Copyright^ 2l 
 
 COPicRIGHX DEPOSIT 
 
GENERAL AND SPECIAL 
 
 PATHOLOGY 
 
 IN 
 
 ABSTRACT 
 
 (Illustrated) 
 
 BY 
 
 V B. WALLGREN, B. S., M. D. 
 
 Assistant Professor of Biology, University 
 
 of Pittsburgh; Pathologist to the 
 
 St. Margaret's and Presbyterian 
 
 Hospitals. Author Histology 
 
 and Bacteriology. 
 
 Second Edition 
 
 Published by 
 
 The Medical Abstract Publishing Company 
 
 Jenkins Arcade Bldg. 
 
 Pittsburgh, Pa. 
 
PREFACE TO FIRST EDITION 
 
 IN preparing this Abstract on Pathol- 
 ogy, the work of Stengel has been 
 freely consulted, together with that of 
 Adami, the Manual of Stenhouse and 
 Pedersen, and others. 
 
 It is not intended to take the place of 
 a text book, but it is hoped that it will 
 be of some use to the student and busy 
 practitioner. 
 
 A. B. Waugren. 
 
 PREFACE TO SECOND EDITION 
 
 The wonderful popularity of Pathology 
 in Abstract has made it necessary to bring 
 out a new edition which contains all upon 
 the subject of Pathology that is found in 
 the larger works. 
 
 The author is actively engaged in Path- 
 ological work in two hospitals, which is 
 a guarantee that all of the advances that 
 have been made are included in this book. 
 
 The illustrations are taken principally 
 from Stengel's Pathology. 
 
 Publisher. 
 
 MAY -6 1918 
 
 ©CIA495814 v " 
 
 Copyrighted by 
 
 The Medical Abstract Publishing Co, 
 
 Pittsburgh, Pa. 
 
 / 
 
-\ ^ l8 PATHOLOGY.** ^* 
 
 PATHOLOGY is the science of disease. 
 It includes 
 
 1. ETIOLOGY. Study of the causes of 
 disease. 
 
 2. MORBID OR PATHOLOGIC ANATO- 
 MY. Study of structural changes. 
 
 a. Gross Pathology. Naked eye ap- 
 pearance of organ or tissue. 
 
 a. Histological Pathology. Miscroscopi- 
 cal appearance. 
 
 3. MORBID OR PATHOLOGIC PHYSI- 
 LOGY. Effects due to disturbance of 
 function. 
 
 Pathologic Chemistry— morbid chemical 
 
 process and products during disturbed 
 
 function. 
 The expressions of abnormal functional 
 
 activity are the Symptoms of 
 
 Disease. 
 DISEASE, is consequent upon an ab- 
 normality in structure or function or 
 both. 
 
 Diathetic (constitutional predisposition) 
 or hereditary (characteristics or tend- 
 encies transmitted from parent to off- 
 spring) conditions may f-equently lead 
 to abnormalities or malformations. 
 
 The ovum can transmit directly either 
 disease or malformations such as 
 syphilis, haemophilia, diabetes in- 
 sipidus and color blindness, supernum- 
 erary digits, webed-fingers and toes, or 
 an individual can inherit through the 
 same channel a predisposition for dis- 
 ease such as gout or tuberculosis. 
 
 The ovum during its growth has also a 
 relation to future disease, in that por- 
 tions "cell rests" may remain unde- 
 veloped till some later period when it 
 may begin to grow abnormally as a 
 tumor. 
 
 The ovum during its development is also 
 subject to accidents which result in 
 
 MALFORMATIONS— TERATOLOGY (A 
 
 monster) 
 
 Anamoly, a slight deviation from the 
 normal structure but not so great as 
 
PATHOLOGY. 
 
 to interfere with proper function. 
 Monstrosity — when malformation is so 
 great as to interfere with function of 
 part or individual. 
 . MALFORMATION DUE TO EXCESS. 
 
 1. In size. 
 
 a. General increase in size of individ- 
 ual, as in a giant. 
 
 b. Overgrowth of tongue. larynx, 
 ringers or toes. 
 
 2. In number. This is brought about by 
 a varying degree of flsson of embryo. 
 Division of ovum gives two complete 
 individuals, more or less separate. 
 If it occurs later in embryo there may 
 be only reduplication of limbs. The 
 growth may be equal or so unequal 
 that one seems but an appendage of 
 the other. 
 
 a. Complete twin-monsters. 
 Xiphopagus — union by xiphoid and 
 
 umbilicus. 
 Sternopagi — union from umbilicus 
 
 upward. Double liver, lungs and 
 
 heart. 
 Prosopothoracopagi, (face). 
 Syncephali (head). 
 United by thorax and head. Single 
 
 oesaphagus, stomach, duodenum 
 
 and heart. Double lungs and 
 
 urinary and sexual organs. 
 Craniopagus — union by cranium. 
 
 Brain may be single or double. 
 Ischiopagus — union by pelvis. 
 Pygopagi — union by buttock. 
 
 b. Double parts. 
 
 Diprosopus — double face; incapable 
 of life. 
 
 Dipyguo — single head and two 
 bodies. Seldom seen in man. 
 
 Parasitic form — one so poorly de- 
 veloped it seems but a parasite 
 on its fellow. 
 
 Supernumerary arms and legs, 
 fingers and toes. 
 
 I. MALFORMATION DUE TO DEFECT. 
 
 1. In cize. 
 a. Dwarf — is defectively small but 
 well proportioned, though the head 
 
MALFORMATIONS. 5 
 
 is usually large, both body and legs 
 are deformed. 
 
 b. Micromelus — limb development is 
 defective. 
 
 c. Microbrachus — arm development is 
 defective. 
 
 d. Micropus — leg development is de- 
 fective. 
 
 e. Microcephalus — small head with de- 
 fective brain development. 
 
 2. In formation of parts. 
 
 a. Homogenous Twins. Where one 
 embryo is developed at the expense 
 of the other. This may be caused 
 by one having a stronger heart or 
 a more rapidly growing allantois. 
 Various conditions of the weaker 
 gives rise to the terms, — 
 
 a. Foetus papyraceus, (parchment 
 like) shriveled up. 
 
 b. Acardiacus — heart not developed. 
 
 c. Omphalosites — receiving its nour- 
 ishment through the allantois 
 being attached to umbilical cord 
 of the other. 
 
 d. Acephalus and Acormus — hav- 
 ing evidences of trunk and limbs 
 but without head, heart or lungs. 
 
 e. Amorphus — shapeless mass cov- 
 ered with skin. 
 
 3. Defective closure of Neural Canal. 
 
 a. Anencephalus, Cranioschisis or 
 Acrania, — brain and bones of crani- 
 um are undeveloped, skull is open 
 and eyes prominent — condition is 
 called "toads head." 
 
 b. "Encephalocele, hernia cerebri, — 
 skull small, brain displaced to out- 
 side. When ventricles are dropsical 
 it is called — 
 
 c. Hydrencephalocele. 
 
 d. Cyclopia or Monophthalmia, — one 
 eye with no retina in forehead, 
 cerebrum has one ventricle. 
 
 e. Agnathia, — no mandible. Often as- 
 sociated with cyclopia. 
 
 f. Spina bifida (cleft spine), — due to 
 nonclosure of neural canal or rup- 
 ture when closed. 
 
; pathology;. 
 
 It is more often found in the lumbar 
 region than cervical, 
 li Rhaehischisis. — Central canal 
 
 of cord, when present, open to ex- 
 terior, inner surface of expanded 
 membranes are continuous with 
 unclosed edges of skin. 
 
 2. Syringocele, — cord when pres- 
 ent is dropsical and in this way 
 forces cord through vertebral 
 arches. 
 
 3. Meningocele, — when arachnoid 
 or subarachnoid is dropsical and 
 spinal meninges alone appear. 
 
 4. Myelomeningocele, — when both 
 cord and meninges protrude. 
 
 4. Defective Ventral closure. 
 
 a. Aprosopus, schistoprospus, — non 
 meeting of cranial and brachial 
 arches, openings in mid-face, hare- 
 lip, cleft palate, hydrocele of neck, 
 cervical nstules, etc. are varities 
 of this defect. 
 
 b. Extroversio Vesicae, — fissure of 
 bladder from failure of the allantois 
 to close. Suprapubic abdominal 
 wall is filled by posterior wall of 
 bladder, Ureters open on its sur- 
 face. Faulty obliteration of allan- 
 toial communication with gut or 
 genital organs may produce im- 
 perforate anus and intestine may 
 communicate directly with bladder, 
 vagina or urethra. Other associated 
 defects may be non closure of pubic 
 bones, absence of urethra and 
 clitoris and vagina of female, while 
 in male the penis is not perfectly 
 developed. 
 
 C. Epispadias, — is where urethra is 
 represented by a groove on the up- 
 per surface of penis. 
 
 d. Hypospadias, — is where urethral 
 opening is on under surface of 
 penis. 
 
 5. Defective Extremities, — from acci- 
 dent as adhesion of amnion, etc. 
 Amelus— all limbs absent. 
 Peramelus — defect in limbs. 
 Phocomelus — hands and feet are at- 
 tached directly to shoulders and 
 hips. 
 
ETIOLOGY. 7 
 
 Abrachius — without upper limbs. 
 Perobrachius — portion of hand or 
 
 arms defective. 
 Apus — without lower limb. 
 Peropus — portion of foot or leg are 
 
 defective. 
 Monobrachus — single arm. 
 Monopus — single leg. 
 Sirenomelia, symmelus or sympus — 
 lower limbs are fused. 
 
 Sympus monopis — limbs fused, 
 
 only one foot. 
 Sympus dipus — two feet fused. 
 Sympus apus — limbs fused but 
 without feet. 
 
 IN. LATERAL TRANSPOSITION OF 
 VISCERA. 
 
 Various organs are found on side op- 
 posite to normal situation. 
 
 ETIOLOGY OF DISEASE. 
 
 I. PREDISPOSING CAUSES.— System or 
 parts is prepared for disease by render- 
 ing it weaker or less resistant. A nor- 
 mal organism is able to cope with the 
 determining causes in disease but the 
 resistance varies according to the in- 
 dividual, race or varying climatic con- 
 ditions. When a certain point of in- 
 tensity in heat or cold or other causes 
 of disease is reached the normal or- 
 ganism is hindered or checked in its 
 resistance and disease or injury re- 
 sults. 
 
 Resistance may be so great that certain 
 diseases are not contracted, this is 
 called immunity in contradistinction to 
 
 Predisposition which is a weakness of re- 
 sistance and may be divided into 
 
 1. Hereditary. 
 
 a. Abnormal weakness transmitted by 
 parent to offspring. 
 
 a. Direct from parent to offspring. 
 
 b. Remote, where trait is latent. 
 
 b. Congenital weakness not direct- 
 ly heriditary but is more or less ac- 
 cidental. 
 
 2. Acquired — from previous disease, 
 vices, etc. 
 
 II. DETERMINING CAUSES— the im- 
 mediate or specific cause. 
 
PATHOLOGY. 
 
 1- TRAUMATISM — from whatever cause; 
 
 effect depends upon the form 
 the severity of injury. 
 
 a. Pressure, — by disturbance of circu- 
 lation or injury to cellular elements, 
 may result in atrophy or a more 
 destructive change — a necrosis or 
 gangrene. 
 
 b. Wounds, — may be so slight as only 
 to cause inflammation and subse- 
 quent regeneration, or so gross as 
 to cause direct injury to tissue con- 
 tinuity in a lesser or greater extent. 
 
 2. PHYSICAL CONDITIONS, 
 a. Heat in excess. 
 
 1. Local excess, — depending upon 
 degree, and varying accordingly, 
 from relaxation of blood vessel 
 walls, necrotic change in cellular 
 elements and exudation of serum 
 with vesicular formation to dis- 
 truction, perhaps with charring, 
 of areas, large or small, with 
 hyperemia or reactive inflamma- 
 tion of surrounding parts. Burns 
 involving one-third or more of the 
 body surface often cause death 
 which is generally produced by 
 formations of poisonous products 
 of tissue distruction or disturbed 
 functions of skin or organs. 
 Immediate death is often from 
 shock. 
 
 2. Exposure to general high temp- 
 erature. 
 
 A constant temperature somewhat 
 higher than the usual temperature 
 will cause body to compensate 
 its increased heat by increase in 
 rate of respirations and pulse. 
 
 Constant high temperatures may 
 cause death by tissue-coagulation, 
 particularly of muscle structures 
 of heart and respiration. 
 
 Constant excessive heat frequently 
 causes conditions known as heat- 
 stroke, sunstroke, insolation and 
 heat exhaustion, due to direct ef- 
 fect of the heat, or products of 
 disturbed metabolism. 
 
 From these, hyperemia, edema or 
 inflammation of meninges may 
 occur. 
 
ETIOLOGY. 9 
 
 b. Cold. — Extreme degrees of cold 
 may cause conditions like those pro- 
 duced by heat. 
 
 There is first vascular constriction 
 then local anemia, which preserves 
 body heat by lessening heat radia- 
 tion; this is followed by vascular 
 paralysis and extreme hyperemia. 
 Cellular exudation and necrosis may 
 occur. These changes are seen in 
 condition called chilblain. In pro- 
 longed cold exposure the activity of 
 various organs is reduced, sensibili- 
 ty weakened and coma gradually 
 supervenes. 
 
 Retention of metabolic excre- 
 ments may be a party to this con- 
 dition. 
 
 The term cold is often used in con- 
 nection with a pharyngitis or 
 coryza but it is merely a predispos- 
 ing factor, by reducing the resist- 
 ing powers of the organism or alter- 
 ing body fluids, thus favoring the 
 activity of bacteria specific to a 
 disease. 
 
 c. Atmospheric Changes. 
 
 a. Increased Atmospheric Pressure 
 
 — as experienced in the work of 
 deep-sea divers or men working 
 in cassions, under pressure of 
 several atmospheres, will fre- 
 quently, on return to normal at- 
 mospheric conditions, suffer from 
 bleeding of mucus membranes, de- 
 pression, delerium and paralytic 
 conditions (cassion disease); this 
 is due to vacuolations in spinal 
 cord, depending of course upon 
 the severity. 
 
 b. Decreased Atmospheric Pres- 
 sure — as experienced by inhabi- 
 tants of high allitudes or in 
 aeronauts. This is accompanied by 
 vascular excitement as hemorr- 
 hages and vomiting; in less mark- 
 ed cases there is nervous excite- 
 ment. The condition is probably 
 due to want of oxygen and to less 
 extent, directly to decreased ex- 
 terior pressure. 
 
 d. Insufficiency of Respiratory Air — 
 
 due to obstruction of air passages 
 
10 PATHOLOGY. 
 
 by disease or foreign bodies. The 
 want of O as in CO 2 poisoning is 
 due to displacement of O in 
 hemoglobin of blood. 
 
 Moderate decrease of air causes 
 asphyxia (labored breathing, 
 
 cynosis, depression and stupor.) 
 
 Complete lack of air produces death 
 by suffocation. Blood is dark and 
 hemorrhages occur. 
 
 A continued want of O may direct- 
 ly or indirectly cause degenerations 
 of tissues. 
 
 e. Electrical Influences. — Electrical 
 discharges may produce various 
 damages to tissues such as burns, 
 etc., often causing shock. The 
 muscles, blood vessels and blood 
 itself may be damaged extensively. 
 The whole nervous system may be 
 disturbed or even undergo degener- 
 ation. Inhibition of heart may 
 cause death. X Rays can cause cel- 
 lular degenerations and necrosis 
 with secondary inflammation. 
 
 3. INTOXICATIONS— POISONS, are 
 
 substances which will disturb the 
 structure or functional activity of a 
 living organism. 
 They may be classified as: 
 
 I. Inorganic, CO, CO 2 Cyanogen, lead 
 mercury, etc. 
 
 II. Organic. 
 
 1. Artificial — chloroform, ether, alcohol, 
 benzine, coffee infusions, etc. 
 
 2. Dietetic — purin poisoning. 
 
 3. Bacterial. 
 
 a. Infectious diseases. 
 
 b. Ptomains. 
 
 1. Decaying meat, canned goods, 
 etc. 
 
 2. Kopraemia. 
 
 4. Poisonous secretions and excretions 
 from insects, snakes and tapeworm, 
 maleria, etc. 
 
 5. Metabolic. 
 
 a. Uraemia. 
 
 b. Acidosis. 
 
 c. Leucomains (substances formed by 
 action of living tissues in course of 
 metabolism. 
 
 d. Internal secretions. 
 
INTOXICATIONS. 11 
 
 1. Diabetes. 
 
 2. Exopthalmic goitre. 
 
 3. Addisons disease. 
 
 4. Acromegaly. 
 
 They may be divided into: — 
 
 A Exogenous Poisons, which enter body 
 through wounds of the skin or sur- 
 faces of the lungs, alementary or genito- 
 urinary tract. From their action they 
 may be divided into: — 
 
 1. Local Poisons. Corrosives, escharotics 
 and caustics. The effect is directly 
 more superficial, producing a more or 
 less disturbance to . cells with which 
 they come in contact, in part by ab- 
 straction of water and in part by their 
 coagulating power. 
 
 These poisons include acids, such as 
 sulphuric, nitric, carbolic and hydro- 
 fluric; alkalies, such as caustic potash 
 or soda and ammonium; gases, such as 
 chlorine and bromine; minerals, such 
 as silver nitrate, mercuric chloride, 
 copper sulphate, etc., and certain or- 
 ganic bodies, such as croton oil and 
 cantharidin. 
 
 2. General Poisons, — manifested by 
 changes in various organs or tissues 
 of body by circulating in the blood. 
 These may be divided into: — 
 
 a. Organic or Parenchymal Poisons. 
 Phosphorus, arsenic, lead, mercury, 
 ergot, etc. The organs generally 
 suffering most are the organs of eli- 
 mination such as the kidneys and the 
 mucous membrane of the intestines, 
 which may show various forms of 
 epithelial cell degeneration. Other 
 organs of body sometimes affected 
 are the liver, spleen, heart and blood 
 vessels. Blood may also be affected 
 secondarily. Toxalbumius of plants 
 or toxic products of bacteria includ- 
 ing bacterial action on various foods 
 (ptomains-putref active compounds) . 
 Decaying meat and shell fish, canned 
 foods, etc., and the venom of serp- 
 ents and various insects are also 
 classed under organic poisons though 
 they may also act as blood or nerve 
 poisons or as all combined. 
 
 b. Blood Poisons. 
 
 1. Those combining with the hemo- 
 
12 PATHOLOGY. 
 
 globin only as carbon monoxide, 
 cyanogen, hydrogen sulphide. 
 
 2. Those which change red blood cell 
 and the coloring matter e. g. potas- 
 sium chlorate, nitroglycerin, ani- 
 lin, nitro-benzol, coal-tar products, 
 arsenuretted hydrogen and poison- 
 ous plants (toad stools). 
 
 3. Those affecting blood and tissue 
 generally such as abrin (from 
 jequirty bean) and recin (from cast- 
 or bean) cause a change in organs 
 and increase coagulability of blood, 
 hence thrombosis. 
 
 4. Those which change blood-plasma 
 or corpuscle, increasing or decreas- 
 ing coagulability, e. g. calcium salts, 
 carbonic acid and fibrin ferment 
 increase coagulability, while albu- 
 mose decreases coagulability. 
 
 c. Nerve Poisons — produce alterations 
 
 in nervous system. Change is gen- 
 erally in central neurons causing a 
 change in size of cells and nucleus 
 with various degenerations or disap- 
 pearance of dendrites and alterations 
 in chromophilic bodies, etc. 
 Some of these poisons are morphine, 
 atropine, alcohol, chloroform, ether, 
 etc. 
 
 The venom of some serpents or ani- 
 mals may act through nervous sys- 
 tem though they are generally blood 
 poisons. 
 
 Ptomains may also act through nerv- 
 ous system. 
 B. Endogenous Poisons, — arising from the 
 cells of the body. On account of the 
 individual being poisoned by himself, 
 as it were, the term autointoxication is 
 used of this group. Poisoning from the 
 bowel contents in chronic constipation 
 (kopraemia) is sometimes called auto- 
 intoxication, but wrongly so for the 
 reason just given. 
 METABOLIC DISTURBANCES. 
 
 1. Decreased food supply; Inanition; 
 Starvation. — The want of food or a 
 gastrointestinal disturbance may lead 
 to insufficient nourishment, causing a 
 loss of body weight by consuming 
 heat producing and energy giving 
 substances. 
 
METABOLISM. 13 
 
 Fats suffer first, then the carbohy- 
 drates. 
 
 Nitrogenous elimination is reduced. 
 The chorides in the urine are de- 
 minished and calcium salts are in- 
 creased with destruction of osseous 
 tissue. The various functions suffer 
 and death may occur from exhaustion 
 or secondary affections (acidosis.) 
 
 2. Increased Food Supply, Overfeeding, 
 
 — depends upon individual conditions 
 and amount of exercise. Excess of 
 proteid food increases excretion of 
 urea. 
 
 Excess of carbohydrates and fats in- 
 crease the deposit of reserve fat and 
 glycogen which may be used later and 
 is physiological but an inordinate 
 storing up of fat is probably 
 pathologic as is frequently seen in 
 Obesity, caused by excessive ingestion 
 of food in those having an active di- 
 gestion and leading sedentary lives. 
 It is undoubtedly due to an inherent 
 abnormal metabolism. 
 
 3. Excessive Tissue distruction, — is in- 
 dependent of amount of food ingest- 
 ed. It is observed in fever, chronic 
 infectious diseases with or without 
 fever, tumors (carcinoma), intoxica- 
 tions and some cases of Graves dis- 
 ease. The nature of the "disturbance 
 is obscure though ordinarily it is 
 due to poisonous substances in the 
 blood. 
 
 4. Acidosis. Acid Intoxication. — Various 
 acid bodies chiefly of acetone group, 
 consisting of B-oxybuteric acid, 
 diacetic and acetone derivatives of 
 proteid decomposition are formed as a 
 result of katabolism and their ac- 
 cumulation in the blood on account 
 of over production, interference with 
 elimination, or a combination of the 
 two, bring on symptoms as rapid 
 respiration ataxia, convulsions and 
 coma. 
 
 The acids above mentioned together 
 with lactic, sarcolactic, sulphuric and 
 phosphoric are generally neutralized 
 by the fixed alkalies (sodium and 
 potassium) and with ammonium and 
 in part excreted as such, the urea 
 of urin is decreased and ammonium 
 
14 PATHOLOGY. 
 
 salts are increased. Some, as sar- 
 colactic acid are decomposed in the 
 body and therefore rarely found in 
 the urine. 
 
 5. Formation of Albumoses, — due to dis- 
 turbed metabolism and is present in 
 the blood and excreted in the urine 
 from fevers, suppurations or in tis- 
 sue distruction of acute yellow 
 atrophy, phosphorus poisoning, etc., 
 ulceration of gastro-intestinal tract 
 and some new growths. 
 
 There is always rapid tissue dis- 
 truction and its presence retards the 
 coagulation of blood and causes 
 leucocytosis. 
 
 6. Aloxin Bases and Uric Acid — deriv- 
 ed from the nuclein of cellular nuclei. 
 Xanthin bases are intermediary pro- 
 ducts which become more or less 
 oxidized to uric acid. Normally uric 
 acid is in excess of bases. Uric acid 
 may be oxidized with the formation of 
 urea. 
 
 Cellular distruction, especially of the 
 . leucocytes is the source of these pro- 
 ducts. 
 
 Gout is in some way dependent upon 
 or associated with aloxin bases and 
 uric acid. 
 
 7. Glycosuria, is the occurance of grape 
 sugar in the urine. It may be trans- 
 ient or trivial in amount or it may 
 manifest itself definitely as Diabetes. 
 It is caused by the inability of the 
 body to consume the carbohydrates 
 and is due probably to a failure of 
 certain preparatory stages in the de- 
 composition of sugar molecule, hence 
 cannot be oxidized by the tissues. 
 
 4. VEGETABLE AND ANIMAL PARA- 
 SITES, on entrance into the body are 
 considered as specific cause of all in- 
 fectious diseases. (See diseases due to 
 bacterial and animal parasites). 
 a. Bacteria (vegetable parasites). 
 The term infectious is applied to all 
 bacterial disease, but when the dis- 
 eases are readily communicated 
 from person to person the term con- 
 tagious disease is used. Immediate 
 contact is not always necessary. 
 The term non-contagious is used 
 when the transference is not ob- 
 
PYREXIA. 15 
 
 served. It is a matter of degree 
 only, as in some cases transference 
 occurs through air, in others con- 
 tact is necessary, in still others 
 secretions or excretions of the dis- 
 eased must be conveyed to the 
 healthy. 
 
 Endemic diseases are restricted to 
 a locality. 
 
 Miasmetic diseases are the same as 
 endemic but are dependent upon the 
 conditions of atmosphere, soil, etc.. 
 for their continuance. 
 
 Epidemic diseases affect a large 
 number of people in a community. 
 Pandemic diseases spread over large 
 areas as country or continent. 
 Bacteria may enter body by swal- 
 lowing or inhalation; through abras- 
 ions in mucous membrances or skir- 
 and in utero from material to foetal 
 blood. The nature and habitat of 
 the bacterium together with sur- 
 rounding conditions will regulate 
 the mode of entrance in individual 
 diseases. 
 b. Animal Parasites, entering the 
 body by invasion cause disease of 
 various kinds. Some present a 
 clinical picture of infectious diseases 
 while other bear little resemblance. 
 
 PYREXIA OR FEVER. 
 
 A. fever is a rise in the temperature of 
 the body above normal (98.6°F) due to 
 increased metabolism especially in the 
 muscles. In health the heat-produc- 
 tion and heat-dissipation are balanced 
 by the nervous system. In fever the 
 production and dissipation are increas- 
 ed though the latter is insufficient. The 
 period of rigor or chill in fever, which 
 is due to reflex spasm of the superficial 
 arteries, though the internal tempera- 
 ture is above normal, the metabolism 
 is somewhat increased as proven by 
 the increase in CO 2 excreted. During 
 the fastigium acne or hot-stage, skin 
 is hot, usually dry and glandular se- 
 cretions are scanty. There is a great 
 increase in the consumption of O and 
 excretion of CO 2 but particularly of 
 urea and extractives showing much 
 
16 PATHOLOGY. 
 
 nitrogeneous waste. 
 There may be a gradual decline of fever 
 (lysis) or an abrupt termination 
 (crisis), which is often associated with 
 sweating, but with restoration of glan- 
 dular function. 
 
 Etiology. Commonly due to poisonous 
 material entering blood in form of bac- 
 teria or their toxines, or products of 
 bacterial growth, which is probably of 
 an albuminous nature. Other albumi- 
 nous bodies resulting from normal or 
 abnormal metabolism, such as albu- 
 moses, peptone, tissue fibrinogen, etc., 
 or ferments, as pepsin, fibrin-ferment, 
 diastase, etc., may also produce fever. 
 All these factors acting upon the nerv- 
 ous system will produce fever, as will 
 also excessive heat as seen in sun- 
 stroke. Rarely is fever produced by in- 
 juries or a disease of central nervous 
 system as in tumors, degenerations, 
 sclerosis, etc. 
 
 Pathological Physiology. Loss of appe- 
 tite, thirst, emaciation, more or less" 
 disturbance of various organs. There 
 is a tendency to inspissation of the 
 blood. The corpuscles are relatively 
 augmented and the specific gravity in- 
 creased. The alkalinity of the blood is 
 more or less reduced. 
 
 Pathological Anatomy. There is a fall 
 in blood pressure. Pulse and respira- 
 tions are increased, due to influence 
 of overheated toxic blood on heart 
 muscle and the centers in medulla. 
 Special lesions, depending upon the 
 character of the disease, as cloudy 
 swelling usually seen in liver, kidney 
 and muscles, particularly the heart 
 muscle, due to toxic blood. The con- 
 dition may pass on to fatty degenera- 
 tion or coagulation necrosis. 
 
 DISTURBANCES OF THE CIRCULA- 
 TION OF THE BLOOD. 
 
 I. GENERAL DISTURBANCES. 
 1. Weak Heart, due to 
 
 a. Weakened heart muscle, from over- 
 strain, fevers or other disease, ac- 
 tion of poisons and insufficient nour- 
 ishment, as in the anemias or nar- 
 
THE BLOOD. 17 
 
 rowing of the coronary artery. 
 
 b. Soft and cloudy, fatty or sclerotic 
 heart muscle. 
 
 c. Functional disturbance of intracar- 
 diac ganglia. 
 
 d. Diseased valves or orifices of heart. 
 Results. Blood will accumulate in the 
 
 venous system. The situation of the 
 engorgement depends upon the part 
 of heart weakened. 
 
 If the left ventricle is weakened the 
 blood backs to the left auricle and 
 lungs. Congestion goes no further, 
 but when right heart fails the right 
 auricle and systemic veins are re- 
 pleted. 
 
 If right heart is first affected there 
 is from the first a general venous 
 congestion. Arterial pressure falls 
 and blood current is slowed and 
 venous pressure is increased. 
 . Overaction of Heart, due tempor- 
 arily to activeness of circulation and 
 elevation of blood pressure. More 
 lasting overaction is caused by over- 
 work, excessive feeding or nervous 
 stimulation, resulting in hypertro- 
 phy of left ventricle, followed by 
 whole heart with consequent over- 
 active circulation. 
 
 . Arterial Disorders. 
 
 a. Organic disturbance. 
 
 1. Sclerosed arteries impede ar- 
 terial circulation. 
 
 The heart compensates by hy- 
 pertrophy. 
 
 When the heart fails venous 
 congestion and dropsy ensue. 
 
 2. Localized conditions in aorta, 
 such as narrowing, pressure by 
 large glands or tumors, aneu- 
 rysms, blood clots may inter- 
 fere with the flow of blood, thus 
 causing stagnation of the blood 
 in the heart, lungs and veins. 
 
 b. Vasomotor disturbances, due to dis- 
 ease of nerve centers or toxic sub- 
 stances which act locally on the 
 vessels or upon the vasomotor cen- 
 ter, causing constriction of the ar- 
 terioles, with elevation of the blood 
 pressure, slowing of the heart and 
 venous congestion follows. 
 
18 PATHOLOGY. 
 
 Contrary to this the arterioles may 
 distend from vasomotor paralysis, 
 with fall of blood pressure and hy- 
 postatic congestion may follow. 
 
 4. Blood Changes. A small decrease in 
 the quantity of the blood is taken care 
 of by the absorption of water from 
 the tissues. A sudden large decrease 
 in the quantity of blood may be fatal 
 by syncope. A change in the char- 
 acter of the blood by the accumula- 
 tion of carbonic acid, and the product 
 of tissue change may impede the cir- 
 culation of blood by the toxic action 
 on the terminal nerve filaments in the 
 vessel walls or directly upon the 
 walls, causing vasomotor contraction. 
 
 II. HYPEREMIA— CONGESTION. Is an 
 
 increase in the quantity of blood in a 
 tissue or organ of the body. It is divided 
 into — 
 
 1. Active, Acute or Arterial Hyper- 
 emia or Congestion. It is due to an 
 increase of the blood flow to part. 
 It occurs physiologically during the 
 functional activity of the organs. 
 Pathologically, it occurs from any 
 condition which interferes with the 
 nervous control of the calibre of the 
 arteries, acting either — 
 
 a. Through their local nerve plex- 
 uses or the vasomotor center in 
 the medulla. 
 
 1. Neuroparalytic hyperemia. 
 Vaso-constrictor fibers of the 
 sympathetic nerves are cut off 
 or compressed by tumors. 
 
 2. Neurotoxic lryperemia. Vaso- 
 dilator in the spinal nerves are 
 stimulated as in neuritis. Toxic 
 causes of fevers may act sim- 
 ilarly through the vasomotor 
 centers, causing superficial hy- 
 peremia — 
 
 b. by local affections of the vessel 
 walls, from injury by — 
 
 1. Heat. 
 
 2. Traumatism. 
 
 3. Inflammation. 
 
 4. Drugs. 
 
 5. Vascular fatigue, following 
 temporary stoppage of the cir- 
 culation, as frequently seen 
 
HYPEREMIA. 19 
 
 on the removal of rubber 
 bandage after a bloodless am- 
 putation or in the abdominal 
 vessels when the pressure of 
 an ascites or large tumor is 
 suddenly relieved. 
 Arterial hyperemia is the initial 
 phenomena of inflammation, but 
 transudation only takes place 
 when the capillary endothelium is 
 damaged. 
 . Passive or Venous Hyperemia is due 
 to obstruction of the outflow of blood 
 through the veins by — 
 Failure of the left heart to provide 
 arterial pressure. 
 
 Failure of the right to empty the 
 veins. 
 
 Weak heart power, following attempts 
 to overcome the obstruction in veins 
 by thrombi, pressure by tumor, etc., 
 or resistance of narrowed arteries 
 (atheroma). 
 
 These conditions bring on what is 
 called — 
 
 Hypostatic Congestion. The blood 
 
 gravitates to dependent parts. It 
 occurs frequently in low fevers. In 
 combination with the continuous 
 pressure on the skin of these parts 
 congestion may result in necrosis 
 with production of bed sores. In- 
 ternally hypostatic congestion af- 
 fects the lungs and pneumonia may 
 follow. The congested areas are 
 dark red (cyanosis). The capillary 
 endothelium is ill nourished and al- 
 lows the plasma of the blood to 
 transude and the part becomes 
 edematous and dropsical. In severe 
 cases the red blood cell escapes by 
 diapedesis. Passive hemorrhage 
 may follow when congestion is very 
 marked. 
 
 Fatty degeneration from imperfect 
 nutrition may occur later. 
 
 If the hyperemia is moderate and 
 long continued, overgrowth of con- 
 nective tissue with pigmentation 
 from broken down blood corpuscles 
 (brown induration) generally fol- 
 lows. 
 
 When there is complete stoppage of 
 
20 PATHOLOGY. 
 
 circulation in a localized area it is 
 
 known as — 
 Stasis, and if not relieved necrosis 
 and gangrene will follow. 
 
 III. ISCHEMIA OR LOCAL ANEMIA is 
 
 the opposite to congestion, i. e., a tissue 
 or organ contains less than its proper 
 quantity of blood. 
 
 1. Direct Ischemia is caused by — 
 
 a. Pressure. 
 
 b. General or local disease. 
 Pressure may be due to bandages 
 
 upon an organ or an area of body 
 or upon the vessels within the tissue 
 itself, as in amyloid disease or 
 tumors. The circulation may be im- 
 peded by sclerosis of vessels or 
 emboli or thrombi within the ves- 
 sel. Nervous influences acting 
 through the vasomotor system, as in 
 some gouty conditions and Ray- 
 naud's disease, may produce a local 
 anemia. 
 
 2. Collateral Ischemia is due to the 
 withdrawal of blood into hyperemic 
 areas in other parts of the body, 
 e. g., anemia of brain consequent to 
 abdominal hyperemia. 
 
 Ischemic areas are pale and cold, with 
 atrophy and loss of function in pro- 
 portion to the amount and perma- 
 nence of the condition. 
 
 IV. HEMORRHAGE is the escape of the 
 
 constituents of the blood from its nat- 
 ural channels. According to the vessels 
 from which the escape takes place it is 
 termed — 
 
 1. Arterial. 
 
 2. Venous. 
 
 3. Capillary. 
 
 4. Parenchymatous when it escapes from 
 all of the vessels. 
 
 From the mode of escape hemorrhage may 
 be divided into — 
 
 1. Hemorrhage per Diapedesim. Ooz- 
 ing through capillary and smaller 
 vein walls without any apparent 
 rupture. The red cells and certain 
 elements of the plasma escape. 
 
 It is caused by the increased blood 
 pressure, either active or passive, 
 or the normal blood pressure with 
 the increased permeability of the 
 
HEMORRHAGE. 21 
 
 vessel walls due to degeneration of 
 same by the action of poisons, in- 
 fectious diseases, moderate injury of 
 vessel, or temporary obstruction to 
 the blood flow into a certain area. 
 Altered states of blood may per- 
 haps play a part when the vessels 
 and pressure are apparently nor- 
 mal. 
 2. Hemorrhage per Rhexin, due to a 
 break in the continuity of an artery 
 or vein. 
 Causes. 
 
 a. Traumatism. 
 
 b. Diseases of blood vessels from 
 poisoning, infectious fevers, etc., 
 degenerations and miliary aneu- 
 rysm involving the intima or 
 media. The outer coat may be 
 eroded by surrounding disease, 
 e. g., phthisical cavities. 
 
 c. Increase of blood pressure. 
 
 1. Absolute. 
 
 a. Emotional excitement. 
 
 b. Hypertrophy of heart. 
 
 c. Paroxysms of whooping 
 cough, etc. 
 
 d. Asphyxia. The blood press- 
 ure is increased from vaso- 
 motor contraction and violent 
 muscular efforts. 
 
 2. Relative. 
 
 Reduction of external pressure, 
 e. g., balloon ascension or vio- 
 lent inspiratory efforts when 
 air cannot enter lungs. 
 
 d. Neuropathic Hemorrhage, seen 
 in — 
 
 1. Some nervous conditions. 
 
 2. Apoplexy. 
 
 3. Epilepsy. 
 
 4. Spontaneous hemorrhage from 
 nose, stomach or into the lungs. 
 This is also included in — 
 
 5. Vicarious hemorrhage from sup- 
 pression of menses. 
 
 6. Stigmatization. 
 
 7. Hemidrosis — sweating of blood. 
 
 e. Hemorrhagic Diathesis — Hemo- 
 philia. 
 
 An hereditary condition. Persons 
 affected are known as "bleed- 
 
22 PATHOLOGY. 
 
 ers." The hemorrhage appears 
 spontaneously or after trivial 
 injuries or operations. 
 
 In part, it is probably due to ex- 
 treme thinness of the vessel 
 walls and altered blood states. 
 
 The condition is sometimes devel- 
 oped as a result of various in- 
 fections and intoxications. 
 
 Classification. 
 
 1. On free surfaces — from locality. 
 
 a. .Epistaxis — nose bleed. 
 
 b. Hemoptysis — from lung. 
 
 c. Hematemesis — from stomach. 
 
 d. Enterorrhagia — from bowel. 
 
 e. Hematuria — urinary organs. 
 
 f. Metrorrhagia — from uterus between 
 menses. 
 
 g. Menorrhagia — from uterus at the 
 menses. 
 
 2. From tissues — from size and nature. 
 
 a. Ecchymosis. Infiltration of blood 
 beneath the surface of skin and 
 mucous membrane. 
 
 1. Petechia — when small and well 
 defined. 
 
 2. Suggillation or sufusion — when 
 large and diffuse. 
 
 b. Hemotoma — blood tumor. 
 
 c. Hemothorax — in pluera. 
 
 d. Hemopericardium — in pericardium. 
 
 e. Hematocele — in tunica vaginalis. 
 
 f. Hematometra — in uterus. 
 Results of Hemorrhage. 
 
 Effused blood in small amount is 
 taken up by the lymphatics. Re- 
 peated small extravassations may 
 lead to secondary anemia. In large 
 amounts the corpuscle gradually 
 breaks down into pigment, which 
 passes into the lymphatics or de- 
 posited at the seat of hemorrhage. 
 The rest of corpuscle (fluid portion) 
 is generally absorbed or may re- 
 main as a cyst. A focus of hemor- 
 rhage may act as a foreign body 
 and become organized. It may also 
 become calcified. It may also un- 
 dergo degenerative changes. 
 Large hemorrhages cause acute 
 anemia, or a very large hemorrhage 
 may cause sudden death by cere- 
 bral anemia. 
 
THROMBOSIS. 23 
 
 V. THROMBOSIS is the clotting of the 
 blood in the blood vessel or heart dur- 
 ing life. 
 Causes. 
 
 1. Alterations In the blood by the in- 
 crease of fibrin forming factors as 
 seen in typhoid fever, sepsis, etc. The 
 activity of some bacteria in thrombi 
 formation is probably due to their 
 hemolytic action and injurious effect 
 on the endothelium. 
 
 Mineral poisoning and autointoxica- 
 tions probably also form thrombi by 
 their hemolytic power. 
 
 2. Alterations in blood current, due to 
 slowing of current from any cause, as 
 narrowing of the vessels, weakness of 
 the heart or pressure, as seen in 
 various fevers and wasting diseases. 
 The current may be slowed from dila- 
 tations of the vessels, as seen in 
 aneurysm or varicose veins; this in 
 time causes degenerative changes of 
 vessel walls, which is in addition gen- 
 erally necessary. 
 
 3. Changes in vessel wall, due to — 
 
 a. Traumatism. 
 
 b. Atheroma. 
 
 c. Inflammations. 
 
 d. Degenerations. 
 
 e. Aneurysms. 
 
 Pathologic Anatomy. 
 
 1. White thrombi are formed from pure 
 fibrin containing some leucocytes and 
 conglutinated plaques. They are gen- 
 erally formed slowly from actively 
 flowing blood. 
 
 2. Red thrombi are formed from fibrin 
 and contain a large proportion of red 
 corpuscles and indicate an almost 
 complete or a temporary stasis of 
 blood with a rapid production of 
 fibrin ferment. 
 
 3. Mixed or Stratified thrombi are made 
 up from alternating red and white 
 formations of thrombi due to the al- 
 ternating slow and more rapid circu- 
 lation of the blood. 
 
 4. Hyaline thrombi is probably a com- 
 pact form of the white. 
 
 Effect. 
 
 1. The blood flow may be compensated 
 by collateral circulation. 
 
24 PATHOLOGY. 
 
 2. Venous obstruction may cause 
 venous congestion and dropsy. 
 
 3. Arterial obstruction may cause 
 eschemia, and degenerations and ne- 
 crosis if blood' flow is not established 
 by collateral circulation. 
 
 4. Obstruction to small arteries may 
 cause hemorrhagic infarction. 
 
 5. Embolism, which, if infected, may 
 produce general pyemia. 
 
 Fate or Changes of Thrombi. 
 
 1. Organization. The thrombus acting 
 as an irritant to the tissues sets 
 up an inflammation with the for- 
 mation of connective tissue, which 
 by its contraction forms new chan- 
 nels, through which circulation is 
 restored, or it may transform the 
 vessel into a fibrous cord. 
 
 2. Degenerations. The thrombi may 
 be emulsified by liquefaction ne- 
 crosis or fatty degeneration and 
 pass into the blood stream as an 
 embolism. Calcification of a throm- 
 bus is frequent. 
 
 3. Septic thrombi. A thrombus in 
 blocking vessels of suppurating or 
 necrosed tissue when infected by 
 micro-organisms and undergoing 
 softening may give rise to, general 
 pyemia or an infectious embolism. 
 
 VI. EMBOLISM. Foreign bodies of vari- 
 ous kinds carried in the blood stream 
 and deposited in the smaller arteries 
 or capillaries so as to produce obstruc- 
 tion are known as emboli. 
 Source. 
 
 1. Thrombi, in portion or whole from 
 heart, large veins of the extremities 
 or pelvis and atheromatous patches 
 in the aorta. 
 
 2. Fat, from bone marrow in fractures. 
 
 3. Parasites. 
 
 4. Masses of bacteria. 
 
 5. Portions of tumor. 
 
 6. Portions of calcareous heart valves. 
 
 7. Portions of liver in accidental rup- 
 ture of the organ. 
 
 8. Placental cells. 
 
 9. Disorganization of blood, as in the 
 pigment particles in malaria. 
 
 10. Small hyaline masses from burns and 
 certain poisoning. 
 
EMBOLISM. 25 
 
 11. Air. from rounds of large veins in 
 
 neck, etc. 
 Seats. Depend upon its source. 
 
 1. An embolus derived from the left 
 heart or from the -aorta passes to the 
 general arterial circulation and finds 
 lodgment in — 
 
 a. Spleen. 
 
 b. Kidney, 
 c Brain. 
 
 d. Other organs — peripheral vessels. 
 
 2. An embolus derived from the general 
 venous circulation is carried to the 
 lungs, occluding the pulmonary circu- 
 lation 
 
 It may also reach the general arterial 
 circulation when foramen ovale or 
 ventricular septum is perforated or 
 by being broken up into emboli so 
 small as to permit passage through 
 pulmonary capillaries. 
 
 3. An embolus derived from the portal 
 circulation may lodge in liver or pass 
 through the liver into the heart and 
 lungs. 
 
 4. An embolus will sometimes be car- 
 ried in the veins in a different direc- 
 tion opposite to the blood flow. This 
 is called — 
 
 Retrograde embolism. It is seen in 
 some pulmonary diseases causing in- 
 creased intrathoracic pressure such 
 as whooping cough, emphysema, etc. 
 Results of an embolism depends upon 
 
 its size and nature. 
 1. From size — (purely mechanical). 
 A large embolus occluding the main 
 branches of the pulmonary or cere- 
 bral artery or one of the coronary 
 arteries may cause sudden death. 
 If the vessel is not wholly occluded 
 secondary thrombosis may complete 
 the occlusion and death may be slow. 
 
 The occlusion of less important ves- 
 sels merely causes local anemia. 
 
 An embolus caught at the bifucation 
 of a vessel may break up into small 
 pieces and produce multiple em- 
 bolism of the branches. 
 
 The obstructed artery contracts on 
 the proximal side of the embolus 
 and dilates on the distal side as do 
 also the anastomosing branches of 
 
 
 
26 PATHOLOGY. 
 
 neighboring vessels and circulation 
 is quickly readjusted without serious 
 or lasting damage to the tissues. 
 The important mechanical result of 
 small emboli is the pathological con- 
 dition called — 
 
 Infarction. 
 
 An Infarct is the necrosed condition 
 produced in the region of distribu- 
 tion of an end artery by its ob- 
 struction by an embolus. 
 
 They occur in the periphery of an 
 organ especially in the kidney, 
 spleen, lungs, retina, base of brain 
 and parts of heart. 
 
 They are harder than the surrounding 
 tissue and wedge-shaped with base 
 towards the periphery of the organ. 
 They are divided into — 
 
 a. White or Anemic Infarcts are yel- 
 low or grayish anemic wedge-shap- 
 ed areas frequently surrounded by a 
 zone of congestion or hemorrhage,.. 
 The anemia is probably due to oc- 
 clusion of the circulation and the 
 area undergoing coagulation necro- 
 sis. 
 
 From the anemic period they may be 
 changed directly, by the over- 
 filling with blood and its extra- 
 vasation, into an hemorrhagic in- 
 farct. The persistence of the anem- 
 ic form is due to the thrombosis of 
 the venules receiving blood from 
 the occluded endartery and anasto- 
 motic capillaries or by the compres- 
 sion of the capillaries by a rapid 
 swelling of the parenchymatous cells 
 of the organ. 
 
 Some authorities contend that anemic 
 infarcts may be formed by the 
 absorption and the removal of col- 
 oring matter of the blood from 
 hemorrhagic infarcts. 
 
 Infarcts of the spleen, kidney and 
 brain are frequently anemic. 
 
 b. Red or hemorrhagic Infarcts are 
 dark red wedge-shaped areas of 
 hemorrhage with coagulation. 
 
 They are probably formed by the 
 overfilling of the vessels from a 
 back flow of blood from the veins 
 or from free capillary anastomosis. 
 The hyperemia produced leads to 
 
EDEMA. 27 
 
 extravasation of the blood from the 
 degenerative changes of the vessels. 
 
 Lung infarcts are nearly always 
 hemorrhagic. 
 
 Results of Infarcts. 
 
 In the red infarcts the extravasated 
 blood breaks into pigment matter 
 and the tissues undergo degenera- 
 tions and is gradually absorbed. 
 Reactive inflammation and organi- 
 zation causes cicatrization with pig- 
 mentation. The anemic infarcts 
 undergo coagulation necrosis and 
 caseation. 
 
 A small amount of calcareous mat- 
 ter is frequently deposited, es- 
 pecially in the brain. In both the 
 anemic and the hemorrhagic form 
 the final result is scar formation, 
 pigmented in the hemorrhagic form. 
 Infarcts niay undergo liquefaction 
 and cyst formation, especially in the 
 brain. They may become infected 
 with micro-organisms. 
 
 2. From nature (which is septic). 
 
 An embolus may contain micro-or- 
 ganisms as is seen in cases of puru- 
 lent softening of thrombi from, — 
 
 a. Local suppuration or necrosis. 
 
 b. Ulcerative endocarditis, etc. 
 These may only cause an infarct 
 
 which may become secondarily in- 
 fected but micro-organisms gener- 
 ally multiply and invade the tissues 
 at once causing, — 
 
 a. Suppuration. 
 
 b. Gangrene. 
 
 c. Metastatic Abscesses. 
 VII. EDEMA AND DROPSY. 
 
 The term Edema is applied to a condi- 
 tion in which there is an accumulation 
 of serum in the cellular tissue. 
 
 It is brought about by an escape of serum 
 through a more or less permeable mem- 
 brane, the capillary walls, in conse- 
 quence of direct filtration, osmosis or 
 diffusion, and probably secretion of 
 endothelial cells of capillaries and the 
 hymphatic spaces. The quantity pres- 
 ent in the tissue depends upon the 
 amount escaping from blood vessels and 
 the amount carried away by the lym- 
 phatic system. 
 
28 PATHOLOGY. 
 
 The term Dropsy is used indiscriminately. 
 More strictly a general accumulation in 
 the subcutaneous tissue and skin is call- 
 ed Anasarca or hyposarca; local trans- 
 udation is called oedema; dropsy of the 
 peritoneal sac is called asites; in 
 pleura — hydrothorax and in the pericar- 
 dinum — hydropericardium, etc. 
 
 Causes 
 
 1. Increased blood pressure, always 
 causes the escape of liquid from ves- 
 sels (transudation) consequently 
 more hymph. In active hyperemia the 
 escaped liquid is carried off by the 
 lymphatics and edema does not occur. 
 In passive congestion, the escape of 
 liquid is greater and lymphatic cir- 
 culation is insufficient and edema or 
 dropsy results. 
 
 This is a process of direct filtration. 
 The transudate consists of water, 
 saline and a relatively small degree 
 of albuminous constituents of plas- 
 ma. 
 
 2. Decreased tissue-elasticity and pres- 
 sure, is probably only a contributing 
 cause. It is a principal cause in 
 edema ex vacuo where in the liquid 
 of blood escapes to fill a place left 
 vacant by disease or atrophy, as seen 
 in subarachnoid spaces and other 
 parts of the central nervous system. 
 
 3. Alterations of the blood, probably 
 act indirectly. Seen in the anemias, 
 which will in itself cause increased 
 permeability of the vessels, by ill 
 nourishment or actually damaged 
 endothelium by circulating toxic sub- 
 stances. 
 
 4. Alterations of the liquids of the tis- 
 sues may cause increase in the diffus- 
 ion of liquids. 
 
 5. Increased permeability of the capil- 
 lary-walls probably plays a part in 
 every case of edema. 
 
 Permeability is due to, — 
 
 a. Diseased capillary walls from 
 
 1. Degenerations, as in Brights dis- 
 ease. 
 
 2. Inflammations. 
 
 3. Traumatism. 
 
 4. Poisons. 
 
 5. Bacterial toxins. 
 
 b. Heredity. 
 
ATROPHY. 29 
 
 Certain nervous conditions such as 
 
 1. Neuritis. 
 
 2. Neuralgia. 
 
 3. Organic disease of the cord. 
 
 4. Nervous irritations. 
 
 6. Obstruction of the lymphatic cir- 
 culation, infrequently produces 
 edemia as the collateral circulation 
 generally carries away the lymph. 
 If a large trunk as thoracic duct or 
 several smaller lymphatics are ob- 
 structed edema may result. The 
 former edema is known as chylous 
 ascites and the latter is seen in 
 elephantiasis. 
 
 Pathologic Anatomy. Depends upon the 
 situation. Liquid varies according to 
 the cause. In transundates due to fil- 
 tration, the liquid is watery with sp. gr. 
 below 1016 and poor in blood corpuscles 
 an albuminous matter. Where disease 
 of the vessel walls, as inflammatory 
 edema, plays a part, the liquid is more 
 dense and contains more corpuscles and 
 albumen. 
 
 The transundate is found in the lymph 
 spaces or in the interstices of the tis- 
 sue. The part is swollen and boggy. 
 The tissue pits on pressure and on sec- 
 tion liquid exudes. This appearance is 
 not so marked in the solid organs like 
 the kidney or liver. 
 
 Under microscope the tissue elements are 
 seen to be pushed apart and the cells 
 themselves may be diseased. 
 
 Results. Function of part is impaired. 
 Death may occur when epiglottis, lungs 
 or brain is involved. Various cell de- 
 generations of part and productive 
 changes in the connective tissue may 
 occur. 
 
 RETROGRESSIVE PROCESSES. 
 
 I. ATROPHY is a condition in which a 
 tissue or organ decreases in size with- 
 out definite disease of its parts. If a 
 tissue or organ is under its normal size, 
 due to defective development the con- 
 dition is called hypoplasia. If an organ 
 or part of body is entirely wanting, the 
 condition is termed Aplasia. 
 
 Causes. 
 
 1. Want of functional demand. 
 
30 PATHOLOGY. 
 
 a. Palsied limbs. 
 
 b. Disturbance to trophic nervous sys- 
 tem. 
 
 c. Physiologic. 
 
 1. Atrophy of thymus gland. 
 
 2. Atrophy of the genital organs at 
 the menopause. 
 
 3. Involution of old age. 
 
 2. Lack of use, as seen in muscle of a 
 limb long confined in splints. 
 
 3. Lack of nutrition from any cause 
 
 either local or general such as, — 
 
 a. Occlusion of vessels. 
 
 b. Continuous pressure, as in athropy 
 of the liver in women from tight 
 lacing, or when an aneurysm esca- 
 vates the vertebrae or the steady 
 contraction of new connective tis- 
 sue as in cirrhosis. 
 
 c. Impoverished blood. 
 
 Pathalogic Anatomy. 
 
 1. Single or true atrophy. Individual 
 cells are decreased in size without 
 manifesting disease. 
 
 2. Numerical. The cells are reduced in 
 number and generally altered by some 
 form of degeneration. 
 
 In atrophy the parenchyma of an or- 
 gan is the first to suffer. 
 
 In the true form the cell may suffer no 
 change except slight pigmentation due 
 to the fact that the normal cell pig- 
 ment does not suffer reduction. 
 
 In other cases there may be a deposition 
 of pigment from the blood and is 
 known as brown atrophy as is often 
 seen in heart muscle of old age or in 
 cachectic disease. 
 
 In other conditions cells may undergo 
 various degenerations. 
 
 Secondarily the connective tissue may 
 suffer degeneration. 
 
 Athrophic organs are often irregular, 
 the consistancy may be more or less 
 reduced or may be hard and tough 
 due to the connective tissue hyper- 
 plasia. The capsule is generally 
 wrinkled. The color is often darker 
 than normal. In the case of brown 
 athrophy it may be decidedly changed. 
 Pathologic Physiology. 
 
 Function of organ is impaired, the 
 
DEGENERATION. 31 
 
 amount of disturbance varyi ng accord- 
 ing with variation in functions of the 
 organ. 
 
 II. DEGENERATIONS AND INFILTRA- 
 TIONS. 
 
 These two conditions may be said to go 
 hand in hand and in individual cases it 
 is often difficult to distinguish between 
 two varieties. 
 
 Degeneration is the retrograde change 
 which takes place in a cell or tissue by 
 which their integrity is altered in the 
 direction of lowered vitality. The pro- 
 toplasm of the cell may be converted 
 into substances abnormal to it in kind 
 and quantity. The cell may break down 
 and be absorbed or its altered debris 
 may remain in one form or another. 
 
 Infiltration is the deposit, in the cell from 
 the blood or other fluids of the body, of 
 a foreign substance which may remain 
 either within the cell as a fat or pig- 
 ment, or it may be found around the 
 cell as in the amyloid degeneration. In- 
 filtration frequently interferes with cells 
 function. 
 
 1. Cloudy Swelling; Albuminous Infiltra- 
 tion; Albuminous, Parenchymatous or 
 Granular Degeneration is an edema of 
 cellular protoplasm with granular 
 change of the protied and production 
 of opacity. 
 
 Causes. 
 
 a. Intoxications. 
 
 1. Bacterial toxines. 
 
 2. Organic substances. 
 
 3. Inorganic substances. 
 
 b. Hyperpyrexia. 
 
 c. Inflammations. 
 
 d. Nutritional disturbances. 
 Pathologic Anatomy. 
 
 The organs are sometimes greatly en- 
 larged, doughy and on section may be 
 found dull gray in color, a little moist, 
 and protruding parenchyma. 
 Microscopically the cell is finely opaque, 
 due to refractile granules. 
 The normal protoplasmic granules may 
 have disappeared and vocuolations may 
 also be observed. The nuclei may be 
 obscured by granulations. 
 The chromatin is diffusely stained, but 
 in the late stages the cell stains very 
 poorly if at all. 
 
32 PATHOLOGY. 
 
 Pathologic Physiology. 
 
 The coagulation is due to precipation or 
 coagulation of a part or all of the cells 
 protied. The function of organ is more 
 or less interferred with. Recovery is 
 frequent. If causes persist fatty de- 
 generation generally follows. 
 Seats. Glandular epithelia and muscle 
 fibers. 
 
 2. Hydropic Degeneration or Dropsical 
 Infiltration is the presence of a fluid 
 in the protoplasm of the cell. 
 Causes,— probably a physical phenom- 
 ena in the dropsies, also a part of 
 cloudy swelling. Burns and other skin 
 lesions. 
 
 Inflammations. 
 
 Pathologic Anatomy. 
 Microscopically, the cells are swollen 
 even to bursting and clear from sep- 
 aration of their contents. The fluid 
 may be between the cells, often com- 
 pressing them noticably. 
 Pathologic Physiology. The protoplasm 
 sooner or later becomes cloudy and 
 often undergoes fatty degeneration. 
 Vacuolation is frequently observed. 
 Seats. 
 Inflamed tissues and cancer. 
 
 3. Fatty Infiltration, is the deposition of 
 fat in cells which normally contain none 
 other deposition, in excess, of fat in 
 cells, normally containing it. 
 
 Causes. 
 
 a. Physiologic. 
 
 1. Puberty. 
 
 2. Pregnancy. 
 
 3. Menopause. 
 
 b. Pathologic. 
 
 1. Inherited tendency. 
 
 2. Luxurious living with lack of ex- 
 ercise. 
 
 3. Exceptional digestive power and 
 faulty combination. 
 
 4. Alcohol. 
 
 5. Cachexias, as the fatty liver some- 
 times seen in phthisis and in the 
 cells of carcinoma. 
 
 6. Organic disease of the nervous sys- 
 tem. 
 
 7. Bone disease. 
 
 8. Fracture, or bone operations. Fat 
 is taken up by the circulation. 
 
DEGENERATION. 33 
 
 9. Diseased or atrophied organs or tis- 
 sues. The deposition may take place 
 around a sclerosed kidney or in 
 bones, also in muscles in pseudo- 
 hypertropic paralysis. 
 
 Pathologic Anatomy. 
 
 The appearance varies with the tissue 
 affected. The connective tissue is 
 usually affected . Microscopically the 
 infiltrated tissue looks like that of nor- 
 mal adipose- tissue. In the connective 
 tissue the deposit of fat may be local- 
 ized or diffuse or in streaks along the 
 planes of fascia or fibrous strands, un- 
 der endothelial membranes, about 
 lymph channels, between muscular 
 fibrillae or under the skin. In the or- 
 gans, such as the kidney, the fat is 
 seen around the tubules; in the liver, 
 in the trabeculae, also in the hepatic 
 cells; in the heart between fiber 
 bundles and under the serous mem- 
 brane. 
 
 In the parenchyma cells the fat is seen 
 as distinct drops within the cell wall. 
 Where there is much fat in the cell 
 the cell protoplasm is crowded to the 
 cell wall, and the nucleus is flattened, 
 though normally distinct, and stains 
 easily. 
 
 Pathologic Physiology. 
 Unless very extreme the functions of 
 cells are not greatly embarrassed and 
 complete recovery is the rule. It may, 
 however, lead to secondary conditions, 
 as mechanical embarrassment or de- 
 generations, which may be serious ac- 
 cording to the organ involved. 
 
 Seats. 
 
 Subcutaneous and subserous tissues, 
 mesenteries and omentum, along fascia, 
 between muscles, kidney, liver and 
 heart. Lungs and central nervous or- 
 gans rarely. 
 
 4. Fatty Degeneration is a destructive 
 chemical change of a cell protoplasm 
 into fat. 
 Causes. 
 
 a. Cloudy swelling. 
 
 b. Intoxications. 
 
 1. Metallic, as mercury, arsenic, lead, 
 etc. 
 
 2. Compounds, carbonic oxid, chlor- 
 ates, coal tar compounds, pyrogallic 
 
34 PATHOLOGY. 
 
 acid, chloroform, etc. 
 3. Toxines of bacteria. 
 
 c. Anemias and cachexias. 
 
 d. Extreme hemorrhage. 
 
 e. Metabolic disease. 
 
 f. Fever if high and prolonged. 
 
 g. Fatty infiltration. 
 
 h. Trophic disturbances. 
 
 Pathologic Anatomy. 
 
 Organs are generally increased in size 
 (except in acute yellow atrophy of 
 liver, etc.), consistency is generally de- 
 creased, the sp. gr. reduced, color is 
 generally pale yellow, though conges- 
 tion or pigmentation will alter this. 
 
 The degenerated areas may be uniform 
 or isolated. On section, fat may drop 
 from knife and cut surface. Microscop- 
 ically, parenchyma cells are primarily 
 affected; connective, tissue may at 
 times be involved. Cells are usually 
 enlarged. The granules of the proto- 
 plasm disappears, to be replaced by 
 fine dark granules, which stain black 
 with osmic acid, and are dissolved by 
 ether or alcohol, but not by acetic acid. 
 The fat is generally seen as numerous 
 droplets, though they may become one 
 drop, as in fatty infiltration. The chro- 
 matin of nuclei becomes diffuse and 
 stains poorly, or it may disappear. 
 
