 degeneration of, 804 
 edema of, 803 
 hemorrhages into, 803 
 hyperemia of, 803 
 
 inflammation of, 806. See also Neu- 
 ritis. 
 leprosy of, 809 
 muscular fibers in, 809 
 regeneration of, 804 
 
 Nerves, sarcoma of, 809 
 
 syphilis of, 808 
 
 tuberculosis of, 808 
 
 tumors of, 809 
 Nervous system, central, injuries of, 760 
 general pathologic anatomy of, 732 
 influence of, in causation of edema, 
 61 
 Neurin, poisoning by, 29 
 Neuritis, 806 
 
 acute interstitial, 806 
 
 chronic hypertrophic interstitial, 808 
 
 chronic interstitial, 807 
 
 parenchymatous, 808 
 
 suppurative, 808 
 Neuroblasts, 724 
 Neuroglia, degeneration of, 739 
 Neuroglioma, ganglionar, 769 
 Neuroma, 154 
 
 amyelinic, 154 
 
 false, 154 
 
 myelinic, 154 
 
 of suprarenal bodies, 566 
 
 plexiform, 154 
 
 true, 154 
 Neuron, description of, 726 
 Neuroparalytic hyperemia, 46 
 Neuropathic arthritis, 703 
 
 hemorrhage, 50 
 
 muscular atrophy, 709 
 Neurotic hyperemia, 46 
 Neutrophiles, 300 
 Neutrophilic granules, 301 
 New-growths, 115. See Tumors. 
 Nigrities of tongue, 471 
 Nissl's method of staining nerve-cells, 
 
 733 
 Nitrate of silver, poisoning by, 24 
 Nitric acid, poisoning by, 24 
 Nitrifying ferments, 193 
 Nitrobenzol, poisoning by, 28 
 Nitroglycerin, poisoning by, 28 
 Nodes of Eanvier, 738 
 Noma, 469 
 
 Non-contagious disease, definition of, 30 
 Non-siderous pigments, 85 
 Normoblasts, 304 
 
 Nourishment, insuflicient, effect of, 31 
 Nuclear solution, 97 
 Nuclei of cells, degenerations of, 97 
 
 of nerve-cells, morbid changes in, 736 
 Nucleo-albuminuria, 609 
 Numerical atrophy, 62 * 
 
 hypertrophy, 114 
 Nutmeg-liver, 522 
 Nutrition, disorders of, 31 
 
 Obesitas cordis, 361 
 Obesity, 32 
 
 associated conditions, 33 
 
 causes of, 32 
 
 pathologic anatomy of, 33 
 Obligate saprophytes and parasites, 189 
 Obstruction, intestinal, 500 
 
 of bronchi, 412 
 Obstructive thrombus, 56 
 Odontinoids, 474 
 
836 
 
 INDEX. 
 
 Odontoma, 131, 474 
 (Edema ex vacuo, 60 
 Oligemia, 307 
 ■Oligochromemia. 313 
 Oligocythemia, ::i3 
 Omentum, dropsy of, 552 
 'Oophoritis. 639 
 
 chronic, 639 
 •Optic thai ami, 726 
 Orchitis, 664 
 
 acute, 665 
 
 chronic. 665 
 Organic poisons, 25 
 Ose, 191 
 
 « >>!iHi>is, escape of fluid by, 59 
 Ossification, 83 
 
 differentiation of, from calcification, 
 83 
 Ossifying myositis. 709 
 
 pachymeningitis, 714 
 
 periostitis, 689 
 Osteitis, 689 
 
 chronic, 690 
 
 condensing, 691 
 Osteo-arthropathy, hypertrophic, 689 
 Osteoblasts, 111 
 Osteochondroma, 129 
 Osteoclasts, 691 
 Osteoid chondroma, 129 
 
 sarcoma, 699 
 Osteoma, 130 
 
 appearance of, 130 
 
 definition of, 130 
 
 dental, 131 
 
 durum, 131 
 
 eburueum, 131 
 
 etiology of. 130 
 
 heteroplastic, 131 
 
 nature of, 132 
 
 of brain. 771 
 
 of lungs, 157 
 
 of mammary gland, 680 
 
 of muscles. 712 
 
 of pleura, 465 
 
 of testicle, 669 
 
 seats of, 131 
 
 spongiosum, 131 
 
 structure of. 131 
 Osteomalacia, 693 
 Osteomyelitis, 344, 689 
 Osteophytes, 130 
 Osteoporosis, inflammatory, 691 
 < Osteopsathyrosis, 692 
 Osteosarcoma, 147 
 
 myeloid, 148 
 Osteosclerosis, 691 
 Ovaries, 637 
 
 absence of, 638 
 
 active hyperemia of, 638 
 
 adenocystoma of, 640 
 
 carcinoraata of, 643 
 
 chondromata of, 640 
 
 congenital abnormalities of, 638 
 
 congestion of, 638 
 
 eysto-adenoma of, 640 
 
 cystoma of papillary, 641 
 
 cvstoinata of, colloid, 640 
 
 Ovaries, cystomata of, glandular, 640 
 myxoid, 640 
 
 dermoid cysts of, 642 
 
 development and anatomic considera- 
 tions, 637 
 
 dislocation of, 638 
 
 fibroma of, 640 
 
 fibrosarcoinata of, 640 
 
 follicular cysts of, 6 40 
 
 hemorrhages into, 638 
 
 hypoplasia of, 638 
 
 inflammation of, 639 
 
 myofibroniata of, 640 
 
 passive congestion of, 638 
 
 sarcoma of, 640 
 
 supernumerary, 638 
 
 tuberculosis of, 639 
 
 tumors of, 640 
 Overaction of heart, effect of, on circula- 
 
 lation, 45 
 Overfeeding, effect of, 32 
 Oviducts. See Fallopian tubes. 
 Oxalate of lime in urine, 611 
 Oxalic acid, poisoning by, 24 
 Oxaluria, 40 
 Oxidizing ferments, 193 
 Oxyphile granules, 300 
 Oxvuris vcrmicularis, 287, 520 
 Ozena, 403 
 Ozeena syphilitica, 403. See Tuberculosa. 
 
 Pacchionian bodies. 721 
 Pachydermia laryngis, 405 
 Pachymeningitis, 713 
 
 cervicalis. 776 
 
 external tuberculous, of cord, 775 
 
 hemorrhagic, 713 
 
 internal hemorrhagic, of cord, 776 
 
 ossifying, 714 
 
 productive, 714 
 
 suppurative, 714 
 Pancreas. 546 
 
 amyloid degeneration of, 547 
 
 atrophy of, 546 
 
 carcinoma of. 549 
 
 circulatory disturbances of, 546 
 
 cirrhosis of. 51- 
 
 congenital abnormalities of, 546 
 
 cysts of, 549 
 
 fat-necrosis of, 547 
 
 hematochromatosis of, 547 
 
 hemorrhage in, 546 
 
 hyperemia of. 546 
 
 inflammation of, 548 
 
 necrosis of. 517 
 
 parenchymatous degeneration of, 547 
 
 pigmentation of. 547 
 
 relation of, to diabetes, 39 
 
 sarcoma of, 549 
 
 syphilis of, 549 
 
 tuberculosis of. 549 
 
 tumors of, 549 
 Pancreatic calculi, 550 
 
 duct. 550 
 
 dilatation of. 550 
 obstruction of, 550 
 
 veins, 550 
 
INDEX. 
 
 837 
 
 Pancreatitis, 548 
 
 acute hemorrhagic, 548 
 suppurative, 548 
 
 chronic indurative, 548 
 
 necrotic, 548 
 Papillary cystoma of ovary, 641 
 
 tumors, 118 
 Papuliferous cystic adenoma of kidney, 
 592 
 
 cystoma of testicle, 670 
 
 cystomata, 178 
 Papilloma, 157 
 
 hard, 158 
 
 of bladder, 604 
 
 of Fallopian tubes, 649 
 
 of intestines, 516 
 
 of larynx, 407 
 
 of mouth, 473 
 
 of penis, 662 
 
 of vagina, 654 
 
 soft, 158 
 Papillomatous tumors of vulva, 660 
 Parachromophoric bacteria, 195 
 Paradoxic embolism, 52 
 Paralysis, general progressive, 757 
 Paramecium coli, 276 
 Parametritis, 624 
 Paraphimosis, 661 
 Parasites, 188 
 
 animal, 265 
 
 embolism by, 52 
 
 in etiologv of disease, 31 
 
 of blood, 324 
 
 of bone, 699 
 
 of bronchi, 413 
 
 of heart, 375 
 
 of intestine, 519 
 
 of kidney, 594 
 
 of larynx, 408 
 
 of liver, 539 
 
 of lungs, 459 
 
 of lymphatic vessels, 401 
 
 of nasal cavities, 404 
 
 of pericardium, 380 
 
 of peritoneum, 558 
 
 of pleura, 467 
 
 of spleen, 333 
 
 of thyroid gland, 562 
 
 of ureter, 598 
 
 of uterus, 637 
 Parasitic disease, definition of, 31 
 
 stomatitis, 471 
 
 theory as to origin of carcinoma, 164 
 Parenchyma-poisons, 25 
 Parenchymatous encephalitis, 753 
 
 glossitis, 471 
 
 goiter, 560 
 
 degeneration, 64. See Cloudy swelling. 
 of heart, 359 
 of kidney, 586 
 of liver, 526 
 of muscles, 711 
 of pancreas, 547 
 
 hemorrhage, 48 
 
 hepatitis, 529 
 
 inflammation, 106 
 
 nephritis, 571 
 
 Parenchymatous nephritis, acute, 572 
 chronic, 575 
 
 neuritis, 808 
 
 tissue, regeneration of, 112 
 Paroophoron, 638 
 Parotitis, 481 
 Parovarium, 638 
 
 cysts of, 643 
 Paroxysmal hemoglobinuria, 609 
 Passive hyperemia, 46 
 
 immunity, 197 
 Pathologic anatomy, definition of, 17 
 
 chemistry, definition of, 17 
 Pathology, definition of, 17 
 
 general, 17 
 
 special, 298 
 Patulous, ductus Botalli, 348 
 Pearl disease, 230 
 Pelvis of kidney, 595 
 calculus in, 596 
 inflammation of, 596 
 malformations of, 595 
 tuberculosis of, 597 
 tumors of, 598 
 Penis, 661 
 
 angioma of, 663 
 
 carcinoma of, 662 
 
 condyloma acuminatum, 662 
 
 congenital abnormalities of, 661 
 
 cysts of, 662 
 
 epithelioma of, 662 
 
 fibroma of, 663 
 
 inflammation of, 661 
 
 injuries of, 663 
 
 lipoma of, 663 
 
 papilloma of, 662 
 
 tuberculosis of, 662 
 
 tumors of, 662 
 Pentastomum denticulatum, 296, 297, 
 539 
 
 tsenioides, 297 
 Peptic ulcer of intestine, 505 
 
 of stomach, 489 
 Peptone, formation of, 35 
 
 poisoning by, 28 
 
 solution, 190 
 Peptonuria, 35 
 Perforative peritonitis, 554 
 Periangiocolitis, 533 
 Periarteritis, 383 
 
 nodosa, 384 
 Peribronchial fibrous pneumonia, 439 
 Peribronchitis, 412 
 Pericarditis, 376 
 
 associated conditions of, 379 
 
 dry, 376 
 
 fibrinous, 376 
 
 hemorrhagic, 378 
 
 interna et externa, 380 
 
 purulent, 378 
 
 serofibrinous, 377 
 
 terminations of, 378 
 Pericardium, 346, 375, 378 
 
 actinomycosis of, 380 
 
 hemorrhages in, 376 
 
 hyperemia of, 376 
 
 inflammation of, 376 
 
838 
 
 INDEX. 
 
 Pericardium, parasites of, 380 
 
 syphilis of, 380 
 
 tuberculosis of, 380 
 
 tumors of, 380 
 Perichondritis of larynx, 405 
 Perihepatitis, 533 
 
 hyperplastic, 556 
 Perilymphangitis, 442 
 Perimastitis, 677 
 Perimetritis, 624 
 Perinephritis, 570 
 Peri-orchitis, 666 
 
 prolifera, 666 
 Periosteal callus, 686 
 Periostitis, 688 
 
 ossifying, 689 
 
 purulent, 689 
 
 simple, 688 
 
 syphilitic, 697 
 Peripheral nervous system, 802 
 Periproctitis, 509 
 Periprostatitis, 671 
 Perisplenitis cartilaginea, 331 
 Perithelioma, 770 
 Peritoneum, 551 
 
 carcinoma of, 557 
 
 circulatory disturbances of, 551 
 
 congenital abnormalities of, 551 
 
 dropsy of, 552 
 
 echinococcus cysts of, 558 
 
 fibromata of, 557 
 
 hemorrhage of, 551 
 
 hyperemia of, 551 
 
 inflammation of, 553. See Peritonitis. 
 
 lipomata of, 557 
 
 parasites of, 558 
 
 sarcoma of, 557 
 
 tuberculosis of, 556 
 
 tumors of, 557 
 Peritonitis, 553 
 
 acute general, 555 
 localized, 554 
 
 chronic, 555 
 
 hemorrhagic, 555 
 
 idiopathic, 553 
 
 micro-organisms of, 554 
 
 perforative, 554 
 Peritrichous bacteria, 185 
 Peritvphlitic abscess, 508 
 Perityphlitis, 508 
 Periurethral abscess, 615 
 Perivascular fibrous pneumonia, 439 
 Pes calcaneus, 700 
 
 equinus, 700 
 
 valgus, 700 
 
 varus, 700 
 Petechia, definition of, 51 
 Petri's dishes, 191 
 Phagedenic ulcer, 105 
 
 ulceration of cervix uteri, 627 
 Phagocytes, 198 
 Phagocytosis, 198 
 Phagolysis, 199 
 Pharyngitis, catarrhal, 475 
 
 chronic catarrhal, 475 
 
 phlegmonous, 476 
 
 pseudomembranous, 476 
 
 Pharyngomycosis leptothricia, 480 
 Pharynx, anemia of, 475 
 diphtheria of, 479 
 edema of, 475 
 glanders of, 480 
 hemorrhages of, 475 
 hyperemia of, 475 
 inflammation of, 475 
 lepra of, 480 
 pressure-necrosis of, 478 
 syphilis of, 480 
 tuberculosis of, 480 
 tumors of, 480 
 Phimosis, 661 
 Phlebectasia, 397 
 Phlebectatic elephantiasis, 398 
 Phlebitis, 396 
 acute, 396 
 chronic, 396 
 Phleholiths, 58, 396 
 Phlebosclerosis, 396 
 Phlegmonous cystitis, 601 
 esophagitis, 483 
 inflammation of vulva, 659 
 pharyngitis, 476 
 stomatitis, 469 
 tonsillitis, 477, 478 
 Phlogogenic bacterial proteins, 192 
 Phloridzin-glycosuria, 38 
 Phosphates in urine, 611 
 Phosphatic calculi, 603 
 Phosphaturia, 40 
 Phosphoric acid, excessive formation of, 
 
 in body, 34, 39 
 Phosphorus, poisonous action of, 25 
 Ph orogenesis, 195 
 Phragmodiothrix, 183 
 Phthisis, fibroid, 449 
 Phylaxins, 201 
 Physometra, 622 
 Pia mater, cerebral, 715 
 anemia of, 715 
 cholesteatomata of, 722 
 edema of, 716 
 endothelioma of, 722 
 hemorrhages of, 715 
 hypei-emia of, 715 
 inflammation of, 716 
 lipoma of, 723 
 syphilis of, 721 
 teratomata of, 723 
 spinal, 777 
 
 calcareous infiltration of, 777 
 hyperemia of, 777 
 inflammation of, 777 
 syphilis of, 778 
 tuberculosis of, 778 
 Pigment-building cells, 88 
 Pigment-metastases, 86 
 Pigmentation, 83 
 
 by cutaneous absorption, 85 
 
 by foreign bodies, 83 
 
 by hemoglobin derivatives, 85 
 
 by salts of silver. 85 
 
 from the exterior, 83 
 
 hematogenous, 85 
 
 hepatogenous, 87 
 
INDEX. 
 
 839 
 
 Pigmentation, metabolic, 88 
 of bone-marrow, 343 
 of choroid plexus, 763 
 of intestines, 502 
 of liver, 525 
 
 of lymphatic glands, 335 
 of mucosa of stomach, 491 
 of nerve-cell, 736 
 of pancreas, 547 
 of red blood-corpuscle, 305 
 of spinal pia, 777 
 of spleen, 332 
 of suprarenal bodies, 565 
 Pigmented sarcoma, 146 
 Pineal gland, 726, 775 
 Pin-worm, 287 
 Pituitary body, 771 
 adenoma of, 774 
 amyloid degeneration of, 773 
 colloid degeneration of, 773 
 cysts of, 774 
 hemorrhage into, 773 
 hyperemia of, 773 
 hypertrophy of, 772 
 inflammation of, 773 
 lymphosarcoma of, 774 
 relation of, to acromegaly, 774 
 sarcoma of, 774 
 softening of, 773 
 syphilis of, 773 
 tuberculosis of, 773 
 tumors of, 773 
 Placenta, 654 
 abnormal development of, 655 
 hemorrhage into, 656 
 inflammation of, 656 
 praevia, 655 
 succenturiata, 655 
 syphilis of, 657 
 tuberculosis of, 657 
 Placental infarcts, 656 
 
 polyps, 657 
 Placentitis, 656 
 Planococcus, 183 
 Planosarcina, 183 
 Plaques jaunes, 753 
 Plasma of blood, 382 
 Plasmodia, 267 
 Plehn's solution, 326 
 Plethora, 306 
 apocoptica, 307 
 hydremica, 307 
 vera, 306 
 Pleura, 460 
 circulatory disturbances of, 460 
 inflammation of, 461 
 parasites of, 467 
 passive hyperemia of, 460 
 petechial hemorrhages of, 460 
 syphilis of, 465 
 tuberculosis of, 465 
 tumors of, 465 
 Pleurisy, 461. See Pleuritis. 
 
 bread-and-butter, 463 
 Pleuritis, 461 
 fibrinous, 462 
 hemorrhagic, 464 
 
 Pleuritis, purulent, 463 
 
 serofibrinous, 463 
 Pleurogenic fibrous pneumonia, 439 
 pneumonia, 425 
 purulent pneumonia, 442 
 Plexiform angiosarcoma, 144 
 
 neuroma, 154 
 Pneumaturia, 608 
 Pneumonia, 425 
 alba, 440, 454 
 aspiration-, 431, 434 
 catarrhal, 430 
 
 bacteria of, 210 
 cheesy, 435 
 
 congenital syphilitic, 440 
 croupous, 425. See Pneumonia, fibrin- 
 ous. 
 bacteriology of, 207 
 deglutition-, 431 
 desiccans, 442 
 fibrinous, 425 
 
 associated lesions in, 429 
 etiology of, 425 
 pathologic anatomy of, 426 
 
 physiology of, 429 
 stage of congestion or engorgement, 
 
 426 
 stage of consolidation or hepatiza- 
 tion, 427 
 stage of resolution in, 428 
 usual characters of, 428 
 usual terminations of, 429 
 fibrous, 437 
 
 peribronchial, 439 
 perivascular, 439 
 pleurogenic, 439 
 secondary, 439 
 hematogenic, 425 
 hypostatic, 431, 434 
 irregular, 210 
 
 lobar, 425. See Pneumonia, fibrinous. 
 lobular, 430 
 migrans, 426 
 pleurogenic, 425 
 productive, 437 
 purulent, 440 
 
 bronchogenic, 440 
 hematogenic, 441 
 pleurogenic, 442 
 tubercular, 210 
 tuberculous, 435 
 Pneumonic tuberculosis, 445 
 Pneumonokoniosis, 83, 437 
 Piieumonomycosis aspergillina, 460 
 Pneumopericardium, 380 
 Pneumopyopericardium, 381 
 Pneumothorax, 461 
 Poikilocytosis, 303 
 Poisons, action of, in general, 23 
 blood-, 28 
 classification of, 24 
 corrosive, 24 
 effect of, 23 
 elimination of, 24 
 fate of, after ingestion, 23 
 immunity to, 23, 24 
 in etiology of disease, 23 
 
840 
 
 INDEX. 
 
