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A Textbook of Veterinary Pathology
A TEXT BOOK
OF
VETERINARY
PATHOLOGY
FOR
STUDENTS AND PRACTITIONERS
BY
A^T^KINSLEY, M. Sc, D. V. S,
Pathologist, Kansas City Veterinary College.
SECOND EDITION
Eevised and Enlarged with 194 Illustrations,
5 inserts and one plate.
CHICAGO
ALEXANDER EGER
1916
Copyrighted at Washington, D. C, by
ALEXANDER EGER
1915
D
PREFACE TO THE SECOND EDITION.
This second edition of Veterinary Pathology has been care-
fully revised and it is hoped that no errors have crept in. The
subject matter has been elongated where it was deemed advis-
able. The chapter on Immunity was revised by Dr. J. W. Kal-
kus, Pathologist of the Washington State College. New illus-
trations have been substituted wherever the subject could be
more clearly demonstrated by so doing.
To his publisher, Alex. Eger, the author desires to express
his appreciation.
A. T. Kinsley.
Kansas City, Mo., September. 1915.
PREFACE.
A knowledge of pathology is essential to practitioners and
to students of medicine. The general considerations of pathol-
ogy, whether in reference to diseases of the human or diseases
of domestic animals, are practically identical. Many textbooks
on this subject are available, but they are especially written for
the practitioner and student of human medicine, and the illus-
trations and examples are all in reference to diseases of the
human. Such textbooks have been used by the author for sev-
eral years in veterinary classes and it was thought that if the
same general pathological principles could be exemplified by
cases and illustrations in veterinary medicine, the subject mat-
ter would be more readily understood by the veterinary student.
This explains the issuance of the present volume.
The writer has endeavored to place every phase of pathol-
ogy from the veterinarian's point of view. The entire subject
matter has been expressed as far as possible in common every
day language, with the hope that all readers will have no trou-
ble in grasping the pathologic facts. An extensive glossary has
been appended and will be of considerable aid because practi-
cally every technical term, with its analysis and definition, will
be found therein.
The author is greatly indebted to Dr. S. Stewart, Dean of
the Kansas City Veterinary College ; Dr. D. M. Campbell, edi-
tor of The American Journal of Veterinary Medicine ; Prof. W.
E. King, Bacteriologist of the Kansas State Agricultural College ;
Dr. F. J. Hall, Chief of the Food Inspection Department Kan-
sas City, Mo., and formerly pathologist of the Medical Depart-
ment University of Kansas ; Dr. L. Rosenwald, formerly patholo-
gist of the Kansas City Veterinary College; Dr.. Geo. F. Babb,
Milk Inspector of the city of Topeka, Kansas ; Dr. D. Cham-
plain, editor of The Milk-Man, for suggestions made by them
concerning the text matter. Also Dr. R. F. Bourne, physiologist
of the Kansas City Veterinary College ; Dr. C. D. Folse, City
Milk and Meat Inspector of Marshall, Texas, and Mr. Chas. Sals-
bery, microscopic laboratory assistant in the Kansas City Vet-
erinary College, for their assistance in the preparation of the
illustrations.
The author consulted various text-books, journals and other
publications while preparing the text for which acknowledge-
ment is hereby made.
If this book supplies the practitioner and the student of veter-
inary medicine with clear, concise statements of veterinary
pathology, the purpose of the book has been fulfilled.
A. T. K.
CONTENTS.
PAGE
Preface to The Second Edition 5
Preface 6
CHAPTER I.
Definitions 19
The Cell 20
CHAPTER H.
General Consideration of Disease 34
Inherited Diseases 35
Acquired Diseases 38
Table of Vegetable Parasites 49
Hypnomycetes 50
Saccharomyces 52
Schizomycetes 54
Animal Parasites 64
Protozoa 64
Helminthes 65
Arthropoda 66
CHAPTER HI.
Immunity : 75
CHAPTER IV.
Malformations 90
CHAPTER V.
Circulatory Disturbances 109
Hemorrhage Ill
Lymphorrhagia 117
Oedema, Dropsy or Hydrops 118
Thrombosis 122
Embolism 128
Ischemia 132
Hyperemia (Passive) 133
Hyperemia (Active 135
CHAPTER VI.
Inflammation 138
CHAPTER VII.
Progressive Tissue Changes 177
Regeneration 177
i
CONTENTS
PAGE
Wound Healing 184
Hypertrophy 189
Hyperplasia 192
Metaplasia 194
CHAPTER Vni.
Retrogressive Tissue Changes 196
Atrophy 197
Cloudy Swelling 301
Fatty Changes 204
Fatty Infiltration 206
Fatty Degeneration 208
Amyloid Changes 211
Hyaline Changes 213
Mucoid Changes 215
Colloid Changes 218
Serous Infiltration 221
Glycogenic Infiltration 222
Uratic Infiltration 224
Keratosis 225
Ossification 227
Calcareous Infiltration 228
Calculi 231
Concrements 239
Pigmentary Changes 242
Excessive Pigmentation 244
Absence of, or Diminished Pigmentation 250
CHAPTER IX.
Necrosis and Death 251-262
Physiologic Death 263
Pathologic Death 264
CHAPTER X.
Tumors 268
Fibroma 279
Myxoma 284
Chondroma 285
Lipoma 287
Osteoma 290
Glioma 291
Odontoma 291
Neuroma 295
Angioma 295
Myoma 298
CONTENTS iii
Sarcoma 300
Papilloma 321
Embryonic Epithelial Tumors 324
Placentoma 334
Teratoma 335
Cysts 338
CHAPTER XI.
Fever 342
CHAPTER XH.
Infective Granulomata 347
Tuberculosis 347
Actinomycosis 358
Glanders 364
Epithelioma Contagiosum 373
Glossary 376
LIST OF INSERTS.
Insert I — Botanical Names Next to page 45
Insert II — Bacteria Next to page 62
Insert III — Protozoa Next to page 63
Insert IV — Helminthes Next to page 66
Insert V — Arthropoda Next to page 71
Insert VI — Explanatory to Plate I Next to page 86
PLATE I.
Immunity 87
A LIST OF THE ILLUSTRATIONS
FIGURE PAGE
I — Diagram of a Typical Cell 21
2, 3 — Amitosis 25-26
4 — Division of Nucleus 26
5 — Division of Cell 27
6 — Cell in Resting Stage 27
7 — Prophase, Showing Division of Centrosome 27
8 — Prophase, Shov»ring Separation of Centrosomes 28
9 — Metaphase 28
10, II, 12, 13 — Indirect Cell Division — Metaphase, Anaphase, Telophase 28-29
14 — Ciliated Epithelium, Trachea 30
IS — Spermatozoa 31
16 — Red Buckeye 47
17 — Astragalus Molissimus (Loco) 48
18 — Trichophyton Tonsurans 50
19 — Aspergillus Fumigatus 51
20 — Saccharomyces Farcimosus 53
21 — Various Forms of Cocci 54
22 — Various Forms of Bacilli 54
23 — Various Forms of Spirilla 55
24 — Flagellate Bacteria 55
25 — Capsulated Bacteria 56
26 — Bacterial Fission 58
27 — Sporulation 59
28 — Bacterium Anthracis 60
29 — Bacillus Tetanus 61
30 — Piroplasma Bigeminum 64
31 — Trypanosoma Evansi 65
32 — Sarcocystis Miescheri 66
33 — Taenia Echinococcus 67
34 — Oxyuris Curvula 68
35 — Trichocephalus Depressiusculus 69
36 — Melophagus Ovinus 70
37 — iQastrophilus Equi 71
38 — Oestrus Ovis 71
39 — Culex Pungens 72
40 — Distoma Hepaticum "72)
41 — Echinorhynchus Gigas ^Z
42 — Hematopinus Phalanges Ovis 76
43 — Pulex Serraticeps 76
44 — Margarapus Annulatus, Female ^^
iv
LIST OF ILLUSTRATIONS
FIGURE PAGE
44 — Margarapus Annulatus, Male "]"]
46 — Margarapus Annulatus, Female laying eggs 'j']
47 — Margarapus Annulatus Larva '^'j
48 — Psoroptes Communis Ovis 79
49. 50 — Demodex Folliculorum Canis (From Kaupp Parasites) 80
51 — Dithoracisamelus 92
52 — Cranio Schisis 94
S3 — Chelo Schisis 95
54 — Palato Schisis 96
55 — Abdomino Schisis 96
56 — Synophthalmia 97
57 — Solipedia 98
58 — Polydactilism 99
59 — Prognathism 100
60 — Schistosis, Melus Anticus loi
61 — Pseudo-hermaphrodite 104
62 — Dicephalic, Calf 106
63 — Dicephalic, Calf 107
64 — Petechial Hemorrhage 113
65 — Hematoma 114
66 — Ascites, Dog 119
67 — Subcutaneous Oedema, Horse 120
68 — Thrombus in Aorta of Horse 125
69 — Thrombus, Red 126
70 — Embolism 129
71 — Infarction, Anemic-spleen 130
72 — Hyperemia Hemorrhage and Oedema Intestine 135
TZ — Hyperemia Kidney 136
74. 75. 76. ^^ — Vascular Variations in Inflammation 147-148-149-150
78 — Types of Cells in Inflammatory Exudates 151
79 — Gastritis 153
80 — Acute Pleurisy 154
81 — Acute Meningitis 156
82 — Gray Hepatization 157
83 — Fibrinous Pleurisy 158
84 — Myositis, Acute 160
85 — Chronic Pneumonia 162
86 — Chronic Hepatitis 165
87 — Pus, from a case of Strangles 168
88 — Suppurative Nephritis 170
89 — Red Hepatization 172
90 — Vascular Regeneration 178
91 — Fibrous Regeneration 179
92 — Wound Healing by first Intention 187
93 — Exuberant Granulation . . 188
VI LIST OF ILLUSTRATIONS
FIGURE PAGE
94 — Hyperplasia Interstitial Testicular Cells 192
95 — Hyperplastic Ureter 193
96 — Fibrous Tissue Ossification 194
97 — Cloudy Swelling 202
98 — Fatty Infiltration, Liver 207
99 — Fatty Degeneration, Liver 210
100 — Amyloid Degeneration, Liver 213
loi — Hyaline Degeneration, Vessels 214
102 — Mucoid Degeneration 217
103 — Colloid Degeneration 219
104 — Colloid Degeneration 220
105 — Keratotic Growth 226
106 — Atheromatous Degeneration 230
107 — Group Calculi 2:^2
108 — Cystic Calculus 234
109 — Urinary Calculi 235
1 10 — Salivary Calculus 236
I II — Inteestinal Calculus 237
112 — Biliary Calculi 238
113 — Hair Balls 240
114 — Inspissated Pus 241
115 — Hemosidern Pigmentation 245
1 16 — Icterus 247
1 17 — Necrosis 254
1 18 — Bacillus Necrophorus 255
1 19 — Ergot of Rye 256
120 — Ergot Poisoning in Cattle 257
121 — Fatty Necrosis 259
122 — Necrotic Center of Tubercle 260
123 — Sarcoma 271
124 — Metastatic Sarcomata 274
125 — Epithelioma 277
126 — Hard Fibroma 281
127 — Soft Fibroma 282
128 — Myxoma 284
129 — Chondroma 286
130 — Lipoma, Horse 288
131 — Lipoma, Ox 289
132 — Osseous Tumor, Maxilla 290
133 — Odontoma, Horse 292
134 — Odontoma, Epithelial 294
135 — Hemangioma, Simplex 296
136 — Hemangioma Cavernosum 297
137 — Hemangioma Hypertrophicum 298
138 — Leiomyoma, Small Intestine 299
LIST OF ILLUSTRATIONS vil
FIGURE PAGE
139 — Leiomyoma, Microscopic 300
140 — Sarcoma, Horse 301
141 — Sarcoma Mediastinum (Sections of Tumor) 302
142 — Sarcoma, Round Cell 303
143 — Lympho-Sarcoma Heart 304
144 — Lympho-Sarcoma 305
145 — Spindle Cell Sarcoma, Mule 306
146 — Spindle Cell Sarcoma 307
147 — Myeloid or Giant Cell Sarcoma 308
148 — Mixed Cell Sarcoma, Horse 309
149 — Mixed Cell Sarcoma, Jaw 310
150 — Mixed Cell Sarcoma, Maxilla 311
151 — Alveolar Sarcoma 312
152 — Endothelioma 313
153 — Endothelioma-Mediastinal 314
154 — Tumor in Ventricle 315
I55> 156 — Nature of Connective Tissue, Leucocytes, iMeoplasm Cells, Etc. 3:16
157 — Grape-Sarcoma, Uterus of Cow 317
158 — Melano-Sarcoma, Hog Skin 318
159 — Melano-Sarcoma, Microscopic, of Horse's Liver 319
160 — Myxo-Sarcoma 320
161 — Papillomatosis, Horse 322
162 — Papilloma, Microscopic 323
163 — Carcinoma-Encephaloid 325
164 — Epithelioma, Microscopic 326
165 — Epithelioma, Microscopic 327
166 — Epithelioma, Pearl Cell 328
167 — Adenoma, Mammary 329
168 — Adenoma, Microscopic 330
169 — Adeno-Sarcoma, Microscopic 331
170 — Cystadenoma 332
171 — Hypernephroma 333
172, 173— Dermoid Cysts 335
174 — Dermoid Cyst, Eye of Steer 336
175 — Dentigerous Cyst 337
176 — Cyst, Abdomen of Mule 339
177 — Uterine Cyst 340
178 — Fever — Crisis and Lysis 343
179 — Continuous Fever 345
180 — Remittent Fever, Curve 345
181 — Intermittent Fever, Curve 346
182 — Bacterium Tuberculosis, Bovine 348
183— Small Cellular Tubercular Liver ' 351
Vin LIST OF ILLUSTRATIONS
FIGURE PAGE
184 — Tuberculosis Lesion 353
185 — Tuberculosis ]\Iammary Gland 354
186 — Ray Fungus (Actinomyces) 359
187 — Actinomycotic Tongue 362
188— Bacterium Mallei 365
189 — 'Glanders, Nasal Septa 368
190 — Glanders, Cutaneous 369
191 — Glanders, Microscopic 370
192 — Epithelioma, Contagiosum ;ij^
193 — Epithelioma, Contagiosum 374
194 — Epithelioma, Contagiosum, Microscopic 375
CHAPTER I.