 The cell membrane sooner or later breaks 
 down and fatty contents and detritus 
 fill the space. Cholesterin, lecithin and 
 fatty crystals are often seen. 
 
 Pathologic Physiology. 
 Fatty degeneration results from an in- 
 filtration of fat derived from the blood 
 and from fat deposits of the body, or 
 from food, and deposited in diseased 
 cells. Fatty degeneration tends to 
 cause secondary changes in the cells 
 protoplasm or the fatty degeneration 
 itself will increase until the cell is de- 
 stroyed. In mild cases where nuclei of 
 cells are not destroyed recovery may 
 take place. Severe grades go on to total 
 necrobiosis. 
 
 Seats. 
 
 Occurs in nearly all tissues. Most fre- 
 
 . quent are the epithelial structures, such 
 as liver, kidneys, heart muscle, central 
 nervous organs. 
 
 "Interstitial and ..parenchymatous tissues 
 
DEGENERATION. 35 
 
 may be involved. 
 Exudates and transudates are liable to 
 the change, and liquid may give the 
 appearance of an emulsion. 
 5. Albuminoid Degenerations. 
 
 This condition represents a proteid 
 metamorphosis. There are four varie- 
 ties, and, though they have several fea- 
 tures in common, especially in their 
 chemical composition and microscopic 
 appearance, they may be distinguished 
 by their reactions and by their prefer- 
 ence for special tissues and sites. 
 a. Mucoid Degeneration is the conversion 
 of cellular protoplasm into mucin. 
 Causes. 
 
 Mucin should not always be consid- 
 ered pathological, as we find it physio- 
 logically in glandular epithelum, um- 
 bilical cord, chorionic villi and the 
 vitreous humor, nor should the hy- 
 persecretion of mucin, as a result of 
 inflammation or irritation of all sorts, 
 be mistaken for mucoid degeneration. 
 
 1. Inflammation. 
 
 2. Myxedema. 
 
 3. Scleroderma. 
 
 4. Tumors. 
 
 The occurrence of mucin in sarco- 
 mata, carcinomata, fibromata, lipo- 
 mata or chondromata is accidental, 
 though occasionally it may be a 
 direct transformation, as is the case 
 in myxomata. 
 Pathologic Anatomy. 
 
 On mucous membrane it appears as a 
 coat of thick, tenacious mucus, with 
 or without congection or other changes. 
 Where it is pent up in the tissues it 
 swells, dilates the chambers and flat- 
 tens the epithelium, and later becomes 
 a thin albuminous fluid and takes on 
 the appearance of a cyst. In connective 
 tissues it may not show the mucin 
 characteristics, but the tissue is soft, 
 elastic and tears easily. 
 . It is insoluble in water, though it will 
 take up water and swell. It is very 
 soluble in alkaline solutions, but is pre- 
 cipitated by alcohol, heat, many of the 
 metals, acetic acid and "on saturation 
 with most neutral salts. 
 Mucin from cystic ovarian neoplasms is 
 often . peculiar, . in that . it , will not pre- 
 
36 PATHOLOGY. 
 
 cipitate with acetic acid, and is there- 
 fore called pseudomucin. 
 
 Microscopically. In mucous membranes 
 the goblet cells are excessive in quan- 
 tity. Death of cell occurs only in ex- 
 treme cases. The cells are much swol- 
 len, with distal end bulged out with 
 mucin. The submucous tissue is usually 
 inflammatory and pus cells containing 
 mucin may be seen. In the connective 
 tissue the mucin lies between the cells, 
 the ground substance of which has dis- 
 appeared. 
 
 The cells themselves, though rarely 
 changed to mucin, may be degenerated 
 otherwise. In tumors the change may 
 be in and between the cells or in the 
 form of cysts. Mucin is fixed by the 
 bichloride of mercury. It stains with 
 most of the basic analin stains. Thio- 
 nin and toluidin blue stain the nucleus 
 blue and the mucin red. It is, how- 
 ever, not entirely distinctive. 
 
 Pathologic Physiology. 
 Causes and modus operandi are not 
 clear. Unless the disease is prolonged 
 the tissue affected may recover. 
 
 In connective tissue the deposit may often 
 be removed by reabsorbtion. In neo- 
 plasms it is probably an evidence of 
 cell death. 
 
 Seats. 
 
 Epithelial tissues of the respiratory and 
 gastro-intestinal tract, salivary glands 
 and uterus, though any epithelial tissue 
 may be involved. 
 
 Skin, any connective tissue, ovarian 
 cysts, carcinomata and any mesoblastic 
 tumor. 
 
 b. Colloid Degeneration is the abnormal 
 appearance in the tissues of a colloid 
 substance, like that found in the thyroid 
 glands. 
 
 Causes are obscure. 
 
 It may arise from or be converted into 
 mucoid material and borders on the 
 hyaline substance. It occurs in 
 goiter and thyroid neoplasms and 
 other organs of the body. 
 
 Pathologic Anatomy. 
 
 The tissue affected is the connective 
 tissue. The organs affected are en- 
 larged, hard or soft. On section the 
 areas involved appear as yellowish- 
 
DEGENERATION. 37 
 
 brown, translucent bodies, sometimes in- 
 visible, sometimes they may be in form 
 of large cysts. 
 
 A serous transudation may accompany 
 the colloid degeneration and dissolve it, 
 so that the cysts may be filled with a 
 chocolate-colored fluid containing pus, 
 blood, cholesterin, sodium chloride and 
 calcium oxalate. 
 
 Microscopically. The material is found in 
 the cells, in the glandular acini and in 
 the connective tissue. 
 
 It is generally arranged in balls or 
 whorls. The cells generally show de- 
 generative changes and inflammation is 
 often present. 
 
 The material shrinks, but is not precipi- 
 tated by acetic acid or alcohol. 
 
 Stains with acid stains. It does not stain 
 with I. & K. I. or methyl-violet. 
 
 Pathologic Physiology is obscure. 
 The substance is undoubtedly formed 
 in loco. It is grave and usually asso- 
 ciated with marked cellular disturb- 
 ance. It may be changed into mucoid, 
 hyaline or be replaced by an exuda- 
 tion. 
 
 Seats. 
 
 Thyroid gland, kidney, prostate, pituit- 
 ary body, parovarium and carcinomata. 
 
 c. Amyloid Degeneration is the appear- 
 ance in the tissues of an amyloid sub- 
 stance. 
 
 Causes. 
 
 1. Suppuration and ulceration, as seen 
 in tuberculosis of lungs and bones, 
 syphilis, various gastro -intestinal ul- 
 cerations and in actinomycosis. 
 
 2. Mixed infections. 
 
 3. Without suppuration (rare) in the 
 cachexias, as in cancer, materia, 
 leukemia, etc. It may sometimes be 
 found without any apparent cause. 
 
 Pathologic Anatomy. 
 
 Organs are enlarged and specific 
 gravity is increased. On section they 
 are firm and smooth. The consistency 
 may vary according to the degree of 
 fibrosis, fatty degeneration, etc. It is 
 generally inelastic. The color is pale, 
 though this may be altered by con- 
 gestion, pigmentation or fatty degen- 
 eration. 
 
38 PATHOLOGY. 
 
 The amyloid substance is translucent, 
 glistening and waxy. 
 
 Microscopically. It is found in the outer 
 surface of the capillary walls, the in- 
 tima and media of the larger blood 
 vessels (the adventitia being rarely af- 
 fected and the endothelia probably 
 never), fixed connective tissue of the 
 organs, elastic tissues and basement 
 membranes of the glandular acini. The 
 material appears as irregular clumps or 
 streaks in the interstitial tissues, often 
 compressing the cells and blood vessels. 
 The cells are generally atrophied and 
 degenerated otherwise. 
 
 The material is insoluble in water, alcohol 
 and weak alkalies. It swells, but is in- 
 soluble in the tissue fluids. 
 
 It stains a light pink or red with gentian 
 violet or iodine green, a mahogany red 
 with Lugol's solution of iodine. The 
 red color is changed to blue by treat- 
 ing with sulphuric acid or chloride of 
 zinc. 
 
 Pathologic Physiology. 
 
 It is a combination of chrondratin sul- 
 phuric acid with a proteid. 
 
 As chrondratlnic acid is normally present 
 in the tissues (bone, cartilage, elastic 
 tissue) of the body it is probably not 
 abnormal, but an abnormal combina- 
 tion of normal substances. 
 
 Local cellular conditions probably favor 
 the deposition of the material by rea- 
 son of their inability to properly dis- 
 pose of the constituent substances 
 brought by the blood. 
 
 Hyaline degeneration may be a prelim- 
 inary stage. 
 
 The functional activity is interfered with 
 by reason of pressure upon the paren- 
 chyma and by vascular disturbances. 
 It may occasion thrombosis by reason 
 of its situation. 
 
 Reabsorbtion has been known to take 
 place, but not when extensive change 
 exists. 
 
 Seats. Glomeruli of kidney, liver, spleen, 
 blood vessels, endocardium, intestinal 
 mucosa, lymph glands, adrenalin bodies, 
 dural tumors and in rare cases the vol- 
 untary muscles and nervous system. 
 
 d. Hyaline Degeneration is the appear- 
 
Fig*. 1. Cloudy swelling' and necrosis 
 
 of the epithelial cells of the renal 
 tubules, due to sublimate poisoning:. 
 (Kargr and Schmor.) 
 
 i .*<« 
 
 r i 
 
 
 Fig. 2. Colloid degeneration of the 
 thyroid gland, showing- masses of col- 
 loid matter in the gland acini. (Kargr 
 and Schmor.) 
 
Fig. 3. Amyloid defeneration of the 
 kidney, showing- amyloid substance in the 
 walls of the blood vessels of the glome- 
 rulus at b, and hyaline tube casts in 
 the renal tubules at g. (Ziegler.) 
 
 : - ^* v '1'*" -*- 
 
 
 -.. vr-, .«*•*. 
 
 
 
 Fig:. 4. Coagulation necrosis of the 
 hepatic cells in a case of puerperal 
 eclampsia. (Karg and Schmor.) 
 
DEGENERATION. 39 
 
 ance in a tissue of a homogenous pro- 
 
 teid substance of an obscure nature. 
 
 Causes. 
 
 It is allied to the other albuminoid de- 
 generation and can pass into each of 
 them. It is also related to coagula- 
 tion necrosis. It occurs under the 
 following pathological conditions — 
 
 1. In muscles during infections and 
 septic processes; also after trauma- 
 tism. 
 
 2. Intoxications, as by lead. 
 
 3. In interstitial hemorrhages and 
 hematoma. 
 
 4. In struma. 
 
 5. Cicatrices. 
 
 6. In blood vessels of old age. 
 
 7. In arteritis. 
 
 8. In disease of endocardium and car- 
 diac valves. 
 
 9. In granulomata. 
 
 10. In neoplasms. 
 
 11. In lungs in pneumonia. 
 
 12. Nephritis. 
 
 13. Coagulation necrosis. 
 
 14. Fibrinous exudation. 
 
 Pathologic Anatomy. 
 
 If extensive enough to be macroscopic 
 the tissue or organ is enlarged, dense, 
 pale and opaque. On the mucous or 
 serous membrane small collections, 
 pseudomembraneous or opaque plaques 
 may be seen. 
 Microscopically, it is found in three sit- 
 uations — 
 
 1. In the blood vessels, where it may 
 be in or beneath the endothelium, 
 surrounding the vessel, or between 
 its coats or fibers. 
 
 2. In the interstitial tissue. 
 
 3. Within the cells. 
 
 Unstained it has a glistening, waxy ap- 
 pearance, but is less translucent than 
 amyloid. It has an affinity for acid 
 anilin stains. It may also take basic 
 stains in a modified manner. 
 A mixture of picric acid and acid 
 fuchsin (Gieson's) will stain it red. 
 Pathologic Physiology is obscure. It con- 
 sists probably of a proteid modified in 
 loco by a disturbed action of cells, or 
 it may be brought by cellular carriers. 
 
 It can be reconverted, absorbed and re- 
 moved. It will not interfere greatly 
 
40 PATHOLOGY. 
 
 with parenchymatous structure. 
 
 It may be converted into other albu- 
 minoid degenerations and may undergo 
 caseation or calcareous infiltration. 
 
 Seats. Cardiovascular system, muscles, 
 mucous and serous membranes, liver, 
 kidney, spleen, ovaries, adrenal bodies, 
 nervous system and neoplasms. 
 
 6. Glycogenic Infiltration is the presence 
 of glycogen in cells which normally 
 contain none or an excess in cells which 
 normally contain it. 
 
 Causes. 
 
 Glycogen is normally present in the 
 
 liver, muscles, leucocytes and blood 
 
 serum. 
 It occurs pathologically in the blood of 
 
 diabetes and cachectic states. 
 Pathologic Anatomy. It is generalby mi- 
 croscopic. The substance is usually 
 found within the cells. It is sometimes 
 found in the intercellular substance and 
 may be free in the blood or fluid of 
 exudates. It is seen as round balls con- 
 centrically striated. 
 If fresh it is soluble in water, but loses 
 its solubility after alcohol fixation. It 
 stains brownish red with iodine, but 
 sulphuric acid does not turn it blue. 
 There is loss of color reaction when 
 treated with ptyalin or amylopsin. 
 Pathologic Physiology is obscure. In neo- 
 plasms and suppurations it is probably 
 deposited. 
 
 Seats. Kidney, blood, purulent collec- 
 tions and inflammatory areas, malig- 
 nant growths of mesoblastic origin. 
 
 7. Calcification is the abnormal deposition 
 in the tissues of earthy salts, chiefly the 
 phosphates and carbonates of lime and 
 magnesia. 
 
 Cause. 
 
 1. Vascular disorders in diseased tissues. 
 
 2. Local necrosis or fibrosis. 
 
 3. Neoplasms. 
 
 4. Degenerations, especially fatty and 
 hyaline. 
 
 5. Old age (due to increased lime re- 
 absorbtion from the skeleton). 
 
 6. Extensive disease of bones. 
 Pathologic Anatomy. No early macro- 
 
DEGENERATION. 41 
 
 scopic signs are present. However, in 
 the gross it is gritty or of stone hard- 
 ness and grates on the knife. On the 
 addition of a dilute mineral acid 
 earthy material will dissolve with for- 
 mation of carbonic acid. 
 
 Microscopically. It is opaque by trans- 
 mitted and glistening by reflected light. 
 The granules are fine and scattered 
 through the intercellular substance. In- 
 frequently the cells show an infiltration 
 with more or less extensive degenera- 
 tions. The granules may coalesce and 
 assume a concentric arrangement 
 (psamomma bodies). 
 
 Calcarious plates are formed in the blood 
 vessels and serous membranes. 
 
 In blood vessels and neoplasms deposits 
 may be great. The color is here white, 
 grayish or yellow. A discoloration is 
 due to pigments. 
 
 It stains by carmine and hematoxylin, but 
 not as a rule with analin dyes. 
 
 Pathologic Physiology. 
 It is considered by some to be due to 
 an escape of carbonic acid from stag- 
 nant lymph, with consequent precipita- 
 tion of the earthy salts; by others to a 
 combination of these salts with the 
 albumins and fatty acids of the degen- 
 erating tissues. 
 
 It is probable that the salts are precipi- 
 tated as insoluble combinations with 
 proteids. The deposits are seldom if 
 ever removed. They will cause degen- 
 erations of adjacent tissues. 
 
 Seats. 
 
 1. Cardiovascular system (affecting 
 chiefly the intima and media). 
 
 2. Hyaline cartilage (except articular 
 cartilage). 
 
 3. In tissues subject to pathologic 
 change. 
 
 4. Ganglion cells of brain. 
 
 5. Renal cells. 
 
 6. Tumors. 
 
 7. Cicatricial tissue. 
 
 The foetuses of extrauterine pregnancy 
 are sometimes calcified and are then 
 known as lithopaedion. 
 
 In some cases true ossification occurs 
 where only calcification might be ex- 
 pected. An accurate differentiation 
 
42 PATHOLOGY. 
 
 from calcification can only be made 
 where osteoblasts are detected after 
 the material is decalcified. 
 Uratic Infiltration. The deposit of urate 
 of sodium in cartilages and fibrous tis- 
 sue of joints, etc., occurs in gout. 
 8. Pigmentation. According to origin and 
 variety of pigments it may be divided 
 into— 
 a. Pigmentation from External Causes. 
 
 1. Entering through air passages and 
 termed pneumonokoniosis. 
 
 a. Coal pigmentation called anthra- 
 cosis. 
 
 b. Iron pigmentation called side- 
 rosis. 
 
 c. Stone pigmentation called calci- 
 cosis. 
 
 d. Vegetable particles. 
 
 e. Animal hairs and furs. 
 
 This is commonly an occupation 
 disease. Inhaled substances are 
 probably caught by the cellular 
 cilia of the bronchial tubes and 
 coughed up or eliminated with the 
 bronchial secretions. Some of the 
 substance penetrates the bron- 
 chial wall or is carried into the 
 submucosa and deposited in this 
 situation by the phagocytes, or it 
 may be carried by the lymph to 
 the peribronchial and mediastinal 
 glands, fibrous tissue of lungs or 
 the subpleural tissue. 
 
 In rare cases the pigment enters 
 the general circulation and is de- 
 posited in the various organs of 
 the body. 
 
 2. Entering through the alimentary 
 canal. Due to an excessive inges- 
 tion of soluble metallic salts, such 
 as silver, etc. If due to silver salts 
 the condition is called argyra. 
 
 b. Pigmentation derived from the hemo- 
 globin called Hematogenous Pigmenta- 
 tion. 
 The pigments are — 
 
 1. Siderous, which is chiefly hemo- 
 siderin. 
 
 2. Non-siderous, derivatives of hema- 
 tin, hematoidin, hemofuscin, me- 
 lanin, etc. 
 
 Hematogenous Pigmentation is divided 
 into — 
 
DEGENERATION. 43 
 
 1. Those in which the hemolytic 
 agents act in the blood; found in — 
 
 a. Pernicious anemia. 
 
 b. Leukemia. 
 
 c. Malaria. 
 
 d. Cachexias. 
 
 e. Infectious and septic processes. 
 
 f. Poisoning. 
 
 The hemoglobin is set free in the 
 blood. It is eliminated by the kid- 
 ney and to a small extent by the 
 intestines. It is converted into bile, 
 a little passing into it unchanged. 
 Some is reduced by the tissues to 
 the siderous and non-siderous, and 
 is then carried by the lymph and 
 blood stream and is deposited by 
 cellular carriers in various places 
 in the body. The depositions are 
 both inter and intracellular. 
 Hemochromatosis is a condition in 
 which a pigment containing iron is 
 deposited in the epithelia of the liv- 
 er and pancreas, and a pigment free 
 from iron in the smooth muscles of 
 the intestines, walls of the blood and 
 lymph vessels and in the connective 
 tissue. Associated with this pigmen- 
 tation was cirrhosis of the organs. 
 The diabete bronze of the French is 
 a widespread form of this pigmen- 
 tation, in which, in addition, other 
 organs and skin are involved. It is 
 accompanied by glycosuria, due to 
 cirrhosis of the pancreas. 
 Alcohol, cachexia and other toxe- 
 mias are of etiologic importance. 
 The deposits in the cells cause de- 
 generations and death of same. 
 The appearance of the organs vary ac- 
 cording to the variety and stage. 
 
 2. Those in which reductions occur in 
 local tissues — 
 
 Local pigmentation. 
 Causes. 
 
 a. Thrombosis. 
 
 b. Interstitial hemorrhage and co- 
 agulation. Pigmentations of in- 
 duration result of venous stag- 
 nation, and congestion are 
 probably of the same origin. 
 
 The pigment is diffused from the 
 blood cell; some is carried away 
 by the plasmatic circulation. 
 
44 PATHOLOGY. 
 
 When areas become enclosed the 
 pigments are formed within. The 
 pigments change and are then 
 carried away by the phagocytes 
 to various parts of the body, es- 
 pecially to the liver, blood modi- 
 fying organs, intestines and 
 glands; the deposits being known 
 as pigment- metastasis. Micro- 
 scopically the pigments are found 
 as small needles, rhombic crystals 
 or amorphous masses or small 
 clumped balls. The color varies 
 from pink to deep red; from yel- 
 low green to brown or black. 
 
 c. Pigmentation derived from the Bile. 
 Hepatogenous Pigmentation. 
 
 It is due to bilirubin and biliverdin. 
 All jaundice is of hepatic origin. The 
 pigments deposited are either in so- 
 lution in the tissues, in precipitation 
 or crystals. The liver, skin, mucous 
 and serous membranes, endarterium. 
 glandular and fatty tissue are very 
 susceptible. 
 
 The color is first yellow, then deepens 
 to olive. 
 
 d. Pigmentation derived from cellular ac- 
 tivity within the organism. Metabolic 
 Pigmentation. 
 
 Pigments are probably formed by mi- 
 gratory and pigment-building cells 
 and deposited by means of the 
 leucocytes and plasma cells. 
 
 The hemoglobin has secondarily some- 
 thing to do with its manufacture 
 with the possible exception of some 
 pigments of melanosarcoma. 
 
 This pigmentation may be — 
 
 1. Local, as seen in — 
 
 a. Nevi. 
 
 b. Moles. 
 
 c. Pregnancy. 
 
 d. Corpus luteum. 
 
 e. Freckles. 
 
 f. Scars. 
 
 g. Certain skin disease. 
 h. Melanosarcomata. 
 
 2. General, as seen in — 
 
 a. Addison's disease.. 
 
 b. Severe anemias and cachexias. 
 
 c. Tuberculosis of peritoneum, in- 
 testines and retroperitoneal 
 
 .;.. . . glands. 
 
NECROSIS. 45 
 
 d. Abdominal neoplasms. 
 
 e. Senility. 
 
 Metabolic pigments are generally de- 
 posited as granules, sometimes crys- 
 tals, in and between the cells. 
 
 9. NECROSIS is the local death of tissue. 
 Necrobiosis is the death of individual 
 cells. 
 
 Causes. 
 
 (1) Circulatory derangements. 
 
 (a) Acute and chronic ischemia, 
 produced by embolism thrombosis, 
 arteriosclerosis, atheroma, extra- 
 arterial blood pressure, cardiac 
 spasms, as ergotism and Ray- 
 naud's disease. 
 
 (b) Venous stagnation. 
 
 (c) Aneredas. 
 
 (d) Cachexias. 
 
 (e) Senility. 
 
 (f) Diabetes. 
 
 (2) Trophic derangements, due to 
 trophic disturbances, as in bed sores 
 and myletic cystitis. 
 
 (3) Intoxications, due to animal, 
 vegetable, bacterial and inorganic 
 poisons. 
 
 (4) Traumatism, due to pressure per 
 se or the pressure of calculi, con- 
 cretions, enteroliths and exostoses. 
 
 (5) Inflammations. 
 Varieties — 
 
 a. Coagulation Necrosis. In this necrosis 
 the proteid of the tissue suffers death 
 from changes similar with coagulation. 
 
 Pathologic Anatomy. 
 
 Macroscopically. The tissue is of a 
 glazed, opaque, waxy appearance, 
 pale and firm. 
 
 Later the tissue becomes grayish and 
 is inclined to soften. 
 
 Microscopically. There is a fixed exu- 
 date in the tissues. Fibrin granules 
 or fibrills are present. Fibrinoids, 
 which do not react to stains like the 
 fibrin, are also seen. 
 
 During the early stage the nuclei stain 
 faintly and is of homogenous appear- 
 ance. The cell disintegrates. The 
 striations disappear in the muscles. 
 All other cells in area suffer the fate 
 ~- of the fixed tissues, 
 
46 PATHOLOGY. 
 
 Pathologic Physiology. 
 
 It is supposed to be due to the union 
 of the dying cell protoplasm with the 
 fibrinogen of the blood. 
 
 Many chemicals may act direct. 
 
 Bacterial products may act fibrino- 
 genetically. A coagulated area may 
 be cast off by ulceration, or it may 
 become liquified, caseated, suppurated, 
 encysted and dissolved or reabsorbed. 
 
 It may finally be converted into scar 
 tissue. Function is more or less com- 
 pletely lost. 
 
 b. Liquefaction Necrosis or Colliquefac- 
 tion is the death of tissue with lique- 
 faction. It is divided into— 
 Primary liquefaction necrosis, as seen 
 
 frequently in the central nervous sys- 
 tem, where it follows pathologic con- 
 ditions which elsewhere would pro- 
 duce coagulation. 
 
 Secondary liquefaction necrosis is a 
 form in which the areas of coagula- 
 tion necrosis, cheesy necrosis, inflam- 
 mation, gangrenous tissue and tumors 
 may become liquefied. 
 Pathologic Anatomy. 
 Early stage is softer than normal tis- 
 sue. The fibrillar tissue begins to dis- 
 solve and the area becomes filled with 
 a liquid the consistency of which de- 
 pends upon the tissue involved. The 
 cells are variously degenerated, and 
 after a while nothing but detritus re- 
 mains. In some cases the exudate may 
 coagulate. The color may be white 
 from emulsified fats; yellow from pig- 
 ments and fat; red or brown from 
 blood pigments, or deeply colored from 
 bile pigments. Liquefactive areas may 
 be discharged, coagulated, reabsorbed, 
 encysted or organized. 
 
 c. Caseation is where coagulation ne- 
 crosis takes on a cheese-like appear- 
 ance. It is typical of tuberculosis and 
 syphilis. It is secondary to coagula- 
 tion necrosis. It results from the ne- 
 crobiotic effects of the tubercle bacillus 
 or the poison of syphilis upon the 
 tubercle or gumma. 
 
 Microscopically. The nuclei disappear 
 and the cells break down into a struct 
 tureless, cheesy mass. 
 
GANGRENE. 47 
 
 Caseated areas may be cast off, reab- 
 sorbed, encysted or calcified. 
 
 d. Fat Necrosis designates a peculiar 
 type of necrosis, which occurs in very 
 stout people, over small areas in the 
 normal fat. It is quite distinct from 
 ordinary fatty metamorphosis. 
 
 It is seen in the abdominal walls and the 
 subperitoneal fat. 
 
 The affected areas are usually not larger 
 in size than a pea, soft or gritty and 
 white in color. The area may be sur- 
 rounded by inflammation. 
 
 Microscopically. The cells lose their 
 transparency, though they still stain 
 with osmic acid. 
 
 There is no agreement as to the cause of 
 this condition. Some contend that it is 
 due to fat splitting ferment of pan- 
 creatic secretion. 
 
 The necrotic portions when not infected 
 may be absorbed or organized, fol- 
 lowed by a cicatrix, or may become 
 calcified. The liquefied portion may be- 
 come encapsulated and remain as a 
 cyst. 
 
 e. Gangrene is the putrefaction of areas 
 of necrosis. It may be classed as — 
 
 1. Primary, when a particular bac- 
 terium produces a direct gangrenous 
 result, as in malignant oedema, 
 anthrax, etc. 
 
 2. Secondary, when saprophytic bac- 
 teria decompose an area already 
 dead. 
 
 Gangrene may be divided into — 
 
 1. Dry gangrene* due to — 
 
 a. Arterial disturbance or occlusion 
 result of arterial obstruction of se- 
 nility, arterial embolism or throm- 
 bosis, freezing, ergotism, Ray- 
 naud's disease. 
 
 b. The moist type, when putrefaction 
 is slow and the fluids evaporate. 
 
 Dry gangrene is circumscribed and 
 ends in mummification. The color 
 is dark or black. Early the color 
 may be yellow or brown. There is 
 little toxic absorbtion in this type. 
 
 2. Moist gangrene generally results 
 from extensive venous occlusion. fc In 
 some cases it may be due to arterial 
 
48 PATHOLOGY. 
 
 occlusion. 
 Causes. 
 
 a. Internal emboli, as in pulmonary 
 arteries and veins. 
 
 b. In the lungs as the result of in- 
 spiratory pneumonia, abscesses, 
 neoplasms, bronchiectasis and in 
 diabetes. 
 
 C. Traumatism and pressure con- 
 tusions, as seen in intussusception 
 and strangulation of bowels; very 
 frequent in vermiform appendix; 
 also as result of torsion in mov- 
 able kidneys, spleen or tumors. 
 
 d. Infections. 
 
 e. Skin disease (rare). 
 
 f. Severe trophic lesions, as decu- 
 bitus, etc. 
 
 Pathologic Anatomy. 
 
 Macroscopically. The consistency 
 of part becomes softer. There is 
 local or widespread emphysema. 
 The color is dark brown. The 
 skin is black and covered with 
 fciebs. 
 
 Coagulation necrosis or an inflam- 
 matory zone may surround the 
 areas, the latter producing a line 
 of demarkation. In some cases, 
 as in the diabetic, neither zone is 
 formed. 
 
 Microscopically all the cells of the 
 tissue are involved. The cells are 
 the first to succumb. Hemorrhages 
 into the area are common. The 
 connective tissue and elastic fibers 
 are liquefied. 
 
 The affected areas contain crystals 
 of pigment, fatty acids, cholestern, 
 leucin, tyrosin, phosphates and 
 carbonates, ammonia and fatty 
 acids, indol and skatol, amins, 
 sulphurated hydrogen, carbonic 
 acid and other gases give rise to 
 pronounced odors. There is more 
 
 . or less toxic absorbtion. 
 
 Pathologic Physiology. 
 
 The condition may progress and 
 cause death, or it may become 
 circumscribed. 
 
 In the. circumscribed a line of de- 
 markation is formed by inflamma- 
 tory reaction. The mass is cast 
 
INFLAMMATION. 49 
 
 off if the area is superficial or 
 encysted if area is internal, which 
 is then followed by reabsorbtion 
 of the contents and calcification 
 of the sac. 
 
 In dry and vascular form of moist 
 the gangrene is generally limited. 
 In the other forms it is progres- 
 sive. 
 
 From the above you will note then 
 that gangrene is circumscribed, 
 progressive or metastatic. 
 
 INFLAMMATION AND REGENER- 
 ATION. 
 
 1. INFLAMMATION is the reaction which 
 occurs in tissues to various forms of 
 irritations, and is characterized by the 
 cardinal symptoms of heat (calor), red- 
 ness (rubor), pain (dolor), swelling 
 (tumor) and later altered function 
 (functio laesae). 
 Etiology. Irritation by — 
 
 1. Mechanical, as in fractures and 
 wounds. 
 
 2. Chemical, as by strong acids. 
 
 3. Electrical. 
 
 4. Thermal or opposite, burns and frost 
 bites. 
 
 5. Microorganisms. 
 
 6. Metabolic, as in gout, etc. 
 
 7. Mental, as in hyponosis, etc. 
 Phenomena of Inflammation. 
 
 1. Vascular changes. 
 
 a. Momentary contraction of the ar- 
 teries. This is probably reflex and 
 is rarely observed. 
 
 b. Dilitation of arteries, due in part 
 to nervous reflex, but probably 
 most to some degeneration of ves- 
 sel walls. The blood courses more 
 quickly at first and is then followed 
 by a slowing of the blood current, 
 with sometimes complete stoppage 
 (stasis), brought about by the dam- 
 aged endothelial cells, , which swell, 
 increase in adhesiveness, . thus en- 
 croaching upon the lumen of the 
 vessel. This condition ' is followed 
 by— 
 
 2. Exudative changes. 
 
 a. Leucocytes in r . the. plasmatic, zone 
 
50 PATHOLOGY. 
 
 of the blood stream increase in 
 number and cling to the vessel 
 wall. 
 b. Leukocytic migration through the 
 vessel wall to the outside and into 
 the tissues. This is brought about 
 by- 
 
 1. The leucocytes' own ameboid 
 movement. 
 
 2. Chemotoxis (positive), the attrac- 
 tive chemical influence at the site 
 of irritation. 
 
 3. Increased permeability of the 
 vessel wall and blood pressure 
 aid to a minor extent. 
 
 Coincidentally with migration there 
 is — 
 C. Exudation of altered blood plasma. 
 The amount and character of which 
 varies with the nature and condi- 
 tion of the tissues affected and the 
 character of the irritant. 
 The exudate is relatively rich in al- 
 bumen and more coagulable than 
 dropsical fluid. 
 d. Diapedesis of Red corpuscle. 
 
 The escape of the red corpuscle 
 from the capillaries is a passive 
 process, being due to blood pressure. 
 It is most marked when stasis has 
 occurred. 
 3. Proliferative changes. Some authori- 
 ties hold that proliferative changes 
 are not in reality a part of inflam- 
 mation, but are for the purpose of 
 tissue repair after inflammation. It 
 will, however, be regarded as a part 
 of inflammation. 
 In the inflammed area, especially at the 
 periphery, the tissue is infiltrated with 
 round cells resembling lymphocytes, 
 or mononuclear leucocytes frequently 
 showing evidences of karyokinesis. 
 They are derived from fixed connec- 
 tive tissue cells and the endothelia of 
 lymph spaces. 
 The newly formed connective tissue cell 
 becomes in part wandering and more 
 or less phagocytic in nature, and in 
 part fixed, and assumes a regenera- 
 tive role, frequently called flbro-blastic 
 cells. The appearance of the tissue at 
 
Fig. 5. Acute appendicitis, with ex- 
 tensive round cell infiltration of all the 
 coats of the appendix. 
 
Fig-. 6. Fibroblasts forming- fibrous 
 tissue. (Ziegler.) 
 
 m 
 
 Fig. 7. Chronic interstitial nephritis; 
 great increase of connective tissue 
 around the glomeruli, renal tubules and 
 blood vessels; from a case of arterio- 
 capillary fibrosis. 
 
INFLAMMATION. 51 
 
 this stage is characteristic and is 
 termed Round-cell infiltration. 
 
 Granulation Tissue. 
 
 Active proliferative changes, multipli- 
 cation of new blood vessels, pre-ex- 
 isting vessels endothelial outgrowth, 
 all surrounded by various forms of 
 round cells constitute granulation tis- 
 sue. It is frequently seen in the floor 
 or ulcers. It is more properly a re- 
 generation. 
 
 4. Degenerative changes. 
 
 The nature of the degeneration de- 
 pends upon the severity of the irri- 
 tation. Very powerful irritants cause 
 necrosis at once. Irritants which 
 merely disorder but do not entirely 
 destroy the cells are apt to cause in- 
 flammation. 
 
 The degenerative changes may be 
 physiologic or there may be structural 
 changes such as cloudy swelling, 
 mucoid degernation, liquefaction, fat- 
 ty or coagulation necrosis. These de- 
 generations though primary are often 
 followed by a secondary degeneration 
 which may serve to spread and in- 
 tensity the original inflammation. 
 Varieties of inflammation. 
 
 a. Catarrhal, mucous inflammation or 
 catarrh, occurs on the mucous mem- 
 branes, as in the nose, throat, 
 bronchi, stomach, bowels, etc. 
 
 The mucosa is congested, a serous ex- 
 udation is discharged from the sur- 
 face, and to some extent it is re- 
 tained in the tissue causing edemat- 
 ous swellings. Tne mucous glands 
 increase their secretion and leucocytes 
 escape. When abundant, as in nasal 
 catarrh, the process may be purulent 
 or suppurative, more frequently 
 mucopurulent. 
 
 When inflammation is chronic there 
 is considerable productive inflam- 
 mation with consequent irregular- 
 thickening or thinning of area in- 
 volved. 
 
 b. Serous Inflammation, is character- 
 ized by an abundant exudate of 
 serum with very little cellular 
 matter. It is frequently seen in 
 pleural or peritonitic effusions and 
 
52 PATHOLOGY. 
 
 as edema of the larynx, etc. 
 All serous effusions are not inflam- 
 matory. 
 
 Some are purely mechanical, as in 
 dropsies. 
 
 Inflammatory effusions differ from 
 dropsical in that they contain more 
 albumin and fibrin. 
 
 C. Fibrinous (croupous) Inflammation, 
 
 is characterized by a thick deposit of 
 fibrin and occurs on the serous sur- 
 faces as in peritonitis, larynx and 
 bronchi in acute infections as in ty- 
 phoid, small-pox and pyaemia and in 
 the lung in pneumonia. 
 The term sero-fibrinous is applied 
 when it is associated with serous 
 exudation and fibrino-purulent when 
 exudate is purulent. 
 
 d. Diphtheric Inflammation, is of the 
 same nature as the fibrinous but diff- 
 ers in that it is much more severe and 
 having associated with the coagu- 
 lated exudate a necrosis of the cells 
 of the part involved. It is typically 
 seen in diphtheria but may also be 
 seen in other conditions. 
 
 The membrane consists of a net- 
 work of fibrin or fibrin masses en- 
 closing degenerated epithelial cells 
 and emigrated leucocytes. 
 
 e. Supperative Inflammation, although 
 generally caused by infection with 
 pyogenic micro organisms, it has also 
 been produced by calomel, croton oil, 
 turpentine, etc. It is characterized 
 by an abundance of emigrated leu- 
 cocytes and the tendency to liquefac- 
 tion. 
 
 The most common bacteria producing 
 it are the pyogenic staphylococci and 
 streptococci but other forms not gen- 
 erally considered pathogenic may 
 also cause it, as the typhoid and coli 
 bacillus, gonococcus and others. 
 Bacteria entering the tissue by means 
 of the blood or otherwise, first cause 
 degeneration or necrosis, congestion 
 follows with exudation of leucocytes 
 and plasma and more or less fibrin 
 formation and finally softening of the 
 whole area involved from the action 
 of the bacteria on the cells, creating 
 a ferment. 
 
INFLAMMATION. 53 
 
 The packed exudative cells and the 
 pressure together with the local 
 anemia produced are additional fac- 
 tors that lead to degenerative changes 
 and pus-formation. The fluid exudate 
 fails to coagulate and form fibrin. 
 
 Pus consists of a liquid part (liquor 
 puris) and a corpuscular part. 
 
 The liquid part is made up of a less 
 coagulable blood plasma containing 
 quantities of albumose. 
 
 The corpuscles are chiefly more or 
 less degenerated polymorphonuclear 
 leucocytes. 
 
 When the suppuration within a tis- 
 sue or organ is circumscribed it is 
 called an, — 
 
 Abscess. The tissues surrounding 
 the area show proliferative changes, 
 forming a sort of retaining wall. In 
 slow forming abscesses the wall is 
 quite firm and is often called pyogenic 
 membrane. 
 
 The abscesses will soften the tissues 
 in the direction of least resistance and 
 discharge their contents onto the sur- 
 face by sinuses. 
 
 The pus may become inspissated by 
 the absorbtion of the liquid part, the 
 remaining matter undergoing various 
 degenerations. The membrane may 
 become organized and thus encap- 
 sulate the abscess. 
 
 Ulcer. An ulcer is of the same con- 
 struction as an abscess except that 
 it appears with erosion upon the skin 
 or mucous surfaces. 
 Suppuration of the skin and sub- 
 cutaneous tissues are localized or 
 diffused. Of the localized we have 
 pustules, furuncles and carbuncles. 
 
 f. Parenchymatous Inflammation is a 
 term applied to inflammations when 
 it attacks the proper tissues of an 
 organ as in nephritis and leads to 
 degeneration of its active cells. 
 
 g. Productive Inflammation. 
 
 The term intestitial inflammation is 
 applied to this form in contradistinc- 
 tion to the parenchymatous form. 
 The proliferative changes predominate 
 over exudation and degeneration. 
 
54 PATHOLOGY. 
 
 When the inflammation becomes 
 chronic the proliferative changes in 
 the tissue predominate more or less. 
 There is essentially some primary de- 
 struction of tissue so that productive 
 process must therefore be regarded 
 as reactive. 
 
 Repair of Wounds. This is brought 
 about by productive inflammation. 
 Where there is but little exudation 
 and proliferated connective tissue 
 cells, it is called healing by immedi- 
 ate union. This is when the lips of 
 the wound are clean and carefully 
 drawn together at once. 
 Where opposition is slightly delayed 
 or less accurate, the exudation is 
 greater, and the healing is more slow, 
 it is called healing by first intention. 
 If the wound is exposed or irritated 
 there will be seen, after 48 hours, 
 small red elevations (granulations) 
 made up of newly formed loops of 
 capillaries covered with round cells 
 and later there may be giant cells. 
 The round cells elongate and form 
 fibrous tissue which contracts and 
 forms ciratrices or scars. 
 The continuity is re-established by 
 old epithelial cell multiplication at the 
 edges of the wound. This is called 
 healing by granulation or second in- 
 tention. 
 
 Adhesions. The formation of ad- 
 hesions following inflammation of 
 serous surfaces, is brought about by 
 the fibriuous primary exudation which 
 causes agglutination of the neighbor- 
 ing surfaces and is then followed by 
 conditions somewhat similar to the 
 healing of wounds. 
 
 Repeated attacks of the parenchyna- 
 tous inflammation results in an in- 
 terstitial inflammation in which the 
 supporting framework of the organ is 
 involved. This connective tissue over- 
 growth results in cirrhosis, fibrosis or 
 induration of the organ. 
 
 General Fibrosis is a tendency to wide 
 spread productive inflammation, sup- 
 posedly due to alcoholic, gouty,. syphil- 
 ic, etc. intoxications It affects the 
 blood vessels especially, also the 
 liver (cirrhosis), kidney (interstitial 
 
REGENERATION. 55 
 
 nephritis), etc. 
 
 This form of inflammation may also 
 attack the epithelia of the skin, 
 mucous membranes adenoid tissues, 
 cartilages, bones or the periosteum. 
 h. Hemorrhagic Inflammation, is an in- 
 flammation in which the exudate is 
 usually rich in red corpuscles. It is 
 distinguished from ordinary inflam- 
 mation in which hemorrhages occur 
 accidentally. 
 
 The cause is probably due to the ir- 
 ritating cause falling principally on 
 the blood vessels or that the patient is 
 suffering from cancer, tuberculosis, 
 hemophilia, etc. 
 
 Purulent inflammation is generally 
 caused by infection with microorgan- 
 isms. 
 
 Resolution. 
 
 Where exudation is small, the emi- 
 grated leucocytyes and the liquid ex- 
 udate re-enter the blood current or 
 escape through the lymphatics. The 
 connective tissue cells remain or be- 
 come wandering cells. 
 When the exudate is abundant, the 
 liquid element is removed by the 
 blood or the lymphatics, but the cells 
 first degenerate and are emulsified, 
 then gradually absorbed. 
 In purulent inflammation the pus is 
 discharged through openings, extern- 
 ally or into the cavities of the body, or 
 may be inspisated. 
 
 If the inflammation of the parench- 
 yma may recover if the degeneration 
 is not too severe, or may be softened 
 and removed. 
 II. REGENERATION is the formation of 
 new cells or tissues to take the place 
 of those destroyed. It may be divided 
 into — 
 
 1. Physiologic. Occurs in the normal 
 organism, counterbalancing the cel- 
 lular wear and tear. 
 
 The cells multiply, but do not go be- 
 yond the point of normal develop- 
 ment. Some unknown restraining in- 
 fluence prohibits the cells from go- 
 ing beyond their limit. The repro- 
 ductive process is probably depend- 
 ent upon the loss of substance. 
 
56 PATHOLOGY. 
 
 Where the normal restraining influ- 
 ence is deficient giant growth results. 
 
 In normal regeneration the process is 
 one of gradual cell multiplication. 
 
 Cell multiplication or division occurs 
 in two vva>s, i. e., it takes place 
 directly by cleavage (amitosis), which 
 seldom takes place, or by the indi- 
 rect method (karyokinesis), which is 
 the usual method. 
 
 2. Pathologic Regeneration is a mas- 
 sive and often atypical reconstruc- 
 tion that follows disease or injuries. 
 
 In this form there seems to be an ab- 
 normal stimulation of the reproduc- 
 tion of cells as well as a reduced re- 
 straining influence. 
 
 Various toxic substances probably stim- 
 ulate the formative process, though 
 in regeneration following mechanical, 
 thermal or toxic causes there is first 
 a destruction of cells. The regenera- 
 tion which follows may be due to 
 relief from accustomed pressure, 
 which may serve to withdraw the re- 
 straining influence. 
 
 Regeneration is the more or less ef- 
 fective effort of nature to replace in- 
 jured or excised tissue. The com- 
 pleteness of the restoration is in the 
 proportion to the tissues lack in 
 higher organization and differentia- 
 tion. 
 
 The lower the type of tissue and the 
 younger the individual the more com- 
 plete the restoration. 
 
 Organization is the method by which a 
 non-infective organic foreign body is 
 absorbed and replaced by connective 
 tissue. It is best seen in thrombi and 
 in small tissues killed by infarcts. 
 
 In a clot the endothelium of the vessels 
 proliferate to form fibroblasts, new 
 vessels from the vasa vasorum grow 
 into the lumen, and with the increase 
 of the young connective tissue there 
 is a disappearance of the clot. 
 
 The same process takes place in an 
 infarct. The new vessels and fibro- 
 blasts are furnished from the vessels 
 and the cells around. 
 
 Metaplasia is the transformation of one 
 form of tissue into another without 
 
HYPERTROPHY. 57 
 
 any intervening stage of regeneration 
 by cellular multiplication. The change 
 may be a transformation of the inter- 
 cellular substance, as when common 
 connective tissue is converted into 
 myxomatous tissue or the fibrillar 
 into cartilaginous or bony tissue. 
 
 The tissue never changes its species, 
 and the character once altered is 
 permanent. 
 
 PROGRESSIVE TISSUE CHANGES. 
 
 . HYPERTROPHY. Is the increase in 
 size of the tissue elements without 
 marked alteration from the normal 
 structure. 
 Causes. 
 
 1. Increase of functional demand, as in 
 hypertrophy of the muscles of ath- 
 letes; hypertrophy of a limb after in- 
 jury to the opposite limb; hypertro- 
 phy of a kidney after disease or re- 
 moval of its fellow. 
 
 2. Disturbances of the nervous sys- 
 tem. 
 
 3. Continued congestion, though this is 
 the means in which it is affected 
 rather than the original cause. 
 Pathologic Anatomy. 
 
 The parts are uniformly increased 
 
 in size. 
 Histologically, hypertrophy may be 
 
 divided into — 
 
 1. Simple or true hypertrophy, in 
 
 which there is an increase in 
 the size of the individual cells. 
 This is seen in the uterus dur- 
 ing pregnancy. 
 
 2. Numerical hypertrophy or hy- 
 perplasia. In this form the cells 
 are of the normal size, but are 
 increased in number. This is a 
 common factor in hypertrophy. 
 It may be limited to one tissue 
 of an organ, principally the con- 
 nective tissue. 
 
 There are all grades between the 
 extremes. Some cases are des- 
 ignated clinically as — 
 
 Hypertrophic enlargement, which 
 is a hyperplasia of the connec- 
 tive tissue, with a tendency to 
 
58 PATHOLOGY. 
 
 atrophy of the organs proper 
 substance, as in hypertrophic 
 cirrhosis of the liver, etc. 
 Pathologic Physiology. 
 
 When there is an increased de- 
 mand upon an organ by reason of 
 disease in itself or in a related 
 organ, or from loss of a correlated 
 organ, the organ undergoes com- 
 pensatory hypertrophy. This is seen 
 in the kidney when the other is 
 diseased or absent; in the heart in 
 valvular disease, and in the en- 
 larged muscles of laborers. 
 
 II. TUMORS. New Growths, Neoplasms, 
 Pseudoplasm. 
 
 A tumor is a growth which consists 
 of a non- inflammatory mass of cells 
 atypical in structure and arrangement 
 and grows at the expense of the 
 body. 
 
 Causes. There are several theories, 
 none clear. 
 
 1. "Cell Rests" (Cohnheim's theory) or 
 defective development. This theory 
 is based upon frequent small errors 
 of development, which would lead to 
 a misplacement of portions of the 
 blastoderm in the tissues, derived 
 from a different layer of the em- 
 bryo. These cell rests differ in func- 
 tion to the part in which they lie, 
 and are therefore liable to sprout 
 when subjected to irritation or their 
 vitality stimulated, with the conse- 
 quent formation of tumors. 
 
 2. Irritation or injuries (Virchow's 
 theory), as seen in epithelioma of 
 chimney sweeps and pipe smokers 
 and carcinoma of breasts, etc. 
 
 3. Infectious character has been con- 
 sidered by some authorities as a 
 cause, in that in certain respects 
 some tumors resemble infectious 
 processes in their effect upon the 
 general health and their tendency to 
 metastasis. 
 
 Other investigators have determined 
 that no ordinary bacterium play any 
 causative part. The possibility of 
 • ultra- microscopic organisms has been 
 considered. Secondary and accidental 
 invasions of • bacteria . into tumors 
 
TUMORS. 59 
 
 may occur and lead to confusion. 
 The transplantation of tumors from 
 one part to another does not differ 
 from ordinary metastasis. It, how- 
 ever, proves only the proliferative 
 tendency of the cells of the growth 
 and not the infectious origin. 
 
 4, Anaplastic. In this theory the tumor 
 results from a retrograde change in 
 the vital properties of cells so that 
 they tend toward the characteristics 
 of the germ- cells and multiply in an 
 indeterminate manner. 
 
 5, Parasites (coccidia) have been de- 
 scribed as occurring in cancer, but 
 this still awaits proof. 
 
 A late theory is that the cancer cell 
 does not spring from pre-existing 
 epithelium, but is a parasite from 
 without. 
 
 Predisposing causes play an important 
 part in the formation of a new 
 growth. We have therefore — 
 
 1. Constitutional predisposition from — 
 
 a. Advanced age. 
 
 b. Lowered vitality from disease, 
 etc. 
 
 2. Family predisposition, formerly re- 
 garded of great importance, was 
 
 probably over-estimated, but can- 
 not entirely be denied. 
 Structure of Tumors 
 
 1. Tumors conform more or less with 
 structure of some one or more tis- 
 sues. 
 
 2. Tumor cells represent some one of 
 several types of normal cells. They 
 differ from normal cell in that — 
 
 a. They may be smaller or larger. 
 
 b. They may be embryonic or un- 
 developed. 
 
 c. They may be asynametrical or 
 abnormal in mitosis. 
 
 d. Inclused leucocytes are often 
 found in tumor cells and have 
 frequently been mistaken for 
 parasites. 
 
 e. In the malignant tumor cell there 
 is not the normal number of 
 chromosomes. 
 
 3. Arrangement of tumor cells differ 
 from that of normal, tissue, in that — 
 
60 PATHOLOGY. 
 
 a. The orderly arrangement of cells 
 and stroma or the intercellular sub- 
 stance is wanting. 
 
 b. Scattered through the stroma and 
 between the tumor cells are vari- 
 ous forms of leucocytes. 
 
 4. Blood vessels of tumor have poorly 
 developed walls, which permits ready 
 emigration of leucocytes. 
 
 5. Regenerative changes is constantly 
 seen in the formation of the connec- 
 tive tissue frame work. 
 
 Shape of tumors. This depends upon 
 the situation, growth and influence 
 of the surrounding parts. They may 
 be divided into — 
 
 1. Circumscribed growths, which may 
 be of various shape, but distinguished 
 by a line of demarkation and often a 
 capsule. 
 
 They usually grow in an expansive 
 manner from the center, pushing the 
 older parts toward the surrounding 
 tissue. 
 
 According to the appearance of the 
 growth the terms miliary, tubercular, 
 nodular are employed to designate the 
 grades when the tumor is buried in 
 the tissue or project more or less 
 from the surface. When the growth 
 has a constricted base the term 
 fungiform is used. When it is at- 
 tached by a narrow pedicle the term 
 polypoid is used. Wart-like growths 
 are called verucose or papillary. 
 Cauliflower growths are called den- 
 dritic. 
 
 2. Infiltrating growths are those in 
 which there is no distinct line of de- 
 markation, and the extent of tissue 
 involvment cannot be definitely de- 
 termined. 
 
 The growth is irregular. Parts of the 
 periphery or original growth may ex- 
 tend, or secondary nodules may form 
 in the neighborhood, afterwards be- 
 coming confluent with the original 
 mass. 
 
 Pathologic Physiology. 
 
 Tumors may be said to be parasitic, 
 in that they live at the expense of 
 the organism. 
 
TUMORS. 61 
 
 Tumors may be classed as — 
 
 1. Benign, when it does not apparently 
 affect the health. They are danger- 
 ous by reason of the pressure to vital 
 parts or the secondary changes to 
 which they are liable. 
 
 2. Malignant, when it shortens life. 
 It infiltrates the surrounding tissue. 
 It tends to recur after removal. 
 
 It spreads to distant organs by the 
 blood vessels and lymphatics (Metas- 
 tasis), or transplantation of a tumor 
 from one part of the body to another. 
 
 A specific poison is formed by the 
 tumor cell, which disturbs the health 
 from the first, and the patient shows 
 a peculiar, sallow complexion know-n 
 as a cachexia. 
 
 Tumors w T hich are ordinarily benign 
 may recur after operation or cause 
 metastasis, the terms — 
 
 1. Primary tumors refer to the orig- 
 inal tumor and the number. They 
 are generally solitary, though they 
 may be multiple, as in carcinoma, 
 appearing in both breasts simul- 
 taneously or in other different parts 
 of the body. 
 
 Benign tumors are usually solitary. 
 
 2. Secondary tumors refer to meta- 
 static growths and are usually mul- 
 tiple. 
 
 Classification of Tumors. There is no sat- 
 isfactory classification. The classifica- 
 tion by Ada mi is given below — 
 
 I. Blastomata, composed of products of 
 aberrant growth of cells and tissues of 
 the individual in whom they are de- 
 veloped. 
 
 Adult tissues may be divided into two 
 types — 
 
 1. Lepidic tissue (rind or membrane), 
 tissue in which there is no stroma 
 with blood and lymph vessels be- 
 tween the individual cells. 
 
 2. Hylic or pulp tissues (crude matter, 
 supporting or packing tissue), tissue 
 in which there is homogenous , or 
 fibrillated inter-cellular substance 
 separating the specific cells. 
 
 Both of these types are derived from 
 the epiblastic, mesoblastic and hy- 
 
62 PATHOLOGY. 
 
 poblastic layers of the embryo. 
 They are derived from the — 
 
 a. Epiblast. 
 
 1. Lepidic. Skin and its glands, 
 portions of eye, ear and brain, 
 etc. 
 
 2 Hylic Nerve and glia cells. 
 
 b. Hypoblast. 
 
 1. Lepidic. Epithelium of the di- 
 gestive tract and associated 
 glands. 
 
 2. Hylic. Intervertebral disc (noto- 
 chord). 
 
 c. Mesoblast. 
 
 1. Lepidic. 
 
 a. Mesothelium — lining of pleura, 
 pericardium, specific cell of 
 suprarenals, kidneys, testis, 
 ovary, epithelium of uterus, 
 fallopian tubes, vagina, vas 
 deferns, etc. 
 
 b. Endothelium — lining of the 
 blood vessels and lymphatics. 
 
 2. Hylic. 
 
 a. Mesenchyme — connective tis- 
 sue, bone, marrow, etc. 
 
 b. Mesothelium — striated muscle. 
 Inasmuch as both hylic and lepidic tissue 
 
 is found in all three layers, blastomata 
 may be classified both embryologically 
 and hystologically into — 
 1. Lepidomata or "Rind" Tumors, 
 a. Primary Lepidomata. 
 
 1. Epilepidomata are overgrowth of 
 tissue derived from epiblastic lin- 
 ing membranes or true epiblast. 
 
 a. Typical. Papilloma, epidermal 
 adenomata (of sweat, salivary, 
 sebaceous and mammary glands, 
 etc.). 
 
 b. Atypical. Carcinoma develop- 
 ing in the same organs and re- 
 regions. 
 
 2. Hypolepidomata. 
 
 a. Typical. Adenoma and papil- 
 loma of the digestive and re- 
 spiratory tract, thyroid, pan- 
 creas, liver, bladder, etc. 
 
 b. Atypical. Carcinoma develop- 
 ing in the same organs and re- 
 gions. 
 
TUMORS. 63 
 
 b. Secondary Lepidomata. Tumors 
 whose characteristic constituents 
 are cells derived in direct descent 
 from the persistent mesothelium of 
 of the embryo. 
 
 1. Mesolepidomata. 
 
 a. Typical. Adenoma of kidney, 
 testicle, ovary, urogenital ducts; 
 adenoma of uterus and prostate; 
 adenomas originating from se- 
 rous membranes, "mesotheli- 
 oma" of pleura, peritoneum, 
 etc. 
 
 b. Atypical. Cancer of the above 
 mentioned organs, squamous 
 endothelioma, so-called, of se- 
 rous surfaces, epithelioma of 
 vagina. 
 
 2. Endothelial Lepidomata. Tumors 
 originating from endothelium of 
 blood and lymph vessels; endothe- 
 lioma, perithelioma. 
 
 1. 2. Hylomata or "Pulp" Tumors. 
 
 a. Epibryiomata. Tumors whose char- 
 acteristic constituents are over- 
 growths of tissue, derived from the 
 embryonic pulp of epiblastic origin. 
 
 1. Typical. True neuroma, glioma. 
 
 2. Atypical. Gliosarcoma. 
 
 b. Hypohylomata. Tumors derived 
 similarly from the embryonic pulp 
 of hypoblastic origin. Chordoma. 
 
 c. Mesohylomata. 
 
 1. Mesenchymal Hylomata. Derived 
 from tissues originating from the 
 persistent mesoblastic pulp or 
 mesenchyme. 
 
 a. Typical. Fibroma, lipoma, 
 chondroma, osteoma, myxoma, 
 leiomyoma. 
 
 b. Atypical. Sarcoma. Derived 
 from mesenchymatous tissues 
 with its various subdivisions, 
 nbrosaroma. spindle cell sar- 
 coma, oat-shaped cell sarcoma, 
 chondrosarcoma, osteosarcoma, 
 myxosarcoma, melanotic sar- 
 coma, etc. 
 
 2. Mesothelial Hylomata. Tumors 
 which are overgrowths similarly 
 of tissues derived from embryonic 
 pulp of definitely mesothelial 
 origin. 
 
64 PATHOLOGY. 
 
 Rhabron^oma. 
 The Histology and the Distribution of the 
 Blastomata. 
 
 1. Fibromata are benign connective tis- 
 sue growths, consisting chiefly of fibers 
 with cells, which become more nu- 
 merous in proportion to the rapidity 
 with which the tumor grows. The 
 growth is usually exceedingly slow. 
 They are destructive only in so far as 
 they are capable of producing mechan- 
 ical injury by pressure. 
 
 In some cases they will recur after re- 
 moval, and in these instances resemble 
 sarcoma. 
 
 a. Hard Fibroma is a dense, tendon 
 like formation, having only a few 
 cells and flat fibers. It is often en- 
 capsulated. It is seen in the perios- 
 teum, particularly of the dental 
 alveoli. 
 
 b. Soft Fibroma is of a soft consistency 
 and of a loose texture. It is seen as 
 a non-capsulated tumor of the skin. 
 Also as polypi of the nose. 
 
 c. Elephantoid Fibromata (mimic ele- 
 phantiasis), multiple tumors of the 
 skin. 
 
 d. Fibroma Moliuscum (M. non-con- 
 tagiosum) is absolutely different from 
 M. contagiosum. It is made up of a 
 great number of small fibromata 
 growing from the skin and are sessile 
 and pedunculated. Microscopically, it 
 is shown to be made up of both loose 
 and dense fibrous tissue. 
 
 e. Cheloid is a dense, fibrous growth, 
 appearing usually, but not always, 
 in cicatrices, and is of the same 
 structure. It may assume a sarco- 
 matous character. 
 
 f. Psammoma, or brain sand tumor, is 
 found in the pineal gland, in the 
 choroid plexus and the dura mater. 
 It is a soft connective tissue, new 
 growth, infiltrated with calcareous 
 globes and spicules. 
 
 The fibromata also include many 
 tumors which have been called neu- 
 romata because they spring from the 
 nerve sheaths. There is, however, no 
 nervous tissue to be found in their 
 
TUMORS. 65 
 
 structure. 
 Seats. Always springing from pre-ex- 
 isting connective tissue. They are 
 found in the subcutaneous connective 
 tissue, submucous tissue, periosteum, 
 tendons and tendon sheaths, and the 
 fibrous covering of the nerves. The 
 uterus, ovaries, kidneys and heart 
 muscle, serous membranes of the 
 chest and abdomen and the central 
 nervous system. 
 
 2. Myxoma, is a tumor made up of stel- 
 late or spindle-shaped, connective tissue 
 cells and an inter-cellular substance 
 containing a mucoid material. Mucoid 
 tissue is physiologically present in the 
 umbilical cord, the foetal subcutaneous 
 tissue and the vitrious of the eye. 
 
 The tumor is soft, flabby and rounded in 
 structure. It is surrounded by a cap- 
 sule. It may sometimes be lobulated, 
 or it may be diffuse, having no capsule. 
 Found in the subcutaneous and sub- 
 mucous tissue and the connective tissue 
 of certain organs, principally the mam- 
 mary gland along the course of nerves, 
 brain and the spinal cord. It may also 
 be found in the subserous tissue. It is 
 usually found alone, but may be asso- 
 ciated with or as a degeneration of 
 lipoma, fibroma, chondroma and ade- 
 noma, the prefix Myxo being used with 
 each of these terms. 
 
 The myxoma is benign, but it may be 
 myxosarcomatous. 
 
 3. Lipoma is a tumor made up of fat 
 tissue, which does not differ greatly 
 from the normal subcutaneous fatty 
 tissue. It resembles greatly the ap- 
 pendices epiploicae. 
 
 The tumor cells are frequently larger 
 and contain more oil than the normal 
 fat cell. 
 
 The tumor is soft to the feel unless it is 
 made tense by fibrous trabeculae run- 
 ning in from its capsule, it is then 
 called a flbrolipoma. 
 
 The capsule may be wanting in some 
 cases, the tumor being then diffuse. 
 
 The tumor may be solitary or multiple. 
 Congenital lipoma are not rare, but it 
 generally appears during adult years or 
 middle life. 
 
66 PATHOLOGY. 
 
 It is benign and of slow growth and 
 usually occurs in the subcutaneous 
 fatty tissue of the back, shoulders, 
 buttocks or limbs, the submucous and 
 the subserous tissue. 
 