 Poisons, necrosis from, 90 
 
 nerve-, 29 
 
 organic, 25 
 
 parenchyma-, 25 
 Polar spore, 184 
 
 field, 111 
 Poliomyelitis, acute anterior, 791 
 
 chronic anterior, 799 
 Polycholia, 545 
 Polychromatophilia, 305 
 Polycythemia, 310 
 Polymastia, 676 
 
 Polymorphonuclear leukocytes, 300 
 Polymorphous heredity, 36 
 Polymyositis, 70S 
 
 secondary acute, 711 
 Polyneuritis. 808 
 Polynuclear leukocytes, 300 
 Polypoid elevations of stomach, 493 
 
 growths of bladder, 604 
 
 outgrowths from tooth-pulp, 474 
 
 tumors, 118 
 Polyps, nasal, 403 
 
 placental, ii.">7 
 
 of uterus, 632 
 sarcomatous, 634 
 Polyuria, 606 
 Pons, anatomy of, 726 
 Porencephaly, 741 
 Portal vein, embolism and thrombosis 
 
 of, 523 
 Port-wine stains, 133 
 Posterior sclerosis of spinal cord, 793 
 Posthitis, 661 
 Post-mortem lividity, 44 
 Potassium chlorate, poisoning by, 28 
 Potato-extract, 190 
 Predisposing causes of disease, 18 
 Predisposition to disease, 18 
 Pregnancy, abdominal, 652 
 
 extra-uterine, 650 
 
 interstitial, 650 
 
 tubal, 650 
 Prepuce, concretions under, 663 
 
 inflammation of, 661 
 Pressure, effect of, on tissues, 19 
 
 -myelitis. 7: to 
 
 -necrosis of pharynx, 478 
 Primary anemias, 315 
 
 gangrene, 95 
 
 thrombus, 56 
 Processes of nerve-cell, degenerative 
 
 changes in, 732 
 Proctitis, 509 
 Productiye inflammation, 105 
 
 myositis, chronic, 709 
 
 pachymeningitis, 714 
 
 pneumonia, 437 
 Proglottides of tape-worms. 278 
 Progressive muscular atrophy, 710 
 
 pernicious anemia. 317 
 
 spinal muscular atrophy, 799 
 
 tissue-changes, 113 
 Projection fibers of brain, 725 
 Prolapse of rectum, 502 
 of uterus, 620 
 of vaginal walls, 652 
 
 Proliferation-cysts, 177 
 Proliferative cystomata, 178 
 Prosencephalon, 724 
 Prostate gland, 671 
 
 abscess of, 671 
 
 atrophy of, 672 
 
 carcinoma of, 675 
 
 concretions in, 672 
 
 cysts of, 675 
 
 fatty degeneration of, 672 
 
 hypertrophy of, 672 
 
 inflammation of, 671 
 
 sarcoma of, 675 
 
 tuberculosis of, 672 
 Prostatitis, 671 
 
 phlegmonous, 671 
 
 simple, 671 
 
 suppurative, 671 
 Proteins produced by bacteria, 192 
 Proteolytic ferments, 193 
 Protozoa, 265 
 Psammoma, 82, 149, 771 
 
 -bodies, 81, 641 
 Pseud arthroses, 687 
 Pseudodichotomy of bacteria, 186 
 Pseudodiphtheria bacillus, 212 
 Pseudohypertrophic muscular atrophy, 
 
 711 
 Pseudoleukemia, 137, 323 
 
 cutis, 150 
 
 infantum, 323 
 Pseudomembranous cystitis, 602 
 
 enteritis. 505 
 
 esophagitis, 482 
 
 gastritis, 486 
 
 pharyngitis, 476 
 
 stomatitis, 469 
 
 vaginitis, 6.33 
 Pseudomonas, 183 
 Pseudomucin, 77 
 Pseudoplasms, 115. See Tumors. 
 Pseudotrichinosis, 708 
 Pseudotuberculosis, 234 
 Psorospermise, 269 
 
 in liver, 539 
 
 in pelvis of kidney, 598 
 Psycnrophilic bacteria, 189 
 Ptomains, poisoning by, 29 
 Puerperal infections of uterus, 628 
 etiology of, 628 
 pathologic anatomy of, 629 
 Pulmonary artery, stenosis and atresia 
 of, 347 
 
 infarcts, 54 
 Pulsion-diverticula of esophagus, 483 
 Punctate cerebral hemorrhage, 747 
 Purulent arthritis, 702 
 
 lymphangitis, 442 
 
 myelitis, hematogenous, 788 
 
 pericarditis, 378 
 
 periostitis, 689 
 
 pleuritis, 463 
 
 pneumonia, 4 10 
 
 vaginitis testis, 667 
 Pustule, malignant, 242 
 Putrefaction, 1!« 
 Pyelitis, 570, 596 
 
INDEX. 
 
 841 
 
 Pyelonephritis, 597 
 
 suppurative, 574 
 Pyemia, 197 
 
 Pyknoniorphous state, 734 
 Pykuosis, 97 
 Pylephlebitis, 524 
 Pyogenic albumosuria, 608 
 
 bacterial proteins, 192 
 
 membrane, 105 
 Pyoid marrow, 344 
 Pyonephrosis, 597 
 Pyosalpinx, 648 
 Pyothorax, 463 
 Pyramidal tract, degeneration of, 750 
 
 Quartan malaria, organism of, 267 
 Quinsy, 478 
 
 Babies, bacteriology of, 262 
 Eacemose adenoma, 160 
 
 cysticerci, 279 
 Eachitic rosary, 684 
 Eachitis, 683 
 Eanula, 473 
 Eanulse, 177 
 Eay fungus, 248 
 Eectocele, 621 
 
 vaginal, 652 
 Eectum, inflammation of, 509 
 
 prolapse of, 502 
 Eecurrent fibroid tumor, 141 
 Eecurring appendicitis, 508 
 Eed atrophy of liver, 522 
 
 blood-corpuscles, 298. See Blood-cor- 
 puscle. 
 nucleated, 304 
 
 granular kidney, 578 
 
 hepatization of lung, 427 
 
 softening of brain, 751 
 Eeducible hernia, 500 
 Eegeneration, 109 
 
 normal, 109, 110 
 
 of bone, 685 
 
 of connective tissues other than fibrous, 
 112 
 
 of fibrous connective tissues, 111 
 
 of nerves, 804 
 
 of parenchymatous tissue, 112 
 
 pathologic, 110, 111 
 Eelapsing appendicitis, 508 
 
 fever, 251 
 Eelative immunity, 197 
 Eemote heredity, 18 
 Eenal calculi, 596 
 
 " rests," 564 
 
 sand, 596 
 Eepair of wounds, 106 
 Eeproductive organs, diseases of, 618 
 Eesolution after inflammation, 109 
 Eespiratory system, diseases of, 402 
 Betention-cysts, 177 
 Eetroflexion of uterus, 620 
 Eetrograde embolism, 52 
 Eetrogressive processes, 62 
 Eetroperitoneal hernia, 499 
 Eetropharyngeal abscess, 476 
 Eetro-uterine hematocele, 624 
 
 Ehabditis stercoralis, 290 
 Ehabdomyoma, 157 
 
 of muscles, 712 
 
 of testicle, 669 
 Ehabdomyosarcoma of kidney, 591 
 Bhachischisis, 728 
 Eheumatism, bacteriology of, 263 
 Eheumatoid arthritis, 702 
 Ehinitis, acute, 402 
 
 atrophica, 403 
 
 chronic, 403 
 
 diphtheritic, 403 
 Ehinoliths, 404 
 Ehinoscleroma, 210 
 
 affections of nasal cavities in, 403 
 Ehopalocephalus carcinomatosus, 272 
 Eice-water stools of cholera, 511 
 Eicin, poisoning by, 27 
 Eickets, 683 
 
 congenital, 685 
 Bound-cell infiltration, 101 
 
 -celled sarcoma, 142 
 
 ulcer of stomach, 489 
 
 worms, 286 
 Eubeola, 261. See Measles. 
 Bupture of bladder, 600 
 
 of intestines, 520 
 
 of liver, 534 
 
 of uterus, 623 
 
 Sacchaeomyces albicans, 471 
 Saccular aneurysm, 391 
 
 bronchiectasis, 413 
 Sago spleen, 332 
 
 Salivary ducts, concretions in, 482 
 cystic dilatation of, 482 
 diseases of, 481 
 
 fistulse, 481 
 
 glands, inflammation of, 481 
 tumors of, 481 
 Salpingitis, 646 
 
 acute, 646 
 
 chronic, 648 
 
 diphtheritic, 647 
 Sanarelli's bacillus, 260 
 Sapremia, 197 
 Saprophytes, 188 
 Sarcina, 183 
 Sarcinse ventriculi, 493 
 Sarcolactic acid, excessive formation of, 
 
 in body, 34 
 Sarcoma, 138 
 
 alveolar, 143 
 
 appearances of, 139 
 
 blood-vessels of, 140 
 
 giant-celled, 147 
 
 myeloid, 147 
 
 of bone, 698 
 
 of brain, 770 
 
 of cervix uteri, 634 
 
 of dura mater of cord, 776 
 
 of Fallopian tubes, 650 
 
 of intestines, 516 
 
 of kidney, 591 
 
 of liver, 536 
 
 of lungs, 457 
 
 of lymphatic glands, 343 
 
842 
 
 INDEX. 
 
 Sarcoma of mammary gland, 680 
 
 of mouth, 473 
 
 of muscles, 712 
 
 of nerve, 809 
 
 of ovaries, 640 
 
 of paucreas, 549 
 
 of peritoueum, 557 
 
 of pituitary body, 774 
 
 of pleura, 465 
 
 of prostate, 675 
 
 of spinal cord, 802 
 
 of spleen, 333 
 
 of stomach, 493 
 
 of suprarenal bodies, 566 
 
 of testicle, 669 
 
 of thymus glaud, 345 
 
 of thyroid glaud, 562 
 
 of tooth-puli'. 474 
 
 of urethra, 618 
 
 of uterus, 634 
 
 of vagina, <>.">! 
 
 of vulva, 660 
 
 osteoid, 699 
 
 pigmented, 146 
 
 round-celled, 142 
 
 seats of, 140 
 
 spindle-celled, 141 
 Sarcomatosis, 140 
 Sarcomatous cylindromata, 145 
 
 polyps of uterus, 634 
 Scarlatina. See Scarlet fever. 
 Scarlet fever, animal parasites of, 274 
 
 bacterium of, 261 
 Scirrhous carcinoma, 172 
 Sclerosis of brain, atrophic, 740 
 diffuse, 739 
 disseminated, 739 
 hypertrophic, 740 
 lobar, 758 
 multiple, 759 
 
 of spinal cord, amyotrophic lateral, 
 798 
 combined, 798 
 posterior, 793 
 Scolex of tape-worm, 278 
 Scrofula, 339 
 Scrotum, 661 
 
 cysts of, 662 
 
 elephantiasis of, 662 
 
 epithelioma of, 662 
 Seat-worm, 287 
 Secondary anemia, 313 
 
 gangrene, 95 
 
 thrombus, 56 
 Segmentation, indirect, 110 
 
 of fibers of heart, 363 
 Seminal vesicles, 675 
 
 diseases of, 676 
 Senile arthritis. 702 
 
 atrophy of uterus, 631 
 
 emphysema of lungs, 422 
 Septicemia, 197 
 Septic endocarditis, 354 
 Sequestrum, 693 
 Serofibrinous pericarditis, 377 
 
 pleuritis, 463 
 Serous arthritis, 702 
 
 Serous inflammation, 103 
 myositis, 707 
 vaginitis testis, 666 
 Serpents, venom of, poisoning by, 27 
 Serpiginous ulcer, 105 
 Serum-reaction of Widal, 217 
 Serumuria, 608 
 Shadow corpuscles, 305 
 " Shaven-.beard " appearance, 513 
 Siderosis, 83, 439 
 Siderous pigments, 85 
 Silver-salts, pigmentation by, 85 
 Slumbering cells of Grawitz, 101 
 Soft chancre, 259 
 papilloma, 158 
 Softening-cysts, 177 
 Sozins, 201 
 Special pathology, 298 
 
 definition of, 17 
 Spermatocele, 670 
 Sphacelinic acid, 26 
 Sphacelus, 97 
 Spina bifida, 781 
 Spinal cord, 775 
 
 abnormal smalluess of, 780 
 
 anatomy of, 778 
 
 anemia of, 785 
 
 aneurysms of, 785 
 
 blood-vessels of, degeneration of 
 
 walls of, 785 
 carcinoma of, 802 
 cysts of, 802 
 
 degenerations of, secondary, 800 
 development of, 723 
 double, 780 
 glioma of, 802 
 hyperemia of. 785 
 inflammations of, 787 
 primary degenerations of, 793 
 sarcoma of, 802 
 
 sclerosis of, amyotrophic lateral, 798 
 combined, 798 
 posterior, 793 
 total absence of, 780 
 tumors of, 802 
 unusual length of, 780 
 varicose veins of. 786 
 white matter of. degeneration of, 799 
 ganglia, disease of, 803 
 Spindle-celled sarcoma. 141 
 
 -shaped aneurysm, 390 
 Spirillacese, 183 
 Spirillum, 183 
 Berolinensis, 223 
 cholerse Asiaticae, 219 
 
 pathogenicitv of, 221 
 Metschnikowi, 2-22 
 of Finkler and Prior, 222 
 tyrogenicum, 222 
 Spi'rochaeta, 183 
 Obemeieri, 251 
 Spirosoma, 183 
 Splanchnoptosis. 492 
 
 Spleen, abnormal development and situ- 
 ation of. 327 
 abscess of. 330 
 amyloid degeueration of, 331 
 
INDEX. 
 
 843 
 
 -Spleen, anemia of, 328 
 
 atrophy of, 331 
 
 calcification of, 332 
 ( carcinoma of, 333 
 
 chronic hyperplasia of, 331 
 inflammation of, 331 
 
 circulatory disturbances in, 328 
 
 congestion of, 328 
 
 cysts of, 333 
 
 embolism of, 328 
 
 hemorrhages in, 328 
 
 hyaline degeneration of, 332 
 
 hyperemia of, 328 
 
 infectious diseases of, 333 
 
 inflammation of, 329 
 
 movable, 327 
 
 pathologic physiology of, 327 
 
 pigmentation of, 332 
 
 sarcoma of, 333 
 
 syphilis of, 334 
 
 thrombosis of, 329 
 
 tuberculosis of, 333 
 
 tumors of, 332 
 Splenemia, 321 
 Splenic anemia, 315 
 
 fever, 242 
 
 stones, 329 
 Splenitis, 329 
 
 circumscribed, 330 
 
 diffuse, 329 
 
 spodogenous, 332 
 Splenization of lung-tissue, 417, 424 
 Spodogenous splenitis, 332 
 Spongioblasts, 723 
 Spores of bacteria, 184 
 
 staining of, 188 
 Squamous cancer of stomach, 497 
 
 epithelioma, 171 
 Staining of bacteria, 186-188 
 
 of blood, 325 
 Staphylococcus epidermidis albus, 203 
 
 pyogenes albus, 203 
 aureus, 202 
 citreus, 203 
 Starvation. 31 
 Stasis of blood, 47 
 Staubzellen, 437 
 Stenosis of biliary ducts, 542 
 
 of esophagus, 483 
 
 of Fallopian tubes, 645 
 
 of heart-valves, 357 
 
 of intestines, 498 
 
 of uterus, 622 
 
 of vagina, 652 
 Stercoral typhlitis, 506 
 Stomach, adenocarcinoma of, 497 
 
 adenomatous proliferation of glands of, 
 494 
 
 alteration in position of, 492 
 
 amyloid degeneration of subniucosa of, 
 492 
 
 anemia of, 485 
 
 anthrax of, 493 
 
 atrophy of, 491 
 
 calcification of mucosa of, 492 
 
 cancer of, 494 
 
 carcinoma of, 494 
 
 Stomach, circulatory disturbances of, 485 
 
 colloid cancer of, 497 
 
 congenital defects of, 485 
 
 cylindrical cancer of, 497 
 
 degeneration of mucous membrane of, 
 491 
 
 dilatation of, 492 
 atonic, 492 
 
 displacements of, 492 
 
 fatty degeneration of cells of, 491 
 
 hemorrhage of, 485 
 
 hyperemia of, 485 
 
 infectious diseases of, 493 
 
 inflammation of, 504 
 of mucosa of, 486 
 
 malignant adenoma of, 497 
 
 peptic ulcer of, 489 
 
 pigmentation of mucosa of, 491 
 
 polypoid elevations of, 493 
 
 round ulcer of, 489 
 
 softening of walls of, 492 
 
 squamous cancer of, 497 
 
 svphilitic gummata of, 493 
 
 thrush of, 493 
 
 tuberculous ulceration of, 493 
 
 tumors of, 493 
 Stomatitis, 468 
 
 aphthous, 468 
 
 associated conditions in, 470 
 
 catarrhal, 46S 
 
 gangrenous, 469 
 
 parasitic, 471 
 
 phlegmonous, 469 
 
 pseudomembranous, 469 
 
 ulcerative, 469 
 Stone-particles, pigmentation by, 83 
 Strangulated hernia, 500 
 Strangulation, internal, of intestines, 500 
 Stratified thrombi, 56 
 Streptococci in kidney, 595 
 Streptococcus, 183 
 
 pyogenes seu erysipelatis, 203 
 
 -toxin, 205 
 Streptothrix, 183 
 
 Madurse, 250 
 Stricture of urethra, 616 
 
 syphilitic, 515 
 Strongylus longevaginatus, 293 
 Struma, 559. See Goiter. 
 
 aberrata suprarenalis, 591 
 
 adenomatosa, 561 
 Strumitis, acute, 559 
 suppurative, 559 
 Submucous abscess of intestine, 505 
 
 fibroids, 632 
 Subperitoneal fibroids, 632 
 Substantia nigra, 726 
 Substantial emphysema of lungs, 420 
 Suffocation, 22 
 Suffusion, definition of, 51 
 Sugar in blood, 37 
 
 in urine, 37 
 Suggillation, definition of, 51 
 Sulphate of copper, poisoning by, 24 
 Sulphates in urine, 613 
 Sulphuric acid, excessive formation of, 
 in body, 34 
 
844 
 
 INDEX. 
 