DEFINITIONS.
Pathology is the science of disease. It is the science which
treats of the nature, causes, progress, symptoms and termina-
tion or result of disease. It includes etiology, i. e., the study
of the causes oi disease, and pathogenesis, that is, the study of
tlie course, al)nonnal functions and lesions produced in disease.
General Pathology is confined to the explanation of the sum-
mary of the facts obtained in the study of special pathology. It
is concerned essentially in the solution of general principles of
those morbid conditions that are common to the entire organism,
as malformation, degeneration, regeneration, inflammation, neo-
formation and fever.
Special Pathology deals with all the abnormalities or diseased
conditions of one part or organ as the diseases of the ear, skin,
etc., and consequently special pathology' is further subdivided
into otologic j^athology, dermatologic pathology, etc.
Pathologic Physiology, is that part of pathology which has to
do whh the investigation and description of abnormal functions
of a diseased organ or animal. The pathologic physiology is,
in many cases, the principle symptom of a disease, e. g., paraly-
sis of the radial nerve. Abnormal function is frecprentlv the
onlv evidence discernible in a disease, e. g., epilepsy.
Pathologic Anatomy, or morbid anatomy, is concerned in the
structural changes in a diseased tissue or organ. Pathologic
changes that have occurred in the structure of a living tissue or
organ are collectively termed lesions. Lesions may be sufficiently
gross that they are readily observed with the unaided eye or
they may be so minute that the microscope is necessary for their
detection. The investigation and the recording of facts observed
in the study of gross and minute lesions are included in gross,
or macroscopic pathologic anatomy and minute, or microscopic
pathologic anatomy respectively.
Human Pathology has to do with the facts observed in the
study of the diseases of the human.
Comparative Pathology, is the name applied to the study of
the diseases of all animals in which the diseases of one genus,
(group of animals) is taken as a standard and the diseases of all
other animals are discussed in comparison with the type selected.
^ Veterinary Pathology, is a discourse on the diseases of domestic
animals.
19
20 VETERINARY PATHOLOGY,
THE CELL.
anatomic:
Structure.
Body.
Nucleus.
Centrosoiiic.
Membrane.
Shape.
Sice.
PHYSIOLOGIC.
Grozvth.
Reproduction.
Motion.
Metabolism.
Anabolisin.
Katabolism.
Irritability.
Structurally, an animal body is composed of definitely ar-
ranged parts, called organs. An organ is a portion of the body
having a particular function and is, structurally, a tissue-complex
in which each tissue has a certain definite proportion and relation.
A tissue is composed of like or similar cells with more or less
intercellular substance interposed. The intercellular substance is
usually a product of the cells. A cell has been defined as a
microscopic mass of protoplasm containing sufficient individ-
uality to possess a life history.
The function of an animal body is the sum total of the corre-
lated functions of its component tissues. The function of a
tissue is the sum total of the function of its cells. Thus a cell
represents the anatomical or structural unit and the physiologic
or functional unit of all animal bodies.
In ancient times disease was thought to be the result of
the entrance into the body of some "evil spirit," and the symp-
toms presented during disease was evidence of the struggle
beween the body and the "evil spirit." During the middle ages,
Hippocrates, "The Father of Medicine," established the Hippo-
cratic Theory of disease. Hippocrates taught, 1st, that the body
was composed of four humors, viz., blood, phlegm, yellow bile
and black bile ; 3nd, that health consisted of the proper balance
of the humors ; and od, that disturbed proportions of the hum-
ors resulted in disease.
Modern pathology is based upon the knowledge of cell activi-
ties. Virchow was the father of cellular pathology. He first
taught the cellular theory to students of pathology and he first
advocated it in published articles. Cellular physiology was really
an outgrowth of cellular pathology. A knowledge of cells is
THE CELL.
21
indispensable in the study of pathology and a brief description
is here appended.
Structure — Cells are variable in structure. The active consti-
tuent of all animal cells is protoplasmic in nature. The essen-
tial parts of animal cells are the cell-body, nucleus and cenrro-
some.
The cell-body is present in pratically all cells. It is com-
posed of semisolid protoplasm, a portion of which is of a stringy
- 3
-4
- S
Fig. 1— Diagram of a T.vpioal Cell, alfir Bolim-nnvir.
Fig. 22. — Various forms of Bacilli.
ago the study of bacteria was looked upon as a fad bj^ the
majority of the people. However, the practical application of
bacteriologic knowledge in medicine, sanitation, the various
arts and agriculture, has caused bacteriology to assume its
present important position as one of the principal biologic
sciences.
Bacteria are found everywhere that animals or higher plants
have grown. They are practically omnipresent.
Bacteria are single celled plants, each individual possessing a
cell body and a cell membrane. The cell body is principally
GENERAL CONSIDERATION OF DISEASE. 55
composed of protoplasm, which may be homogeneous or granu-
lar. In some instances non-protoplasmic particles may be pres-
ent. Chromatin, the essential nuclear material, is regularly dis-
tributed throughout the entire cell body and no doubt functions
the same as a nucleus. Granules that are intensely stained
with methylene blue occur in the body of some bacteria, but
their significance is not known. The cell bodies of some bacteria
contain starch granules while those of others contain sulphur
^V
1^5 \^-s. 'h
Fig 23. — Various forms of Spirilla.
granules. The cell membrane is of a protoplasmic nature and
is probably formed by condensation of the protoplasmic cell
body, whereas cellulose constitutes the cell membrane of the
cells of higher plants. Some species possess organs of locomo-
tion called flagella, which are delicate protoplasmic projec-
tions of the cell body or cell membrane. Some bacteria, per-
haps all, possess a capsule which appears as a gelatinous sub-
stance and is probably derived from the cell membrane. The
-4^ ^
Fig. 24. — Flagellate bacteria of various forms
cell body is the essential structure and presides over metabol-
ism, reproduction and practically all other functions. Circu-
latory, nervous and excretory organs are obviously not required
in such simple forms of life. The cell membrane protects the
cell body.
Bacteria are very small, one eight millionth part of a cubic
inch has been estimated as the least mass capable of being de-
tected with the naked human eye. This space will contain about
2,000,000 ordinary bacteria. The dimensions of bacteria are ex-
nressed in the term micron which is the unit of microscopical
measurement. (A micron is 1/35.000 of an inch and is desig-
nated by the Greek letter "Mu".) The Bacterium tuberculosis
averages about 2.5 microns in length and about .5 microns in
56 VETERINARY PATHOLOGY.
width, i. e., 1,000 tuberculosis organisms placed end to end
would make one inch in length or it would take 50,000 of these
bacteria placed side by side to make a linear inch. Some spher-
ical bacteria are less than one micron in diameter, e. g., the
pyogenic micrococci average .8 of a micron in diameter.
Different individuals of the same species may vary considerably
in size, thus the Bacterium anthracis may vary from four to
ten microns in length. Some diseases are probably the result
of infection with micro-organisms that are so small they can-
not be detected by the use of present day microscopes and they
also pass through the best known germ-proof filters. These in-
fectious agents are designated as invisible or ultra-microscopic
and may be present in a "filterable virus."
Fig. 25. — Bacteria, showing capsule.
Morphologically bacteria are very simple. Three principal
types of bacteria are recognized according to their form, viz :
the rod shaped (Bacilli), spherical (Cocci), and the spirals,
(Spirilla). Another type, characterized by branching forms,
(Chlamydo-bacteria), has a few representatives but their classi-
fication as bacteria has been questioned. The representatives
of each of the three principal groups, Bacilli, Cocci and
Spirilla, are constant in their morphology so long as the environ-
ments remain the same, i. e., the progeny of bacilli are bacilli,
etc. Again, each individual is constant in its form, increase in
size being the only change that occurs. Frequently, however,
unfavorable conditions may cause pleomorphism among indi-
vidual organisms.
Perhaps the best accepted morphologic classification of bac-
teria is as follows : —
1. Coccaceae, spherical shaped bacteria.
2. Bacteriaceae, rod or cylindrical shaped bacteria.
3. Spirillaceae, spiral shaped bacteria.
GENERAL CONSIDERATION OF DISEASE. 57
4 Chlamydo-bacteriaceae, branching or irregular forms of
bacteria.
According to their biologic characteristics, bacteria may be
classified as follows : —
Aerobic or anaerobic.
Chromogenic or non-chromogenic.
Zymogenic or non-zymogenic.
Saprogenic or non-saprogenic.
Photogenic or non-photogenic.
Thermogenic or non-thermogenic.
Saphrophytic or non-saphrophytic.
Parasitic or non-parasitic.
Pathogenic or non-pathogenic.
Pyogenic or non-pyogenic, etc.
Bacteria, like other living things, grow and reproduce under
favorable conditions. They grow until they attain a certain size
then they divide, i. e., a cell divides into two equal halves, each
half representing an individual bacterium which in turn grows
and ultimately divides into two equal halves, etc., thus bacteria
grow and multiply. The rate of growth and division is com-
paratively rapid. The Bacillus subtilis, under favorable con-
ditions may pass through the life cycles incident to attaining
its growth and dividing, thus doubling in number, every 30 min-
utes. Barber has found that Bacillus coli communis, under
optimum conditions may divide by fission, in seventeen min-
utes. Beginning with one bacterium, it has been estimated that
if division occurred once per hour and continued for three days,
the progeny would weigh 7,417 tons. Some other cells, notably
the undifferentiated cell in the animal embryo, may divide as
rapidly as bacteria, but they do not become developed, and so
far as known, there are no other cells that complete the entire
cycle of growth and reproduction in so short a time. This
method of reproduction is called fission. Fission occurs in the
three principal forms of bacteria. Among the Bacteriaceae and
Spirallaceae. the division takes place in the transverse diameter,
while the Coccaceae may divide in one, two or three planes.
Bacteria grow and divide by fission as long as favorable
conditions are supplied. When the environments are unfavor-
able the organisms cease growing and do not increase m num-
ber. Some species produce spores when conditions become
unfavorable for further growth and fission. Bacterial spores,
generallv characterized by being small, highly refractive oval
shaped bodies, are more condensed than the original cell body
protoplasm. Spore formation is first indicated by the appearance
58 VETERINARY PATHOLOGY.
of small granules in the protoplasm of the parent cell. These
granules collect and ultimately coalesce thus forming the spore.
The spore may form in the center of the bacterium or near one
end. After the spore is formed the remainder of the bacterial
body becomes disintegrated. Spores are much more resistant
to external injurious influences than are bacteria. The resist-
ance of spores is due to the fact that they contain less water
than bacteria, moreover they enjoy the protection of a thick
covering or cell wall. Spores are inactive, i. e., they remain dor-
mant until placed in favorable media and under favorable con-
ditions when they germinate and develop as the vegetative form.
One bacterium produces only one spore which in turn produces
Fig, 26. — Bacteria, showing fission.
only one bacterium and hence spore formation is not a means
of multiplication, but is rather a natural means of preservation
or continuation of the species. Those species of bacteria in
which no spores are formed usually have a greater resistance to
injurious influences than do the vegetative forms of the species
which are capable of producing spores.
Bacterial food requirements are quite variable. Some types
of bacteria require preformed organic compounds and others
appear to have the power of synthesizing the simplest com-
pounds and available elements into new compounds upon which
they subsist. Until recently it was supposed that synthesis was
confined to chlorophyllaceous plants but some species of bac-
teria are now known to possess the power of building complex
compounds from simple materials, e. g., the nitrifying bacteria
Parasitic bacteria and most saprophytic bacteria as a rule 're-
quire preformed organic compounds for their food. Some soil
GENERAL CONSIDERATION OF DISEASE. 59
bacteria and many water bacteria appear to live and thrive on
simple inor.e;anic substances. In fact most bacteria are capable
of adapting themselves to an inorganic food medium. Food sub-
stances must be in a dilute form in order that bacteria may
subsist upon them. This is probably because of the osmotic
differences of bacteria and their surroundings. Some chemic
substances, usually considered as destructive to bacteria, when
sufficiently diluted are food for certain bacteria, thus the Bacillus
pantotropus produces formalin and then uses it for food. It is
said that Bacillus pantotropus may live and thrive in a 1 to
15,000 solution of formalin. Bacteria as a rule require food
media of neutral or slightly alkaline reaction, (as shown by
Fig. 27. — Showing spore formation.
litmus paper) though some grow readily in acid media. While
foods are required in small quantities only for each bacterium,
yet because of their rapid multiplication and the resulting enorm-
ous numbers, the quantity of food substances consumed by them
becomes of considerable importance.
Most foods of bacteria like those of animals or higher plants,
must undergo modification preparatory to assimilation. As
previously stated, bacteria do not possess a digestive tube,
neither do they have the power of enveloping particles of food
as do some protozoa. Bacterial digestion is an extracellular
process, i. e., the bacterium digests food substances that are
outside of its own body. This process is the same as the
digestion in higher animals, the digestive tube in the latter
being outside of the body tissues. Bacterial digestion is the
result of activity of ferments produced by the body protoplasm
and in this respect is comparable with equine digestion which
60 VETERINARY PATHOLOGY.
is the result of activity of ferments produced by protoplasm
of the salivary, gastric, pancreatic cells, etc. Some bacterial
digestive ferments are very similar if not identical to the
digestive ferments of higher animals.