 The mammary gland and kidneys are the 
 most frequent seats in the organs of 
 the body. 
 
 4. Xanthoma is a benign tumor made up 
 of modified fatty tissue resembling em- 
 bryonic adipose tissue, with more or 
 less round cell infiltration. 
 
 a. Xanthoma vulgare occurs frequently 
 in or near the eyelids in the form of 
 yellow, flat elevations. 
 
 b. Xanthoma diabeticorum is found in 
 diabetic patients. It is similar to the 
 above, but is more inflammatory and 
 rarely affects the eyelids or the face. 
 
 5. Chondroma is a tumor composed of 
 cartilage. It consists of distinct 
 forms, which differ somewhat in ap- 
 pearance. 
 
 a. Ecchondromata, or cartilagenous 
 outgrowths, spring from the cartilage 
 and appear as irregular outgrowths, 
 or may be wart-like in form, or may 
 occur in rows or groups. They may 
 be loosely or firmly attached, and are 
 seen in rheumatoid arthrites, where 
 they may become detached, or they 
 may be seen on the surfaces of the 
 costal or laryngeal cartilages, where 
 they are firmly attached. 
 
 b. Enchondromata, cartilageous tumors 
 or chrondromata proper, are the 
 more common form and begins in 
 some other form of connective tissue. 
 
 They occur in bones or the periosteum 
 and have a rounded or lobular ap- 
 pearance. 
 
 Chondromata, in all probability, arise 
 from "cell rests," and are unexpect- 
 edly found to occur in the parotid- 
 gland and in the testicle. 
 
 Enchondroses occurs in the neighbor- 
 hood of bones, in muscles and ten- 
 dons and in organs mentioned above. 
 
 The ecchondroses are most frequently 
 found about the long bones, partic- 
 ularly at their epiphyseal attachment. 
 
 All forms are hard, though secondary 
 
TUMORS. 67 
 
 softening may occur. Associated mu- 
 cous, sarcomatous or other softer tis- 
 sue will regulate its consistency. 
 
 Histologically, the cartilage cells are 
 found inclosed in a hyaline or fibrous 
 matrix. The cells are frequently with- 
 out a capsule and not regularly ar- 
 ranged. The inter-cellular substance, 
 which is abundant, is frequently gela- 
 tinous, mucoid or fibrous. 
 
 When the tumor is associated with 
 myxoma and sarcoma the structure 
 varies. They are then called mixed 
 tumors. When there is calcification 
 and true ossification it is called os- 
 teochondroma. 
 
 Osteoid chondroma is the name given 
 to it when the inter- cellular substance 
 suggests bone structure, but actual 
 ossification has not occurred. 
 
 The tumor is usually benign. 
 
 Metastasis may occur. 
 
 6. Osteoma is a tumor composed of os- 
 seous tissue. The pathologic growth 
 of bone is seen as a senile change, and 
 also results from chronic irritation and 
 inflammation, as seen in the deltoid 
 muscle, from carrying a rifle, and around 
 inflamed joints. Osteoma is closely 
 allied to the chondroma and, like the 
 chondromata, two forms are distin- 
 guished. 
 
 a. Exostoses and osteophytes are out- 
 growths differing in shape and ap- 
 pearance only. The exostosis is a di- 
 rect outgrowth from bone of a more 
 or less warty character. 
 
 The osteophytes are extensive, bony 
 deposits upon bones and are less 
 closely attached. They are formed 
 either of spongy or compact bone. 
 When spongy, it grows from the 
 epiphyseal cartilage. When compact, 
 it grows from and beneath the perios- 
 teum. 
 
 They are divided into— 
 
 1. Ostoma durum, hard. 
 
 2. Osteoma spongiosum, soft. 
 
 3. Osteoma eburueum, when exceed- 
 ingly dense. 
 
 When arising and consisting of den- 
 tine it is known as odontoma. 
 
 b. Enostoses (osteoma proper or hetro- 
 
68 PATHOLOGY. 
 
 plastic osteomata) are those which 
 are separated from the bone, as when 
 they appear in the medullary canal 
 and in the serous membranes. 
 Osteoma are found in connection with 
 bone, cartilage or the connective tis- 
 sue near bone. 
 
 They are sometimes found in other 
 connective tissues, serous membranes 
 or organs as testicles and the parotid 
 gland. 
 
 The growth is benign. Secondary de- 
 generations may occur and are some- 
 times associated with other tumors, 
 such as chondroma, myxoma, fibroma 
 and sarcoma. 
 
 7. Myoma is a tumor composed of mus- 
 cular tissue. 
 It is divided into — 
 
 a. Leiomyoma or Myoma laevicellulare 
 is made up of unstriated muscle 
 fibers running in various directions. 
 There is generally some fibrous tissue 
 associated with it. If cut transversely 
 there may or may not be a round 
 nucleus, depending upon where the 
 cell is cut. 
 
 If cut longitudinally a rod-shaped 
 nucleus will be seen, the spindle out- 
 line of the cell may be indistinct. 
 
 There is a distinct capsule to the 
 tumor. 
 
 Its chief seat is in the uterus and its 
 apendages, though frequently it oc- 
 curs in the prostate and alimentary 
 tract. Rarely it is found in the walls 
 of blood vessels, the nipple and the 
 skin. 
 
 The tubercula dolorosa (Wood's tumor) 
 of the skin is a myoma probably de- 
 rived from the arrector pili muscle. 
 
 It is benign and the growth slow. 
 Only dangerous by reason of strangu- 
 lation or occlusion, as in digestive 
 tract and weight in other cases. 
 
 b. Rhabdoma or myoma striocellulari is 
 a tumor of rare congenital form com- 
 posed more or less of striated muscle 
 fiber, together with a bulk of other 
 tissue, which is generally sarcoma- 
 tous. 
 
 It is probably an inclusion from the 
 
TUMORS. 69 
 
 embryonic muscle plates. 
 
 It occurs chiefly in the kidney and tes- 
 ticle. 
 
 In structure its appearance is that of 
 a spindle cell sarcoma, with more or 
 less striped muscle fibers of an em- 
 bryonic character. 
 
 It is malignant in proportion to the 
 sarcomatous element present. 
 
 8. Neuroma is a tumor consisting of nerve 
 tissue made up of principally medul- 
 lated and non-medullated nerve fibers. 
 Ganglion cells in the tumor are ex- 
 tremely rare. 
 
 Ordinarily growth of the perineurium or 
 endoneurium are called neuromata, but 
 these are purely fibromata. If with 
 these there are any nerve fibers present 
 the term fibroneuromata is used. 
 The terms — 
 
 a. True neuromata is used when the 
 growth is strictly nervous, which is 
 exceedingly rare. 
 
 It is called — 
 
 1. Myelinic when composed of med- 
 ullated nerve fibers. 
 
 2. Amyelinic when composed of 
 non-medullated nerve fibers. 
 
 b. False neuromata is used when the 
 growth is of the nerve sheath, to- 
 gether with the nerve fibers. 
 
 The peripheral nerves are most fre- 
 quently involved, but involvment 
 may also be near their roots or the 
 terminal fibers within the organs. 
 
 The tumor is painful, but benign. 
 
 9. Glioma is a tumor composed of neu- 
 roglia. It is usually a solitary, round 
 tumor, gradually merging into the sur- 
 rounding nervous tissue, consisting of 
 small spheroidal cells and the typical 
 spider cells of neuro'glia. 
 
 The protoplasm is scanty, while occa- 
 sional fibers may render it moderately 
 dense. 
 
 The tumor is very vascular and hemor- 
 rhage is frequent and followed by apo- 
 plectic symptoms. Softening may oc- 
 cur. 
 
 Embryologically, it is an epithelial struc- 
 ture, and therefore may be associated 
 with sarcoma, though it is of slow 
 
70 PATHOLOGY. 
 
 growth and essentially benign it causes 
 great damage by its pressure on the 
 nerve fibers or centers. 
 
 It occurs in the brain and less fre- 
 quently in the spinal cord. The cranial 
 nerves are sometimes involved. 
 
 Glioma of the Retina is primary, but may 
 extend so as to involve the eyeball. It 
 occurs most frequently in children, 
 and family predisposition in some cases 
 seems to play an important part. The 
 growth is malignant in character. 
 
 Glioma Ganglionare is a mixed tumor 
 composed of neuroglia and nerve fibers, 
 with large ganglionar nerve cells. 
 
 It occurs as multiple nodular masses 
 scattered through the brain or cord. 
 The nerve roots and suprarenal cap- 
 sules are sometimes the seat of these 
 tumors. 
 
 It may resemble the ordinary glioma. 
 Its nature is the same as that of glioma. 
 
 10. Haemangioma or Simple angioma is a 
 tumor composed of new blood vessels. 
 It is divided into — 
 
 a. Capillary, Plexiform angioma or an- 
 gioma teleangiectaticum is made up 
 of arteries, veins and capillaries, 
 which may have thicker walls than 
 normal and be dilated or sacculated. 
 
 It is most frequently found in the skin 
 and forms the naevus, birth mark or 
 port wine stain. 
 
 It is usually conigenital, but may grow 
 larger after birth. 
 
 A condition where the vessels are much 
 thickened and tortuous, forming the 
 so-called "earth worm feel," bunches 
 under the skin, is frequently seen in 
 the varicosity of the legs, etc., and 
 most frequently seen in hemorrhoids. 
 
 b. Cavernous angioma shows a connec- 
 tive tissue trabeculae, enclosing en- 
 larged spaces lined with endothelium 
 and filled with blood. 
 
 They are tumor-like formations of a 
 dark venous color, and are usually 
 found in the skin or subcutaneous tis- 
 sues. They are also found in the 
 orbit, liver, spleen and kidney. 
 
 It may be conigenital, but more fre- 
 quently arises later in life. 
 
Fig-. 8. Myxoma, showing- stellate 
 cells separated by a gelatinous (mucoid) 
 intercellular material. 
 
 fe^£ V *%0 'i; 
 
 Fig. 9. Ch.ond.roma of the hyaline 
 type. 
 

 
 Fig-, 10. Cavernous angioma, (Warren.) 
 
 Fig. 11. Adenoma of the mammary 
 gland, with cystic enlargement of acini 
 and abundant interglandular hyperplasia 
 of connective tissue. 
 
TUMORS. 71 
 
 It is a distinct tumor, which may show 
 a distinct capsule. 
 
 The plexiform angioma may be asso- 
 ciated with lipoma, glioma and sar- 
 coma. 
 
 The angioma generally are essentially 
 benign, and may continue throughout 
 life, though hemorrhage, inflamma- 
 tory or necrotic changes may take 
 place. 
 
 11. Lymphangioma is a tumor composed 
 of dilated lymph vessels or lymph 
 spaces, the latter more often involved. 
 It is similar to the haemangioma and 
 
 favors the same sites. 
 Elephantiasis congenital mollis is a con- 
 dition in which the subcutaneous tis- 
 sues are edematous with cystic for- 
 mations. 
 Congenital cystic hygroma is a dilita- 
 
 tion of the lymph spaces. 
 Macroglossia is an enlargement of the 
 
 tongue. 
 Macrocheilia is an enlargement of the 
 
 lips. 
 Naevus lymphaticus is an enlargement 
 
 of the skin. 
 The above conditions are congenital en- 
 largements dependent upon abnormal 
 enlargement of the lymph spaces. 
 Lymphangioma ^avernosum and caver- 
 noma are the names sometimes given 
 to these cases of dilated lymph spaces. 
 It is a rare condition in which actual 
 enlargement and varicosity of lymph 
 vessels are found. It is, however, seen 
 as a general process in elephantiasis. 
 The acquired dilated lymphatics may 
 attain a considerable size, and this 
 rupture may lead to a dangerous 
 lymphorrhea. The lymph may in this 
 way be discharged externally, or it 
 may be discharged into the various 
 serous cavities. Rupture" along the 
 urinary tract will occasion chyluria. 
 It is a benign process generally. 
 12. Lymphadenoma is a more or less ma- 
 lignant new growth of the lymph glands 
 or other lymphoid tissue, and has the 
 structure of lymphatic tissue. Clinic- 
 ally, it is called Hodgkins' Disease or 
 Pseudoleukemia. 
 
72 PATHOLOGY. 
 
 It can be considered as a form of sar- 
 coma, or at least closely allied. It 
 has been called lymphosarcoma, also 
 malignant lymphoma and lymphoma. 
 
 It presents itself as enlarged lymphatic 
 glands of a single group or a number 
 of groups in different parts of the 
 body. 
 
 A few or all of the glands in a group 
 may be involved. The glands retain 
 their shape, and as a rule do not ex- 
 tend beyond their capsule. 
 
 It may be soft or hard, according to 
 the amount of connective tissue and 
 the cellular infiltration and prolifera- 
 tion present. 
 
 The glands may be distinct or fused 
 together. The tumor varies in size 
 and shows up as knobby enlarge- 
 ments under the skin. 
 
 Microscopically, the glands in the 
 earlier stages show a hyperplasia of 
 lymphoid tissue, with a great number 
 of small cells (lymphocytes). 
 
 Later large cells with pale nuclei ap- 
 pear. These are probably proliferated 
 cells from the lymph sinuses. These 
 may enlarge to become mononuclear 
 or polynuclear giant cells, and at this 
 time there is formed a reticular net- 
 work, which increases till the gland 
 becomes hard. 
 Large areas of syncetial tissue (nu- 
 cleated protoplasm) may be seen. 
 The spleen may be involved, also the 
 bone marrow, also the liver, kidneys, 
 lungs, and the gastro-intestinal mu- 
 cosa may be involved with new for- 
 mations of the same character as that 
 which takes place in the lymphoid 
 tissue. 
 13. Adenoma is a tumor which in struc- 
 ture corresponds more or less to epithe- 
 lial glands, but not in its function, as 
 it is without proper secretion. 
 It may arise from any active gland or 
 
 from glandular "cell rests." 
 In appearance it is moderately firm, 
 usually single and circumscribed; 
 sometimes it is surrounded by a 
 fibrous capsule. 
 Its epithelium is sometimes irregular, 
 without a basement membrane and 
 
TUMORS. 73 
 
 therefore abnormal, but it frequently 
 conforms to glandular structure. 
 There are two varieties — 
 
 a. Tubular, in which the glandular sys- 
 tem consists of tube formations lined 
 with columnar epithelial cells. 
 
 b. Racemose or alveolar, in which the 
 acini are closely aggregated and cir- 
 cular in outline, containing columnar, 
 cubical or polyhedral cells. 
 
 On account of its encapsulation in the 
 breast and its superficial location 
 in the rectum it is benign. In the 
 stomach and when it affects the 
 submucosa of the rectum it is very 
 k malignant. It may undergo cystic 
 
 change from the mucoid secretion 
 (adenocystoma) or take on malig- 
 nant characters by carcinomatous 
 growth (adenocarcinoma). When 
 there is a preponderance of fibrous 
 tissue around the acini it is called 
 adenofibroma. 
 
 14. Papilloma is a benign tumor, which 
 appears on the skin, such as warts, 
 corns and horns, and on the mucous 
 surfaces. 
 
 There are two varieties — 
 
 a. Hard papilloma, occurring on the 
 
 skin. 
 
 b. Soft papilloma, appearing on the 
 mucous membrane. 
 
 Papilloma is made up of a center or 
 ground work of connective tissue 
 containing blood vessels and cov- 
 ered by epithelium. 
 
 In the skin the growth appears as 
 exaggerated papilla. A tendency to 
 branching gives to it a cauliflower 
 appearance; each branch contains 
 a connective tissue framework and 
 epithelial covering of stratified 
 squamous cells, which show a tend- 
 ency to horny change. 
 
 In the mucous membrane the papil- 
 lomata differ according to the situa- 
 tion. 
 
 Papilloma may greatly resemble an 
 epithelioma, but can be readily dis- 
 tinguished by the fact that papil- 
 lomas growth is always superficial 
 and always shows some connective 
 
74 PATHOLOGY. 
 
 tissue stroma, while the epithelioma 
 grows into the deep tissues. 
 15. Carcinoma or cancer is a very malig- 
 nant tumor, consisting of groups of 
 epithelial cells arranged into solid 
 blocks or columns separated by so- 
 called alveoli of connective tissue, in 
 which blood vessels alone are found. 
 The epithelial proliferation shows a 
 tendency to extend beyond its anat- 
 omical limits. 
 
 The structure of the cancer may be 
 compared somewhat to a sponge, the 
 sponge forming the alveoli, the can- 
 cer cells filling up the holes. 
 
 The histology of the cell, however, 
 
 varies in different situations and in 
 
 different forms. 
 The epithelial cells vary in size from 
 
 medium to large and have a large 
 
 clear nucleus. 
 
 The cell differs as to the structure in- 
 volved. If of the skin the cells are 
 large and usually of a squamous va- 
 riety. If of the mucous membranes 
 they are often cylindrical or col- 
 umnar and with a tendency to the 
 formation of cuboidal or polyhedral, 
 which is generally present in cancer 
 of the glandular organs. Secondary 
 changes may change the appearance 
 of the cells. The cancers of the skin 
 may tend to arrange the epithelia in 
 concentric whorls and tend to be- 
 come glistening from horny trans- 
 formation. 
 
 The nucleus may be clear and quite 
 structureless, or the nucleus may be 
 distinct with a definite chromatin 
 network. 
 
 Karyokinetic figures may be abundant 
 and frequently atypical. Degenera- 
 tive changes may alter the nucleus 
 as well as the body of the cell. The 
 stroma is produced from the connec- 
 tive tissue of the part at which the 
 epithelium begins to grow abnormally, 
 and is never found between the in- 
 dividual cells, only around groups of 
 them. The cells have no direct blood 
 supply, but communicate freely with 
 the lymphatics, through which meta- 
 stasis, of the epithelium alone, oc- 
 curs. The nearest lvmnh elands are 
 
TUMORS. 75 
 
 therefore usually found enlarged and 
 hardened. 
 
 The metastatic epithelial cell attaches 
 itself to a part and forces the connec- 
 tive tissue to become its framework 
 whether it be that of fibrous tissue, 
 cartilage or bone. 
 
 Macroscopically, carcinoma differ in 
 appearance in different parts of the 
 body. On the surface of the body 
 they appear as nodular, flat eleva- 
 tions. 
 
 In the skin the nodules may be hard 
 and smooth, or they may undergo 
 ulceration. In the mucous membrane 
 the growth is soft and polypoid 
 ulceration may occur. 
 
 In glandular organs the carcinoma are 
 more or less nodular in form, or may 
 be as irregular infiltrations. 
 
 In consistency the tumor is described 
 by the proportion of the cells to the 
 connective tissue, as — 
 
 Simple carcinoma, when the cells and 
 the connective tissue are equal in 
 amount, or nearly so. 
 
 Hard, chronic or scirrhous, where there 
 is a great preponderance of connec- 
 tive tissue. 
 
 Soft, medullary, acute or encephaloid, 
 where there are large masses of cells 
 with little stroma (brain-like in con- 
 sistency). 
 
 The scirrhous is of slow growth, but 
 infiltrates the tissue widely. Meta- 
 stasis and gland involvment is late. 
 
 The situations in which carcinoma oc- 
 cur are the mouth, in alimentary tract 
 at the pylorus, ileocaecal valve 
 larynx, gall bladder, uterus and some- 
 times the other genito -urinary or- 
 gans, liver and the lungs. 
 
 Varieties of Carcinoma. 
 
 a. Epithelioma is divided into — 
 1. Squamous Epithelioma, which occurs 
 in the skin or mucous membranes 
 wherever stratified squamous epi- 
 thelium exists normally. It spe- 
 cially favors the junction of the 
 skin and mucous membrane. The 
 frequent seats are the lips, eso- 
 phagus, larynx and cervix uteri. 
 It is also seen in the anus and vulvi 
 
76 PATHOLOGY. 
 
 and on the hands and feet of the 
 aged. 
 
 The lower cells of the Malpighian 
 layer sends down cylinders of 
 epidermis, which are cut off by 
 connective tissue overgrowths and 
 become "cell rests," which give rise 
 to the concentric epithelial perles, 
 epidermal globes, etc. 
 
 Oblique sections of the normal epi- 
 dermal prolongation or the glands 
 should not be mistaken for the 
 "cell rests." 
 
 Epithelioma cells are large with 
 prickle edge and frequent vacuola- 
 tions of their substance. 
 
 Metastasis is frequent, but it is not 
 so malignant as the glandular car- 
 cinoma. 
 2. Cylindrical Epithelioma is made up 
 of columnar or cylindrical epithe- 
 lium. 
 
 It is frequently seen in the mucous 
 membranes of the gastro-intestinal 
 tract and the uterus. The growth 
 starts from the cells of the tubular 
 glands or the surface. 
 
 The structure is more or less of a 
 tubular character, composed of a 
 layer of epithelial cells or a num- 
 ber of epithelial cell layers with 
 the outer layer of columnar cells. 
 The acini of the growth becomes 
 filled with various shaped prolif- 
 erated epithelial cells, or the 
 tubular character of the acini may 
 be lost. 
 
 The carcinomata of the kidney, liver 
 and mammary gland may be of the 
 cylindrical form. This form re- 
 sembles the glandular form, more 
 than does the squamous, in its ma- 
 lignancy. 
 
 Rodent ulcer may be considered as a 
 form of epithelioma of slow growth. 
 It may begin as a wart or fissure 
 of the skin and become a chronic 
 ulcer, generally situated on the 
 sides of the nose and around the 
 orbit. It has a hard, overhanging 
 edge. 
 
 It shows no metastasis, nor are the 
 glands involved. Prickle cells or 
 

 Fig-. 12. Epithelioma of skin, showing: 
 concentric arrangement and degeneration 
 of cells. 
 
 Fig. 13. Careinoma of uterus. 
 
Figr. 14. Scirrhous carcinoma. 
 
 Medullary carcinoma of 
 
TUMORS. 77 
 
 perles are not found. 
 
 b. Glandular carcinoma resembles race- 
 
 mose glands, being made up of 
 alveoli containing epithelial cells in 
 several layers, which fill the lumen, 
 and a connective tissue stroma. 
 
 They may be divided into three forms — 
 
 1. Simple, made up of epithelium and 
 
 stroma, resembling more or less the 
 structure of normal glands. 
 
 2. Medullary or soft is made up of an 
 
 excessive amount of epithelium in 
 the form of solid plugs or columns 
 of epithelial cells. 
 
 3. Scirrhous is where there is a mix- 
 
 ture of acini and epithelial cells, 
 but with an excess of fibrous tissue, 
 which renders it hard. 
 The glandular variety of carcinoma 
 is more or less nodular or infil- 
 trating and glistening white in 
 color. On section a milky fluid ex- 
 udes, which is made up of an al- 
 buminous fluid, degenerated cells 
 and oil droplets. 
 
 It is found in the pylorus, other mu- 
 cous surfaces, mammary gland, 
 pancreas, kidneys, ovaries and tes- 
 ticles. 
 
 Metastasis occurs. 
 
 c. Colloid cancers are seen in the stom- 
 
 ach and intestinal tract, mammary 
 gland and ovaries. It is jelly-like 
 and of a transparent, glistening ap- 
 pearance. 
 
 Microscopically, there is a mucoid de- 
 generation of the epithelial cells and 
 the connective tissue. In some cases 
 the epithelium alone is involved. 
 
 Direct extension is a frequent method 
 of spreading. The entire abdominal 
 cavity may become filled with the 
 material. 
 16. Sarcoma is a malignant tumor made 
 up of connective tissue cells with 
 little inter-cellular substance. It is 
 more or less rounded in form and 
 often encapsulated. It may. however, 
 be irregular, infiltrating and there- 
 fore without a capsule. 
 
 In consistency it is flesh-like, hard or 
 soft, depending upon the proportion 
 of cells and inter-cellular substance, 
 
78 PATHOLOGY. 
 
 or according to the amount of asso- 
 ciation with fibroma, chondroma, 
 myxoma, etc., and with adenoma. 
 
 It is white or gray and on section a 
 whiteish, liquid exudes. 
 
 Dilated blood vessels may give it a 
 hemorrhagic appearance or actual 
 hemorrhage may take place with for- 
 mation of cysts, bloody or serous. 
 Necrosis, mucoid change or liquefac- 
 tion necrosis may render the sar- 
 coma soft and cystic. 
 
 Secondary sarcomata are nodular in 
 character and usually have a cap- 
 sule. White or pinkish in color, firm, 
 but with a tendency to central 
 necrosis or softening. In some cases 
 where the body is studded with white 
 spots, like those of miliary tuber- 
 culosis, the condition is called sar- 
 comatosis. 
 
 In structure the main type of cells are 
 round, cylindrical, spindle shaped or 
 polymorphous. The nucleus is vesic- 
 ular, though sometimes granular, and 
 occupies a large proportion of the 
 cell. If the growth is rapid, karyo- 
 kinetic figures may be abundant. 
 
 The arrangement of cells is very ir- 
 regular. The inter-cellular substance 
 is homogenous with a few fibers in 
 the spindle variety, but few if any 
 in the other forms. 
 
 The distinctive feature of the growth 
 is the presence of connective tissue 
 and blood vessels between the indi- 
 vidual cells which have no direct con- 
 nection with the lymphatics. Meta- 
 stasis is therefore by the blood ves- 
 sels, hence appears earlier than in 
 carcinoma. 
 
 Sarcoma springs from pre-existing con- 
 nective tissue, such as the subcutane- 
 ous, intermuscular, periosteal, tendi- 
 nous, bone, cartilage, fat, lymphatic 
 glands, submucous and serous sur- 
 faces. 
 
 They are also found in the kidney, 
 liver, spleen, thyroid gland and 
 testis. 
 Varieties of Sarcoma. 
 
 a. Round-celled sarcoma is made up 
 
TUMORS. 79 
 
 of small or large round cells with 
 little intercellular substance. 
 
 It springs from any form of connec- 
 tive tissue, but frequently affects 
 the skin (moles and warts) and 
 bones, and is of a soft consistency. 
 
 The small cell variety is softer than 
 the larger. Both are very ma- 
 lignant; the smaller is perhaps the 
 most malignant of all varieties. 
 
 1. Lympho sarcoma is a variety of 
 
 the round cell sarcoma. It re- 
 sembles the structure of a 
 lymphatic gland. It is character- 
 ized by a reticular stroma formed 
 by stellate cells, which are united 
 by their prolongations. 
 It occurs in the lymphatic glands 
 and lymphadenoid tissues of the 
 mucous membranes. The thymus 
 gland and other organs may be 
 affected. 
 
 Lymphosarcoma, unlike lymphade- 
 noma, shows a tendency to ex- 
 tend beyond the normal limita- 
 tions of the gland or its other 
 structure. 
 
 Chloroma is a round cell sarcoma, 
 which occurs in the periosteum 
 of the bones of the head and 
 secondarily in other parts of the 
 body. On section it is first green 
 in color, then by exposure to the 
 air it is changed to gray. 
 
 Clinically, it is associated with 
 symptoms of leukemia or pseu- 
 doleukemia. 
 
 2. Alveolar sarcoma is a variety of 
 
 the round celled sarcoma, though 
 there is also spindle cells pres- 
 ent. 
 
 Its characteristic features is the 
 acinus structure, composed largely 
 of spindle-shaped cells with some 
 fibrillar, intercellular substance, 
 filled with large round cells, hav- 
 ing a more or less epitheloid ap- 
 pearance. 
 
 It is frequent in the skin, spring- 
 ing from warts and moles. It oc- 
 curs also in lymph glands and 
 serous membranes, etc. 
 
80 PATHOLOGY. 
 
 b. Spindle cell sarcoma is made up of 
 
 large or small spindle-shaped cells, 
 with slender or sometimes branched 
 ends. 
 
 The cells may be angular or stellate. 
 The cells may run in parallel col- 
 umns or they may run in different 
 directions. The spindle celled sar- 
 coma is of a denser consistency 
 than the round celled sarcoma, 
 and usually more grayish or flesh- 
 colored. It is often associated 
 with fibromata, with which it may 
 be confused. 
 
 It is found in the denser connective 
 tissue of periosteum, tendons and 
 fascia. 
 
 It is less malignant than the round 
 variety and shows no tendency to 
 metasasis, but recurs after re- 
 moval. 
 
 c. Angiosarcoma or Perithelioma is a 
 
 sarcoma which arises from the 
 adventitia of blood vessels. It re- 
 sembles carcinoma. 
 
 The tumor is generally quite vascu- 
 lar and is seen in the serous mem- 
 branes and skin, and especially in 
 the salivary glands. Its character- 
 istic feature is the round-cell 
 masses surrounding the blood ves- 
 sels. 
 
 Plexiform angiosarcoma is the name 
 given to it when each vessel of a 
 vascular network is surrounded by 
 a coat of sarcoma cells. 
 
 Alveolar angiosarcoma is the name 
 given to it when the vascular net- 
 work encloses the sarcoma cells in 
 such a way as to give rise to an 
 alveolar form. These forms are 
 found in the sarcomata of warts 
 and moles and are prone to mela- 
 notic change. 
 
 The endothelium of the blood vessels 
 is sometimes the origin of vascular 
 sarcoma and is a rare variety of 
 endothelioma. 
 
 They are liable to degenerations, 
 such as myxomatous and hyaline. 
 
 Angiosarcoma is somewhat benign. 
 Metastasis as a rule is rare, but 
 
Fig-. 16. Small round-celled sarcoma; 
 in the center is seen a blood vessel with 
 its wall of endothelium. 
 
 Fig-. 17. Lymphosarcoma of nasal mu- 
 cous membrane; a, on left side a blood 
 vessel, on right side reticulum; b, cells 
 of reticulum; c, sarcoma cells. (Zieg*- 
 ler.) 
 
Fig-. 18. Angiosarcoma with myxoma- 
 tous degeneration (cylindroma) ; the fig- 
 ure represents one of the blood vessels 
 with the sarcomatous cells springing" 
 from its walls and outside of these 
 myxomatous tissue. 
 
 
 Fig-. 19. Cylindroma, showing a num- 
 ber of blood vessels whose walls have 
 become converted into hyaline material. 
 
TUMORS. 81 
 
 the alveolar and the melanotic 
 variety are very malignant. 
 
 d. Cylindroma is a variety of the peri- 
 
 thelioma and receives its name 
 from the cylinders of sarcomatous 
 cells growing around the blood 
 vessels. 
 
 Sarcomatous cylindromata, may be 
 
 simple sarcoma, which has under- 
 gone hyaline or myxomatous 
 degeneration, or the two combined 
 more or less, but nearly always it 
 is the angiosarcomata which pre- 
 sents the condition. 
 
 The sarcoma cells surrounding the 
 blood vessels are converted into 
 hyalomyxomatous tissue, resulting 
 in branching columns of the ma- 
 terial which traverses the sar- 
 coma. 
 
 Angiosarcomata myxomatodes is the 
 term used when the walls of the 
 blood vessels themselves are the 
 seat of hyaline change, the 
 sarcoma cells are pushed aside. 
 
 Cylindroma occur in the salivary 
 glands, brain, lachrymal glands and 
 sometimes in the subcutaneous tis- 
 sue. 
 
 It is more or less benign. 
 
 e. Endothelioma begins in the endo- 
 
 thelium of blood or lymph vessels 
 and spaces. It occurs in the se- 
 rous membranes, as the pleura, 
 peritoneum and meninges, but it 
 may be found in the skin, walls 
 of blood vessels, periosteum, bone 
 marrow, lymphatic glands, gums, 
 ovary, testicle, liver and salivary 
 glands. 
 It has, by its growth along the ves- 
 sels, a more or less tubular or 
 acinus-like aggregation of endo- 
 thelial cells. Frequently it orig- 
 inates from the endothelium sur- 
 rounding the blood vessels. The 
 endothelium of the perivascular 
 lymph spaces proliferate and form 
 a growth around the blood ves- 
 sels, which is really an angiosar- 
 coma or perithelioma, and by its 
 mucoid or hyaline degeneration 
 cylindroma may take its origin. 
 
82 PATHOLOGY. 
 
 f. Melanosarcoma, Melanotic sarcoma, 
 
 Melanoma, Chromatophoroma or 
 Pigmented sarcoma is a very ma- 
 lignant tumor, consisting of round 
 or spindle cells, or both, in which 
 there is abundant melanin (chro- 
 matophores) and stroma. 
 
 The pigment gives to it a dark 
 color. It is found in the skin, es- 
 pecially in pigmented moles or 
 warts and in the choroid of the 
 eye and the pia mater. 
 
 The tumor is extremely malignant, 
 grows very rapidly and shows 
 early and wide metastasis, espe- 
 cially the lymphatic glands and 
 later the liver. 
 
 This tumor is a definite growth and 
 is not merely a pigmented sar- 
 coma. 
 
 g. Giant-celled sarcoma, Myeloid sar- 
 
 coma, Osteosarcoma is made up of 
 large round or spindle cells inter- 
 mingled with large multinuelear 
 cells which resemble the myelo- 
 plaques of bone. 
 
 The tumor generally grows in con- 
 nection with bone, does not show 
 metastasis and as a rule does not 
 recur after removal. 
 
 The giant cells may be said to be 
 due to irritation of the spicules of 
 bone or the deposit of blood pig- 
 ment, and are therefore mere ac- 
 cidents in a round or spindle cell 
 sarcoma. 
 The maxillary bone is most fre- 
 quently involved. An epuiis grow- 
 ing from the dental alveoli is of 
 this nature. 
 17. Cysts are pathologic formations, con- 
 sisting of a more or less definite 
 wall, enclosing a liquid or semi- 
 liquid substance, which differs in 
 character from the surrounding parts. 
 Some cysts are true tumors; others 
 are quite different in nature. Some 
 cysts do not have a definite capsule, 
 hence we distinguish — 
 St. True cysts, which are enclosed by a 
 capsule and is lined by epithelium 
 GT endothelium. 
 
TUMORS. 83 
 
 b. Cystoids (cyst-like formations), 
 which are merely a circumscribed 
 collection of softened material. 
 
 Cysts may be classified as— 
 
 1. Retention cysts are formed when 
 
 the outlet of any secreting struc- 
 ture is obstructed, as when the 
 duct of a sebaceous gland of the 
 skin is closed, causing the so- 
 called sebaceous cyst or wen. 
 Ranule is the term used when 
 the cyst is due to the closure 
 of the salivary or small mucous 
 glands or ducts under the 
 tongue. 
 Cysts are also formed by the clos- 
 ure of the uriniferous tubules, 
 tubules of ovary or in par- 
 ovarium, in acini and ducts of 
 the mammae, pancreas and other 
 glands. 
 
 2. Softening cysts are due to degen- 
 
 erative softening of the normal 
 or pathologic tissues. 
 
 It may be the result of hemor- 
 rhage, the blood clot is inspis- 
 sated and followed by exudation 
 of serum in the area. 
 
 This form is common in all the 
 different kinds of tumors. 
 
 Softening cysts may also be due 
 to foreign bodies. The tissues 
 having been injured by the same, 
 they undergo necrosis with the 
 formation of a capsule by con- 
 nective tissue reaction. Fre- 
 quently seen as a result of para- 
 sitic invasion. 
 
 3. Proliferation Cysts. This forma- 
 
 tion is very much like true 
 tumors. They are sometimes 
 called epithelial cysts. They oc- 
 cur in glandular organs, such as 
 the ovary and mammary gland, 
 or they may appear in any gland. 
 
 They may represent an adenoma- 
 tous or carcinomatous new 
 growth. 
 
 They result from obstruction to 
 the excretory ducts and the irri- 
 tation of the retained secretion. 
 Congenital abnormalities may 
 
84 PATHOLOGY. 
 
 also play a part in their forma- 
 tion. 
 It may be in the form of a single 
 cyst, or it may be multiple, or 
 the large cyst may be divided by 
 compartments into many and 
 filled with a serous, gelatinous 
 or hemorrhagic fluid. 
 
 Secondary degenerations may oc- 
 cur. They may be benign, but 
 often there is a tendency to ma- 
 lignancy, frequently undergoing 
 a carcinomatous change, which 
 spreads or becomes metastatic. 
 
 II. TERATOMATA is a tumor of a pe- 
 culiar, mixed character, representing 
 the products of growth of one indi- 
 vidual within the tissue of another in- 
 dividual of the same species. It is 
 probably due to some congenital mis- 
 development. It may be — 
 
 Endogenous, in which superficial tis- 
 sues are retained in the internal 
 parts. 
 
 Ectogenous, in which there is a sep- 
 arate foetal deposition, as the origin 
 of the tumor. This is seen when 
 there is a separate and well-devel- 
 oped foetus within the developed or- 
 ganism (a foetus in foetu). 
 
 1. Dermoids or Dermoid cysts are cystic 
 
 formations which are found in the 
 skin in the regions of the neck and 
 sacrum and in the ovary, less often 
 in the brain, testis, orbit and lungs. 
 
 They are filled with a semi-fluid, 
 cheesy mass, consisting of epithelial 
 cells, fatty matter, hair, teeth, mus- 
 cle, bone, and glandular structure 
 also occur. 
 
 A tumor called cholesteotoma of a 
 glistening, whitish nature and com- 
 posed of concentric layers of cells re- 
 sembling epithelium, with occasional 
 crystals of cholesterin, is sometimes 
 found in the membranes and sub- 
 stance of the brain, is classed by 
 Ziegler as teratoid growths. 
 
 Similar growths are found in the kid- 
 neys, testicles, parotid gland, ovary 
 and middle or external ear. 
 
 2. Syncytioma malignum or Deciduoma 
 
 malignum or Sarcoma Deciduocellu- 
 
BACTERIA. 85 
 
 la re is a very malignant tumor of the 
 decidua. 
 
 It of course occurs during pregnancy 
 and originates at the site of the 
 decidua serotina, but rapidly spreads 
 to the uterus and then by metastasis 
 through the blood vessels to the ex- 
 ternal genitalia, frequently the lungs 
 and less often the liver, spleen and 
 other organs. 
 
 The nature of the tumor is still un- 
 determined. It is probably a foetal 
 structure composed of large and 
 small cells. The larger cells growing 
 from the syncytium and the smaller 
 cells from the outer epiblastic cov- 
 ering of the chorionic villi (Langh- 
 an's cells). 
 
 It is therefore carcinomatous, though 
 its metastasis suggests sarcoma. It 
 is very vascular and therefore sub- 
 ject to hemorrhage. 
 
 BACTERIA AND DISEASES DUE TO 
 BACTERIA. 
 
 FUNCTIONS AND PRODUCTS OF 
 BACTERIA (Vital Actions). 
 
 The vital actions of bacteria are de- 
 structive ones, splitting up higher 
 nitrogenous and non-nitrogenous 
 compounds into simpler substances. 
 Sometimes such changes are destruc- 
 tive to the bacteria themselves, as 
 when lactic and butyric acids are 
 formed in the media. 
 
 As producers of disease bacteria cause 
 various pathologic conditions, pro- 
 ducing diseases known as infectious 
 diseases, and the germs are called 
 pathogenic bacteria. 
 
 The germs which do not cause any 
 pathological conditions are called 
 non-pathogenic bacteria. 
 The substances found in media of bac- 
 terial growth are — 
 1. Proteins, which are components of the 
 bacterial cell proper and may cause 
 suppuration (Pyogenic), fever ( Pyro- 
 gen ic) and inflammatory processes 
 (Phlogenic). 
 
 Some examples of this is mallein (de- 
 rived from the bacillus of glanders), 
 and tuberculine (derived from the 
 
86 PATHOLOGY. 
 
 bacillus of tuberculosis). 
 These when injected into subjects sick 
 with the disease are pyrogenic, but 
 in healthy subjects they have very 
 little or no effect. 
 
 2. Ferments, secretions of the cell, pos- 
 sess the power of breaking up the 
 more highly organized nitrogenous and 
 non-nitrogenous compounds into sim- 
 ple and more diffusible substances. 
 The action of ferments upon non- 
 nitrogenous compounds is called fer- 
 mentation. 
 The action of ferments upon non- 
 nitrogenous compounds is called pu- 
 trif action, which often produces odor- 
 ous gases and ptomains (complex al- 
 kaloids resembling those found in 
 plants). 
 
 The principal bacterial ferments are— 
 Proteolytic, transforming albumin into 
 more soluble substances, gelatin 
 liquefaction is an example; diastatic 
 transforms starches into sugar; in- 
 verting changes a sugar that does 
 not undergo fermentation into one 
 that does; emulsifying formed by a 
 few microbes, e. g., micrococcus pyo- 
 genes tenuis; coagulating coagulates 
 milk; others produce both a coagula- 
 tion and a dissolving ferment 
 (casease), which dissolves the coagu- 
 lation; hydrolytic breaks up urea into 
 ammonium carbonate and hippuric 
 acid into glycocol and benzoic acid; 
 fat splitting splits fats into glycerin 
 and fatty acids; oxidizing reduces the 
 nitrates of the soil into ammonia, 
 etc.; nitrifying changes albuminoids 
 into skatol, indol, leucin, and these 
 into ammonia, ammonia into nitrites, 
 and nitritis into nitrates. 
 
 3. Substances that are the result of the 
 action of bacteria upon the medium 
 of growth — 
 a. Toxins are poisonous substances 
 akin to the venom of serpents and 
 other animals, and to certain pois- 
 onous principles of plants. It has 
 been estimated that 1-1000 gm. of 
 tetanus toxin will kill a horse 
 weighing 1,200 pounds. 
 They were first called ptomains or 
 
BACTERIA. 87 
 
 cadaveric alkaloids, but this term 
 is now applied to poisons which 
 form in decomposing meat, cheese, 
 etc., as a result of chemical change 
 caused by bacteria. They have 
 .also been termed toxalbumins, as 
 ' they give all the reactions of albu- 
 mins. 
 
 It is probable, however, that a tox- 
 albumin is but a combination of 
 the toxin and the substances de- 
 rived from the medium of growth. 
 
 Toxines may be divided into — 
 
 1. Those which are within the body 
 of the bacteria and are set free 
 by the disintegration of the or- 
 ganism. Pathogenic bacteria 
 comprise most of this group. 
 Anti-bacterial sera is used to 
 combat this type. 
 
 2. Those in which the toxines are 
 excreted by the bacteria and are 
 found in the surrounding media. 
 Anti-toxic sera is used to com- 
 bat this type. 
 
 b. Pigments. Bacteria have the prop- 
 erty of forming pigments in them- 
 selves (chromophoric, or they form 
 a chromogenic body which when 
 free gives rise to color (chromo- 
 paric). 
 
 C. Photogenesis, phenomenon of phos- 
 phorescence, e. g., condition seen 
 in decaying fish, etc. 
 
 d. Fluorescence. A play of colors is 
 
 found in some bacterial cultures. 
 
 e. Odors are produced by some germs, 
 
 some pleasant and others foul. 
 
 f. Gas is formed by anaerobic bacteria, 
 
 especially noxious and odorless. 
 Effect of Bacteria, generally known as 
 Infections. 
 When bacteria have gained an entrance 
 into the animal body they may pro- 
 duce effects in two ways— 
 1. Local Effects. The local effects of bac- 
 teria are of two kinds — 
 a. Mechanical. By their mere presence 
 in the tissues bacteria may cause 
 tissue changes of two kinds — 
 t. Proliferation, due to irritation. 
 2. Thrombosis (by rapid multiplica- 
 tion) and its consequent conditions, 
 
88 PATHOLOGY, 
 
 b. Toxic. The local toxic effects of bac- 
 teria are due to the action of their 
 toxins upon the cells with which 
 they are in direct contact, and may 
 be,— 
 
 1. Proliferation. • 
 
 2. Cell degeneration, and 
 
 3. Necrobiosis. 
 
 2. General Effects (Intoxications). 
 
 The general effects of bacteria upon 
 the body are due entirely to the cir- 
 culation of their toxines in the blood. 
 This may occur in two ways, viz., 
 from — 
 
 a. Primary focus (point of entrance). 
 Bacteria may remain at the point of 
 
 entrance and elaborate toxins 
 which are absorbed and circulated 
 by the blood, causing disease, e. g., 
 tetanus, diphtheria and the sapre- 
 mia due to pyogenic organisms. 
 
 b. Secondary foci. 
 
 Bacteria may also circulate in the 
 body fluids and find lodgment in 
 any of the organs, causing both 
 local tissue changes and general in- 
 toxication, e. g., Bacillus of Eberth 
 (typhoid fever), Pneumococcus of 
 Frankel (pneumonia), Diplococcus 
 intracellulars of Weichselbaum 
 (cerebro-spinal fever), Streptococus 
 (septicemia and pyemia). 
 Conditions Necessary to Infection are — 
 
 1. The micro-organism must be patho- 
 genic. It must be a parasite. 
 
 2. Toxins elaborated by the micro-organ- 
 ism must be present in sufficient 
 amount. 
 
 3. Animal infected must be susceptible. 
 
 SUSCEPTIBILITY. 
 Susceptibility varies. It may be — 
 
 1. Natural, to a certain race. 
 
 2. Aquired, to those conditions being 
 
 present which lower vitality. 
 
 3. Inherited, by reason of inherited 
 tendency. 
 
 IMMUNITY. 
 -.- Immunity denotes that condition of 
 ■ an organism which enables it to 
 
 resist an- attack of the - particular 
 bacteria and their- toxic secretions 
 against - which they -are- said to be 
 immune,,. •;,■••• ...... 
 
IMMUNITY. 89 
 
 The varieties of immunity are 
 
 1. Natural, as an inheritance from im- 
 
 mune ancestors. 
 
 a. Absolute immunity is rare. 
 
 b. Relative immunity is common. It 
 
 may be individual or racial, e. g., 
 dogs and Algerian sheep are resist- 
 ent to anthrax. 
 Lower animals are immune from cer- 
 tain diseases common to man, e. g., 
 sphilis. 
 
 2. Acquired. 
 
 a. Active immunity. 
 
 1. Naturally acquired by a previous 
 
 infection. 
 
 2. Artificially acquired by — 
 
 a. Inoculations with weakened, at- 
 
 tenuated cultures of bacteria, 
 e. g., vaccins of variola and 
 anthrax. 
 
 The attenuation is produced by 
 successive artificial cultivations. 
 
 Virulence is lessened by passing 
 cultures through animals less 
 susceptible or immune. 
 
 b. Inoculation of small doses of 
 
 very virulent micro-organisms. 
 Successive inoculations with 
 gradually increased doses of the 
 virus creates an immunity suf- 
 ficient to resist 10 times the 
 toxic dose. 
 
 c. Injecting gradually increased 
 
 doses of the sterilized or fil- 
 tered products of bacteria. 
 Cultures are sterilized by heat 
 or filtered through germ filters. 
 The sterilized cultures or the fil- 
 trate still contain the toxins. 
 
 b. Passive immunity is acquired by the 
 injection of the serum of animals 
 that have been rendered immune by 
 the artificial methods. 
 
 THEORIES OF IMMUNITY. 
 
 The theories most acceptable at the 
 present time are modifications of 
 MetchnikofTs Phagocytic and Ehr- 
 lich's "side chain." 
 MetchnikofTs Phagocytic op Cellular 
 Theory. 
 The term "phagocyte" is given to any 
 cell capable of incorporating bacteria 
 
90 PATHOLOGY. 
 
 and of destroying them by a process 
 of digestion. 
 
 Phagocytic cells comprise — 
 
 1. Microphages, polymorphonuclear leu- 
 
 cocytes. 
 
 2. Macrophages are all other leuco- 
 
 cytes, endothelial cells and connec- 
 tive tissue corpuscles, having pha- 
 gocytic power. 
 
 When animals are subjected to an 
 irritant ' phagocytosis occurs. The 
 leucocytes are attracted by chemo- 
 taxis to the zone of irritation and 
 envelop the irritating substance. 
 
 The organisms that escape from one 
 cell are seized by others, but if 
 their multiplication is excessive 
 they overpower the phagocytic leu- 
 cocytes and invade the blood 
 serum. The blood serum and the 
 body fluids are likewise bacteri- 
 cidal, due to the disintegration of 
 phagocytes — phagoiysis; the prop- 
 erties of these cells being imparted 
 to the serum. This property is due 
 to two constituents of the plasma. 
 The one (the specific immune 
 body) circulates in the plasma and 
 resists a temperature of 100 de- 
 drees C. The other, or "cytase" 
 (digestive ferment), derived from 
 the disintegrated phagocytes, cor- 
 responds to Buehner's "alexins" 
 and Ehrlich's "lysins." It is de- 
 stroyed at 60 degrees C. 
 
 Ehrlich's "side chain" theory derives its 
 name from its analogy to what hap- 
 pens in the Benzol ring when its re- 
 placeable hydrogen atoms are substi- 
 tuted by "side chains." The theory 
 itself is based upon the mechanism 
 of cell nutrition in its relation to the 
 mode of production of specific anti- 
 toxines. Each cell contains an active 
 central nucleus and outer groups of 
 molecules or "side chains" (recep- 
 tors). These outer groups make up 
 the main feature of the scheme, 
 since the receptors receive the nu- 
 trient molecules (haptophores) by 
 which the cellexists. The receptors 
 have an affinity for the haptophores, 
 but do not combine with these only. 
 
OPOSONINS. 91 
 
 The cells may, by means of the re- 
 ceptors, take up in addition any num- 
 ber of isomeric non-nutritious bodies, 
 and if any of these happen to be 
 toxic (toxophore) and sufficiently ac- 
 tive in quality and quantity, the 
 cell's function is inhibited or de- 
 stroyed. 
 
 Intoxications being due to a toxin, the 
 toxophore attaches itself to the re- 
 ceptor and reacts actively upon the 
 cell proper. 
 
 The receptor being destroyed, the cell 
 reproduces a greater number of new 
 ones than are required by the cell 
 itself, therefore they accumulate in 
 the blood and lymph. The surplus 
 receptors (antitoxins) preserve their 
 affinity for their specific toxophores 
 and hold the toxin in captivity, as it 
 were, before it can reach the cell 
 proper, thus immunizing the cell 
 against the poison. The destruction, 
 by the blood serum, of the bacteria 
 (bacteriloysis), worn-out blood cells 
 (haemolysis), muscle cells (myolysis), 
 etc., is probably brought about by a 
 destructive solvent element called 
 the "compliment" (lysins, alexins or 
 cytase) and an "immune body" (An- 
 boceptor), which attaches itself to 
 the cells or the bacteria to be dis- 
 solved, and acts as a link between 
 them and the compliment. It is in 
 this way that the compliment, which 
 has no affinity for the cellular ele- 
 ments, is brought into contact with 
 the cells to be dissolved. 
 Opsonic Theory. 
 
 Wright and others have demonstrated 
 certain thermolabile bodies, the ac- 
 tive products of the tissues and 
 serum under the stimulation of the 
 toxin, which, acting upon bacteria, 
 sensitize them for phagocytosis. 
 These substances have been called 
 opsonins. ■ 
 
 They have a haptophore group which 
 attaches themselves to the bacteria 
 and an opsoniferous group which re- 
 sembles the complements. Chemic- 
 ally, they are unstable, as they un- 
 dergo changes at 60 degrees C. or by 
 the action of light. 
 
92 PATHOLOGY. 
 
 OTHER REACTIONS OF IMMUNITY. 
 
 Specific precipitins are substances which 
 are precipitated when immune bodies 
 are brought into contact with the 
 specific body of whose stimulation it 
 is formed. In other words, the blood 
 serum of animals immune against 
 certain bacteria or their albumins 
 will give a precipitate when added 
 to the cultures of these organisms or 
 their albumins. The nature of this is 
 not understood. 
 
 Agglutinins. If certain bacterial cultures 
 be added to the blood serum of an 
 animal whose illness is due to that 
 particular organism the bacteria will 
 become clumped in motionless masses. 
 This condition is taken advantage of 
 by Widal for diagnostic purposes — 
 typhoid fever, etc. 
 
 DISEASES DUE TO BACTERIA. IN- 
 FECTIOUS DISEASES. 
 
 An infection is the invasion of the 
 body by a disease producing micro- 
 organism. The time when the germ 
 enters the body is not always known 
 to the patient, and some time usually 
 elapses between the time of actual 
 entrance and the appearance of the 
 resulting symptoms. This time is 
 called the period of incubation. 
 
 There is, at this time, no great dis- 
 tinction between the terms infection 
 and contagion unless it is that in 
 contagion it is used to denote infec- 
 tion by personal contact. 
 
 SUPPURATIVE DISEASES. 
 
 1. STAPHYLOCOCCUS GROUP may be 
 
 divided into — 
 
 a. Staphylococcus pyogenus aureus is 
 
 found in lesions such as furuncles, 
 abscesses, carbuncles and ulcera- 
 tions of the skin or mucous mem- 
 branes. It is frequently seen in 
 suppurative inflammations, such as 
 malignant endocarditis, osteomy- 
 litis, appendiceal abscesses, etc. 
 It is generally found in focal lesions. 
 Other organisms may also be as- 
 sociated in these lesions. 
 
 b. Staphylococcus pyogenes albus is 
 
 far less virulent than the aureus 
 
BACTERIA. 93 
 
 and is frequently found as a harm- 
 less parasite of the skin. Asso- 
 ciated with other micro-organisms 
 it occurs generally in abscesses and 
 suppurative diseases. 
 
 c. Staphylococcus pyogenes citreus is 
 
 not very common nor virulent. 
 
 2. STREPTOCOCCUS GROUP. Under 
 
 the streptococcic group are included 
 various bacteria that resemble each 
 other very closely. 
 
 a. Streptococcus pyogenes is found dis- 
 
 tributed much the same as is the 
 staphylococci, but not generally in 
 the healthy body. 
 
 It is found upon the mucous mem- 
 branes or in the various secretions 
 or excretions of the body, and oc- 
 curs occasionally in focal lesions. 
 
 It may occur in generalized septo- 
 pyemia, infectious endometritis and 
 sometimes in ulcerative endocar- 
 ditis. 
 
 It may occur in persons with a previ- 
 ous good health or in the course of 
 infectious diseases, such as scar- 
 latina, measles and la grippe; also 
 in sore throats resembling diph- 
 theria (pseudodiphtheria). It is 
 always found in all cases of ery- 
 sipelas. 
 
 b. Streptococcus intracellulars menin- 
 
 gitidis, also called meningococcus 
 or diplococcus meningitidis, is found 
 in meningeal pus, nasal mucus, 
 sputum and urine of those sick 
 with epidemic cerebro-spinal men- 
 ingitis. 
 Other micro-organisms associated in 
 meningitis are the pneumococcus, 
 streptococcus and staphylococcus 
 pyogenes, typhoid and colon 
 bacilli, influenza bacillus, etc. 
 
 3. GONOCOCCUS OF NEISSER is a 
 
 diplococcus which occurs in the pus. 
 epithelial cells and deeper structures 
 of the urethra in gonorrhoea, of 
 which it is the specific cause. Gon- 
 orrhoea is generally a local disease, 
 but it may extend to the neighbor- 
 ing structures, as the testis, uterus 
 and tubes. It may also, secondarily, 
 cause arthritis, peritonitis, endocar- 
 
94 PATHOLOGY. 
 
 ditis, conjunctivitis, etc.; the latter 
 (gonorrhoeal opthalmia) is a^ very 
 grave affection. It may also give rise 
 to peripheral abscesses, suppurative 
 adenitis, etc. 
 
 4. DIPLOCOCCUS PNEUMONIA, pneu- 
 
 mococcus, micrococcus lanceolatus, 
 streptococcus pneumania seu lance- 
 olatus. This micro-organism is of 
 lanceolate shape, and in the sputum, 
 lungs and in the blood it is com- 
 monly found in pairs, with its broad 
 ends adjacent and the pointed ends 
 out. 
 
 The specific character of this organism 
 has not been determined definitely 
 according to Koch's rules, though it 
 is considered the usual cause of 
 croupous pneumonia. 
 
 The germ first produces local lesions 
 within the lung, then systemic infec- 
 tion and general intoxication when 
 the organism gains access to the 
 blood. It may now also produce sec- 
 ondary lesions in other organs. The 
 germ has been found in other condi- 
 tions, such as meningitis, pleurisy, 
 inflammation of other serous sur- 
 faces, abscesses, otitis media and 
 arthritis. 
 
 Irregular forms of lobar pneumonia 
 may be caused by the streptococcus 
 or the staphylococcus, influenza 
 bacillus, typhoid bacillus and Fried- 
 lander's bacillus of pneumonia. 
 
 5. BACILLUS PNEUMONIA OF FRIED- 
 
 LANDER occurs as a distinct bacil- 
 lus, usually in pairs and surrounded 
 by a capsule. It was at one time re- 
 garded as the cause of croupous pneu- 
 monia. 
 
 It may sometimes be the cause of the 
 catarrhal or lobular form, or the ir- 
 regular forms of pneumonia of the 
 ordinary croupous pneumonia. It. 
 however, probably occurs as a mixed 
 infection. 
 
 When a pneumonia is due primarily to 
 this bacillus it is very virulent, caus- 
 ing a peculiar visid exudate in the 
 lung. 
 
 Other organisms found in broncho 
 pneumonia are the streptococcus 
 
BACTERIA. 95 
 
 pyogenes, occasionally the influenza, 
 coli communis, typhoid, glanders and 
 the plague bacillus. 
 
 6. BACILLUS RHINOSCLEROMATIS is 
 
 allied to Friedlander's bacillus and 
 causes a condition called Rhino- 
 scleroma, which presents itself as 
 nodular thickenings of the skin of 
 the nose and lip, and sometimes 
 spreading to neighboring parts, as 
 the mucous membranes of the mouth, 
 pharynx or larynx. The mucous 
 membranes are prone to ulcerate, the 
 skin rarely. 
 
 The cells involved may suffer hyaline 
 degeneration. 
 
 7. BACILLUS OF DIPHTHERIA (Klebs- 
 
 Loeffler Bacillus) is the specific cause 
 of diphtheria, which is primarily a 
 local disease of the tonsils, pharynx, 
 larynx and mucous membranes or 
 skin, and produces a pseudomem- 
 brane, which is made up of a fibrinous 
 exudate in which are massed epithe- 
 lial cells, other tissue elements and 
 infiltrating leucocytes. The affected 
 membranes undergo coagulation ne- 
 crosis or granular degeneration. The 
 action of the toxins may produce in- 
 ternal or viseral lesions during its 
 course or during convalescence. De- 
 generation of the nerves and muscles 
 with later paralysis, which may be 
 temporary or total, together with ne- 
 crotic lesions in the liver or other 
 organs, myocarditis or myocardial 
 degenerations, renal degenerations 
 and nephritis are all complications 
 met with. 
 
 The organisms are found locally— that 
 is, in the pseudomembranes in enor- 
 mous numbers, but only exception- 
 ally are they found in the blood or 
 in the internal organs. 
 
 A non-pathogenic diphtheria bacillus 
 is found in the pharynx of healthy 
 people as well as in other parts of 
 the body. It is also found in the 
 various forms of rhinitis, conjunc- 
 tivitis and non-diphtheitic angina. 
 
 The germ differs from the virulent 
 diphtheria bacillus, in that it is 
 harmless and also in its morphology. 
 
96 PATHOLOGY. 
 
 It is called the pseudodiphtheria 
 bacillus, and its exact relation to the 
 Klebs-Loffler bacillus is still unset- 
 tled. 
 Other organisms, such as the strepto- 
 cocci and staphylococci and the pneu- 
 mococci, may be associated with the 
 bacillus of diphtheria and take a 
 prominent part in the local or gen- 
 eral pathologic process of the dis- 
 ease. 
 8. BACILLUS TYPHOSUS, B. TYPHI 
 ABDOMINALIS, is the specific cause 
 of typhoid fever (enterica or enteric 
 fever). It is a very motile bacillus 
 containing 18 to 20 peripheral flagella. 
 It is short, somewhat plump and has 
 rounded ends. It occurs both within 
 and without the human body. Within 
 the body it occurs in lesions of the 
 intestine and intestinal contents and 
 is often present in the spleen, liver 
 and kidneys. It is regularily found 
 in the blood and is almost present in 
 the gall bladder. 
 It also occurs in the lungs, parotid 
 gland and other organs and post 
 typhoidal abscesses. 
 
 The brunt of the attack usually falls 
 upon the solitary and agminated 
 glands of the intestines which show 
 every change from inflammation and 
 superficial ulceration to a deep 
 necrosis with perforation and 
 peritonitis. 
 
 The ulceration is generally located 
 at the lower end of the ilium but 
 may be as far up as the jejunum 
 and as low down as the rectum. 
 
 The necrosed condition frequently 
 causes hemorrhage which is often 
 fatal. 
 
 The typhoid ulcer is usually oblong 
 with its long axis parallel with that 
 of the bowel in contradistinction to 
 the tuberculous (annular) ulcer which 
 is transverse. 
 
 A similar affection is found in the 
 mesenteric glands and the spleen 
 which is nearly always more or less 
 enlarged. 
 
 The inflammatory condition extends to 
 the surrounding mucous membranes 
 
BACTERIA. 97 
 
 causing catarrhal change (diarrhoea) 
 and the toxin produced by the bacillus 
 may cause focal necroses of the 
 vicera, infarction and thrombosis with 
 the conditions which follows such as 
 gangrene of the lung and bowel and 
 embolism of different organs. 
 
 The infection may be followed by 
 pneumonia, myocarditis, inflamed kid- 
 neys and ovaries, and suppurative in- 
 flammation of most any organ, 
 periosteum of bone or the connective 
 tissues. 
 
 Protective vaccination (Haffkine's 
 method), consisting of an emulsion of 
 killed bacilli, has been variously 
 practiced without definite result as 
 yet. 
 
 9. BACILLUS COL! COMMUNIS gener- 
 
 ally spoken of as Bacillus of the "coli 
 group" in as much there are various 
 bacteria which are closely allied to 
 one another and some with different 
 names which are probably identical. 
 The bacillus coli communis is an or- 
 ganism that greatly resembles the 
 typhoid bacillus. 
 