 Sulphuric acid, poisoning by, 24 
 Supernumerary ovaries, 638 
 Suprarenal bodies, 564 
 
 accessory, 564 
 
 adenoma of, 566 
 
 amyloid degeneration of, 565 
 
 carcinoma of, 566 
 
 congenital abnormalities of, 564 
 
 fatty degeneration of, 565 
 
 general effects of diseases of, 566 
 
 glioma of, 566 
 
 hemorrhage from, 566 
 
 inflammation of, 566 
 
 neuroma of, 566 
 
 pigmentation of, 565 
 
 sarcoma of, 566 
 
 syphilis of, 565 
 
 tuberculosis of, 565 
 
 tumors of, 566 
 Suppurative bacterial diseases, 202 
 cholangitis, 542 
 encephalitis, 755 
 enteritis. 505 
 inflammation, 104 
 lymphadenitis, 336 
 myositis, 708 
 
 chronic, 708 
 nephritis, ."71 
 neuritis. 308 
 pachymeningitis. 714 
 pyelonephritis, 574 
 Sympathetic nervous system, develop- 
 ment of, 724 
 Syncytioma malign um, 175 
 Syncytium, 176, 655 
 Synovitis pannosa, 702 
 Syphilis, 254 
 congenital, 258 
 of arachnoid and pia, 721 
 of arteries, 388 
 
 of brain. 714 
 of bone, 697 
 of brain, 768 
 of bronchi, 413 
 of dura mater, 714 
 
 cord. 776 
 of esophagus, 484 
 of Fallopian tubes, 649 
 of heart, 375 
 of intestines, 515 
 of joints. 705 
 of kidney, 590 
 of larynx, 406 
 of liver, 534 
 of lungs. 454 
 of lymphatic glands. 341 
 
 vessels, 400 
 of mammary gland, 678 
 of mouth, 472 
 of muscles, 712 
 of nasal cavities, 403 
 of nerves, 808 
 of pancreas, 549 
 of pericardium. 380 
 of pharynx, 480 
 
 of pia and arachnoid of cord, 778 
 of pituitary body, 773 
 
 Syphilis of placenta, 657 
 
 of pleura, 465 
 
 of spleen, 334 
 
 of suprarenal bodies, 565 
 
 of testicle, 668 
 
 of thymus gland, 345 
 
 of thyroid gland, 562 
 
 of tongue, 472 
 
 of trachea, 409 
 
 of urethra, 618 
 
 of uterus, 631 
 
 of vagina, 654 
 
 of vulva, 660 
 
 secondary lesions of, 255 
 
 tertiary lesions of. 256 
 Syphilitic bubo, 255 
 
 gummata of stomach, 493 
 
 periostitis, 697 
 
 pneumonia, congenital, 440 
 
 stricture. 515 
 Syphilomata, 256 
 Syringomyelia, 782 
 
 Tabes dorsalis, 793 
 
 mesenterica, 341 
 Ttenia Algeriana, 282 
 
 cucumerina, 282 
 
 echinococcus, 282 
 
 elliptica, 282 
 
 flovopunctata, 282 
 
 Madagascariensis, 282 
 
 nana, 281 
 
 saginata, 280 
 
 solium, 279 
 
 tenella, 282 
 Tape-worms, 277 
 
 dwarf, 281 
 Teeth, affections of, 474 
 Temperature, high, effect of, 20 
 Tendon-sheaths, inflammation of, 706 
 Tenosynovitis. 706 
 
 gonorrheal, 616 
 Teratoma, 179 
 
 of pia and arachnoid, 723 
 Tertian fever, parasite of, 267 
 Testicles, 663 
 
 adenoma of, 669 
 
 adenosarcoma of. 669 
 
 atheromatous cvst of, 671 
 
 atrophy of. 663 * 
 
 benign fungus of. 665 
 
 calcification of, 664 
 
 carcinoma of, 669 
 
 caseation of. 664 
 
 chondrocarcinoma of, 670 
 
 chondroma of, 669 
 
 congenital abnormalities of, 663 
 
 cysts of, 670 
 
 dermoid cysts of, 671 
 
 echinococcus cysts of, 671 
 
 fattv degeneration of. 664 
 
 fibroma of, 669 
 ! hyperemia of, 664 
 
 hypertrophy of. 664 
 
 inflammation of. 664. See Orchitis. 
 
 lepra of. 669 
 
 myxoma of, 669 
 
INDEX. 
 
 845 
 
 Testicles, myxomatous degeneration of, 
 664 
 osteoma of, 669 
 papuliferous cystoma of, 670 
 rhabdomyoma of, 669 
 sarcoma of, 669 
 syphilis of, 668 
 syphilitic fungus of, 669 
 tuberculosis of, 667 
 tumors of, 669 
 Tetanih, 247 
 Tetanotoxin, 247 
 Tetanus 246 
 
 antitoxin of, 247 
 bacillus of, 246 
 Thalainencephalon, 724 
 Thermophilic bacteria, 189 
 Thiothrix, 183 
 Third ventricle of brain, 726 
 Thoracic duct, diseases of, 401 
 Thrombi, ball, 57 
 calcification of, 58 
 canalization of, 58 
 degeneration of, 57 
 marantic, 55 
 organization of, 58 
 purulent softening of, 58 
 simple softening of, 58 
 stratified, 56 
 Thrombo-arteritis, 384 
 Thrombophlebitis, 396 
 Thrombosis, 55 
 fermentation-, 55 
 of bone, 688 
 of brain, 751 
 of cavities of heart, 350 
 of coronary artery, 351 
 of intestines, 503 
 of kidney, 570 
 of liver, 523 
 of muscles, 707 
 of spleen, 329 
 of thoracic duct, 401 
 Thrombus, lateral, 56 
 obstructive, 56 
 primary, 56 
 secondary, 56 
 Thrush, 471 
 
 of esophagus, 484 
 of stomach, 493 
 Thymus gland, diseases of, 345 
 Thyroid disease, general results of, 562 
 gland, 558 
 abscess of, 559 
 actinomycosis of, 562 
 adenoma of, 562 
 anatomic considerations, 558 
 carcinoma of, 562 
 circulatory disturbances in, 559 
 congenital defects of, 559 
 general results of disease of, 562 
 hyperemia of, 559 
 inflammation of, 559 
 sarcoma of, 562 
 syphilis of, 562 
 tuberculosis of, 562 
 tumors of, 562 
 
 Tissue-changes, progressive, 113 
 
 -destruction, excessive, 33 
 
 -elasticity, decreased, a cause of edema, 
 60 
 Toadstools, poisoning by, 28 
 Tongue, actinomycosis of, 473 
 
 furring of, 468 
 
 geographical, 467 
 
 nigrities of, 471 
 
 syphilis of, 472 
 
 tuberculosis of, 471 
 Tonsil, abscess of, 478 
 
 hypertrophv of, 478 
 Tonsillitis, 477 
 
 catarrhal, 477 
 
 follicular, 477 
 
 lacunar, 477 
 
 phlegmonous, 477, 478 
 Tophi of gout, 36 
 Toxalbumins, 194 
 
 from plants, poisoning by, 27 
 Toxic products of bacteria, action of, 27 
 
 effects of, 196 
 Toxin-immunity, 199 
 
 of diphtheria, 213 
 Toxins, 194 
 Toxophylaxins, 201 
 Toxosozins, 201 
 Trachea, 408 
 
 circulatory disturbances of, 408 
 
 inflammations of, 408 
 
 malformations of, 408 
 
 syphilis of, 409 
 
 tuberculosis of, 409 
 
 tumors of, 409 
 Traction-diverticula of esophagus, 483 
 Transitional leukocytes, 299 
 Traumatic hemorrhage, 50 
 
 theory of cause of carcinoma, 164 
 Traumatism in etiology of disease, 19 
 Trematodes, 293 
 Trichina spiralis, 288 
 
 in larynx, 408 
 Trichiniasis, 289 
 Trichobacteria, 185 
 Trichocephalus dispar, 290 
 Trichomonas caudata, 275 
 
 elongata, 275 
 
 flagellata, 275 
 
 intestinalis, 275 
 
 vaginalis, 275 
 Trilocular heart, 347 
 True hypertrophy, 114 
 
 neuroma, 154 
 Tubal abortion, 651 
 
 pregnancy, 650 
 Tube-cast in nephritis, 581 
 Tubercle-bacillus, 223 
 
 lymphoid, 229 
 
 miliary, 227 
 
 structure and evolution of, 228 
 
 toxic properties of, 233 
 Tubercula dolorosa, 155 
 Tubercular leprosy, 236 
 
 pneumonia, 210 
 Tuberculin of Koch, 234 
 Tuberculosis, 223 
 
846 
 
 INDEX 
 
 Tuberculosis, acute pneumonic, 446 
 avian, 235 
 bacillus of, 223 
 bronchogenic, 444 
 chronic pneumonic, 447 
 fowl-, 235 
 gallivarum, 235 
 hematogenic, 451 
 latent, 233 
 lymphogenic, 453 
 miliary, 232 
 of arteries, 388 
 of bladder, 602 
 of bone, 694 
 of brain, 767 
 of bronchi, 413 
 of choroid plexus, 762 
 of dura mater, 714 
 
 of cord, 775 
 of epididymis, 667 
 of esophagus, 484 
 of Fallopian tubes, 648 
 of heart, 375 
 of intestine, 514 
 of joints, 704 
 of kidney, 590 
 of larynx, 406 
 of liver, 534 
 of lungs, 443 
 
 bronchogenic, 443, 444 
 of lymphatic glands, 338 
 of lymphatics, 400 
 of mammary gland, 678 
 of mouth, 471 
 of muscle, 712 
 of nasal cavities, 403 
 of nerves, 808 
 of ovary, 639 
 of pancreas, 549 
 of pelvis of kidney, 597 
 of penis, 662 
 of pericardium, 380 
 of peritoneum , 556 
 of pharynx, 480 
 
 of pia and arachnoid of cord, 778 
 of pituitary body. 773 
 of placenta, 657 
 of pleura, 465 
 of prostate, 672 
 of seminal vesicles, 676 
 of spleen, 333 
 of suprarenal bodies, 565 
 of testicle, 667 
 of thoracic duct, 401 
 of thymus gland, 345 
 of thyroid gland, 562 
 of tongue, 471 
 of trachea, 409 
 of urethra, 618 
 of uterus, 630 
 of vagina, 654 
 of vas deferens, 668 
 of veins, 399 
 of vulva, 660 
 pneumonic, 445 
 
 relations of human, to animal, 227 
 seats of, 232 
 
 Tuberculous meningitis, 719 
 
 pneumonia, 435 
 
 ulceration of stomach, 493 
 Tubo-ovarian cysts, 650 
 Tubular adenoma, 160 
 Tumor-dyscrasia, 164 
 Tumors, 115 
 
 benign, 119 
 
 circumscribed, 118 
 
 classification of, 120 
 
 dendritic, 118 
 
 fungiform, 118 
 
 fungoid, 118 
 
 infiltrating, 118 
 
 malignant, 119 
 
 mixed, 129 
 
 of arachnoid and pia, 721 
 
 of biliary ducts, 544 
 
 of bladder, 604 
 
 of bone, 698 
 
 of brain, 768 
 
 of bronchi, 413 
 
 of choroid plexus, 763 
 
 of dura mater, 715 
 of cord, 776 
 
 of esophagus, 484 
 
 of Fallopian tubes, 649 
 
 of gall-bladder, 544 
 
 of heart, 375 
 
 of intestine, 516 
 
 of joints, 705 
 
 of kidney, 590 
 
 of larynx, 407 
 
 of liver, 536 
 
 of lungs, ir>, 
 
 of lymphatic glands, 341 
 
 vessels, 400 
 of mammary gland, 679 
 of mouth, 473 
 of muscles, 712 
 of nasal cavities, 403 
 of nerves, 809 
 of ovaries, 640 
 of pancreas, 549 
 of pelvis of kidney, 598 
 of penis, 662 . 
 
 of pericardium, 380 
 of peritoneum, 557 
 of pharynx, 480 
 of pituitary body, 773 
 of pleura, 465 
 of salivary glands, 481 
 of seminal vesicles, 676 
 of spinal cord, 802 
 of spleen, 332 
 of stomach, 493 
 of suprarenal bodies, 566 
 of teeth, 474 
 of testicle, 669 
 of thoracic duct, 401 
 of thymus gland, 345 
 of thyroid gland, 562 
 of trachea, 409 
 of ureter, 598 
 of urethra, 618 
 of uterus, 632 
 of vagina, 654 
 
INDEX. 
 
 847 
 
 Tumors of veins, 398 
 
 of vulva, 660 
 
 papillary, 118 
 
 polypoid, 118 
 
 verrucose, 118 
 Typhlitis, 506 
 
 stercoral, 506 
 Typhoid fever, 214, 511 
 bacillus of, 214 
 complications of, 513 
 Typhus fever, bacteriology of, 262 
 
 icteroides, 260 
 
 recurrens, 251 
 Tyroma, meningeal, 720 
 Tyrosin in urine, 35, 613 
 Tyrotoxicon, 29 
 
 Ulcee, 105 
 
 indolent, 105 
 
 peptic, of intestines, 505 
 
 phagedenic, 105 
 
 serpiginous, 105 
 Ulceration of intestines, 505 
 Ulcerative dysentery, 510 
 
 endocarditis, 354 
 
 esophagitis, 483 
 
 gastritis, 486 
 
 stomatitis, 469 
 Ulcers of bronchi, 412 
 Ulcus ex digestione, 489 
 Umbilical cord, abnormalities of, 655 
 
 velamentous insertion, 655 
 Urate of sodium, deposit in tissues, 83 
 Urates in urine, 612 
 Uratic infiltration, 83 
 Urea, formation of, 33 
 Uremia from nephritis, 585 
 Ureter, 595 
 
 dilatation of, 595 
 
 inflammation of, 597 
 
 malformations of, 595 
 
 obstructions of, 595 
 
 parasites of, 598 
 
 tumors of, 598 
 Ureteritis, 597 
 Urethra, 614 
 
 carcinoma of, 618 
 
 congenital abnormalities of, 614 
 
 cysts of, 618 
 
 inflammation of, 614 
 
 injuries of, 617 
 
 sarcoma of, 618 
 
 stricture of, 616 
 
 tuberculosis of, 618 
 
 tumors of, 618 
 Urethritis, 614 
 
 anterior, 615 
 
 associated lesions of, 615 
 
 posterior, 616 
 Uric acid calculi, 603 
 
 crystals in urine, 611 
 excretion of, in gout, 37 
 formation of, 36 
 Urinary bladder. See Bladder. 
 
 calculi, 603 
 results of, 604 
 
 organs, congenital anomalies of, 567 
 
 Urine, abnormal conditions of, 606 
 
 bacteria in, 610 
 
 bilirubin in, 613 
 
 carbonates in, 613 
 
 chemic changes in, 611 
 
 cholesterin in, 613 
 
 color of, 606 
 
 cystin in, 613 
 
 fat-crystals in, 613 
 
 hippuric acid in, 612 
 
 indigo in, 613 
 
 in nephritis, 581 
 
 leuciu in, 613 
 
 oxalate of urine in, 611 
 
 phosphates in, 611 
 
 quantity of, 606 
 
 reaction of, 606 
 
 sediments of, 611 
 
 specific gravity of, 606 
 
 sulphates in, 613 
 
 tyrosin in, 613 
 
 urates in, 612 
 
 uric acid crystals in, 611 
 
 xanthin in, 613 
 Uriniferous tubules, concretions in, 589 
 Urobilinuria, 607 
 Uschinsky's fluid, 190 
 Uterus, 618 
 
 adenoma of, 634 
 malignant, 634 
 
 amyloid degeneration of, 631 
 
 anteflexion of, 620 
 
 anteversion of, 620 
 
 bicornis, 619 
 
 carcinoma of, 634 
 
 congenital abnormalities, 619 
 
 cvsts of, 637 
 
 dilatation of, 622 
 
 erosions of, 627 
 
 fatty degeneration of, 631 
 
 fibroid of, 632 
 polyps of, 632 
 
 fcetalis seu infantalis, 619 
 
 hemorrhages of, 624 
 
 hyperemia of, 623 
 
 hyperplasia of mucous membrane of, 
 631 
 
 hypertrophy of, 631 
 
 hypoplasia of, 619 
 
 inflammation of, 624 
 
 inversion of, 622 
 
 lateral displacements of, 620 
 
 leiomyoma of, 632 
 
 myofibroma of, 632 
 
 parasites of, 637 
 
 polyps of, 632 
 
 prolapse of, 620 
 
 puerperal atrophy of, 631 
 infections of, 628 
 
 retroflexion, 620 
 
 rupture of, 623 
 
 sarcoma of, 634 
 
 senile atrophy of, 631 
 
 septus, 619 
 
 stenosis of, 622 
 
 syphilis of, 631 
 
 tuberculosis of, 630 
 
848 
 
 INDEX. 
 