Digested foods or food substances in solution pass into the
bacterial body by osmosis.
Bacterial respiration is a simple process. The exchange of
gas is probably accomplished by means of the transfusion of
fluids containing the respiratory gas. Bacteria may vary in their
oxygen requirement. Aerobic bacteria are those that require
oxygen as a respiratory gas. Some bacteria will not develop
Fig. 2S — Bacterium Antliracis.
in the absence of free oxygen, obligatory aerobes. Although
it was originally supposed that all forms of life required free
oxygen this is now known to be an erroneous idea. Thus, the
anaerobic bacteria require the absence of free oxygen ; and some
organisms, — obligatory anaerobes — require the absolute absence
of uncombined oxygen. Other bacteria, facultative aerobes or
anaerobes, are not so selective in their oxygen requirements,
e. g., some are capable of immediate adaptation to a medium
containing free oxygen. It is probable that anaerobic bacteria
require oxygen as a respiratory gas but the oxygen is obtained
from oxygen compounds that are decomposed by these bacteria,
the oxygen probably being consumed while in the nascent state.
Moisture, temperature and light are other physical condi-
tions that afifect bacterial development. A very few bacteria
Oeneral consideration of disease.
61
will remain active in substances containing less than twenty
per cent of water. The optimum conditions relative to moisture,
requires the presence of about 80 per cent of water. This fact is
observed in the preparation of dried food stuffs and is the essen-
tial reason why dessicants favor wound healing or retard infec-
tion. The temperature range of the various bacteria is wide.
Some bacteria live and thrive at a temperature near the boiling
point, others at a freezing temperature. Pathogenic bacteria, in
general, require the temperature of their host. The chicken has
a very high normal temperature (107° to 108° F.), and this
Fig. 29. — Bacillus Tetanus.
may explain its immunity to practically all the diseases that
aft'ect other domestic animals. All bacteria require the absence
of light for their best development. By adaptation some have
become capable of growing and thriving in daylight.
The effects of bacterial growth and the products evolved
during bacterial growth vary according to the micro-organism
in question and its environment. Heat and light are two forms
of energy produced by bacterial activity. The heating observed
in manure piles, alfalfa, hay and various grains in the stack is
thought to be the result of bacterial action. In the above sub-
stances, the contained moisture favors the growth of bacteria and
the growth of zymogenic bacteria is always dependent upon
chemic changes in which complex compounds are reduced to
62 VETERINARY PATHOLOGY.
simpler ones. Such chemical changes are accompanied by the
evolution of heat. In all fermentation, in which the substances
acted upon are converted into simple compounds, heat is liber-
ated. Light or phosphorescence may be produced by bacteria.
The phosphorescence of decayed wood, ocean water, hesh, etc.,
may accompany the growth of light producing bacteria. Light is
a form of energy and bacterial light or phosphorescence is the
result of the conversion of some other form of energy usually
kinetic energy, into ether vibrations or light. The production
of heat and light are of little importance in comparison with
other bacterial products and activities.
Pigments of various kinds are produced by several different
species of bacteria. These pigments may be an excretion or a
secretion or they may possibly represent synthetic extracellular
products or enzymotic by-products. The importance of bac-
terial pigments is largely confined to the discolorization of food
substances. Thus the Micrococcus roseus, Bacillus prodigiosus,
and Bacillus erythrogenes, produce a red pigment in milk. The
red pigment in the milk is sometimes mistaken for bloody milk.
Other bacteria produce a variety of pigmentation in food sub-
stances. These pigments are variable in composition ^nd solu-
bility. Generally speaking the bacterial pigments are not
injurious when consumed. Practically all pigment producing
bacteria are aerobic.
The principal action of most bacteria is the result of the
activity of ferments or enzyms produced by the bacterial pro-
toplasm. Some of these bacterial ferments may produce their
specific activity while inside the bacterial body, others bring
about specific changes after being secreted and eliminated from
the bacterial body. The end products resulting from the activity
of bacterial enzyms or ferments are variable and depend upon
the specific enzym or ferment also on the composition of the
substances acted upon. Acids or alkalies represent the end
products of many of the bacterial decompositions. Carbohy-
drates are usually converted ultimately into an acid, carbon
dioxide and water. Protein substances may be converted into
dififerent simpler introgenous compounds or into carbon dioxide,
water and ammonia by the activity of many different bacteria.
Putrefaction is a bacterial decomposition of nitrogenous sub-
stances and occurs in the absence of air. The end products
of putrefaction are extremelv variable: hvdrogen, carbon dioxide,
nitrogen, hydrogen sulphid, and ammonia, are some of the com-
mon gases that escape from a putrefying carcass ; amido com-
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BRANCH
PROTOZOA,
Unicellular animal organ-
isms, asexual, reproduce
by fission, sporulatlon. or
budding.
ORDER
SPOROZOA,
Reproduce by sporulation,
no flagella, no cillia.
INFUSORIA,
Possess cilia or flagella,
reproduce by fission and
budding.
CLASS
COCCIDIA.
SARCOSPORIDIA.
FLAGELLATA.
HYPOTRICHA.
INSERT III.
FAMELY GENUS SPECIES
PSOROSPERMIDAB.
SARCOSPORIDAE.
CERCOMONIDAE.
Coccidlum ovlforme
Coccidlum cunlcull
Coccldium avium
Sarcocystls MIeschert
Sarcocystls tenella
Balblanla glgantea
Lanablla Intcstlnalla
Monoccrcomonas hepatica
Trypanosoma equlperdum.
Trypanosoma Evansl.
Trypanosoma equlnum.
TRTPANOSOMATIDAE. Trypanosoma Brucel.
HOST PART INFESTED
Rabbits, G. pigs and man Liver and Intestine.
Rabbit. Llcberkuhn's slands and intestine.
Fowls. Liver and Intestine
Pig. Muscles.
Horse, ox, sheep, and pig. Muscles.
Ox, sheep and dog. Connective tissue.
Sheep and dog
Pigeons.
Horse.
Horse.
Horse.
Horse.
Intestine.
Liver.
Blood.
Blood.
Blood.
Blood.
ANKULATA,
Specialized worms com-
posed of ring like sege-
menls, simple head end
pyes. usually everslble
dentated pharj-nx. straight
alimentary canal, well de-
veloped nervous system.
HIRUNDINEA,
Slightly flattened on dor-
sal and voniral surface,
sucker at each end.
GNATHOBDELLA,
GNATHOBDELLIDBA, Hlrudo medlcinalis
HIrudo troctlna.
Hlrudo decora
HIrudo Tagala
Haemopis sangulsuga
Man and horse.
Man and horse.
Man and horse.
Man and animals.
Horse
Skin.
Skin.
Skin.
Anterior respiratory tract and Intes-
tine.
GENERAL CONSIDERATION OF DISEASE. 63
pounds, pepton, skatol and indol represent aromatic compounds ;
ptomains probably represent one of the most important putre-
factive products. Ptomains are basic chemic substances pro-
duced by decomposition of nitrogenous compounds. They are
usually formed outside the body, although they may be formed
by putrefaction of the contents of the intestine. Ptomain pois-
oning is usually the result of consumption of foods contaminated
with ptomains, although it may result from the absorption of
ptomains formed within the intestine. Sufficient ptomains may
also be absorbed from necrotic tissue to produce injurious efifects.
The chemic substances produced by pathogenic bacteria are
probably of more importance than any other bacterial com-
pounds. Although they have been extensively studied the com-
position of most of these compounds is still unknown. Three
groups of pathogenic bacterial products deserve mention, they
are (1) bacterial toxins, (2) endotoxins and (3) bacterial pro-
teids.
1. Bacterial toxins are soluble, synthetical, poisonous,
chemic substances elaborated by the bacterial protoplasm and
liberated into the surrounding media. The chemic composi-
tion of bacterial toxins is unknown. They are very similar in
many respects to enzyms. They are specific, i. e., a given
organism always produces a definite toxin. According to
Ehrlich bacterial toxins are composed of two combining groups,
one the haptophore which combines with the receptors, of the
animal cells and forms a medium through which the other group,
toxophore, acts. They are the principal product in some infec-
tion, e. g., tetanus. (Infection is the invasion into a living body
of pathogenic micro-parasites, and the sum total of the disturb-
ance produced bv their presence in the body.) During infection
the body attempts to neutralize bacterial toxins by the produc-
tion of a substance termed an antitoxin.
2. Endotoxins are poisonous chemic products formed and
retained within the bacterial body. They become liberated only
when the bacteria are destroyed and distintegrated. Although
the chemistry of endotoxins is not known, they are probably
constant in composition and produce specific symptoms in in-
fected animals. The animal body does not produce antibodies
that neutralize endotoxins, but opsonins are produced in the
tissues of animals immunized to endotoxins. Endotoxins are
the principal injurious substances produced by pyogenic cocci.
Bacterium tuberculosis, the organisms causing glanders, pneu-
rnonia, and other specific infections.
64 VETERINARY PATHOLOGY.
3. Bacterial proteids are insoluble nitrogenous constituents
of the bacteria cell protoplasm. They are not well understood.
(See insert No. 3.)
ANIMAL PARASITES.
The animal parasites, capable of producing disease in an-
imals, are quite numerous and represent the following branches
of the animal kingdom : — protozoa, helminthes, and arthropoda.
Fig. 30. — Piroplasnia liiKeniinum in the red bl>od corpuscles.
Protozoa.
Protozoa are microscopic single celled animals. They are
very simple in structure, being composed of a mass of proto-
plasm with or without a cell membrane. The cell membrane,
when present, consists of concentrated protoplasm The pro-
tozoa having a cell membrane are constant in shape, as the Try-
panosoma Evansi, and those not possessing a cell membrane
vary in shape from a sphere to an irregular flat mass and are
capable of changing their shape whenever occasion demands.
Protozoa are larger than bacteria.
Protozoa require food similar to the foods of higher animals.
Particles of food may be inclosed or incorporated by them pre-
paratory to digestion. Digestion is accomplished by means of
ferments elaborated and secreted by the protozoa. The digested
foods pass by osmosis into the protozoa, the undigested portion
being extruded by rearrangement of the cell protoplasm. Res-
piration takes place by exchange of gases through the surface
protoplasm of the protozoa. They reproduce by fission, budding,
conjugation or sporula+ion.
Protozoa are universally distributed. They all require con-
siderable moisture. In fact most of them live either in fresh or
salt water. A few only are parasitic.
GENERAL CONSIDERATION OF DISEASE.
65
The specific action of pathogenic protozoa in the produc-
tion of disease is not understood. Some may have a mechanical
effect only but the evidence concerning others indicates that
most of them produce an injurious chemic substance.
Helminthes.
This branch of the animal kingdom contains many species
that are parasitic. Structurally, animal parasites are much
simpler than the closely related nonparasitic animals. The sim-
plicity of parasites is a result of adaptation to environments in
v^hich essential structures of the nonparasitic type, useless to the
Fig. 31. — Trypanosoma £vailBi in a bloodsmear from a horse affected with surra.
parasitic type, atrophy because of disuse. The parasitic hel-
minthes are of the simplest structure, their nervous, digestive
and respiratory systems being very rudimentary.
Their food is obtained from their host. Some animal para-
sites, as the tapeworm (Taenia) absorb digested food stuff from
the intestine of their host, others subsist upon the host's blood,
(Uncinaria), and till others consume tissue juices and lymph,
(Trichina spiralis). The reproduction of helminthes is accom-
plished by means of ova, or by the production of living larvae.
The life history or cycle of helminthes is ver}^ interesting. In
some cases the organism is parasitic in different animals during
the different stages of its life cycle ; for instance the Taenia cras-
sicolilis inhabits the liver of the rat during its cystic stage and
the intestine of the cat during the adult stage.
Helminthes produce injury to their host by consuming food,
by sucking blood and by liberating injurious chemic substances.
66
VETERINARY PATHOLOGY.
Arthropoda.
This branch includes many parasitic representatives, as flies
and mosquitoes (diptera), fleas (siphonaptera) lice (hemip-
Flg. 32. — Sarcocystis Miescheri. Drawing made with Camera lucida.
1. Cross section sarcocyst, muscle cell enclosing carcocyst ruptured.
2. Cross section of heart muscle cell.
3. Fibrous connective tissue.
tera), itch mites and ticks (acarina). The entire order, siphon-
aptera and hemiptera. most of the order acarina, and many rep-
resentatives of the order diptera are parasitic. Of the parasitic
arthropoda some are temporary and some are permanent para-
BBANCH CLASS
OKDES
GENUS SPECIES
HOS^
'l»LATTHEiI.MlKTHES. .
Flat worma, nearlj all
bermaphodltea.
NEMATUBLMIKTHES,
Round worms, nonies-
I tnented, leze* •eparate.
CESTODA,
Ribbon shaped, segment-
have no fixation apparatus
have no digestion apparatus
on head. Adult lives In In-
testines.
TKEMATODA,
Fiat worms, nonsegment-
ed, have digestive canal,
no anus, have one or two
suckers on ventral surface.
AC ANTHOCEPH A LA,
Slender worms, complete
digestive canal, are found
In all tissues of domestic
animals except bone.
JTEMATODA.
Slender worms, complete
digestive canal, are found
in all tissues of domestic
animals except bone.
TAENIIDAE,
Head always has four
suckers between which Is
found a depression or a
proboscis. Segments usu-
ally have their gentlal op-
enings on margin.
BOTHRIOCEPHALIDAE,
Found mostly In flshes.
DISTOMIDAE.