 It is normally found in the gastro in- 
 testinal tract and biliary passages. 
 It seems to benefit the body in that 
 it restrains, to a certain extent, the 
 growth of putrefactive and possibly 
 pathogenic organisms. In certain con- 
 ditions of the body it develops rap- 
 idly and increases in virulence, and 
 when it wanders from its proper 
 habitat into damaged tissues it is cap- 
 able of producing Inflammatory or 
 suppurative conditions. It is found 
 in various diseases, the gastrointesti- 
 nal track, biliary passages and 
 urinary system such as cystitis, 
 pyelitis and pyelonephritis and of 
 other viscera, also in peritonitis, from 
 the escape of the bacillus through the 
 intestinal wall or a ruptured intestine 
 or secondary to enteritis, pleurisy, 
 endocarditis and other inflammatory 
 diseases. 
 
 10. BACILLUS PARATYPHOSUS or 
 PARA COLON GROUP is closely al- 
 lied to the typhoid and coli com- 
 munis, though they differ in some es- 
 
98 PATHOLOGY. 
 
 sential particulars. 
 
 Para colon or Paratyphoid infection has 
 been described, as resembling typhoid 
 fever clinically, by several writers, 
 but the tendency at the present time 
 is to regard it as distinct in a bae- 
 teriologic sense rather than in a clini- 
 cal or pathological sense. 
 
 The classification of paratyphoid in- 
 fection as a subvariety of typhoid in- 
 fection is probably warranted. 
 
 11. SPIRILLUM CHOLERA ASIATICAE, 
 
 Asiatic cholera spirillum, Vibrio chol- 
 era asiaticae, Koch's comma baccillus, 
 is found only in the intestinal contents 
 and mucosa and produces the "rice 
 water" stools of choleraic patients. 
 The intestine shows congestion fibrin- 
 ous inflammation and necrosis. 
 The toxins absorbed from the bowel 
 give rise to the extreme toxemia with 
 congestion and necrosis of the 
 viscera. 
 
 The rapid and copious intestinal dis- 
 charges lead to inspissation of the 
 blood and the collapsed appearance 
 invariably found. 
 
 Protective vaccination gives encourag- 
 ing results. 
 
 12. BACILLUS MALLEI, Bacillus of 
 glanders, is the specific cause of the 
 inflammatory infection of the nasal 
 mucosa called glanders, in horses and 
 asses which is sometimes communi- 
 cated to other animals and man. The 
 organism resembles the tubercle 
 bacillus to a certain extent. 
 
 The mucosa of the nose is characterized 
 by its slightly elevated nodules at 
 first, these later show a marked tend- 
 ency to soften and become irregular 
 ulcers. The lymphatic glands of the 
 neck, and elsewhere, enlarge and sup- 
 purate. It may attack the skin but 
 the lesions here are more sluggish. 
 
 In man, similar nodules and ulceration 
 may be found in the nose, larynx or 
 trachea. The skin is attacked in the 
 form of pustules, boils and abscesses. 
 
 Nodules may also form in the viscera 
 and there may be arthritis and 
 ostemylitis. 
 
BACTERIA. 99 
 
 13. BACILLUS OEDEMATIS MALIGNE, 
 Vibron Septique, Bacillus of malign- 
 ant edema. The bacillus resembles 
 that of anthrax, but more slender. 
 It is the specific cause of an intense 
 infection causing 1 inflammation and 
 is called malignant edema, which is 
 seen in certain animals and man. 
 
 The bacillus occurs in the subcutaneous 
 tissues near the point of entrance, 
 also in the muscles and peritoneal 
 cavity at the time of death. 
 
 It is not found in the blood as it is 
 anaerobic. 
 
 The subcutaneous tissues undergo rapid 
 supperation and necrotic inflammation 
 with rapid emphysema and gangren- 
 ous alterations and pus formation or 
 extensive hemorrhagic infiltration. 
 
 14. BACILLUS ANTHRACIS, is a strepto 
 bacillus, the specific cause of anthrax. 
 It occurs most frequently in cows 
 and sheep. 
 
 In animals it is called spleenic fever; 
 in man malignant pustule and wool 
 sorters disease. The mode of infection 
 in animals is most frequently the 
 gastrointestinal tract, the microor- 
 ganism being swallowed with the food. 
 They may, however, gain entrance 
 through the lungs or, which is most 
 common in man, through external 
 abrasions. The bacillus occurs in all 
 the local lesions and from these 
 they are carried to the blood and or- 
 gans such as spleen, liver, kidneys 
 and lungs. 
 
 The lesions produced by anthrax are 
 more or less local but occasion a gen- 
 eral septicemia. When infected 
 through abrasions of the skin, the 
 inflammatory process is intense, the 
 areas are often covered and sur- 
 rounded by bulbous vesicles and at- 
 tended with edema, 
 
 The surface may become eroded with 
 discharge of sanious liquid and crust 
 formation. 
 
 When infected through the gastro- 
 intestinal tract, the mucosa and sub- 
 mucosa is affected like the above. 
 The lesions are first hemorrhagic, 
 then swelling follows, ulceration of 
 
100 PATHOLOGY. 
 
 surface and profuse diarrhoea with 
 discharges may occur. 
 
 When infected through the lungs, the 
 bacilli lodge in the alveoli, rapid cel- 
 lular exudation with edema and 
 hemorrhagic infiltration follows. Sero- 
 sanguinolent pleurisy, enlargement of 
 the mediastinal glands and some- 
 times a hemorrhagic extravasation in- 
 to the mediastinal spaces occurs. 
 
 15. BACILLUS AEROGENES, is an ana- 
 erobic bacillus which somewhat re- 
 sembles the bacillus of malignant 
 edema. It is about as thick as the 
 bacillus of anthrax, adjacent ends are 
 slightly rounded or square and it oc- 
 curs singly, in pairs, clumps or short 
 threads. 
 
 It is the specific cause of Infectious em- 
 physema (gaseous gangrene, gas- 
 phlegmon, emphysematous necrosis). 
 
 Infection takes place through some in- 
 jury or abrasion. It has been met 
 with during the puerperium, probably 
 from uterine infection, and it is prob- 
 able that many cases of air-embolism 
 from douching the uterus after la- 
 bor are realy this form of infection. 
 
 The lesions are wide spread. At the 
 point of entrance there is edematous 
 infiltration with bloody fluid and 
 emphysema due to gas formation. 
 Necrosis and gangrenous softening of 
 tissues occur rapidly. The entire sur- 
 face of the body may become 
 emphysematous as does the my- 
 ocardium kidneys, liver and spleen. 
 
 The blood of the heart and vessels pre- 
 sent a foamy condition, due to gas 
 formation. 
 
 The bacilli are found in the gas vesicles. 
 
 16. ACTINOMYCES BOVIS. Ray-fungus, 
 is an anaerobic organism. The specific 
 cause of "Lump Jaw" in cattle and 
 horses, it also infects man. 
 
 The streptothrix, cladothrix, etc. was 
 at one time classed as this organism 
 but this has been disproved, as they 
 are aerobic. 
 
 The manner of infection has not been 
 determined. In the tissues affected 
 there is round-celled infiltration, and 
 proliferative changes in. the connect- 
 
BACTERIA. 101 
 
 ive tissue surrounding 1 the organism 
 with sometimes secondary softening, 
 necrosis or suppuration. The granu- 
 lation tissue is rich in leucocytes 
 and foci with purulent collections 
 may develope. 
 
 In cattle the disease affects the lower 
 jaw more often than the upper or 
 other bones, the tissues of the neck, 
 tongue, etc. 
 
 In man it is seen in the gums, cheeks, 
 mouth, lungs, intestine and the other 
 internal organs. 
 
 The lesion is first a hard red papule 
 which increases and later breaks 
 down forming necrotic or suppurative 
 excavations. Scar formation may ex- 
 tend to some parts while the necrosis 
 may go on in other directions, so that 
 irregular cavities are established. 
 
 In the pus or necrotic tissues the so- 
 called sulphur granules of the or- 
 ganism are found. The disease tends 
 to become limited or retarded and 
 sometimes this is completely effected. 
 
 17. STREPTOTHRIX MADURAE, is an 
 
 organism somewhat allied to the 
 actinomyces. and is the specific cause 
 of mycetoma or madura foot of In- 
 dia. It affects the foot, and its mode 
 of infection is generally by injuries 
 from thorn wounds, etc. The hands 
 or other parts are rarely affected. 
 
 There is first a nodular swelling which 
 spreads. Later there is softening 
 with rupture and a discharge of thin, 
 watery pus containing grayish or red- 
 dish granules or black granules like 
 gun powder. 
 
 In the later stages, discharging sinuoses 
 may remain. New nodules are form- 
 ed and softened, the affected mem- 
 bers are greatly deformed. Death 
 occurs from exhaustion. 
 
 18. BACILLUS TETANI, is a rod-like 
 anaerobic bacillus, frequently swollen 
 at one end due to the presence of a 
 rounded spore. It is the specific cause 
 of Tetanus. The' organism is fre- 
 quently found in garden earth, in- 
 testinal discharges of animals, and 
 articles about stables. 
 
 Mode of infection occurs through 
 
102 PATHOLOGY. 
 
 puncture made by nails, splinters and 
 the like. 
 
 There is no characteristic lesion. The 
 germ generally remains at the site of 
 inocculation and here produces its 
 toxina which are called tetano- 
 spasmin, the most prominent and 
 causes the spasm; tetanolyism a 
 hemolytic substance. 
 
 There is a vascular congestion, chroma- 
 tolysis of the spinal ganglion cells 
 and death. 
 
 An antitoxin has been prepared and 
 successfully, but the disease is gener- 
 ally so far advanced before it is 
 recognized as to render the antitoxin 
 nearly useless. 
 
 19. SPIROCHAETAE OBERMEIERI, is a 
 spinal organism found in the fresh 
 blood, and is the specific cause of 
 Relapsing fever (typhus recurrens). 
 
 The germ is found in the blood during 
 the attack, but not during the inter- 
 mission. The spleen is congested and 
 greatly enlarged, frequently present- 
 ing areas of anemic infarctious and 
 nercrosis or fatty degeneration. 
 
 20. BACILLUS OF INFLUENZA, Peiffer's 
 bacillus, is an extremely small and 
 usually single bacillus which is the 
 specific cause of Influenza or La 
 Grippe. It occurs in the sputum. 
 There is no specific lesion. 
 
 There is an intense catarrhal processes 
 and at times a pneumonia. There is 
 sometimes inflammatory lesions and 
 hemorrhagic infiltrations in the mem- 
 branes of the brain. 
 
 21. PLAGUE BACILLUS, is a small mo- 
 tite bacillus, somewhat resembling the 
 bacillus of influenza. 
 
 It is the specific cause of the Bubonic 
 plague or pest. The bacillus is found 
 in the lymphatic glands, buboes, blood 
 and the various organs of those 
 affected with the disease. Rats, flies, 
 etc. die during epidemics and help 
 to spread the disease by infecting the 
 soil and dust about dwellings. 
 
 Infection in man is most frequent 
 through injuries of the skin such as 
 scratches, etc, though it may occur 
 through the lungs. 
 
 The lymph glands are attacked and 
 
BACTERIA. 103 
 
 suppurate (bubo), taking place prin- 
 cipally in the inguinal or axiliary 
 regions (bubonic type), or secondarily 
 at the root of the lungs through a 
 primary brouchopneumonia (pneumon- 
 ic type), or a general septicaemic 
 type, here suppuration is not so com- 
 mon. 
 Haffkine's preventive inoculations have 
 been used with good results. 
 
 22. OIDIUM ALBRICANS, is a budding 
 fungus which is the specific cause of 
 Thrush in new born infants or in 
 older children. The disease is char- 
 acterized by a milk-deposit on the 
 mucous membrane of the mouth. 
 
 The organism is found in the air and 
 various articles of food. 
 
 23. LEPTOTHR1X BUCCALIS, is norm- 
 ally found in the mouth and occas- 
 ionally penetrate and multiply in the 
 crypts of the pharynx, producing a 
 chalk-like nodule or deposit. It may 
 cause secondary inflammation. 
 
 24. BACILLUS OF TUBERCULOSIS, is 
 
 a rod-shaped organism often occur- 
 ing in pairs, arranged end to end 
 but not attached. It may appear 
 straight or more or less curved and 
 may branch. It is found in man, 
 cattle and fowl, and is the specific 
 cause of Tuberculosis in its various 
 forms. The organism may be said to 
 be divided into a "human" (which is 
 described above) and a bovine bacil- 
 lus which is shorter and thicker than 
 the human and does not exhibit a 
 curved or branching form, which is 
 common in the human. 
 
 The tuberculin of the bovine is alka- 
 line, in reaction while that of the 
 human is strongly acid. It seems 
 likely that the human, bovine, avians 
 and other animal species of tubercu- 
 losis are simply variations of one com- 
 mon organism. 
 
 The organism probably occurs and 
 multiplies only in the body and 
 excreta of diseased individuals. The 
 sputa or other excreta containing the 
 bacillus may dry and retain the 
 bacillus in a dormant state which is 
 still potential. It is also found 13 
 
104 PATHOLOGY. 
 
 the lesions of all parts of the body. 
 The mode of infection is generally by 
 direct inoculation or by the inhala- 
 tion or the swallowing of germs, or 
 by intra uterine transference through 
 the placenta. 
 
 When the tubercle bacillus is received 
 into a tissue or organ, it being a 
 foreign body, it acts as an irritant 
 to the tissues which react and the 
 so-called tubercle is formed. 
 
 With the appearance of the germ into 
 the tissues, there is a polynuclear 
 leucocytosis into the area from the 
 neighboring vessels, together with a 
 development of epithelioid cells, which 
 look like epithelium, from the fixed 
 connective tissue cells or the endo- 
 thelium of the lymphatics or blood 
 vessels. Some of these cells, either 
 by union, or the proliferation of their 
 nuclei with a growth, but not a di- 
 vision of their protoplasm, form giant 
 or myeloid cells which are inclosed 
 in a structureless intercellular 
 stroma produced by themselves. 
 
 The tubercle formed is of a grayish 
 somewhat translucent pearly body and 
 is called the miliary tubercle. It is 
 avascular and in its further evolution, 
 hyaline degeneration, coagulation 
 necrosis, fatty change, and finally 
 a transformation into a cheesy mass, 
 the so-called caseous necrosis (now 
 yellow in color) takes place. 
 All this is due to a specific action of 
 the living bacillus, and in part to the 
 avascularity of the tissues. 
 The giant cell, although very conspicu- 
 ous, is not characteristic of tubercu- 
 losis as it is found in many inflam- 
 mations, foci of chronic irritation 
 and tumors. 
 The giant cells are early victims to the 
 
 necrosis. 
 
 When the infection is slight and the 
 
 individual is resistant, the tubercle 
 
 undergoing complete necrosis and is 
 
 ;. transformed into a cheesy mass, the 
 
 :;-. surrounding connective tissue may 
 
 * : 4- eventually cause encapsulation of the 
 
 . ...tubercle, and if calcification of the 
 
 ..". "-.cheesy, mass ensues, there may be a 
 
m m 
 
 
 Fig-. 20. Melanosarcoma, mainly 
 round-celled; from a nodule in the skin. 
 
 
 Fig-. 21. Giant-celled sarcoma. (War- 
 ren.) 
 
*>*:# v 
 
 
 Fig-. 22. Miliary tubercles in the liver, 
 showing- abundant round cells in the 
 peripheral parts, epithelioid and giant 
 cells within. 
 
 Fig*. 23. Tuberculous lymphatic glands 
 
 a, lymphadenoid tissue; b, largre round 
 cells (epithelioid); e, large spindle cells. 
 (Ziegler.) 
 
TUBERCULOSIS. 105 
 
 permanent arrest of the activity in 
 the nodule. This is often seen post- 
 mortem, the patient having died from 
 some other cause. If, however, in the 
 necrosis, cavities, sinues, fistulas and 
 ulcers are formed, these conditions 
 are difficult to heal, or when during 
 this condition, breaking down is com- 
 mon, it infects the contiguous sur- 
 faces or distant organs by means of 
 the lymph or blood vessels, the bacil- 
 li are thus introduced into the cir- 
 culation, an acute fatal infection oc- 
 curs which is known as general 
 miliary tuberculosis, seen on section 
 of the various organs. 
 
 Besides the tubercle there are inflam- 
 matory lesions which occur between 
 the tubercles and vary according to 
 the anatomic character of the parts 
 affected. 
 
 In the lungs, the tubercle may be in- 
 conspicuous, while the infiltrated lung 
 tissues, surround the tubercles and 
 filling in the spaces between them, 
 gives the organ a definite appearance. 
 
 An inhalation of a considerable number 
 of tubercle bacilli may be followed by 
 a rapid pneumonia without any tub- 
 ercular formations. 
 
 The caseous change is important in that 
 liquefaction and cavity formation 
 may result which is particularly fre- 
 quent in bones, skin, glands and kid- 
 ney. 
 
 Frequent seats of tuberculosis are the 
 lungs, lymphatic glands, bones and 
 joints, mucous membranes of larynx 
 and intestines, serous membranes, 
 prostrate, testicle, ovaries, fallopian 
 tubes, kidneys, uterus, suprarenal 
 capsules, brain, liver and spleen. In 
 some of the latter sites it is prac- 
 tically always secondary. , 
 
 Latent Tuberculosis. A lesion may be- 
 come encapsulated and limited, and 
 remain so for years without giving 
 rise to clinical symptoms, will sub- 
 sequently break through its capsule 
 and give rise to wide spread infec- 
 tion, local or general. Such is seen 
 in the post bronchial glands, etc. 
 
 Lupus Vulgaris is a chronic tubercu- 
 
106 PATHOLOGY. 
 
 losis which affects the skin in its 
 entire depth. Wide and ugly 
 cicatrices are often formed gradually. 
 
 Scrofula or Struma formerly looked up- 
 on as a distinct disease predisposing 
 to tuberculosis is now known to be 
 tuberculosis occuring in different 
 forms and situations. 
 
 Pseudo tuberculosis or false tubercle is 
 a condition which resembles the real 
 tubercular nodule but is caused by a 
 non infective irritant. 
 
 25. BACILLUS LEPRAE is a bacillus 
 which closely resembles the tubercle 
 bacillus and is the specific cause of 
 leprosy, (Lepra or Elephantiasis 
 Graecorum). 
 The microorganism is found in the lep- 
 rous lesions and in the nasal mucus. 
 In the tissues. The germ is found 
 within the large cells of the specific 
 granulation tissue (lepra cells). 
 
 Leprosy occurs in two forms 
 
 a. Tubercular or lepra tubercularis is 
 found as small or large nodular ele- 
 vations in the skin of the face and 
 the extensor surfaces of the arms 
 and limbs, etc. 
 
 These nodules are at first reddish in 
 color with some inflammatory re- 
 action. 
 
 Later the redness is lost and slow 
 growing or stationary indolent les- 
 ions result. 
 
 They may become ulcerous and do 
 not heal readily, or they may be 
 
 converted into cicatrices which 
 causes great deformities. 
 
 The appearance of the face is char- 
 acteristic and is known as leontiasls 
 leprosa. 
 
 The mucous membrane and some of 
 the internal organs may be involved. 
 
 b. Anaesthetic form is very insiduous 
 in its onset and attacks the con- 
 nective tissue and peripheral nerve 
 fibers. 
 
 In this form the lesions are less con- 
 spicuous, but symptoms such _ as 
 hyperesthesia and neuralgic pains, 
 with later ulcerations partly trophic 
 in nature. Interference with the 
 trophic influence of the nerves lead 
 
SYPHILIS. 107 
 
 to ulceration with loss of the parts 
 below the lesions. 
 There are whitish or brownish spots 
 in the skin which may be slightly 
 elevated. 
 
 The anaesthetic and the tubercular 
 varieties are commonly coexistant. 
 The nodules appearing in the liver, 
 spleen and testes are similar to the 
 nodules of the skin. The nodules of 
 the lungs, kidneys, intestines and 
 of the serous surfaces are held by 
 many to be tuberculosis and the 
 result of secondary infection. 
 Other secondary infections are the re- 
 sult of injuries to the superficial 
 lesions, admiting pyogenic infec- 
 tion. 
 
 The term lepra mutilaus and lepra 
 gangraenosa are applied to such. 
 
 The Leproma or lepra nodule resem- 
 bles that of tuberculosis in struct- 
 ure, but differs in its greater 
 vascularity and absence of tend- 
 ency to cheesy necrosis. The 
 abundant blood vessels and a tend- 
 ency to complete organization with 
 formation of fibrous tissue is mark- 
 ed. 
 
 The bacilli occur within the cells 
 and sometimes between them. They 
 are in large groups and multiply 
 within the cell. The protoplasm of 
 which undergoes swelling and de- 
 generation. The nucleus is broken 
 down and the cell is converted into 
 a sac containing the bacilli and 
 broken down protoplasm. This is 
 called the lepra cell. Giant cells 
 may be formed. 
 
 26. SPIROCHAETA PALLIDA is a deli- 
 cate, actively motile, faintly retractile 
 spiral, long, thread-like organism, 
 tapering at both extremities and ter- 
 minating in pointed ends. It is al- 
 most universally accepted as the 
 specific cause of syphilis. It has been 
 found in the initial lesions, the sec- 
 ondary papules, the enlarged 
 lymphatic glands, the mucous patches, 
 etc., but not as yet in the tertiary 
 lesions nor in patients undergoing 
 active treatment. 
 
108 PATHOLOGY. 
 
 Infection occurs by direct inoculation 
 in sexual intercourse, though it may 
 be conveyed in many other ways, as 
 during surgical operations on syphilit- 
 ic patients; in the process of tattoo- 
 ing or vaccination, when the saliva 
 or vaccine lymph from diseased pers- 
 ons was employed; by kissing or the 
 use of drinking vessels that have been 
 employed by the diseased. 
 
 The new born may be syphilitic by reas- 
 on of the presence of the disease in 
 father or mother. 
 
 Syphilis may be divided into three 
 stages: 
 
 a. Primary lesion, the hard indu- 
 rated or Hunterian chancre, appears 
 in from 10 to 42 days (average 24) 
 after inoculation at the point of 
 infection, which is generally the 
 genital organs, lip, tongue, tonsils, 
 pharynx, examining finger, etc. 
 
 It begins as a red, inflamed papule 
 or as a vesicle, which ruptures and 
 produces an erosion. 
 
 When it appears as a papule the sur- 
 face becomes eroded and super- 
 ficial ulceration follows. 
 
 The lesion is very hard or indurated, 
 which will distinguish it from the 
 soft chancre or chancroid. 
 
 Microscopically, the lesion at first 
 presents small areas of round cell 
 infiltration in the deep layers of 
 the skin or mucous membranes and 
 in the neighborhood of blood ves- 
 sels. 
 
 The connective tissue proliferates 
 and spindle or irregular embryonic 
 connective tissue cells mingled 
 with round lymphoid cells or sur- 
 round foci of the latter. A thicken- 
 ing of the blood vessels may be 
 seen. The tissue elements are 
 usually separated by an infiltrated 
 liquid which leads to the primary 
 vesicle or erosion. 
 
 The induration is probably due to 
 connective tissue hyperplasia, 
 sclerosis of the vessels and tense 
 infiltration of serous liquid. (• 
 
 b. Secondary lesions make their ap- 
 pearance at a variable period of 
 
SYPHILIS. 109 
 
 time after the eruption of the 
 initial lesion, and consist of a 
 swelling and induration of the 
 neighboring lymphatic glands 
 (syphilitic bubo). 
 The superficial glands of the entire 
 body then become swollen and in- 
 durated. At the same time erup- 
 tions appear on the skin and mu- 
 cous membrane. The skin lesion 
 may appear in various forms of 
 papules, macules and scaly erup- 
 tions, symmetrically arranged on 
 both sides of the body and cause 
 but little irritation. 
 
 The skin is frequently said to be cop- 
 pery. On the mucous membranes 
 and neighboring skin the most 
 characteristic lesion is the condy- 
 loma latum, or mucous patch, which 
 appears as an elevated patch with 
 superficial erosion or ulceration. 
 
 The surface has a necrotic appear- 
 ance. It is similar in its structure 
 to the initial lesion. The later 
 tendency to connective tissue hy- 
 perplasia is less marked than it is 
 in the initial lesion. 
 
 c. Tertiary lesions appear gradually 
 after the secondary lesion. They 
 may be divided into— 
 
 1. Localized lesions, which take on 
 the ordinary inflammatory 
 changes with a tendency to 
 fibrous tissue overgrowth and 
 thickening or definite nodules 
 (gummata or syphilomata). These 
 vary in size from small tubercles 
 (miliary gummata) to tumors of 
 an orange in size or larger. It is 
 hard and frequently elastic. On 
 section it may be gelatinous or 
 mucoid in appearance, but there 
 is nearly always considerable in- 
 duration either as a capsular en- 
 closure or bands, which extend 
 from the center to the periphery. 
 
 The gummata may soften and be- 
 come converted into puriform 
 collections, or when superficially 
 placed suppuration, fatty or ne- 
 crotic softening may lead to su- 
 perficial ulceration that may re- 
 
110 PATHOLOGY. 
 
 main, become cicatrized or disap- 
 pear by absorbtion. 
 2. Diffuse syphilitic changes, in this 
 condition may be ranked athe- 
 romatous thickening of the in- 
 tima of blood vessels, certain 
 changes in the liver, spleen, kid- 
 neys, heart muscle and nervous 
 system. 
 
 The tissues of the affected organ 
 are indurated, the connective tis- 
 sue shows more or less pro- 
 nounced hyperplasia. 
 
 Congenital syphilis may be found in 
 the new born or may develop after 
 birth. The condition may cause the 
 child to die in utero or it may cause 
 it premature death. The foetus may 
 be macerated prior to expulsion. 
 Sclerotic lesions of the organs are 
 conspicuous. Superficial lesions of 
 the skin as vesicles or bullae, fis- 
 sures, etc., are also seen. 
 
 The hereditary form with character- 
 istic lesions of the bones, teeth, etc., 
 does not show itself till later. 
 
 DISEASES DUE TO UNDETERMINED 
 BACTERIA. 
 
 1. SOFT CHANCRE OR CHANCROID is 
 
 an infectious venereal sore occurring 
 upon the external genitalia, due pos- 
 sibly to the bacillus of Ducrey and 
 Urma. Various other organisms, such 
 as the streptococci and staphylo- 
 cocci, gonococcus and other organ- 
 isms, are often associated. 
 
 The condition is usually a simple ulcer, 
 with suppurating base and edges, 
 which discharges freely, may reinfect, 
 the patient in other regions, or it 
 may take on a malignant phagedemic 
 or serpiginous character. 
 
 The neighboring lymph glands usually 
 enlarge and may undergo suppura- 
 tion (bubo). 
 
 2. SCARLET FEVER, or SCARLATINA, 
 
 is probably due to a micro-organism 
 which multiplies rapidly in the blood. 
 This is proven by the rapid, fatal 
 cases which show no local lesion of 
 any severity. There have been vari- 
 ous organisms considered as the 
 cause, but none proven to be specific. 
 
MEASLES. Ill 
 
 Among them were the streptococci 
 
 and protozoan organisms. 
 Intense lesions of mucous membranes 
 
 and glands are generally present. 
 
 Suppuration of the glands and severe 
 
 inflammations of the throat, middle 
 
 ear, larynx and trachea, endocaditis 
 
 and pericarditis is quite frequent. 
 
 Diphtheria and pneumonia are not 
 
 rare complications. 
 Parenchymatous nephritis is common, 
 
 and focal necrosis of organs is seen 
 
 in fatal cases. 
 
 3. MEASLES, or RUBEOLA, is probably 
 
 due to some micro-organism. A 
 bacillus resembling that of influenza 
 and a protozoan organism have been 
 considered, but not determined. 
 A catarrhal inflammation of the faucial, 
 nasal and conjunctival membranes 
 and the bronchial mucosa are cus- 
 tomary lesions. There is associated 
 congestion and inflammatory enlarge- 
 ment of the lymph glands. Second- 
 ary degenerations and focal necroses 
 also appear. 
 
 4. MUMPHS. The bacteriology is uncer- 
 
 tain. It is an acute inflammation of 
 the paroted or the submaxillary 
 gland. It rarely terminates in sup- 
 puration or on recovery in indura- 
 tion. 
 
 5. YELLOW FEVER, or Typhus Ic- 
 
 teroides, is an infectious disease gen- 
 erally transmitted through the bite 
 of a mosquito — the Stegomyia fascia. 
 The specific organism is undeter- 
 mined. 
 
 The bacillus icteroides, once considered 
 as the cause, is now looked upon as 
 a secondary invader. Various other 
 organisms have been considered. 
 
 The liver suffers extensive, fatty de- 
 generation and appears mottled on 
 section. 
 
 The kidneys undergo parenchymatous 
 degeneration with extravasation of 
 blood. Hemorrhages of the mucous 
 and serous surfaces are frequent, par- 
 ticularly of the gastric mucosa. The 
 brain and the meninges are con- 
 gested. Rigor mortis occurs early. 
 
 6. WHOOPING COUGH. Micro-organ- 
 
112 PATHOLOGY. 
 
 ism is not determined. Lesions of a 
 persistent bronchitis are present, but 
 are not characteristic. 
 
 7. TYPHUS FEVER (Ship, Jail, Emi- 
 
 grant fever) is rare and of unknown 
 cause. The condition suggests an in- 
 tense infection and intoxication. The 
 blood is often dark colored and pu- 
 trifies rapidly. There may be inflam- 
 mation of the lungs and bronchi, cere- 
 bral and meningeal congestion, and 
 albuminous degeneration of the mus- 
 cles, liver and kidneys. The spleen 
 is enlarged, often soft and may be 
 infarcted. 
 
 8. RABES. HYDROPHOBIA. The causa- 
 
 tive micro-organism is undetermined. 
 It flourishes in the saliva and salivary 
 glands of rabid animals, chiefly 
 wolves, cats and dogs, and is inocu- 
 lated by their fangs. The virus 
 travels along the nerve sheaths to 
 the spinal cord and medulla, in which 
 it resides. There is gangliomic cell 
 degeneration in the medulla and pons, 
 loucocytic congestion of their peri- 
 vascular lymphatics and atrophy of 
 the pneumogastric nerve. 
 
 9. RHEUMATISM. Acute articular rheu- 
 
 matism is probably an infectious con- 
 dition. Its real nature, however, is 
 undetermined. Many still consider it 
 due to faulty metabolism, but the 
 evidence is strongly in favor of Poyn- 
 ton and Pains' diplococcus rheuma- 
 ticus, which has frequently been dem- 
 onstrated in the areolar tissue below 
 the synovial membrane in arthritis, 
 in endo and pericardial lesions, in the 
 meninges, in chorea and cerebral 
 rheumatism. 
 
 10. MALTA FEVER, Mediterranean fever, 
 Gibraltar fever, Febris Undulans, oc- 
 curs along the Mediterranean coasts. 
 It is not contagious. The organism 
 enters the body through the respira- 
 tory and intestinal tract. 
 
 The membrane of the small intestine 
 is red, and the solitary follicles and 
 Pyers patches are sometimes swollen. 
 
 The mucosa of the large intestine is 
 dark red, with small round or large 
 irregular ulcerations, causing hemor- 
 
PARASITES. 113 
 
 rhage. The spleen is enlarged and 
 hyperemia 
 11. BERI BERI occurs in the tropics and 
 sub-tropics. There is a degeneration 
 and inflammation of the peripheral 
 nerves, punctate hemorrhages of the 
 serous surfaces, parenchymatous and 
 fatty degeneration of the heart mus- 
 cle and enlargement of the liver and 
 spleen. 
 
 DISEASES CAUSED BY ANIMAL 
 PARASITES. 
 
 1. RHIZOPODA. 
 
 f. AMOEBA DYSENTERIAE is an or- 
 ganism made up of a clear, refractile 
 ectoplasm and a finely or coarsely 
 granular endoplasm, frequently show- 
 ing a vacuole and sometimes a nu- 
 cleus. It has ameboid movement. 
 It is found in the stools of dysenteric 
 patients, in the tissues of the bowel 
 wall near the dysenteric ulcers and 
 also in secondary liver abscesses. 
 
 2. AMOEBA CO LI is less distinct than 
 
 a. the dysenteriae in its ectoplasm, 
 endoplasm and pseudopodia. "Vac- 
 uoles are usually absent. It has a 
 distinct nucleus with well-defined nu- 
 clear membrane. It is present in the 
 faces in 50 per cent, of healthy per- 
 sons. 
 
 3. AMOEBA URINALIS is found during 
 
 cystitis. Other amoeba are found in 
 the mouth, especially about the teeth. 
 
 4. CERCOMONAS HOMINIS is an or- 
 
 ganism with a pear-shaped body, 
 having a cilia on its small anterior 
 end, a flagellum on its broad posterior 
 end. It is found in diarrhoeal condi- 
 tions, cholera, etc. 
 
 5. TRICHOMONAS INTESTINALIS is a 
 
 granular pear-shaped organism, with 
 an anterior blunt end and a posterior 
 end that is prolonged into a sharp 
 tail. The organism contains one or 
 two vacuoles. There are 10 to 12 
 cilia situated on one side near its 
 anterior end. 
 It has been found in diarrhoea. 
 & TRICHOMONAS VAGINALIS is small- 
 er than the T. intestxnalis. It has 
 
114 PATHOLOGY. 
 
 from 3 to 4 flagella and 6 or 7 short 
 lateral cilia. 
 It is found in the vaginal discharges 
 of vaginitis and in those of women 
 of unclean habits. It may be mis- 
 taken, by the inexperienced, for the 
 spermatozoon. 
 
 7. TRYPANOSOME, Trypanosoma gam- 
 blense is found in the horse and cat- 
 tle of the tropics, and is also found 
 in the blood of man. 
 
 It is a minute worm-like body, with 
 one end drawn out into a flagellum 
 and the other end bluntly conical. 
 The body is short, thick and gran- 
 ular, with an attached undulating 
 membrane. A vacuole is found near 
 its posterior end. 
 
 It exists in the blood of man for a 
 long time without causing any symp- 
 toms. It then enters the cerebro- 
 spinal fluid and causes the charac- 
 teristic symptoms — trypanosomiasis — 
 irregular and relapsing fever, con- 
 stantly frequent pulse and respira- 
 tion; oedema, enlarged and tender 
 spleen; emaciation, weakness and 
 progressive drowsiness, which deep- 
 ens into coma and ends in death. 
 
 It is the sleeping sickness of the 
 Congo. 
 
 The transmission of the parasite is 
 effected mainly by the bite of the 
 tse-tse fly (glossina palpalis). 
 8. PARASITES OF MALARIA. The 
 parasite gains entrance to the blood 
 in the saliva of the female mosquito 
 of the genus anopheles, which have 
 taken the blood of malarial subjects 
 into its stomach, where sexual re- 
 production takes place as follows: 
 The flagellate form (microgame- 
 tocytes) are developed and the 
 flagella (microgametes), each con- 
 taming one part of the nuclear sub- 
 .. stance of the parent cell, are dis- 
 " charged, and, moving toward the 
 ■ other parasites which do not form 
 flagella (macrogametes), fertilize 
 these by penetrating the body of the 
 latter. The fertilized parasites invade 
 the tissues, segment and develop a 
 . ..:capsule r - then called an oocyst, which 
 
MALARIA. 115 
 
 contains sporozooits, the result of 
 segmentation of the parasite. These 
 reach the salivary glands and are 
 injected into the blood of the next 
 person bitten. 
 Three distinct species of the malarial 
 parasite have been identified. 
 
 a. Plasmodium vivax is the organism 
 
 of the tertian fever. The cycle of 
 development in the blood begins 
 with a small hyaline spherule, at- 
 tached to or with a red blood cell. 
 Pigment particles (melanin, derived 
 from altered hemoglobin) appear 
 within the parasite. The currents 
 in the protoplasm render the pig- 
 ment motile. 
 
 The body increases in size and the 
 corpuscle containing it becomes 
 pale. The body continues to in- 
 crease in size to or beyond that of 
 the normal corpuscle. They are ac- 
 tively ameboid until full grown. 
 
 The pigment collects in the center 
 and the organism forms a rosette 
 and then divides into 15 or 20 
 rounded segments or merozoites 
 (new spores). The red cell is de- 
 stroyed and the merozoites are lib- 
 erated, enter other red cells and 
 begin the cycle afresh. Then the 
 chill or ague-fit is ushered in. 
 
 The cycle is completed in 48 hours. 
 
 b. Plasmodium malariae is the organ- 
 
 ism of the quartan fever. It dif- 
 fers from the P. vivax, in that the 
 corpuscle does not enlarge or be- 
 come as pale; the pigment is less 
 in quantity and usually coarse. 
 
 Segmentation is more regular and 
 forms a wheel-like figure with 6 to 
 12 merozoites. 
 
 The cycle occupies 72 hours. 
 
 A mixture of the tertian and quartan 
 orms yield a daily paroxysm — 
 Quotidian fever. 
 
 c. Plasmodium praecox is the organ- 
 
 ism of the estivo-atumnal fever, 
 and also of tropical or malignant 
 forms. It is smaller than" the other 
 forms, with less, but coarse, pig- 
 ment. It occupies only about 1-3 of 
 the the red corpuscle,, and. . divides 
 
116 PATHOLOGY. 
 
 into 15 merozoites in 48 hours. Seg- 
 mentation taking place generally 
 within the spleen, bone marrow, 
 liver and capillaries of the brain. 
 
 Gametocytes are a feature in the 
 later stage of this type of infec- 
 tion. At first they are oval bodies, 
 then they become crescents with 
 centrally placed pigment. 
 
 Gametocytes are significant of long- 
 standing infection. They do not 
 form when the infection is recent 
 and asexual development is active. 
 
 Changes induced are destruction of 
 the red cell with its haemoglobin. 
 The haemosiderin resulting there- 
 from is deposited in the liver, 
 spleen and bone marrow. 
 
 The pigmented spleen is enlarged, 
 congested and soft. Phagocytosis 
 is present. 
 
 The liver and kidneys show paren- 
 chymatous degeneration. 
 
 9. COCCIDUM CUNICULI is a small body 
 
 with a delicate outer coat and a 
 tough inner double-contoured cap- 
 sule. The body is filled with gran- 
 ular material sometimes aggregated 
 in the center. Sporulation takes 
 place outside of the body. The pro- 
 toplasm divides into 4 capsulated 
 spores containing granular resting 
 body between two cicle-shaped 
 daughter-spores. Endogenous spor- 
 ulation may take place. The organ- 
 ism is sometimes seen in the liver 
 of man as cystic nodules, which 
 spring from the bile ducts or some- 
 times as diffuse involvment of the 
 liver with cirrhosis, causing jaundice. 
 They have also been seen in the in- 
 testines, heart and kidneys. 
 
 10. BALANTIDIUM COLI or PARAMECI- 
 
 UM CO LI is a long, slightly ovoid 
 body closely betset with cilia. The 
 protoplasm is granular, contains a 
 nucleus and two contractile vacubles. 
 It is natural in the hog and is some- 
 times found in diarrhoeal discharges 
 in man. 
 
 11. MOLLUSCUM CONTAGIOSUM or 
 EPITHELIOMA CONTAGIOSUM, is 
 
 an infectious disease of the skin and 
 
VERMES. 117 
 
 appears as white or pink papules. The 
 lesions have been found to contain 
 bodies resembling coccidia. 
 
 The disease is found on the face, neck, 
 chest, gentals or scattered over the 
 whole body sometimes on the mucous 
 membrane. 
 
 12. VARIOLA (Smallpox) and VACCINIA 
 
 (Cow pox). Various micrococci have 
 been assigned as the cause for this 
 disease but a protozoan parasite of 
 the order sporozoa is now being con- 
 sidered gravely. 
 
 All authorities do not agree as to the 
 difference of variola and vaccinia. In- 
 oculation of man by cowpox confers 
 an immunity from small pox. 
 
 There are two stages of the disease, 
 the invasion of the blood and the ap- 
 pearance of the eruption which is 
 successively papular, vesicular and 
 pustular with the formation of crusts. 
 When it is confined to the epidermis 
 no disfiguration results; when the 
 true skin is affected, scars with pock- 
 marks result. 
 
 There may be secondary hemorrhages 
 and inflammation of the mucous mem- 
 branes; and parenchymatous degen- 
 eration of the liver, kidney and spleen. 
 
 Secondary infections with various 
 micrococci or other organisms are 
 common and may play an important 
 part in pustulation and complications 
 as septicemia, pneumonia, hemorrhag- 
 ic septicemia, erysipelas, etc. 
 
 13. VARICELLA or CHICKEN POX, is a 
 mild exanthem the etiology is even 
 less determined than that of smallpox. 
 
 II. VERMES (Worms) 
 
 1. CESTODES OR TAPE WORMS, have 
 two stages of existence, the larval 
 state, found in one species of animals 
 (the Intermediate host) and the adult 
 state, usually in another species (the 
 host). 
 
 The adult worm is found in the in- 
 testinal tract of man and lower ani- 
 mals. It consists of a head by which 
 the worm clings to the mucous sur- 
 face, neck and a body which consists 
 of separate links or progolottedes. 
 The latter are complete organisms 
 
118 PATHOLOGY. 
 
 containing a complicated hermaphro- 
 ditic genital apparatus which pro- 
 duces eggs. These are partly dis- 
 charged from the segments, into the 
 intestinal tract, through a genital 
 pore, but escape into the outer world 
 when the ripe segments are separated 
 from the body of the worm. 
 The egg or ovum encloses an imma- 
 ture larval organism which, when re- 
 ceived into a suitable host, penetrates 
 the tissues and lodges in the muscles 
 or organs and forms cysts, the well 
 known measles of measly pork, beef 
 or fish. This closes the asexual stage 
 of its life. They contain a head or 
 scolex inverted into a sac, filled with 
 a clear watery liquid. 
 When the flesh, contaminated with 
 larval worms, is eaten, the cysts are 
 disolved and the scolex fastens itself 
 upon the mucous membrane of the 
 intestine and the body of the worm, 
 is slowly or rapidly formed. 
 Tape worms may exist in the intes- 
 tines of man without causing any 
 disturbance. 
 
 Frequently digestion is interfered with 
 and pain and various reflex conditions 
 may arise which may result from the 
 worm acting as a foreign body or 
 from toxins generaled by the worm 
 normally or by its death. 
 
 a. Taenia Saginata (beef tapeworm) 
 is transmitted usually singly, to the 
 intestines of man by infected in- 
 sufficiently cooked beef. The worm 
 is from 10 to 20 feet in length with 
 100 to 2000 segments which are 
 greater in length than breadth 
 when mature. The head is 1-12 inch 
 in length, containing no rostellum 
 and no hooklets, but 4 suckers. The 
 uteras is a central canal with be- 
 tween 20 or 30 branches. 
 Papilla with genital pore is on the 
 side of the segment, alternations ir- 
 regular. Short oval ova are almost 
 mature when discharged. 
 
 b. Taenia Solium, is rare in America 
 but common in parts of Europe. It 
 is transmitted in numbers to the 
 intestine of man by infected in- 
 sufficiently cooked pork. The worm 
 
VERMES. 119 
 
 is from 7 to 10 feet in length with 
 700 to 1000 segments which are of 
 greater length than breadth when 
 mature. 
 
 The head is 1-24 inch in length. 
 Rostellum contains 26 or 28 hook- 
 lets in double row, 4 suckers. The 
 uteras is a central canal with about 
 10 branches. Papilla with genital 
 pore is situated on the side of seg- 
 ments, side alternating. 
 The ova are spherical and almost 
 mature when discharged, 
 c. Taenia Echinococcus, is transmitted 
 in numbers to the intestine of the 
 dog and wolf by infected viscera of 
 sheep. The worm is x ,4 inch in 
 length with 4 segments. 
 The head is 1-26 inch, about the 
 same as that of taenia solium but 
 smaller; has 4 suckers. The uteras 
 is a wide cavity in the last seg- 
 ment. Papilla with genital pore 
 is on the side of the last segment. 
 The ova are spherical. 
 
 Man harbors the full grown intes- 
 tinal worm, but he may also be the 
 victim of the hydrated stage, as the 
 worm in this stage inhabits the 
 intestine of the dog, its eggs may 
 accidentally be swallowed by man. 
 The larva, set free, will enter the 
 veins and become encysted in the 
 liver, rarely in the lungs, kidneys 
 and brain. 
 
 Here it developes as an ichinococcus 
 cyst, made up of an outer coat — ■ 
 ectocyst and an inner muscular coat 
 with blood vessels — endocyst — from 
 which will develope secondary or 
 daughter cysts (brood capsules) 
 from whose walls scolices grow. 
 Sometimes, even granddaughter 
 cysts are produced — (echinococcus 
 hydatidosus). 
 d. Bothriocephalus Latus, rare in the 
 United States but common in parts 
 of Europe. It is transmitted to the 
 intestine of man by insufficiently 
 cooked lake fish. 
 
 The worm is from 10 to 25 feet in 
 length with 3000 to 4000 segments, 
 which are greater in breadth than 
 in length. The head is 1-10 inch 
 
120 PATHOLOGY. 
 
 in length, club-shaped and oval, no 
 hooklets, 2 suckers. The uteras is a 
 tube, arranged in loops giving the 
 appearance of a rosette. The geni- 
 tal pore is in the center (ventral). 
 Ova are oval with operculum, im- 
 mature, develope in the water where 
 they swim about. 
 
 This worm, when in numbers, may- 
 cause intestinal obstruction. It ex- 
 cretes poisonous substances which 
 being absorbed are the cause of a 
 severe anemia. 
 e. Hymenolepis Nana (dwarf tape 
 worm), is transmitted to the intes- 
 tine of man by means of an insect 
 or snail (not certain). It is about 
 y 2 inch in length. Segmented. Head 
 is round; rostellum contains 22 or 
 30 hooklets, situated in a circle. The 
 genital pore is on the same side of 
 all the segments. The ova are oval. 
 
 2. NEMATODA OR ROUND WORMS. 
 
 a. Ascaris Iumbricoides, common 
 round worm, single or in numbers, 
 of the small intestine. 
 
 It is transmitted to man from in- 
 fected drinking water or food. 
 They may migrate to the gall ducts, 
 stomach, esphagus, larynx or nasal 
 cavities. 
 
 They are light brown in color, and 
 have a central mouth, with 3 lips, 
 at one end and taper to a point at 
 the other end. The male is about 
 6 inches in length, the female about 
 12 inches. 
 
 They are common in the tropics and 
 commonly infest unclean people, 
 children, negroes and lunatics. 
 Tne eggs are produced in great 
 numbers and develope in a month. 
 They may cause intestinal ob- 
 struction, colic, convulsions and re- 
 flex nervous disturbances. 
 
 b. Oxyuris Vermicularis (thread, seat 
 or pin worm), is very common in 
 man. The male is 24 mm. in length 
 and the female 10 mm. 
 
 The posterior end of the male is 
 
 blunt and curved, the female 
 
 elougated. 
 
 The eggs are produced in great 
 
 numbers and are oval or elleptical 
 
VERMES. 121 
 
 in shape. 
 
 It is developed directly from the 
 eggs. When ripe the female moves 
 toward the rectum and is expelled. 
 It is common in children and may 
 cause inflammatory troubles or may 
 produce a diarrhoea. A vaginitis 
 may also be produced by migration 
 of the worm. 
 
 c. Trichinella spiralis, occurs as 
 larvae in the muscles or organs of 
 man and lower animals. The adult 
 type is attained in the intestine of 
 man. The male is about 1-18 inch 
 in length; the female V 8 inch. At 
 the posterior end, there is a refract- 
 ive cloaca and two projections. 
 The encapsulated larva is eaten 
 with insufficiently cooked pork, the 
 capsule becomes disolved in the 
 stomach and they then mature in 
 the bowels in 3 days. The young 
 are hatched within the uteras, dis- 
 charged alive and pass through the 
 intestinal wall into the muscles 
 where it coils itself and becomes 
 surrounded by a capsule. The 
 complete cycle takes place in 18 
 days. 
 
 Infection of the bowel is ushered 
 in by a violent diarrhoea and vomit, 
 with occasional collapse. When in 
 the muscles (trichinosis) there is 
 fever and severe pains like that of 
 rheumatism. 
 
 d. Ankylostomum Duodenale or 
 Dochmius Duodenalis, is a round 
 worm, the female is over y 2 inch in 
 length and , twice the diameter of 
 the male which is less than y 2 inch 
 in length. 
 
 The head is rounded and armed 
 with two perpendicular and 
 four incurved teeth with which 
 it pierces and hooks itself to the 
 duodenal mucosa. It is also cuped 
 to act as a sucker. The caudal 
 end of the male is expanded. 
 The eggs are recognizable by their 
 pigmentation within the shell and 
 appear in great numbers with the 
 stools. If they meet with proper 
 conditions, as warm climate and 
 damp earth they hatch quicklv 
 
122 PATHOLOGY. 
 
 and the embryos are set free. 
 They now develop and are ready to 
 re-enter a human host by penetra- 
 tion of the skin and thence to the 
 blood vessels and is carried to the 
 lung. It here leaves the blood ves- 
 sel and undergoes further change 
 which enables it to resist the gastric 
 juice, enters an air vesicle and then 
 by means of a bronchus, the 
 trachea, osophagus and stomach fi- 
 nally reaches the small intestine 
 where sexual characters are as- 
 sumed. 
 
 The usual intestinal symptoms fol- 
 low its entrance with an addition of 
 intense anemia (egyptian chlorosis), 
 general wasting and often followed 
 by death. 
 
 e. Strongyloides Intestinalis, occurs 
 in two forms — Parasitical genera- 
 tion (auguilla intestinalis), lives in 
 the upper intestinal tract, boring 
 deeply into the mucous membrane.* 
 Eggs develop and the larvae pass 
 out with the feces and develop in 
 about 30 hours into the, — 
 
 Free living generation (anguilla ster- 
 ocoratis). There are therefore two 
 methods of reproduction, that of di- 
 rect transformation of the rhabditi- 
 form larvae into filariform and then 
 into adults and the indirect, through 
 the intermediate generation. 
 Infection occurs through tainted 
 water and food. The embryo may 
 penetrate through the skin. 
 It is common in tropical countries 
 and has recently been found in the 
 United States. 
 
 f. Trichocephalus Trichiurus or Whip 
 worm, is found in the cecum of 
 man and sometimes in the vermi- 
 form appendix and small intestine. 
 It is very common but does not 
 usually cause serious disturbances, 
 though it may bring on intestinal 
 or reflex nervous symptoms. It is 
 about % inches in length, with a 
 thin thread-like anterior portion 
 and a thicker posterior portion 
 which is curled upon itself. * 
 
 g. Filaria or Thread worms, are 
 found only in the tropics. 
 
VERMES. 123 
 
 1. Filaria Medinensis or Dracuncul- 
 us Meinensis (Guinea worm), 
 gains entrance into the intestines 
 of man through small crustaceans, 
 which they infest, which are 
 swallowed in the drinking of 
 water. 
 
 It infests the subcutaneous tis- 
 sues and the skin. It may reach 
 50 to 80 cm. in length and when 
 mature causes abscesses of the 
 skin. 
 
 2. Filaria Bancrofti or F. Sanguinis 
 horn in is (Hominis Nocturna). 
 The female is about Sy 2 inches 
 long and about 1-100 inch in dia- 
 meter. The male is shorter and 
 seldom found. The embryos ap- 
 pear in the blood, urine, lymph 
 and tissue as thread like struct- 
 ures. 
 
 The adult form (male and female 
 found together), lives in the 
 lymphatics of the legs, scro- 
 tum and retroperitoneal glands. 
 They occur only during the night, 
 unless the patient rests during 
 the day. 
 
 They generally appear in the 
 blood at about 6 P. M., and are 
 most numerous at midnight and 
 disappear completely before 7 A. 
 M. They may be in such num- 
 bers (or their eggs) as to block 
 the lymph vessels, causing statis 
 of lymph stream with enormous 
 overgrowth of the scrotum 
 (lymphscrotum, Elephantiasis 
 
 Arabum) and the neighboring tis- 
 sues. 
 
 Chyle containing filaria embryos 
 may appear in the urine from 
 rupture of the lymphatics. 
 They also cause haematuria, 
 lymph abscesses and chylous hy- 
 drocele. 
 
 They are generally transmitted to 
 man by mosquitoes sucking in- 
 fected blood and dying in drinking 
 water, in this way conveying the 
 infecton. 
 
 Filaria diurna appear in the blood 
 during the day. 
 
 Filaria Persians never leave the 
 blood. 
 
124 PATHOLOGY. 
 
 3. TREMATODES OR FLUKE WORMS, 
 
 are small flat tongue- shaped suctorial 
 worms, usually hermaphrodite with a 
 blind intestine and a ventral suck- 
 ing cup, by which it attaches itself. 
 
 a. Fasciola Hepatica, Distoma Hepati- 
 cum or Liver-fiuke, is 15 to 35 mm. 
 long and 6 to 20 mm. broad, pointed 
 at each end, with 2 suckers on an- 
 terior end and a beak-like head. 
 
 It is found in the bile-ducts and gall 
 bladder of sheep (sheep-rot), only 
 occasionally in man. 
 
 b. Opistrochis Sinensis and Feiinens 
 resemble one another and are found 
 in the bile ducts and gall bladder 
 of domestic dogs and cats, and man 
 of foreign countries. 
 
 c. Schistomum Hematobium, Distoma 
 Haematobium or biiharzia haemato- 
 bia, is found in those living along 
 the east coast of Africa. The male 
 worm is 12 to 14 mm. in length, 1 
 mm. thick. The body, back of the 
 large ventral sucker is flattened and 
 curved to form a grove in which the 
 female is attached. 
 
 The female is 16 to 18 mm. long 
 and 13 mm. thick. 
 The worm enters the body in larvae 
 condition with drinking water and 
 when developed is found in the 
 portal, splenic, mesenteric, rectal 
 and vesicle veins. 
 
 At the seat of location it causes in- 
 flammation and ulceration, and 
 hemorrhage. 
 
 In the uterus and bladder there is 
 inflammation, papillary growths, 
 deposits of urinary salts, and ob- 
 struction of ureters, with pyelitis, 
 etc. 
 III. ARTHROPODIA, air-breathing ana- 
 mal parasites belonging to the group 
 Arachnoidea and insecta are also met 
 with in man. 
 
 The purely external parasite, infesting 
 the skin are mites, — ich-mite (acarus 
 scabiei) female burrows in the skin, 
 deposits its eggs and gives rise to itch- 
 ing. Eggs are hatched and the 3^oung 
 mite continues the process; the louse 
 (pediculus) ; bed bug (cimex lectuar- 
 ius); and the flea (pulex irritans). 
 The internal parasites are 
 
THE BLOOD. 125 
 
 The larvae (Linguatula Rhinaria) 
 form of pentaslonium taenioides, 
 which is occasionally found in the liver 
 and rarely in the spleen, intestinal 
 walls, lung and kidney of man, where 
 it creates a small nodular lesion which 
 consists more or less of the degener- 
 ated parasites lying in an encapsulated 
 cheesy or semicalcified mass. 
 The adult form lodges in the nasal 
 cavities of dogs, etc. and produces eggs 
 containing the embryos which pass out 
 with the nasal secretions and in this 
 way gain access to the alimentary 
 tract of man. 
 
 The larvae of various flies are some- 
 times deposited in wounds, nasal and 
 pharynageal chambers. They develop 
 and cause local inflammation which is 
 called myiasis. 
 
 SPECIAL PATHOLOGY. 
 DISEASES OF THE BLOOD. 
 
 The ERYTHROCYTES or the RED 
 BLOOD CELLS in health are 7 to 8 m. 
 in diameter and number 5,000,000 per 
 c. mm. in man and 4,500,000 in women 
 with variations depending upon the 
 time of day and the relation to the 
 taking of food. 
 
 The WHITE CELLS or LEUCOCYTIS in 
 health vary considerably as to number 
 but may be averaged between 6,000 and 
 8,000 per c. mm. They are classified 
 according to their size and the appear- 
 ance of their nuclei; more especially, 
 however, from their reaction to aniline 
 dyes. 
 
 If the cells protoplasm is acid they have 
 an affinity for basic stains and are 
 called Basophile Cells. If they, on the 
 other hand, have an affinity for acid 
 stains they are called Acidphile, Oxy- 
 phile or Eosinophile cells. 
 Those, which react to neither stain, 
 but to a mixture of the two, are called 
 
 NeutrophFFe Cells. 
 
 Therefore we have the following classi- 
 fication 
 
126 PATHOLOGY. 
 
 1. Basophiles. 
 
 a. Lymphocytes, constitute about 22- 
 25% of the leucocytes, when over 
 this, condition is called lymphocy- 
 tosis. In size they are about the 
 same as that of the red blood cell, 
 they contain a large deeply stained 
 nucleus which almost fills the cell. 
 
 b. Large mononuclear leucocytes 
 constitute about 2-4% of the 
 leucocytes. They are about twice 
 the size of the red cell. The 
 nucleas stains poorly and is sit- 
 uated at the side of cell. Transit- 
 ional forms show neutrophilic 
 granules with lobing of the nucleus. 
 
 c. Mast Cells, constitute about 0.5% 
 of leucocytus. They may vary in 
 size and have va*rious shaped nuclei. 
 Their basophile granules are heavily 
 stained. 
 
 .2 Neutrophils constitute about 70 to 
 72%) of leucocytes. They are poly- 
 nuclear or polymorphonuclear. The 
 nucelus stains deeply. 
 
 3. Eosinophiles constitute about 2 to 4% 
 of leucocytes. They vary in size from 
 that of the red cell to the large 
 mononuclear cell. They have amoe- 
 boid movement. Bilobed nucleus 
 takes the stain faintly. Protoplas- 
 mic granules takes the stain strong- 
 ly. 
 PATHOLOGIC FORMS OF THE BLOOD 
 
 CELLS. 
 
 1. THE RED CELLS. 
 
 a. Microcytes, are 1-4 inch in diamet- 
 er, undersized and poor in haemo- 
 globin. 
 
 b. Megalocytes, are 10-20 inch in di- 
 ameter, oversized, deficient or rich 
 in haemoglobin. 
 
 c. Poikilocytes, irreguarlity of form. 
 
 d. Erythroblasts, nucleated red cells. 
 They are divided into 
 
 1. Microblasts— exceedingly small in 
 
 2. Normoblasts— size of normal red 
 cell. 
 
 3. Megaloblasts— large and irregu- 
 lar. 
 
HYDREMIA. 127 
 
 Degenerations of the nucleated red 
 cell may occur as 
 
 Karyolysis — solution of the chro- 
 matin. 
 
 Karyorrhexis — fragmentation of the 
 nucleus. 
 
 Pyknosis — clumping or condensa- 
 tion of the nuclear structure. 
 
 Granular degeneration, vacuolation 
 and nuclear atrophy. 
 
 Karyokinetic figures. 
 
 e. Shadow corpuscles, cell has lost its 
 color. 
 
 f. Ring bodies, are probably the re- 
 mains of a previous existing nu- 
 cleus. 
 
 THE WHITE CELLS. 
 
 a. Mast cells, are nearly always 
 pathologic. 
 
 b. Myelocytes, mononuclear, either 
 neutrophilic or eosinophilic, they are 
 3 or 4 times the size of the red 
 blood cells, with a large, pale, oval 
 nucleus, which is placed to one side. 
 These cells are identical with the 
 large granular cells of the bone 
 marrow. 
 
 PLETHORA, is a supposed excessive 
 quantity of blood. It has been describ- 
 ed as 
 
 1. Plethora Vera, a supposed increase 
 in the quantity of blood without any 
 change in quality. It is found in in- 
 dividuals living in luxury, who have 
 a high color and a vigorous circula- 
 tion. The term "full blooded" is now 
 applied and is probably due to fullness 
 of superficial vessels. 
 
 2. Plethora apocoptica, is a local in- 
 crease in blood. 
 
 3. Plethora hydraemica, the quanity of 
 blood is increased by dilution. 
 
 OLIGEMIA, is a reduction in the quantity 
 of blood as seen temporarily after 
 hemorrhage. It may also possibly oc- 
 cur in certain cachetic and anemic 
 diseases. 
 
 HYDREMIA, is a diluted or watery con- 
 dition of the blood from excessive 
 drinking of water, or hemorrhage, when 
 the plasma is rapidly renewed by 
 osmosis. 
 
128 PATHOLOGY. 
 
 ANHYDREMIA. The plasma of blood is 
 thickened by a loss of the watery ele- 
 ment, as a result of excessive sweating 
 or discharge of water from the bowels, 
 kidney, etc. 
 
 LIPEMFA. Fat occurs free in the blood 
 plasma, normally, to slight extent dur- 
 ing digestion and pathologically in 
 chronic nephritis, diabetes, pulmonary 
 tuberculosis, alcoholism, etc. 
 
 ME LAN EN! A. Dark pigment or granu- 
 lar matter appears in the blood as a 
 result of maleria and certain fevers. 
 
 HEMOCYTOLOYSIS, HEMOGLOB1NE- 
 
 MIA. Destruction of the red blood cell. 
 
 The haemoglobin is liberated and dis- 
 olved in the plasma. 
 
 Causes. It occurs normally in the liver 
 where the hemoglobin is changed in- 
 to bile pigment. 
 
 Pathologically it occurs in severe 
 malaria, relapsing fever, pneumonia 
 and hemorrhagic infections and var- 
 ious poisons. 
 
 Pathologic Anatomy. The blood is often 
 dark in color and shown microcytosis, 
 megalocytosis, poikelocytosis, frag- 
 mentation and vacuolation. 
 
 Pathologic Physiology. Internal respir- 
 ation is disturbed, dyspuora, various 
 nervous symptoms, increased coagul- 
 ability of the blood and formations of 
 thrombi in arteroles and capillaries. 
 
 POLYCYTHEMIA or ERYTHROCYTOS- 
 
 IS, is an increase in the number of red 
 cells. It may be 
 
 1. Actual — overproduction, which is rare. 
 
 2. Relative — from a decrease in the 
 quantity of plasma as in certain 
 cardiac conditions with slow failure of 
 compensation; residents of high alti- 
 tudes; new born; cases of cholera, etc., 
 where liquid discharges is great. 
 