 Uterus, tumors of, 632 
 unicornis, 620 
 upward dislocation of, 620 
 
 Vaccinia, animal parasites of, 273 
 Vacuolation of red blood-corpuscle, 305 
 Vacuolization of nerve-cell, 735 
 Vagina, 652 
 
 carcinoma of, 654 
 
 circulatory disturbances of, 653 
 
 cysts of, 654 
 
 fibroma of, 654 
 
 hyperemia of, 653 
 
 inflammation of, 653. See Vaginitis. 
 
 myofibroma of, 654 
 
 papilloma of, 654 
 
 sarcoma of, 654. 
 
 stenosis of, 652 
 
 syphilis of, 654 
 
 tuberculosis of, 654 
 
 tumors of, 654 
 Vaginal cystocele, 652 
 
 rectocele. 652 
 
 wall, prolapse of, 652 
 wounds and fistulas of, 652 
 Vaginitis, 653 
 
 acute catarrhal, 653 
 
 chronic catarrhal, 653 
 
 exfoliative, 653 
 
 pseudomembranous, 653 
 
 testis, 664, 666 
 hemorrhagic, 667 
 purulent, 667 
 serofibrinous, 666 
 serous, 666 
 Valvular defects, 348 
 Varicella, micro-organism of, 274 
 Varicose aneurysm, 395 
 
 veins of spinal cord, 786 
 Varicosity, 397 
 
 Variola, animal parasites of, 273 
 Vas deferens, inflammation of, 667 
 
 tuberculosis of, 668 
 Vascular goiter, 561 
 
 theories of inflammation, 98 
 Vein-stones, 396 
 Veins, 395 
 
 calcification of, 396 
 
 dilatation of, 397 
 
 fatty degeneration of, 396 
 
 inflammation of, 396 
 
 tuberculosis of, 399 
 
 tumors of, 398 
 Venereal wart, 157 
 Venom of serpents, poisoning by, 27 
 Venous hemorrhage, 48 
 
 hyperemia, 46 
 Ventricular septum, defects of, 348 
 Verrucose endocarditis, 354 
 
 tumors, 118 
 Vesica bipartitis, 599 
 Vesicular emphysema of lungs, 420 
 
 Vibrio cholerse Asiatics, 219 
 Vibrion septique, 240 
 Vicarious emphysema of lungs, 420 
 Virchow's theory of inflammation, 98 
 
 classification of tumors, 120 
 
 theory of tumors, 116 
 Voluntary muscles, diseases of, 706 
 Volvulus, 501 
 Vulva, 659 
 
 abscess of, 659 
 
 adenoma of, 660 
 
 carcinoma of, 661 
 
 chancroids of, 660 
 
 circulatory disturbances of, 659 
 
 cy#ts of, 661 
 
 diphtheria of, 660 
 
 elephantiasis of, 660 
 
 fibroma of, 660 
 
 fibromyxoina of, 660 
 
 gangrene of, 660 
 
 hematoma of, 659 
 
 hyperemia of, 659 
 
 inflammation of, 659 
 
 lipoma of, 660 
 
 myofibroma of, 660 
 
 papillomatous tumors of, 660 
 
 sarcoma of, 660 
 
 syphilis of, 660 
 
 tuberculosis of, 660 
 
 tumors of, 660 
 
 wounds of, 659 
 Vulvitis, 659 
 
 Wart, 157 
 
 venerea], 157 
 Waxy casts in nephritis, 582 
 Wens, 177 
 
 White blood-corpuscles, 298. See Leuko- 
 cytes. 
 
 infarct, 53 
 
 matter of cord, degeneration of, 799 
 
 softening of brain, 751 
 Whooping-cough, bacteriology of, 261 
 Widal reaction, 217 
 Wool-sorters' disease, 242 
 Wounds, repair of, 106 
 
 Xanthin, 36 
 
 diabeticorum, 126 
 
 iu urine, 613 
 Xanthoma, 126 
 
 diabeticorum, 126 
 
 vulgare, 126 
 
 Yellow fever, 260 
 antitoxin of, 261 
 bacillus of, 260 
 softening of brain, 751 
 
 Ziehl's solution, 187 
 Zuckergussleber, 534, 556 
 
CATALOGUE 
 
 OF THE 
 
 MEDICAL PUBLICATIONS 
 
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 W* B* SAUNDERS, 
 
 No. 925 WALNUT STREET, PHILADELPHIA. 
 
 Arranged Alphabetically and Classified under Subjects. 
 
 *TpHE books advertised in this Catalogue as being sold by subscription are usually to be 
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 letter. Money sent in any other way is at the risk of the sender. 
 
 
 See pages 30, 31, for a List of Contents classified according to subjects. 
 
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 American Text-Book of Genito-Urinary and Skin Diseases. Page 4. 
 
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 Anders' Practice of Medicine — Revised Edition. See page 6. 
 
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 Church and Peterson's Nervous and Mental Diseases. See page 9. 
 
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 Griffith on The Baby — Revised Edition. See page 12. 
 
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 Chapin's Compendium of Insanity. See page 8. 
 
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 and Walter S. Haines, M.D., Professor of Chemistry, Pharmacy, 
 and Toxicology in Rush Medical College, Chicago. In Preparation. 
 
 AN AMERICAN TEXT=BOOK OF OBSTETRICS. 
 
 By 15 Eminent American Obstetricians. Edited by Richard C. Nor- 
 
 ris, M.D.; Art Editor, Robert L. Dickinson, M.D. One handsome 
 
 imperial octavo volume of over 1000 pages, with nearly 900 beautiful 
 
 colored and half-tone illustrations. Cloth, $7.00 net; Sheep or Half 
 
 Morocco, $8.00 net. Sold by Subscription. 
 
 " Permit me to say that your American Text-Book of Obstetrics is the most magnificent 
 
 medical work that I have ever seen. I congratulate you and thank you for this superb work, 
 
 which alone is sufficient to place you first in the ranks of medical publishers." — ALEXANDER 
 
 J. C. Skene, Professor 0/ Gynecology in the Long Island College Hospital, Brooklyn, N. Y. 
 
 " This is the most sumptuously illustrated work on midwifery that has yet appeared. In 
 
 the number, the excellence, and the beauty of production of the illustrations it far surpasses 
 
 every other book upon the subject. This feature alone makes it a work which no medical 
 
 library should omit to purchase." — British Medical Journal. 
 
 " As an authority, as a book of reference, as a ' working book ' for the student or prac- 
 titioner, we commend it because we believe there is no better." — American Journal of the 
 Medical Sciences. 
 
 Illustrated Catalogue of the "American Text-Books " sent free upon application. 
 
Medical Publications of W. B. Saunders. 5 
 
 AN AMERICAN TEXT=BOOK OF PATHOLOGY. 
 
 Edited by John Guiteras, M.D., Professor of General Pathology and 
 of Morbid Anatomy in the University of Pennsylvania ; and David 
 Riesman, M.D., Demonstrator of Pathological Histology in the 
 University of Pennsylvania. In Preparation. 
 
 AN AMERICAN TEXT=BOOK OF PHYSIOLOGY. 
 
 By i o of the Leading Physiologists of America. Edited by William 
 H. Howell, Ph.D., M.D., Professor of Physiology in the Johns Hop- 
 kins University, Baltimore, Md. One handsome imperial octavo 
 volume of 1052 pages. Illustrated. Cloth, $6.00 net; Sheep or Half 
 Morocco, $7.00 net. Sold by Subscription. 
 
 " We can commend it most heartily, not only to all students of physiology, but to every 
 physician and pathologist, as a valuable and comprehensive work of reference, written by 
 men who are of eminent authority in their own special subjects." — London Lancet. 
 
 " To the practitioner of medicine and to the advanced student this volume constitutes, 
 we believe, the best exposition of the present status of the science of physiology in the 
 English language." — American Journal of the Medical Sciences. 
 
 AN AMERICAN TEXT-BOOK OF SURGERY. Second Edition. 
 
 By 13 Eminent Professors of Surgery. Edited by William W. Keen, 
 M.D., LL.D., and J. William White, M.D., Ph.D. Handsome 
 imperial octavo volume of 1250 pages, with 500 wood-cuts in the text, 
 and 39 colored and half-tone plates. Thoroughly revised and enlarged, 
 with a section devoted to " The Use of the Rontgen Rays in Surgery." 
 Cloth, $7.00 net; Sheep or Half Morocco, $8.00 net. Sold by Sub- 
 scription. 
 " Personally, I should not mind it being called THE Text-Book (instead of A Text- 
 Book) , for I know of no single volume which contains so readable and complete an account 
 of the science and art of Surgery as this does." — Edmund Owen, F.R.C.S., Member of 
 the Board of Examiners of the Royal College of Surgeons, England. 
 
 " If this text-book is a fair reflex of the present position of American surgery, we must 
 admit it is of a very high order of merit, and that English surgeons will have to look very 
 carefully to their laurels if they are to preserve a position in the van of surgical practice." — 
 London Lancet. 
 
 AN AMERICAN TEXT=BOOK OF THE THEORY AND PRACTICE 
 OF MEDICINE. 
 
 By 12 Distinguished American Practitioners. Edited by William 
 Pepper, M.D., LL.D., Professor of the Theory and Practice of Medi- 
 cine and of Clinical Medicine in the University of Pennsylvania. Two 
 handsome imperial octavo volumes of about 1000 pages each. Illus- 
 trated. Prices per volume : Cloth, $5.00 net ; Sheep or Half Morocco, 
 $6.00 net. Sold by Subscription. 
 
 " I am quite sure it will commend itself both to practitioners and students of medicine, 
 and become one of our most popular text-books." — Alfred Loomis, M.D., LL.D., Pro- 
 fessor of Pathology and Practice of Medicine, University of the City of New York. 
 
 " We reviewed the first volume of this work, and said : ' It is undoubtedly one of the 
 best text-books on the practice of medicine which we possess.' A consideration of the 
 second and last volume leads us to modify that verdict and to say that the completed work 
 is in our opinion the best of its kind it has ever been our fortune to see. " — New York Medical 
 Journal. 
 
 Illustrated Catalogue of the "American Text-Books" sent free upon application. 
 
6 Medical Publications of W. B. Saunders. 
 
 AN AMERICAN YEAR-BOOK OF MEDICINE AND SURGERY. 
 
 A Yearly Digest of Scientific Progress and Authoritative Opinion in all 
 branches of Medicine and Surgery, drawn from journals, monographs, 
 and text-books of the leading American and Foreign authors and 
 investigators. Collected and arranged, with critical editorial com- 
 ments, by eminent American specialists and teachers, under the general 
 editorial charge of George M. Gould, M.D. One handsome imperial 
 octavo volume of about 1200 pages. Uniform in style, size, and 
 general make-up with the "American Text-Book" Series. Cloth, 
 $6.50 net ; Half Morocco, $7.50 net. Sold by Subscription. 
 
 " It is difficult to know which to admire most — the research and industry of the distin- 
 guished band of experts whom Dr. Gould has enlisted in the service of the Year-Book, or the 
 wealth and abundance of the contributions to every department of science that have been 
 deemed worthy of analysis. . . . It is much more than a mere compilation of abstracts, 
 for, as each section is entrusted to experienced and able contributors, the reader has the 
 advantage of certain critical commentaries and expositions . . . proceeding from writers 
 fully qualified to perform these tasks. . . . It is emphatically a book which should find 
 a place in every medical library, and is in several respects more useful than the famous 
 ' Jahrbiicher ' of Germany." — London Lancet. 
 
 ANDERS' PRACTICE OF MEDICINE. Second Edition. 
 
 A Text-Book of the Practice of Medicine. By James M. Anders, 
 M.D., Ph.D., LL.D., Professor of the Practice of Medicine and of 
 Clinical Medicine, Medico- Chirurgical College, Philadelphia. In one 
 handsome octavo volume of 12S7 pages, fully illustrated. Cloth, 
 #5.50 net; Sheep or Half Morocco, $6.50 net. 
 
 " It is an excellent book, — concise, comprehensive, thorough, and up to date. It is a 
 credit to you ; but, more than that, it is a credit to the profession of Philadelphia — to us." 
 James C. Wilson, Professor of the Practice of Medicine and Clinical Medicine, Jefferson 
 Medical College, Philadelphia. 
 
 " I consider Dr. Anders' book not only the best late work on Medical Practice, but by 
 far the best that has ever been published. It is concise, systematic, thorough, and fully up 
 to date in everything. I consider it a great credit to both the author and the publisher." — 
 A. C. Cowperthwaite, President of the Illinois Homeopathic Medical Association. 
 
 ASHTON'S OBSTETRICS. Fourth Edition, Revised. 
 
 Essentials of Obstetrics. By W. Easterly Ashton, M.D., Pro- 
 fessor of Gynecology in the Medico-Chirurgical College, Philadelphia. 
 Crown octavo, 2 5 2 pages ; 75 illustrations. Cloth, $1. 00; interleaved 
 for notes, $1.25. 
 
 [See Saunders 1 Question- Compends, page 21.] 
 
 " Embodies the whole subject in a nut-shell. We cordially recommend it to our read 
 ers." — Chicago Medical Times. 
 
 BALL'S BACTERIOLOGY. Third Edition, Revised. 
 
 Essentials of Bacteriology ; a Concise and Systematic Introduction 
 to the Study of Micro-organisms. By M. V. Ball, M.D., Bacteriol- 
 ogist to St. Agnes' Hospital, Philadelphia, etc. Crown octavo, 218 
 pages; 82 illustrations, some in colors, and 5 plates. Cloth, $1.00; 
 interleaved for notes, $1.25. 
 
 [See Saunders'' Question- Compends, page 21.] 
 
 " The student or practitioner can readily obtain a knowledge of the subject from a perusal 
 of this book. The illustrations are clear and satisfactory." — Medical Record, New York. 
 
Medical Publications of W. B. Saunders. 7 
 
 BASTIN'S BOTANY. 
 
 Laboratory Exercises in Botany. By Edson S. Bastin, M.A., 
 late Professor of Materia Medica and Botany, Philadelphia College of 
 Pharmacy. Octavo volume of 536 pages, with 87 plates. Cloth, $2.50. 
 
 "It is unquestionably the best text-book on the subject that has yet appeared. The 
 work is eminently a practical one. We regard the issuance of this book as an important 
 event in the history of pharmaceutical teaching in this country, and predict for it an unquali- 
 fied success." — Alumni Report to the Philadelphia College of Pharmacy. 
 
 "There is no work like it in the pharmaceutical or botanical literature of this country, 
 and we predict for it a wide circulation." — Atnerican Journal of Pharmacy. 
 
 BECK'S SURGICAL ASEPSIS. 
 
 A Manual of Surgical Asepsis. By Carl Beck, M.D., Surgeon to 
 St. Mark's Hospital and the New York German Poliklinik, etc. 306 
 pages; 65 text-illustrations, and 12 full-page plates. Cloth, $1.25 net. 
 
 " An excellent exposition of the ' very latest ' in the treatment of wounds as practised 
 by leading German and American surgeons." — Birmingham (Eng.) Medical Review. 
 
 "This little volume can be recommended to any who are desirous of learning the details 
 of asepsis in surgery, for it will serve as a trustworthy guide." — London Lancet. 
 
 BOISLINIERE'S OBSTETRIC ACCIDENTS, EMERGENCIES, AND 
 OPERATIONS. 
 Obstetric Accidents, Emergencies, and Operations. By L. Ch. 
 
 Boisliniere, M.D., late Emeritus Professor of Obstetrics, St. Louis 
 Medical College. 381 pages, handsomely illustrated. Cloth, $2.00 net. 
 
 " It is clearly and concisely written, and is evidently the work of a teacher and practi- 
 tioner of large experience." — British Medical Journal. 
 
 " A manual so useful to the student or the general practitioner has not been brought to 
 our notice in a long time. The field embraced in the title is covered in a terse, interesting 
 way." — Yale Medical Journal. 
 
 BROCKWAY'S MEDICAL PHYSICS. Second Edition, Revised. 
 Essentials of Medical Physics. By Fred J. Brockway, M.D., 
 Assistant Demonstrator of Anatomy in the College of Physicians and 
 Surgeons, New York. Crown octavo, 330 pages; 155 fine illustrations. 
 Cloth, $ 1. 00 net ; interleaved for notes, #1.25 net. 
 
 [See Saunders 1 Question- Compends, page 21.] 
 
 " The student who is well versed in these pages will certainly prove qualified to com- 
 prehend with ease and pleasure the great majority of questions involving physical principles 
 likely to be met with in his medical studies." — American Practitioner and News. 
 
 "We know of no manual that affords the medical student a better or more concise 
 exposition of physics, and the book may be commended as a most satisfactory presentation 
 of those essentials that are requisite in a course in medicine." — New York Medical Journal. 
 
 " It contains all that one need know on the subject, is well written, and is copiously 
 illustrated." — Medical Record, New York. 
 
 BURR ON NERVOUS DISEASES. 
 
 A Manual of Nervous Diseases. By Charles W. Burr, M.D., 
 Clinical Professor of Nervous Diseases, Medico-Chirurgical College, 
 Philadelphia; Pathologist to the Orthopedic Hospital and Infirmary 
 for Nervous Diseases ; Visiting Physician to St. Joseph's Hospital, etc. 
 In Preparation. 
 
8 Medical Publications of W. B. Saunders. 
 
 BUTLERS MATERIA MEDICA, THERAPEUTICS, AND PHAR- 
 MACOLOGY. Second Edition, Revised. 
 A Text-Book of Materia Medica, Therapeutics, and Pharma- 
 cology. By George F. Butler, Ph.G., M.D., Professor of Materia 
 Medica and of Clinical Medicine in the College of Physicians and 
 Surgeons, Chicago; Professor of Materia Medica and Therapeutics, 
 Northwestern University, Woman's Medical School, etc. Octavo, 860 
 pages, illustrated. Cloth, $4.00 net; Sheep, $5.00 net. 
 
 " Taken as a whole, the book may fairly be considered as one of the most satisfactory 
 of any single-volume works on materia medica in the market." — Journal of the American 
 Medical Association. 
 
 " The work is executed in a clear, concise, and practical manner, and should meet with 
 a hearty endorsement from the students of our up-to-date colleges. The book will be found 
 a valuable work of reference for the practitioner." — American Medico-Surgical Bulletin. 
 
 CASSELBERRY ON THE NOSE AND THROAT. 
 
 Diseases of the Nose and Throat. By W. E. Casselberry, Pro- 
 fessor of Laryngology and Rhinology in the Northwestern University 
 Medical School, Chicago. /;/ Preparation. 
 
 CERNA ON THE NEWER REMEDIES. Second Edition, Revised. 
 Notes on the Newer Remedies, their Therapeutic Applications 
 and Modes of Administration. By David Cerna, M.D., Ph.D., 
 formerly Demonstrator of and Lecturer on Experimental Therapeutics 
 in the University of Pennsylvania ; Demonstrator of Physiology in the 
 Medical Department of the University of Texas. Rewritten and 
 greatly enlarged. Post-octavo, 253 pages. Cloth, $1.25. 
 
 " The appearance of this new edition of Dr. Cerna's very valuable work shows that it 
 is properly appreciated. The book ought to be in the possession of every practising physi- 
 cian." — New York Medical Journal. 
 
 CHAPIN ON INSANITY. 
 
 A Compendium of Insanity. By John B. Chapin, M.D., LL.D., 
 
 Physician-in-Chief, Pennsylvania Hospital for the Insane ; late Physi- 
 cian-Superintendent of the Willard State Hospital, New York ; Hon- 
 orary Member of the Medico-Psychological Society of Great Britain, 
 of the Society of Mental Medicine of Belgium. i2mo, 234 pages, 
 illustrated. Cloth, $1.25 net. 
 The author has given, in a condensed and concise form, a compendium of Diseases of 
 the Mind, for the convenient use and aid of physicians and students. The work will also 
 prove valuable to members of the legal profession and to those who, in their relations to the 
 insane and to those supposed to be insane, often desire to acquire some practical knowledge 
 of insanity presented in a form that may be understood by the non-professional reader. 
 
 CHAPMAN'S MEDICAL JURISPRUDENCE AND TOXICOLOGY. 
 Second Edition, Revised. 
 Medical Jurisprudence and Toxicology. By Henry C. Chapman, 
 M.D., Professor of Institutes of Medicine and Medical Jurisprudence 
 in the Jefferson Medical College of Philadelphia. 254 pages, with 55 
 illustrations and 3 full-page plates in colors. Cloth, $1.50 net. 
 