All have two suckers, an
anterior and ventral.
ECHINORTNCHIDAE,
Found in digestive canal
of vertebrates.
ASCARIDAE,
Large firm body, resemble
earth worms, mouth Is
surrounded by three lips.
Usually found In small In-
testine.
Taenia saginatta uan
(Cyst; Cystlcercus celluloiie, of pig.)
Taenia soUum ji^n
(Cyst: Cysticercus bovls, of ox.)
Taenia perfoliata • v.»./
Taenia mamlllana
Taenia plicata
Taenia denticulata
Taenia expansa
Taenia fimbrlata
Horse
Horse
Horse
Ox
Ox and sbesp
Sbe»p
PART DfFBSTnf
Intestine
Intestine
Intestine
Intestine
Intestine
Intestine
Duodenum and gall ducfr
Dog
fox
Small intestine
Small intestine
OXTURIDAB,
Cylindroid body,
pointed, mouth
stomach large.
tall
nude,
STRONGTLIDAE,
Body cylindroid, mouth
either nude, armed or
papillated, oseophagus
large.
TRICHOTRACHELIDAE,
Body slender in anterior
portion, enlarged poster-
iorly for containing iQtes-
tlne, mouth nude, anus
terminal, all live In Intes-
tine.
FILARIDAE, . .
Long thread like body,
mouth or triangular .oeso-
phagus small
GNATHOSTOMIDAB,
Head distinct, oviparous.
Taenia marglnata ^
(Cyst; Cysticercus tenuicollls of rumlnanta)
Taenia coenurus do?. wolf and .u*
(Cyst. Coenurus cerebralls In spinal coid and brain of sheep )
Taenia echinococcus Dog and wolf Small Intestine
(Cyst; Echinococcus polymorphous, of herbivora and omnlvora )
Taenia cucumerina Dog
(Cyst; (1) Cryptocystis Irichodcctis of Trichodectes latus.)
(Cyst; (2) Cryptocystis pulecldes of Pulex serratlceps.)
^"^"" rc'>%t, cysticercus ovl. .heep.) °^^ S*»^' ^"'""»*
Bothrbcephalus latue Man, dog, cat Intestine
Distona hepaticum
Distoma lanceolatum
Dlstoma Amerlcanum
Amphlstoma cervi
Paragonlmus Westermanll
Echinorhynchus gisas
Ascaris megalocephal.us
Ascaris bovls
Ascaris ovis
Ascarlsuilla
Ascaris marglnata
Ascaris mystax
Oxyurls curvula
Oxyurls mastigodes
Strongylus Arnfeldi
Strongylus micrurus
Strongylus pulmonaris
StrongjluB fllarla
Strongylus rufeecens
Strongylus paradoxus
Strongylus OsteragI
Strongylus contortus
Strong>-lus flllcollls
Strongylus glgas
Strongylus vasorum
Sclerastoma equinum
Sclerastoma tetracanthum
Sclerastoma hypostomura
Syngamus trachealls
Stephanurus dentatu»
T.Tnclnarla trigonocephala
Undnarla cernua
Undnarla radlatus
Trichocephalus afflnis
Trichocephalus crenatus
Trichocephalus depressiusculue
Trichina spiralis
Fllarla papulosa
Fllarla cervlna
Pilaris Immltls
Splroptera megastoma
Spiroptera microstoma
Splroptera reticulata
Splroptera scutata
Splroptera sanguinolenta
Gnathoitoraum eheiracanthua
Herbivora and omnlvora Gall ducts
Sheep, ox, goat, pig. ass. Gall ducts
dog
Sheep and ox Liver
Ruminants Kumen
Man. dog, pig and cat Lungs
Pig
Solipeds
Ox
Sheep
Pig
Dog
Cat
Horse
Horse
SoUpeds
Bovtnes
Calf
Sheep, goat, camel, deer
Shee", goat and deer
Pig
Ox
Sheep, goat
Sheep and soat
Horse, ox, dog and man
Dog
Horse, ox, dog and man.
SoUpeds
Sheep and goat
Birds and chickens
Pig
Dog and fox
Sheep and goat
Bovlnes
Ox, sheep and goat
Pig
Dog
Pig
Horse
Ox and deer
Dog
Horse
Horse
Horse
Ox, sheep and goat
Dog
Pig. dog and eat
Small intestine
Small Intestine
Intestine
Intestine
Intestine
Intestine
Intestine
Posterior bowel
Posterior bowel
Bronchi and lungs
Bronchi and lungs
Bronchi
Bronchi and lungs
Bronchi
Bronchi
Abomasum
Abomasum and duodenum
Small Intestine and abomasum'
Kidneys and drinary organs
Heart
Intestine
Large Intestine
Large intestine
Trachea
Region of kidney and liver
small Intestine
Small Intestine
Small intestine
Caecum
Large Intestine
Caecum
Muscles
Peritoneal and plural cavltlri
Peritoneum
Right heart and pulmonary arter-
ies
Right stomach
Stomach , . ..
Flexor tendons asd cervical Ujfc*
mcnts
Oesophageal wall
Tumors of. stomach, SUllet and
aorta
Sastric mucosa
GENERAL CONSIDERATION OF DISEASE.
67
sites, and with one or two exceptions they are all external para-
sites.
The structural peculiarities that differentiate arthropoda from
the other branches of the animal kingdom are their jointed ap-
pendages, segmented body, and bilateral symmetry.
The parasitic arthropoda obtain their food from their hosts.
Some of them consume epidermal scales and hair, e. g., the
horse louse (Trichodectes pilosus) and feathers, e. g., the
Figr. 33. — Taenia Echinococcus. Niles & Neuman.
a. Adult tapeworm. After Neuman. b. Part of hog's liver showing cystic form.
chicken louse (Menopon pallidum) others abstract blood, e. g.,
the hog louse (Hematopinus suis), itch mite (Sarcoptes scabei
variety canis), and still others may consume tissue cells other
than blood cells as epithelium. Reproduction of arthropoda is
about the same as it is in helminthes.
Disease resulting from infestation of arthropoda is due
primarily to irritation induced mechanically or by chemic pro-
ducts of the parasites, secondarily to loss of blood.
Extension of Disease. — By extension of disease is meant the
inv^asion and affection of adjacent structures and even remote
68
VETERINARY PATHOLOGY.
tissues of the body. Some diseases are necessarily local, i. e.,
the cause is not capable of being transferred to adjacent or re-
mote structures, e. g., ocular filariosis. Other diseases are in
their earlier stages local, but later the cause may be transferred
to some other part and produce secondary diseased foci or
Fig. 34. — Oxyuris Curvula, after Niles.
a. Adult worm.
b. Cephalic extremity.
c. Caudal area.
metastases, e. g., tuberculosis. The extension of disease may be
produced as follows :
First, by the cause of the disease passing along the natural
channels and establishing secondary diseased foci, thus. Bray
reports that calves become afifected with necrotic gastritis and
enteritis when allowed to swallow the necrotic tissue during an
attack of necrotic stomatitis.
Second, by the spread of the cause into adjacent tissues, e. g. :
Extension in like tissue, as in muscular tissue, is termed contin-
GENERAL CONSIDERATION OF DISEASE.
69
uity and is exemplified in psorospermosis, while extension from
one tissue to another of a different type, as from muscular to
connective tissues, is called contiguity and is evidenced in acti-
nomycosis.
Third, by the lymph and lymphatic nodes, e. g. tuberculosis.
Fourth, by the blood stream in which case the mestastases
will be in the lungs, liver, or kidney, — e. g.,
anthrax. The incorporation of microl)ian
agencies by leucocytes is frequently the
means by which infection is extended, in
fact it is probable that the leucocytes are
the principal factor in lymph and blood
extension of infective processes in the
body.
Fifth, by passing along the nerve fibres
as in rabies.
Termination of Disease. — Termination
is the ending or outcome of the condition
or existing disease. Disease terminates as
follows :
Recovery. — Disease terminates in re-
covery when the body tissues are effectually
repaired and all structures have assumed
their normal function. Diseases resulting from irritating or
non-nutritious foods are corrected by expulsion or neutraliza-
tion of the causative agent either by vomition, purgation or
chemical union and by repair of the injured tissues, after which
normal functioning continues. Tissue afflicted with mechanical
injuries as wounds, recover when the destroyed portions have
been replaced and the normal function has been resumed. Dis-
locations terminate in recovery when the dislocations have
been reduced and the parts assume their normal function. A
horse recovers from pneumonia when the inflammatory exudate
has been removed from the alveolar spaces and all injured
tissues have been repaired and the normal functioning has been
re-established. In general, recovery is the result of the comple-
tion of the protective and reparative processes of the various
tissues of the animal body.
Partial recovery. — If the normal functioning is not assumed
after a disease has run its course, recovery is said to be incom-
plete or partial. Partial recovery is observed in old animals or
in those that have been depleted because of complications or
previous disease. Some diseases are essentially destructive and
their influence in the tissue results in incomplete repair, as in
Fig. 35. — Tricliooeplialus
Depressiusculus
of a Dog, after Railliet.
70
VETERINARY PATHOLOGY.
tuberculosis, glanders, dourine, bovine contagious pleuro-pneu-
monia, etc. Injuries and acute inflammation of the parieties of
Fig^. 36. — Melopliagus Ovinus, after Niles.
Dorsal view of adult. d. Terminal segmant of leg
Ventral view of adult. e. Shell of pupa.
Mouth parts enlarged. f. Pupa.
hollow organs frequently terminate in the formation of cicatrical
tissue thus contracting the lumen of these organs. This is com-
mon in injuries of the oesophagus, intestine, trachea, and ure-
thra. Adhesions succeeding pericarditis, pleuritis, and periton-
itis are examples of partial recovery.
BRANCH CLASS
ORDER
h
u
CO
Z
INSECT A ( HEX APOD A) .
Air breathers, when adult
have three pairs of legs,
and distinct head, thorax
and abdomen.
ABACHNIDA
Ail- breathers with caphai-
othorax and abdomen,
have when adult four
pairs of legs. Those here
Included are oviparous.
DIPTERA
Have two wings, two hal-
teres, sucking mouth parts,
and complete metamor-
phosis, includes flies and
mosquitoes.
HEMIPTERA
Wings often absent, when
present one pair thick and
one pair thin. , Suc,kjng
mouth parts, incomplete
metamorphosis, and include
the blood sucking lice.
MALLOPHAGA
Wingles lice with sucking
moutli parts, and incom-
plete metamorphosis.
SIPHONAPTERA
Wingless fleas with suck-
ing mouth parts, and com-
plete metamorphosis.
ACARtNA
Usually short thick, non-
articulated bodies, possess
camerostoma. larva usual-
ly hexapodal, sexes Bepa-
rate.
MUSCIDAE
Have soft probosis adapt-
ed for suction, styJet of an-
tennae plumose to the end.
TABANIDAE i
Broad and slightly flat-
tened body, large head, I
muscular wings, larva car I
nivarous, are oviparous. '
STOMOXIDAE
Closely resembles the mus-
cidae
SIMULIIDAE ,
Thick body, bulging tho-
rax, M
Fig-. 41. — Eehinorhynchus Gigras, after Niles.
a. Cephalic extremity .showing hooks.
b. Worm with portion of mucous membrane of intestine attached.
tion to emerging vessels of the heart. Nerve paralysis may be
the result of poisonous products derived from infectious agen-
cies, or chemic poisons derived from katabolism, or hemorrhagic
extravasates.
74 VETERINARY PATHOLOGY.
2. Apnoea, or respiratory failure. This may be the result of
paralysis of respiratory nerves or muscles, spasms of respiratory
muscles, rupture of diaphragm, or occlusion of the respiratory
tubes.
3. Apoplexy, or hemorrhage into the brain tissue. This is
probably the specific cause of death in apoplectiform anthrax.
4. Hemorrhage, especially rapid loss of large quantities of
blood. Any of the above may act independently in producing
death, but are probably more frequently complicated one with
another.
CHAPTER III.
IMMUNITY.
DEFINITION.
IMPORTANCE.
VARIETIES.
Inherited, (Natural).
Definition.
Examples.
Cause.
Cell Action, {Metchnikoff & Sternberg).
Chcniic Substance, {Ehrlich & Buchner).
ACQUIRED, (Artificial).
Definition.
E.vainples.
J'arieties.
Active.
Definition.
Varieties, (Toxic), (Opsonic), (Bacterial)
Etiology.
Recovery from attack of disease.
Inoculation zvith virus.
Inoculation with vaccine.
Inoculation z(.fith bacterin.
Inoculation zvith toxi)i.
Inoculation simultaneously zvith virus and antibody.
Passive.
Definition.
Etiology.
Inoculation zvitli ajitibodv.
THEORIES.
Exhaustion.
Retention.
Phagocytosis.
Humoral.
Ehrlich's Lateral Chain Theory.
Immunity literally means proof against disease, i. e., it is
the name of the condition that enables an animal to resist the
action of pathogenic micro-organisms, or to be unaffected by
their products. Immunity is only a relative term, the condition
is not absolute and permanent neither is it constant and con-
tinuous. Whenever an animal is unable to adjust itself to its
environments it becomes susceptible to the effects of the causa-
tive agents of diseases, i. e., its immunity, at least acquired
immunity, is suspended.
The term immunity is ordinarily used in reference to infec-
tive diseases, i. e. those diseases resulting from the invasion of
microparasites ; although it may be used in designating the
resistance to the action of zootoxin, such as snake venom, and
possibly also of the poisonous substances ejected by centipedes
7^
Veterinary pathologv.
and scorpions, as well as the phytotoxins, such as ricin, abrin,
crotin, and robin.