 LEUCOCYTOSIS, is an increase in the 
 number of leucocytos above their normal 
 relation to the red cells. 
 Causes, it occurs 
 
 Normally in the new born, in preg- 
 nency and during digestion. 
 Pathologically in 
 
 1. Inflammatory and infectious dis- 
 eases such as croupous pneumonia, 
 
ANEMIA. 129 
 
 suppurations, inflammation of ser- 
 ous membranes as peritonitis, pleur- 
 isy, meningitis and in infectious 
 fevers generally except typhoid, in- 
 fluenza, malaria and acute tubercu- 
 losis. 
 2. Cachetic conditions, at end of 
 wasting disease, malignant tumors, 
 hemorrhage, massage and cold 
 baths, medicines. 
 
 Character of the Blood. The number 
 of leucocytes may increase moder- 
 ately, 10,000 to 20,000 or excessively 
 50,000 to 100,000 per c. mm. The 
 polymorphonuclear elements are 80 
 to 85% or may be 90 to 95% instead 
 of 65 or 70%. 
 
 Pathologic Physiology. It is probably 
 for protection. 
 
 HYPOLEUKOCYTOSIS or LEUKOPENIA 
 
 is a definciency in the number of leu- 
 coctyes, as is seen to a moderate de- 
 gree in various diseases such as tuber- 
 culosis, typhoid fever, some pneumonias, 
 cachexia, inanition, progressive per- 
 nicious anemia, etc. 
 
 Authorities do not agree as to whether 
 there is an actual leukolysis or a dis- 
 turbance in the distribution of the 
 leucocytes. 
 ANEMIA, literally want of blood, is a 
 general term for a variety of conditions 
 in which blood is wanting in one con- 
 stituent or another. 
 
 The conditions oligocythemia (reduc- 
 tion in red cells) and oligochromemia 
 (reduction in coloring matter of the 
 corpuscel) are usually associated. 
 The anemias arise from two conditions, 
 asynthesis (defective formation) and 
 haemolysis (blood destruction), and may 
 be classified into 
 1. PRIMARY ANEMIAS. 
 
 a. CHLOROSIS, "green sickness", is 
 due to retarded hemogenesis and is 
 characterized by a peculiar pallor of 
 the individual and a marked reduc- 
 tion of the haemoglobin and occurs 
 in young girls and women. 
 Causes. 
 
 Faulty developments and want of 
 proper hemogenic power. Beginning 
 menstruation. Other causes given 
 
130 PATHOLOGY. 
 
 are heredity, constitutional predispo- 
 sition, as poorly developed girls, hy- 
 poplasia of the vascular and genera- 
 tive systems, emotional excitement, 
 homesickness, grief, intestinal intox- 
 ications, constipation and menstrual 
 disorders. 
 
 Pathologic Anatomy. 
 
 The blood is paler than normal and 
 watery. Sp. gr. is low, coagulability 
 is increased and number of red cells 
 may be normal, but the proportion of 
 hemaglobin is decreased in amount. 
 In prolonged cases the number of red 
 cells are reduced in number, and the 
 hemaglobin is from 30 to 20%. The 
 cells may be irregular and nucleated. 
 Secondary diseases may develop, as 
 myocardiac degenerations and dilata- 
 tion. The spleen is frequently slight- 
 ly enlarged. The skin is yellowish or 
 greenish. 
 
 Pathologic Physiology. It resembles 
 the secondary anemias so far as the 
 general health is concerned. 
 
 b. PROGRESSIVE PERNICIOUS ANE- 
 MIA is an anemia which tends to 
 increase in severity to a fatal end. 
 It shows no deficiency of hemo- 
 globin, but an enormous destruction 
 of the red cells. 
 
 It occurs in childhood or old age, but 
 
 generally in middle age. 
 
 Causes. Pregnancy, lactation, gastro- 
 intestinal disease of various sorts 
 from ulcerations to carcinoma, etc., 
 and intoxications to the various 
 parasites, hemorrhages, systemic 
 diseases, as syphilis, malaria, tuber- 
 culosis, etc. Depressing emotions, 
 fright, exposure and unsanitary 
 surroundings act as contributary 
 causes. 
 
 Pathologic Anatomy. The blood is 
 pale in color, though it may be 
 dark. Sp. gr. is reduced. Oli- 
 gocythemia progresses rapidly, the 
 red corpuscles may sink to 1,000,000 
 or less. Microcytes, megalocytes, 
 poikilocytes, microblasts, normo- 
 blasts and megaloblasts are present, 
 with a preponderance of the latter 
 form as a rule. Karyokinetic fig- 
 
LEUKEMIA. 131 
 
 ures and polychromatphilia are 
 also present. 
 
 Secondary changes: The marrow of 
 the long bones is red, softened and 
 often hemorrhagic. The spleen is 
 sometimes enlarged. The liver, 
 kidneys and heart undergoes fatty 
 degeneration, which also frequently 
 causes punctate hemorrhages from 
 the blood vessels. There may also 
 be a degeneration of the posterior 
 and lateral columns of the cord. 
 
 There is pigmentation of the liver, 
 spleen and kidneys and other or- 
 gans from the active hemolysis. 
 
 c. LEUKEMIA or LEUCOCYTHEMIA 
 
 is a disease of the hemogenic organs. 
 It is characterized by an increase in 
 the number of leucocytes and the 
 pathologic changes in the bone mar- 
 row, spleen and lymphatic glands. 
 
 Causes. Infection of some nature. 
 Diseases such as syphilis, malaria, 
 rickets, etc., and probably heredity, 
 may be regarded as predisposing 
 causes. 
 
 Pathologic Anatomy. 
 
 The blood is light in color. Sp. gr. 
 is lowered, the alkaline reactive is 
 less decided and coagulation is 
 slow. The number of leucocytes 
 varies from 100,000 to 300,000 per 
 c. mm. in moderate cases to 1,000,000 
 or more in severe cases. The nor- 
 mal ratio of 1 white cell to 450 red 
 may become 1 to 10 or even 1 to 1. 
 
 The lesions of the solid organs occur 
 principally in the spleen, bone mar- 
 row and lymphatic glands. There- 
 fore the terms lienal or splenic, 
 medullary or myelogenous and 
 
 lymphatic leukemia are applied. 
 
 Primarily, all forms of leukemia 
 probably begin in the bone mar- 
 row. 
 
 No sharp distinction can be made 
 because the forms are generally 
 mixed, but as a suggestion to the 
 tissues most affected leukemia may 
 be divided into two types — 
 1. Splenomedullary or Splenomye- 
 logenous or Myeloid form shows 
 changes in the spleen and the 
 
132 PATHOLOGY. 
 
 bone marrow. The spleen is en- 
 larged and dense from hyper- 
 plasia of the Malpighian tufts 
 and infiltration with masses of 
 leucocytes. 
 
 Hemorrhages, infarction, degenera- 
 tion and necrosis may result. 
 
 The bone marrow also shows hy- 
 perplasia. The proportion of the 
 white cells to the red are 1 to 3 
 or 1 to 2 or even 1 to 1. Large 
 mononuclear leucocytes predom- 
 inate over the lymphocytes and 
 the polymorphonuclear elements 
 which are also increased. The 
 myelocytes are usually present in 
 great numbers. The eosinophiles 
 are increased, but not in per- 
 centage proportion. Mast cells 
 are present in excess of those 
 found in health. Karyokinetic 
 leucocytes are found in small 
 numbers. 
 
 2. Lymphatic form or Lymphatic 
 leukemia involves the lymph 
 glands. These are hyperplastic 
 and may enlarge to the size of 
 hen eggs. The spleen escapes. 
 Leucocytosis is not so marked 
 as it is in the myeloid type. The 
 lymphocytes predominate. There 
 is also an increase in the large 
 mononuclear and the polymorpho- 
 nuclear also. 
 
 Myelocytes occur in small numbers. 
 Nucleated red cells may be pres- 
 ent. 
 
 Acute Lymphatic leukemia strongly 
 suggests an infectious condition. 
 Its duration is from a few weeks 
 to a few months. 
 
 Secondary lesions, as lymphoid in- 
 filtrations of the liver, kidneys, 
 lungs, heart and other tissues, 
 are noted in the lymphatic form, 
 and secondary degenerations of 
 heart, liver and kidneys may re- 
 sult. Sclerosis of the spinal cord 
 may also be met with. 
 
 Pathologic Physiology. It is progres- 
 sively destructive. The blood con- 
 tains toxic substances, as xanthin 
 bodies and acids. Albumoses are 
 
ANEMIA. 133 
 
 present. Urine may contain an ex- 
 cess of xanthin bases and uric acid. 
 
 d. HODGKINS' DISEASE (Pseudoleu- 
 kemia) (see infections) stimulates 
 true leukemia in the enlargement of 
 the lymph glands, but there is no, or 
 a very moderate, increase in the 
 number of leucocytes. 
 
 2. SECONDARY ANEMIA, or SYMPTO- 
 MATIC ANEMIA, designates anemic 
 conditions due to some underlying 
 disease. 
 
 Cause. 
 
 Hemorrhage; parasites in the in- 
 testine or in the blood; infectious 
 diseases; poisons, such as lead, 
 arsenic, phosphorous, coal-tar prod- 
 ucts, etc.; organic diseases, and 
 new growths, and unsanitary con- 
 ditions. 
 
 Pathologic Anatomy. The condition 
 of the blood varies according to 
 the nature of the anemia. In 
 moderate cases the number of red 
 cells are 4,000,000 to 3,000,000 per 
 C. mm., with the haemoglobin 
 correspondingly reduced. In the 
 graver forms the red cells are 
 decreased to 2,500,000 or 2,000,000 
 per C. mm., with the haemo- 
 globin very markedly reduced. 
 The blood is pale and the corpus- 
 cles show various irregularities. 
 A small number of nucleated red 
 cells may be present. The lymph- 
 ocytes may increase relatively 
 and actually in severe cases. The 
 myelocytes may be present. 
 Parenchymatous and fatty degen- 
 eration of the heart, kidneys and 
 liver may be associated. 
 
 Pathologic Physiology. The con- 
 sumption of oxygen and the elim- 
 ination of carbon dioxide are nor- 
 mal, but to accomplish this more 
 active circulation and greater 
 energy of the tissues are needed. 
 This may cause the degeneration 
 of organs stated above and also 
 the characteristic symptoms, as 
 dyspnoea, palpitations, etc. 
 
 * In the severe forms there is an 
 increased tissue waste and 
 
134 PATHOLOGY. 
 
 greater discharge of nitrogen 
 than is digested. 
 
 DISEASES OF THE LYMPHATIC 
 TISSUES. 
 
 SPLEEN. 
 
 1. Abnormal Development and Situation. 
 
 It may be absent or there may be 
 accessory spleens, or there may be a 
 number of small bodies (spleens). 
 It may be freely movable as a float- 
 ing spleen. In this case a twisting 
 of the pedicle may cause its strangu- 
 lation. 
 
 2. Vascular Disturbances. 
 
 a. Anemia, from general anemia. The 
 
 spleen is small, firmer and paler 
 than normal. 
 
 b. Hyperaemia. 
 
 1. Active during digestion or from 
 
 intense congestion. 
 
 2. Passive, seen in cirrhosis of liver, 
 
 cardiac failure, emphysema or the 
 obstruction to large venous chan- 
 nels. 
 
 The spleen is large, dark red and 
 the capsule is distended; later 
 there is thickening of the cap- 
 sule and trabeculae, with subse- 
 quent contraction, and is then 
 called cyanotic induration. 
 
 Hemorrhages, embolism, infarction, 
 etc., also occur. Thrombosis of 
 the spleenic vein may also occur. 
 Calcified thrombi are called 
 spleenic stones. 
 
 3. Inflammations, or Spleenitis, may be 
 
 divided into — 
 a. Diffuse Spleenitis. Enlargement of 
 the spleen occurs during the course 
 of infectious diseases, such as 
 typhoid, malaria, septicemia, ty- 
 phus and relapsing fevers, and to 
 less extent in pneumonia, scarlet 
 fever, smallpox and influenza. 
 
 There is at first a congestion, and 
 if the process advances the spleen 
 may become soft. On section it is 
 lighter in color than normal. The 
 capsule may be distended or 
 wrinkled. 
 
THE SPLEEN. 135 
 
 The cells of the spleenic pulp are 
 increased, and there is a hyper- 
 plasia of the stroma, trabeculae 
 and endothelial cells of spaces. In 
 the later stages degenerations may 
 become prominent. 
 
 It frequently terminates in complete 
 resolution. It may, however, per- 
 sist, or frequent infection may 
 cause chronic inflammatory hyper- 
 plasia, as seen in the so-called 
 ague cake spleen of malaria. 
 
 Rupture from distention or suppura- 
 tion may also occur. 
 
 b. Circumscribed Spleenitis, or Ab- 
 scess of the spleen, may be caused 
 by an acute diffuse spleenitis, or 
 by an extension from neighboring 
 structures, as septic emboli or 
 traumatic injuries. 
 
 Abscess may also result from per- 
 foration of gastric ulcers or in- 
 flammation from other places. 
 
 Small abscesses may be absorbed or 
 inspissated with a cheesy or ne- 
 crotic residue. Large abscesses 
 may be discharged by perforation 
 into the stomach or intestines, or 
 break into the peritoneal or pleural 
 cavities, causing septic inflamma- 
 tions of same. 
 
 4. Atrophy of the pulp and proliferation 
 
 of the stroma is met with in old age. 
 The capsule is thickened and 
 wrinkled. 
 
 5. Degenerations. 
 
 a. Amyloid begins in the Malpighian 
 bodies and walls of blood vessels. 
 They are pale and grayish in color, 
 resembling boiled sago, the so-called 
 Sago-grain spleen. 
 
 b. Hyaline, associated with the amy- 
 
 loid and independent of the latter. 
 
 6. Pigmentation results from chronic con- 
 
 gestion or repeated attacks of acute 
 spleenitis. 
 The pigment may also enter from with- 
 out through the circulation. 
 
 7. Calcification in the capsule results 
 
 from chronic snleenitis, infarcts, tu- 
 bercular or syphilitic areas and para- 
 sitic cysts. 
 
 8. Tumors. Lymphadenoma, primary and 
 
136 PATHOLOGY. 
 
 secondary sarcoma, secondary car- 
 cinoma, endothelioma, cysts, fibroma, 
 angioma and lymphangioma. 
 
 9. Parasites, echinococcus, cysts, and 
 cysticerci. 
 
 10. Infectious diseases, tuberculosis and 
 syphilis. 
 
 LYMPHATIC GLANDS. 
 
 1. Atrophy, from old age and various 
 
 marasmic conditions. 
 
 2. Hypertrophy, very closely allied to 
 
 lymphadenoma. 
 
 3. Degenerations. Patty, amyloid, hya- 
 
 line, calcification, necrosis and pig- 
 mentation. 
 
 4. Lymphadenitis, or Inflammation of the 
 
 lymph glands. 
 
 a. Acute is due to irritants being car- 
 
 ried through the lymph channels 
 or blood vessels as a result of some 
 local or general infection. 
 
 The glands are enlarged and con- 
 gested. There is an accumulation 
 of leucocytes, a desquamation of 
 the cells of the sinuses and an ex- 
 udate of lymph. 
 
 It may end in resolution, or when 
 the infective cause is of great in- 
 tensity necrosis or suppuration may 
 occur. 
 
 b. Chronic Lymphadenitis may follow 
 
 from the acute form or from con- 
 stant irritation of inhaled particles, 
 or digestive disturbances caused by 
 improper food, or long-continued 
 irritation by particles carried from 
 some focus of disease. 
 
 5. Infectious Diseases. 
 
 a. Tuberculosis (Scrofulous glands). It 
 
 appears as small grayish nodules 
 within the gland, sometimes with 
 hyperemia and inflammation. They 
 increase in size and undergo case- 
 ous changes. Eventually the entire 
 gland is converted into a cheesy 
 mass, which may liquefy and dis- 
 charge through the ruptured cap- 
 sule. 
 
 b. Syphilis. The enlarged glands are 
 
 not so great as those of tubercu- 
 losis. They remain hard and do 
 not suppurate. In the tertiary 
 period gummata (bubo tertiaris) 
 
Fig-. 24. Tuberculous lymphatic gland; 
 
 a, recent tubercle with giant cell (c) ; 
 a, inferior caseous tubercle with giant 
 cell (c) ; b, lymphadenoid tissue; d, 
 epithelioid cell. (Ziegler.) 
 
THYMUS GLAND. 137 
 
 may be seen, especially in the 
 glands near diseased viscera. 
 
 c. Leprosy and Actinomycosis may also 
 involve the glands. 
 
 6. Tumors. Lymphadenoma or lympho- 
 sarcoma, primary and secondary sar- 
 coma and secondary carcinoma. 
 
 BONE MARROW. 
 
 1. Atrophy, in old age and marasmic con- 
 
 ditions. 
 
 2. Hpertrophy, in anemic diseases. 
 
 The marrow becomes soft and red in 
 color. In extreme cases it may be 
 dark red and liquid. Fat cells may 
 be greatly reduced or wanting and 
 various sized marrow cells take their 
 place. Pigment cells or red corpus- 
 cles and nucleated red cells are also 
 seen. 
 
 3. Degenerations. 
 
 a. Fatty infiltration, from general 
 
 obesity, also seen in marantic in- 
 dividuals or atrophy of bony tis- 
 tues. 
 
 b. Mucoid degeneration and necrosis 
 
 may be part of inflammation. 
 
 c. Pigmentation from blood destruc- 
 
 tion. 
 
 4. Osteomyelitis, or Inflammation of the 
 
 marrow, is of an infectious origin and 
 occurs during the course of various 
 infectious diseases, or as a result of 
 traumatism and direct infection. 
 
 The usual changes met with in inflam- 
 mation elsewhere is characteristic 
 here. 
 
 The marrow is redder than normal, and 
 generally there is punctate hemor- 
 rhage. 
 
 The white corpuscles or lymphoid cells 
 are increased. Areas of necrosis and 
 granular degeneration of cells may 
 be seen. The marrow may be puru- 
 lent. 
 THYMUS GLAND. 
 
 1. Congenital Abnormalities. The gland 
 
 may be absent, irregular or hyper- 
 trophied. 
 
 2. Vascular Disturbances. Congestion 
 
 and punctate hemorrhages have been 
 seen in death from asphyxia. 
 
138 PATHOLOGY. 
 
 3. Inflammation. Abscesses from general 
 
 pyemia or extension of suppurative 
 affections. 
 
 4. Infectious Diseases. Syphilis, as gum- 
 
 mata in the new born. The gumma 
 may caseate and soften so as to re- 
 semble an abscess. 
 Miliary or caseous tuberculosis may 
 also invade the gland. 
 
 5. Tumors. Lymphosarcoma, round-cell 
 
 sarcoma and epithelioma. 
 
 DISEASES OF THE CIRCULATORY 
 SYSTEM. 
 
 HEART. 
 
 1. Congenital Diseases and Deformities. 
 
 a. Abnormalities in position and size. 
 
 b. Defective development. 
 
 1. Auriculo-ventricular septa may be 
 
 wanting, etc. 
 
 2. Stenosis and atresia of the pul- 
 
 monary artery, aorta and auricu- 
 loventricular orifices. 
 
 3. Defective ventricular or auricular 
 
 septum. 
 
 4. Patulous Ductus Botalli. 
 
 5. Valvular defects, as but two semi- 
 
 lunar valves at aortic or pulmo- 
 nary orifices, etc. 
 Pathologic Physiology. These con- 
 ditions disturb the circulation, 
 overfill the venous channels, 
 produce an abnormal mixture 
 of venous and arterial blood 
 and congenital cyanosis and 
 morbus coerulens (blueness or 
 cyanosis) results. 
 Imperfect circulation causes 
 thickening of lips and nose and 
 clubbing of the finger ends, etc. 
 
 2. Circulatory Disturbances. 
 
 a. Thrombosis of Cavities of the Heart. 
 When thrombi are formed some 
 time before death they appear as 
 deposits upon the heart wall, are 
 yellowish or whitish in color and 
 are attached between the muscu- 
 lar trabeculae. 
 Secondary changes of the thrombi, 
 as softening, may cause cyst-lil*^ 
 cavities to be formed. 
 
THE HEART. 139 
 
 The thrombi may project from the 
 surface in polypoid, form, or they 
 may be free ball thrombi or globu- 
 lar thrombi. 
 
 The condition may disturb the cir- 
 culation by weakening the heart 
 muscle or by obstruction of the 
 valve orifices. It may also lead to 
 embolism. 
 
 b. Thrombosis and Embolism of the 
 Coronary Arteries. 
 
 When an embolism lodges or a 
 thrombus is formed in the artery 
 the area supplied by the artery be- 
 comes anemic. The muscular fibers 
 of the area becomes white, then 
 yellow from softening, and. is called 
 Myomalacia cordis. 
 
 Small areas may heal by absorbtion 
 with the formation of a scar, which 
 may remain or lead to aneurysmal 
 dilatation or the rupture of the 
 heart may take place. 
 
 3. Atrophy. Seen in advanced age. 
 
 though it may be seen in the young. 
 It results from senility and cachetic 
 or wasting diseases, as tuberculosis, 
 carcinoma, etc. 
 
 The heart is small and the capsule 
 is wrinkled and thickened. The ves- 
 sels are tortuous. The muscle fibers 
 are small and contain pigment. 
 
 4. Hypertrophy and dilatation are usually 
 
 associated and result from the same 
 causes, as general over- stimulation 
 as in hysteria, exopthalmic goitre, 
 etc.; excessive eating and drinking; 
 excessive beer drinking, and peri- 
 cardial adhesions. 
 
 Sudden strains may cause acute dila- 
 tation, and when the heart is de- 
 generated the sudden strain may 
 cause pure acute dilatation as seen 
 in the course of infectious fevers. 
 
 Causes acting on the left ventricle are 
 arteriosclerosis, aneurysms of aorta, 
 chronic Bright' s disease and exces- 
 sive exercise or laborious occupations, 
 as blacksmithing, etc. Causes acting 
 upon the right ventricle are emphy- 
 sema, fibroid phthisis and pleural 
 
140 PATHOLOGY. 
 
 synechiae. 
 Pathologic Anatomy. 
 
 a. Concentric hypertrophy, The 
 
 walls are thickened and the cavi- 
 ties are somewhat smaller than 
 normal. 
 
 b. Simple hypertrophy. The walls 
 
 are thickened, but the cavities are 
 normal. 
 
 c. Eccentric hypertrophy or Hyper- 
 trophy with dilatation. The walls 
 are thickened and the cavities are 
 increased in size. 
 
 d. Pure dilatation, without any hy- 
 pertrophy. 
 
 5. Diseases of the Endocardium. 
 
 a. Acute endocarditis, generally affects 
 the endocardium of the valves, but 
 the endocardium of the cavities may 
 also be affected. 
 
 Causes. Various micro-organisms, 
 acute rheumatism, scarlet fever, 
 pneumonia, puerperal sepsis, Bright's 
 disease and malnutrition from carcin- 
 oma and nervous affections. 
 Pathologic Anatomy. The common 
 seats of acute endocarditis in order of 
 frequency are the mitral valve, 
 aortic valve, pulmonary valve, endo- 
 cardium of left ventricle, left auricle 
 and right ventricle. 
 It may be divided into 
 
 1. Simple or verrucose or beingn en- 
 docarditis. First there is an opaque 
 area, later small nodules, like beads, 
 appear and finally these assume 
 wart-like fibrous elevations. 
 
 2. Ulcerative, septic, mycotic, diph- 
 theritic, or malignant endocarditis, 
 appears as very irrgeular fibrinous 
 deposits, or there may be no de- 
 posit, or if present it may be de- 
 tached and necrosis and ulceration 
 of endocardium follows. Secondary 
 deposits of fibrin may cover the ul- 
 cer or the fibrin may be heaped up 
 at the edges of the ulcer. 
 
 The simple form may be healed by 
 gradual absorbtion or the breaking 
 off of the deposit and its dissemina- 
 tion in the circulation. The endo- 
 cardium is thickened bv fibro-blastin 
 
THE HEART. 141 
 
 cells and connective tissue. If the 
 process is deep, the area involved 
 will be distorted. Large deposits 
 may calcify and remain. An entire 
 valve or cordae tendineae may be 
 destroyed or aneurysms may be 
 formed by the penetration of one 
 layer only. 
 
 The malignant type affecting the 
 endocardium of the cavities may 
 lead to myocarditis. 
 
 The most serious danger is embol- 
 ism. 
 
 Pathologic Physiology. Acute endo- 
 carditis may be the center of disem- 
 ination of infectious material, and 
 disease may run its course as an 
 obscure septicemia. 
 
 b. Chronic Endocarditis, usually affects 
 the valves of the heart, distorting 
 them, and constitutes chronic valvular 
 heart disease. 
 
 Causes. It may continue from the 
 acute or it may be chronic from the 
 onset as arteriosclerosis and athero- 
 ma. Advanced years and laborious 
 occupation, chronic alcoholism, gout, 
 lead poisoning, syphilis, diabetes, etc., 
 are also causative agents. 
 
 Pathologic Anatomy. There is slow 
 connective tissue growth in the sub- 
 stance of the valves. The valves may 
 unite by their surface vegetations, 
 causing stenosis, or there may be a 
 deposit of lime which causes further 
 rigidity. Pieces of the vegetation or 
 the calcareous valve may become de- 
 tached and cause embolism in other 
 organs. 
 
 Hypertrophy of the heart results. This 
 of course varies with the condition 
 of health and with the seriousness 
 of the lesion. If the general health is 
 good, there will generally be com- 
 mensurately adequate hypertrophy, 
 and if the lesion is not sufficient to 
 interfere with the circulation of the 
 coronary arteries, hypertrophy is well 
 maintained. 
 
 Eventually however the heart muscle 
 degenerates, the cavities dilate and 
 the circulation fails. This leads to 
 
142 PATHOLOGY. 
 
 changes in the lungs, liver and kid- 
 neys. 
 
 Pathologic Physiology. Chronic en- 
 docarditis (valvular disease) causes 
 more or less profound mechanical dis- 
 orders of the circulation, the severity 
 depending upon the condition of the 
 heart muscle more than upon the se- 
 verity of the valve lesion. 
 "When compensatory hypertrophy fails 
 various organs of the body suffer con- 
 gestion. The lungs are first to suffer, 
 if the lesion is of the left heart, prop- 
 er respiration is prevented and 
 dyspnea (cardiac asthma), cough and 
 expectoration results. In extreme 
 cases, edematous exudation and 
 cyanotic induration takes place. 
 
 When the right fails, the liver, spleen, 
 gastrointestinal mucosa, kidneys and 
 peripheral circulation is congested. 
 Metabolic disturbances occur and the 
 respiratory exchange of gases is re- 
 duced. 
 
 6. Diseases of the Myocardium. 
 
 a. Circulatory Disturbances. 
 
 1. Anemia, from general anemia and 
 obstruction of the coronary arteries. 
 
 2. Hyperemia, from obstruction of re- 
 turn blood to the right heart and 
 failure of compensation in disease 
 of heart. 
 
 3. Hemorrhages, from obstruction to 
 coronary arteries, intense my- 
 ocarditis, surrounding abscesses or 
 hemorrhagic diathesis and various 
 intoxications. 
 
 b. Degenerations. Parenchymatous or 
 cloudy swelling, Amyloid, hyaline, 
 fatty infiltration or obesetas cordis 
 and fatty degeneration. 
 
 s. Myocarditis or Inflammation of the 
 heart muscle, may be divided into 
 
 l.Acute myocarditis, 
 a. Acute circumscribed M., or ab- 
 scess of the heart occurs in con- 
 nection with penetrating endo- 
 cardial lesions or associated with 
 pericarditis. The infection gen- 
 erally takes place through the 
 coronary circulation. 
 
THE HEART. 143 
 
 b. Acute Diffuse M., occurs in var- 
 ious forms of infectious fevers as 
 in typhoid fever, diphtheria, scar- 
 let fever, acute rheumatism, 
 puerperal sepsis, etc. 
 
 Under favorable conditions the acute 
 diffuse and non suppurative form 
 will terminate in resolution. Pro- 
 liferative changes, however, are 
 likely to advance to organization 
 and the formation of localized areas 
 of sclerosis. Death may be caused 
 by dilatation of the cavities and 
 cardiac failure. 
 
 2. Chronic myocarditis or Fibrous 
 myocarditis may be diffuse or cir- 
 cumscribed. 
 
 Causes. It may be primary but gen- 
 erally secondary and is dependent 
 upon the interference with the 
 coronary circulation and alterations 
 in the character of the blood sup- 
 ply, as in areas of sclerosis and 
 atheroma of the coronary or when 
 the blood supply to the arteries is 
 interfered with by faulty heart 
 valves. 
 
 There is a slow general or local 
 production of connective tissue and 
 the muscle atrophies and disappears. 
 
 The heart becomes less contractile, 
 from the muscular loss and more 
 rigid from the increase of con- 
 nective tissue, with the degenera- 
 tion of muscle fibers, in conse- 
 quence of the pressure of the new 
 formed tissue, dilatation may take 
 place if the area is extensive. 
 
 Angina pectoris, is a paroxysm of 
 se^ ere uniform pain which occurs in 
 consequence of the fibroid heart. 
 This is particularly marked when 
 fibroid heart is associated with ad- 
 vanced sclerosis of the coronary 
 arteries. The cause of the pain is 
 uncertain. It may be due to em- 
 bolism or thrombosis of the branch- 
 es of the coronary arteries. 
 
 7. Infectious Diseases. 
 
 Tuberculosis, occurs as acute mili- 
 ary tuberculosis and as caseous 
 tubercules from tubercular adenitis. 
 
144 PATHOLOGY. 
 
 Syphilis, is rare, but gummata may 
 be present. 
 
 Actinomycosis, by extension or 
 embolism. 
 
 8. Tumors. The primary are rare. 
 Sarcoma, fibroma, lipoma, myxo- 
 ma and myoma. Secondary are 
 more common, sarcomata and 
 carcinomata. 
 
 9. Parasites. Echinococcus cysts and 
 cysticerci of taenia. 
 
 PERICARDIUM. 
 1. Pericarditis. 
 Causes. 
 
 a. Primary, are due to irritants car- 
 ried by the blood as in rheumatism, 
 scarlet fever, small pox, influenza 
 and intense septic infections, and 
 acute or chronic nephritis. 
 
 b. Secondary, are due to extensions of 
 inflammation from the pleura, lung, 
 mediastinal glands, sternum, 
 esophagus, stomach or the heart. 
 
 Pathologic Anatomy. 
 
 a. Fibrinous or Dry pericarditis. 
 
 b. Serofibrinous Pericarditis. 
 
 c. Purulent Pericarditis or Pyoperi- 
 cardium. 
 
 d. Hemorrhagic Pericarditis, seen in 
 persons of lowered vitality or those 
 suffering from scurvy, purpura, etc. 
 The pericarditis accompanying 
 tuberculosis or cancer of the 
 pericardium is prone to this type. 
 
 Termination. Any of the forms may 
 persist for a considerable time with- 
 out change. The fibrinous or the 
 serofibrinous, after the absorbtion 
 of the liquid, variety may produce 
 an agglutination of the visceral and 
 parietal pericardium, with a grad- 
 ual extension of the inflammatory 
 process till there is fibrous adhes- 
 ions binding the two layers and at 
 times with complete obliteration of 
 the sac. 
 
 If the inflammation is slight and the 
 layers are kept apart by the serous 
 exudate the areas of inflammation 
 become thickened by new-formed 
 
THE ARTERIES. 145 
 
 fibrous tissue and sclerotic spots re- 
 main upon the surface of the peri- 
 cardium and are often called milk 
 spots, or portions of the fibrinous 
 exudate may remain unabsorbed 
 and with the thickened membrane 
 suffer calcareous infiltration. 
 
 The purulent form may be discharged 
 by rupture, into the esophagus, 
 stomach, pleura or even the bron- 
 chi, with subsequent adhesions of 
 the two layers of the sac. Grad- 
 ual inspissation may also take place 
 and the cheesy residue may re- 
 main or become calcareous. 
 
 Pericarditis may also occasion dis- 
 ease of the neighboring structures. 
 
 It is always accompanied by some 
 superficial myocarditis. 
 
 2. Infectious Diseases. Tuberculosis, 
 syphilis and actinomcosis *may also 
 affect the pericardium. 
 
 3. TUmors. Secondary carcinoma and 
 sarcoma. Lipoma and fibroma are 
 rare. 
 
 4. Parasites. Hydatid cysts and sys- 
 tecerci are occasionally seen. 
 
 5. Pneumopericardium, from perfora- 
 tion of sac, in fracture of ribs or 
 foreign bodies or from the rupture 
 of ulcers of esophagus or stomach. 
 
 ARTERIES. 
 
 1. Hypertrophy, as seen in established 
 
 collateral circulation. 
 
 2. Atrophy. Seen in general atrophy of a 
 
 part or from pressure or anemic 
 areas. 
 
 3. Degenerations. Fatty degeneration, 
 
 calcareous infiltration, hyaline and 
 amyloid degenerations. 
 
 4. Inflammations. 
 
 a. Acute Suppuration or Necrotic Ar- 
 teritis. Seen in areas of suppura- 
 tive inflammation from extension 
 or from lodgment of infected em- 
 boli or infection of thrombi within 
 the vessel wall. When extension is 
 from without, the adventitia and 
 then the media undergo round cell 
 infiltration and collections of pus 
 may be seen in the larger vessels. 
 
146 PATHOLOGY. 
 
 It may extend to the intima and 
 even perforate the vessels and cause 
 hemorrhage. 
 The suppurative process does not di- 
 rectly involve the intima, but leu- 
 cocytes emigrate into it and cause 
 degenerative changes. 
 
 When the process begins from with- 
 in, as through softened thrombi or 
 infectious emboli, there is first ne- 
 crotic or degenerative destruction 
 of the intima and the subsequent 
 round cell infiltration of the media 
 and adventitia. 
 
 b. Acute productive arteritis occurs 
 
 from thrombosis within the non- 
 infected blood vessel and is called 
 thrombo-arteritis. It is by this 
 means that wounds of vessels, etc., 
 are closed. 
 
 It also results from tissue changes 
 surrounding the arteries, in diseases 
 of organs leading to connective tis- 
 sue overgrowth. The condition is 
 chronic rather than acute. 
 
 Peri arteritis nodosa, or Arteritis no- 
 dosa proliferans, is a rare form 
 leading to the formation of fibrous 
 nodules. It affects the entire thick- 
 ness of the wall and shows nodose 
 thickening of the adventitia. 
 
 c. Arteriosclerosis, Endarteritis chron- 
 
 ica deformans, Atheroma, is a 
 
 chronic degenerative and inflamma- 
 tory disease of the arteries. 
 Causes. It is a physiologic process 
 of old age. It generally begins at 
 middle life. When it is severe 
 and begins early it may be due 
 to syphilis, gout, chronic alcohol- 
 ism and chronic nephritis. Mus- 
 cular exertion, cachexia from 
 carcinoma, tuberculosis or in- 
 anition. It may follow acute in- 
 fections. 
 
 Pathologic Anatomy. 
 
 1. Circumscribed or nodular is com- 
 mon in the aorta and large ves- 
 sels. Small nodular elevations are 
 formed on the inner lining of the 
 vessels. They are first of a trans- 
 lucent, grayish color and are cov- 
 
THE ARTERIES. 147 
 
 ered by unchanged endothelium, 
 later they degenerate and become 
 a dull white or yellowish color, 
 then harden with calcification 
 (atheromatous plate). It may, 
 however, undergo degenerative 
 softening and break into the ves- 
 sel, leaving a necrotic, ulcerated 
 patch (atheromatous ulcer). This 
 may now be followed by a cal- 
 careous change with fibrinous 
 deposits over its surface. The 
 sclerosed areas may be few and 
 separated, or they may be nu- 
 merous and thickly set. 
 
 Microscopically, the nodules con- 
 * sist of dense sclerotic tissue. The 
 intercellular substance becomes 
 hyaline in character, then the 
 cells undergo fatty degeneration. 
 Then the whole area suffers fatty 
 or myxomatous degeneration and 
 breaks down into a mass in which 
 fat drops and cholesterin plates 
 are found. Calcareous material is 
 now deposited. 
 
 2. Diffuse affects more or less uni- 
 formly a large part of the ar- 
 terial system. The changes re- 
 semble those of the nodular form. 
 There is a widespread thicken- 
 ing of the arterial coats, which at 
 first affects only the subendothe- 
 lia, but later the entire wall. 
 
 In the diffuse form the media may 
 suffer fatty degeneration and cal- 
 cification with hypertrophy of the 
 muscle fibers. A connective tis- 
 sue hyperplasia may be seen in 
 the adventitia. 
 
 In the nodular form the media is 
 usually thinner than normal. 
 
 In the smaller vessels hyperplasia 
 of the intima may almost com- 
 pletely close the vessels (endar- 
 teritis obliterans). The vessels 
 may be completely closed by a 
 union of the vessel walls or by 
 the formation of a thrombus and 
 its organization. 
 
 In the larger vessels the loss of 
 elasticity by the fibrous tissue 
 formation and degenerations may 
 
148 PATHOLOGY. 
 
 lead to diffuse dilation of the ves- 
 sel or localized aneurysmal sacs. 
 The vessels may rupture spon- 
 taneously. Thrombi may be dis- 
 charged into the circulation and 
 become emboli. 
 
 Diffuse arteriosclerosis is followed 
 by hypertrophy of the heart. 
 
 When small vessels of various or- 
 gans are involved degeneration 
 and reactive connective tissue hy- 
 perplasia results. This is seen in 
 softening of the brain and fibroid 
 changes in the heart and kidney. 
 
 5. Infectious diseases, syphilis and tuber- 
 
 culosis may also attack the arteries. 
 
 6. Aneurysm is a more or less local dila- 
 
 tation of an arterial wall and may 
 be divided into — 
 
 a. False or Spurious Aneurysm, due to 
 
 rupture of the vessel and the en- 
 closing of the blood outside the 
 artery by an adventitious wall. It 
 generally results from trauma. A 
 blood tumor or hematoma may be 
 formed. When an artery and vein 
 are injured the blood may enter the 
 vein and distend it .(aneurysmal 
 varix). If the artery and vein com- 
 municate by an intermediate sac it 
 is called varicose aneurysm. 
 
 6. True Aneurysm is the dilatation of 
 the arterial walls. 
 
 Causes. Weakened vessel wall and 
 blood pressure from any cause. 
 It is most common in those whose 
 arteries are sclerosed, the causes 
 of which may also be given here, 
 though a hereditary weakness of 
 the arterial coats might also be 
 considered as congenital aneu- 
 rysms have been seen. 
 However, aneurysms appear gener- 
 ally at that period of life when 
 early senile change and excessive 
 muscular exertion overlap one an- 
 other. 
 Acute degenerative changes may 
 also lead to aneurysm. It may 
 also result from traumatism. 
 
 Pathologic Anatomy. Aneurysms may 
 
ANEURYSM. 14'J 
 
 be divided into three varieties — 
 
 i. Ectatic aneurysm is a more or less 
 uniform dilatation of all the coats 
 of the vessel. It may be fusi- 
 form or spindle shaped, cylindri- 
 cal and cirsoid (tortuous), the lat- 
 ter when seen in the scalp, where 
 they stand out prominently be- 
 neath the skin, the term anasto- 
 motic A. is also applied. 
 
 The intima and adventitia are 
 thickened, and there are generally 
 atheromatous patches on the in- 
 tima. The media is thinner than 
 normal and may be wanting in 
 some places. 
 
 2. Saccular Aneurysm. A local weak- 
 
 ening leads to the formation of 
 a pouch, which frequently com- 
 municates with the artery by a 
 narrowed orifice. 
 
 The media weakens and gradual 
 dilatation of the intima and ad- 
 ventitia follow. The sac grows 
 larger and larger and rupture 
 may take place. A reactive hy- 
 perplasia of the surrounding tis- 
 sue may act as a secondary re- 
 taining wall, and the cavity con- 
 tains more or less an abundance 
 of clots, which may by their or- 
 ganization completely heal the 
 aneurysm if it is small. 
 
 In the large aneurysms the sur- 
 rounding tissues are pushed aside 
 or compressed and may suffer 
 necrosis. An aortic aneurysm may 
 erode the ribs, sternum and ver- 
 tebrae. It may compress the 
 spinal cord, or it may rupture 
 into various parts of the body. 
 
 Communications may be estab- 
 lished with large venous trunks. 
 
 3. Dissecting Aneurysm is common in 
 
 aorta and results from degenera- 
 tions and traumatism. The in- 
 tima ruptures and the blood bur- 
 rows between the coats for a con- 
 siderable distance. The dissection 
 usually takes place in the media. 
 The adventitious canal may be- 
 come lined with endothelial 
 
150 PATHOLOGY. 
 
 VEINS. 
 
 1. Circulatory Disturbances. Thrombosis, 
 
 etc. 
 
 2. Degenerations. Fatty and calcifica- 
 
 tion. 
 
 3. Inflammations. 
 
 a. Acute Phlebitis results from simple 
 
 but particularly infectious inflam- 
 mation in the neighborhood of the 
 vein. If the outer coat is first in- 
 volved the term periphlebitis, as 
 seen in Plegmasia albadoiens 
 (milk leg), is given. The veins 
 show under the skin as blue 
 streaks running in various direc- 
 tions. 
 
 Cellular inflammation may extend to 
 the media and occasionally the in- 
 tima, and thrombosis may occur, 
 which may become infected and 
 cause septic emboli. 
 
 If the condition begins within the 
 vein by reason of a primary throm- 
 bus the term thrombophlibitis is 
 given. If a thrombus is organized 
 or partly so calcification may take 
 place and phleboliths or vein stones 
 are formed. 
 
 Microscopically, the changes are sim- 
 ilar to tnose which occur in 
 thrombo arteritis. 
 
 b. Chronic Phlebitis, or Phlebosclerosis, 
 
 corresponds to chronic arteritis or 
 arteriosclerosis. 
 
 4. Phlebectasia, Varicosity, Dilatation of 
 
 the Veins. 
 Causes. Mechanical obstruction to cir- 
 culation or weakness of the walls, 
 as seen in dependent portions of 
 the body as legs, rectum, neck of 
 bladder, spermatic cord, scrotum 
 and vagina. Cirrhosis of liver, con- 
 stipation, pelvic tumors, dilatation 
 of veins of rectum, causing hem- 
 orrhoids, are frequent. Abdom- 
 inal tumors, pregnancy or anything 
 causing obstruction to the venous 
 return in lower extremity causes 
 varicosity of the veins of the leg. 
 
 Pathologic Anatomy. Veins become 
 dilated, elongated and assume a 
 
THE LYMPHATICS. 151 
 
 tortuous character, sometimes 
 even pouched. Its walls and sur- 
 rounding tissue are thickened by 
 chronic inflammation, mechanic- 
 ally produced. Rupture may take 
 place and lead to fatal hemor- 
 rhage. The skin becomes inflamed 
 and may break down and pro- 
 duce the varicose ulcer. 
 5. Infectious Diseases. Tuberculosis and 
 syphilis may also attack the veins. 
 
 LYMPHATIC CHANNELS. 
 
 1. Lymphangitis, or Inflammation of the 
 
 Lymphatic vessels, as secondary to 
 inflammatory affections of surrounding 
 parts. Red lines indicate the position 
 and course of the inflamed lympha- 
 tics. There is swelling, endothelial 
 cell multiplication and later accumu- 
 lation of leucocytes within the vessel, 
 and the channel may be more or less 
 uniformly filled with pus. Peri- 
 lymphangitis usually accompanies the 
 process, and if the septic process is 
 violent phlegmonous inflammation oc- 
 curs. : 
 Thrombosis may occur and cause ob- 
 struction. The process may ter- 
 minate in resolution or suppuration 
 with involvement of the surrounding 
 tissue. The resolution may be im- 
 perfect and the connective tissue may 
 obliterate the channels, or the walls 
 may not be entirely restored and 
 dilatation results. 
 
 2. Lymphangiectasia, or Dilatation of the 
 
 Lymphatics. 
 
 a. Acquired. Obstruction by pressure, 
 
 thrombosis or by filariae; inflam- 
 mation, as seen in elephantiasis. 
 The skin is thickened greatly and the 
 surface is lobulated. 
 
 b. Congenital may appear as circum- 
 
 scribed or diffuse forms. The dif- 
 fuse appears as edematous swell- 
 ings of the subcutaneous and re- 
 sembles elephantiasis. 
 
 The localized lymphatic dilatations 
 are the same as the new growths 
 called lymphangioma. 
 
 3. Infectious Diseases. Tuberculosis and 
 
 syphilis. 
 
152 PATHOLOGY. 
 
 4. Tumors. Lymphangiomata, endothe- 
 
 liomata and metastatic carcinomata. 
 
 5. Parasites. Filiaria Bancrofti. 
 THORACIC DUCT. 
 
 1. Thrombosis in association with inflam- 
 
 mation of duct, sometimes without 
 it. This may cause occlusion and 
 dilatation of its lower part, also of 
 the lymphatics. Chylous ascitis may 
 result. Collateral circulation gener- 
 ally prevents serious consequences. 
 
 2. Dilatation from cardiac failure with 
 
 engorgement of the greater veins, 
 impeding the outflow of lymph. Back- 
 ward pressure of the blood through 
 the superior vena cava may distend 
 the upper part of the duct with blood. 
 
 3. Inflammation of duct is associated with 
 
 various inflammations of the ab- 
 domen and pelvis, invasions of irri- 
 tants and extension from abdominal 
 disease, pleurisy, etc. 
 
 4. Infectious Diseases. Tuberculosis is 
 
 met with. 
 
 5. Tumors. Primary, as sarcoma and 
 
 fibroma, rare. 
 Secondary carcinoma is more common. 
 
 DISEASES OF THE RESPIRATORY 
 SYSTEM. 
 
 NASAL CAVITIES. 
 
 1. Congenital Abnormalities, deviated 
 
 septum, atresia of parts or complete 
 absence of nose is rare. 
 Hair lip and cleft palate may involve 
 the nasal cavities. 
 
 2. Circulatory Disturbances. Active and 
 
 passive hyperemia, which may ter- 
 minate in inflammation in the former, 
 and both may cause hemorrhage. 
 Hemorrhage (epistaxis) may also he 
 caused by inflammation of the mu- 
 cous membrane or as a result of 
 blood diseases. 
 
 3. Inflammation. 
 
 a. Acute Nasal Catarrh, Acute rhinitis, 
 Coryza, results commonly from 
 exposure to cold. It may occur as- 
 sociated with various infections, as 
 influenza, etc. The mucosa is red 
 and dry, and a serous, then mucous, 
 
THE LARYNX. 153 
 
 then muco -purulent exudation is 
 discharged. 
 
 b. Chronic Rhinitis follows several 
 acute attacks, particularly in the 
 scrofulous, tuberculous or syphilitic. 
 
 The mucosa becomes thickened 
 (hypertrophic rhinitis), which may 
 undergo atrophy (atrophic rhinitis), 
 in which the exudate is scanty and 
 appears as dry, greenish crusts, 
 which may ulcerate and become of- 
 fensive (ozena). Offensive dis- 
 charges may be due to syphilis 
 (ozena syphilitica) or tuberculosis 
 ozena (tuberculosa). 
 
 4. Infectious Diseases. 
 
 Diphtheritic rhinitis follows diph- 
 theria usually. 
 
 Syphilitis is seen as simple rhinitis con- 
 genially and as mucous patches or 
 gummata. 
 
 Tuberculosis is seen generally as 
 "scrofulous catarrhs" of children. 
 Lupus of the face may extend to the 
 nose. 
 
 Glanders, leprosy and rhinoscleroma are 
 also met with. 
 
 5. Tumors. Polyps, simple generally, but 
 
 fibroid, myxomatous or sarcomatous 
 may occur. Chondromata, sarcomata 
 and epithelial or glandular cancers 
 are sometimes found. 
 
 6. Parasites, Larvae of various flies will 
 
 cause severe inflammation. 
 
 7. Foreign bodies may be encrusted with 
 
 lime salts (Rhinoliths). 
 
 LARYNX. 
 
 1. Circulatory Disturbances. Anemia, ac- 
 
 tive and passive hyperemia and hem- 
 orrhage are met with. 
 Edema of the epiglottis or other parts 
 may be met with in Bright' s or heart 
 disease. 
 
 2. Inflammation. 
 
 a. Acute catarrhal laryngitis result of 
 irritation, and is associated with 
 the various infections. The mem- 
 brane is red and swollen. There i. r ; 
 a mucous or a muco-purulent se- 
 
154 PATHOLOGY. 
 
 cretion. In severe forms ecchymosis 
 or erosion may occur. It may cause 
 disturbance of breathing if severe, 
 and children may suffer from spas- 
 modic contractions of laryngeal 
 muscles with paroxysmal dyspnea 
 (false croup). 
 
 b. Chronic catarrhal laryngitis may fol- 
 
 low the acute form or begin grad- 
 ually from other irritations. The 
 mucous membrane is thickened, 
 granular and even papillomatous. 
 Fibroid thickening may result from 
 irritations of foreign bodies. 
 
 c. Edematous laryngitis, or Edema of 
 
 the larynx, is generally due to in- 
 flammations from violent irritations, 
 infections, severe chronic local 
 lesions of tuberculosis and syphilis 
 and perichondritis. 
 
 d. Perichondritis is usually secondary 
 
 to syphilic, tubercular or carcino- 
 matous, etc., affections of the 
 larynx. 
 
 3. Infectious Diseases. Diphtheritic and 
 
 croupous inflammations as result of 
 diphtheria, typhoid fever, scarlet 
 fever, smallpox, etc. Tuberculosis, 
 syphilis, leprosy and glanders. 
 
 4. Tumors. Papillomatous fibromata, fib- 
 
 roma, carcinoma. 
 
 5. Parasites. Larvae of trichinella 
 - spiralis, lumbricoides, echinococcus 
 
 cysts. 
 
 TRACHEA. 
 
 1. Malformations. 
 
 a. Congenital, absence, abnormalities in 
 length or diameter or structure. 
 
 b. Acquired. Diffuse or local dilatation, 
 constriction from tumors or aneu- 
 rysms and cicatricial contraction. 
 
 2. Inflammations are associated with 
 laryngitis and bronchitis and are from 
 the same cause. 
 
 3. Infe-ctious Diseases. Syphilis and tu- 
 berculosis. 
 
 4. Tumors. Ecchondroses and osteomata, 
 chondromata and secondary cancers. 
 
 BRONCHI. 
 
 1. Circulatory disturbances, same as 
 larynx. 
 
TRACHEA. 155 
 
 2. Inflammations. 
 
 a. Acute catarrhal bronchitis is due to 
 
 exposure, irritating gases and ex- 
 tension of tracheal catarrhs. It is 
 associated with typhoid fever, 
 measles, whooping cough, etc. It 
 may be secondary to pulmonary dis- 
 eases, and various micro-organisms 
 have been found in bronchitis. The 
 mucous membrane is red and dry, 
 then a mucous or muco-purulent 
 exudate is formed. If the exuda- 
 tion is excessive the condition is 
 called bronchorrhea. 
 
 It may be serous or purulent and 
 very offensive and is then called 
 fetid bronchitis. 
 
 b. Chronic catarrhal bronchitis occurs 
 
 from repeated attacks of the acute 
 and also in the old or those with 
 cardiac weakness. It is frequently 
 associated with chronic lung dis- 
 ease. 
 
 The ciliated cells are replaced by 
 columnar, and the mucous mem- 
 brane undergoes hypertrophy. The 
 bronchus is thickened by cellular 
 infiltration and overgrowth of 
 fibrous tissue. 
 
 c. Fibrinous bronchitis is frequently as- 
 
 sociated with laryngeal or tracheal 
 diphtheria, but may also be due to 
 inhalation of irritants. It occurs 
 in the finer bronchi as a result of 
 croupous and catarrhal pneumonia. 
 The^e is also a form which is char- 
 acterized by periodical attacks in 
 which fibrinous casts are formed 
 and discharged. 
 
 Small spirals (Curschman's spirals) 
 containing or associated with them, 
 small octahedral crystals (Charcot 
 g^id Leyden crystals). 
 
 3, Bronchiectasis, or Dilatation of the 
 
 bronchi, is due to weakness of the 
 walls, from chronic bronchitis gen- 
 erally, or increased pressure within 
 the bronchi or to both. 
 
 When a part of the lungs is atelectic 
 the obstruction to the entrance of air 
 leads to dilatation above the collapsed 
 area. 
 
156 PATHOLOGY. 
 
 Accumulated secretions in the tubes by 
 their weight may sometimes cause 
 bronchiectasis. Fibrous adhesions be- 
 tween bronchus and pleura may also 
 cause it. 
 
 If the dilatation is localized it is called 
 saccular bronchiectasis; when it is 
 uniformly enlarged it is called cylin- 
 drical or fusiform. 
 
 The mucous membrane may be almost 
 normal in appearance, but it is gen- 
 erally thickened and irregular. There 
 may be polypoids and ulcerations. 
 The exudation is copious, purulent 
 and often fetid. It may sometimes be 
 thick and cheesy. 
 
 4. Infectious Diseases. Tuberculosis and 
 syphilis. 
 
 5. Tumors. Polypoids, primary cancers, 
 leukemic nodules, lymphosarcoma, 
 fibroid chondroma and lipoma .may be 
 met with. 
 
 LUNGS. 
 
 1, Congenital Disturbances. One lung 
 may be absent, or the parenchyma un- 
 developed, while the bronchi are in a 
 cystic condition. Accessory lobes of 
 the lung have been seen. 
 
 2. Circulatory Disturbances. 
 
 a. Anemia from general anemia, pres- 
 sure on lung and obstruction to blood 
 vessels. The lungs are pale or mot- 
 tled in appearance in old people; the 
 latter is Cue to pigment. 
 
 b. Active Hyperemia, or Congestion. 
 
 Exercise increases the flow of blood 
 to the lungs, and if extreme it may 
 cause rapid death (Apoplexia pul- 
 monum vascularis). Irritating in- 
 halations and Collateral hyperemia 
 may occur when the lung or other 
 parts of the body become anemic 
 through obstruction of circulation 
 to the part. 
 
 The lung is dark red and the blood 
 
 will flow from the sectioned sur- 
 face. Alveoli may contain free blood 
 and it may be seen in the spu- 
 tum. 
 
 c. Passive hyperemia occurs from con- 
 
 ditions preventing the outflow of 
 Uie blood from the lungs, as in va.l- 
 
LUNGS. 157 
 
 vular disease or weakness of the 
 
 left ventricle. The hindrance to the 
 outflow of the blood in the veins 
 leads to similar passive congestion. 
 It is found in the dependent parts 
 of the lungs in cases of great 
 asthenia and is called hypostatic 
 congestion. It may lead to hyposta- 
 tic pneumonia if irritants are in- 
 spired, etc. 
 
 The lung is dark red and heavy. On 
 section it is moist, due to an infil- 
 tration of serous exudate and blood. 
 
 In chronic cases the tissue is dry 
 and indurated. Red and white 
 blood cells are found within the 
 alveoli and interstitial tissue. In 
 later stages the red cell may re- 
 enter the circulation or break down 
 and remain as pigment granules. 
 There is then hyperplasia and in- 
 duration of connective tissue, which 
 is called cyanotic induration. 
 
 d. Edema, from passive hyperemia, 
 
 general septic conditions, vasomo- 
 tor relaxation and stenosis of 
 larynx. 
 The lungs are dark red when edema 
 is due to passive congestion. In 
 other forms the lungs are light in 
 color, grayish; frothy serous fluid 
 exudates on section in both cases. 
 
 e. Hemorrhage. In severe congestion or 
 
 inflammation, hemorrhagic or in- 
 fectious diseases and high blood 
 pressure small punctate hemor- 
 rhages may be met with. 
 
 When hemorrhage is due to conges- 
 tion and is mixed with serous ef- 
 fusion the lung looks like an hy- 
 peremic spleen ((spleenization). 
 Large hemorrhages into the lungs 
 may result from traumatism or 
 aneurysmal rupture. 
 
 Small or large hemorrhages may be 
 due to lesions of the nervous sys- 
 tem at the base of the brain. 
 
 Hemorrhage discharged externally 
 through the bronchial tubes is gen- 
 erally due to tuberculosis in its 
 later stages. It may occasionally 
 be due to congestion of the lungs, 
 erosion of small blood vessels by 
 
158 PATHOLOGY. 
 
 gangrene, abscess, etc., or vicarious 
 menstruation. 
 
 f. Hemorrhagic infarcts may occur in 
 
 the lungs as it does in other places 
 from obstruction to arteries by em- 
 boli. 
 
 g. Embolism without infarction may 
 
 be met with. Traumatic disturb- 
 ance of fatty tissue or the break- 
 ing of bone may cause a fat em- 
 bolism. If large branches of the 
 pulmonary artery or several vessels 
 are obstructed sudden death may 
 result, or there may be only great 
 dyspnoea and oppression. 
 
 3. Hypertrophy. True hypertrophy is 
 rare. Partial hypertrophy of the lungs 
 muscular tissue may occur when there 
 is obstruction in air passages so that 
 great expiratory force is required. 
 
 4. Atrophy. Occurs only as a part of 
 emphysema. 
 
 5. Aatelectasis applies to a non-inflated 
 or collapsed lung. 
 
 a. Congenital atelectasis is found in the 
 
 new born in which the lung or 
 part of lung has never been prop- 
 erly expanded by air as the result 
 of general weakness or compres- 
 sion of the thorax, or cerebral hem- 
 orrhage. 
 It may be due to obstruction to the 
 air passages by meconium, etc. 
 
 b. Atelectasis in after life, in which 
 
 the lung is compressed or collapsed 
 by pleural effusions. deformed 
 chests, tumors, aneurysms, etc. It 
 is also caused by obstruction to 
 the bronchi. 
 
 If the larger bronchi are occluded the 
 atelectasis is of considerable ex- 
 tent. 
 
 If the smaller bronchi and atelectasis 
 are occluded lobular areas of ate- 
 lectasis are developed. This is fre- 
 quently seen in broncho-pneu- 
 monia. 
 
 In some cases the obstruction to the 
 bronchi may prevent , inspiration, 
 but not expiration, so that there is 
 a gradual collapse. In other cases 
 both the expiration and the inspira- 
 
EMPHYSEMA. 159 
 
 tion are prevented with a gradual 
 absorption of the air within the 
 vesicles. 
 
 Pathologic Anatomy. 
 
 Atelectatic areas are dark in color, 
 reduced in size. On section the 
 surface is smooth and generally 
 dry (called carnification), though 
 passive hyperemia may be pres- 
 ent and when bloody liquor flows 
 from the cut surface the term 
 spleenization is given to it. 
 The lung does not crepitate and 
 sinks when placed in water. If 
 the condition has persisted for 
 some time the connective tissue 
 overgrowth from the septa causes 
 induration and permanent col- 
 lapse. The lung is then hard, dark 
 in color due to pigment of disin- 
 tegrated blood. The bronchi may 
 be compressed, but sometimes 
 atelectatic bronchiectasis may re- 
 sult from increased pressure of 
 air in the bronchi by reason of 
 the collapsed state of the lung 
 tissue. 
 
 6. Emphysema is an increase of air con- 
 tained within the normal tubes and 
 alveoli or in the interstitial connec- 
 tive tissue of the lungs. It may be 
 divided into, — 
 
 a. Vesicular emphysema, is an over- 
 distention of the alveoli and air 
 sacs of the lungs. It may be divided 
 into, — 
 
 1. Acute Vesicular emphysema, due to 
 excessive air pressure within the 
 alveoli consequent upon conditions 
 such as inflammatory swelling or 
 mucous secretions within the 
 bronchi, etc., thus impeding ex- 
 piration, but not sufficient to ob- 
 struct the inspiration and over- 
 distention of alveoli and air sacs 
 results. 
 
 When the entrance of air into cer- 
 tain parts is impeded by obstruc- 
 tion, diseased bronchi or pulmo- 
 nary consolidation, localized em- 
 physema of other parts results, 
 this is called vicarious emphy- 
 sema. 
 
 Pathologic Anatomy. The alveoli an£ 
 
160 PATHOLOGY. 
 
 air sacs are simply distended. The 
 tissues are paler than normal and 
 gives a cotton-like feel when 
 pressed between the fingers. 
 
 2. Chronic Vesicular Emphysema, 
 
 Substantial Emphysema, is com- 
 mon in old people. Attacks of 
 broncho-pneumonia and other in- 
 flammatory and congestive condi- 
 tions of lungs act as predisposing 
 causes. These conditions lead to 
 weakness and loss of the elas- 
 ticity of the lung tissue. 
 
 The direct exciting cause is prob- 
 ably increased air pressure within 
 the alveoli by reason of increase 
 in expiratory force, as in whoop- 
 ing cough, the constant cough of 
 chronic bronchitis, blowing of 
 wind instruments and constant 
 straining in pelvic disorders, etc. 
 
 Pathologic Anatomy. Lung is en- 
 larged and often distended, edges 
 rounded, light in color, and cot- 
 ton-like feel to the fingers. On 
 section alveoli are distended into 
 cavities of various sizes. When 
 large spaces are seen near the 
 pleural surface the term bullous 
 emphysema is used. The emphy- 
 sema may be local or generalized. 
 
 Microscopically, the vesicles and 
 alveoli are enlarged and may be 
 joined together or the inter-vesic- 
 ular and inter-alveolar septa are 
 atrophied or destroyed. The blood 
 vessels are reduced in number. 
 
 Associated Conditions. The chest is 
 in a constant state of inspiration 
 (barrel shaped). The diaphragm 
 is depressed, the liver is below the 
 normal level, and heart is almost 
 covered in front and pressed back- 
 ward. 
 
 Pathologic Physiology. Obstruction 
 to capillary circulation leads to hy- 
 pertrophy of the right heart, later 
 dilatation of the right ventricle 
 and drpsy with cyanosis may re- 
 sult. 
 