 " The best book of its class for the undergraduate that we know of." — New York 
 Medical Times. 
 
Medical Publications of W. B. Saunders. 9 
 
 CHURCH AND PETERSON'S NERVOUS AND MENTAL DISEASES. 
 Nervous and Mental Diseases. By Archibald Church, M.D., 
 Professor of Mental Diseases and Medical Jurisprudence in the North- 
 western University Medical School, Chicago ; and Frederick Peter- 
 son, M.D., Clinical Professor of Mental Diseases in the Woman's 
 Medical College, New York ; Chief of Clinic, Nervous Department, 
 College of Physicians and Surgeons, New York. In Preparation. 
 
 CLARKSON'S HISTOLOGY. 
 
 A Text=Book of Histology, Descriptive and Practical. By 
 
 Arthur Clarkson, M.B., CM. Edin., formerly Demonstrator of 
 Physiology in the Owen's College, Manchester; late Demonstrator of 
 Physiology in Yorkshire College, Leeds. Large octavo, 554 pages; 
 22 engravings in the text, and 174 beautifully colored original illustra- 
 tions. Cloth, strongly bound, $6.00 net. 
 
 " The work must be considered a valuable addition to the list of available text- books, 
 and is to be highly recommended." — New York Medical Journal. 
 
 "This is one of the best works for students we have ever noticed. We predict that the 
 book will attain a well-deserved popularity among our students." — Chicago Medical Recorder. 
 
 "The volume is a most valuable addition to the armamentarium of the teacher." — 
 Brooklyn Medical Journal. 
 
 CLIMATOLOGY. 
 
 Transactions of the Eighth Annual Meeting of the American 
 Climatological Association, held in Washington, September 22-25, 
 1891. Forming a handsome octavo volume of 276 pages, uniform with 
 remainder of series. (A limited quantity only.) Cloth, $1.50. 
 
 COHEN AND ESHNER'S DIAGNOSIS. 
 
 Essentials of Diagnosis. By Solomon Solis-Cohen, M.D., Pro- 
 fessor of Clinical Medicine and Applied Therapeutics in the Philadel- 
 phia Polyclinic ; and Augustus A. Eshner, M.D., Professor of Clinical 
 Medicine in the Philadelphia Polyclinic. Post-octavo, 382 pages; 55 
 illustrations. Cloth, $1.50 net. 
 
 [See Saunders 1 Question- Compends, page 21.] 
 
 "We can heartily commend the book to all those who contemplate purchasing a 'com- 
 pend.' It is modern and complete, and will give more satisfaction than many other works 
 which are perhaps too prolix as well as behind the times." — Medical Review, St. Louis. 
 
 CORWIN'S PHYSICAL DIAGNOSIS. 
 
 Essentials of Physical Diagnosis of the Thorax. By Arthur 
 M. Corwin, A.M., M.D., Demonstrator of Physical Diagnosis in Rush 
 Medical College, Chicago ; Attending Physician to Central Free Dis- 
 pensary, Department of Rhinology, Laryngology, and Diseases of the 
 Chest, Chicago. 200 pages, illustrated. Cloth, flexible covers, $1.25 net. 
 
 " It is excellent. The student who shall use it as his guide to the careful study of 
 physical exploration upon normal and abnormal subjects can scarcely fail to acquire a good 
 working knowledge of the subject." — Philadelphia Polyclinic. 
 
 "A most excellent little work. It brightens the memory of the differential diagnostic 
 signs, and it arranges orderly and in sequence the various objective phenomena to logical 
 solution of a careful diagnosis." — Journal of Nervous and Mental Diseases. 
 
10 Medical Publications of W. B. Saunders. 
 
 CRAGIN'S GYNAECOLOGY. Fourth Edition, Revised. 
 
 Essentials of Gynaecology. By Edwin B. Cragin, M.D., Attend- 
 ing Gynaecologist, Roosevelt Hospital, Out-Patients' Department, New 
 York, etc. Crown octavo, 200 pages; 62 fine illustrations. Cloth,. 
 $1.00; interleaved for notes, $1.25. 
 
 [See Saunders' Question- Compends, page 21.] 
 
 " A handy volume, and a distinct improvement on students' compends in general. No 
 author who was not himself a practical gynecologist could have consulted the student's needs 
 so thoroughly as Dr. Cragin has done." — Medical Record, New York. 
 
 CROOKSHANK'S BACTERIOLOGY. Fourth Edition, Revised. 
 
 A Text=Book of Bacteriology. By Edgar M. Crookshank, M.B., 
 Professor of Comparative Pathology and Bacteriology, King's College, 
 London. Octavo volume of 700 pages, with 273 engravings and 22 
 original colored plates. Cloth, $6.50 net; Half Morocco, $7.50 net. 
 
 " To the student who wishes to obtain a good resume of what has been done in bacteri- 
 ology, or who wishes an accurate account of the various methods of research, the book may 
 be recommended with confidence that he will find there what he requires." — London Lancet. 
 
 Da COSTA'S SURGERY. Second Ed., Revised and Greatly Enlarged. 
 Modern Surgery, General and Operative. By John Chalmers 
 DaCosta, M.D., Clinical Professor of Surgery, Jefferson Medical 
 College, Philadelphia ; Surgeon to the Philadelphia Hospital, etc. 
 Handsome octavo volume of 900 pages, profusely illustrated. Cloth, 
 $4.00 net; Half Morocco, $5.00 net. 
 
 "We know of no small work on surgery in the English language which so well fulfils 
 the requirements of the modern student." — Medico-Chirurgical Journal, Bristol, England. 
 
 DE SCHWEINITZ ON DISEASES OF THE EYE. Third Edition, 
 Revised. 
 Diseases of the Eye. A Handbook of Ophthalmic Practice. 
 
 By G. E. de Schweinitz, M.D., Professor of Ophthalmology in the 
 Jefferson Medical College, Philadelphia, etc. Handsome royal octavo 
 volume of 700 pages, with 256 fine illustrations and 2 chromo-litho- 
 graphic plates. Cloth, $4.00 net ; Sheep or Half Morocco, $5.00 net. 
 
 " A clearly written, comprehensive manual. One which we can commend to students 
 as a reliable text-book, written with an evident knowledge of the wants of those entering 
 upon the study of this special branch of medical science." — British Afedical Journal. 
 
 " A work that will meet the requirements not only of the specialist, but of the general 
 practitioner in a rare degree. I am satisfied that unusual success awaits it." — William 
 Pepper, M.D., Professor of the Theory and Practice of Medicine and Clinical Medicine, 
 University of Pennsylvania. 
 
 DORLAND'S OBSTETRICS. 
 
 A Manual of Obstetrics. By W. A. Newman Dorland, M.D., 
 Assistant Demonstrator of Obstetrics, University of Pennsylvania; 
 Instructor in Gynecology in the Philadelphia Polyclinic. 760 pages; 
 163 illustrations in the text, and 6 full-page plates. Cloth, $2.50 net. 
 
 " By far the best book on this subject that has ever come to our notice." — American 
 Medical Review. 
 
 " It has rarely been our duty to review a book which has given us more pleasure in its 
 perusal and more satisfaction in its criticism. It is a veritable encyclopedia of knowledge, 
 a gold mine of practical, concise thoughts." — American Medico- Surgical Bulletin. 
 
Medical Publications of W. B. Saunders. 11 
 
 FROTHINGHAM'S GUIDE FOR THE BACTERIOLOGIST. 
 
 Laboratory Guide for the Bacteriologist. By Langdon Froth- 
 ingham, M.D.V., Assistant in Bacteriology and Veterinary Science, 
 Sheffield Scientific School, Yale University. Illustrated. Cloth, 75 cts. 
 
 " It is a convenient and useful little work, and will more than repay the outlay neces- 
 sary for its purchase in the saving of time which would otherwise be consumed in looking 
 up the various points of technique so clearly and concisely laid down in its pages. " — Ameri- 
 can Medico- Stirgical Bulletin. 
 
 GARRIGUES' DISEASES OF WOMEN. Second Edition, Revised. 
 Diseases of Women. By Henry J. Garrigues, A.M., M.D., Pro- 
 fessor of Gynecology in the New York School of Clinical Medicine ; 
 Gynecologist to St. Mark's Hospital and to the German Dispensary, 
 New York City, etc. Handsome octavo volume of 728 pages, illus- 
 trated by 335 engravings and colored plates. Cloth, $4.00 net; 
 Sheep or Half Morocco, $5.00 net. 
 
 " One of the best text-books for students and practitioners which has been published in 
 the English language ; it is condensed, clear, and comprehensive. The profound learning 
 and great clinical experience of the distinguished author find expression in this book in a 
 most attractive and instructive form. Young practitioners to whom experienced consultants 
 may not be available will find in this book invaluable counsel and help." — Thad. A. 
 Reamy, M.D., LL.D., Professor of Clinical Gynecology, Medical College of Ohio. 
 
 GLEASON'S DISEASES OF THE EAR. Second Edition, Revised. 
 Essentials of Diseases of the Ear. By E. B. Gleason, SB., 
 M.D., Clinical Professor of Otology, Medico-Chirurgical College, 
 Philadelphia ; Surgeon-in-Charge of the Nose, Throat, and Ear Depart- 
 ment of the Northern Dispensary, Philadelphia. 208 pages, with 
 114 illustrations. Cloth, $1. 00; interleaved for notes, $1.25. 
 [See Saunders 1 Question- Compends, page 21.] 
 
 " It is just the book to put into the hands of a student, and cannot fail to give him a 
 useful introduction to ear-affections ; while the style of question and answer which is adopted 
 throughout the book is, we believe, the best method of impressing facts permanently on the 
 mind. ' ' — Liverpool Medico- Chirurgical Journal. 
 
 GOULD AND PYLE'S CURIOSITIES OF MEDICINE. 
 
 Anomalies and Curiosities of Medicine. By George M. Gould, 
 M.D., and Walter L. Pyle, M.D. An encyclopedic collection of 
 rare and extraordinary cases and of the most striking instances of 
 abnormality in all branches of Medicine and Surgery, derived from an 
 exhaustive research of medical literature from its origin to the present 
 day, abstracted, classified, annotated, and indexed. Handsome im- 
 perial octavo volume of 968 pages, with 295 engravings in the text, 
 and 12 full-page plates. Cloth, $6.00 net; Half Morocco, $7.00 net. 
 Sold by Subscription. 
 
 " One of the most valuable contributions ever made to medical literature. It is, so far 
 as we know, absolutely unique, and every page is as fascinating as a novel. Not alone for 
 the medical profession has this volume value : it will serve as a book of reference for all who 
 are interested in general scientific, sociologic, or medico-legal topics." — Brooklyn Medical 
 Journal. 
 
 "This is certainly a most remarkable and interesting volume. It stands alone among 
 medical literature, an anomaly on anomalies, in that there is nothing like it elsewhere in 
 medical literature. It is a book full of revelations from its first to its last page, and cannot 
 but interest and sometimes almost horrify its readers." — American Medico- Surgical Bulletin. 
 
12 Medical Publications of W. B. Saunders. 
 
 GRIFFIN'S MATERIA MEDICA AND THERAPEUTICS. 
 
 Manual of Materia Medica and Therapeutics. By Henry A. 
 Griffin, A.B., M.D., Assistant Physician to the Roosevelt Hospital, 
 Out-Patient Department, New York City. In Preparation. 
 
 GRIFFITH ON THE BABY. Second Edition, Revised. 
 
 The Care of the Baby. By J. P. Crozer Griffith, M.D., Clini- 
 cal Professor of Diseases of Children, University of Pennsylvania; 
 Physician to the Children's Hospital, Philadelphia, etc. nmo, 404 
 pages, with 67 illustrations in the text, and 5 plates. Cloth, $1.50. 
 
 " The best book for the use of the young mother with which we are acquainted. . . . 
 There are very few general practitioners who could not read the book through with advan- 
 tage. ' ' — Archives of Pediatrics. 
 
 "The whole book is characterized by rare good sense, and is evidently written by a 
 master hand. It can be read with benefit not only by mothers but by medical students and 
 by any practitioners who have not had large opportunities for observing children." — Ameri- 
 can Journal of Obstetrics. 
 
 GRIFFITH'S WEIGHT CHART. 
 
 Infant's Weight Chart. Designed by J. P. Crozer Griffith, M.D., 
 Clinical Professor of Diseases of Children in the University of Penn- 
 sylvania, etc. 25 charts in each pad. Per pad, 50 cents net. 
 
 A convenient blank for keeping a record of the child's weight during the first two years 
 of life. Printed on each chart is a curve representing the average weight of a healthy infant, 
 so that any deviation from the normal can readily be detected. 
 
 GROSS, SAMUEL D., AUTOBIOGRAPHY OF. 
 
 Autobiography of Samuel D. Gross, M.D., Emeritus Professor of 
 Surgery in the Jefferson Medical College, Philadelphia, with Remi- 
 niscences of His Times and Contemporaries. Edited by his Sons, 
 Samuel W. Gross, M.D., LL.D., late Professor of Principles of Sur- 
 gery and of Clinical Surgery in the Jefferson Medical College, and 
 A. Haller Gross, A.M., of the Philadelphia Bar. Preceded by a 
 Memoir of Dr. Gross, by the late Austin Flint, M.D., LL.D. In 
 two handsome volumes, each containing over 400 pages, demy octavo, 
 extra cloth, gilt tops, with fine Frontispiece engraved on steel. Price 
 per volume, $2.50 net. 
 
 " Dr. Gross was perhaps the most eminent exponent of medical science that America 
 has yet produced. His Autobiography, related as it is with a fulness and completeness 
 seldom to be found in such works, is an interesting and valuable book. He comments on 
 many things, especially, of course, on medical men and medical practice, in a very interest- 
 ing way." — The Spectator, London, England. 
 
 HAMPTON'S NURSING. 
 
 Nursing: Its Principles and Practice. By Isabel Adams Hamp- 
 ton, Graduate of the New York Training School for Nurses attached 
 to Bellevue Hospital ; Superintendent of Nurses, and Principal of the 
 Training School for Nurses, Johns Hopkins Hospital, Baltimore, Md. 
 i2mo, 484 pages, profusely illustrated. Cloth, $2.00 net. 
 
 " Seldom have we perused a book upon the subject that has given us so much pleasure 
 as the one before us. We would strongly urge upon the members of our own profession the 
 need of a book like this, for it will enable each of us to become a training school in him- 
 self. ' ' — Ontario Medical Journal. 
 
Medical Publications of W. B. Saunders. 13 
 
 HARE'S PHYSIOLOGY. Third Edition, Revised. 
 
 Essentials of Physiology. By H. A. Hare, M.D., Professor of 
 Therapeutics and Materia Medica in the Jefferson Medical College of 
 Philadelphia; Physician to the Jefferson Medical College Hospital. 
 Containing a series of handsome illustrations from the celebrated 
 " Icones Nervorum Capitis" of Arnold. Crown octavo, 239 pages. 
 Cloth, $1.00 net; interleaved for notes, $1.25 net. 
 
 [See Saunders'' Question- Compends, page 21.] 
 
 " The best condensation of physiological knowledge we have yet seen." — Medical 
 Record, New York. 
 
 HART'S DIET IN SICKNESS AND IN HEALTH. 
 
 Diet in Sickness and in Health. By Mrs. Ernest Hart, formerly 
 Student of the Faculty of Medicine of Paris and of the London School 
 of Medicine for Women ; with an Introduction by Sir Henry 
 Thompson, F.R.C.S., M.D., London. 220 pages; illustrated. Cloth, 
 $1.50. 
 
 " We recommend it cordially to the attention of all practitioners ; both to them and to 
 their patients it may be of the greatest service." — New York Medical Journal. 
 
 HAYNES' ANATOMY. 
 
 A Manual of Anatomy. By Irving S. Haynes, M.D., Adjunct 
 Professor of Anatomy and Demonstrator of Anatomy, Medical Depart- 
 ment of the New York University, etc. 680 pages, illustrated with 42 
 diagrams in the text, and 134 full -page half-tone illustrations from 
 original photographs of the author's dissections. Cloth, $2.50 net. 
 
 " This book is the work of a practical instructor — one who knows by experience the 
 requirements of the average student, and is able to meet these requirements in a very satis- 
 factory way. The book is one that can be commended." — Medical Record, New York. 
 
 HEISLER'S EMBRYOLOGY. 
 
 A Text=Book of Embryology. By John C. Heisler, M.D., Pro- 
 fessor of Anatomy in the Medico-Chirurgical College, Philadelphia. 
 In Preparation. 
 
 HIRST'S OBSTETRICS. 
 
 A Text=Book of Obstetrics. By Barton Cooke Hirst, M.D., 
 Professor of Obstetrics in the University of Pennsylvania. In Prepa- 
 ration. 
 
 HYDE AND MONTGOMERY ON SYPHILIS AND THE VENEREAL 
 DISEASES. 
 Syphilis and the Venereal Diseases. By James Nevins Hyde, 
 M.D., Professor of Skin and Venereal Diseases, and Frank H. Mont- 
 gomery, M.D., Lecturer on Dermatology and Genito-Urinary Diseases 
 in Rush Medical College, Chicago, 111. 618 pages, profusely illustrated. 
 Cloth, $2.50 net. 
 
 " We can commend this manual to the student as a help to him in his study of venereal 
 diseases. ' ' — Liverpool Medico- Chirurgical Journal. 
 
 "The best student's manual which has. appeared on the subject." — St. Louis Medical 
 and Surgical Journal. 
 
14 Medical Publications of W. B. Saunders. 
 
 JACKSON AND GLEASON'S DISEASES OF THE EYE, NOSE, AND 
 THROAT. Second Edition, Revised. 
 Essentials of Refraction and Diseases of the Eye. By Edward 
 Jackson, A.M., M.D., Professor of Diseases of the Eye in the Phila- 
 delphia Polyclinic and College for Graduates in Medicine ; and — 
 Essentials of Diseases of the Nose and Throat. By E. Bald- 
 win Gleason, M.D., Surgeon-in-Charge of the Nose, Throat, and 
 Ear Department of the Northern Dispensary of Philadelphia. Two 
 volumes in one. Crown octavo, 290 pages; 124 illustrations. Cloth, 
 $1.00; interleaved for notes, $1.25. 
 
 [See Saunders' Question- Compends, page 21.] 
 
 " Of great value to the beginner in these branches. The authors are both capable men, 
 and know what a student most needs." — Medical Record, New York. 
 
 KEATING'S DICTIONARY. Second Edition, Revised. 
 