Immnnity, more than any other problem, directly concerns
the medical profession and indirectly the international commer-
Fig. 42. — Hematopinus phalanges ovis, after Niles.
a. Adult. b. Egg cemented to hair.
cial welfare. It was a laboratory fad of the pathologists until
they demonstrated to the practitioners that it was feasible to
produce immunity in man and animals. Veterinarians have now
Fig. 43.— Pulex Serraticeps, after Tu«jgor.
IMMUNITY,
11
almost universally accepted the proposition and have at their
command the means by which they can immunize animals
against the ravages of some of the fatal infective diseases to
which they are susceptible. The increased confidence of the
people is in turn enabling scientists to investigate new phases
of the subject. Although immunization has been known and
made use of more or less for centuries as vaccination against
"^^"^^^^s^m.
.^
Fig. 44. — Margrarapiis Anmilatus, female. Fig. 45. — Margarapus Annulatus, male.
Fig. 46. — Margarapus Annulatus,
female laying egjji.
Fig. 47. — Margrarapus Annulatus, Larva.
smallpox by the Chinese before the Christian era, yet the essen-
tial ph3^siologic, chemic or pathologic basis for immunity is
still unknown.
Immunity may be natural (inherited) or artificial (acquired).
Natural immunity is an inherited property possessed by or-
ganisms (animals). The horse has a natural immunity to hog
cholera, the ox to glanders and the hog to tick fever. The
concise and exact cause of natural immunitv is unknown. It
is probably the result of cellular activity in the immune animal,
an activitv the nature of which is not understood. Some inves-
tigators, ]\Ietchnikoff in particular, attribute natural immunity
to phagocytosis (cellular hypothesis), others maintain that insus-
78 VETERINARY PATHOLOGY.
ceptibility to disease is a result of the antagonistic action of the
body fluids (humoral hypothesis). Ehrlich's lateral chain the-
ory assumes that the cells of immune animals are not capable
of combining Avith the toxins of bacteria, i. e., they have no
receptor molecules and hence those animals are not receptive,
they are immune. Whether we accept the cellular hypothesis,
the humoral hypothesis, or Ehrlich's lateral chain theory, the
fact remains that natural mimunity is a characteristic or prop-
erty of parental origin that is transmitted to the offspring and
is present at the time of birth.
Natural immunity may be the result of an acquired toler-
ance due to natural selection and heredity. There is a marked
variation in susceptibility and resistance in individuals of a given
species. A continuous or repeated exposure of susceptible ani-
mals to a given pathogenic microparasite will result either in
destruction of those animals or the production of an immunity,
i. e., those individuals most resistant will survive and their
resistance will become more and more fixed and will finally be
transmitted to the offsprmg and hence be a natural immunity.
Thus all native Cubans are practically immune to yellow fever
because at the time yellow fever was first introduced into Cuba
the least resistant individuals died of the malady, the most
resistant individuals survived and lived in the presence of the
diseases almost continually after yellow fever was introduced
into Cuba (It was not eliminated until after the Spanish-Amer-
ican war). Consequently the Cubans for several generations
developed in the midst of yellow fever and only the resistant
''ndividuals survived. This resistance finally became so firm
that it was transmitted to their offspring and was then a nat-
ural immunity.
The resistance possessed by dogs to most diseases is ex-
plained in a similar way to the Cubans' resistance to yellow
fever. Thus the dog has descended from the jackal and the
wolf, two types of animals that have lived largely upon the
carcasses of animals dead of various diseases. As the animals
fed on carcasses they fought, thus inoculating each other, so in
the beginning the least resistant individuals died, the more resis-
tant animals survived. Thus the constant fighting and inocu-
lating has established in them a firm resistance that is trans-
mitted to their progeny as a natural immunity. This immunity
has become so fixed that it does not vary even in the domestic
dog. The above is a plausible explanation of race or species
immunity. The exact origin of individual immunity is considered
IMMUNITY.
79
by some to be an acquired tolerance, i. e.. an acquired immunity,
and by others, as simply an individual resistance not developed
by having the disease to which the q-iven individual is immune.
Acquired immunity is an artficially produced condition by
virtue of which the animal is capable of resisting- disease, and
Fig. 48. — The scat) mite of sheep. Psoroptes Coiiiiiiunis Ovis, magnified 150 diameter'?.
is produced in an animal either in utero or after birth, and may
be active (toxic, opsonic or bacterial), or passive (antitoxic).
Active acquired immunity is, no doubt, the result of cellular
action and may be produced as follows : —
1. By an animal becoming infected and recovering from an
attack of the disease, e. g. blackleg.
2. By inoculation of a susceptible animal with a small
quantity of the virulent causative microparasites, thus produc-
ing the disease in a mild form. This is practiced in immunizing
cattle against tick fever.
3. By inoculating a susceptible animal with an attenuated
virus, (vaccine.) Horses, mules, cattle, and sheep are immun-
ized to anthrax by a vaccine.
4. By inoculation of susceptible animals with a bacterin
80
VETERINARY PATHOLOGY.
(dead bacteria) colts are immunized to strangles by the use of a
strepto bacterin.
5. By repeated inoculations of a susceptible animal with
small quantities of a toxin of a specific pathogenic microparasite,
tetanus toxin or other active poison as snake venom. This
method is used only in the production of antitoxins or in immun-
izing animals against zootoxins and phytotoxins.
Fig. 49. — Deniodex Folliculoruni,
variety Canis.
Field showing various stages of
development.
a. Ova.
b. Pupa.
c. Adult.
d. A piece of Scab.
Fig. 50. — Demodex Folliculonim,
variety Canis.
Adult Male, magnified 400 times-
showing wide head, with ros
trum, short legs (3 articles
each) 2 claws and elongated
body.
6. By simultaneous inoculation with a virus and an antitoxin
(antibodies, bactericidal substances, etc.). In the Philippine
Islands this method is employed in immunizing cattle against
rinderpest, and it is also being successfully used in the immun-
ization of hogs, against cholera.
Toxic immunity is the resistance to poisonous substances as
toxins of bacterial origin, zootoxins and phytotoxins. It is
common to hear sheep herders speak of dogs that are immune
to the venom of rattlesnakes. The dogs are bitten frequently
while doing duty on the range and although the reaction from
the first inoculation is intense and may even kill, each succeed-
ing inoculation produces less reaction until finally the dogs may
IMMUNITY. 81
be bitten or the venom inoculated with impunity. Immunity to
intoxication diseases such as tetanus are of this type. The ab-
sence of action of various therapeutic agents that have been
given repeatedly may be explained on the principles similar to
those involved in the production of immunity in dogs to snake
venom. Toxic immunity is the result of the presence in the
body fluids of an antibody (Antitoxin.)
Opsonic immunity is the resistance of an infected animal due
to a substance, opsonin that facilitates the destruction of bacteria
by leucocytes. This is the type of immunity manifested in the
human that is immune to typhoid, and the various animals that
are immune to suppurative processes caused by the pyogenic
micrococci.
Bacterial immunity is the resistance an infected animal mani-
fests to the bacterial invader. It is the result of bacteriolytic
substances in the body fluids. Pfeififer demonstrated that
bacteria are destroyed when introduced into an immune animal.
He introduced the spirilla of Asiatic cholera into the peritoneal
cavity of guinea pigs and noted that the bacteria were soon
rendered immobile, became swollen and granular and were finally
disintegrated. This phenomena has been designated PfeilTer's
leaction.
Passive acquired immunity consists essentially of the presence
in the tissues or body fluids of substances inimical to' micro-
parasitic activity, or substances capable of union with micro-
parasitic products, (toxins) thus rendering them inert. This
type of immunity is of short duration. It is usually produced
by the inoculation of susceptible animals with antitoxin. In-
jured animals inoculated with tetanus antitoxin at the time of
injury are thus immunized to tetanus for a brief period.
Acquired immunity, like natural immunity, is variable and
inconstant. The production of active acquired immunity entails
more risk than the production of passive acquired immunity.
The causative agents or their toxic products are vised in obtain-
ing an active immunity and thus disease may be produced and
the animal life sacrificed while the anti-toxin is used in the
production of a passive immunity, without danger of the pro-
duction of disease although transient disturbances may result
from hemolysins, contained in the blood in which there is anti-
toxin.
Theories of acquired immunity. — Many theories have been
advanced in explanation of acquired immunity. The chief of
which are as follows: —
82 VETERINARY PATHOLOGY.
1. The Exhaustion Theory. — This theory was championed by
Pasteur, who proposed it about 1880. It is based upon the
supposition that there are certain substances in the animal body
that are food for micro-parasites and that these substances are
not regenerated. Hence when they have been consumed the
micro-parasites cease to develop and the animal becomes im-
mune. This theory is not tenable because immunity can be
produced by bacterial products and by dead bacteria neither of
which consume substances from the tissues of an animal immun-
ized.
2. The Retention Theory. — In the study of bacteriology it
has been found that bacteria, like most other organisms, can
not develop in the presence of a large quantity of their own
excrements. This theory presupposes that bacterial products
remain in a body after it has been infected and that these
prodvicts prevent the future development of like bacteria. This
theory does not explain the production of an immunity with
toxines and is not supported by any scientists at the present
time. The theory was proposed by Chauveau.
3. The Phagocytosis Theory. — This theory was proposed
independently by Sternberg and Metchnikofif about 1881. The
theory was the outgrowth of the experimental study of the
action of leucocytes upon bacteria and yeast, in which it was
found that certain leucocytes are active in the destruction of
various bacteria, yeast and tissue debris. These investigators
designated those leucocytes active in the destruction of bacteria,
phagocytes. Phagocytosis is a state or condition characterized
by the development of phagocytes and the display of their special
function. The supporters of this theory hold that the cells,
which are active in the production of leucocytes transmit the
property of phagocytosis to their progeny and thus immunity
is perpetuated after it has been acquired. That phagocytes do
incorporate bacteria and other foreign substances is not denied
but it has not been demonstrated whether phaogocytosis is the
cause or the result of immunity.
This theory does not explain immunity from such diseases as
tick fever. The microzoon of tick fever inhabits and usually
destroys the red corpuscles. The leucocytes are probably not
afifected by them. In fact, the presence of the Piroplasma bigem-
inum in leucocytes has not been noted. More recently Wright
and Douglas have demonstrated that certain substances in the
blood serum are necessary to prepare bacteria for phagocytic
action. These substances have been designated opsonins.
Opsonins are chemic substances in blood serum that render
IMMUNITY. 8J
bacteria subject to the action of phagocytes. Opsonins resem-
ble the amboceptors of Ehrlich in action, but they are not iden-
tical with them. The action of opsonins is evidenced in pneu-
monia, pyogenic infections, tuberculosis and probably in other
diseased conditions. The opsonic index indicates the relative
power of resistance due to phagocytic action in an animal body.
4. Humoral Theory. — After the phagocytic theory had been
found insufficient, immunity was explained from a chemic view
point. The supporters of this theory, among whom Buchner
was active, demonstrated the bactericidal action of blood serum
and lymph obtained from immune animals. Their demonstra-
tions established the fact that immunity is due to a chemic
substance, possibly an enzyme. But the origin and specific ac-
tion of the chemicals in the production of immunity was not
determined. The bacteriolytic substance of the body fluid called
complement, was found to be destroyed by a temperature of
55°C.
5. EhrlicJi's Lateral Chain Theory. — Ehrlich maintains that
every living cell contains an active central body which produces
unknown chemical substances that combine with and extend
nutriment to the cell. These chemical substances, marginal
chemic groups or lateral chains as they are variously called, for
convenience of description are designated — receptors. These re-
ceptors are specific in their nature ; i. e.. there are certain groups
of receptors that combine with certain kinds of nutritive sub-
stances. Likewise there are present normally in the body cells
certain groups of receptors which combine with disease produc-
ing substances, e. g., toxins, which in turn destroy the body cells.
It is thought that receptors for certain diseases are absent in
certain species of animals and that because of this, there exists
a natural immunity ; e. g., the dog is immune to hog cholera be-
cause his body cells do not have the specific receptors for that
disease. If, on the other hand, the receptors that are normally
present be increased in amount, an acquired immunity develops.
Whenever there is an increase of the receptors in the body they
become freed from the cells and are found in solution in the body
fluids as antibodies. Experimentation has shown that antibodies
are produced by the tissues as a result of the injection of a great
variety of substances. These substances are known as antigens.
Therefore, an antigen is any substance that when introduced into
the body will stimulate the tissues to the production of antibodies.
An antibody may be defined as any substance present in the
body that has the property of antagonizing, neutralizing, precipi-
tating, agglutinating or dissolving the substance (antigen) which
84 VETERINARY PATHOLOGY.
has induced the production of such antibody. For example, the
toxin of the tetanus bacillus when injected in minute, non-lethal
doses, stimulates the production of antitoxin by the tissues ; the
toxin is the antigen, the antitoxin is the antibody. Likewise,
blood serum when injected into a different species of animal
would be an antigen and the precipitating substance produced
by the tissues as a result, is the antibody.
The following are some of the known antigens with their
antibodies. This list is by no means complete but serves our
purpose for the student of general pathology.
Antigens, Antibodies.
Toxins Antitoxins
Agglutinogens Agglutinins
Precipitogens Precipitins
Lysogens Lysins or Cytolysins.
For convenience of study and because of difference in consti-
tution Ehrlich has divided receptors into three separate varieties
known as receptors of the First, Second, and Third orders.
Ehrlich's receptors of the first order, — (antitoxins).
Toxins. — Toxins are antigens that when introduced into the
body will stimulate the cells to the production of antitoxins.
Excepting the fact that they give some of the protein reactions
the chemical nature of toxins is not understood, but they can be
demonstrated by certain biological tests.