 3. Senile Emphysema is a result of the 
 
 atrophic process of old age and 
 - , is due to thinning of .the inter- 
 
PNEUMONIA. 161 
 
 vesicular septa. The lung is light 
 in color and collapses readily. 
 
 b. Interstitial Emphysema, is air within 
 the fibrous tissue of the lung and 
 occurs in affections where there is 
 obstruction to expiration combined 
 with forcible expiratory efforts, as 
 severe cough (whooping cough), 
 straining during labor or blowing of 
 wind instruments, etc., causing the 
 rupture of the inter-vesicular septa 
 and extravasation of air, which 
 eventually passes into the inter- 
 lobular and subpleural connective 
 tissue, where it appears as small 
 movable blebs. The process may 
 extend to the root of the lungs, 
 mediastinal tissues or subcutan- 
 eous tissue of the neck. 
 Rupture into the pleural cavities re- 
 sults in pneumothorax. 
 7. Inflammation or Pneumonia. 
 
 a. Fibrinous, Croupous or Lobar Pneu- 
 monia is an acute infection, involv- 
 ing a lobe or more of one or both 
 lungs, generally caused by the 
 diplococcus pneumonia, and is char- 
 acterized by a fibrinous exudation 
 within the air vesicles and terminal 
 bronchioles. 
 
 Causes. Specific cause (see Diseases 
 Caused by Bacteria). 
 
 Predisposing causes, — exposure to 
 cold, injury to lungs by trauma- 
 tism, fatigue and systemic depres- 
 sion. 
 
 Pathologic Anatomy. The seat of in- 
 volvement is the lower lobe of 
 the right lung; lower lobe of left 
 lung and apices are less frequently 
 involved. There is a tendency to 
 involvement of a whole lobe uni- 
 f o r m 1 y and simultaneously, 
 though it may vary and a more 
 or less lobular form may develop, 
 or it may spread from one part 
 of the lung to another (pneumonia 
 migrans. 
 -''- Typical cases may be divided into 
 the following stages, — 
 
 1. Congestion or Engorgement. 
 
 There is intense congestion with 
 exudation of serous liquid and 
 blQQ$ corpuscle:-} into the: alveoli 
 
162 PATHOLOGY. 
 
 and terminal bronchioles. The 
 area involved is dark red in color, 
 swollen and heavy. There is a 
 certain loss of the normal crepi- 
 tation. The pleura over the area 
 is $ull. On section bloody liquid 
 exudes. 
 
 Micraecopically, the blood vessels of 
 septa are distended and project 
 inward toward the alveoli. Red 
 blood corpuscles, some leucocytes 
 and detached epithelial cells are 
 found in the alveoli. 
 
 2. Consolidation or Hepatization. The 
 
 diseassed part is liver-like, swollen 
 and marked on the surface by the 
 ribs. On section it is at first red 
 in color (red hepatization), later 
 white or gray or variegated in 
 elderly persons (gray hepatiza- 
 tion. The cut surface is dry and 
 granular from projecting plugs of 
 fibrin. The blood vessels are less 
 prominent than in the first stage. 
 Leucocytes increase in number. 
 
 3. Resolution. The cells of the exu- 
 
 date undergo fatty degeneration 
 and the exudate itself becomes 
 gradually softened and the lung 
 becomes mo: A st. The material is 
 carried off by the lymphatics or 
 is expectorated. Puriform liquid 
 is present. Crepitation is re-es- 
 tablished. 
 
 The epithelial cells of the alveoli 
 and bronchioles proliferate, and 
 the lung is restored to its previ- 
 ous condition. 
 
 In some cases throughout the dis- 
 ease there may be severe conges- 
 tion and even edema of the lung. 
 In drunkards or in the cachetic 
 the exudate may be hemorrhagic, 
 and in some cases proliferative 
 changes in the septa are promi- 
 nent. 
 
 Pathologic Physiology. There is gen- 
 erally an associated pleurisy. Car- 
 diac and respiratory embarrass- 
 ment is probably due to the ac- 
 tion of toxines on the nervous 
 system. In fatal cases white clots 
 are often found in the chambers 
 
PNEUMONIA. 163 
 
 of fhe heart. 
 
 Myocardial degenerations, nephritis, 
 albumin and albumosis may be 
 sometimes found in the urine. 
 The chlorides of the urine are 
 usually diminished. The spleen is 
 enlarged and soft. Pericarditis 
 and endocarditis is common. 
 Meningitis may be noted. Inflam- 
 mations of the bronchi, larynx, 
 stomach and intestines and blad- 
 der may be met with. 
 
 Secondary infections may lead to 
 abscess or the affected area may 
 become gangrenous. Resolution 
 may be so delayed and productive 
 changes may occur, that a car- 
 nification of lung results and is 
 then called fibrous pneumonia. 
 
 b. Catarrhal Broncho-pneumonia, Lobu- 
 lar Pneumonia, is an acute inflam- 
 mation in localized areas of the 
 lung tissue in consequence of in- 
 flammation of the terminal bron- 
 chioles. 
 
 Causes. Some bacterium (diplococcus 
 pneumonia in 50% of cases). 
 (See Bacterial Diseases). 
 
 It occurs in the course of measles, 
 whooping cough, influenza or other 
 fevers attended with bronchitis. 
 It extends by contiguity and con- 
 tinuity or aspiration of irritating 
 bronchial secretions. 
 
 Pathologic Anatomy. 
 
 1. Simple Catarrhal Broncho-pneu- 
 monia. The pleural surface pre- 
 sents areas of dark, light-red or 
 grayish color, surrounded by em- 
 physema and here and there areas 
 of atelectasis. Both lungs are 
 generally involved. The small 
 bronchi and arterioles contain a 
 muco-purulent secretion, and the 
 areas of consolidation are smooth 
 and moist. The walls of the ter- 
 minal bronchioles and alveoli are 
 swollen and contain a fluid exu- 
 date with disquamated epithelial 
 cells. The septa present round 
 cell infiltration, and the blood 
 vessels are surrounded by emi- 
 grated leucocytes. 
 
164 PATHOLOGY. 
 
 In some cases lobar involvement by 
 confluence of the lobular areas 
 (pseudo-lobar pneumonia) takes 
 place. If the micro-organisms 
 are extremely virulent, suppura- 
 tion and gangrene may result. 
 Fetid foci or purulent collections 
 surrounded by areas of conges- 
 tion and inflammatory edema may 
 result. 
 
 Resolution may be slow, with pro- 
 liferation of connective tissue 
 and sclerotic hardening, and con- 
 traction of the lung tissue re- 
 sults. 
 
 2. Hypostatic Pneumonia occurs as a 
 
 terminal affection in many dis- 
 eases. It begins as a hypostatic 
 congestion and hemorrhagic 
 edema of the dependent portions 
 of the lungs. Irritants enter 
 through the bronchi and inflam- 
 mation of the terminal bron- 
 chioles and air vesicles results. 
 It is more fibrinous than the or- 
 dinary broncho-pneumonia and 
 the process is more diffuse. 
 
 3. Aspiration Pneumonia. Inhaled 
 
 dust, etc., when it reaches the 
 - finer bronchi and bronchioles set 
 up a local irritation and conges- 
 tion, with disquamation of the 
 epithelial cells, and an emigra- 
 tion of leucocytes. When the in- 
 halation is excessive, as in the 
 occupation of coal mining and 
 steel grinding, etc., it rarely stops 
 with the catarrhal inflammation. 
 
 The irritant penetrates the walls 
 and a pneumonia is produced, 
 which is more properly a fibrous 
 pneumonia. 
 
 c. Cheesy or Tuberculous Pneumonia 
 
 is an acute or subacute pneu- 
 monia caused by the tubercle bac- 
 illus. 
 
 ., V Cause. Tubercule bacillus. It is more 
 
 ;.f ■ , common in children than in men. 
 
 V" A tuberculous gland or cavity 
 
 - ruptures into a bronchus and the 
 
 ...--■ infective material is disseminated 
 
 !, throughout the lung. The germ 
 
 may be inhaled from without or 
 
PNEUMONIA. 165 
 
 from foci in the larynx or noso. 
 
 Pathologic Anatomy. It is a lobular 
 process. If the infection is 
 abundant the areas involved may 
 be so close as to resemble the 
 lobar form. There is no tend- 
 ency to resolution, but, on the 
 contrary, it leads to progressive 
 cheesy degeneration and the for- 
 mation of cavities. Limited areas 
 are sometimes healed by reactive 
 fibrous overgrowth, encapsulat- 
 ing the diseased area and trans- 
 forming the whole into a fibrous 
 mass. 
 
 . Fibrous Pneumonia, or Productive 
 Pneumonia, is a chronic process 
 and results from continued irrita- 
 tion. It is characterized by over- 
 growth of connective tissue, involv- 
 ing small or large areas of the lung 
 tissue. 
 
 Causes and Classification. 
 
 1. Pneumonokoniosis. Ordinarily most 
 of the dust inhaled is lodged on 
 the walls of the upper respira- 
 tory passages and is discharged 
 free with the sputa or in the 
 leucocytes and emthelial cells 
 (dust cells, Staubzellen). 
 
 If small particles reach the ter- 
 minal bronchioles, catarrhal in- 
 flammation with proliferation of 
 the epithelium and exudation of 
 leucocytes is occasioned, which 
 may envelop the dust particles 
 and remove it by expectoration. 
 
 When the dust inhaled has sharp 
 edges, as in coal, iron and marble 
 dust, etc., and is in great quan- 
 tity, it is difficult in removal. It 
 penetrates the walls and passes 
 between the epithelial cells and 
 occasions a zone of inflamma- 
 tory exudation which organizes 
 and is enclosed by a fibrous cap- 
 sule. 
 
 Some particles float free in the 
 lymph or enclosed in leucocytes 
 and enter the lymphatic vessels, 
 where it may be arrested at vari- 
 ous points and occasion fibrous 
 thickening of the vessel walls, or 
 
166 PATHOLOGY. 
 
 produce an indurative enlarge- 
 ment of the lymphatic glands at 
 the root of the lung and sur- 
 rounding bronchi. 
 
 Pathologic Anatomy. In moderate 
 cases the lung presents small 
 areas of thickening with pucker- 
 ing. On section the areas are 
 hard and grayish in color. They 
 may be darkly pigmented from 
 the particles themselves or from 
 hemorrhagic pigmentation. The 
 fibrous tissue is stellate or con- 
 centrically arranged around a 
 nucleus of foreign matter. Cal- 
 cification is sometimes seen. 
 
 Extensive induration is rare. "When 
 met with the vesicular character 
 of the lung tissue is lost. Con- 
 nective tissue bands follow the 
 bronchi and radiate into the 
 lungs, which is contracted. Ex- 
 tensive adhesions to the chest 
 wall often causes deformities of 
 the chest. 
 
 2. Secondary Fibrous Pneumonia is 
 
 sometimes seen as secondary to 
 the fibrinous or catarrhal pneu- 
 monia or atelectasis. It is caused 
 by reactive inflammation of the 
 septa. It is also seen in some 
 cases of caseous pneumonia and 
 chronic phthisis. Chronic conges- 
 tion of the lung may lead to dif- 
 fuse sclerosis of the lung. 
 
 3. Pleurogenic Fibrous Pneumonia 
 
 will follow chronic pleurisy. Tra- 
 beculae of fibrous tissue extends 
 from the sclerotic pleura into the 
 lung tissue. 
 
 4. Peribronchial and Perivascular 
 
 Fibrous Pneumonia is seen with 
 the pleurogenic form or the over- 
 growth of connective tissue 
 around the bronchi and vessels 
 which specially results from 
 syphilis. 
 
 Moderate forms of this pneumonia 
 may occur in association with 
 the others. 
 
 e. Purulent Pneumonia is an acute 
 form caused by pyogenic micro-or- 
 
GANGRENE OF LUNG. 167 
 
 ganisms and is characterized by- 
 purulent and hemorrhagic exuda- 
 tion in the connective tissue, 
 lymphatic channels or terminal 
 bronchioles and alveoli. The infec- 
 tion may reach the lungs through 
 the bronchi (Bronchogenic purulent 
 pneumonia); the blood vessels 
 (Hematogenic purulent pneumonia), 
 or the subpleural lymphatics (Pleu- 
 rogenic or Lymphogenic pneu- 
 monia). 
 
 In the bronchogenic and hematogenic 
 forms the pleura is intensely in- 
 flamed over the areas and extensive 
 purulent pleurisy (Empyema) may 
 occur. 
 
 Extensive abscesses may be formed 
 which, frequently break into the 
 bronchi or sometimes into the 
 pleural sac. 
 
 Local or diffuse necrosis or gangrene 
 may occur. Recovery may take 
 place by absorption or discharge of 
 the exudate, but as a rule it is 
 fatal. 
 
 In the pleurogenic form there is first 
 infection of the lymphatics, and 
 then it extends into the lung in the 
 form of yellow streaks or bands, 
 pushing aside the lobules, which 
 gives rise to the term pneumonia 
 desiccans. 
 
 Widespread pyemic or toxic lesions 
 are often found associated with 
 purulent pneumonia; this is gener- 
 ally a part of the primary disease. 
 Secondary infections as malignant, 
 endocarditis, septic nephritis, ett., 
 may occur. 
 
 . Gangrene results from putrifactive bac- 
 teria in necrotic areas of the lung 
 tissue. 
 
 Causes. Extension of adjacent care- 
 ous conditions; extension of necrotic 
 process of gastric or oesophageal 
 ulcers and cancers; inspiration of in- 
 fective material from the upper air 
 passage; infective material may reach 
 .the lung through the blood; pneu- 
 monia, tuberculosis and hemorrhagic 
 infarction. 
 
 It may appear circumscribed or dif- 
 
168 PATHOLOGY. 
 
 fuse. In the circumscribed the blood 
 vessels escape the gangrenous process 
 unless they are occluded by throm- 
 bosis, but the bronchi are generally 
 penetrated. 
 
 It may extend or a fibrous capsule 
 may limit it, and after discharging 
 through a bronchus scar formation 
 may terminate the disease. 
 
 The diffuse gangrene does not differ 
 much except that it is less intense 
 and more widespread. Spots of hem- 
 orrhagic infiltration, softening and 
 formation of cavities may be seen. 
 The sputa is muco-purulent. yellow- 
 ish gray or brownish in color and 
 very fetid. 
 
 9. Infectious Diseases. 
 
 a. Tuberculosis. (See Bacterial Dis- 
 eases). 
 
 Infection takes place through bron- 
 chial tubes, blood vessels or the 
 lymphatic system, hence we have,— 
 
 1. Bronchogenic Tuberculosis. When 
 the infective material is inhaled 
 and reaches the terminal bron- 
 chioles there is set up a limited 
 area of caseous or tuberculous 
 pneumonia or by penetration of 
 the bacilli between the epithelial 
 cells, causes tubercular changes 
 in the perialveolar and peribron- 
 chial connective tissue (miliary 
 tubercules). The authorities do 
 not agree as to which of these 
 processes are more apt to arise. 
 It is probable that there is a 
 mixture of the two. 
 
 Degeneration soon takes place. The 
 areas, beginning as small foci or 
 as larger areas of lobular tuber- 
 culous pneumonia, change in 
 color from a gray to yellow and 
 caseate. Coincidently, round- 
 cell infiltration and proliferative 
 changes take place in the tissues 
 surrounding the diseased areas. 
 
 The more acute the disease the 
 more apt is the degenerative 
 caseation to take place and the 
 less likely regeneration to occur. 
 
 In favorable cases the tubercles 
 
TUBERCULOSIS. 169 
 
 may be encapsulated and con- 
 verted into fibrous nodules. 
 
 Varieties. 
 
 a. Acute Pneumonic Tuberculosis is 
 
 more common in children than 
 in adults. There must be a high 
 degree of susceptibility and a 
 great number of virulent bacilli. 
 
 The infection may be derived by 
 direct inhalation or be discharged 
 from older caseous areas of the 
 lungs.. 
 
 Pathologic Anatomy. It is gen- 
 erally lobular, but an entire lobe 
 may be involved. The base or 
 apex may be involved. On sec- 
 tion the lung is at first variegated 
 from the formation of minute 
 patches and lobular areas of 
 caseous pneumonia (grayish) and 
 surrounding congestion of lung 
 tissue. 
 
 The cut bronchiole shows a 
 cheesy exudate surrounded by 
 peribronchial caseation. Small 
 miliary tubercules may be seen in 
 edges of the pneumonic patches. 
 As the process advances the lung 
 tissue is more extensively involved 
 and uniformly gray or yellowish 
 and consolidated. Complete de- 
 struction of the areas take place 
 and cavities, appearing generally 
 as necrotic excavations, are form- 
 ed. The pleura over the lung is 
 inflamed and covered with a 
 fibrinous or fibrino-purulent ex- 
 udate, or it may be studded with 
 tubercles. 
 
 If the process is less active there 
 may be evidence of reparative 
 change. 
 
 Encapsulation of areas and cal 
 cification may occur. Fibrous 
 overgrowth may convert it into a 
 scar mass. Cheesy area, if mere- 
 ly enclosed with fibrous tissue, 
 may remain quiescent for a time 
 and then break through the wall 
 and infect anew. 
 
 b. Chronic Pneumonic Tuberculosis 
 
 is the ordinary pulmonary 
 
 phthisis. It generally begins in 
 
 . the apices, though in - children 
 
170 PATHOLOGY. 
 
 the base of lung is likely to be 
 first affected. 
 
 Pathologic Anatomy. If there is 
 a bronchitis the bacilli may ad- 
 here and cause a tubercular 
 bronchitis with ulceration and 
 later involvement of the sur- 
 rounding tissues. Ordinarily, 
 however, the bacilli lodge in the 
 bronchioles or alveoli, as in the 
 acute form, and cause lobular 
 areas of caseous pneumonia sur- 
 rounded by tubercles formed along 
 the lymphatic vessels and outgo- 
 ing from the first formed foci. 
 There is a great tendency to in- 
 crease the disease by aspiration 
 of the caseous material into other 
 parts of the lung and by the 
 lymphatics. 
 
 On section the lung is found to 
 be more or less consolidated in 
 areas. These areas are opaque, 
 grayish or yellowish in appearance 
 and in which can be seen bronchi 
 as open spaces filled with a muco- 
 purulent liquid. 
 
 Areas of fibrinous or cellular 
 pneumonia, which may be due 
 to secondary infections, may be 
 formed; it differs from the caseous 
 in its granular or gelatinous ap- 
 pearance and their liability to 
 partial or complete resolution. 
 
 A tendency to degeneration and 
 softening together with the pro- 
 cess of repair may be seen as in 
 the acute form. The changes are 
 less rapid and connective tissue, 
 proliferation and fibrous tissue, 
 formation is greater than in the 
 acute. 
 
 The necrotic process leads to 
 the cavities or vomicae, which are 
 characteristic and contain putrid 
 secretions, consisting of broken- 
 .down, cheesy matter pus cells, de- 
 generated epithelial cells, elastic 
 tissue fibers, tubercle bacilli, pyo- 
 genic bacteria and sometimes 
 mold fungi. The cavities are 
 formed by bronchiectasis or by 
 liquefaction of the caseous areas 
 not in connection with a bronchial 
 tube. Single cavities may grow 
 
TUBERCULOSIS. 171 
 
 larger by constant ulceration, due 
 not only to caseous tuberculous 
 degenration, but also to mixed in- 
 fection. The walls of the cavities 
 are formed by reparative fibrous 
 proliferation and are covered by a 
 "pyogenic membrane." Blood ves- 
 sels in the areas may show 
 aneurysmal dilatation, erosion of 
 these will streak the sputum in 
 the early stage while rupture of 
 the vessels produce the hemorr- 
 hage in the later stage. 
 
 Connective tissue formation, en- 
 capsulating the area, may limit 
 the disease, or it may be com- 
 pletely fibrosed, as in, 
 
 C. Fibroid Phthisis, which may be- 
 gin before or after the cavity 
 formation, tends to counteract 
 caseation and destruction. If it 
 begins in the early stage a well- 
 formed capsule will separate the 
 area from the surrounding tis- 
 sue, and by its tendency to 
 shrink the material may be- 
 come calcareous and the dis- 
 ease process is completely ar- 
 rested. 
 
 If the capsule is not firm the dis- 
 ease, after having been quies- 
 cent for a varying period of time, 
 will be perforated by a fresh 
 extension and an acute or 
 chronic course of the disease 
 will be established. If the foci 
 of the disease are minute the 
 fibrous tissue proliferation con- 
 verts it into a sclerotic mass 
 instead of capsule formation. 
 
 Complications of Bronchogenic 
 Tuberculosis. Involvement of the 
 pleura; swallowing of the sputa is 
 liable to produce intestinal tuber- 
 culosis; upper air passages may be 
 involved; blood dissemination of 
 the infection may cause lesions 
 of the vessels, pericardium, endo- 
 cardium and general miliary tub- 
 erculosis; acute pneumonia, and 
 hypertrophy of the left ventricle. 
 
 2. Hematogenic Tuberculosis occurs 
 when a tubercular focus in the 
 cervical or peribronchial lymph 
 gland or foci at apices of lungs, 
 
172 PATHOLOGY. 
 
 etc., rupture into a blood vessel. 
 It is a part of general tubercu- 
 losis. The organs most frequent- 
 ly infected are spleen, liver, kid- 
 ney, choroid coat of eye, men- 
 inges and most of all the lung. 
 Pathologic Anatomy. Is the forma- 
 tion of miliary tubercles and their 
 acute or chronic changes, etc. 
 
 3. Lymphogenic Tuberculosis. Di- 
 rect infection to the lungs may 
 take place by means of the lymph 
 channels, as in tuberculous 
 pleurisy, which may be primary 
 or secondary to tuberculous dis- 
 ease of the vertebrae or ribs. 
 It may also be carried by the thor- 
 acic duct from the lymphatic 
 glands of the abdomen and pos- 
 terior mediastinum and caseous 
 vertebrae to the blood vessels 
 and then to lungs as a hemato- 
 genic infection. 
 
 Pathologic Anatomy. Typical tu- 
 bercles are scattered along the 
 lymph vessels in the interlobu- 
 lar septa and surround the blood 
 vessels and bronchi. 
 
 b. Syphilis. 
 
 1. Diffuse syphilitic infiltration of the 
 
 lungs is seen in the "still-born." 
 It appears as a more or less lobar 
 consolidation and induration of 
 the lung tissue. The lung is light 
 gray and airless (pneumonia 
 alba). 
 
 2. Syphilitic Gummata may be asso- 
 
 ciated with the diffuse form of 
 congenital syphilis, or it may be 
 present without the diffuse va- 
 riety. It is sometimes seen in the 
 adult. 
 
 3. Syphilitic fibrous induration of the 
 
 lung has been described. 
 
 c. Glanders. Infection takes place by 
 inhalation and rarely through the 
 blood. The lesion may be a diffuse 
 grayish or purulent infiltration with 
 abscess formation, or they may be of 
 a nodular character, of the size of a 
 hemp seed or a pea, in various parts 
 of the lung and show early degenera- 
 tion. 
 
PLEURA. 173 
 
 10. Tumors. Connective tissue tumors, — 
 fibroma, lipoma, chondroma, osteoma. 
 Sarcoma (primary and secondary are 
 more common. 
 
 Epithelial tumors, — carcinoma, the pri- 
 mary is the more common, while sec- 
 ondary is less frequent; adenoma has 
 been described. 
 
 Cysts, — congenital and are probably 
 merely dilatatious of bronchi have 
 been described. Dermoids are rare. 
 
 PLEURA. 
 
 1. Circulating Disturbances. 
 
 a. Passive Hyperemia, is seen in dis- 
 eases interfering with respiration, 
 pressure upon azygos vein, and in- 
 trathoraic pressure. 
 
 b. Petechial Hemorrhage, is seen in in- 
 tense congestion, blood disorders and 
 hemorrhage diathesis. 
 
 c. Hemothorax, free blood in the pleural 
 cavity from wounds, fracture of ribs 
 and rupture of aneurysms. If infec- 
 tion does not take place the blood is 
 generally absorbed rapidly. 
 
 d. Hydrothorax, or dropsy of the pleural 
 cavity, may be a part of general 
 edema. It is a serous effusion. Usu- 
 ally bilateral but may be unilateral. 
 The pleura frequently undergoes some 
 opacity and loss of luster. There may 
 be edema of the subpleural fibrous 
 tissue. Compression of the lungs and 
 displacement of adjacent viscera is 
 produced. 
 
 e. Pneumothorax, air in pleural cavity, 
 from rupture of tuberculous cavities, 
 gangrenous areas, softened infarcts or 
 abscesses of the lung, or rupture of 
 emphysematous air vesicles allowing 
 air to enter the pleural sac. 
 
 It may also follow the rupture of an 
 empyema into the lung. It may be 
 due to penetrating wounds. 
 The air is frequently absorbed, but if 
 infection takes place, purulent exuda- 
 tion from the pleura is caused and the 
 condition is then called pyopneumo- 
 thorax. The adjacent organs are 
 often displaced. 
 
 2. Plexitis, Pleurisy or Inflammation of 
 the Pleura. 
 
174 PATHOLOGY. 
 
 Causes: 
 
 a. Local causes, inflammatory exten- 
 sion from the various pneumonias, 
 gangrene and tuberculosis; extension 
 from pericarditis or mediastinal dis- 
 ease and inflammatory affections of 
 the spine, ribs or chest walls. 
 Inflammatory extension from the ab- 
 domen or its organs may take place. 
 Perforation of gastric ulcers, etc., and 
 abscess of the liver or spleen in rare 
 cases may cause it. 
 
 b. General causes, results from infec- 
 tion or intoxication reaching the 
 pleura from the blood, e. g. pyemia 
 and septicemia, rheumatism, acute 
 infectious diseases and Bright's dis- 
 ease, and acute inflammation. 
 
 Cold and traumatism are predis- 
 posing factors only. 
 
 Various microorganisms causing in- 
 flammation are met with. 
 It may be secondary to pneumonia or 
 tuberculosis, or the germs of these 
 diseases may be found in primary 
 pleurisy without affection of the 
 lungs. 
 Pathologic Anatomy. There are sever- 
 al varieties of pleurisy but one gen- 
 erally merges into the other. 
 
 a. Fibrinous Pleuritis. The pleura is 
 congested, lusterless and followed by 
 a fibrinous exudation. The pleural 
 surfaces become agglutinated which 
 when separated are roughened so as 
 to give rise to the term "bread and 
 butter pleurisy." 
 
 This process may involve small areas 
 only, or it may be extensive. If 
 small areas only are involved ab- 
 sorption takes place so that the 
 pleura is restored to its normal con- 
 dition. If it is extensive organiza- 
 tion takes place so that the pleura 
 are bound together by connective tis- 
 sue, which is later developed into 
 sclerotic bands. When it occurs re- 
 peatedly, as in tuberculosis, and is 
 not extensive, the pleura may be 
 thickened in spots from connective 
 tissue proliferation. 
 
 b. Serofibrinous Pleurisy may be a sec- 
 ondary condition to the fibrinous, or 
 it may begin as a serous exudation 
 
THE MOUTH. 175 
 
 into the sac. The fluid is heavier 
 than dropsical and contains flakes 
 and shreds of fibrin. 
 The lungs are pressed backward and 
 the adjacent organs are displaced. 
 
 c. Purulent Pleuritis, Empyema, Pyo- 
 thorax, results from micro-organ- 
 ismal infection. It may begin as such, 
 or as a primary serofibrinous pleu- 
 risy, with secondary infection from 
 various sources. The contents of the 
 pleura may rupture into the lung or 
 bronchi and sometimes through the 
 chest wall. 
 
 A rare termination is absorption of 
 the pus or gradual inspissation, re- 
 maining as cheesy detritus, which 
 may become calcareous. 
 
 d. Hemorrhagic Pleurisy generally re- 
 sults from tuberculous infection or 
 malignant disease of lungs or pleura. 
 It may also result in old and cachec- 
 tic individuals or in those suffering 
 from scurvy, purpura, etc. 
 
 The liquid varies from a light bloody 
 serum to nearly pure blood. 
 
 e. Chronic Pleurisy. This term may be 
 used in cases of thickening of the 
 pleural membrane following the vari- 
 ous forms, but strictly, when the 
 thickening is of a progressive pro- 
 ductive character. In both cases the 
 pleura is thickened by fibrous over- 
 growth, which may be uniform or 
 localized, or in the form of adhe- 
 sions. 
 
 . Infectious diseases. Tuberculosis and 
 syphilis. 
 
 . Tumors are rare. Fibromata, lipomata., 
 chondromata, osteomata, primary 
 and secondary sarcomata and second- 
 ary carcinomata. 
 
 . Parasites. Echinococcus cysts, amoe- 
 bacoli. 
 
 DISEASES OF THE DIGESTIVE 
 SYSTEM. 
 
 DISEASES OF THE MOUTH. 
 1. Stomatitis or Inflammation. 
 
 a. Catarrhal Stomatitis is caused by 
 irritants, — chemical, physical, me- 
 
176 PATHOLOGY. 
 
 chanical or bacterial, or some cases 
 of lowered vitality. 
 
 The mucous membrane of the mouth 
 is at first red, dry and hot; later 
 there is considerable liquid exuda- 
 tion. Teeth impressions are found 
 on the tongue, lips and cheeks, the 
 gums are swollen and painful. If 
 the condition is intense, cysts due 
 to distended mucous glands and ero- 
 sions may appear. If it is long con- 
 tinued, white slightly elevated spots 
 may be seen, which result from 
 epithelial hyperplasia (leukoplakia). 
 In gastro-intestinal and other dis- 
 eases epithelial disquamation is ac- 
 tive with retention of the cells on 
 the surface, which, mixed with food, 
 bacteria, etc., causes the "furring of 
 the tongue." 
 
 Localized disquamation gives rise to 
 the so-called "geographical tongue." 
 
 b. Apthous Stomatitis is seen in chil- 
 dren and is due to malhygiene, de- 
 bility or gastro-intestinal and other 
 diseases. It is a form of herpes. 
 Small whitish spots on an inflamed 
 base are found on the mucous mem- 
 brane, especially of the lower lips 
 and gums. 
 
 They are usually descrete, but some- 
 times confluent. The spots are com- 
 posed of desquamated epithelium, 
 with occasional fibrin. Ulceration is 
 seldom seen. 
 
 Pednar's Apthae are small ulcers 
 seen at the lateral portions of the 
 palate, sometimes on the soft palate, 
 and are probably due to traumatism 
 occurring in the act of sucking. 
 
 c. Ulcerative Stomatitis. In children it 
 is the result of malnutrition and lack 
 of cleanliness of the mouth. Various 
 micro-organisms normally found in 
 the mouth under certain conditions 
 aid in its production. Cachectic con- 
 ditions, as scurvy, etc., mercury and 
 other forms of poisoning, leads to 
 extensive ulcerations. 
 
 It may also be secondary to necrotic 
 conditions of the bones or suppura- 
 tive inflammation about the roots of 
 the teeth. The gums are reddened 
 .and soft with sometimes hemorrhagic 
 
STOMATITIS. 177 
 
 infiltration and epithelial destruction, 
 resulting in ulcers. 
 
 Suppuration may occur and loosen 
 or even dislodge the teeth. 
 
 Pyorrhoea Alveolaris begins around 
 the necks of the teeth and second- 
 arily involves the gums, results from 
 some constitutional disease allied to 
 gout. 
 
 The ligament of the tooth is inflamed 
 and retraction and suppuration of 
 the gums follows. 
 
 d. Pseudomembranous Stomatitis is 
 
 usually secondary to pharyngeal 
 diphtheria. 
 
 e. Phlegmonous Stomatitis is seen in 
 the . lips and results from trauma- 
 tism, with intense infection or sec- 
 ondary condition after erysipelas or 
 other cellular inflammations of the 
 face. The lips and cheeks are swol- 
 len and suppuration may occur with 
 abscesses rupturing into the mouth. 
 A chronic form of the deeper tissues 
 of the lips may cause hypertrophy. 
 
 f. Gangrenous Stomatitis, Noma, Can- 
 crum oris, occurs in ill-nourished 
 children. It affects the mucous mem- 
 brane in the form of a sloughing 
 ulcer, with inflammatory induration 
 of the entire thickness of the cheek. 
 The skin is at first dark red, bluish 
 or greenish, followed by gangrene. 
 It follows measles in about one-half 
 of all cases. Putrefactive changes 
 cause an almost intolerable fetor. In- 
 tense septic infection and intoxica- 
 tion attends. 
 
 2. Infectious Diseases. 
 
 Thrush, Mycotic Parasitic Stomatitis, 
 Parasitic Stomatitis, generally affects 
 poorly nourished and hand-fed chil- 
 dren and is due to the oidium albi- 
 cans. (See Parasitic Diseases). The 
 mucous membrane is inflamed, white 
 spots appear here and there due to 
 a mixture of mycelial threads of the 
 parasite and degenerated epithelial 
 cells and other micro-organisms. 
 Tuberculosis, Syphilis and Actinomy- 
 cosis are also met with. t 
 3. Tumors. Papillomatous growths, 
 
 fibroma, lipoma, myxoma, chondroma, 
 
178 PATHOLOGY. 
 
 lymphadenoma, carcinoma, hemangi- 
 oma and lymphangioma. 
 Cysts from obstruction of mucous 
 glands. 
 
 Ranule, is a cyst that is formed by 
 dilatation of the gland ducts, as seen 
 in the ducts of mucous, sublingual, sa- 
 livary or submaxillary glands. 
 
 DISEASES OF THE TONGUE. 
 
 1. Acute Glositis, from irritation caused 
 by burns, stings of insects, traumatism, 
 "foot and mouth disease" and various 
 micro-organisms. The tongue is red 
 and enlarged. Superficial or deep ab- 
 scesses are occasionally formed. 
 
 2. Chronic Glositis, from repeated attacks 
 of the acute, irritation from excessive 
 use of tobacco and alcohol, injury from 
 bad teeth, and it has occurred from 
 myxodema and cretinism. The tongue 
 is enlarged and ulcerated at the edges. 
 
 3. Macroglossia (muscular hypertrophy) 
 may be unilateral or bilateral and due 
 to lymphangioma. 
 
 4. Atrophy and Degeneration from nerv- 
 ous diseases. 
 
 5. Infectious Diseases, as tuberculosis, 
 syphilis and actinomycosis. 
 
 6. Tumors. Same as in mouth. 
 
 DISEASES OF THE SALIVARY 
 GLANDS. 
 
 1. Salivation, or Hypersecretion, is due 
 
 to nervous disturbances, diseases as 
 hydrophobia and smallpox, etc., cer- 
 tain drugs and metals, pregnancy and 
 some uterine disease. 
 True idiopathic salivation is rare. 
 
 2. Xerostoma, or dry mouth, is due to 
 
 arrest of flow from the salivary or 
 buccal glands. The mucous membrane 
 is dry and slimy. The tongue is dry 
 and red. It is caused by some nerv- 
 ous influence. 
 
 3. Inflammation. 
 
 a. Parotitis may be an independent in- 
 fection mumps or secondary to 
 various infections, as typhoid fever, 
 typhus fever or pyemia. 
 In mumps the gland is swollen and 
 tensely distends the capsule. The 
 
THE TEETH. 179 
 
 exudate is serous and is removed by 
 absorption. 
 
 Secondary infection of the gland 
 tends to abscess formation. Chronic 
 induration may remain. 
 b. Angina Ludovici, or Ludvigs Angina, 
 is a septic inflammation, usually of 
 the submaxillary arid adjacent parts. 
 It results from streptococcic infection 
 in the course of various diseases, 
 principally scarlet fever. It may re- 
 sult from a carious process at the 
 roots of the teeth. It terminates by ab- 
 scess formation with perforation. 
 Necrosis or gangrene may result. 
 
 4. Tumors. Sarcoma, chondroma, fibroma, 
 myxoma, lipoma, concretions and 
 cystic dilatations of the ducts 
 (Ranula) and salivary fistula results 
 from trauma or abscess. 
 
 TEETH. 
 
 1. Anomalous Development, absence, in 
 size, number, delay in eruption, irregu- 
 larity in formation and maldevelop- 
 men£, as in case of congenital syphilis 
 (Hutchinson's teeth), which are wedge- 
 shape, the cutting edge is smaller than 
 crown, and has a concave notch. These 
 teeth are not entirely peculiar to 
 syphilis. 
 
 2. Caries of Teeth is due to malnutri- 
 tion, digestive disturbance and un- 
 cleanliness. 
 
 Micro-organisms, leading to acid fer- 
 mentation, soften the enamel and oc- 
 casion fissures, which give entrance to 
 other bacteria. There is gradual dis- 
 integration of the enamel and dentine, 
 with formation of granular detritus, in 
 which are numerous bacteria. The 
 process penetrates to the pulp and sec- 
 ondary inflammation or pulpitis is set 
 up. 
 
 Caries may sometimes begin from 
 within. 
 
 3. Inflammation of Pulp is associated 
 with caries or independently. The pulp 
 is red, swollen, hemorrhagic, with later 
 suppuration. The process spreads 
 through the roots of the teeth to the 
 alveolar periosteum, with sometimes ab- 
 scess formation about the teeth. This 
 may spread to the gums (alveolar ab- 
 
180 PATHOLOGY. 
 
 scess) and rupture on the surface. 
 4. Tumors. Odontomata resemble den- 
 tine and arise from the pulp during de- 
 velopment. They form irregular out- 
 growths of the crown or root. Odon- 
 tonoids are smaller outgrowths, resem- 
 bling enamel, dentine or the cement 
 substance, and are seen in later life. 
 Sarcomata and fibromata arise from 
 the pulp during development, or from 
 the connective tissue around the root. 
 Polypoid outgrowths are hypertrophied 
 granulations. 
 
 Giant-celled sarcoma, known as epulis, 
 spring from the alveolar process of the 
 jaw. 
 
 Cysts arise from the primary follicles 
 in which teeth are developed. 
 
 DISEASES OF THE PHARYNX AND 
 TONSILS. 
 
 Inflammations of the Pharynx. 
 
 1. Catarrhal Pharyngitis, or Angina, or 
 Sore Throat, is due to irritations, as 
 hot liquids, chemicals, exposure to 
 cold and infections. It may affect the 
 entire pharynx or be limited to the 
 tonsils. The mucous membrane is 
 bright red and sometimes swollen, with 
 a tenacious exudate composed of mu- 
 cous and desquamated cells. There 
 may be vesicular elevations, which 
 sometimes rupture and form super- 
 ficial ulcers. There may be extravasa- 
 tions of hemorrhage. 
 
 Herpes angina is like herpes of the 
 skin. 
 
 2. Chronic Catarrhal Pharyngitis results 
 from repeated attacks of the acute or 
 excessive use of the voice, smoking and 
 alcohol. The mucous membrane is at 
 first swollen, but later it becomes 
 atrophic, with hyperplastic lymph fol- 
 licles or distended mucous glands ap- 
 pearing as slight granular elevations. 
 The submucous veins are enlarged and 
 tortuous. 
 
 3. Phlegmonon Pharyngitis is due to 
 
 wounds or is associated with infections, 
 as pseudo-membraneous tonsilitis and 
 pharyngitis, smallpox, pustules of 
 pharynx or pharyngeal glands. The 
 soft palate, uvula and arches are swol- 
 len and distended. There may be deep 
 
THE TONSILS. 181 
 
 cyanosis and edematous exudation. 
 Suppuration generally follows and 
 sometimes gangrenous necrosis. There 
 is often general septicemia. 
 Retropharyngeal Abscess is secondary 
 to trauma or infectious pharyngitis. 
 Occasionally it is produced by caries 
 of the vertebrae, embolism during some 
 infectious fevers, or the infective germ 
 may enter the lymph stream through 
 the tonsils. 
 
 4. Pseudo-membranous Pharyngitis is 
 
 caused by the bacillus diphtheria or to 
 various other organisms or irritations 
 from gases or steam, etc. 
 If non-diphtheretic it is common with 
 scarlet fever, measles and other infec- 
 tions, and seems to be due to the 
 streptococcus. The throat appears like 
 that of diphtheria, but extensive ne- 
 crosis is more common. The mucous 
 membrane and other parts, especially 
 the tonsils, are swollen and edematous, 
 with later necrotic changes. 
 
 White or yellowish patch or patches 
 appear in the throat, which coalesce as 
 a rule and extend over the tonsil, 
 fauces and uvula, or to the mouth, nose 
 and larynx. The pseudo-membrane is 
 firmly attached. 
 
 Microscopically, the deposit is made 
 up of meshes of fibrin containing de- 
 generated leucocytes and epithelial 
 cells, bacteria, etc. The deep tissues 
 are intensely congested with round cell 
 infiltration. The adjacent lymph glands 
 are enlarged and may suppurate with 
 sometimes extensive cellulitis and sup- 
 puration of the floor of mouth. 
 
 Inflammation of the Tonsils or Tonsilitis 
 
 may occur associated with tonsilitis or 
 may be independent. 
 
 1. Catarrhal Tonsilitis is similar to ca- 
 tarrhal pharyngitis. 
 
 2. Follicular Tonsilitis, Lacunar or Croup- 
 ous Tonsilitis involves the normal or 
 chronic hypertrophied tonsils, and is 
 due to causes similar to pharyngitis. 
 White or yellowish spots appear, which 
 are the lacunar or crepts distended 
 with degenerated epithelial cells and 
 bacteria, as staphylococci, streptococci, 
 pneumococci, tubercle bacilli, diph- 
 
182 PATHOLOGY. 
 
 theria bacilli, etc.; all play a part in 
 the etiology. 
 
 Ulceration may occur. The contents of 
 the lacunae are discharged, or adhere 
 like pseudo-membranes, or remain in- 
 spissated and even calcify. 
 Bacteria may penetrate the tonsil and 
 cause, — 
 
 3. Phlegmonous Tonsilitis, Abscess of the 
 Tonsil, Quinsy, is due to an infection. 
 It may result from the catarrhal or fol- 
 licular, or may be associated with the 
 phlegmonous inflammation of the 
 pharynx. One or both tonsils may be 
 affected. The tonsil is greatly swollen, 
 red and its parenchyma is infiltrated 
 with leucocytes and serum. Pus may 
 form in the tonsillar or peritonsillar 
 tissue. Rupture of the abscess may 
 take place into the pharynx, or it may 
 open on the neck at the angle of the 
 jaw, or it may extend down the neck 
 into the mediastinum. The internal 
 caroted artery may be perforated. The 
 submaxillary and cervical lymph glands 
 are enlarged. There is frequently mild 
 septicemia, myocarditis and nephritis 
 may result. There appears to be a 
 close connection between rheumatism 
 and quinsy. 
 
 4. Hypertrophy of the Tonsil results from 
 repeated attacks of the catarrhal or 
 follicular tonsilitis. The tonsils are 
 irregularly enlarged and harder than 
 normal. The connective tissue is in- 
 creased and the lymphoid follicles are 
 hyperplastic. Pressure upon the orifices 
 of the crypts may obstruct and cause 
 lacunar tonsilitis. The contents of the 
 crypts are prone to be retained and 
 calcified where the tonsils are hyper- 
 trophied. 
 
 Hypertrophied tonsils are frequent in 
 badly nourished children and is asso- 
 ciated with hvnerplasia of lingual ton- 
 sil and adenoids of the nasopharynx. 
 
 Infectious Diseases of the Pharynx and 
 Tonsils. 
 
 Diphtheria (see Bacterial Diseases), 
 tuberculosis, syphilis, glanders, lepra, 
 typhoid ulcers and pharyngomycosis 
 leptothricia (leptothrix buccalis). 
 Tumors. Polypoid tumors, hyperplastic 
 adenoid growths, fibroma, lipoma, chon- 
 
ESOPHAGUS. 183 
 
 droma, papilloma, sarcoma and epithe- 
 loma. 
 
 DISEASES OF THE ESOPHAGUS. 
 
 1. Congenital Defects. The esophagus 
 may be divided by a septum, or it may 
 be absent altogether. It may open 
 into trachea, or it may open onto the 
 external surface of the neck. 
 
 2. Circulatory Disturbances. Anemia, 
 active hyperemia and passtive conges- 
 tion. 
 
 3. Inflammations. 
 
 a. Catarrhal Esophagitis. There is hy- 
 peremia and desquamation of epithe- 
 lium and scant liquid secretion, 
 caused by trauma, swallowing acid, 
 alkaline or hot liquids. 
 
 b. Chronic Catarrhal Esophagitis from 
 long-continued passive congestion 
 and alcoholism. 
 
 c. Pseudo-membranous Esophagitis, 
 diphtheria or pseudo-membranous 
 pharyngitis. 
 
 d. Ulcerative Esophagitis from pustules 
 of smallpox, irritation of foreign 
 bodies. Small or large ulcers may be 
 present. Peptic ulcers may be found 
 in the lower end. 
 
 4. Stenosis is due to pressure of tumors 
 or aneurysms, lodgment of foreign 
 bodies, tumors of esophageal walls or 
 stricture following ulcers, etc. 
 
 5. Dilatation. 
 
 a. Simple Dilatation or Ectasia, is gen- 
 erally seen at the lower end and is 
 due to obstructions at the cardiac 
 end of the stomach. 
 
 b. Diverticula. 
 
 1. Pulsion Diverticula is generally 
 situated at the upper portion of 
 the esophagus and is due to pres- 
 sure from within, the muscular 
 coat being thinned. 
 
 2. Traction Diverticula are generally 
 situated at the lower end of eso- 
 phagus and are due to adhesions 
 of diseased bronchial glands and 
 subsequent contraction. Perfora- 
 tion may occur with septic infec- 
 tion of pleura, pericardium and 
 
184 PATHOLOGY. 
 
 lungs. Large arteries may be per- 
 forated. 
 
 6. Perforation and Rupture from necrotic 
 or suppurative processes of the eso- 
 phagus or adjacent structures, aneu- 
 rysms of thoracic aorta, etc. 
 
 7. Infectious Diseases. Tuberculosis 
 (rare), syphilis, typhoid ulcerations, 
 thrush. 
 
 8. Tumors. Fibroma, myoma, lipoma and 
 sarcoma are rare. Papilloma and car- 
 cinoma. 
 
 DISEASES OF THE STOMACH. 
 
 1. Congenital Defects. Atresia of pylorus, 
 division by septa, hour glass contrac- 
 tion and sometimes absence. 
 
 2. Circulatory Disturbance. 
 
 a. Anemia, as part of general anemia. 
 
 b. Hyperemia. 
 
 1. Active. Functional during diges- 
 tion. Inflammations and irritating 
 agents. Punctate hemorrhages may 
 occur. 
 
 2. Passive. Heart disease and ob- 
 struction to portal circulation. Mi- 
 nute hemorrhages may occur. When 
 congestion has existed for some 
 time dark or bluish punctate pig- 
 mentation occurs and chronic gas- 
 tritis results. The changes are 
 more marked near the pyloric end. 
 
 c. Hemorrhage. Small hemorrhages 
 may occur from active and passive 
 congestion, inflammation, infectious 
 or hemorrhagic diseases. Large 
 hemorrhages occur from congestion 
 in cardiac disease or cirrhosis of 
 the liver, gastric ulceration or car- 
 cinoma. The vomit of blood which 
 is in a semi-digested condition 
 (coffee ground vomit) is significant 
 of carcinoma. 
 
 Melaena Neonatorum. The blood 
 vomit of the new born is due to 
 gastric hemorrhages of disturbed 
 circulation in insufficient respira- 
 tion and possibly infectious hem- 
 orrhage diseases. 
 
 3. Inflammation. 
 
 a. Acute Gastritis, Acute Inflammation 
 of the Mucosa, is due to chemical, 
 
STOMACH. 185 
 
 mechanical or thermal irritations and 
 sometimes to infection. The mucous 
 membrane is red, swollen and cov- 
 ered with mucous. The gastric se- 
 cretion is reduced and the mucous 
 and peptic cells are granular and 
 swollen. The inter-tubular tissue is 
 infiltrated with round cells. The 
 lymphatic tissue of the mucosa is 
 hyperplastic. The seat is more fre- 
 quently near the pyloric end. 
 
 b. Pseudo-membranous Gastritis is due 
 to corrosive poisons, smallpox, ty- 
 phoid fever and septicemia, diph- 
 theria, etc. There is an irregular 
 pseudo-membrane, with sometimes 
 necrosis and ulceration. 
 
 c. Ulcerative Gastritis, from extreme 
 congestion and acute gastritis, 
 pseudo-membranous gastritis, septic 
 embolism, and rarely infectious ul- 
 ceration from tuberculosis, anthrax 
 and typhoid fever. 
 
 d. Chronic Gastritis. 
 
 Causes. Repeated attacks of the 
 acute, errors in diet, abuse of al- 
 cohol, tobacco, anemia, gout, tuber- 
 culosis, diabetes, albuminuria, ulcer, 
 dilatation, chronic heart disease and 
 cirrhosis of the liver. 
 Pathologic Anatomy. The mucous sur- 
 face is rough and wrinkled. Mucosa 
 is of a grayish color, the veins are 
 enlarged and there may be ecchy- 
 mosis or small hemorrhages. There 
 is cloudy swelling or atrophy of the 
 gland cells so that the different cells 
 can not be recognized. The glands 
 may be obliterated, inflammatory 
 processes press upon and destroy the 
 tubules, bringing on a condition of 
 sclerosis of the mucosa and sub- 
 mucosa. The stomach walls may be 
 thin and the stomach itself dilated, 
 or the wall may be thickened and 
 the stomach actually reduced in size. 
 
 There is occasionally complete 
 atrophy of the secreting tissue, the 
 mucosa is then smooth, with occa- 
 sional erosion of its surface. 
 
 Pathologic Physiology of Gastritis. All 
 
 forms of gastritis disturb the func- 
 tions of the stomach, giving rise to 
 the terms indigestion and dyspepsia, 
 
186 PATHOLOGY. 
 
 due to abnormal secretion of the gas- 
 tric glands, reduced motor power of 
 walls and altered nervous mechan- 
 ism. 
 
 In some instances the amount of hy- 
 drochloric acid remains normal, in 
 others there is absence of acid and 
 then again both acid and ferments 
 are lacking. 
 
 The general metabolism suffers and 
 emaciation and systemic depression 
 follows. 
 
 Toxic substances produced in the 
 stomach may contribute to the meta- 
 bolic disturbances. 
 4. Gastric Ulcer, Peptic or Round Ulcer. 
 
 About 60% of cases occur in females, 
 
 and young women seem particularly 
 
 liable. 
 
 Causes. Anemia and general malnutri- 
 tion. The ulcers are due to the ac- 
 tion of the gastric juice upon the 
 parts of lowered vitality, and in- 
 creased acidity is probably an impor- 
 tant factor. 
 
 Areas of lowered vitality may be due 
 to embolism or thrombosis with in- 
 farction. Spasms of the blood vessels 
 and thickening of the vessel walls, 
 trauma, etc. 
 
 Pathologic Anatomy. The number of 
 ulcers present varies, but generally 
 there is only one. The situation is, 
 as a rule, in the lesser curvature 
 on the posterior wall near the pyloric 
 end. They may, however, be found 
 at the fundus or at the cardiac end. 
 They vary in size from a few m m. 
 to 5 cm., and have sloping edges 
 (funnel form), with the apex toward 
 the muscular coat. The edges are 
 irregular and rough, but may be 
 smooth and rounded. 
 Ulcers may cause perforation, fatal 
 hemorrhages, deformity by contrac- 
 tion and loss of much secreting 
 structure. 
 
 In the healing of ulcers scars are 
 formed, which have usually a char- 
 acteristic stellate shape. 
 If the ulcers are large, extensive con- 
 traction results. Hour-glass contrac- 
 tion of the stomach or pyloric sten- 
 osis may occur, with resulting sec- 
 ondary conditions, as dilatations, etc. 
 4. Atrophy is caused by senility, chronic 
 
STOMACH. 187 
 
 gastritis, chronic diseases, as pernicious 
 anemia, etc., gastric dilatation and 
 contraction of cardiac orifice of stom- 
 ach. 
 
 5. Degenerations. Fatty degeneration, 
 pigmentation, amyloid degeneration, 
 calcification and gastro-malacia (sim- 
 ple softening of walls) is usually a 
 post mortem condition. 
 
 6. Alterations in Position and Size. The 
 stomach may be displaced into the 
 thoracic cavity through rupture of the 
 diaphragm (diaphragmatic hernia); 
 through the abdominal walls when 
 these are congenitally deficient, and 
 downward (gastroptosis) from dilata- 
 tion, adhesions, tight lacing, enlarge- 
 ment of spleen or relaxed abdominal 
 walls. 
 
 Dilatation or Gastrectasia. 
 Causes. Cicatricial contraction at py- 
 lorus; cancer at or near the pylorus; 
 fibroid hypertrophy and contraction 
 at the pyloric end from gastritis, 
 pressure of an aneurysm, movable 
 kidney or tumor. A dilatation of 
 stomach called atonic dilatation may 
 be caused by over-eating, excessive 
 beer drinking v> chronic gastric ca- 
 tarrh, exhausting diseases and gen- 
 eral muscular debility. It is due to 
 weakening of the stomach walls. It 
 may also be caused by abnormal ad- 
 hesions of the stomach. 
 Pyloric stenosis may at first be com- 
 pensated for by hypertrophy of the 
 muscles of the stomach, then the 
 stomach dilates, food stagnates and 
 ferments (Sarcinae ventriculae are 
 often present and lactic, butryic and 
 acetic acids, sulphuretted hydrogen 
 may result) and dilatation is in- 
 creased. The mucosa is thin and oft- 
 en degenerated and atrophic. 
 
 7. Infectious Diseases. Tuberculosis ul- 
 cerations, syphilic gummata or ulcera- 
 tion may occur, anthrax and thrush. 
 
 8. Tumors. 
 
 Connective tissue tumors. Fibroma, 
 myoma, lipoma, may be seen and 
 sarcoma is rare. 
 
 Epithelial tumors. 
 
 a. Polypoid elevations and adenoma- 
 tous proliferations. 
 
188 PATHOLOGY. 
 
 to 
 
 b. Carcinoma is a frequent tumor of 
 the stomach. Hard or scirrhous, soft 
 or medullary, adenocarcinomata or 
 adenoma, cylindrical-celled and squa- 
 mous-called carcinoma. 
 
 The cancers are most frequently sit- 
 uated at or near the pylorus. Stag- 
 nation of food and fermentation re- 
 sults. Hcl is absent. Lactic acid 
 secretion is pronounced. Stomach di- 
 lates. A long thread-like bacillus 
 (Oppler-Boas) is present and is sup- 
 posed, by a few, to occur only in 
 cancer of the stomach. Metabolism 
 is disturbed, etc. 
 
 DISEASES OF THE INTESTINES. 
 
 1. Congenital and Acquired Abnormali- 
 ties. 
 
 a. Total absence has been seen in mon- 
 strosities. 
 
 b. Narrowing or distortion is more fre- 
 quent. 
 
 c. There may be congenital enlarge- 
 ments of the intestines and localized 
 dilatations, notably Merckle's diver- 
 ticulum, which represents the re- 
 mains of omphalomesenteric duct. 
 This may be open at the umbilicus 
 and diverticula may be formed as a 
 result of constipation or localized 
 weakening of the muscular walls, al- 
 lowing a protrusion of the mucosa. 
 
 d. There may be congenital abnormali- 
 ties of position, e. g., ascending color, 
 and cecum, situated on the right side, 
 etc. 
 
 e. Enterocystoma is a congenital 
 cystic condition sometimes seen a; 
 the umbilicus from cystic dilatation 
 of parts of omphalomesenteric sys- 
 tem of the foetus. 
 
 f. Narrowing or stenosis may be seen 
 and is due to pressure of tumors or 
 displaced viscera, cicatricial constric- 
 tions from ulcerations or to neo- 
 plasms. 
 
 Narrowing of the lumen may be due 
 to carcinoma or tumors within. 
 
 g. Hernia is a displacement of any of 
 the viscera from the cavity in which 
 it normally lies. 
 
INTESTINES. 1SH 
 
 Causes. 
 
 1. Congenital, occasionally. 
 
 2. Acquired. A weakness of the ab- 
 dominal wall and abnormal mova- 
 bility of the intestine acts as a pre- 
 disposing cause, while a strain acts 
 as an exciting cause. 
 
 Varieties. 
 
 Internal Hernia is displacement of vis- 
 cera into other cavities within the 
 body, as into the thorax diaphrag- 
 matic hernia; into retroperitoneal 
 space (retroperitoneal hernia). 
 
 External Hernia is a displacement of 
 the viscera through the abdominal 
 wall and may be divided into: — 
 
 1. Inguinal Hernia. Protrusion 
 through external inguinal ring. The 
 intestine descends through the in- 
 guinal canal sometimes as far as 
 scrotum (indirect inguinal heria), 
 or protrusion takes place directly 
 through the internal inguinal ring 
 and may present itself under the 
 skin or descend through the lower 
 part of inguinal canal into scrotum 
 (direct inguinal heria). 
 
 2. Femoral Hernia is frequently seen 
 in women. The intestine pushes 
 through the femoral ring and pre- 
 sents itself on the inner side of 
 the thigh at the saphenous open- 
 ing. 
 
 Other varieties are, — ventral, vag- 
 inal, rectal, perineal, ischiatic or 
 obturator, 
 
 Hernia consists of a sac (perito- 
 neum) and its contents, which is 
 intestines or portions of omentum 
 or both. Secondary changes, as 
 inflammations of the sac and in- 
 testines, which may lead to fibrous 
 adhesions, contracting the sac and 
 binding the intestines in place. 
 Hernia may be divided into, — 
 Reducible, or irreducible, in accord- 
 ance to ability of replacing con- 
 tents into peritoneal cavity or not. 
 If there is pressure at the neck of 
 the sac by inflammatory exudation 
 or constrictions or accumulations 
 within the bowel so as to obstruct 
 the circulation of the intestinal 
 
190 PATHOLOGY. 
 
 hernia. Intense passive congestion 
 and inflammation of the peritoneal 
 coat follows and gangrenous ne- 
 crosis frequently results. This is 
 called Strangulated hernia. 
 
 2. Intestinal Obstruction. 
 
 a. Internal Strangulation by peritoneal 
 adhesions or the intestine slipping 
 through openings or perforations of 
 the mesentery or omentum. 
 
 This causes great dilatation of the 
 intestine above the obstruction and 
 collapse of the intestine below. 
 Congestion and peritonitis, necrosis 
 and perforation may occur at the 
 point of stricture. 
 
 b. Volvulus is a twist of some part of 
 the intestinal canal and due to ab- 
 normal laxity of the mesentery, 
 which predisposes, and general strain 
 or abdominal compression acts as the 
 exciting cause. 
 
 The vessels may become obstructed 
 and hemorrhagic infarction is often 
 seen. Gangrene of bowel may re- 
 sult. 
 
 c. Intussusception, or Invagination, is a 
 
 slipping of one part of intestine into 
 an adjoining part. The upper part 
 of the intestine is induplicated and 
 pushed into the lower part. It is 
 due to irregular peristalsis from 
 atony of one part with increased ac- 
 tivity of another part. Polypoid 
 tumors within the bowel are dragged 
 by peristalsis from the upper part of 
 bowel into the lower part. It is more 
 common in children than in adults. 
 The invagination most frequently 
 takes place in the iliocecal region. 
 The serous surfaces tend to unite by 
 peritonitis, and the invagination por- 
 tion may become gangrenous and be 
 discharged, which may result in re- 
 covery. Otherwise perforation pro- 
 duces fatal peritonitis. 
 
 d. Prolapse of Rectum is due to weak- 
 ness of the sphincter and other parts 
 of the wall with straining. It is fre- 
 quently seen in infants and some- 
 times in adults. It may be occa- 
 sional or constant. • 
 
 Secondary inflammation, ulceration 
 
INTESTINES. 191 
 
 and even necrosis may result. 
 
 3. Circulatory Disturbances. 
 
 Active and passive hyperemia, hemor- 
 rhage, edema, embolism and thrombosis 
 are often seen. 
 
 Hemorrhoids result from varicose veins 
 of the rectum and are generally 
 found in or outside of the sphincter 
 muscle, and are designated as inter- 
 nal or external hemorrhoids. They are 
 due to obstruction to the venous cir- 
 culation from cirrhosis of the liver, 
 repeated pregnancies, pelvic tumors or 
 chronic constipation. 
 
 The hemorrhoid presents itself as a 
 congested small polypoid elevation, 
 consisting of slightly or greatly di- 
 lated veins, between which is a more 
 or less amount of inflammatory con- 
 nective tissue. Thrombosis within the 
 cavities often occurs. Infection of the 
 veins may occur and hemorrhoid en- 
 larges and becomes inflamed and ede- 
 matous. 
 
 4. Inflammation. 
 
 Enteritis, or Inflammation of the Intes- 
 tines, involves particularly the mucosa 
 and submucosa of any part of the 
 gastro-intestinal tract, and is most fre- 
 quent in children and the aged. 
 
 Causes. Irritating foods; poisons of 
 various kinds; poisons produced by 
 improper digestion and fermentation; 
 bacteria, of which the normal colon 
 bacillus plays an important part, in 
 that it increases in violence under cer- 
 tain conditions, but other organisms 
 undoubtedly play an important part. 
 
 Pathologic Anatomy. 
 
 a. Catarrhal Enteritis. The mucosa is 
 swollen and of a light red color. The 
 arteries are distended and sometimes 
 there may be petechial hemorrhages. 
 On the surface there is a mucous 
 exudate containing desquamated and 
 degenerated epithelial cells and emi- 
 grated leucocytes. The contents of 
 the intestine is liquid by serous exu- 
 dation. 
 
 The solitary or agminated follicles 
 are enlarged and the term follicular 
 enteritis is given. 
 