 A New Pronouncing Dictionary of Medicine, with Phonetic 
 Pronunciation, Accentuation, Etymology, etc. By John M. 
 Keating, M.D., LL.D., Fellow of the College of Physicians of Phila- 
 delphia ; Vice-President of the American Paediatric Society ; Editor 
 " Cyclopaedia of the Diseases of Children," etc.; and Henry 
 Hamilton, Author of "A New Translation of Virgil's ^Eneid into 
 English Rhyme," etc.; with the collaboration of J. Chalmers Da- 
 Costa, M.D., and Frederick A. Packard, M.D. With an Appendix 
 containing Tables of Bacilli, Micrococci, Leucoma'ines, Ptomaines; 
 Drugs and Materials used in Antiseptic Surgery ; Poisons and their 
 Antidotes ; Weights and Measures ; Thermometric Scales ; New 
 Official and Unofficial Drugs, etc. One volume of over 800 pages. 
 Prices, with Denison's Patent Ready-Reference Index: Cloth, $5.00 
 net; Sheep or Half Morocco, $6.00 net; Half Russia, $6.50 net. 
 Without Patent Index: Cloth, $4. 00 net; Sheep or Half Morocco, 
 $5.00 net. 
 
 " I am much pleased with Keating's Dictionary, and shall take pleasure in recommend- 
 ing it to my classes." — Henry M. Lyman, M.D., Professor of the Principles and Practice 
 of Medicine, Rush Medical College, Chicago, III. 
 
 " I am convinced that it will be a very valuable adjunct to my study-table, convenient 
 in size and sufficiently full for ordinary use." — C. A. Lindsley, M.D., Professor of the 
 Theory and Practice of Medicine, Medical Deft. Yale University. 
 
 KEATING'S LIFE INSURANCE. 
 
 How to Examine for Life Insurance. By John M. Keating, 
 M.D., Fellow of the College of Physicians of Philadelphia; Vice- 
 President of the American Paediatric Society ; Ex-President of the 
 Association of Life Insurance Medical Directors. Royal octavo, 211 
 pages ; with two large half-tone illustrations, and a plate prepared by 
 Dr. McClellan from special dissections ; also, numerous other illustra- 
 tions. Cloth, $2.00 net. 
 
 " This is by far the most useful book which has yet appeared on insurance examination, 
 a subject of growing interest and importance. Not the least valuable portion of the volume 
 is Part II, which consists of instructions issued to their examining physicians by twenty-four 
 representative companies of this country. If for these alone, the book should be at the right 
 hand of every physician interested in this special branch of medical science." — The Medical 
 News. 
 
Medical Publications of W. B. Saunders. 15 
 
 KEEN ON THE SURGERY OF TYPHOID FEVER. 
 
 The Surgical Complications and Sequels of Typhoid Fever. 
 
 By Wm. W. Keen, M.D., LL.D., Professor of the Principles of Sur- 
 gery and of Clinical Surgery, Jefferson Medical College, Philadelphia; 
 Corresponding Member of the Societe de Chirurgie, Paris ; Honorary 
 Member of the Societe Beige de Chirurgie, etc. Octavo volume of 
 386 pages, illustrated. Cloth, $3.00 net. 
 
 This monograph is the only one in any language covering the entire subject of the 
 Surgical Complications and Sequels of Typhoid Fever. It will prove to be of importance 
 and interest not only to the general surgeon and physician, but also to many specialists — laryn- 
 .gologists, gynecologists, pathologists, and bacteriologists. 
 
 KEEN'S OPERATION BLANK. Second Edition, Revised Form. 
 An Operation Blank, with Lists of Instruments, etc. Required 
 in Various Operations. Prepared by W. W. Keen, M.D., LL.D., 
 Professor of the Principles of Surgery in Jefferson Medical College, 
 Philadelphia. Price per pad, containing blanks for fifty operations, 
 50 cents net. 
 
 KYLE ON THE NOSE AND THROAT. 
 
 Diseases of the Nose and Throat. By D. Braden Kyle, M.D., 
 Clinical Professor of Laryngology and Rhinology, Jefferson Medical 
 College, Philadelphia; Consulting Laryngologist, Rhinologist, and 
 Otologist, St. Agnes' Hospital ; Bacteriologist to the Philadelphia 
 Orthopedic Hospital. In Preparation. 
 
 LAINE'S TEMPERATURE CHART. 
 
 Temperature Chart. Prepared by D. T. Laine, M.D. Size 8x13^ 
 inches. A conveniently arranged Chart for recording Temperature, 
 with columns for daily amounts of Urinary and Fecal Excretions, 
 Food, Remarks, etc. On the back of each chart is given in full the 
 method of Brand in the treatment of Typhoid Fever. Price, per pad 
 of 25 charts, 50 cents net. 
 
 " To the busy practitioner this chart will be found of great value in fever cases, and 
 ■especially for cases of typhoid." — Indian Lancet, Calcutta. 
 
 LOCKWOOD'S PRACTICE OF MEDICINE. 
 
 A Manual of the Practice of Medicine. By George Roe Lock- 
 wood, M.D., Professor of Practice in the Woman's Medical College 
 of the New York Infirmary, etc. 935 pages, with 75 illustrations in 
 the text, and 22 full-page plates. Cloth, $2.50 net. 
 
 " Gives in a most concise manner the points essential to treatment usually enumerated 
 in the most elaborate works." — Massachusetts Medical Journal. 
 
 LONG'S SYLLABUS OF GYNECOLOGY. 
 
 A Syllabus of Gynecology, arranged in Conformity with " An 
 American Text=Book of Gynecology." By J. W. Long, M.D., 
 Professor of Diseases of Women and Children, Medical College of 
 Virginia, etc. Cloth, interleaved, $1.00 net. 
 
 " The book is certainly an admirable resume of what every gynecological student and 
 practitioner should know, and will prove of value not only to those who have the ' American 
 Text-Book of Gynecology,' but to others as well." — Brooklyn Medical Journal. 
 
16 Medical Publications of W. B. Saunders. 
 
 MACDONALD'S SURGICAL DIAGNOSIS \ND TREATMENT. 
 
 Surgical Diagnosis and Treatment. By J. W. Macdonald, M.D. 
 Edin., L.R.C.S., Edin., Professor of the Practice of Surgery and of 
 Clinical Surgery in Hamline University ; Visiting Surgeon to St. 
 Barnabas' Hospital, Minneapolis, etc. Handsome octavo volume of 
 800 pages, profusely illustrated. Cloth, $5.00 net; Half Morocco, 
 $6.00 net. 
 
 "A thorough and complete work on surgical diagnosis and treatment, free from pad- 
 ding, full of valuable material, and in accord with the surgical teaching of the day." — The 
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 " The work is brimful of just the kind of practical information that is useful alike to 
 students and practitioners. It is a pleasure to commend the book because of its intrinsic 
 value to the medical practitioner." — Cincinnati Lancet- Clinic. 
 
 MALLORY AND WRIGHT'S PATHOLOGICAL TECHNIQUE. 
 
 Pathological Technique. A Practical Manual for Laboratory Work 
 in Pathology, Bacteriology, and Morbid Anatomy, with chapters on 
 Post- Mortem Technique and the Performance of Autopsies. By Frank 
 B. Mallorv, A.M., M.D., Assistant Professor of Pathology, Harvard 
 University Medical School, Boston; and James H. Wright, A.M., 
 M.D., Instructor in Pathology, Harvard University Medical School, 
 Boston. Octavo volume of 396 pages, handsomely illustrated. Cloth, 
 $2.50 net. 
 
 " I have been looking forward to the publication of this book, and I am glad to say that 
 I find it to be a most useful laboratory and post-mortem guide, full of practical information, 
 and well up to date." — William H. Welch, Professor of Pathology, Johns Hopkins Uni- 
 versity, Baltimore, Md. 
 
 MARTIN'S MINOR SURGERY, BANDAGING, AND VENEREAL 
 DISEASES. Second Edition, Revised. 
 Essentials of Minor Surgery, Bandaging, and Venereal 
 Diseases. By Edward Martin, A.M., M.D., Clinical Professor of 
 Genito-Urinary Diseases, University of Pennsylvania, etc. Crown 
 octavo, 166 pages, with 78 illustrations. Cloth, $1.00; interleaved for 
 notes, $1.25. 
 
 [See Saunders' Question- Compends, page 21.] 
 
 "A very practical and systematic study of the subjects, and shows the author's famil- 
 iarity with the needs of students." — Therapeutic Gazette. 
 
 MARTIN'S SURGERY. Sixth Edition, Revised. 
 
 Essentials of Surgery. Containing also Venereal Diseases, Surgi- 
 cal Landmarks, Minor and Operative Surgery, and a complete de- 
 scription, with illustrations, of the Handkerchief and Roller Bandages. 
 By Edward Martin, A.M., M.D., Clinical Professor of Genito- 
 Urinary Diseases, University of Pennsylvania, etc. Crown octavo, 338 
 pages, illustrated. With an Appendix containing full directions for the 
 preparation of the materials used in Antiseptic Surgery, etc. Cloth, 
 |i.oo; interleaved for notes, $'1.25. 
 
 [See Saunders 1 Question- Compends, page 21.] 
 
 " Contains all necessary essentials of modern surgery in a comparatively small space. 
 Its style is interesting, and its illustrations are admirable." — Medical and Surgical Reporter. 
 
Medical Publications of W. B. Saunders. 17 
 
 McFARLAND'S PATHOGENIC BACTERIA. Second Edition, Re- 
 vised and Greatly Enlarged. 
 Text=Book upon the Pathogenic Bacteria. By Joseph McFar- 
 land, M. D. , Professor of Pathology and Bacteriology in the Medico- 
 Chirurgical College of Philadelphia, etc. Octavo volume of 497 pages, 
 finely illustrated. Cloth, $2.50 net. 
 
 " Dr. McFarland has treated the subject in a systematic manner, and has succeeded in 
 presenting in a concise and readable form the essentials of bacteriology up to date. Alto- 
 gether, the book is a satisfactory one, and I shall take pleasure in recommending it to the 
 students of Trinity College." — H. B. Anderson, M.D. , Professor of Pathology and Bac- 
 teriology, Trinity Medical College, Toronto. 
 
 MEIGS ON FEEDING IN INFANCY. 
 
 Feeding in Early Infancy. By Arthur V. Meigs, M.D. Bound 
 in limp cloth, flush edges, 25 cents net. 
 
 " This pamphlet is worth many times over its price to the physician. The author's 
 experiments and conclusions are original, and have been the means of doing much good." — 
 Medical Bulletin. 
 
 MOORE'S ORTHOPEDIC SURGERY. 
 
 A Manual of Orthopedic Surgery. By James E. Moore, M.D., 
 Professor of Orthopedics and Adjunct Professor of Clinical Surgery, 
 University of Minnesota, College of Medicine and Surgery. Octavo 
 volume of 356 pages, handsomely illustrated. Cloth, $2.50 net. 
 
 A practical book based upon the author's experience, in which special stress is laid 
 upon early diagnosis, and treatment such as can be carried out by the general practitioner. 
 The teachings of the author are in accordance with his belief that true conservatism is to 
 be found in the middle course between the surgeon who operates too frequently and the 
 orthopedist who seldom operates. 
 
 MORRIS'S MATERIA MEDICA AND THERAPEUTICS. Fifth 
 Edition, Revised. 
 Essentials of Materia Medica, Therapeutics, and Prescription 
 Writing. By Henry Morris, M.D., late Demonstrator of Thera- 
 peutics, Jefferson Medical College, Philadelphia; Fellow of the College 
 of Physicians, Philadelphia, etc. Crown octavo, 288 pages. Cloth, 
 $1.00; interleaved for notes, $1.25. 
 
 [See Saunders'' Question- Compends , page 21.] 
 
 " This work, already excellent in the old edition, has been largely improved by revi 
 sion. " — American Practitioner and News. 
 
 MORRIS, WOLFF, AND POWELL'S PRACTICE OF MEDICINE. 
 Third Edition, Revised. 
 Essentials of the Practice of Medicine. By Henry Morris, M.D., 
 late Demonstrator of Therapeutics, Jefferson Medical College, Phila- 
 delphia ; with an Appendix on the Clinical and Microscopic Examina- 
 tion of Urine, by Lawrence Wolff, M. D. , Demonstrator of Chemistry, 
 Jefferson Medical College, Philadelphia. Enlarged by some 300 essen- 
 tial formulae collected and arranged by William M. Powell, M.D. 
 Post-octavo, 488 pages. Cloth, $2.00. 
 
 [See Saunders' Question- Compends, page 21.] 
 
 " The teaching is sound, the presentation graphic ; matter full as can be desired, »nd 
 style attractive." — American Practitioner and News. 
 2 
 
18 Medical Publications of W. B. Saunders. 
 
 MORTEN'S NURSE'S DICTIONARY. 
 
 Nurse's Dictionary of Medical Terms and Nursing Treat- 
 ment. Containing Definitions of the Principal Medical and Nursing 
 Terms and Abbreviations ; of the Instruments, Drugs, Diseases, Acci- 
 dents, Treatments, Operations, Foods, Appliances, etc. encountered 
 in the ward or in the sick-room. By Honnor Morten, author of 
 " How to Become a Nurse," etc. i6mo, 140 pages. Cloth, $1.00. 
 
 " A handy, compact little volume, containing a large amount of general information, all 
 of which is arranged in dictionary or encyclopedic form, thus facilitating quick reference. 
 It is certainly of value to those for whose use it is published." — Chicago Clinical Review. 
 
 NANCREDE'S ANATOMY. Fifth Edition. 
 
 Essentials of Anatomy, including the Anatomy of the Viscera. 
 By Charles B. Nancrede, M.D., Professor of Surgery and of Clini- 
 cal Surgery in the University of Michigan, Ann Arbor. Crown octavo, 
 388 pages; 180 illustrations. With an Appendix containing over 60 
 illustrations of the osteology of the human body. Based upon Gray's 
 Anatomy. Cloth, $1.00; interleaved for notes, $1.25. 
 [See Saunders" Question- Compends, page 21.] 
 
 " For self-quizzing and keeping fresh in mind the knowledge of anatomy gained at 
 school, it would not be easy to speak of it in terms too favorable." — Atnerican Practitioner. 
 
 NANCREDE'S ANATOMY AND DISSECTION. Fourth Edition. 
 Essentials of Anatomy and Manual of Practical Dissection. 
 
 By Charles B. Nancrede, M.D., Professor of Surgery and of Clinical 
 Surgery, University of Michigan, Ann Arbor. Post-octavo ; 500 pages, 
 with full-page lithographic plates in colors, and nearly 200 illustrations. 
 Extra Cloth (or Oilcloth for the dissection-room), $2.00 net. 
 
 " It may in many respects be considered an epitome of Gray"s popular work on general 
 anatomy, at the same time having some distinguishing characteristics of its own to commend 
 it. The plates are of more than ordinary excellence, and are of especial value to students 
 in their work in the dissecting room." — Journal of the Atnerican Medical Association. 
 
 NORRIS'S SYLLABUS OF OBSTETRICS. Third Edition, Revised. 
 Syllabus of Obstetrical Lectures in the Medical Department 
 of the University of Pennsylvania. By Richard C. Norris, 
 A.M., M.D., Demonstrator of Obstetrics, University of Pennsylvania. 
 Crown octavo, 222 pages. Cloth, interleaved for notes, $2.00 net. 
 
 "This work is so far superior to others on the same subject that we take pleasure in 
 calling attention briefly to its excellent features. It covers the subject thoroughly, and will 
 prove invaluable both to the student and the practitioner." — Medical Record, New York. 
 
 PENROSE'S DISEASES OF WOMEN. Second Edition, Revised. 
 A Text=Book of Diseases of Women. By Charles B. Penrose, 
 M.D., Ph.D., Professor of Gynecology in the University of Pennsyl- 
 vania ; Surgeon to the Gynecean Hospital, Philadelphia. Octavo 
 volume of 529 pages, handsomely illustrated. Cloth, $3.50 net. 
 
 "I shall value very highly the copy of Penrose's 'Diseases of Women' received. 
 I have already recommended it to my class as THE BEST book." — Howard A. Kelly, 
 Professor of Gynecology and Obstetrics, Johns Hopkins University, Baltimore, Md. 
 
 " The book is to be commended without reserve, not only to the student but to the 
 general practitioner who wishes to have the latest and best modes of treatment explained 
 with absolute clearness." — Therapeutic Gazette. 
 
Medical Publications of W. B. Saunders. 19 
 
 POWELL'S DISEASES OF CHILDREN. Second Edition. 
 
 Essentials of Diseases of Children. By William M. Powell, 
 M.D., Attending Physician to the Mercer House for Invalid Women 
 at Atlantic City, N. J. ; late Physician to the Clinic for the Diseases of 
 Children in the Hospital of the University of Pennsylvania. Crown 
 octavo, 222 pages. Cloth, $1.00; interleaved for notes, $1.25. 
 [See Saunders' Question- Compends, page 21.] 
 
 "Contains the gist of all the best works in the department to which it relates."— 
 American Practitioner and News. 
 
 PRINGLE'S SKIN DISEASES AND SYPHILITIC AFFECTIONS. 
 Pictorial Atlas of Skin Diseases and Syphilitic Affections 
 (American Edition). Translation from the French. Edited by 
 J. J. Pringle, M.B., F.R.C.P., Assistant Physician to the Middlesex 
 Hospital, London. Photo-lithochromes from the famous models in 
 the Museum of the Saint-Louis Hospital, Paris, with explanatory wood- 
 cuts and text. In 12 Parts. Price per Part, $3.00. Complete in 
 one volume, Half Morocco binding, $40.00 net. 
 
 "I strongly recommend this Atlas. The plates are exceedingly well executed, and 
 will be of great value to all studying dermatology." — Stephen Mackenzie, M.D. 
 
 ' ' The introduction of explanatory wood-cuts in the text is a novel and most important 
 feature which greatly furthers the easier understanding of the excellent plates, than which 
 nothing, we venture to say, has been seen better in point of correctness, beauty, and general 
 merit." — New York Medical Journal. 
 
 PYE'S BANDAGING. 
 
 Elementary Bandaging and Surgical Dressing. With Direc- 
 tions concerning the Immediate Treatment of Cases of Emergency. 
 For the use of Dressers and Nurses. By Walter Pye, F.R.C.S., late 
 Surgeon to St. Mary's Hospital, London. Small 121110, with over 80 
 illustrations. Cloth, flexible covers, 75 cents net. 
 i( The directions are clear and the illustrations are good." — London Lancet. 
 "The author writes well, the diagrams are clear, and the book itself is small and port- 
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 RAYMOND'S PHYSIOLOGY. 
 
 A Manual of Physiology. By Joseph H. Raymond, A.M., M.D., 
 Professor of Physiology and Hygiene and Lecturer on Gynecology in 
 the Long Island College Hospital ; Director of Physiology in the 
 Hoagland Laboratory, etc. 382 pages, with 102 illustrations in the 
 text, and 4 full-page colored plates. Cloth, $1.25 net. 
 
 " Extremely well gotten up, and the illustrations have been selected with care. The 
 text is fully abreast with modern physiology." — British Medical Journal. 
 
 RONTGEN RAYS. 
 