A number of plants and animals are known to produce toxins
among which the following bacteria are important :
Bacillus diphtheriae, the cause of diphtheria.
Bacillus tetani. the cause of tetanus or lockjaw.
Bacillus botulinus, the cause of certain cases of botulism or
meat-poisoning.
Bacillus pyocyaneus, the cause of blue pus.
Ricin is a toxin found in the castor-oil bean, abrin comes
from the jequirity bean and robin from the bark of the locust.
Toxins have also been demonstrated in the venom of snakes,
scorpions and spiders.
A toxin is composed of two parts — a thermostabile (heat re-
sistant) part, known as the haptophore or combining group, and
a thermolabile (destroyed by heat at 56°C. for half an hour)
group, designated as the toxophore. By careful heating at a
lower temperature the toxophore only can be destroyed ; in such
a case the remaining haptophore group is known as a toxoid. A
toxoid has the property of stimulating the body cells to the pro-
duction of antitoxin but cannot exercise a toxic effect.
IMMUNITY, 85
Antitoxins. — If a large quantity of toxin, e. g. tetanus toxin,
be injected into the body of a horse it will combine through the
medium of its haptophorous group with all the available recep-
tors (these being limited in amount in normal susceptible ani-
mals) and cause death of the organism by destruction of its cells.
If on the other hand only a small quantity of toxin be introduced,
there will be injury instead of destruction of cells which together
with their neighbors will be stimulated to the production of new
receptors. Subsequent injections of increasing amounts of toxin
further stimulate the production of receptors, which become
freed from the cells as antitoxin in the tissues. These free re-
ceptors or antitoxin, as they are now known, combine with the
toxin which they neutralize and immunity is the result. Anti-
toxins as a rule are more stable than toxins but they can be de-
stroyed by heat at 60°C. if sufficiently prolonged. Unlike toxins
they are composed of only one group known as the haptophore
or combining group.
Ehrlich's receptors of the second order. (Agglutinins and
Precipitins.)
It has been found that the blood of an animal immunized to
certain diseases, e. g. glanders, when added to a culture of the
specific organism causes the bacteria to clump together. This
phenomenon is known as agglutination and the substance respon-
sible for the process is called agglutinin. Likewise it has been
discovered that protein substances used as antigens cause the
production in the body of substances, known as precipitins
which, when mixed with the protein in solution, will form a pre-
cipitate. Unlike antitoxins, agglutinins and precipitins are di-
vided into two portions — a combining or haptophore group, and
an active agglutinating or precipitating — zymophore group. The
zymophore group is unstable, and may be destroyed by heating
to a temperature of 60° to 75° C. When an agglutinin has thus
lost its zymophore group the remaining haptophore is known as
an agglutinoid. Likewise, a precipitoid is the combining group
of a precipitin after its zymophore has been destroyed.
Antigens which cause the production of agglutinins are
known as agglutinogens. Most foreign cells, as red blood cor-
puscles, other body cells, protozoa and bacteria act as agglutino-
gens \vhen injected into the body. The following pathogenic
bacteria cause agglutinin production: Bacillus typhosis. Bacil-
lus mallei. Bacillus pestis. Spirillum Cholera, Bacillus tubercu-
losis, and others. Advantage is taken of this fact and the ag-
glutination test is used as a method of diagnosis in diseases pro-
duced by some of these organisms.
86 VETERINARY PATHOLOGY.
Antigens which stimulate the production of precipitins are
known as precipitogens. Precipitogens are colloid substances
in solution and are represented by such materials as, blood
serum, milk, meat juices, egg white, etc.
Agglutinogens are composed of a haptophore group only.
Ehrlich's receptors of the third order. (Lysins or Cytoly-
sins.)
Lysins are antibodies which have the power of dissolving or
disintegrating their respective antigens. Lysins may be sub-
divided with reference to their antigens, into bacteriolysins,
hemolysins, etc. Antigens which cause the production of lysins
are known as lysogens and are represented by a variety of bac-
teria, foreign cells as red blood corpuscels, etc. Lysogens are
composed of a haptophore group only.
Receptors of the third order or lysins are composed of two
elements. A thermostabile substance which has two combining
or haptophore groups and hence known as an ambocepter, and a
thermolabile substance known as the complement or alexin.
The amboceptor is specific ; i. e., it will combine only with that
variety of lysogen which has caused its production. It is a com-
bining element only and its presence is necessary for the lytic
action of the complement. The two haptophore groups of the
ambocepter are of dilTerent action ; one is known as the cytophile
and combines only with the lysogen ; the other is called the com-
plementophile and unites with the complement. Complement
is found in varying quantities in all normal blood. It is non-
specific — i. e., it is capable of combining with any variety of
amboce])ter and through this combination cause lysis. The
complement has been found to consist of two groups — the hapto-
phore, which combines with the amboceptor, and the zymophore
or lytic group. Careful heating destroys the zymophore and the
remaining haptophore is known as complementoid.
Plate 1 represents graphically the production of the various
orders of receptors and a careful study of the figures will enable
the reader to grasp the subject more readily.
Toxic immunity is explained by Ehrlich as follows : Toxins
are composed of two essential chemic groups which are desig-
nated haptophores and toxophores. The haptophore of the
toxin has an aflfinity for the cell receptors. The union of the
toxin haptophore and the cell receptor forms a medium through
which the toxin toxophore passes to the central part of the cell
where it exerts its action.
The toxin haptophores are not injurious except as they enable
the destructive toxin toxophore to reach the central cell mass.
Graphic Representation of the Various Forms of Immunity According to Ehrlich's
Lateral Chain Theorj'.
iFig. 1. — A — The bacterial cell or other substance which produces antigen,
a, in the form of soluble toxin, al.
B — The body cell which produces side chains or receptors of the first order,
z, in the form of antitoxin, zl.
a2 — toxin uniting with receptor, z, injuring the body cell and stimulating it
to the production of more receptors.
zl — free antitoxin which at z3 is seen to be coinbining with and neutralizing
the toxin a3.
b — toxophore group and c haptophore groui3 of toxin molecule.
c3 — toxoid after careful heating of toxin and destruction of toxophore bl.
c3 — toxoid combining- with receptor; such a combination does not produce a
toxic effect.
Kg:. 2. — A — Bacterial cell, foreign serum or whatnot which contains the
antigen a, in the form of agglutinogen or precipitogen al.
B — Body cell which produces receptors z, in the form of agglutinin or pre-
cipitin zl.
a2 — agglutinogen or precipitogen combining with the receptor z, and stimu-
lating the body cell to the production of more receptors.
zl — freed receptor in the form of agglutinin or precipitin which is seen to
combine at z2 with the antigen. This union results in agglutination or precipita-
tion.
X — haptophore group and y zymophore group of the antibody; careful heating
will destroy the zymophore group and the remaining haptophore grotlp, xl, is
known as the agglutinoid or precipitoid.
x2 — agglutinoid or precipitoid combining with the antigen. Agglutination or
precipitation does not result from such union.
Fig:. 3. — A — Bacterial cell, red blood corpuscle or other body cell which con-
tains antigen; a, in the form of lysogen al.
B — Body cell which produces receptors z in the form of amboceptors zl and
complement y, which together are known as lysin.
a2 — lysogen combining with the ambocepter and stimulating the body cell
to the production of more ambocepters.
y — complement, which is found in all normal serum.
zl — freed amboceptor which is composed of two haptophore groups known as
the cytophile xl, and the complementophile x2.
C — shows a combination of lysogen, amboceptor and complement; this union
results in lysis of the cell A.
D — shows a combination of the lysogen and amboceptor only; the cell A is
not destroyed by such union.
The complement is composed of a zymophore group vl and a haptophore t2.
Careful heating destroys the zymophore and the remaining haptophore is knows
as a complementoid v4.
Immunity,
8^
Rg-.l.
mg-.3
VBawlnffVy, H.C.Lure.
88 VETERINARY PATHOLOGY.
Toxin toxophores in the absence of toxin haptophores are inac-
tive. The result of the union with, or action of, the toxin toxo-
phore upon a cell may produce immediate destruction of the
cell or it may stimulate the cell to produce more receptors. The
presence of toxin in the body fluids stimulates the body cells
to produce receptors in excess. The increased receptors may
remain in connection with the central body or they may become
detached and float in the body fluids. Free receptors in blood
serum is the essential active principle of antitoxin. Toxic im-
munity may be better understood by giving an example.
Examples. — Tetanus is an intoxication disease due to the pro-
duction of toxins by localized bacterial activity of the tetanus
bacillus. Immunity to tetanus is dependent upon the neutraliza-
tion of the tetanus toxin. The tetanus toxin is composed of hap-
tophores and toxophores. The body cells possess receptors capa-
ble of union with the tetanus toxin haptophores. The union of
cell receptors and tetanus toxin haptophores enables the tetanus
toxin toxophore to act upon the central mass of the body cell,
thus stimulating them to form more receptors. The excess recep-
tors become detached and float free in the body fluids and com-
bine with the tetanus toxin haptophore. thus preventing the lat-
ter from combining with the attached cell receptors. The te-
tanus toxophores are not capable of combining with the central
mass of the body cells except through the medium of tetanus
toxin haptophores and if the tetanus toxin haptophores are
locked up with the detached cell receptors, the tetanus toxo-
phores remain inactive and the animal is not inconvenienced by
their presence and is immune.
Toxic immunity is therefore dependent upon first, sufificient
free receptors to lock up the haptophores thus inhibiting the
action of the toxophore or second, upon the absence of hapto-
phores.
Bacterial inunnnity. — From the phenomena observed in Pfeif-
fer's reaction Ehrlich has proposed an hypothesis in explanation
of bacterial immunity. As previously stated, normal blood serum
contains bacteriolytic substances (see humoral theory). Comple-
ments are destroyed by a temperature of 55°C. The blood serum
of immune animals possess another substance, in addition to
complement, not destroyed, by heating to 55°C. These are called
amboceptors. According to Ehrlich, amboceptors, like toxins,
are composed of two different combining groups, also designated
haptophores and toxophores. The complemental substance of
normal serum is not capable of action upon bacteria. The ambo-
ceptor haptophore has an affinity for the complement of normal
IMMUNITY. 89
serum. The amboceptor toxophore has an affinity only for bac-
teria, but is not injurious to them. The amboceptor toxophore
combined with or acting upon bacteria produces a condition
favorable for the action of the combined amboceptor haptophore
and complement, i. e., this enables the complement to cause dis-
integration of bacteria. The amboceptor thus renders condi-
tions favorable, i. e., makes it possible for the bacteriolytic sub-
stance, the complement, to exert destructive action upon bacteria,
the amboceptor acting as middle man.
Opsonic immunity. — Opsonins are produced by some animal
tissue, probably muscle. Opsonic production is the result of
stimulation with endotoxins. Endotoxins are products or are an
integral part of bacteria. Opsonins increase the destroying
power of leucocytes or diminish the resistance of bacteria.
CHAPTER IV.
MALFORMATIONS.
DEFINITION.
ETIOLOGY.
I'ntniisic (heredity).
Extrinsic.
Pressure.
Amniotic Adhesion.
Excessive Motion.
Malnutrition.
CLASSES.
Single.
Result of Arrested Development.
Result of Excessive Development.
Result of Transposed Visceral Organs.
Result of Persistent Foetal Structures.
Result of Mixed Sexual Organs.
Double or Multiple.
Symmetrical Duplicities.
Complete.
Incomplete.
Asymmetrical Duplicities.
Multiple.
During the embryonic stage of intra-uterine life the special-
ized tissues and organs are formed. The foetal period is the
time during which the structures formed in the embryonic stage
grow and develop. At birth the young of a given species are of
a definite shape, contour and type ; the form or type which is
most common is accepted as normal ; and deviations from the
normal are designated malformations, anomalies or develop-
mental errors. Many new strains and breeds of stock have been
the result of developmental errors becoming a fixed peculiarity.
Thus the polled cattle, the Boston bull-dog, the Mexican (hair-
less) dog, and the five toed chicken had their origin.
Etiology. — Malformations may be brought about by pre-
existing influences in the maternal cells, (internal or intrinsic
causes), or from external influences (external or extrinsic
causes).
Internal or Intrinsic Causes. — Internal causes are inherited
peculiarities, i. e., heredity and atavismal influences. These are
probably not the usual causes of malformation in domestic ani-
mals for malformed individuals excepting cryptorchidism and
animals afYected with prognathism and some other of lesser de-
fects are rarely used for breeding purposes.
90
MALFORMATIONS. 91
External or Extrinsic Causes of malformations are pressure,
amniotic adhesions, excessive motion, insufficient or abnormal
nutrition, infectious diseases, etc. External causes exert their
influence during the embryonic or formative period and they
must act in a mild degree or death of the embryo and abortion
follows.
Typical malformations are approximately of the same form
and are usually produced by similar causes. Atypical mal-
formations are variable in form and may be produced by a variety
of causes.
A complete description of all malformations is beyond the
scope of general pathology. A general classification with a de-
scription and origin of the most striking malformations is all
that will be attempted in this chapter.
Malformations may be divided into two classes : 1st, Single
malformations, and 2nd, Double or multiple malformations.
Single malformations are those affecting a single individual.
Single malformations may be grouped into five classes as fol-
lows : Malformations resulting from; (a) arrested growth or
development; (b) excessive growth or development; (c) trans-
position of visceral organs; (d) persistent foetal structures; (e)
mixture of sexual organs.
ARRESTED DEVELOPMENT. — Malformatious caused bv arrested
development may involve an entire individual or any part of
an individual. Arrested development of the entire individual
results in the formation of an irregular, fleshy mass, called a
mole, in place of the normal foetus. Moles may be carried in
the uterus for the entire period of gestation. In some instances
a mole and a normal foetus may be delivered at the same time.