192 PATHOLOGY. 
 
 The desquamation of the epithelium 
 may be more marked than the mu- 
 cous exudation, shreds of mucous 
 may be discharged and the term 
 croupous enteritis is given this form. 
 
 b. Suppurative Enteritis differs from 
 the above, in that there is a greater 
 emigration of leucocytes in the exu- 
 date, and in intense cases the sur- 
 face may be covered with pus. The 
 mucosa and submucosa show round 
 cell infiltration and submucous ab- 
 scesses, or ulcers are sometimes 
 seen. The solitary follicles tend to 
 break down and form follicular ulcers. 
 
 c. Pseudo-membranous Enteritis in- 
 volves the large intestine and is es- 
 pecially seen in dysentery. Diph- 
 theria with pseudo-membranous de- 
 posits may occur. 
 
 d. Chronic Enteritis is due to repeated 
 attacks of the acute, chronic conges- 
 tion, tuberculosis, dysentery and er- 
 rors in diet. The pathologic changes 
 are in some cases identical with those 
 of the acute form. In others the 
 changes are more pronounced, ulcera- 
 tion, pigmentation from hyperemia 
 and blood extravasation, thickening 
 and induration from proliferative 
 connective tissue changes in the 
 glandular tissue, or thinning and 
 wasting of the villi and follicles and 
 contraction from healing ulcers. 
 
 In the later stages atrophy may en- 
 sue, which may affect the mucosa 
 alone, but often involves the muscu- 
 laris also. 
 
 Pathologic Physiology. 
 
 General systemic intoxication may 
 result from absorption of bacterial 
 products, may produce depression or 
 shock by local irritation acting 
 through the nervous system. 
 
 Exudation into the intestine may de- 
 plete the vascular system and cause 
 failure of the circulation. 
 
 Peristaltic movements may be ar- 
 rested and constipation results, 
 though peristalsis is generally in- 
 creased and enormous exudation 
 produces diarrhoea. Digestion fails 
 from the disease of the bowel and 
 
APPENDICITIS. 193 
 
 premature expulsion of the intestinal 
 contents. 
 
 Marked disturbance of health re- 
 sults. 
 Duodenitis is associated with gastritis 
 and is prone to obstruct the bile duct 
 by inflammatory thickening and the 
 accumulation of mucous at the 
 mouth of the duct, and by this ob- 
 struction gives rise to catarrhal 
 jaundice. 
 
 Inflammation of the Ileum is of the 
 
 same character as enteritis, with 
 conspicuous follicular form. It is 
 common in children suffering from 
 infectious fevers, as scarlet fever and 
 diphtheria. The Pyers patches are 
 enlarged and sometimes ulcerated 
 
 Typhilitis or cecitis inflammation of 
 the cecum. It is of the simple ca- 
 tarrhal variety and is due to irrita- 
 tion produced by constipation (ster- 
 coral typhilitis). 
 
 If the constipation is severe or ob- 
 struction takes place ulceration may 
 occur. 
 
 Appendicitis may be a primary condi- 
 tion or it may be due to direct ex- 
 tension of typhilitis; or the thicken- 
 ing of the mucosa and the accumu- 
 lation of mucous in consequence of 
 the typhilitis, which may cause ob- 
 struction of the appendix. The re- 
 tained appendiceal contents, together 
 with the increased action of bac- 
 teria, such as the colon bacillus, 
 streptococcus, staphylococcus, etc., 
 produces distention and congestion, 
 the bacteria penetrate the mucosa 
 and appendicitis results. In cases 
 where fecal concretions and foreign 
 bodies are found within the appen- 
 dix they may be considered not as a 
 direct cause, but by their irritation or 
 injury to the mucosa the entrance of 
 bacteria is rendered more easy. It 
 may also be considered that the con- 
 cretions found within the appendix 
 have been formed from mucous or 
 desquamated epithelial cells after the 
 disease has begun. The part which 
 the obstruction of the appendiceal 
 arterial supply plays in the etiology 
 of the disease is probably secondary. 
 
194 PATHOLOGY. 
 
 Pathologic Anatomy. 
 
 a. Catarrhal Appendicitis. The mu- 
 cosa is slightly swollen and eroded, 
 the muscularis and serosa may be 
 congested and edematous, the appen- 
 diceal contents is retained and is 
 more or less muco-purulent. 
 
 b. Necrotic or Gangrenous Appendi- 
 citis. The mucosa is rapidly de- 
 stroyed with extension of the process 
 into the muscularis and serosa, and 
 results in a local fibrinous peritoni- 
 tis, which serves to retard the in- 
 fective process and prevents diffuse 
 peritonitis. If gangrene is very rapid 
 with early rupture of appendix and 
 escape of abundant bacteria, general 
 peritonitis results before a wall can 
 be formed. 
 
 c. Interstitial Appendicitis. There is 
 more or less of a productive connec- 
 tive tissue change in all cases of ap- 
 pendicitis, but in this particular form 
 the change is particularly conspicu- 
 ous in all the coats and frequently 
 terminates in chronic thickening of 
 the appendix. 
 
 Colitis is generally due to irritation by 
 fecal accumulation. The sigmoid 
 flexure is the common seat. 
 There is a thickening of the mu- 
 cous membrane and abundant mu- 
 cous exudation, later there is atrophy 
 and sometimes ulceration. Masses of 
 mucous or casts of the bowel may be 
 discharged (Mucous colitis). 
 
 Proctitis, or Inflammation of the Rec- 
 tum, is due to irritation of fecal 
 matter, parasites, etc., tumors, hem- 
 orrhoids, etc. It may be a part of a 
 colitis with like conditions. Ulcera- 
 tive processes may extend to sur- 
 rounding tissues and cause abscesses 
 with a fistulous communication with 
 the rectum or exterior. 
 5. Infectious Diseases. 
 
 a. Dysentery is a specific inflammation 
 of the large intestine. It may be 
 endemic or epidemic. 
 
 Causes. In mild cases tainted foods 
 and products of fermentation, with 
 probably specific bacteria, poisons 
 like mercury, etc., may cause it. 
 
CHOLERA. 195 
 
 In the ulcerative form of the tropics, 
 the amoeba coli is considered the 
 cause. 
 
 Pathologic Anatomy. 
 
 1. Catarrhal Dysentery. There is 
 congestion, swelling and edema of 
 the mucous membrane, petechial 
 hemorrhages and follicular en- 
 largements or ulcers are met with. 
 
 2. Ulcerative Dysentery. The mu- 
 cosa is very much swollen by a 
 serous or sero-hemorrhagic infil- 
 tration and covered with a sticky 
 mucous or muco-purulent exudate. 
 The ulcers become chronic and in- 
 dolent. There is great thickening 
 of the bowel. 
 
 3. Diphtheretic Dysentery. A pseudo- 
 membrane of a grayish or brown- 
 ish character appears on the mu- 
 cosa. It is more or less necrotic 
 and covers the entire wall of the 
 colon or rectum, or is scattered in 
 small areas here and there upon a 
 thickened catarrhal surface. In 
 mild cases the membrane is super- 
 ficial; in severe cases it may ex- 
 tend into the submucosa, and if 
 detached leaves an irregular ulcer, 
 which later becomes dirty-gray or 
 brownish in color. Gangrenous 
 dysentery is applied to the most 
 violent form. 
 
 In all cases the bowel is thickened. 
 Occasional perforation may occur 
 with peritonitis, periproctitis, etc. 
 Embolism or ascending thrombosis 
 of the portal vein frequently causes 
 liver abscess. 
 
 b. Cholera. (See Bacterial Diseases). 
 The mucosa is red and swollen, with 
 frequent petechial ecchymosis. There 
 is extensive degeneration of the 
 epithelium, which is probably a co- 
 agulation necrosis. The solitary fol- 
 licles or Pyers patches are enlarged 
 and sometimes ulcerate. There is a 
 great quantity of serous exudation 
 containing flakes of desquamated 
 and degenerated epithelium, which 
 gives rise to the "rice water" stools. 
 In later stages pseudo- membranous 
 inflammation may be met with, and 
 probably results from secondary in- 
 
196 PATHOLOGY. 
 
 fection. Lobular pneumonia is a fre- 
 quent complication. 
 
 c. Typhoid Fever. (See Bacterial Dis- 
 eases). 
 
 d. Syphilis is most frequently seen in 
 the rectum, where it may appear in 
 the form of warty elevations or as a 
 chancre, mucous patches and gum- 
 matous nodules or infiltrations. The 
 mucosa and submucosa is thickened 
 and ulcerated, secondary cicatriza- 
 tion and stenosis (syphilitic stricture) 
 results. 
 
 It may also be seen in the small 
 intestine and the colon in the form 
 of localized or diffuse gummata, with 
 sometimes ulceration, particularly in 
 congenital syphilis. 
 
 e. Anthrax and Actinomycosis. (See 
 Bacterial Diseases). 
 
 f. Enteromycosis results from ingestion 
 of putrid meat, fish, sausages, etc. 
 The lesions are similar to catarrhal 
 enteritis or croupous or pseudo- 
 membranous inflammation or erosion 
 or ulceration. The acute general 
 symptoms are probably produced by 
 bacterial poisons in the foods rather 
 than by the bacteria themselves. 
 
 6. Tumors. 
 
 Connective Tissue Tumors. Fibroma, 
 myxoma and lipoma. Sarcoma is 
 rare. 
 
 Epithelial Tumors. Inflammatory pa- 
 pilloma, adenoma and carcinoma. 
 
 7. Parasites. Tubercle bacillus, glander 
 bacillus, typhoid bacillus, streptothrix, 
 actinomycosis, bacillus coli communis. 
 Protozoa, as coccidial psorospermia, 
 Lamblia intestinalis and amoeba dys- 
 enteria. The Tania saginata and so- 
 lium, Dibothriocephalus latus. Ascario 
 lumbricoides, Ankylostomum duodenale. 
 Oxyuris vermicularis and Trichinella 
 spiralis. The larva of various flies, etc. 
 
 Rupture of the Intestine may be due 
 
 to traumatism or penetrating 
 wounds, ulcerations, such as duo- 
 denal (peptic), appendiceal, typhoid, 
 tubercular, dysenteric ulcers, etc. 
 Foreign bodies may be swallowed and 
 lodge in the intestine. Fecal con- 
 
LIVER. 197 
 
 cretions or enteroliths, which con- 
 sist of a nucleus of epithelial cells, 
 mucous, hairs and earthy salts. They 
 may cause great irritation and even 
 perforation. 
 
 LIVER. 
 
 1. Circulatory Disturbances. 
 
 a. Anemia. As a part of general anemia, 
 pressure on liver from disease of its 
 substance or compression of blood 
 vessels. 
 
 b. Hyperemia. 
 
 1. Active, — physiologic during diges- 
 tion, and associated with inflamma- 
 tory abdominal diseases. 
 
 2. .Passive, — from obstruction to cir- 
 culation of cardiac or pulmonary 
 disease, pleural effusions or adhes- 
 ions, thrombosis of inferior vena- 
 cava. 
 
 The liver is enlarged, edges are 
 rounded and color is darker than 
 normal. 
 
 On section, the central veins are 
 seen to be congested and surround- 
 ed by lighter areas. If the process 
 persists, secondary fatty degenera- 
 tion or atrophy of peripheral zone 
 takes place which gives rise to the 
 term nut- meg liver. There may be 
 small hemorrhages into the sub- 
 stance beneath the capsule. If 
 in the late stages degeneration and 
 reduction in size takes place and 
 the liver becomes dark red in color 
 from deposit of blood pigment, the 
 term red atrophy is given. 
 If there is a hyperplasia of connec- 
 tive tissue between the lobules and 
 acini with pigmentation, the term 
 cyanotic induration is given. 
 The hepatic function is 1 disturbed 
 and jaundice results from pressure 
 on the biliary ducts and capillaries. 
 
 c. Embolism and Thrombosis of the 
 portal vein occurs in various diseases 
 of the gastrointestinal tract particular 
 ulcerative enteritis. 
 2. Atrophy, senility, inanition and or- 
 ganic diseases, pressure, etc. Portions 
 of the liver or the greater part of its 
 structure may be involved. The liver 
 
198 PATHOLOGY. 
 
 is uneven and more or less pigmented. 
 The liver cells are decreased in size 
 and granular. The acini may disappear 
 and hyperplasia of the stroma and pro- 
 liferation of the biliary ducts may oc- 
 cur. Acute yellow atrophy — see below. 
 Red atrophy — see congestion. 
 
 3. Degeneration. 
 
 a. Pigmentation, Hemotogenous, biliary 
 and rarely anthracotic pigmentation 
 occurs. 
 
 b. Fatty Infiltration, may be physiologic 
 in children and overfed persons. 
 Pathologically it occurs from the us- 
 ual causes. 
 
 c. Parenchymatous or cloudy swelling. 
 
 d. Fatty degeneration, and 
 
 e. Amayloid, in consequence of syphilis- 
 
 f. Dropsical Infiltration, in intense in* 
 fection and intoxication. 
 
 g. Acute Yellow Atrophy, which is the 
 most advanced fatty degeneration oc- 
 curring in the liver. 
 
 Causes. It is most frequently seen in 
 young women, especially those who 
 use alcohol in excess. Intoxications, 
 by phosphorus, alcohol and bacteria. 
 Syphilis seems to act as a cause 
 and parturition acts as a determining 
 cause. 
 
 Pathologic Anatomy. The liver may 
 at first be increased in size, but gen- 
 erally it is decreased, soft and friable. 
 On section it is of a brownish or 
 grayish color (due to degenerated 
 and pigmented hepatic cells) with 
 bright red areas here and there (due 
 to foci of hemorrhagic infiltration or 
 pigmentation). 
 • The hepatic cells undergo rapid fatty 
 degenerations or necrosis and are re- 
 placed by yellow pigment particles. 
 It leads to intense cholemia. 
 
 4. Inflammations or Hepatitis. 
 
 a. Parenchymatous Hepatitis, is due to 
 infections and intoxications. The liv- 
 er cells undergo a certain amount of 
 degeneration. 
 
 b. Acute Intestitial Hepatitis or Liver 
 Abscess, is due to microorganisms, as 
 amoeba of dysentery, staphylococcus, 
 streptococcus, bacillus coli communis, 
 
LIVER. 199 
 
 etc., gaining access to the liver, di- 
 rectly, by penetrating wounds or gas- 
 tric or duodenal ulcers, etc., or in- 
 directly through the circulation or by 
 invasion along the bile ducts. 
 
 It is probably brought about most 
 frequently by ulcerations of the in- 
 testine, particularly dysentery, the 
 germ being carried to the liver 
 through the circulation. 
 
 In the tropics, traumatism without 
 any apparent contusion may occasion 
 abscess. It is probably due to micro- 
 organisms entering the injured part 
 from the biliary passages. 
 
 Pathologic Anatomy. 
 
 The traumatic or dysenteric abscess- 
 es are solitary. They begin as small 
 grayish or yellowish spots. Softening 
 takes place and a cavity is formed 
 which is filled with a creamy pus 
 often having a reddish appearance. 
 The cavity may increase to enormous 
 proportions and may be partially ta- 
 bulated. Multiple abscesses may 
 sometimes be present. If the cavity 
 is small, pus may be absorbed and a 
 cicatrix may result, or pus may be 
 inspissated and encapsulation may en- 
 sue. Large abscesses may rupture 
 into the stomach, intestines or the 
 cavities. 
 
 Metastatic abscesses or those due to 
 extension of infection from the ducts 
 etc., are multiple and of small size. 
 
 c. Chronic Interstitial Hepatitis or 
 Cirrhosis of the liver, is a diffuse 
 hyperplasia of the interlobular con- 
 nective tissue, sometimes extending 
 into the acini or causes secondary 
 changes in the liver cells. 
 Causes. Alcohol and overeating con- 
 tributes, syphilic, malaria or tuber- 
 culosis. Some authorities have as- 
 signed bacteria, entering the portal 
 circulation from the intestines, as a 
 cause. 
 
 Pathologic Anatomy. 
 
 1. Atrophic Cirrhosis ("Gin -drinker's 
 liver") is the ordinary form. 
 In the early stages the liver is 
 often enlarged but later it is con- 
 tracted, hard granular and irresru- 
 
200 PATHOLOGY. 
 
 lar on the surface. Bands of dull 
 gray or white connective tissue sur- 
 round the yellowish or brownish 
 acini and compress them so that 
 they rise above the surface. 
 Microscopically there is at first 
 round cell infiltration and connec- 
 tive tissue proliferation. The com- 
 pression of the acini may cause 
 them to denegerate. New formed 
 biliary ducts may be present. 
 
 The portal circulation is obstruct- 
 ed and congestion of the spleen and 
 gastro -intestinal mucosa with 
 
 ascites follows. 
 
 If the obstruction is extreme, col- 
 lateral circulation may relieve the 
 portal congestion. The communica- 
 tion may be between the gastric and 
 esophageal veins and between the 
 hemorrhoedal veins and the veins of 
 Retzius with the retroperitoneal 
 veins. The veins of the round liga- 
 ment may communicate with the 
 veins at the umbilicus. Jaundice is 
 rare, as the bile ducts are rarely 
 compressed. 
 
 Pathologic Physiology. Gastroin- 
 testinal disturbances from obstruc- 
 tion to the portal circulation, and 
 metabolic disturbances. 
 
 2. Hypertrophic Cirrhosis, is more of- 
 ten seen in warm climates. 
 
 The liver is uniformly enlarged, 
 smooth and indurated. On section 
 it is of a yellowish or greenish 
 color. Interlobular proliferated con- 
 nective tissue is present and ex- 
 tends into the acini every where be- 
 tween the columns of hepatic cells. 
 Proliferated bile-ducts are seen 
 within the new formed connective 
 tissue. There is frequent prolifer- 
 ation of the liver cells. 
 Jaundice is prominent. Obstruction 
 to the portal circulation is rarely 
 marked. 
 
 3. Biliary Cirrhosis, is consequent up- 
 on obstruction of the biliary ducts. 
 Toe liver is swollen from retention 
 of the bile and is sometimes con- 
 gested. Stagnation of the bile takes 
 place and the irritating substances 
 produced leads to reactive inflam- 
 mation. The appearance of th« 
 
GALL, BLADDER. 201 
 
 liver is much like that of the hy- 
 pertrophic form. There is marked 
 proliferation around the interlobu- 
 lar biliary capillaries and multipli- 
 cation of new bile ducts and hepatic 
 cells may be seen from the first. 
 If the gall ducts are absolutely ob- 
 structed and active fermentative 
 changes in the bile has occured. 
 rapid fatty degeneration and acute 
 atrophy of the liver results. 
 
 Perihepatitis or Inflammation of the 
 Capsule of the liver, may be an ex- 
 pression of syphilitic infection or oc- 
 cur alone or in association with 
 peritoneal thickening. 
 
 It may be associated with cirrhosis. 
 The capsule is thickened and may 
 cause atrophy of the underlying 
 hepatic substance. 
 
 5. Infectious Diseases. 
 
 a. Tuberculosis, is always secondary 
 and is of the miliary form. The 
 tubercles arise in the interlobular tis- 
 sue or from the acini. 
 
 b. Syphilis, is seen as diffuse infiltra- 
 tions and cirrhosis or in the form of 
 gummata. It occasions overgrowth of 
 connective tissue around parenchy- 
 matous distruction which becomes 
 necrosed with subsequent contraction. 
 This causes the irregular tucking in 
 of the liver surface, pathognomonic of 
 syphilis. 
 
 c. Leprosy is rare. 
 
 6. Tumors. Fibromata, lipomata, myo- 
 ._ mata, angiomata, sarcomata (gener- 
 ally secondary), lymphadenomata, ade- 
 nomata, carcinomata (general second- 
 ary), and cysts, — are rare. 
 
 7. Parasites. Amoeba dysenteria, Psoros- 
 permiae, Fasciola hepatica, Dicrocoelum 
 lanceatum, Schistosomum haematobium. 
 Ascarides and the Taenia echinococcus 
 causing the echinococcus cysts (see 
 Parasitic Diseases). 
 
 BILIARY DUCTS AND GALL BLADDER. 
 
 1. Inflammations, 
 a. Cholangitis or inflammation of the 
 biliary ducts, is due to duodenal ca- 
 tarrh or irritation, of gall stones, 
 foreign bodies from the intestine or 
 parasites or bacteria. 
 
202 PATHOLOGY. 
 
 The mucosa is swollen, edematous 
 and secretes abundant mucous. The 
 duct is obstructed with retention of 
 bile and jaundice. 
 
 b. Suppurative Cholangitis, may occur 
 in consequence of infectious diseases, 
 but generally from obstruction to the 
 common or the hepatic duct. Bac- 
 terial invasion and sometimes from 
 rupture of liver abscess into the bile 
 ducts may cause it. The pyogenic 
 micrococci and Bacillus Coli com- 
 munis are frequently found in sup- 
 purative cholangitis. 
 
 The ducts are filled with decomposed 
 bile or a puriform liquid and the 
 large ducts, especially, present an 
 ulcerated or necrotic appearance. 
 
 c. Chronic cholangitis, may follow an 
 intense attack of the acute, but gen- 
 erally it is due to chronic obstruc- 
 tion of the ducts and retention of the 
 bile. 
 
 Intense inflammatory lesions follow- 
 ing the passage of stones may cause a 
 cicatricial stenosis. 
 
 d. Cholecystitis or inflammation of the 
 gall bladder, results from an extens- 
 ion of cholangitis or the irritation of 
 retained bile or gall stones. It is 
 common in typhoid fever and the 
 Bacillus typhosis may be found in 
 the contents of the gall bladder. The 
 wall is thickened, mucous membrane 
 is swollen and ulcerated. The gall 
 bladder may be filled with pus 
 (empyema of the gall bladder). Rup- 
 ture may take place into the periton- 
 eal cavity, viscera or externally. 
 
 2. Stenasis of the ducts, result from acute 
 inflammations, chronic cholangitis with 
 cicatricial overgrowth of connective 
 tissue, impaction of gall stones or for- 
 eign bodies, pressure of aneurysms or 
 tumors, adhesions from peritonitis, all 
 lead to retention of bile and dilation 
 of ducts above, with consequent en- 
 largement of the liver and jaundice. 
 
 Obstruction to cystic duct, generally 
 from stone, may occasion dilatation 
 of the gall bladder with dropsical 
 liquid due to passive hypermia and 
 condition is called dropsy of the gall 
 bladder. 
 
GALL STONES. 203 
 
 3. Gall Stones or Cholelithiasis, results 
 from inspissation of bile or the deposit 
 of various substances from the bile. 
 
 Causes. Advanced years, female sex, 
 sedentary life and high living are fact- 
 ors in the etiology. Inflammations 
 leading to obstruction and retardation 
 of the outflow of bile and desquamation 
 of epithelium with mucous forms the 
 nuclei of the stone are also considered 
 as causes. Bacteria also play an im- 
 portant part, particularly the Typhoid 
 bacillus. 
 
 Pathologic Anatomy. The stone may 
 be single or multiple. They vary in 
 size from minute granules to calculi 
 several cm. in diameter. If single, they 
 are rounded or oval; if multiple, each 
 stone is marked with facets; if formed 
 in the bile dutcs they are elongated. 
 The minute granules (biliary sand) are 
 made up of biliary pigments in combi- 
 nation with calcium salts. 
 
 Large stones are made up of a central 
 nucleus composed of epithelium or 
 mucous and inspissated bile surrounded 
 by a radiating and crystaline zone of 
 cholesterin. This may be surrounded 
 by biliary pigment. 
 
 In some cases the stone is formed of 
 biliary pigment and calcium salts. The 
 stones are formed in the gall bladder or 
 ducts. They may occasion no disturb- 
 ance, or they may cause frequent at- 
 tacks of biliary colic from their passage 
 to the bowel. They may become im- 
 pacted in the duct at its entrance into 
 the bowel or in the mouth of the cystic 
 duct. 
 
 Various secondary changes may occur 
 in the gall bladder and liver. 
 
 4. Jaundice, or Icterus, is a discoloration 
 of the skin or other parts from the 
 pressure in the blood of biliary pig- 
 ments. It may be divided into:— 
 
 a, Hepatogenous (obstructive, mechan- 
 ical), from catarrhal enteritis and 
 colangitis. This is called catarrhal 
 jaundice. It may be brought about 
 by obstruction to the ducts from any 
 cause. 
 
 Congestion of the liver may lead to 
 "aundice by the overfilled blood ves- 
 
204 PATHOLOGY. 
 
 sels or by reabsorption of the bile, 
 b. Hematogenous jaundice, once re- 
 garded as due to disintegrated blood 
 in general circulation, but now the 
 pigment formation is recognized as 
 only taking place in the liver. 
 Active hemolysis is, however, an im- 
 portant element and is seen in yellow 
 fever, acute yellow atrophy and jaun- 
 dice of the new born and various in- 
 toxications. 
 
 Some believe that the hepatic cells 
 may reverse their secretion so as to 
 discharge the bile into the lymphatics 
 instead of the bile capillaries, but 
 this is not as yet proven. 
 Pathologic Anatomy. The biliary ca- * 
 pillaries are distended and the he- 
 patic cells are pigmented. The bile 
 is absorbed by the lymphatics and 
 given to the general circulation. The 
 skin and external mucous membrane 
 are discolored. The urine is dark 
 brown or green in color. "When the 
 bile fails to enter the intestine the 
 stools are of a putty color. 
 In the hematogenous jaundice the 
 color of the stools is, to a certain 
 extent, maintained. 
 
 PANCREAS. 
 
 1. Circulatory Disturbances. 
 
 a. Active hyperemia occurs during di- 
 gestion and acute inflammation. 
 
 b. Passive hyperemia occurs from ob- 
 struction to the portal circulation. 
 
 c. Hemorrhage occurs as minute 
 petechiae or diffuse infiltrations, 
 from passive congestion or hemor- 
 rhagic and infectious diseases. 
 Extensive hemorrhage sometimes oc- 
 curs as an idiopathic affection. 
 
 2. Atrophy occurs from old age and 
 marasmic conditions. 
 
 3. Degenerations. 
 
 a. Parenchymatous, from acute infec- 
 tions. The organ is enlarged, soft 
 and sometimes congested. 
 
 b. Amyloid is rare. 
 
 c. Pigmentation occurs in the atrophic 
 organ of old age, hemorrhagic in- 
 filtration and subsequent disorganiza- 
 
PANCREAS. 205 
 
 tion of the extravasated blood. 
 
 d. Necrosis, of small areas from hem- 
 orrhage or inflammations. The whole 
 organ may sometimes undergo gan- 
 grenous necrosis. 
 
 Fat necrosis is most frequently found 
 in association with acute or chronic 
 pancreatitis, tumors of the pancreas 
 or obstruction of its ducts. It may 
 occur independently. 
 
 e. Hyaline degeneration is seen in the 
 islands of Langerhans, which may 
 suffer atrophy or degeneration, in- 
 dependently or associated with 
 chronic interstitial pancreatitis. 
 
 4. Inflammation or Pancreatitis. 
 
 a. Acute hemorrhagic pancreatitis oc- 
 curs more frequently in young per- 
 sons and is due to infection of the 
 pancreas or its ducts. The pancreas 
 is swollen, lobules are enlarged and 
 the interlobular tissues are com- 
 pressed. Hemorrhagic infiltration is 
 constant, but varies in extent. 
 
 b. Acute suppurative or necrotic pan- 
 creatitis results from direct exten- 
 sion of septic processes, as gastric 
 or duodenal ulceration, purulent col- 
 lections in peritoneum, etc., or it may 
 result as an independent affection 
 from the intestinal tract. 
 
 Swelling is generally marked with 
 more or less softening and some- 
 times necrotic foci. Complete gan- 
 grene may sometimes occur. 
 
 c. Chronic indurative pancreatitis or 
 cirrhosis may be hematogenous in 
 origin, resulting from syphilis and 
 alcoholism, or from prolonged irri- 
 tation in consequence of entrance of 
 intestinal contents or partial stenosis 
 of its duct. It is analogous to 
 chronic hepatitis and leads to sim- 
 ilar induration or cirrhosis. 
 
 Pathologic Physiology. There is a 
 disturbance of the internal secretion 
 with relation to the consumption of 
 sugar. When the secretion stops or 
 diminishes glycosuria or diabetes re- 
 sults. 
 
 5. Infectious Diseases. 
 
 Syphilis, in form of diffuse induration 
 or gumma ta. 
 
206 PATHOLOGY. 
 
 Tuberculosis, in form of miliary tu- 
 bercles in case of generalized tuber- 
 culosis. 
 6. Tumors. Carcinoma, sarcoma is oc- 
 casionally seen and is generally sec- 
 ondary. 
 Cysts. 
 
 Obstruction to the pancreatic duct from 
 tumors, calculi, inflammation or con- 
 tracting tissue of chronic pancreatitis 
 may lead to dilatations of the duct and 
 sometimes cause cystic formations. 
 
 Pancreatic calculi are made up of a 
 carbonate or phosphate of lime and are 
 of irregular shape. 
 
 PERITONEUM. 
 
 1. Circulatory Disturbances. 
 
 a. Hyperemia, both active and passive, 
 is met with from general causes. 
 
 b. Hemorrhage, as punctate extravas- 
 ations in septic and hemorrhagic dis- 
 eases and in parts of the peritoneum 
 covering intense inflammatory lesions 
 of adjacent parts. It may also be 
 due to intense passive congestion. 
 Certain intoxications, as phosphorus, 
 snake venom, etc. 
 
 Traumatism may cause large hem- 
 orrhage into the peritoneal cavity. 
 
 c. Dropsy of the peritoneum or ascites 
 
 may occur as part of general anas- 
 arca in cardiac or renal disease, or to 
 obstruction of the portal circulation, 
 as in cirrhosis of the liver. 
 
 2. Inflammations of the peritoneum or 
 Peritonitis. 
 
 a. Acute Peritonitis. 
 
 Causes. Bacteria or bacterial prod- 
 ucts. Among the bacteria are the 
 streptococcus pyogenes, staphylococ- 
 cus pyogenes, coli communis, diplo- 
 coccus pneumonia, bacillus of Fried- 
 lander and the gonococcus. 
 The bacteria gain entrance through 
 the blood, Fallopian tubes, invasion 
 through walls or perforation of the 
 viscera or external walls. 
 Pathologic Anatomy may be divided 
 into: — 
 1. Acute localized peritonitis is seen 
 
PERITONEUM. 207 
 
 when bacteria escape gradually and 
 in small numbers through the in- 
 testine walls, or when perforation 
 is secondary to the production of 
 an exudate, which limits the ex- 
 tent of the infection. 
 
 It is most frequently seen in asso- 
 ciation with disease of the tubes 
 or uterus or in the region of the 
 appendix. 
 
 The exudate may remain fibrinous, 
 but generally becomes fibrino-puru- 
 lent in the later stages. In cases 
 of perforative peritonitis, localized 
 encapsulated abscesses are com- 
 monly met with. 
 
 The exudate may be removed by 
 the pus emptying into the bowel 
 or in rare cases it discharges ex- 
 ternally. It may become gradually 
 inspissated. The fibrinous exudate 
 is frequently absorbed with remain- 
 ing fibrous tissue adhesions. 
 
 2. Acute general peritonitis results 
 from the discharge of large quan- 
 tities of infective matter from a 
 perforation of the bowel or other 
 organs, or it may be due to a 
 breaking down of the fibrinous wall 
 of a localized peritonitis. 
 
 The peritoneum, particularly the 
 visceral, is congested and luster- 
 less, with a varying quantity of 
 serous exudation. It is generally 
 scanty and flakes, or thin coatings 
 of fibrinous exudate appears upon 
 the walls of the intestine, which are 
 matted together. Later, emigration 
 of leucocytes or pus cells renders 
 the exudate more yellow. Adjacent 
 coils of the intestine are agglu- 
 tinated and pockets, containing a 
 sero-purulent liquid, may be formed 
 between them. 
 
 In the most violent form of the 
 local or general peritonitis the ex- 
 udate assumes a putrid character 
 and the deposit upon the serosa 
 or the serosa may undergo necrotic 
 change. 
 
 b. Chronic peritonitis may be the ter- 
 mination of a localized acute form. 
 It may be due to inflammatory thick- 
 
208 PATHOLOGY. 
 
 ening of the peritoneum adjacent to 
 organs the seat of disease. 
 If due to localized peritonitis it 
 usually presents itself in the form of 
 fibrous thickenings or adhesions, and 
 occasionally calcareous plates are 
 found in the thickened peritoneal cov- 
 erings of the bowel, etc. If it is 
 due to diffuse acute peritonitis the 
 adhesions are widespread and the 
 peritoneum is more or less diffusely 
 thickened and more or less liquid ef- 
 fusion may be present. In some cases 
 the peritonitis arises as a chronic 
 process from the beginning. The 
 cause for this is obscure. Syphilis 
 sometimes seems to be a factor. The 
 peritoneum is uniformly thickened, 
 but in some cases presents small nod- 
 ular lesions, suggesting miliary tuber- 
 cles. In several instances serous ef- 
 fusion, have led to the diagnosis of 
 tuberculous peritonitis. Microscopic 
 examination shows a fibrous structure, 
 and is negative to tuberculosis. 
 
 3. Infectious Diseases. 
 
 Tuberculosis of the peritoneum is 
 usually secondary to tuberculosis of 
 some abdominal viscera or of a more 
 distant organ. 
 
 It is primary in rare instances. 
 Marked inflammatory changes are as- 
 sociated with the specific tubercle. 
 In some cases extensive adhesions are 
 met with and the tubercles tend to 
 agglutinate, forming considerable 
 
 cheesy masses. 
 
 Miliary tuberculosis without any in- 
 flammatory changes may occur. 
 Tuberculosis of the peritoneum may 
 terminate by complete resolution, but 
 the peritoneum is left somewhat thick- 
 ened. 
 
 4. Tumors. Fibromata, lipomata, sarco- 
 mata, carcinoma ta (usually secondary). 
 
 5. Parasites. Echinococcus, Filaria, Lin- 
 guatula Rhinaria. Cysticercus cellu- 
 losae. 
 
209 
 
 DISEASES OF THE URINARY 
 SYSTEM. 
 
 KIDNEYS. 
 
 1. Malformations. One kidney may be 
 absent and in rare instances both may 
 be absent. They may be congenitally 
 lobulated and in some cases three kid- 
 neys have been observed. The kidneys 
 may be united into one horse-shoe 
 shaped organ. 
 
 They may be abnormally attached or 
 may be movable or floating. 
 
 2. Circulatory Disturbances. 
 
 a. Anemia, as a part of general anemia 
 or by pressure upon its arteries by 
 growths, etc. The organ is pale and 
 shows various atrophic and degen- 
 erative changes. 
 
 b. Hyperemia. 
 
 1. Active Hyperemia is due to in- 
 flammation from chemical or infec- 
 tious irritation. The kidney is en- 
 larged and dark red in color, with 
 sometimes punctate hemorrhages. 
 
 2. Passive Hyperemia is due to con- 
 ditions impeding the circulation. 
 The organ is enlarged and darkened 
 in color, especially in the pyramids. 
 
 c. Hemorrhage. Small hemorrhages 
 (punctate) may occur from intense 
 active or passive hyperemia, also in 
 nephritis. 
 
 Large hemorrhages are the result of 
 trauma. 
 
 d. Edema occurs from obstruction to 
 the venous circulation. Congestion is 
 associated. Cases of simple edema 
 may result from obstruction to the 
 
 urinary outflow. 
 
 e. Thrombosis is rare, but embolism is 
 
 quite common. 
 
 3. Inflammation or Nephritis. 
 
 Causes. Parenchyma poisons, as ar- 
 senic, mercury, phosphorus, cantharidis, 
 etc. Infectious diseases, as scarlet 
 fever, diphtheria, cholera, septicemia, 
 
210 PATHOLOGY. 
 
 etc. Chronic infections, as syphilis, tu- 
 berculosis, etc., and auto-intoxications, 
 as gout, etc. 
 Pathologic Anatomy. 
 a. Acute Parenchymatous Nephritis or 
 Acute Bright's Disease. 
 
 1. Acute Degenerative Nephritis. The 
 
 kidney is enlarged and pale. The 
 cortex is thickened and the cap- 
 sule strips easily. The epithelium 
 of the convoluted tubule and some- 
 times the capsule of the glomeruli 
 is swollen, cloudy and desquamated. 
 Emigrated leucocytes and some- 
 times red cells are found in the 
 tubules and Malpaghian capsule. 
 
 2. Acute Glomerulomphritis. In this 
 form the glomeruli are primarily 
 affected. There is a proliferation 
 of the vascular endothelium within 
 the tuft. Polymorphonuclear leu- 
 cocytes and lymphocytes may be 
 present. Hemorrhage into the cap- 
 sular space and necrosis of the cells 
 of the capsule and tuft may occur, 
 This form occurs most commonly 
 in scarlet fever. 
 
 3. Acute Diffuse Nephritis. Ordinary 
 Bright's Disease. It generally oc- 
 curs as a termination to either of 
 the other two forms. The kidney 
 has the general characteristics of 
 the other forms. The capsule strips 
 easily, the organ is enlarged and 
 uniformly gray or yellow in color. 
 Hemorrhages may give it a dark 
 red color. There is more or less 
 degeneration of the epithelium of 
 the convoluted tubules and Mal- 
 pighian bodies. Associated with the 
 epithelial changes may be evidences 
 of interstitial changes, and con- 
 nective tissue proliferation is also 
 seen. In the cases where there is 
 a hemorrhagic tendency the term 
 acute hemorrhagic nephritis is often 
 used. 
 
 b. Acute Interstitial Nephritis. 
 
 1. Non-suppurative (Acute Interstitial 
 Nephritis) occurs during infectious 
 diseases. The changes may be dif- 
 
BRIGHT'S DISEASE. 211 
 
 fuse or in areas only. The tissues 
 of the corticulo- medullary junction, 
 glomerular region or those beneath 
 the capsule are marked with con- 
 nective tissue proliferation, leuco- 
 cytes and lymphocytes. 
 
 2. Suppurative Nephritis results from 
 metastatic involvement, extension 
 from pyelitis or adjacent suppura- 
 tive disease. Small foci or larger 
 abscesses result, which empty 
 themselves into the tubules and 
 pelvis and sometimes the entire or- 
 gan breaks down. 
 
 c. Chronic Parenchymatous Nephritis 
 
 results from repeated acute attacks, 
 infectious diseases, alcoholism, auto- 
 intoxications, etc. The kidney is en- 
 larged, capsule strips easily and the 
 color is grayish or yellowish. It is 
 often called large white kidney. 
 The kidney may sometimes be red 
 in color or areas of yellow or gray 
 appearing within congested portions 
 give to it the term chronic hemor- 
 rhagic nephritis. 
 
 Small cysts may form in the sub- 
 stance, upon the surface by disten- 
 tion of the tubules or Bowman's cap- 
 sules. 
 
 In the late stages degeneration of 
 the epithelium is pronounced, the or- 
 gan is light in color and interstitial 
 changes render the kidney more firm 
 and reduced in size. 
 According to the amount of fatty 
 parenchymatous change, fatty con- 
 tracting kidney, or according to the 
 amount of interstitial overgrowth — 
 secondary interstitial nephritis, is 
 often applied. 
 
 d. Chronic Interstitial Nephritis or 
 Chronic Bright's Disease, or Chronic 
 Granular Kidney, results from a pri- 
 mary affection, as gout, alcohol, etc., 
 and as a result of arteriosclerosis. 
 The arteries are sclerosed and the 
 cortex of the kidney degenerates in 
 patches. The kidney is hard, red, 
 atrophied in areas and somewhat con- 
 tracted. 
 
 In advanced cases it is very small 
 
212 PATHOLOGY. 
 
 and indurated. The surface is nodu- 
 lar, capsule thick and adherent to the 
 atrophied cortex. There is marked 
 increase of fibrous tissue, which is 
 abundant along the tubules and 
 around the glomeruli, which tend to 
 atrophy and may disappear. 
 
 The epithelium of the tubules de- 
 generate and disappear, to be re- 
 placed by a cubical non-secreting 
 form. The tubules may dilate and 
 contain in many places epithelium 
 undergoing fatty, granular or hyaline 
 degeneration, which forms casts. 
 The tubules may dilate so as to form 
 cysts. 
 
 Pathological Physiology. Gastroin- 
 testinal disturbances. In the acute 
 form the urine is decreased and may 
 be mixed with blood. In the chronic 
 form nitrogenous elimination may be 
 reduced. Urea is decreased and uric 
 acid is generally decreased in quan- 
 tity. In all cases there is an albu- 
 minuria and the presence of tube 
 casts, which may be divided into: — 
 
 Hyaline casts (clear rounded bodies), 
 seen in simple congestion and in 
 icterus. They are abundant in acute 
 and chronic forms of nephritis. 
 
 Cellular casts, most frequent are 
 granular or hyaline casts covered with 
 epithelial cells, and are seen in the 
 acute parenchymatous nephritis. 
 Leucocytic casts are found in puru- 
 lent pyelonephritis. 
 
 Blood casts are made up of red blood 
 cells or blood pigment, and are seen 
 in acute and chronic hemorrhagic 
 nephritis. 
 
 Granular casts are composed of 
 broken-down epithelial cells and are 
 common in chronic nephritis; may 
 also occur in the acute form. 
 
 Cylindroids are thread-like formations 
 resembling casts, but have long taper- 
 ing ends. They occur in irritations 
 that are not sufficient to cause ne- 
 phritis. They are also found in ne- 
 phritis. They are also supposed to 
 .. 'be produced from other parts of the 
 
URETERS. 213 
 
 genito-urinary system, as from the 
 glands of Cowper. 
 
 Results of Nephritis. From the in- 
 fectious or toxic cause, acute de- 
 generative or inflammatory lesions of 
 the heart muscle and dilatations may 
 occur. Acute inflammations of the 
 serous membranes. 
 
 Subacute or chronic nephritis may 
 cause hypertrophy of the heart. 
 The arteries become sclerosed. 
 Edema and dropsy, from disease cf 
 the blood vessels. 
 
 Uremia is the clinical manifestation, 
 probably caused by the retention of 
 toxic substances in the blood, which 
 are ordinarily excreted with the 
 urine. 
 
 4. Atrophy may be congenital or may be 
 due to old age or nephritis. 
 
 5. Hypertrophy may take place in one 
 kidney when the other is congenitally 
 wanting, diseased or has been removed. 
 
 6. Degenerations. Parenchymatous, fatty 
 infiltration and degeneration, calcifica- 
 tion, glycogenic infiltration, amyloid 
 degeneration. 
 
 7. Infectious Diseases. Tuberculosis and 
 Syphilis. 
 
 8. Tumors. Fibroma, lipoma, leiomyoma, 
 congenital adenoma (remnant of the 
 suprarenal capsule), sarcoma, adenoma 
 (rare), papuliferous cystic adenoma, 
 carcinoma (rare), cysts. 
 
 9. Parasites. Bacteria occur in various 
 affections. Of the animal parasites the 
 echinococcus cysts, filariae, eggs of 
 Fasciola hepatica, amoeba and infu- 
 soria. Round worms and the oxyuris 
 may migrate or enter through fistulae. 
 
 PELVIS OF THE KIDNEY AND URE- 
 TER. 
 
 The pelvis or ureter may be absent or 
 malformed. The ureter may be ob- 
 structed by congenital atresia, twists 
 or disease. The ureters may be dilated 
 from the above causes and the secre- 
 tion still going on may convert the 
 kidney into somewhat of a cyst con- 
 taining a clear liquid, partly urine and 
 
214 PATHOLOGY. 
 
 partly transudate, to which condition 
 the term hydronephrosis is given, j Cal- 
 culi frequently occur in the pelvis of 
 the kidney from the precipitation of 
 various normal or abnormal constit- 
 uents of the urine. They may vary in 
 size from small particles (renal sand 
 or gravel) to large stones made up of 
 uric acid, oxalate of lime and some- 
 times calcium carbonate and triple 
 phosphates. 
 
 Inflammation of the Pelvis, or Pyelitis, 
 
 results from irritations of ingested 
 poisons, as cantharidis, turpentine, etc., 
 and more frequently from irritation of 
 a calculus. The inflammation may ex- 
 tend into the kidney (pyelonephritis). 
 If there is complete obstruction and the 
 pelvis becomes dilated and filled with 
 pus the term pyonephrosis is given. 
 Inflammation of the Ureter, or Ure- 
 teritis, may occur under the same con- 
 ditions as pyelitis. 
 
 BLADDER. 
 
 The bladder may be absent or divided 
 by a septum; both conditions are rare. 
 A common condition (exstrophy), an- 
 terior wall of the abdomen over the 
 bladder and the bladder is wanting and 
 the ureters are exposed to view. 
 Fistulous openings between the blad- 
 der and adjacent cavities are often 
 met with from disease or injury. Dila- 
 tation may result from stenosis of its 
 neck or urethra, or paralysis in conse- 
 quence of disease of the spinal cord 
 or nerves. Diverticulae may be ac- 
 quired, which are sometimes large and 
 afford concealment for calculi. 
 The bladder may become hypertrophied 
 from obstruction to the urinary flow. 
 Rupture may take place from over- 
 distention or trauma. 
 
 1. Circulatory Disturbances. Anemia, ac- 
 tive and passive hyperemia are met 
 with from the usual causes, and hem- 
 orrhages from severe congestion or in- 
 flammation, ulceration, tumors, cal- 
 culi, etc., and hemorrhagic diseases are 
 also met with. 
 
 2. Inflammation of the Bladder, or 
 Cystitis, may be acute or chronic and 
 
BLADDER. 215 
 
 is caused by irritants excreted with 
 the urine, infections as gonorrhoea, 
 etc., injury as by calculus, etc. 
 It may be divided into: — 
 
 a. Muco-purulent Cystitis. In acute 
 cases the mucous membrane is swol- 
 len, blood vessels are injected and 
 the surface is covered with a muco- 
 purulent exudate containing pus cells 
 and desquamated epithelium. In 
 chronic cases the submucosa is thick- 
 ened and the muscularis is hyper- 
 trophied and fibrous tissue bands rib 
 the surface. Erosions and ulcerations 
 may occur. 
 
 b. Phlegmonous Cystitis results from 
 infections or retention of the urine 
 in paraplegia. Perforation of walls 
 with paracystitis or phlegmonous in- 
 flammation of the surrounding tissues 
 may occur. 
 
 c. Pseudo- membranous Cystitis occurs 
 in severe infectious diseases and may 
 present itself as typical pseudo-mem- 
 branes or in combination with the 
 phlegmonous. 
 
 3. Infectious Diseases, as secondary tu- 
 berculosis and in rare cases syphilitic 
 ulcers are seen. 
 
 4. Calculi are frequently found and are 
 due to precipitation from the constit- 
 uents of the urine as the result of 
 stagnation and fermentative changes. 
 They form in the pelvis of the kidney 
 and gradually enlarge in the bladder. 
 Foreign bodies, parasites, etc., may 
 sometimes act as nuclei to the stones. 
 The common varieties of stones are 
 uric acid, the r phosphatic, oxalates are 
 less common and cystin and xanthin 
 are rare. 
 
 5. Tumors. Fibroma, myoma, myxoma, 
 adenoma, secondary carcinoma, pri- 
 mary carcinoma (rare), and sarcoma is 
 very rare. 
 
 URETHRA. 
 
 1. Inflammation of the Urethra, or 
 
 Urethritis, may be acute or chronic. 
 The acute is generally due to a specific 
 micro-organism (gonococcus). It may, 
 however, be non-specific from chemical 
 
216 PATHOLOGY. 
 
 or mechanical irritation associated with 
 infection. 
 
 It usually affects the mucosa at or near 
 the meatus and then spreads rapidly 
 to the posterior parts. The mucosa Is 
 congested, red, swollen, with a yellow 
 or greenish purulent exudate. The 
 crypts swell and are distended with a 
 purulent exudate. 
 
 Microscopically, it has the features of 
 an intense purulent catarrh. 
 Associated Lesions. Prostatitis, epididy- 
 mitis, orchitis, purulent conjunctivitis 
 when pus is brought into contact with 
 the conjunctiva, gonorrheal arthritis 
 and gonorrheal tenosynovitis and occa- 
 sionally pericarditis, endocarditis and 
 myocarditis, etc., are all caused by 
 metastasis. 
 
 Stricture in the membranous portion is 
 frequent. This is a result of produc- 
 tive inflammation of the mucosa and 
 submucosa. 
 
 Gleet is a slight discharge of mucous 
 exudate in chronic urethritis. There is 
 generally no gonococci, but occasionally 
 a few may be found. The urine con- 
 tains flocculent shreads (clap-threads) 
 resembling cylindroids and often cov- 
 ered with pus cells. 
 
 2. Infectious Diseases. Gonorrhoeal 
 urithritis. (See above and Bacterial 
 Diseases). Tuberculosis. Syphilis, the 
 chancre may occur, but usually under- 
 goes rapid ulceration. 
 
 3. Tumors. Small polypoid, carcinoma, 
 sarcoma (rare), retention cysts. 
 
 DISEASES OF THE DUCTLESS 
 GLANDS. 
 
 THYROID GLAND, may be congenitally 
 absent in an idiot or a cretin. It may 
 be undersized or of an irregular shape 
 or separated into lobules. 
 The gland stands in close etiological re- 
 lationship to certain general conditions 
 as: — 
 
 Cretinism. The gland is congenitally 
 absent, deficient, or early becomes 
 functionless. It is sometimes goiter- 
 
THYROID GLAND. 217 
 
 ous. The condition usually developes 
 soon after birth. 
 
 The cretin is physically and mentally 
 undeveloped. The head is large, lips 
 and tongue thick, subcutaneous tis- 
 sue is flabby, abundant and some- 
 times myxedematous. 
 Myxedema. Develops in later life, 
 sometimes following goiter, gumma, 
 tumors, etc., of the thyroid gland. 
 The eyelids, subcutaneous tissue of the 
 face and neck are swollen, later in- 
 volvement of the limbs and body oc- 
 curs. The skin is pallid and dry, the 
 hairs fall out and nervous symptoms 
 are developed and the intelect dis- 
 turbed. 
 
 Graves Disease or Exophthalmic 
 Goitre. The gland is enlarged; there 
 is palpitation of the heart, exophthal- 
 mos and muscular tremor. It is prob- 
 ably due to over-production of thyroid 
 secretion. Some authorities hold that 
 the condition is primarily nervous. 
 
 1. Inflammation, may be mild or severe. 
 It results from trauma or infection. A 
 degree of inflammation is frequently 
 met with in infectious fevers as diph- 
 theria, typhoid, etc. Recovery by reso- 
 lution or abscess may take place which 
 may rupture into the larynx or cellular 
 tissue of the neck. 
 
 2. Goiter or Struma, is the term given 
 to enlargement of the thyroid gland 
 resembling tumors but not classed as 
 such. 
 
 Cause. Certain localities, drinking 
 water and an infectious cause have 
 been considered but not demonstrated. 
 Pathologic Anatomy. 
 
 a. Parenchymatous Goitre. The glandu- 
 lar tissue undergoes more or less ac- 
 tive hyperplasia. The gland is gen- 
 erally uniformly enlarged but may 
 show lobular elevations. Cystic 
 forms may occur and are designated 
 as cystic goiter. Ordinarily the 
 acini contain the normal amount of 
 colloid material but sometimes the 
 acini are greatly distended with the 
 colloid material and the name colloid 
 goiter is given. Connective tissue 
 changes may be slight or very con 
 spicuous in some cases. 
 In thickening of the capsule and 
 
218 PATHOLOGY. 
 
 preponderance of stroma, the term 
 fibrous goitre is applied, 
 b. Vascular Goitre, is applied when the 
 enlargement is characterized by great 
 dilatation of the blood vessels with- 
 in the gland. The glandular tissue 
 may not show any change or it may 
 be similar to that of the parenchy- 
 matous. The gland is enlarged and 
 may pulsate. It is met with as an 
 important pathological condition in 
 many cases of Graves disease. 
 
 3. Infectious Diseases. 
 
 Tuberculosis, as miliary tubercles or 
 caseous nodules. 
 Syphilis, in form of gumma. 
 Actinomycosis is rare. 
 
 4. Tumors. Adenoma, carcinoma, sar- 
 coma secondary tumors are rare. 
 
 5. Parasites. Ecchinococcus cysts (rare). 
 SUPRA RENAL GLANDS. 
 
 1. Congenital Abnormalities. The glands 
 may be congenitally absent, may be 
 small or composed of separate portions 
 some of which may be found within 
 the capsule of the kidney, causing a 
 tumor (Grawitz hypernephroma). 
 
 2. Circulatory Disturbances. 
 Hemorrhage (rare) is associated with 
 hemorrhagic diseases, anemias, trau- 
 matism, or obstruction to the venous 
 circulation, etc. 
 
 3. Degenerations. Pigmentation, fatty and 
 amyloid degenerations. 
 
 4. Inflammation during the course of 
 infectious diseases is sometimes seen. 
 
 5. Infectious Diseases. 
 
 Tuberculosis, as miliary tubercules in 
 the course of general tuberculosis, also 
 as a fibro-caseous form in which the 
 gland is enlarged, hard, nodular or 
 irregular in outline. The capsule is 
 thickened, the gland substance is dry, 
 yellow and cheesy or puriform. This 
 condition is found in the presence of, — 
 .Addisons Disease, in which the skin 
 of exposed parts of the body and flexor 
 surfaces is characterized by a brown- 
 ish pigmentation. The pigmentation is 
 at first mottled then becomes uniform. 
 Brownish or purplish spots are fre- 
 quently seen on the mucous membranes. 
 Together with this is great weakness, 
 
TESTICLES. 210 
 
 stomachic disturbance and cardio- 
 vascular asthenia. 
 6. Tumors. Sarcoma, adenoma, carcino- 
 ma, glioma and neuroma (rare), sec- 
 ondary sarcoma and carcinoma. 
 
 DISEASES OF THE REPRODUCTION 
 SYSTEM. 
 
 PENIS. 
 
 1. Congenital Malformations. Absence is 
 rare. It may be double or have , two 
 canals or it may be abnormally small. 
 The urethra may terminate on the un- 
 der surface of the penis (hypospadias) 
 or on the dorsum (epispadias). 
 
 The prepuce may be elongated and con- 
 stricted, producing phimosis. 
 
 2. Inflammation, is due to injury or in- 
 fection. 
 
 Balanitis is term given when the glans 
 is inflamed and posthitis, when the 
 prepuce alone is inflamed. Conditions 
 are caused by foreign substances or 
 the decomposition of smegma from un- 
 cleanliness. 
 
 If the prepuce is constricted in front 
 of the glans, it is called phimosis and if 
 behind the glans it is called para- 
 phimosis. 
 
 3. Infectious Diseases. 
 
 Syphilitic chancre, soft chancres or 
 chancroid are frequent. 
 Tuberculosis is rare. 
 
 4. Tumors. Papilloma or condyloma acu- 
 minatum occurs in association with 
 gonorrhoea, syphilis, irritations, etc. 
 carcinoma, sarcoma, angioma, lipoma 
 and cysts. 
 
 SCROTUM, may be imperfectly united. 
 Elephantiasia is a common disease of 
 the East. The scrotum may become very 
 large and epithelioma is not uncom- 
 mon. Dermoid cysts are sometimes 
 found. ' 
 
 TESTICLES. 
 
 1. Congenital Abnormalities. Absence 
 (anorchia) rare, small (microrchia), 
 there may be one (monorchia), 
 more than two (polyorchia), or they 
 may be undescended (cryptorchia). 
 
220 PATHOLOGY. 
 
 I 
 
 2. Atrophy and Hypertrophy, may be 
 
 seen from the usual causes. 
 
 3. Degenerations, as fatty, myxomatous, 
 calcification and caseation are met 
 with. 
 
 4. Circulatory Disturbances, such as ac- 
 tive and passive hyperemia and em- 
 bolism which may be followed by 
 necrosis or gangrene has been seen. 
 
 5. Inflammation of the testicle (orchitis), 
 and the epididymis (epididymitis) are 
 common. They may be acute or 
 chronic and are due to injuries or in- 
 fections. The infection may be due to 
 extension from some adjacent part or 
 to gonorrhoeal inflammation of the 
 urethra. It may also be due to infec- 
 tions as typhoid fever, parotitis, 
 pyaemia, small pox, etc. 
 
 The organ is swollen and hyperemic. 
 A hydrocele may result from envolve- 
 ment of the covering. Abscesses may 
 form or the inflammation may take on 
 a chronic form; the end is more or less 
 complete distruction of the testicle. 
 Permanent enlargment or gradual 
 atrophy from chronic inflammation may 
 ensue. 
 
 6. Infectious Diseases. 
 
 Tuberculosis of the testicle and 
 epididymis is usually secondary. 
 Syphilis, as circumscribed gummata. 
 Lepra is met with. 
 
 7. Tumors, Filroma, rhabdomyoma, sar- 
 coma and carcinoma. The rare tumors 
 are chondroma, osteoma, myxoma and 
 adenoma. 
 
 Cysts as dermoid and retention are 
 
 met with. 
 9. Parasites. Echinococcus cysts are 
 
 rare. 
 PROSTATE GLAND. 
 
 1. Inflammation or Prostatitis, may be of 
 traumatic origen but usually it is due 
 to some infection as during the course 
 of gonorrhoea, cystitis, proctitis, etc. 
 Abscesses may result or it may be fol- 
 lowed by atrophy. 
 
 2. Atrophy, is rare before middle life but 
 occurs in the aged. 
 
 3. Hypertrophy is frequently seen in old 
 age and may involve the entire gland or 
 only one lobe. Enlargment may be due 
 
OVARIES. 221 
 
 to a hyperplasia of the tissue or to new 
 
 formations. Most common form is the 
 
 hypertrophy of the glandular strutcure 
 
 in which the epithelium and acini are 
 
 increased. 
 
 The fibrous tissue predominates in the 
 
 interstitial form. 
 
 Urination is often interfered with. 
 
 4. Concretions, may be seen in old age, 
 and vary in size from microscopic 
 granules to bodies the size of millet 
 seeds. 
 
 5. Infectious Diseases. Tuberculosis in 
 association with tuberculosis elsewhere. 
 
 6. Tumors. Adenoma, sarcoma, carcin- 
 oma, cysts. 
 
 SEMINAL VESICLES. 
 
 1. Inflammation, is usually due to some 
 infection as gonorrhoea, epididymitis 
 or prostatitis. A chronic inflammation 
 of the vessels may result from the 
 acute form and cause contraction or 
 thickening of the walls. 
 
 2. Tuberculosis, is usually secondary to 
 the disease elsewhere. 
 
 3. Tumors^ Primary carcinoma (rare), 
 secondary carcinoma more common. 
 Retention cysts. 
 
 OVARIES. 
 
 1. Congenital Abnormalities. One or 
 both ovaries may be absent; they may 
 be congenitally small or displaced, her- 
 mia ovarii may occur or suppernumer- 
 ary ovaries have been found. 
 
 2. Circulatory Disturbances, active and 
 passive hypermia and hemorrhages into 
 the substance is met with. 
 
 3. Inflammation or Oophoritis, is gener- 
 ally a secondary infection and is due 
 to an extension from the uterus, tubes 
 or pelvic cavity or it may be carried 
 by the blood. The most pathogemic 
 germs are the gonococcus, streptococcus 
 and the staphylococcus. The organ be- 
 comes enlarged and soft. Its surface 
 may be covered with serum or pus or 
 abscesses may be formed within. A 
 chronic form with fibrous tissue for- 
 mation and subsequent contraction or 
 atrophy of the organ occurs. 
 
 Tuberculosis, may be primary but more 
 commonly secondary to disease of other 
 parts. 
 
222 PATHOLOGY. 
 
 5. Tumors.. Carcinoma, fibroma, 
 chondroma, angioma and cysts. The 
 cysts may be due to non-ruptured 
 Grafian follicles which go or increas- 
 ing in size and contain a clear fluid 
 with sometimes blood. Dilatation of the 
 parovarian tubules give rise to the 
 socalled Parovarian cysts. 
 A c?7st of the ovary called papillomatous 
 cystoma is made up of a number of 
 cysts from the walls of which grow 
 numerous papillae which may fill the 
 cystic cavities. 
 
 Dermoid cysts are more frequent in the 
 ovary than in other parts. 
 
 FALLOPIAN TUBES. 
 
 1. Congenital Abnormalities. They may 
 be absent, or deformed. 
 
 2. Stenosis, may occur congenitally or 
 be acquired. This may cause dilatation. 
 
 3. Circulatory Disturbances. Active and 
 passive hyperemia, and hemorrhage oc- 
 curs normally during the menstrual per- 
 iod and pathologically when due to in- 
 fections. 
 
 4. .Inflammation or Salpingitis, is caused 
 by an infection by the gonococcus, 
 streptococcus, colon bacillus and 
 pneumococcus. The infection gen- 
 erally extends from the uterin cavity. 
 The mucous membrane is first involved 
 with the formation -of an exudate of a 
 mucous or purulent character depend- 
 ing upon the severity. The contents 
 of the tube may escape into the uterus 
 or into the peritoneal cavity. The tube 
 may become occluded and then dilated 
 with fluids to which the terms hydro- 
 salpinx, pyosalpinx, or haematosalpinx 
 are given according to their nature. 
 The walls may become distorted and 
 thickened. They may contain small 
 abscesses. 
 
 5. Infectious Diseases, as tuberculosis 
 (primary or secondary) and syphilis in 
 the form of gummata or diffuse sclerosis 
 may occur. 
 
 6. Tumors. Fibroma, carcinoma, papil- 
 loma, sarcoma. Cysts, as hydrosalpinx 
 and small cysts of the fimbria, formed 
 
 r in Multers ducts (hydatids of Morgagni) 
 
 : may be seen. Tubo-ovarian cysts^are 
 
 "formed by distention of the abo^ominal 
 
UTERUS. : 223 
 
 end of the tube when the u.nbria are 
 attached to the ovary. 
 UTERUS. 
 
 1. Abnormalities. Absence is rare. There 
 may be congenital hypoplasia or ar- 
 rested development may be due to a 
 failure to increase in size at the age of 
 functional activity and the name uterus 
 foetalis seine infantilis is applied. In- 
 complete fusion of Muller's ducts causes 
 an anomaly in the uterus or vagina, 
 e. g. uterus unicornus or bicornus. 
 Atresia may be congenital or acquired 
 by reason of ulceration or laceration. 
 Malpositions as antiflection, retroflec- 
 tion, antiversion, retroversion and pro- 
 lapse are met with. 
 