 Archives of the Rontgen Ray (Formerly Archives of Clinical 
 Skiagraphy). Edited by Sydney Rowland, M.A., M.R.C.S., and 
 
 W. S. Hedley, M.D., M.R.C.S. A series of collotype illustrations, 
 with descriptive text, illustrating the applications of the new photo- 
 graphy to Medicine and Surgery. Price per Part, #1.00. Now ready: 
 Vol. I., Parts I. to IV.: Vol. II. , Parts I., II. 
 
Saunders' 
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 1. ESSENTIALS OF PHYSIOLOGY. By H. A. Hare, M.D. Third edition, 
 
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 2. ESSENTIALS OF SURGERY. By Edward Martin, M.D. Sixth edition, 
 
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Saunders' New Series of Manuals* 
 
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 PHYSIOLOGY. By Joseph Howard Raymond, A.M., M.D., Professor of Physiology 
 and Hygiene and Lecturer on Gynecology in the Long Island College Hospital; 
 Director of Physiology in the Hoagland Laboratory, etc. Illustrated. Cloth, $1.25 net. 
 
 SURGERY, General and Operative. By John Chalmers DaCosta, M.D., Clini- 
 cal Professor of Surgery, Jefferson Medical College, Philadelphia; Surgeon to the 
 Philadelphia Hospital, etc. Second edition, thoroughly revised and greatly enlarged. 
 Octavo, 900 pages, profusely illustrated. Cloth, $4.00 net ; Half Morocco, $5.00 net. 
 
 DOSE=BOOK AND MANUAL OF PRESCRIPTION=WRITING. By E. Q. 
 
 Thornton, M.D., Demonstrator of Therapeutics, Jefferson Medical College, Phila- 
 delphia. Illustrated. Cloth, #1.25 net. 
 
 SURGICAL ASEPSIS. By Carl Beck, M.D., Surgeon to St. Mark's Hospital and 
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 MEDICAL JURISPRUDENCE. By Henry C. Chapman, M.D. Professor of Insti- 
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 delphia. Illustrated. Cloth, $1.50 net. 
 
 SYPHILIS AND THE VENEREAL DISEASES. By James Nevins Hyde, M.D., 
 Professor of Skin and Venereal Diseases, and Frank H. Montgomery, M.D., 
 Lecturer on Dermatology and Genito-Urinary Diseases in Rush Medical College, 
 Chicago. Profusely illustrated. (Double number.) Cloth, $2.50 net. 
 
 PRACTICE OF MEDICINE. By George Roe Lockwood, M.D., Professor of 
 Practice in the Woman's Medical College of the New York Infirmary; Instructor in 
 Physical Diagnosis in the Medical Department of Columbia College, etc. Illustrated. 
 (Double number.) Cloth, $2.50 net. 
 
 MANUAL OF ANATOMY. By Irving S. Haynes, M.D., Adjunct Professor of 
 Anatomy and Demonstrator of Anatomy, Medical Department of the New York 
 University, etc. Beautifully illustrated. (Double Number.) Cloth, $2.50 net. 
 
 MANUAL OF OBSTETRICS. By W. A. Newman Dorland, M.D., Assistant 
 Demonstrator of Obstetrics, University of Pennsylvania ; Chief of Gynecological Dis- 
 pensary, Pennsylvania Hospital, etc. Profusely illustrated. (Double number.) Cloth, 
 $2.50 net. 
 
 DISEASES OF WOMEN. By J. Bland Sutton, F.R.C.S., Assistant Surgeon to 
 Middlesex Hospital and Surgeon to Chelsea Hospital, London ; and Arthur E. 
 Giles, M.D., B.Sc. Lond. , F.R.C.S. Edin., Assistant Surgeon to Chelsea Hospital, 
 London. Handsomely illustrated. (Double number.) Cloth, $2.50 net. 
 
 VOLUMES IN PREPARATION. 
 
 NOSE AND THROAT. By D. Braden Kyle, M.D., Clinical Professor of Laryn- 
 gology and Rhinology, Jefferson Medical College, Philadelphia ; Consulting Laryngolo- 
 gist, Rhinologist, and Otologist, St. Agnes' Hospital ; Bacteriologist to the Philadel- 
 phia Orthopedic Hospital and Infirmary for Nervous Diseases, etc. 
 
 NERVOUS DISEASES. By Charles W. Burr, M.D., Clinical Professor of Nervous 
 Diseases, Medico-Chirurgical College, Philadelphia; Pathologist to the Orthopaedic 
 Hospital and Infirmary for Nervous Diseases ; Visiting Physician to the St. Joseph 
 Hospital, etc. 
 
 *** There will be published in the same series, at short intervals, carefully-prepared works 
 on various subjects by prominent specialists. 
 
 Pamphlet containing specimen pages, etc. sent free upon application. 
 
24 Medical Publications of W. B. Saunders, 
 
 SAUNDBY'S RENAL AND URINARY DISEASES. 
 
 Lectures on Renal and Urinary Diseases. By Robert Saundbv, 
 M.D. Edin., Fellow of the Royal College of Physicians, London, and 
 of the Royal Medico-Chirurgical Society ; Physician to the General 
 Hospital ; Consulting Physician to the Eye Hospital and to the Hos- 
 pital for Diseases of Women; Professor of Medicine in Mason College, 
 Birmingham, etc. Octavo volume of 434 pages, with numerous illus- 
 trations and 4 colored plates. Cloth, $2.50 net. 
 
 " The volume makes a favorable impression at once. The style is clear and succinct. 
 We cannot find any part of the subject in which the views expressed are not carefully thought 
 out and fortified by evidence drawn from the most recent sources. The book may be cordially 
 recommended." — British Medical Journal. 
 
 SAUNDERS' POCKET MEDICAL FORMULARY. Fifth Edition, 
 Revised. 
 
 By William M. Powell, M.D., Attending Physician to the Mercer 
 House for Invalid Women at Atlantic City, N. J. Containing 1800 
 formulae selected from the best-known authorities. With an Appen- 
 dix containing Posological Table, Formulas and Doses for Hypo- 
 dermic Medication, Poisons and their Antidotes, Diameters of the 
 Female Pelvis and Fcetal Head, Obstetrical Table, Diet List for Various 
 Diseases, Materials and Drugs used in Antiseptic Surgery, Treatment 
 of Asphyxia from Drowning, Surgical Remembrancer, Tables of 
 Incompatibles, Eruptive Fevers, Weights and Measures, etc. Hand- 
 somely bound in flexible morocco, with side index, wallet, and flap. 
 $1.75 net. 
 
 " This little book, that can be conveniently carried in the pocket, contains an immense 
 amount of material. It is very useful, and, as the name of the author of each prescription 
 is given, is unusually reliable." — Medical Record, New York. 
 
 SAUNDERS' POCKET MEDICAL LEXICON. Fourth Edition, 
 Revised. 
 A Dictionary of Terms and Words used in Medicine and 
 Surgery. By John M. Keating, M.D., Fellow of the College of 
 
 Physicians of Philadelphia; Editor of the "Cyclopaedia of Diseases 
 of Children," etc.; Author of the "New Pronouncing Dictionary of 
 Medicine;" and Henry Hamilton, Author of "A New Translation 
 of Virgil's ^Eneid into English Verse;" Co- Author of the "New 
 Pronouncing Dictionary of Medicine." 32mo, 280 pages. Cloth, 
 75 cents; Leather Tucks, $1.00. 
 
 " Remarkably accurate in terminology, accentuation, and definition." — Journal oj the 
 American Medical Association. 
 
 SAYRE'S PHARMACY. Second Edition, Revised. 
 
 Essentials of the Practice of Pharmacy. By Lucius E. Sayre, 
 M.D., Professor of Pharmacy and Materia Medica in the University of 
 Kansas. Crown octavo, 200 pages. Cloth, $1.00; interleaved for 
 notes, $1.25. 
 
 [See Saunders 1 Question- Compends, page 21.] 
 
 ' ' The topics are treated in a simple, practical manner, and the work forms a very useful 
 student's manual." — Boston Medical and Surgical Journal. 
 
Medical Publications of W. B. Saunders. 25 
 
 SEMPLE'S LEGAL MEDICINE, TOXICOLOGY, AND HYGIENE. 
 Essentials of Legal Medicine, Toxicology,, and Hygiene. By 
 
 C. E. Armand Semple, B. A., M. B. Cantab., M. R. C. P. Lond., 
 Physician to the Northeastern Hospital for Children, Hackney, etc. 
 Crown octavo, 2 1 2 pages ; 130 illustrations. Cloth, $1. 00; interleaved 
 for notes, $1.25. 
 
 [See Saunders' Question- Compends, page 21.] 
 
 " No general practitioner or student can afford to be without this valuable work. The 
 subjects are dealt with by a masterly hand." — London Hospital Gazette. 
 
 SEMPLE'S PATHOLOGY AND MORBID ANATOMY. 
 
 Essentials of Pathology and Morbid Anatomy. By C. E. 
 
 Armand Semple, B.A., M.B. Cantab., M.R.C.P. Lond., Physician to 
 the Northeastern Hospital for Children, Hackney, etc. Crown octavo, 
 174 pages; illustrated. Cloth, $1.00; interleaved for notes, $1.25. 
 [See Saunders' Question- Compends, page 21.] 
 
 " Should take its place among the standard volumes on the bookshelf of both student 
 and practitioner." — London Hospital Gazette. 
 
 SENN'S GENITOURINARY TUBERCULOSIS. 
 
 Tuberculosis of the Genito=Urinary Organs, Male and Female. 
 
 By Nicholas Senn, M.D., Ph.D., LL.D., Professor of the Practice of 
 Surgery and of Clinical Surgery, Rush Medical College, Chicago. 
 Handsome octavo volume of 320 pages, illustrated. Cloth, $3.00 net. 
 
 " An important book upon an important sutvject, and written by a man of mature judg- 
 ment and wide experience. The author has given us an instructive book upon one of the 
 most important subjects of the day." — Clinical Reporter. 
 
 " A work which adds another to the many obligations the profession owes the talented 
 
 author." — Chicago Medical Recorder. 
 
 SENN'S SYLLABUS OF SURGERY. 
 
 A Syllabus of Lectures on the Practice of Surgery, arranged 
 in conformity with " An American Text=Book of Surgery." By 
 
 Nicholas Senn, M.D., Ph.D., Professor of the Practice of Surgery and 
 of Clinical Surgery in Rush Medical College, Chicago. Cloth, $2.00. 
 
 " This syllabus will be found of service by the teacher as well as the student, the work 
 being superbly done. There is no praise too high for it. No surgeon should be without 
 it." — New York Medical Times. 
 
 SENN'S TUMORS. 
 
 Pathology and Surgical Treatment of Tumors. By N. Senn, 
 
 M.D., Ph.D., LL.D., Professor of Surgery and of Clinical Surgery, 
 Rush Medical College ; Professor of Surgery, Chicago Polyclinic ; 
 Attending Surgeon to Presbyterian Hospital; Surgeon-in- Chief, St. 
 Joseph's Hospital, Chicago. Octavo volume of 710 pages, with 515 
 engravings, including full-page colored plates. Cloth, $6.00 net; 
 Half Morocco, $7.00 net. 
 
 " The most exhaustive of any recent book in English on this subject. It is well illus- 
 trated, and will doubtless remain as the principal monograph on the subject in our language 
 for some years. The book is handsomely illustrated and printed, and the author has given a 
 notable and lasting contribution to surgery." — Journal of the American Medical Association. 
 
26 Medical Publications of W. B. Saunders. 
 
 SHAW'S NERVOUS DISEASES AND INSANITY. Third Edition, 
 Revised. 
 Essentials of Nervous Diseases and Insanity. By John C. 
 Shaw, M.D., Clinical Professor of Diseases of the Mind and Nervous 
 System, Long Island College Hospital Medical School ; Consulting 
 Neurologist to St. Catherine's Hospital and to the Long Island College 
 Hospital. Crown octavo, 186 pages; 48 original illustrations. Cloth, 
 $1.00 ; interleaved for notes, $1.25. 
 
 [See Saunders' Question- Compends, page 21.] 
 
 " Clearly and intelligently written." — Boston Medical and Surgical Journal. 
 
 " There is a mass of valuable material crowded into this small compass. 1 ' — American 
 Medico- Surg ical Bulletin . 
 
 STARR'S DIETS FOR INFANTS AND CHILDREN. 
 
 Diets for Infants and Children in Health and in Disease. By 
 
 Louis Starr, M.D., Editor of "An American Text-Book of the 
 Diseases of Children." 230 blanks (pocket-book size), perforated 
 and neatly bound in flexible morocco. $1.25 net. 
 
 The first series of blanks are prepared for the first seven months of infant life ; each 
 blank indicates the ingredients, but not the quantities, of the food, the latter directions being 
 left for the physician. After the seventh month, modifications being less necessary, the diet 
 lists are printed in full. Formula; for the preparation of" diluents and foods are appended. 
 
 STELW AGON'S DISEASES OF THE SKIN. Third Edition, Revised. 
 Essentials of Diseases of the Skin. By Henry W. Stelwagon, 
 M.D., Clinical Professor of Dermatology in the Jefferson Medical 
 College, Philadelphia; Dermatologist to the Philadelphia Hospital; 
 Physician to the Skin Department of the Howard Hospital, etc. 
 Crown octavo, 270 pages; 86 illustrations. Cloth, $1.00 net; inter- 
 leaved for notes, $1.25 net. 
 
 [See Saunders 1 Question- Compends, page 21.] 
 
 " The best student's manual on skin diseases we have yet seen." — Times and Register. 
 
 STENGEL'S PATHOLOGY. 
 
 A Manual of Pathology. By Alfred Stengel, M.D., Physician 
 to the Philadelphia Hospital ; Professor of Clinical Medicine in the 
 Woman's Medical College; Physician to the Children's Hospital; 
 late Pathologist to the German Hospital, Philadelphia, etc. In 
 Preparation. 
 
 STEVENS' MATERIA MEDICA AND THERAPEUTICS. Second 
 Edition, Revised. 
 A Manual of Materia Medica and Therapeutics. By A. A. 
 
 Stevens, A.M., M.D., Lecturer on Terminology and Instructor in 
 Physical Diagnosis in the University of Pennsylvania; Demonstrator 
 of Pathology in the Woman's Medical College of Philadelphia. Post- 
 octavo, 445 pages. Cloth, $2.25. 
 
 "The author has faithfully presented modern therapeutics in a comprehensive work, 
 and, while intended particularly for the use of students, it will be found a reliable guide and 
 sufficiently comprehensive for the physician in practice." — University Medical Magazine. 
 
Medical Publications of W. B. Saunders. 27 
 
 STEVENS' PRACTICE OF MEDICINE. Fifth Edition, Revised. 
 A Manual of the Practice of Medicine. By A. A. Stevens, A.M., 
 M.D., Lecturer on Terminology and Instructor in Physical Diagnosis 
 in the University of Pennsylvania ; Demonstrator of Pathology in 
 the Woman's Medical College of Philadelphia. Specially intended 
 for students preparing for graduation and hospital examinations. Post- 
 octavo, 511 pages; illustrated. Flexible leather, $2.50. 
 
 "The frequency with which new editions of this manual are demanded bespeaks its 
 popularity. It is an excellent condensation of the essentials of medical practice for the 
 student, and may be found also an excellent reminder for the busy physician." — Buffalo 
 Medical Journal. 
 
 STEWART'S PHYSIOLOGY. 
 
 A Manual of Physiology, with Practical Exercises. For 
 Students and Practitioners. By G. N. Stewart, M.A., M.D., 
 D.Sc, lately Examiner in Physiology, University of Aberdeen, and 
 of the New Museums, Cambridge University ; Professor of Physiology 
 in the Western Reserve University, Cleveland, Ohio. Octavo volume 
 of 800 pages; 278 illustrations in the text, and 5 colored plates. 
 Cloth, $3.50 net. 
 
 " It will make its way by sheer force of merit, and amply deserves to do so. It is one 
 ■of the very best English text-books on the subject." — Londo7t Lancet. 
 
 "Of the many text-books of physiology published, we do not know of one that so 
 nearly comes up to the ideal as does Prof. Stewart's volume." — British Medical Journal. 
 
 STEWART AND LAWRANCE'S MEDICAL ELECTRICITY. 
 
 Essentials of Medical Electricity. By D. D. Stewart, M.D., 
 Demonstrator of Diseases of the Nervous System and Chief of the 
 Neurological Clinic in the Jefferson Medical College; and E. S. 
 Lawrance, M.D., Chief of the Electrical Clinic and Assistant Demon- 
 strator of Diseases of the Nervous System in the Jefferson Medical 
 College, etc. Crown octavo, 158 pages; 65 illustrations. Cloth, 
 $1.00; interleaved for notes, $1.25. 
 
 [See Saunders' Question- Compends, page 21.] 
 
 " Throughout the whole brief space at their command the authors show a discriminating 
 knowledge of their subject." — Medical News. 
 
 STONEY'S NURSING. Second Edition, Revised. 
 
 Practical Points in Nursing. For Nurses in Private Practice. 
 
 By Emily A. M. Stoney, Graduate of the Training-School for Nurses, 
 Lawrence, Mass.; late Superintendent of the Training-School for 
 Nurses, Carney Hospital, South Boston, Mass. 456 pages, illustrated 
 with 73 engravings in the text, and 8 colored and half-tone plates. 
 Cloth, $1.75 net. 
 
 " There are few books intended for non-professional readers which can be so cordially 
 endorsed by a medical journal as can this one." — Therapeutic Gazette. 
 
 " This is a well-written, eminently practical volume, which covers the entire range of 
 private nursing as distinguished from hospital nursing, and instructs the nurse how best to 
 meet the various emergencies which may arise, and how to prepare everything ordinarily 
 needed in the illness of her patient." — American Journal of Obstetrics and Diseases of 
 Women and Children. 
 
 " It is a work that the physician can place in the hands of his private nurses with the 
 assurance of benefit." — Ohio Medical Journal. 
 
28 Medical Publications of W. B. Saunders, 
 
 SUTTON AND GILES' DISEASES OF WOMEN. 
 
 Diseases of Women. By J. Bland Sutton, F.R.C.S., Assistant 
 Surgeon to Middlesex Hospital, and Surgeon to Chelsea Hospital, 
 London; and Arthur E. Giles, M.D., B.Sc. Lond. , F.R. C.S. Edin., 
 Assistant Surgeon to Chelsea Hospital, London. 436 pages, hand- 
 somely illustrated. Cloth, $2.50 net. 
 
 "The book is very well prepared, and is certain to be well received by the medical 1 
 public. ' ' — British Medical Journal. 
 
 "The text has been carefully prepared. Nothing essential has been omitted, and its 
 teachings are those recommended by the leading authorities of the day. ' ' — Journal of tht 
 American Medical Association. 
 
 THOMAS'S DIET LISTS AND SICK=ROOM DIETARY. 
 
 Diet Lists and Sick=Room Dietary. By Jerome B. Thomas, 
 M.D., Visiting Physician to the Home for Friendless Women and 
 Children and to the Newsboys' Home ; Assistant Visiting Physician 
 to the Kings County Hospital. Cloth, $1.50. Send for sample sheet. 
 " The idea is good, and the lists are copious." — London Lancet. 
 