Moles have been observed in mares, more rarely in cows.
Malformations resulting from arrested development of a part
may be manifested by the entire absence of the part (aplasia),
by underdevelopment of the part, (hypoplasia), or by a lack
of union or fusion of tissue (schistosis and atresia). The fol-
lowing malformations are the result of local aplasia.
Accphalus. A name applied to a headless monstrosity.
Acephalus is probably the result of amniotic adhesions.
Atrichia. A defect in which there is no hair. This results
from some disturbance of cutaneous development.
Amyelns. A malformation in w^hich the spinal cord is absent.
Defects of the primitive streak or failure of production of the
neural canal interferes with or prohibits the formation of the
spinal cord and is the cause of amyelus.
92
VETERINARY PATHOLOGY.
Acardia. A heartless monstrosity.
Agastria. A malformation in which the affected individual
has no stomach. This may be due to lack of sacculation of the
embryonic gut.
Acaiidia. A malformed individual in which the defect con-
sists in the absence of the tail. An acaudia fox terrier bitch
was recently observed, her mother whelped one or two tailless
puppies at each whelping". This bitch recently whelped an
acaudiac puppy.
Aprosopiis. An individual having no face.
Dithoracisamelus.
Fig-. 5]. — This picture taken wlien calf was five months old. The animal was able
to get about by walking in an upright position and could gain its feet
unassisted. Case observed by Dr. Smith V. Ewers.
Aguatlius. A term used to designate an individual in Avhi:h
the inferior maxilla is absent. This is common in lambs.
Amclus. The name of a limbless or legless individual. Ame-
lus is the result of arrested development of leg buds and is usual-
ly caused by unequal intrauterine pressure or amniotic adhesions.
M onopygusamclus. A monstrosity in which one posterior leg
is wanting. This is due to arrested development of leg buds,
probably due to amniotic adhesions.
Dipygusamclus. The name of a malformed animal in which
both posterior legs are absent. Result of arrested development
of leg buds.
MALFORMATIONS.
93
MonotJioracisaiiielits and dithoracisamelus are monstrosities
in which one and both front legs arc al)sent respectively.
Apits. A name applied to a malformation in which the feet
are absent. This may be the result of intrauterine amputation
or amniotic adhesions.
Monopygnsapus is an individual in which one hind foot is
wanting" and a dipygusapus, an individual in which both hind
feet are absent.
M onothoracisapus, and dithoracisapus, are names implying the
absence of one or both front feet.
The following malformations are the result of under develop-
ment or undergrowth. (Hypoplasia).
Micro cephalns, a term used to designate an individual hav-
ing a diminished sized head, also used to designate the small
head itself. This is probably the result of diminished nutrition
to the head and anterior part of the body during embryonic and
foetal development.
Micro-cardia. A name applied to an individual having a small
heart. This may be due to excessive pressure.
Micro ophthalmia. A term used to indicate a malformation in
which the eye or eyes are smaller in size than the normal. Tl.is
is probably the result of insufificient nutrition.
Micrognathy. The name of an individual having a diminutive
inferior maxilla. These are caused by undue pressure or insufficient
nutrition.
Micromehis. A malformation so named because of the dimin-
ished size of all legs. This is caused either by diminished nutrition
or undue pressure.
The following are illustrations of arrested development mani-
fested by absence of imperfect tissue union, thus producing
fissures (schistoses), or resulting in fusion of parts that are
normally separate (synactoses). Fissures of the body cavities
are due to increased accumulation of fluids in internal organs,
increased size of internal organs, prolapse of viscera before
body walls have united, the presence of amniotic folds between
cleft edges or lack of sufficient tissues to close the margins.
Cranioschisis. The name of a condition produced by fail-
ure of development and union of the cranial bones and resulting
in a cleft. The meninges and in some instances the brain tissue
may be exposed or there may be protusion of the meninges and
also of the nerve tissue, thus producing meningocele or men-
ingo-encephalocele.
94
VETERINARY P.XTHOLOGV.
Craniorrhachischisis. A malformed individual so called because
of a fissure of the spine and cranium accompanied by exposure or
protrusion of the spinal cord or brain.
RacJiiscJiisis. A condition in which there is a cleft of the
spinal column. This malformation is usually the result of some
defect in the margins of the neural groove. If the fissure ex-
tends the entire length of the spinal column the resulting con-
dition is called holoschisis. If the fissure does not extend the
entire length of the spinal column, the condition is termed
meroschisis (Gr. ]\Ieros=part, and schisis:=splitting.) The
spinal meninges may protrude through the spinal column fissure
Figr. 52. — Cranioschisis — Calf.
producing splna-bifida. A hernia of the spinal meninx that con-
tains cerebrospinal fluid is termed spinal meningocele, and if the
cord and meninges protrude, it is called a myelomeningocele.
Cheiloschisis, is the condition resulting from arrested develop-
ment of the soft tissues covering the maxilla. This is the condition
popularly termed hair lip. It is an inconvenience because it inter-
feres with sucking the teat, the source of nutrient of the new born
mammal. The defect may also involve the maxilla producing
cheiliognathoschisis.
Palatoschisis. A defect in which the palatine processes have
imperfectly developed, thus leaving a fissure through which
there is free communication between the nasal and buccal
MALFORMATIONS.
95
cavities. This condition is commonly spoken of as cleft palate.
Tlioracoschisis. A condition resulting from failure of union
of the thoracic walls. The thoracic viscera, the lung, heart and
large vessels may protrude through the fissure thus producing
ectopiacordis or ectopiacordispulmonaris.
Fig'. 53. — C'heiloseliiwis.
AbdouiinoscJiisis, is the condition caused by failure of union of
the abdominal parieties. The condition is frecjuently accom-
panied by protusion of the abdominal viscera through the fissure.
The abdominal fissure may involve only a portion of the cavity
or it may be complete. Ectopia gastrium is the condition result-
ing from protusion of the stomach through an abdominal fis-
sure ; ectopia vesicae, protrusion of bladder, etc.
Hypospadias is a condition resulting from arrested develop-
ment of the penis and scrotum. Tlie principle defect in hypos-
padias consists of a variable cleft in the posterior and inferior
96
VETERINARY PATHOLOGY.
>'?'
?Q6«
'"'»- w: '■-'.>5....
Fig. 54. — I'alatdscliisis.
surface of the penis and scrotum. This cleft which represents the
urethra is Hned with mucous meml^rane and into it urine i^'
discharged. This is the most common malformation of tlic
male genital organs. Raymond Pearl reported his observation
Fig. 55. — Abdominoschisis.
MALFORMATIONS. 97
on a case of hypospadias in a lamb in the American Veterinary
Review.
Synoplithahiiia, or cyclopia (Gr. Kuklops=mythical single eye
monster), is a condition resulting from the fusion of the optical
vesicles. Arrested development of the anteriar cerebral vesicles
allows the optical vesicles to contact and in some instances there is
one large double eye centrally located or there may be two eyes
occurring in a centrally located orbit. Cyclopia is usually associated
with defects of the nose.
Synactosis is a general term denoting a condition caused by
the fusion of parts or organs that are normally separate.
Synmelus. A malformation caused by the fusion of two legs
into one irregular member.
Synophthalmia or Cy<'lopia.
Syiidactyliis. An individual having the digits fused or grown
together. An illustration of syndactylism is the soliped hog.
The soliped hog usually has two separate digits of three pha-
langes each and the ossa pedes are encased in a single hoof.
Synmehisdipus. A malformation having fused legs and two feet.
Synmelusmonopiis. An individual having fused legs and only
one foot.
Synruclusapus. A monster having fused legs and no feet.
Synorcliisiu. A malformed animal in which the testicles are
fused.
Arrested development may be evidenced by the nonappear-
ance of the lumen in any of the natural hollow organs, (atresia).
The mouth is formed by an ingrowth of the ectoderm and the
buccal cavity extends inward until it meets the anterior elonga-
tion of the embryonic gut. Later the partition separating the
buccal cavity and the cavity of the embryonic gut is absorbed
and thus the cavities become continuous. Failure of the exten-
98
VETERINARY PATHOLOGY.
sion of the mouth cavity and its fusion with the embryonic gut
constitutes the condition atresia oris.
Atresia iridis. A defect in the eye (hie to the absence of an
( pening (pupil).
Atresia ocuii, a malformation in which there is no opening
between the eyelids.
Atresia anus is a condition in which there is an imperforate
;inus, that is, there has been failure of union and fusion of the
anal ingrowth and the rectal outgrowth. Atresia anus is of
'alher frequent occurrence and usually the defect is easily re-
lieved.
Fig. 57. — A condition of i^iilipedia in a liog.
Atresia urethra. Imperforation of the urethra.
MALFORMATIONS RESULTING FROM EXCESSIVE DEVELOPMENT OR
OVERGROWTLI. — Excessive development is usually evidenced as a
multiplicity of digits or phalanges though there may be multi-
plicity of any structure.
Polydactylism. — The name applied to a malformed individual
in wdiich there is an excessive number of digits. Indi\-iduals
having supernumerary digits are frequently observed. Tlic
condition is probably more frequently observed in hogs than
in other animals. Polydactylism, however, occurs occasionally
in the ox and horse.
PolynielustJioracicus. — This is a malformation in which the
afifected animal has one or more extra fron.t legs. An interest-
ing case was observed in a cow in which there was an irregular
MALFOKMATIONS.
99
bone attached to the right scapula, and extending across the
median Hne. This bone articulated with an irregular supernum-
erary scapula and also with the spine of the left scapula. This
irregular formed scapula articulated with another bone which
was similar to a humerus on the distal end of which there was
a rudimentary ulnar. The condition of supernumerary posterior
legs is termed polymeluspygus.
Dicaudis. — An individual having two tails. This type of
malformation is not very common. It is probably the result of
a division or cleavage of the caudal segments during embryonic
formation.
Fig. 5S. — Pol.vdaetylism in a hog.
Multiplicity of internal organs is occasionally observed. Thus
several cases of partially double spleens have been reported.
An interesting case of malformation was observed in a hog, the
defect consisting of a double oenis. This individual may have
been called a dipenis.
Malformations from excessive growth may be applied to the
entire animal when it is excessively large (giants). Malforma-
tions resulting from the overgrowth of a part are frequent, thus
one foot, one leg, the head or any other part may be overgrowm.
Darwin, (in Plants and Animals under Domestication), men-
tions a cat that he observed which had incisor teeth one and
one half inches in lene:th.
100
VETERINARY PATHOLOGY.
Fig. 59. — riosnathism, common name "undershot."
TRANSPOSITION OF VISCERAL ORGANS, (situs visccrum invcrsus).
Very rarely animals are observed in which the visceral organs
are re-arranged, i. e., those organs that normally occur on the
left side of the body are found on the right side. A sheep in
prime condition was observed which was normal in appearance
MALFORMATIONS.
101
except its head was turned slightly to the left and the atlas was
ankylosed to the occipital, thus giving it but little vertical
motion. The right shoulder was anterior to the left. The vis-
cera were entirely reversed ; the heart was hanging toward the
right ; the four compartments of the stomach were transposed,
the rumen being on the right side, and the spleen being in con-
tact with the right side of the diaphragm ; the liver was on the
left side and the right kidney was posterior to the left which
was swinging free as the right usually does.
Figr. so. — Seliistosis inelus anticus or dinieliis anticiis — Male.
(Drawing made from a photograph.)
Transposition of visceral organs probably results from an
irregularity to the allantoic veins and their continuation. In
normal development the right vein atrophies and the left vein
becomes larger in early embryonic life and if for any reason
the left vein atrophies and the right vein becomes longer then
the visceral organs tend to develop in the reverse position.
PERSISTENT FOETAL STRUCTURES. — All the malformations are
grouped into this class that retain embryonic or foetal structures
abnormal to extra-uterine forms of life,
102 VETERINARY PATHOLOGY.
Foramen ovale. — An occasional case is observed in which there
is a persistent foramen ovale. The right and left auricles com-
municate through the foramen ovale during the foetal stage of
life. This communication normally ceases at the time of birth.
The foramen may not entirely close and thus the blood in the
left ventricle will be mixed. Such a case was observed by A.
Leslie, the patient being a pure bred 15 months old Guernsey
heifer. The foramen ovale had persisted, it was oval and one-
half inch in diameter. This case also presented an interventri-
cular communication.
Cryptorchids — (Gr. Kruptein=to hide and orchis-testicle) are
probably the most frequent malformations resulting from the
persistence of a foetal structure. The testicles of domestic ani-
mals are formed within the abdominal cavity during embryonic
life and later migrate, except in fowds. birds, etc., to their per-
manent position in the scrotum. Cryptorchids are animals in
which the testicle was properly formed, but did not descend
to the scrotum. Dr. DeWolf carefully inspected 4671 male
hogs and found 38 single and 7 double cryptorchids.
Cloacal persistence. — During embryonic life the rectum and uro-
genital tract terminate in one common cavity known as the
cloaca. The cloaca persists throughout life in the avidae, but
not in mammalia. H. Brassy Edwards, M. R. C. V. S., reported
a case in the veterinary Journal of an imperforate anus in a
brindle bull bitch pup 10 days old. There was no trace of an
anus and the prominence usually felt in the perineal region of
imperforate anus was also absent. On operation the rectum
and uterus were found to be fused, thus producing a cloaca. Dr.
P. Phillipson of Holbrook, Nebr., reported a colt in which there
was a cloacal formation. In this case the floating colon fused
with the uterus and the vagina was a common opening of the
digestive tract and the genito-urinary tract.
Cervical ectopia cordis. — This is the name of a malformation in
which the heart is located in the cervical region. The heart
is normally formed in the embryo in the cervical region and if
the anterior thoracic wall closes prematurely, the heart remains
in that region.