 2. Circulatory Disturbances. The uterus 
 is physiologically hyperemic during 
 menstruation and occurs pathologically 
 in all forms of acute inflammation of 
 the organ. 
 
 Passive hypermia occurs from general 
 venous stasis but especially from dis- 
 location of the uterus which causes 
 pressure upon the veins. 
 
 3. Atrophy, occurs naturally from old age. 
 It may follow frequent pregnancies and 
 certain diseases and is caused by fatty 
 degeneration and absorbtion of the 
 muscular element. 
 
 4. Hypertrophy, is physiologic during 
 pregnancy. It may remain enlarged. It 
 may occur in association with inflam- 
 mation or from chronic congestion. The 
 body of the uterus or the cervix may be 
 enlarged independently of each other. 
 
 5. Inflammation. 
 
 a. Endometritis, when the mucous 
 membrane is involved. It may be 
 acute or chronic. The acute is 
 caused by traumatism; infection by 
 the gonococcus, staphylococcus, 
 diphtheria bacillus, etc. It may oc- 
 cur during specific fevers. 
 The mucosa is swollen, congested, 
 epithelium disquamating and the 
 surface covered with mucopurulent 
 discharge. Corpuscles exudate and 
 the stroma is infiltrated with cells. 
 The chronic form follows the acute 
 or may be due to foreign bodies. There 
 is infiltration of cells and the glands 
 are enlarged. The glands may be oc- 
 
224 PATHOLOGY. 
 
 eluded causing cystic degeneration. 
 
 There is hyperplasia of connective tis- 
 sue. 
 b. Metritis, when the walls of the uter- 
 us is involved. It is a result of an 
 extension from endometritis, an in- 
 fection or traumatism. 
 The organ is enlarged, congested, tis- 
 sue softened, blood and lymph ves- 
 sels dilated, cellular infiltration. The 
 walls may contain small abscesses and 
 there may be thrombi in the venous 
 sinuses. There is connective tis- 
 sue hyperplasia. The muscular ele- 
 ments may be degenerated and a 
 small hard uterus results. 
 
 6. Infectious Diseases. 
 
 Puerperal Infections, occur during the 
 puerperium and are due to the entrance 
 of microorganisms, generally the 
 streptococcus, but the staphylococcus, 
 a bacillus resembling the coli communis, 
 bacillus of tetanus and the gonococcus 
 
 have also been found. 
 Syphilis of the cervix has been seen as 
 a chancre or a tertiary lesion. 
 
 7. Tumors. Leiomyoma, lipoma, fibroma, 
 sarcoma, carcinoma, papilloma, condy- 
 loma, adenoma and cysts. 
 
 VAGINA. 
 
 1. Abnormalities, as prolapse primarily or 
 in conjunction with prolapse of the 
 uterus, bladder or rectum. Fistulous 
 openings connecting it with adjacent 
 hollow organs or malformations the re- 
 sult of injury are also met with. 
 
 2. Inflammation, Vaginitis or Colpitis re- 
 sults generally from gonorrhoeal infec- 
 tion but mechanical and chemical irri- 
 tants may also cause it. Diphtheria, 
 tuberculosis and syphilis may act as 
 a cause. 
 
 3.i Tumors. Fibroma, myofibroma, sar- 
 coma, carcinoma, papilloma and cysts. 
 
 VULVA. Injuries give rise to lacerations, 
 inflammation, edema and sometimes a 
 haematoma. Diphtheria, gonorrhoea, 
 tuberculosis, chancres, gummata, chan- 
 croids and gangrenes are met with. 
 Elephantiasis, fibroma lipoma, myofib- 
 roma, sarcoma, epithelioma, myxoma, 
 cysts and venereal warts are the tum- 
 ors usually found, -.•,.' 
 
MAMMARY GLAND. 82S 
 
 MAMMARY GLAND. 
 
 1. Congenital Abnormalities. The nipples 
 may be absent or they may be multiple. 
 The gland may be absent or there may 
 be supernumerary glands (polymastia). 
 
 2. Circulatory Disturbances. 
 
 Hypermia occurs physiologically during 
 the menstrual period and at beginning 
 lactation, and pathologically from in- 
 flammation, etc. 
 
 Hemorrhages result from traumatism, 
 sometimes it occurs from intense in- 
 flammation or tumor formation. 
 
 3. Inflammation or Mastitis. It may be 
 acute (Acute Mastitis, which tends to 
 suppuration) or chronic (Chronic 
 Mastitis, which is a diffuse induration). 
 It is generally caused by some infection 
 but may be due to traumatism.. Some 
 authorities claim the infection may 
 reach the lacteal ducts through the 
 general circulation, but the infection 
 probably always enters through fissures 
 about the nipple. The organisms most 
 frequently found are the staphylococci 
 and the streptococci. 
 
 4. Atrophy, occurs physiologically after 
 the menopause or it may be due to 
 abscess or tumor formation. 
 
 5. Hypertrophy, is sometimes seen in girls 
 at puberty. All the constituents of the 
 gland may be involved or dilatation of 
 the lymph channels or degenerative 
 changes may simulate true hypertrophy. 
 Functional activity (galactorrhoea) may 
 be increased. 
 
 6. Infectious Diseases as tuberculosis and 
 syphilis are met with. 
 
 7. Tumors. Fibroma, myxoma, fibromyx- 
 oma, lipoma, 
 
 Sarcoma is frequently of the round cell 
 variety and occurs as a diffuse form 
 or as circumscribed nodules. It is not 
 infrequently associated with fibroma 
 and myxoma. 
 
 Adenoma, may be independent or as- 
 sociated with fibroma, sarcoma or 
 others. Carcinoma may develop from 
 the tubules or from the acini of the 
 glands and is of the medullary, simple, 
 scirrhous and myxomatous variety. 
 Retention cysts.. are also met with. 
 
226 PATHOLOGY. 
 
 DISEASES OF THE MUSCLES. 
 
 1. Inflammation or Myositis. 
 
 a. Acute Myositis, is divided, into — 
 
 1. Localized Acute Myositis, is caus- 
 ed by an injury or by an infection 
 carried to a muscle or by extension 
 of inflammation from adjacent 
 parts or by obstruction to the cir- 
 culation as by an embolism. 
 There may be an exudation of ser- 
 um into the tissue (serous myositis) 
 or an extravasation of blood 
 hemorrhagic myositis), or suppura- 
 tion (suppurative myositis). 
 
 There is hyperemia and swelling. 
 
 2. Disseminated acute myositis or 
 Polymysitis, is due to some in- 
 fection. It has been seen in asso- 
 ciation with some of the infectious 
 fevers. It has probably been re- 
 garded in connection with these con- 
 ditions as a muscular rheumatism. 
 The muscles are first hyperemic, 
 followed by serous infiltration and 
 leucocytic exudation. Fibers may 
 undergo fatty or ganular degenera- 
 tion. Coagulation necrosis and 
 vacuolations may occur. 
 
 b. Chronic Myositis, may be divided in- 
 to:— 
 
 1. Chronic Suppurative myositis, may 
 result from acute suppuration and 
 is often seen in association with 
 tuberculosis and actinomycosis. 
 
 2. Chronic Productive Myositis, re- 
 sults from the acute type or from 
 disease in the neighborhood of 
 muscles or disease in the muscles 
 themselves. It is characterized by 
 an increase of the connective tis- 
 sue. The muscle is enlarged, tender 
 and firm. Degeneration of the 
 muscle is in proportion to the con- 
 nective tissue change. The fibers 
 show cloudy swelling, hyaline 
 changes or fatty degeneration, 
 fragmentation or vacuolar forma- 
 tion. 
 
 3. Ossifying Myositis, is a variety of 
 productive myositis in which bone 
 is found in the substance of 
 muscles. It occurs in muscles sub- 
 jected to irritation or strain as in 
 
MUSCLES. 227 
 
 the delloid muscle of soldiers and 
 the adductor muscles in horsemen. 
 Growths of bone may extend into 
 muscles from diseased bone or 
 periosteum. Nearly all the muscles 
 of the body may be affected. 
 The first formation is in the form 
 of a small spicule which increases 
 in size until the muscle may be con- 
 verted into a bony mass. In some 
 cases there is a connective tissue 
 overproduction with less activity in 
 bone formation. 
 Atrophy. 
 
 a. Neuropathetic Muscular Atrophy, 
 is due to disease of the anterior horns 
 of the gray matter of the cord, and, 
 where this is the underlying patho- 
 logic condition, the term progressive 
 muscular atrophy is applied. There is 
 a progressive atrophy of the muscles 
 of the hands, arms, shoulders and less 
 frequently the body and buttocks. 
 The muscle fibers show various forms 
 of degeneration. At the same time, 
 reactive proliferation is seen in the 
 connective tissue between the fibers. 
 The muscle fibers themselves may 
 proliferate extensively. 
 
 A scondary neuropathetic muscular 
 atrophy may occur in spinal diseases 
 as syringomyelia, etc., and degenera- 
 tions following cerebral disease which 
 is similar to the primary form though 
 it differs clinically. 
 
 Injuries or disease of motor nerves 
 may lead to local atrophies by sep- 
 arating the muscle from the centers 
 within the cord. 
 
 b. Myopathic Muscular Atrophy, is seen 
 in the young and is frequently 
 heriditary. It begins in the buttocks, 
 thighs or calves, sometimes in the 
 shoulders. It may be divided into, — 
 
 1. Simple atrophic form, in which the 
 change is like that of the neuro- 
 pathic. 
 
 2. Pseudo hypertrophic form. The 
 muscles enlarge but are soft and 
 flabby. The child may look like an 
 athlete but is extremly weak. There 
 is considerable intermuscular pro- 
 liferation of the connective tissue, 
 with marked fatty infiltration. In 
 some muscles, the fibers may be ac- 
 
228 PATHOLOGY. 
 
 tually enlarged but it is undoubted- 
 ly degenerative. 
 c. Simple Muscular Atrophy, may be 
 due to senility or lack of exercise. 
 The muscular fibers are deminished in 
 size with some connective tissue pro- 
 liferation. In the senile cases, brown 
 atrophy may occur. 
 
 3. Degenerations. Parenchymatous, fatty 
 degeneration and infiltration, amyloid 
 (rare), calcification, coagulation necrosis 
 or hyaline degeneration. 
 
 4. Infectious Diseases. Tuberculosis (cold 
 abscesses in psoas abscess) in associa- 
 tion with tuberculosis of bone, lymph 
 glands, etc. 
 
 Syphilis as gummata, glanders, 
 actinomycosis and anthrax. 
 
 5. Tumors. Fibromata, myxomata, lipo- 
 mata, osteomata, chondroma and sec- 
 ondary carcinoma. 
 
 6. Parasites. Trichinosis, cysticercus in- 
 vasion and hydatid disease. 
 
 DISEASES OF THE BONES. 
 
 1. Rickets or Rachitis, is a constitution- 
 al condition attended with overproduc- 
 tion of the cellular elements of the 
 bones and lack of their normal calcifi- 
 cation. 
 
 Causes, are obscure, though it is gen- 
 erally conceded that there is some in- 
 herited tendency with a lack of proper 
 nourishment and unhygienic conditions. 
 The disease generally begins during the 
 first j'ear of life and continues through 
 the second and third years. 
 Pathologic Anatomy. The production of 
 cellular elements of bone is increased, 
 especially at the epiphyses. The bones 
 are enlarged and tender at the ends. 
 There is also a deficiency in the for- 
 mation of bone. The bones of the 
 skull and long bones are soft and easily 
 bent and deformed. The fontanelles 
 
 'remain open a long time. Osteophytes 
 may form and the skull bones remain 
 soft (craniotabes). The anterior ends 
 of ribs are enlarged and form a row of 
 nodes (rickety rosary). The chest is 
 
 . often pigeon breasted. 
 
 I When the calcification commences it 
 
BONES. 229 
 
 is greater than normal and the bones 
 are thus too hard, deformed and en- 
 larged in places. The vertebrae and 
 pelvic bones are markedly deformed. 
 2. Inflammations. 
 
 a. Periostitis, is an inflammation of the 
 periosteum. 
 
 Causes. Traumatism, by giving di- 
 rect entrance to infections or by 
 lowering the resistance of an area 
 with subsequent infection. 
 Hematogenous infection without local 
 injury is often seen. 
 Infective periostitis may result from 
 extension of inflammation in the 
 neighborhood of bones or from 
 osteomyelitis. More or less periostitis 
 occurs in all forms of bone diseases. 
 
 Pathologic Anatomy. 
 
 1. Simple Periostitis. The periosteum 
 is swollen, red, and may be in- 
 filtrated with blood. There is round 
 cell infiltration and proliferation of 
 the periosteal tissue. If the process 
 is extensive andl long continued, 
 fibroid thickening is observed. 
 
 2. Purulent Periostitis, may be cir- 
 cumscribed or diffuse and is due to 
 some pyogenic organism acting 
 through the blood. The condition 
 extends rapidly, involves the bone 
 and usually the medulla. Soon after 
 the beginning of the inflammation, 
 the periosteum is destroyed and 
 more or less of the bone may ne- 
 crose. The periosteum throws out 
 new bone which may form a sheath 
 around the necrosed portion. 
 
 3. Ossifying Periostitis or Chronic 
 Periostitis. Occurs in association 
 with chronic osteitis. It is met 
 with principally in syphilis. There 
 is a proliferation of the osteogenetic 
 layer of the perosteum, then partial 
 ossification and complete bone for- 
 mation with firm attachment to the 
 bone. Bony excrescences, exostoses 
 or osteophytes are formed. 
 
 In some cases of pulmonary tuber- 
 culosis, there is a toxin in the blood 
 that gives rise to a periostitis in 
 the extremities to which the term 
 hypertrophic osteo-arthropathy is 
 ^ sometimes given. 
 
230 PATHOLOGY. 
 
 b. Osteitis. (inflammation of the 
 bones), is frequently caused by in- 
 juries, periostitis, or other inflamma- 
 tory diseases. It is also caused by 
 febril diseases and occurs in rheu- 
 matism, syphilis and tuberculosis. 
 Acute infective inflammation is also 
 met with. The blood to part is in- 
 creased. The vessels of the bone, 
 periosteum and medulla enlarge. The 
 Haversian canals become vascular and 
 capillary loops are formed. Spaces 
 are formed in the bone by the soft- 
 ening and absorbtion of its sub- 
 stance. Contained within the spaces 
 is granuation tissue and large multi- 
 nuclear cells which assist in the ab- 
 sorbtion of the bone and convert it 
 into a cancellous condition. During 
 this time at the medulla and the 
 periosteum, new bone is being formed 
 in which are numerous osteoblasts en- 
 gaged in the bone formation. If the 
 inflammation is limited in extent and 
 duration, the new bone may be ab- 
 sorbed. If the inflammation is pro- 
 longed, the new bone becomes or- 
 ganized and is denser than normal 
 (osteosclerosis or condensing osteitis). 
 If the process is acute, an abscess 
 may be formed and if very acute the 
 circulation of the periosteum and 
 Haversian canals are obstructed by 
 the exudates and oedema results 
 which ends in necrosis. 
 A disease which is a form of osteoscl- 
 erosis causes irregular thickening 
 and enlargment of the bones of the 
 head and face is designated as 
 leontiasis ossium. 
 
 Osteitis Deformans. Cause obscure. 
 Some trophic disturbance plays a part. 
 It is a condition which affects the 
 skull, vertebrae and certain long 
 bones, causing enlargment and elas- 
 ticity on account of which there is 
 great deformity. The compact bone 
 is absorbed with confluence of the 
 Haversian canals and formation un- 
 * calcified osseous tissue. The medul- 
 lary canal is filled with vascular con- 
 nective tissue and pus cells. Giant- 
 cell sarcoma may occupy the medulla. 
 Osteomy litis. In the acute form of a 
 single type as fractures and amputa- 
 tions, there may be enough bone to 
 close the medullary canal and adja- 
 
BONES. 231 
 
 cent bone undergo rapid suppuration 
 and necrosis. 
 
 The chronic form leads to bone thick- 
 ening along the medullary canal and 
 to its narrowing which may go on to 
 occlusion. In some cases there is 
 chronic suppuration and necrosis. 
 
 3. Atrophy, may result from disease as a 
 paralyzed extremity or from a bone not 
 in use by reason of deformity or in- 
 jury; severe cachexia or long confine- 
 ment to bed, chronic disease of joints. 
 Disturbance of trophic nerves and cer- 
 tain nervous conditions as cretinism and 
 insanity have been met with as a cause. 
 There seems to be an idiopathic form 
 which brings on a condition of bone 
 fragility (fragilitas ossium or osteop- 
 sathyrosis) from the increase of its 
 narrow spaces and general porosity. 
 
 4. Hypertrophy. A local hypertrophy may 
 be caused from muscular development 
 and exercise or strain on the bone. 
 Giantism. Certain bones or the bones 
 of the entire skeleton may be involved. 
 The bones are enlarged, thick and ir- 
 regular. The condition usually begins 
 about puberty. 
 
 Acromegaly, is allied to giantism but 
 the bones of forearms, hands, legs, feet, 
 upper and lower jaws and the nose are 
 marked in their enlargment. The 
 etiology is obscure through enlarg- 
 ment of the pituitary body, also the 
 persistence of the thymus gland has 
 been considered as factors but this is 
 still unsettled. 
 
 5. Degenerative Conditions. 
 
 a. Necrosis, is due to periostitis, 
 osteitis and osteomyelitis, which leads 
 to an interruption of the blood sup- 
 ply to the bone. Embolic obstruc- 
 tion of the blood vessels may also 
 cause it. The more acute and intense 
 the inflammatory process the more 
 likely is the necrosis. 
 The surface, cancellous portion or the 
 entire thickness of the bone may be 
 involved. The line of demarkation of 
 the living bone with that of the dead 
 bone is softened and rarified, and 
 granulation tissue is formed. These 
 processes go on until the dead por- 
 tion (sequestrum) is loosened. The 
 periosteum is forming new bone which 
 
232 PATHOLOGY. 
 
 may encase the sequestrum and pre- 
 vent its escape, unless this is 
 brought about through openings or 
 cloacae that exist in the new bony 
 case. A peculiar form of necrosis is 
 produced by phosphorus fumes and 
 affects the maxillary bone. 
 Syphilis and tuberculosis may also 
 produce necrosis. 
 b. Osteomalacia, is a disease of adult 
 life and is most frequently seen in 
 females, particularly in the puerperal 
 woman. The real causes are not 
 known. The bone salts are absorbed, 
 the medullary and Haversian canals 
 are enlarged, the bone trabecullae dis- 
 appear and the corticular layer be- 
 comes thin. 
 
 The long bones contain red narrow 
 and fractures readily. In the later 
 stages the bone becomes soft and 
 bends quite easily. Deformities may 
 become great. During the late stage 
 there is only a jelly-like substance 
 within the periosteum. It proves fatal 
 in about two years. 
 
 5. Infectious Diseases. 
 
 a. Tuberculosis, is more frequent in the 
 young and may be acute or chronic. 
 The tubercles are found in the 
 periosteum, the bone or the medulla. 
 The cancellous tissue is particularly 
 liable. The areas are gray in color, 
 surrounded with congested and swol- 
 len tissue. Caseation of area takes 
 place. Bone trabecular are broken 
 down. Giant cells are found in the 
 tubercles, osteoclasts appear on the 
 bone lamella and granulation tissue 
 is formed. 
 
 By extension new foci are formed. 
 The diseased bone may separate 
 through caseation and caries is the 
 usual course. The inflammatory pro- 
 cess may produce an abscess which 
 sometimes invades the soft parts as a 
 cold abscess (psoas abscess). The 
 tubercular bone abscess has generally 
 a pyogenic membrane and the con- 
 tents of the abscess may be cheesy 
 matter or pus. Tuberculosis of the 
 bones has a tendency to invade the 
 . joints. 
 
 b. Syphilis. The periosteum is fre- 
 : . quently involved. There is thicken- 
 
JOINTS. 233 
 
 ing, with an infiltration of cellular 
 matter which may undergo gummy 
 or mucoid degeneration and super- 
 ficial necrosis. 
 
 Syphilis of the bone attacks the can- 
 cellous tissue mainly. The gumma- 
 tous material extends into the Haver- 
 sian canals, erode the bony, lamellae 
 and enlarge the canals, thus giving 
 to the bone a worm eaten appear- 
 ance. The bone is thickened near the 
 gummatous formation, becomes 
 
 sclerosed and necrosed with forma- 
 tion of sequestra. The gumma may 
 form in the medullary canal or ends 
 of bones and invade the joints. 
 In congenital syphilis, there is char- 
 acteristic alterations at the junction 
 of the epiphyses with the diaphyses of 
 the long bones. The epiphyses may 
 be completely seperated from the 
 shaft. Nodes are often formed 
 around the anterior fontanells and 
 the nasal bones are often diseased as 
 in the tertiary form. 
 6. Tumors. Exostoses, fibroma, lipoma, 
 myxoma, angioma, chondroma, osteo- 
 ma, sarcoma, carcinoma (usually sec- 
 ondary), and cysts, in connection 
 with tumors and hydatids occasionally. 
 
 DISEASES OF THE JOINTS. 
 
 1. Inflammation. 
 
 a. Acute Arthritis, is due to trauma; 
 disease in vicinity or hematogenous 
 which may occur in the course of 
 infectious diseases as scarlet fever, 
 small pox, pyemia, etc. Acute 
 articular rheumatism may also be 
 added to this group. 
 It may be of a dry or fibrinous, a 
 serous and a seropurulent nature. 
 The synovial membrane is congested, 
 the cartilages and ligaments are also 
 more or less involved. The term 
 synovitis implies synovial involve- 
 ment and panarthritis is a general 
 involvement. Fibrin is deposited on 
 the surface in the dry form. In the 
 serous form, the exudation is purely 
 serous while in the real seropurulent, 
 form, empyema of the point results. 
 Resolution takes place in mild cases. 
 
234 PATHOLOGY. 
 
 In the severe cases, the articulating 
 cartilages may ulcerate or necrosis 
 may result, leading to ostitis or 
 osteomylitis. Disorganization of 
 
 joints may take place. 
 
 b. Chronic Arthritis may be due to 
 the acute. It also '^occurs in the 
 course of gout and certain nervous 
 diseases. It may be divided into, — 
 
 1. Chronic Serous Arthritis, or 
 Hydrops articulorum. The synovial 
 membrane is thickened and more 
 or less injected (synovitis pannosa). 
 The joint is filled with thin syn- 
 ovia. 
 
 2. Chronic puruient arthritis is due 
 to infection, and is the outcome 
 of an acute sero-purulent or puru- 
 lent arthritis. It terminates in ex- 
 tensive disorganization of the 
 joint. A fibrous ankylosis is the 
 favorable outcome. 
 
 Arthritis deformans or rheumatoid 
 arthritis, is generally seen in those 
 past middle age. The cartilages 
 are softened, ulcerated or eroded 
 and have an irregular rough sur- 
 face. Hyperplasia of cartilage cells 
 takes place with subsequent degen- 
 eration and absorption. The car- 
 tilage is reduced and the ends of 
 the bones are bare. The synovial 
 membrane and ligaments thicken, 
 the articulating surface is absorbed 
 and proliferated in the form of ex- 
 ostoses and osteophytes, and the 
 joint is deformed and thickened. 
 Subluxations are common and an- 
 kylosis may follow. 
 It is seen in the metacarpophalan- 
 geal joints of hands and feet. 
 Other joints may be involved. 
 
 c. Chronic dry arthritis, with ulcera- 
 tion or senile arthritis, is similar to 
 the rheumatoid arthritis, but more 
 slow. It is common in the hip joint. 
 There is gradual absorption of the 
 cartilages and exposed surfaces of 
 the bone, with subsequent sclerosis 
 and hyperplasia of the surrounding 
 bone. 
 
 d. Neuropathic arthritis resembles the 
 other forms, but is very slow. It is 
 seen in the course of spinal diseases 
 such as locomotor ataxia and sy- 
 
BRAIN. 235 
 
 ringomyelia. It is painless and sug- 
 gests a degeneration or trophic dis- 
 order. 
 
 3. Gouty Arthritis. There is a deposit of 
 crystals of the urate of sodium and 
 calcium in the cartilage cells and inter- 
 cellular substance of the articulations. 
 The deposit may also take place in the 
 connective tissue of the joints in more 
 severe cases. The deposit gives rise 
 to the attacks (gouty paroxysm) 'which 
 is marked by inflammatory processes 
 in the joint. The synovial membrane 
 is hyperemic, with serous effusion and 
 sometimes inflammatory manifesta- 
 tions. The cartilages may become 
 eroded and suppuration may take place. 
 The metatarso-phalangeal joint of the 
 great toe is particularly liable to be 
 involved. 
 
 4. Infectious Diseases. 
 
 Tuberculosis, when primary, begins in 
 the synovial membrane. It may be 
 secondary to tuberculosis of bone when 
 any part of the joint is first involved. 
 The former is usually the case in chil- 
 dren and the latter in adults. 
 Syphilis may occur in the hereditary 
 form. In later life gummata may in- 
 vade the joint. 
 
 5. Tumors. Sarcoma, exostosis, hydatids 
 (rare). 
 
 TENDON SHEATHS AND BURSAE. 
 
 Tenosynovitis and Bursitis is like the 
 inflammation of joints. 
 House- maid's knee is a chronic bursitis 
 with dropsical effusion, due to chronic 
 irritation, and is analogous to hydrops 
 articulorum. 
 
 Ganglion is a condition of the tendon- 
 sheaths which presents itself as a 
 rounded cystic nodule on the back of 
 hands and wrist. It is due to a local- 
 ized dropsical condition of the tendon 
 sheath. 
 
 DISEASES OF THE BRAIN AND ITS 
 MEMBRANES. 
 
 BRAIN. 
 
 1. Circulatory Disturbances. 
 
 a. Anemia. Acute anemia results from 
 severe hemorrhage or hyperemia in 
 
236 PATHOLOGY. 
 
 other parts of the body. It is sup- 
 posed to exist in fainting, during 
 hysterical crises and in sleep. 
 Chronic anemia occurs in severe 
 cachexias and sometimes in atheroma 
 of the cerebral arteries. 
 Local anemia may result from throm- 
 bosis and embolism. 
 
 b. Hyperemia is associated with in- 
 flammatory or toxic conditions. 
 
 1. Active hyperemia may be divided 
 into, — 
 
 Local active hyperemia, usually as- 
 sociated with meningitis, and may 
 be limited to the superficial part 
 of the cortex. It may also occur 
 after thrombosis. 
 
 General active hyperemia is sup- 
 posed to be associated with un- 
 usual activity of the mind. 
 In acute infections, such as typhoid 
 fever, excessive irritation of the 
 cerebral substance may occur, 
 which gives rise to symptoms some- 
 what like those of meningitis. It 
 is termed meningismus and is due 
 to hyperemia. 
 
 2. Passive hyperemia is associated 
 with valvular heart disease or 
 chronic lung disease, or may be 
 caused by tumors pressing upon the 
 jugular vein, or intracranial condi- 
 tions, as brain tumors, etc. "Where 
 passive hyperemia exists there is 
 nearly always edema of the brain. 
 Apoplexia serosa is a local edema 
 of the brain found near the areas 
 of softening. 
 
 c. Apoplexy may be divided into three 
 varieties. In all varieties there is a 
 thickened intima and muscular coat, 
 causing obliteration of the vessels or 
 an atheromatous condition, with the 
 formation of thrombi on the rough- 
 ened surface, or give rise to aneu- 
 rysmal dilatation of the vessel. Por- 
 tions of brain with occluded or rup- 
 tured vessel and formation of clot 
 gives rise to well-marked focal symp- 
 toms. 
 
 Apoplexy is due to, — 
 1. Hemorrhage (cerebral hemorrhage) 
 may be divided into, — 
 
BRAIN. 237 
 
 Punctate hemorrhage, due to al- 
 teration in walls of blood vessels 
 or of the degree of blood pressure, 
 causing extravasation of blood into 
 surrounding tissues. The principal 
 causes are hyperemia and disease 
 of the vessel walls. 
 Massive hemorrhage occurs usually 
 from the branches of the middle 
 cerebral artery, which are the fre- 
 quent seats of miliary aneurysms. 
 The blood collects in the form of 
 an irregular dark mass. The size 
 of the clot varies with its location 
 and the amount of extravasated 
 blood. The time of the absorption 
 of the clot varies according to its 
 size. It begins to lose its color in 
 two or three weeks, and in about 
 twelve weeks it is reduced to a 
 yellowish mass. The damaged brain 
 tissue undergoes fatty degenera- 
 tion. 
 2. Thrombosis and Embolism. 
 
 Thrombosis probably occurs most 
 frequently in the basilar artery, 
 while embolism occurs in the ar- 
 tery of the Sylvian fissure. That 
 portion of the brain deprived of its 
 blood supply undergoes fatty de- 
 generation. The area becomes yel- 
 lowish and is known as yellow 
 softening. The embolism may be- 
 come infected, as in ulcerative en- 
 docarditis and pyemia, so that in 
 addition to the pathological changes 
 already present inflammatory proc- 
 esses are set up. 
 2. Inflammation. 
 
 a. Encephalitis is an acute inflamma- 
 tion, which is probably of an infec- 
 tious origin. It occurs during the 
 course of scarlet fever, measles, 
 pneumonia, influenza, etc. It may be 
 limited to large or small areas, and 
 many foci of inflammation may be 
 present. In the affected parts the 
 neurones are found to be degen- 
 erated. In the course of time the 
 tissue becomes sclerosed, and if a 
 system of neurons are destroyed 
 symptoms, as imbecility, paralysis of 
 muscles, defect in speech, etc., en- 
 sues. If only a few neurons are de- 
 stroyed partial recovery may take 
 place by the absorption of the small 
 
38 PATHOLOGY. 
 
 clots and infiltrations. The gHa and 
 connective elements are increased 
 and sclerosed patches follow the at- 
 tempts at repair. Adhesions between 
 the meninges and cortex may be 
 formed. 
 
 Cerebral abscess may be caused by 
 an injury with or without a fracture. 
 An abscess may form several weeks 
 after an injury. Otitis media of the 
 chronic form is the usual cause of 
 abscess. An abscess may also result 
 by metastasis from some other part 
 of the body. 
 
 Single abscesses are generally of slow 
 growth, large in size, with a thick 
 capsule. Small abscesses are usually 
 numerous and are of metastatic form. 
 An abscess may be latent for years, 
 is never absorbed and ruptures into 
 the ventricle or on the surface of the 
 brain, which is frequently followed 
 by meningitis and thrombosis of the 
 sinuses. i 
 
 The micro-organisms found in the 
 pus are the streptococci, staphylo- 
 cocci and pneumococci. Occasionally 
 the bacillus pyocyaneus and the tu- 
 berculosis. 
 b. Meningoencephalitis, or General Pro- 
 gressive Paralysis, is more common in 
 men than in women. Syphilis seems 
 to play an important part in its eti- 
 ology. In addition excesses in alcohol 
 and sexual indulgence is also consid- 
 ered as a cause. 
 
 The meninges are hyperemic and 
 many capillaries are occluded. The 
 vessels cell elements are overpro- 
 duced. Vessels dilate and fibrous tis- 
 sue are formed around them. There 
 is a degeneration of the neurones and 
 the nucleated cells of the neuroglia 
 are increased. 
 
 The cortical cells and their dendrites 
 undergo fatty degeneration. 
 The changes in the neuroglia, cere- 
 bral cells and the vessels cause a gen- 
 eral atrophy of the brain. The en- 
 tire brain may lose one-fourth its 
 weight. The meninges become thick- 
 ened and the cerebral fluid is in- 
 creased in quantity. There may also 
 be sclerosis of the posterior columns 
 of the cord. 
 
BRAIN. 239 
 
 The disease is not directly due to 
 syphilis, but an attack of syphilis 
 generally precedes it. Some cases 
 fail to give any syphilitic history. 
 c. Chronic encephalitis is a variety of 
 sclerosis, but may take on a scar 
 formation. 
 It may be divided into, — 
 
 1. Lobar sclerosis is usually an ex- 
 tensive but circumscribed process 
 affecting the whole or part of one 
 or more lobes of the brain. The 
 affected area is usually diminished 
 in size. The consistency is greatly 
 increased, the tissue is almost like 
 cartilage. 
 
 Microscopically, there are some 
 changes found in other forms of 
 sclerosis. The cause seems to be 
 due to some fetal vascular disturb- 
 ance. 
 
 2. Multiple, Insular or Disseminated 
 Sclerosis. Cause is obscure. The 
 greater number of authorities be- 
 lieve it to be of vascular origin, 
 i. e., the patches are due to some 
 toxic agent, while some think it due 
 to an overgrowth of neuroglia and 
 that myelin fibers suffer from pres- 
 sure; others think it is a defect 
 in the development of the nerve 
 fiber, with the medullary sheath 
 imperfect or wanting. 
 
 There are many small patches of 
 sclerosis scattered through the cen- 
 tral nervous system. The patches 
 vary insize and are irregular in 
 shape. They occur in the cortex, 
 but most frequently in the central 
 white matter of the brain. The 
 basal ganglia are common seats. In 
 the cord the patches involve several 
 tracts. There is no secondary de- 
 generations in the affected tracts, 
 as the process does not affect the 
 axones. The neurone sheath and 
 the adventitious tissue of the brain 
 and cord are not sclerosed unless 
 the gray matter is involved. The 
 patches are more vascular than the 
 normal tissue and are of pink color; 
 in the later stages they become 
 nearly white. The blood vessels are 
 thickened. 
 If a patch extends to the gray mat- 
 
240 PATHOLOGY. 
 
 ter there is fatty degeneration of 
 the cell elements. The nerve fibers 
 as they pass through the patches 
 are compressed and reduced in size. 
 The medullary sheath is interrupted 
 and undergoes fatty degeneration 
 and an occasional axon is de- 
 stroyed. 
 
 3. Infectious Diseases. 
 
 Tuberculosis occurs in the form of mili- 
 ary tubercles, or the so-called solitary 
 tubercle, or tyroma, which is made up 
 of a rounded mass of grayish or yellow 
 color, showing fresh gray tubercles at 
 the periphery. Early caseation is usual. 
 Syphilis, as gummata or as a diffuse 
 vascular disease, with secondary de- 
 generation and softening or sclerosis of 
 a diffuse or focal character. 
 Actinomycosis is secondary and may 
 take the form of a chronic abscess or 
 may be tumor like. 
 
 4. Tumor. Glioma, sarcoma, fibroma 
 lymphangioma, osteoma, p'sammoma, 
 carcinoma. Cysts in connection with 
 other cysts or may sometimes be para- 
 sitic in origin. 
 
 VENTRICLES. 
 
 Hydrocephalus is an excess in quan- 
 tity of the cerebro-spinal fluid in the 
 ventricles. It may be either external 
 or internal. The external is caused by 
 exudation of serum from the meninges 
 and the internal is caused by the ac- 
 cumulation of fluid in the ventricles. 
 Hydrocephalus may be divided into, — 
 
 a. Acute, which is caused by a menin- 
 gitis. 
 
 b. Chronic, which is usually caused by 
 a mild meningitis and the obstruction 
 of the outlets to the ventricles at the 
 aqueduct of Sylvius and the foramen 
 of Munroe. 
 
 THE MEMBRANES OF THE BRAIN. 
 
 Dura Mater. 
 
 1. Circulatory Disturbances. Active and 
 passive hyperemia occur in association 
 with gumma, tumors and other focal 
 diseases; while hemorrhages are usually 
 due to trauma and are extra or intra- 
 dural. A collection of . blood between 
 the skull and the dura is sometimes 
 - called internal cephalhematoma. 
 
MENINGES. 241 
 
 2. Inflammation or Pachymeningitis may 
 
 be acute or chronic and is divided 
 into, — 
 
 a. Hemorrhagic Pachymeningitis is 
 
 found more often in the aged than 
 in the young. Alcoholism and trauma 
 are etiological factors. 
 A grayish membrane, with brown 
 spots composed of hematoidin, ap- 
 pears on the inner surface of the 
 dura. Later there is diapedesis of 
 blood corpuscles or actual hemor- 
 rhage may occur. 
 
 b. Suppurative Pachymeningitis occurs 
 in consequence of trauma, caries or 
 other disease of the skull. Sometimes 
 it may be due to internal or middle 
 ear disease. 
 
 c. Productive Pachymeningitis is of a 
 fibrous or ossifying character. It may 
 follow the two other forms. 
 
 3. Infectious Diseases. 
 
 Tuberculosis is in form of miliary tu- 
 bercles, in association with disease else- 
 where. It may be primary in some 
 cases. 
 
 Syphilis, as a diffuse productive pachy- 
 meningitis or gumma. 
 
 4. Tumors. Alveolar sarcoma, angiosar- 
 coma, fibroma, small round cell sar- 
 coma, gliosarcoma and carcinoma. 
 Cysts, as meningocele. 
 
 The Pia and Arachnoid. 
 
 1. Circulatory Disturbances. 
 
 Anemia, active and passive hyperemia 
 from the usual causes. Hemorrhages, 
 as small punctate in meningitis, 
 scurvy, purpura, etc.; large are found 
 between the pia and arachnoid from 
 trauma and rupture of aneurysms. 
 The blood may become inspissated, or 
 it may be encapsulated with absorp- 
 tion of pigment, causing a cyst (hy- 
 groma). Edema of the membranes 
 or collections of liquid in the sub- 
 arachnoid space may be due to pas- 
 sive congestion. 
 
 2. Inflammation, or Leptomeningitis, is 
 always infectious and may be acute or 
 chronic. 
 
 a. Septic meningitis occurs during the 
 course, of septic disease or wounds. 
 It may appear during pneumonia, ty- 
 
242 PATHOLOGY. 
 
 phoid fever, eruptive fevers, emv 
 pyema, erysipelas and ulcerative en- 
 docarditis. The germs usually found 
 are the streptococcus, staphylococcus 
 and the pneumococcus. 
 A part or the entire membrane may 
 be affected. The convexity of the 
 brain is more likely to suffer. 
 There is hyperemia at first, then an 
 exudation of serum, which may cause 
 oedema of the cortex and separation 
 of the layers of the meninges. 
 Fibrin is also deposited as flakes on 
 the pia, and pus collects in the 
 meshes and on the surface of the 
 membrane. 
 
 Abscesses of the cortex may form and 
 the inflammation may extend into the 
 ventricles. 
 
 Tuberculosis and syphilis also cause 
 a meningitis. (See Infectious Dis- 
 eases below). 
 b. Epidemic Cerebro-Spinal Meningitis, 
 or Spotted Fever, results from an in- 
 fection by the diplococcus intra- 
 cellularis • meningitidis of Weichsel- 
 baum, and in this is its only differ- 
 ence from the septic form. The In- 
 flammatory process generally begins 
 on the frontal lobes and extends back- 
 ward and downward, the basal menin- 
 ges being involved late in the course 
 of the disease. 
 
 3. Infectious Diseases. 
 
 Tuberculous Meningitis is usually a 
 secondary infection. The base of the 
 brain is more likely to suffer, the spaces 
 become filled with tubercles and inflam- 
 matory products. Rarely there is pus; 
 but the pia is studded with tubercles, 
 and there is exudation of fibrin, lymph 
 and serum. The closure of the fissure 
 of Sylvius will cause the ventricles to 
 become greatly distended. 
 Syphilitic Meningitis. The meninges 
 near the crura is the favorite location. 
 It occurs in the form of gummatous 
 infiltrations. 
 
 Flattened nodular thickening of gray or 
 pinkish color, with a tendency to ne- 
 crotic change, appear in the arachnoid 
 and pia. 
 
 4. Tumors. Pacchionian bodies, endothe- 
 lioma, cholesteatomata, lipoma and 
 teratomata. 
 
243 
 
 DISEASES OF THE SPINAL CORD 
 AND MEMBRANES. 
 
 THE SPINAL CORD. 
 
 1. Congenital Abnormalities. Absence 
 (amyelia) exists only with anen 
 cephalus. The cord may be abnormally 
 small (micromyelia) ; it may be double 
 (diastematomyelia); it may be of un- 
 usual length; it may be heterotopic, 
 i. e., a doubling of one of the horns, or 
 disorganization of one or both horns, 
 or of fissures extending into its sub- 
 stance; the central canal of cord may be 
 dilated; the imperfect closure of the 
 posterior processes of the vertebrae 
 may give rise to clefts, which are known 
 as rachischisis, and if the membranes 
 of the cord protrude to form a sac or 
 hernia it is called spina bifida. 
 
 2. Circulatory Disturbances. 
 
 a. Hyperemia may be present. It may 
 result from long decubitus and in 
 early stages of inflammations of the 
 cord and meninges. Excessive venery 
 may also cause it. 
 
 b. Anemia arises from narrowing of the 
 vessels in meningitis or occlusion of 
 the vessels by embolism, also by rea- 
 son of a general anemia. 
 
 c. Varicose Veins are sometimes found 
 as a sort of plexiform angioma. This 
 has been seen sometimes after birth 
 and is frequently seen in myelitis and 
 sclerosis. 
 
 d. Hemorrhages are rare. They occur 
 from injury and in connection with 
 myelitis or in death by drowning or 
 strangulation. Minute extravasations 
 are found in the white and gray mat- 
 ter from asphyxial states. Large 
 hemorrhages, not due to injury, be- 
 gin in the gray substance. The blood 
 clot may lacerate the tissues. 
 
 The irritation caused by hemorrhages 
 is followed by inflammatory reaction. 
 A condition in which the central canal 
 is dilated and contains blood is called 
 hematomyelia. It results from trau- 
 matism or some vascular degenera- 
 tion 
 
244 PATHOLOGY. 
 
 3. Inflammation. 
 
 a. Myelitis may be divided into, — 
 
 1. Acute Myelitis is due to pressure 
 on the cord by tumors or from a 
 curvature of the spine, or injuries, 
 violent muscular action, exposure to 
 cold, toxic blood conditions or ex- 
 cessive functional activity. 
 
 At first the vessels are dilated and 
 gives the part a red color (red soft- 
 ening). The coloring matter of 
 the blood extravasations undergo 
 changes and yellow softening ap- 
 pears. Later the cord becomes 
 grayish from absorption of products 
 of fatty degeneration. 
 The nerve fibers are degenerated 
 early into masses of myelin and 
 granular matter, which contains red 
 and white cells and fragments of 
 axis cylinders. 
 
 The gray matter contains round 
 cells, nuclei of other cells, and the 
 tissue is very granular. The nerve 
 cells are swollen and contain fatty 
 matter, while their processes are 
 small or have disappeared. The in- 
 terstitial tissue takes on a fibrous 
 appearance, with the nerve pro- 
 cesses of Deiter's cells extending 
 between the nerve elements. The 
 myelin sheaths are degenerated to 
 a varying degree, and the axis cyl- 
 inders are granular and swollen. 
 As the disease progresses the gray 
 matter disappears and the perivas- 
 cular exudate shows fatty degenera- 
 tion. 
 
 In the gray degeneration vacuoles 
 are found in the neuroglia. 
 
 2. Chronic Myelitis develops slowly 
 and ma- be due to the acute form, 
 repeatea exposures to cold, various 
 injuries, a hereditary tendency, 
 continued over-exertion, tumors, 
 chronic disease of bones, meningitis, 
 alcoholism, gout and syphilis may 
 all act as etiological factors. The 
 cord is wasted. The white matter 
 seems grayish and the gray matter 
 dark. It may be transverse or dis- 
 seminated. There may be several 
 isolated foci of disease, or there 
 may be a sclerosed ring around the 
 cord. The disease is interstitial, the 
 
SPINAL CORD. 245 
 
 connective tissue is increased, with 
 but few nerve elements present. 
 In some part of white matter the 
 interstitial tissue is increased and 
 contain nuclei and various shaped 
 cells. Deiter's cells are often pres- 
 ent. As the condition progresses 
 the nerve fibers and cells gradually 
 disappear, and the axis cylinders 
 are of irregular shape and break 
 up in portions. 
 
 The blood vessel walls are thick- 
 ened and ganglion cells swell, then 
 shrink, become irregular, lose their 
 projections and disappear. 
 
 b. Polyiomyelitis, or Atrophic Spinal 
 Paralysis, may be divided into, — 
 
 1. Acute Anterior Polyiomyelitis, In- 
 fantile Paralysis, or Acute Atrophic 
 Spinal Paralysis, occurs almost ex- 
 clusively in young children. It is 
 undoubtedly due to some blood 
 state. It appears after some ex- 
 posure to cold subsequent to some 
 other infectious disease and has ap- 
 peared as an epidemic. The nature 
 of the poison is unknown. There is 
 an acute inflammation of the an- 
 terior cornua of the cord. The ves- 
 sels are distended and minute ex- 
 travasations into the substance may 
 be seen. 
 
 The neuroglia is swollen, ganglion 
 cells are granular and the processes 
 indistinct. Granular corpuscles. 
 If the cervical and lumbar enlarge- 
 ments are involved there is soften- 
 ing. 
 
 If the process is slight there may 
 not be much destruction of 
 nerve elements. The inflammatory 
 changes extend into other portions 
 of the cord and cause degeneration 
 of other tracts, especially the lat- 
 eral. In severe cases the motor 
 nerve cells almost entirely disap- 
 pear, with later distinct degenera- 
 tion of their nerve fibers. 
 The cord at the diseased level is 
 reduced in size. The muscles sup- 
 plied by the diseased nerves are 
 paralyzed and undergo atrophy. The 
 muscles may contract and give rise 
 to various deformities in the limbs. 
 
 2. Chronic Poliomyelitis, Chronic 
 
246 PATHOLOGY. 
 
 Spinal Muscular Atrophy, Progres- 
 sive Muscular Atrophy, Wasting 
 Palsy, is most frequent between the 
 ages of 25 and 45 years. It results 
 from a slow degeneration of the 
 motor cells in the anterior cornua 
 of the cord. There seems to be a 
 hereditary tendency in its etiology, 
 but prolonged emotional excitement, 
 and syphilis seems to bear some 
 connection to it. 
 
 The motor cornual cells are atro- 
 phied, the nerve fibers are degen- 
 erated and the muscles supplied by 
 these nerves undergo wasting. The 
 disease is probably a degeneration. 
 The muscles are reduced in size 
 and are pale. The muscle fibers 
 may be narrowed or they may un- 
 dergo fatty degeneration and have 
 disappeared in some instances. 
 In many of the nerve fibers the 
 myelin undergoes fatty change and 
 the axis cylinder disappears, noth- 
 ing but connective tissue threads 
 remain. 
 
 The affected portions of cornua are 
 wasted and softened. 
 The ganglion motor cells are 
 changed in outline with loss of their 
 processes or the cells have disap- 
 peared. 
 Posterior Sclerosis, Locomotor Ataxia, 
 Tabes Dorsal is, occurs generally be- 
 tween the ages of 20 and 50 years. It 
 is more frequent in the male than the 
 female. Syphilis can be traced as a 
 cause in from 70 to 90 per cent, of 
 the cases. Exposure to wet and cold 
 and excessive fatigue have been ad- 
 vanced as a possible cause. There is 
 a degeneration of the central and peri- 
 pheral sensory nerve elements. The 
 posterior columns of the cord are of 
 a graj r ish color, due to an over-pro- 
 duction of connective tissue. The 
 columns are reduced in size. The de- 
 generation of the nerve elements and 
 the increase of connective tissue are 
 confined mainly to the posteromedian 
 columns, but other columns, espe- 
 cially those of the lumbar region, may 
 be involved to some extent. The 
 overgrowth of connective tissue is 
 known as sclerosis, though it is more 
 properly a hardening. 
 
SPINAL CORD. 247 
 
 In advanced cases the posterior 
 vesicular columns and nerve cells in 
 the posterior cornua also degenerate 
 according to the severity of the case. 
 The pia mater is generally thickened 
 and the posterior nerve roots and 
 ganglia are nearly always degenerated 
 to some extent. 
 
 The nuclei of Goll and Burdach may 
 also be affected. 
 
 Extensive morbid changes may be 
 present in the peripheral sensory 
 nerves and in the optic nerves. Other 
 cranial nerves may also suffer. 
 
 Spastic Spinal Paralysis, Primary Lat- 
 eral Sclerosis. The cause is obscure. 
 Syphilis, infectious diseases, lead pois- 
 oning and exposure to cold have been 
 considered as etiological factors. 
 There is a chronic degeneration of 
 the anterior and lateral pyramidal 
 tracts. In the lumbar region the de- 
 generation is limited almost entirely 
 to the lateral tracts; higher up the 
 cord the anterior tracts are involved. 
 The morbid changes are the same as 
 in the other degenerations of the cord. 
 
 Amytrophic Lateral Sclerosis is a com- 
 bination of pathologic conditions found 
 in primary lateral sclerosis and 
 chronic anterior poliomyelitis. 
 
 Ataxia Paraplegia is a combination of 
 the pathologic conditions found in 
 lateral sclerosis and locomotor ataxia. 
 
 Friedreich's Disease, or Hereditary 
 Ataxia, is a combination degenera- 
 tion of the lateral and posterior col- 
 umns. 
 
 Syringomyelia and Hydromyelia. 
 
 At one time these two conditions were 
 considered different, but now they are 
 considered practically the same. The 
 condition is due to a non-perfect clos- 
 ure of the central canal of the spinal 
 cord during its development. The 
 cord may contain one or more cavi- 
 ties, or it may extend through its 
 entire length. The cavities encroach 
 upon the posterior coruna. 
 The condition may also be caused by 
 hemorrhage from injury or the break- 
 ing down of gliomatous tissue. The 
 cavities are surrounded by a layer of 
 embryonal neuroglia tissue. 
 The white matter of the cord is de- 
 
248 PATHOLOGY. 
 
 ficient. The condition is met with in 
 the upper portion of the cord, and as 
 the cavities increase in size the wall 
 will give way and the fluid contents 
 will then extend to other tissues of 
 the cord. The fluids are the products 
 of necrosis, cerebro-spinal fluid and 
 the remains of hemorrhages. 
 The white tissue is dark, with sec- 
 ondary degeneration of the tracts. 
 Some posterior roots may be de- 
 stroyed. 
 4. Tumors. Glioma, sarcoma, carcinoma 
 (secondary). Cysts are rare. 
 
 THE MEMBRANES OF THE CORD. 
 
 Dura Mater. The pathological processes 
 are generally secondary to some dis- 
 ease of the vertebral column. The most 
 important is tuberculosis, which gives 
 rise to, — 
 
 External tuberculous pachymeningitis, 
 a collection of cheesy material, un- 
 dergoing softening or necrosis or con- 
 tains pus cells. The dura is thickened 
 and does not differ from tuberculosis 
 in other serous membranes. 
 Syphilis occurs as discreet gumraata 
 or as regular and diffuse thickenings 
 of the inner membrane. 
 Tumors. Sarcoma, myxoma, lipoma, 
 fibroma. 
 
 Pia and Arachnoid. 
 
 1. Circulatory Disturbances. Active and 
 passive hyperemia from the usual 
 causes. 
 
 2. Degenerations, as calcareous and pig- 
 mentary infiltrations. 
 
 3. Inflammation. 
 
 a. Acute Leptomeningitis, or Acute In- 
 flammation, is often secondary to 
 cerebral meningitis. It may be in- 
 dependent, as a result of a local 
 suppurative process, and may be 
 serous and purulent in character. In 
 the purulent an exudation is found 
 on the inner surface of the dura and 
 in the subarachnoidian space. If 
 death does not occur adhesions may 
 form between the dura and arach- 
 noid. 
 
 b. Chronic Leptomeningitis is usually 
 associated with sclerosis of the cord. 
 It may also follow some other in- 
 
NERVES. 249 
 
 flammatory process, with formation 
 
 of adhesions between the dura and 
 arachnoid. 
 
 Continuous pressure upon the dura 
 from injury to the spinal column, etc., 
 
 may result in thickening of the mem- 
 brane. 
 
 4. Infectious Diseases. 
 
 Tuberculosis, as miliary nodules or 
 small cheesy masses. Solitary 
 
 tubercles may occur in any part of 
 the spinal cord. 
 
 Syphilis, appears as thickening of the 
 membrane with multiple gummata 
 projecting into the substance of the 
 cord or involving the dura mater. 
 
 DISEASES OF THE PERIPHERAL 
 NERVOUS SYSTEM. 
 
 THE GANGLIA OF THE CRANIAL AND 
 SPINAL NERVES. t 
 
 Ganglia of the Cranial Nerves, may be 
 diseased from extension of pathologic 
 processes. They are also subject to 
 inflammatory changes. There is de- 
 generation of the myelin sheaths and 
 the nerve fibers in the ganglia. The 
 cells of the ganglia occasionally un- 
 dergo atrophy. The vessels are 
 sclerotic. The changes are probably 
 secondary to lesions in the peripheral 
 sensory nerves. 
 
 Spinal ganglia. Slight degeneration has 
 been noted as a result of locomotor 
 ataxia and peripheral neuritis. The 
 ganglia, however, are more frequently 
 involved by disease of the surrounding 
 bones as cares, producing tubercular 
 softening, or sarcoma, by pressure pro- 
 ducing atrophy of the ganglia. 
 
 THE NERVES. 
 
 1. Circulatory Disturbances. 
 
 Hyperemia, — from acute inflammation. 
 Hemorrhage, — from congestion or in- 
 juries. 
 
 Edema, — from nerves traversing inflam- 
 matory areas. 
 
 2- Atrophy, in consequence of pressure 
 or from disease of the nerves (neuritis) 
 
250 PATHOLOGY. 
 
 or the central nervous system. Atrophy 
 is sometimes seen in old age. 
 
 3. Inflammation or Neuritis, may be di- 
 vided into, — 
 
 a. Local Neuritis, is due to cold, pres- 
 sure on nerve from any cause or 
 extension of inflammation from an 
 adjoining tissue. 
 
 The nerve is swollen and red. The 
 sheath or the nerve fiber may be af- 
 fected. 
 
 The sheath undergoes fatty degen- 
 eration. 
 
 The fiber may become atrophied. 
 If the fibers are affected the myelin 
 breaks up and the axis cylinder be- 
 comes irregular, granularly degen- 
 erated and fragmented. 
 If certain nerves are affected, spec- 
 ial names are given, as sciatica, 
 Bell's paralysis, brachial neuritis, 
 etc. 
 
 b. Multiple Neuritis (a number of nerve 
 trunks are affected at the same time), 
 may be due to sudden cold after ex- 
 ertion, specific fevers, poisons as lead, 
 arsenic and alcohol, diabetes, cancer, 
 beri beri, etc. 
 
 The pathologic changes are similar to 
 the localized form. 
 
 4. Infectious Diseases. 
 
 Tuberculosis of the trunks is due to 
 direct extension. It affects the roots 
 and occurs in the course of tubercular 
 spinal or cerebral pachymeningitis. The 
 connective tissue is first affected, the 
 nerve fibers degenerate slowly. 
 Syphilis. The nerve roots are chiefly 
 involved. There is connective tissue 
 outgrowth with pressure which causes 
 degeneration of the nerve fibers. Gum- 
 mata is sometimes seen upon the cran- 
 ial nerves. 
 
 Leprosy. Large epithelioid cells con- 
 taining vacuoles filled with the lepra 
 bacillus are found within the connec- 
 tive tissue of the nerve fibers. 
 The small cutaneous nerves are affected 
 and anesthesia and trophic changes in 
 the skin are produced. 
 
 5. Tumors. Neuroma, sarcoma, muscle 
 fibers are sometimes found within the 
 sheath. 
 
INDEX. 
 
 Actinomycosis, 100. 
 
 Adenoma, 72. 
 Amoeba, 113. 
 Aneurysm, 148. 
 Anemia, 129. 
 Anhydremia, 128. 
 Apoplexy, 236. 
 Appendicitis, 1&3. 
 Arteries, 145. 
 Atrophy, 29. 
 
 Bacillus, 95. 
 
 Coli, 97. 
 
 Diphtheria, 95. 
 
 Influenza, 102. 
 
 Lepra, 106. 
 
 Mallei, 98. 
 
 Malignant 
 edema, 99. 
 
 Bubonic 
 plague, 102. 
 
 Tetanus, 101. 
 
 Tuberculosis, 
 103. 
 
 Typhoid, 96. 
 Bacteria, 85. 
 Beri Beri, 113. 
 Blastomata, 61. 
 Bladder, 214. 
 Blood Cells, 125. 
 Blood diseases, 125. 
 Bone diseases, 67- 
 
 228. 
 Bone marrow, 137. 
 Brain diseases, 235. 
 
 Carcinoma, 74. 
 Chancroid, 74. 
 
 Chancre, 108. 
 Cholera, 195. 
 Chondroma, 66. 
 
 Degenerations, 31. 
 
 Albuminous, 35 
 
 Calcareous, 40. 
 
 Fatty, 32. 
 
 Glycogenic, 40. 
 
 Hydropic, 32. 
 Dipeococci, 94 
 Dropsy, 27. 
 Dysentry, 194. 
 
 Edema, 27. 
 Embolism, 24. 
 Endothelioma, 81., 
 Endocardium, 140. 
 Enteritis, 191. 
 Esophagus, 183. 
 Epithelioma, 75. 
 Etiology of dis- 
 ease, 7. 
 
 Fallopian tubes, 
 
 222. 
 Ferments, 86. 
 Fever, 16. 
 Fibromata, 64. 
 
 Gall bladder, 201. 
 
 Gangrene, 47. 
 Glioma, 69. 
 Glands, 
 
 Thyroid,. 216. 
 
 Suprarenal, 218. 
 
 Salivary, 178. 
 
riaemangioma, 70. 
 
 Heart, 16-138. 
 Hemorrhage, 20. 
 Hodgkin's disease, 
 
 133. 
 Hydraemia, 127. 
 Hylomata, 63. 
 Hydraemia, 17. 
 Hypertrophy, 57. 
 
 Inflammation, 
 161. 
 Lymphatic chan- 
 nels, 151. 
 Lymphatic glands. 
 
 136. 
 Lymphangioma, 71. 
 Lymphadenoma, 71 
 
 Immunity, 88. 
 Infiltrations, 31. 
 Inflammation, 49. 
 
 Diphtheritic, 52. 
 
 Fibroid, 52. 
 
 Suppurative, 52 
 Intoxications, 10. 
 Intestines, 188. 
 Ischaemia, 20. 
 
 Jaundice, 203. 
 Joint diseases, 233. 
 
 Kidneys, 209. 
 
 Atrophy, 210. 
 Brights of, 210. 
 Hypertrophy, 
 209. 
 
 Larynx, 153. 
 Leucocytes, 28. 
 Lepidomata, 62. 
 Leukemia, 131. 
 Lipomata, 65. 
 Liver, 197. 
 
 Atrophy, 197. 
 Cirrhosis, 199. 
 Degeneration, 
 
 198. 
 Hyperemia, 197. 
 hypertrophy, 
 
 200. 
 Inflammation, 
 
 198. 
 Tuberculosis, 
 201. 
 Lung, 156. 
 
 Congestion, 156. 
 Edema, 157. 
 Embolism, 158. 
 Emphysema, 
 
 159. 
 Gangrene, 167. 
 Hemorrhage, 
 158. 
 
 Malformations, 4. 
 
 Malta fever, 112. 
 Malaria, 114. 
 Mammary gland. 
 
 225. 
 Metabolism, 12. 
 Measles, 111. 
 Meningitis, 240. 
 Mouth disease, 175. 
 Molluscum 
 
 contagio<3um, 116. 
 Myoma, 68. 
 Myocardium, 142. 
 Myxomata, 65. 
 Myelitis, 244. 
 
 Nasal cavities, 152. 
 Xecrosis, 45. 
 Neuroma, 69. 
 Nerve diseases, 249. 
 Neuritis, 250. 
 
 Oesophagus, 183. 
 Osteoma, 67. 
 Osteophytes, 67. 
 Ovaries, 221. 
 Oidium albicans, 
 103. 
 
 Pancreas, 204. 
 Parasites, 14. 
 Papilloma, 73* 
 Penis, 219. 
 Pericardium, 144. 
 Peritoneum, 206. 
 Phagocytic cells, 90. 
 Pharynx, 180. 
 Pleura, 173. 
 Plethora, 127. 
 Pneumonia, 161. 
 
 Broncho, 163. 
 
 Fibrous, 165. 
 
 Hypostatic, 164. 
 Poisons, 10. 
 Proteins, 85. 
 
Prostate gland, 
 220. 
 
 Rabies, 112. 
 Regeneration, 55. 
 Resolution, 55. 
 Rheumatism, 112. 
 Rhizopoda, 113. 
 Rickets, 228. 
 
 Sarcoma, 77. 
 Salivary glands, 178. 
 Scarletina, 110. 
 Scrotum, 219. 
 Seminal vesicles. 
 
 221. 
 Spirochaeta, 102- 
 
 107. 
 Spinal cord, 243. 
 Spleen, 134. 
 Spirillum, 98. 
 Stomatitis, 175. 
 Stomach, ±84. 
 Staphylococci, 92. 
 Streptococci, 93. 
 Susceptibility, 88. 
 Suppuration, 92. 
 Syphilis, 108-172. 
 
 Teeth, 179. 
 Teratomata, 84. 
 Testicles, 219. 
 Thrombosis, 23. 
 Thrush, 177. 
 Thymus gland, 137. 
 
 Tonsils, 181. 
 Tongue. 178. 
 Trachea, 154. 
 Typhoid fever, 96. 
 Typhus fever, 112. 
 Tumors, ^58. 
 
 benign, 61. 
 
 malignant, 61. 
 
 Urinary diseases, 
 
 209. 
 Urethra, 215. 
 Uterus, 223. 
 
 Vagina, 224. 
 Vaccinia, 117. 
 Varicella, 117. 
 Variola, 117. 
 Veins, 150. 
 Vermes, 117-125. 
 Volvulus, 190. 
 Vulva, 224. 
 
 Whooping cough, 
 111. 
 
 Worms, 117-125. 
 Wound repair, 54. 
 
 Xanthoma, 66. 
 Yellow fever, 111, 
 
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