 "Its practical usefulness places it among the requirements of every practitioner." — 
 Chicago Medical Recorder. 
 
 THORNTON'S DOSE=BOOK AND PRESCRIPTION=WRITINQ. 
 
 Dose=Book and Manual of Prescription=Writing. By E. Q. 
 
 Thornton, M.D., Demonstrator of Therapeutics, Jefferson Medical 
 College, Philadelphia. 334 pages, illustrated. Cloth, $1.25 net. 
 
 "Full of practical suggestions; will take its place in the front rank of works of this- 
 3( »rt . ' ' — Medical Record, New York. 
 
 VAN VALZAH AND NISBET'S DISEASES OF THE STOMACH. 
 Diseases of the Stomach. By William W. Van Valzah, M.D. , 
 Professor of General Medicine and Diseases of the Digestive System 
 and the Blood, New York Polyclinic; and J. Douglas Nisbet, M.D., 
 Adjunct Professor of General Medicine and Diseases of the Digestive 
 System and the Blood, New York Polyclinic. Octavo volume of 674 
 pages, illustrated. Cloth, $3.50 net. 
 
 VIERORDT'S MEDICAL DIAGNOSIS. Fourth Edition, Revised. 
 Medical Diagnosis. By Dr. Oswald Vierordt, Professor of Medi- 
 cine at the University of Heidelberg. Translated, with additions, 
 from the fifth enlarged German edition, with the author's permission, 
 by Francis H. Stuart, A. M., M. D. Handsome royal octavo volume 
 of 600 pages; 194 fine wood-cuts in text, many of them in colors. 
 Cloth, $4.00 net; Sheep or Half Morocco, $5.00 net; Half Russia, 
 $5.50 net. 
 
 " A treasury of practical information which will be found of daily use to every busy 
 practitioner who will consult it." — C. A. LlNDSLEY, M.D., Professor of the Theory and 
 Practice of Medicine, Yale University. 
 
 " Rarely is a book published with which a reviewer can find so little fault as with the 
 volume before us. Each particular item in the consideration of an organ or apparatus, which 
 is necessary to determine a diagnosis of. any disease of that organ, is mentioned ; nothing 
 seems forgotten. The chapters on diseases of the circulatory and digestive apparatus and 
 nervous system are especially full and valuable. The reviewer would repeat that the book is 
 one of the best — probably the best — which has fallen into his hands." — University Medical 
 Magazme. 
 
Medical Publications of W. B. Saunders. 29 
 
 WARREN'S SURGICAL PATHOLOGY AND THERAPEUTICS. 
 
 Surgical Pathology and Therapeutics. By John Collins Warren, 
 M.D., LL.D., Professor of Surgery, Medical Department Harvard 
 University; Surgeon to the Massachusetts General Hospital, etc. 
 Handsome octavo volume of 832 pages; 136 relief and lithographic 
 illustrations, 33 of which are printed in colors, and all of which were 
 drawn by William J. Kaula from original specimens. Cloth, $6.00 
 net; Half Morocco, $7.00 net. 
 
 "There is the work of Dr. Warren, which I think is the most creditable book on 
 Surgical Pathology, and the most beautiful medical illustration of the bookmaker's art, that 
 has ever been issued from the American press." — Dr. Roswell Park, in the Harvard 
 Graduate Magazine. 
 
 " The handsomest specimen of bookmaking that has ever been issued from the American 
 medical press." — American Journal of the Medical Sciences. 
 
 " A most striking and very excellent feature of this book is its illustrations. Without 
 exception, from the point of accuracy and artistic merit, they are the best ever seen in a work 
 of this kind. Many of those representing microscopic pictures are so perfect in their coloring 
 and detail as almost to give the beholder the impression that he is looking down the barrel 
 of a microscope at a well-mounted section." — Annals of Surgery. 
 
 WEST'S NURSING. 
 
 An American Text=Book of Nursing. By American Teachers. 
 Edited by Roberta M. West, late Superintendent of Nurses in the 
 Hospital of the University of Pennsylvania. In Preparation. 
 
 WOLFF ON EXAMINATION OF URINE. 
 
 Essentials of Examination of Urine. By Lawrence Wolff, M.D., 
 Demonstrator of Chemistry, Jefferson Medical College, Philadelphia, 
 etc. Colored (Vogel) urine scale and numerous illustrations. Crown 
 octavo. Cloth, 75 cents. 
 
 [See Saunders 1 Question- Compends, page 21.] 
 " A very good work of its kind — very well suited to its purpose." — Times and Register. 
 
 WOLFF'S MEDICAL CHEMISTRY. Fourth Edition, Revised. 
 
 Essentials of Medical Chemistry, Organic and Inorganic. 
 
 Containing also Questions on Medical Physics, Chemical Physiology, 
 Analytical Processes, Urinalysis, and Toxicology. By Lawrence 
 Wolff, M.D., Demonstrator of Chemistry, Jefferson Medical College, 
 Philadelphia, etc. Crown octavo, 218 pages. Cloth, $1.00; inter- 
 leaved for notes, $1.25. 
 
 [See Saunders' Question- Compends, page 21.] 
 
 ' ' The scope of this work is certainly equal to that of the best course of lectures on 
 Medical Chemistry." — Pharmaceutical Era. 
 
CLASSIFIED LIST 
 
 Medical Publications 
 
 W. B. SAUNDERS, 
 
 925 Walnut Street, Philadelphia. 
 
 ANATOMY, EMBRYOLOGY, 
 HISTOLOGY. 
 
 Clarkson — A Text-Book of Histology, 9 
 Haynes — A Manual of Anatomy, . . . 13 
 Heisler — A Text- Book of Embryology, 13 
 Nancrede — Essentials of Anatomy, . . 18 
 Nancrede — Essentials of Anatomy and 
 
 Manual of Practical Dissection, ... 18 
 Semple — Essentials of Pathology and 
 
 Morbid Anatomy, 25 
 
 BACTERIOLOGY. 
 
 Ball — Essentials of Bacteriology, ... 6 
 Crookshank — A Text-Book of Bacteri- 
 ology, 10 
 
 Frothingham — Laboratory Guide, . . II 
 Mallory and Wright — Pathological 
 
 Technique, 16 
 
 McFarland — Pathogenic Bacteria, . . 17 
 
 CHARTS, DIET-LISTS, ETC. 
 
 Griffith— Infant's Weight Chart, ... 12 
 Hart — Diet in Sickness and in Health, . 13 
 
 Keen — Operation Blank, 15 
 
 Laine — Temperature Chart. . . .15 
 Meigs — Feeding in Early Infancy, . . 17 
 Starr — Diets for Infants and Children, . 26 
 Thomas — Diet-Lists and Sick-Room 
 Dietary 28 
 
 CHEMISTRY AND PHYSICS. 
 
 Brockway — Essentials of Medical Phys- 
 ics, .... 7 
 
 Wolff — Essentials of Medical Chemistry, 29 
 
 CHILDREN. 
 
 An American Text-Book of Diseases 
 
 of Children, . . 3 
 
 Griffith— Care of the Baby, 12 
 
 Griffith — Infant's Weight Chart, ... 12 
 
 Meigs — Feeding in Early Infancy, . . 17 
 
 Powell — Essentials of Dis. of Children, 19 
 
 Starr — Diets for Infants and Children, . 26 
 
 DIAGNOSIS. 
 
 Cohen and Eshner— Essentials of Di- 
 agnosis, 9 
 
 Corwin — Physical Diagnosis, .... 9 
 
 Macdonald — Surgical Diagnosis and 
 Treatment, 16 
 
 Vierordt— Medical Diagnosis, .... 28 
 
 DICTIONARIES. 
 
 Keating — Pronouncing Dictionary, . . 14 
 
 Morten — Nurse's Dictionary, . . . . IS 
 
 Saunders' Pocket Medical Lexicon, . 24 
 
 EYE, EAR, NOSE, AND THROAT. 
 
 An American Text- Book of Diseases 
 
 of the Eye, Ear, Nose, and Throat, . 3 
 Casselberry — Dis. of Nose and Throat, 8 
 De Schweinitz — Diseases of the Eye, . 10 
 Gleason — Essentials of Dis. of the Ear, II 
 Jackson and Gleason — Essentials of 
 
 Diseases of the Eye, Nose, and Throat, 14 
 Kyle — Diseases of the Nose and Throat. 15 
 
 GENITOURINARY. 
 
 An American Text-Book of Genito- 
 urinary and Skin Diseases, 4 
 
 Hyde and Montgomery — Syphilis and 
 the Venereal Diseases, 13 
 
 Martin — Fssentials of Minor Surgery. 
 Bandaging, and Venereal Diseases, . 16 
 
 Saundby — Renal and Urinary Diseases, 24 
 
 Senn — Genito- Urinary Tuberculosis, . 25 
 
 GYNECOLOGY. 
 
 American Text- Book of Gynecology, 4 
 Cragin — Essentials of Gynecology, . . 10 
 Garrigues — Diseases of Women, ... n 
 Long — Syllabus of Gynecology, ... 15 
 Penrose — Diseases of Women, .... 18 
 Sutton and Giles — Diseases of Women, 28 
 
 MATERIA MEDICA, PHARMACOL- 
 OGY, AND THERAPEUTICS. 
 
 An American Text-Book of Applied 
 
 Therapeutics 3 
 
 Butler — Text-Book of Materia Medica, 
 
 Therapeutics and Pharmacology, ... 8 
 Cerna — Notes on the Newer Remedies, 8 
 Griffin — Materia Med and Therapeutics, 12 
 Morris — Essentials of Materia Medica 
 
 and Therapeutics, . . 17 
 
 Saunders' Pocket Medical Formulary, 24 
 Sayre — Essentials of Pharmacy, ... 24 
 Stevens — Essentials of Materia Medica 
 
 and Therapeutics, 26 
 
 Thornton — Dose-Book and Manual of 
 
 Prescription-Writing 28 
 
 Warren — Surgical Pathology and Ther- 
 apeutics, 29 
 
 MEDICAL JURISPRUDENCE AND 
 TOXICOLOGY. 
 
 An American Text-Book of Legal 
 Medicine and Toxicology, 4 
 
 Chapman — Medical Jurisprudence and 
 Toxicology, & 
 
 Semple — Essentials of Legal Medicine. 
 Toxicology, and Hygiene, 25 
 
Medical Publications of W. B. Saunders. 
 
 31 
 
 NERVOUS AND MENTAL 
 DISEASES, ETC. 
 
 Burr — Nervous Diseases, 7 
 
 Chapin — Compendium of Insanity, . . 8 
 Church and Peterson — Nervous and 
 
 Mental Diseases, 9 
 
 Shaw — Essentials of Nervous Diseases 
 
 and Insanity, 26 
 
 NURSING. 
 
 An American Text-Book of Nursing, 29 
 
 Griffith — The Care of the Baby, ... 12 
 
 Hampton— Nursing, 12 
 
 Hart — Diet in Sickness and in Health, 1 3 
 
 Meigs — Feeding in Early Infancy, . . 17 
 
 Morten — Nurse's Dictionary 18 
 
 Stoney — Practical Points in Nursing, . 27 
 
 OBSTETRICS. 
 
 An American Text-Book of Obstetrics, 4 
 Ashton — Essentials of Obstetrics, . . 6 
 Boisliniere— Obstetric Accidents, Emer- 
 gencies, and Operations, 7 
 
 Borland — Manual of Obstetrics, . . . 10 
 
 Hirst— Text-Book of Obstetrics, ... 13 
 
 Norris — Syllabus of Obstetrics 18 
 
 PATHOLOGY. 
 
 An American Text-Book of Pathology, 5 
 Mallory and Wright — Pathological 
 
 Technique, 16 
 
 Semple — Essentials of Pathology and 
 
 Morbid Anatomy, . 25 
 
 Senn — Pathology and Surgical Treat- 
 ment of Tumors, 25 
 
 Stengel — Manual of Pathology, . . 26 
 Warren — Surgical Pathology and Thera- 
 peutics, 29 
 
 PHYSIOLOGY. 
 
 An American Text-Book of Physi- 
 ology, 5 
 
 Hare — Essentials of Physiology, ... 13 
 
 Raymond — Manual of Physiology, . . 19 
 
 Stewart — Manual of Physiology, ... 27 
 
 PRACTICE OF MEDICINE. 
 
 An American Text-Book of the The- 
 ory and Practice of Medicine, .... 5 
 
 An American Year-Book of Medicine 
 and Surgery, ... . . 6 
 
 Anders — Text-Book of the Practice of 
 Medicine, . . .6 
 
 Lockwood — Manual of the Practice of 
 Medicine, . . .... 15 
 
 Morris — Essentials of the Practice of 
 Medicine, ... 17 
 
 Rowland and Hedley — Archives of 
 the Roentgen Ray, 19 
 
 Stevens — Manual of the Practice of 
 Medicine, 27 
 
 SKIN AND VENEREAL. 
 
 An American Text-Book of Genito- 
 urinary and Skin Diseases, 3 
 
 Hyde and Montgomery — Syphilis and 
 the Venereal Diseases, 13 
 
 Martin — Essentials of Minor Surgery, 
 Bandaging, and Venereal Diseases, . 16 
 
 Pringle — Pictorial Atlas of Skin Dis- 
 eases and Syphilitic Affections, ... 19 
 
 Stelwagon — Essentials of Diseases of 
 the Skin, 26 
 
 SURGERY. 
 
 An American Text-Book of Surgery, 5 
 An American Year-Book of Medicine 
 
 and Surgery 6 
 
 Beck — Manual of Surgical Asepsis, . . 7 
 DaCosta — Manual of Surgery, .... 10 
 
 Keen — Operation Blank 15 
 
 Keen — The Surgical Complications and 
 
 Sequels of Typhoid Fever, 15 
 
 Macdonald — Surgical Diagnosis and 
 
 Treatment, 16 
 
 Martin — Essentials of Minor Surgery, 
 
 Bandaging, and Venereal Diseases, . 16 
 Martin — Essentials of Surgery, .... 16 
 
 Moore — Orthopedic Surgery, 17 
 
 Pye — Elementary Bandaging and Surgi- 
 cal Dressing, 19 
 
 Rowland and Hedley — Archives of 
 
 the Roentgen Ray, 19 
 
 Senn — Genito-Urinary Tuberculosis, . 25 
 Senn - Syllabus of Surgery, . . . . 25 
 Senn — Pathology and Surgical Treat- 
 ment of Tumors, 25 
 
 Warren — Surgical Pathology and Ther- 
 apeutics, 29 
 
 URINE AND URINARY DISEASES. 
 
 Saundby — Renal and Urinary Diseases, 24 
 Wolff— Essentials of Examination of 
 Urine, 29 
 
 MISCELLANEOUS. 
 
 Bastin — Laboratory Exercises in Bot- 
 any, 7 
 
 Gould and Pyle — Anomalies and Curi- 
 osities of Medicine, 11 
 
 Keating — How to Examine for Life 
 Insurance, 14 
 
 Keen — Surgical Complications and Se- 
 quels of Typhoid Fever, 15 
 
 Rowland and Hedley — Archives of 
 the Roentgen Ray, 19 
 
 Saunders' Medical Hand-Atlases, . . 2 
 
 Saunders* New Series of Manuals, 22, 23 
 
 Saunders* Pocket Medical Formulary, 24 
 
 Saunders' Question-Compends, . . 20, 21 
 
 Senn — Pathology and Surgical Treat- 
 ment of Tumors, ... . . 25 
 
 Stewart and Lawrance — Essentials of 
 Medical Electricity, ....... 27 
 
 Thornton — Dose-Book and Manual of 
 Prescription-Writing, 28 
 
 Van Valzah and Nisbet — Diseases of 
 the Stomach, 28 
 
In Preparation for Early Publication. 
 
 AN AMERICAN TEXT=BOOK OF DISEASES OF THE EYE, EAR, NOSE, 
 AND THROAT. 
 
 Edited by G. E. DE Schweinitz, M.D., Professor of Ophthalmology in the Jeffer- 
 son Medical College, Philadelphia; and B. Alexander Randall, M.D., Professor 
 of Diseases of the Ear in the University of Pennsylvania and in the Philadelphia 
 Polyclinic. 
 
 AN AMERICAN TEXT=BOOK OF PATHOLOGY. 
 
 Edited by John Guiteras, M.D., Professor of General Pathology and of Morbid 
 Anatomy in the University of Pennsylvania; and David Riesman, M.D., Demon- 
 strator of Pathological Histology in the University of Pennsylvania. 
 
 AN AMERICAN TEXT=BOOK OF LEGAL MEDICINE AND TOXICOLOGY. 
 
 Edited by Frederick Peterson, M.D., Clinical Professor of Mental Diseases in 
 the Woman's Medical College, New York ; Chief of Clinic, Nervous Department, 
 College of Physicians and Surgeons, New York ; and Walter S. Haines, M.D., 
 Professor of Chemistry, Pharmacy, and Toxicology in Rush Medical College, Chicago, 
 Illinois. 
 
 STENGEL'S PATHOLOGY. 
 
 A Manual of Pathology. By Alfred Stengel, M. D., Physician to the 
 Philadelphia Hospital; Professor of Clinical Medicine in the Woman's Medical 
 College ; Physician to the Children's Hospital ; late Pathologist to the German 
 Hospital, Philadelphia, etc. 
 
 CHURCH AND PETERSON'S NERVOUS AND MENTAL DISEASES. 
 
 Nervous and Mental Diseases. By Archibald Church, M.D., Professor of 
 Mental Diseases and Medical Jurisprudence in the Northwestern University Medical 
 School, Chicago ; and Frederick Peterson, M.D. , Clinical Professor of Mental 
 Diseases in the Woman's Medical College, New York ; Chief of Clinic, Nervous 
 Department, College of Physicians and Surgeons, New York. 
 
 HEISLER'S EMBRYOLOGY. 
 
 A Text=Book of Embryology. By John C. Heisler, M.D., Professor of 
 Anatomy in the Medico-Chirurgical College, Philadelphia. 
 
 KYLE ON THE NOSE AND THROAT. 
 
 Diseases of the Nose and Throat. By D. Braden Kyle, M. D.. Clinical Pro- 
 fessor of Laryngology and Rhinology, Jefferson Medical College, Philadelphia; Con- 
 sulting Laryngologist, Rhinologist, and Otologist, St. Agnes' Hospital ; Bacteriologist 
 to the Philadelphia Orthopedic Hospital and Infirmary for Nervous Diseases, etc. 
 
 HIRST'S OBSTETRICS. 
 
 A Text=Book of Obstetrics. By Barton Cooke Hirst, M.D., Professor of 
 Obstetrics in the University of Pennsylvania. 
 
 WEST'S NURSING. 
 
 An American Text-Book of Nursing. By American Teachers. Edited by 
 Roberta M. West, Late Superintendent of Nurses in the Hospital of the University 
 of Pennsylvania.