Hymen persistence. — The extent of the hymen is quite variable.
Ordinarily the hymen consists of a fold in the vaginal mucous
membrane from which a delicate web like structure may com-
pletely divide the vagina. In some instances the hymen is com-
posed of dense fibrous tissue which interferes with or prevents
successful copulation
MALFORMATIONS. 103
MIXTURE OF SEXUAL ORGANS, HERMAPHRODITISM. — The SCXUal
glands, ovaries and testicles, and the external genitals, of both
sexes, are derived from four similar embryonic structures. The
influence or factors determining sex are not known. During
embryonic development the sexual determination is not distinct,
the individual possessing more or less complete sexual organs
typical of both the male and the female. Animals in which
there is a combination of sexual organs are termed hermaphro-
dites. According to the development of sexual organs, herma-
phrodites are designated as true and pseudo or false herma-
phrodites.
A true hermaphrodite possesses secreting sexual glands of both
sexes, i. e., they have secreting ovarian and testicular tissues.
The external genitals of the true hermaphrodite may be bisex-
ual or unisexual. True hermaphrodites are rare, and fertility
of such animals is doubtful. True hermaphroditism may be
lateral, bilateral or unilateral.
Lateral hermaphroditism is the condition in which there is an
ovary on one side and a testicle on the other. The following
example illustrates this type. The animal was a two year old
bovine and had an ovary suspended by the left broad ligament
and a testicle suspended by the right broad ligament. The two
glands had their normal appearance, typical of ovarian and tes-
ticular tissues. This type of hermaphroditism is rare.
Bilateral hermaphroditism is typified by the presence on both
sides of an ovary and a testicle, or a single organ on each side
containing ovarian and testicular tissues. This type of her-
maphroditism also is rare.
Unilateral hermaphroditism is characterized by the presence of
a single organ, as an ovary or testicle on one side and an ovary
and testicle on the other side or an organ containing ovarian and
testicular tissue on one side. This type is not common.
Pseudo, or false hermaphrodites, are individuals having one
distinct type of sexual glandular tissue and in which the exter-
nal genitals partake of the nature of both sexes. This type of
malformation is more common in the male and is usually the
result of persistence of Miillers canal and the further develop-
ment of the uterus and Fallopian tubes. Tn pseudohermaphro-
ditism the testicles are usually retained in the abdominal cav-
ity. There are usually Fallopian tubes, vagina and uterus, the
completeness of which is variable. The appearance of the testi-
cle is variable according to the development of the female ex-
ternal genitals. Pseudohermaphroditism is much less frequent
in the female than in the male.
104
VETERINARY PATHOLOGY.
A rather well marked case of a pseudohermaphroditic horse
was obtained and carefully observed for some time after which
it was destroyed and the type and relation of the sexual organs
Fig. 61. — I'seudo-Iierinaphroilite.
were determined by dissection. In this animal the head and
neck while not decisive of either sex in general rather favored
the male in conformation. There was quite a well marked vulva
and the much elongated clitoris projected about four inches
postero-inferiorly and closely resembled a penis. The uterus
was quite rudimentary and the reproductive glands were located
near the normal location of the internal inguinal ring and had
MALFORMATIONS. 105
very little resemblance to either testicle or ovary. Microscopic
examination did not solve the difficulty for the glands were a
conglomerate of small cysts. The mammary gland was fairly
well developed.
Double or Multiple Malformations. — Under this caption those
malformations will be considered that involve two or more in-
dividuals developing simultaneously. Marchand's classification
of duplicate monsters is adhered to in the following discussion.
The entire subject of duplicate monsters may be subdivided into
1st, symmetrical duplicity, 2nd, asymmetrical duplicity, and 3rd,
multiplicity.
SYMMETRICAL DUPLICITY. — The individuals, in symmetrical
duplicity are, in the beginning, similar and symmetrical. Each
of the symmetrical duplicates is derived from separate, similar,
equal anlagen of a single fertilized ovum or bisection of a single
anlagen. This class of malformations may be divided into two
groups : — viz., complete and incomplete duplicities.
Complete duplicity. — Complete duplicates are in the beginning
alike and complete and the individuals may remain separate
thus forming twins, (free duplicities,) or they may be united,
thus forming double monsters.
Twins, (free duplicates), develop in a single chorin though
each individual usually has a separate amnion and allantois.
Monochorionic duplicates may develop equally or unequally,
depending upon the division of nourishment. The above dis-
cussion primarily applies to uniparous animals. However, by
varying the number it is equally applicable to multipares. Twins
may also result from simultaneous fertilization of two ova.
Double monsters are mono-chorionic duplicities in which the
bodies are united. The two bodies may be equal or unequal in
size, depending upon the distribution of nourishment. Double
monsters are the result of partial fission of a fertilized ovum,
partial fusion of two separate anlagen of a single ovum, or par-
tial fusion of two fertilized ova. The attachment of the two
bodies of the double monsters may be posterior, middle or anter-
ior.
Posterior union may be dorsal or ventral. In the former the
union occurs at the pelvis, and the dorsal surfaces of the bodies
are usually in apposition ; such a monster is called a pygopagus.
Pygopagi have two umbilical cords which fuse to form a single
cord ; coccyx and sacrum are single, rectum and anus usually
single ; spinal cord double anteriorly, fused posteriorly forming
a single filum terminale ; urogenital system usually double. Ven-
tral posterior union may be confined to the pelvic region.
106 VETERINARY PATHOLOGY.
(ischiopagus), or it may extend anteriorly to and including the
thoracic cavity, (thoracisischiopagus) The two bodies in ven-
tral posterior union are so united that their venter surfaces are
in opposition. Ischiopagi, usually have a single umbilicus and
cord ; pelvic organs may be single or multiple ; there is usually
no anus. If one of the bodies is small or rudimentary, it is desig-
nated a parasite, (ischiopagusparasiticus). Thoracoischiopagi,
may have single or double thoracic viscera; the abdominal vis-
cera are usually double.
Middle union in double monsters occurs on the venter sur-
face from the umbilicus and extends anteriorly. There is usu-
ally a single umbilicus ; the abdom.inal viscera is usually double ;
thoracic viscera single or double, depending upon the area of
union ; middle union may occur at the xiphoid cartilage, (xipho-
pagus), involve the entire sternum, (sternopagus), or the entire
thoracic venter surface, (thoracopagus), x'phopagi may survive,
the ".Siamese Twins,'' were of this type. Thoracopagi are fre-
quently unecjual in size, the smaller one being designated as a
parasite.
Anterior union may be dorsal or ventral or the union may be
on the anterior surface of the head. Dorsal, anterior union rare-
ly occurs, the attachment being on the frontal region. These
malformations are designated Craniopagi. Ventral anterior
MALFOR^FATIONS.
107
union occurs occasionally. The union in this type is along the
venter cervical region and extends onto the venter thoracic re-
gion. The sternum and oesophagus are single ; larynx, trachea
and stomach may be single or double ; intestine double ; there
may be two faces or the faces may be fused. Fused-face mon-
sters resulting from union of the venter anterior cervical or
cephalic regions are called syncephali.
-,.,«'trW^:?^-_?^?7^^ wwr^p»,v
Incomplete duplicity is the name applied to those malformations
in which the greater part of the body is single, duplication oc-
curring in only a part. The duplicity may involve any part.
These malformations are not easily differentiated from malfor-
mations resulting from multiplicity of parts as polydactylism.
ASYMiMETRicAL DUPLICITY are those malformations resultmg
from the development of two separate, dissimilar, unecpial
anlagen of a single ovum, the development of a fertilized polar
body or the development of an isolated group of segmentation
cells. In asymmetrical duplicity one bodv is rudimentary or
under-developed, (the parasite), and the other body develops
normally or nearly so, (the autosite). The parasite always re-
mains attached to the autosite or is included bv it. Parasitic
108 VETERINARY PATHOLOGY.
duplicity may occur in any region. Thus the parasite may pro^
ject from the orbit, mouth, shoulder or it may be included in the
thoracic or abdominal cavities.
MULTIPLICITY is the name applied to designate the development
of more than two separate individuals in a single chorion. Mul-
tiplicity is of rare occurrence. One single case has been authen-
tically reported in the human in the form of a tricephalus.
CHAPTER V.
CIRCULATORY DISTURBANCES.
Normal blood circulation is dependent upon normal rate,
rhythm and force of tlie heart, normal caliber of the blood ves-
sels and the normal resistance offered by them and the quantity
and the quality of the blood.
Variation of Heart Action.— A marked variation in the heart
activity results in imperfect circulation. Depressed or diminislied
heart action is more common than increased heart action. Di-
minished functional activity is most frequently caused by in-
flammation of the endocardium, myocardium, epicardium or per-
icardium. Valvular stenosis and valvular insufficiency are the
result of endocarditis. Myocarditis diminishes the activity of
the heart and if the inflammation is long continued the muscle
cells are destroyed and then replaced by fibrous tissue thus per-
manently impairing the force of the heart. Inflammation of the
epicardium and pericardium may be accompanied by volumin-
ous exudation which distends the pericardial sac and produces
sufficient pressure to hinder diastole, or the exudate may be-
come coagulated and later organized attaching the sac to the
surface of the heart and thus hindering cardiac systole. Cardiac
activity may be diminished by the collection of fluid in the
pleural cavity, malformed thoracic cavity, tumors, occlusion of
coronary arteries, fatigue and thrombic formation upon the car-
diac valves. Diminished cardiac activity results in a diminished
quantity of blood being sent out from the heart and an accumu-
lation of waste products in the tissues.
Increased functional activity of the heart is usually only tem-
porary excepting in those animals affected with cardiac com-
pensatory hypertrophy. The most common cause of increased
cardiac activity is reflex stimulation. Increased activity due
to reflex stimulation may terminate in exhaustion and syncope
in a relatively short time. Increased functional activity, due
to a cardiac compensatory hypertrophy resulting from increased
resistance as in emphysema, chronic nephritis, etc., may result
in permanent over action of the heart.
Anatomical changes in the cardiac-structure, as hypertrophy,
fatty degeneration, fragmentation, fibrous formation, or necrosis
109
110 VETERINARY PATHOLOGY.
may be evident when the functional activity of the heart is
varied.
Vascular Variations. — The amount of blood passing into or
out of a given organ is determined by the caliber of the blood
vessels, provided the heart action and general blood pressure
remain normal. Variations in the caliber of normal blood ves-
sels depend primarily upon the response of the vessel muscu-
lature to vaso-motor stimulation. Blood pressure is dependent
upon the elasticity of the arteries and the force of the heart. In
general, pathologic vascular variations are the result of, first,
disturbed arterial elasticity ; second, variation of the normal cal-
iber of the vessels and ; third, abnormal permeability of the vas-
cular walls.
Arteriosclerosis is a condition in Avhich the elasticity of the
vessel walls is lessened or destroyed. In the production of
arteriosclerosis there is vascular dilatation succeeded by supen-
dothelial fibrous formation which continues until the lumen of
the dilated vessel is reduced to its normal size. The hyper-
plastic fibrous tissue may later become calcified. Sclerotic ar-
teries are thick, stifif and nonelastic. Sclerosis is most common
in arteries although it occurs in veins.
The vascular caliber may be diminished by muscular con-
traction or by hypertrophied vessel walls. In animals afifected
with chronic nephritis there is contraction of the systemic ar-
teries resulting in compensatory cardiac hypertrophy. Arterial
constriction is also common in the peripheral vessels of animals
afifected with carbon dioxide poisoning. Local diminution of
vascular caliber may be produced by parietal thrombi. The
vascular caliber may be increased by paralysis of the vaso-motor
nerves, a condition which is sometimes observed in animals that
have received inj-uries in the cervical region.
Increased permeability of vessel walls usually results from
insufficient nutriment to the vascular structures and occurs most
frequently in small vessels, i. e., capillaries and venules. In-
creased permeability usually accompanies venous hyperemia,
although it may exist independent of variations in the quantity
of blood. Thus oedema is common in hydremic individuals.
Variations in Quantity and Quality of Blood. — The quantity
of blood in a part is determined by the caliber of the supplying
vessel and by the blood pressure. Acute general anemia re-
sults in a diminished blood pressure which, if not corrected in
a short time, terminates fatally. Chronic general anemia is ac-
companied by a slightly diminished blood pressure and a re-
tarded blood current.
CIRCULATORY DISTURBANCES. Ill
The most important variations in the quality of blood that
concerns the student of general pathology are due to the varia-
tions of the percentage of water contained. Hydremia is ac-
companied by disturbances of the renal function and by oedema.
Anhydremia is productive of a slow^ weak pulse and the sec-
ondary changes resulting therefrom. Excess of carbon dioxide
or urea in the blood stimulates the vaso-constrictor nerves thus
causing arterial contraction.
HEMORRHAGE.
DEFINITION.
ETIOLOGY.
Predisposition (liciiiopliiUa).
Ruptured vessel.
Rlie.ris or diahrosis.
Increased permeability.
Diapedesis.
VARIETIES.
Location.
Tissue.
Petechia (flea bite) pin point.
Ecchymosis (over-Hozv) from pin point to sice of dime.
Suggillation (sivelling) bruise.
Effusion.
Hematoma (blood tumor).
Infarction.
Surface — Skin, mucous, membrane, serous membrane.
Epista.vis.
Hemaiemesis.
Hemoptysis.
Hematuria.
Hematidrosis.
Hematonietra.
Hematocele.
Metrorrhagia.
Hemathorax.
Hemocoelia, etc.
Vessels.
Cardium.
Arteries.
Veins.
Capillaries.
APPEARANCE.
Macroscopic.
Microscopic.
Tissue hemorrhage.
Clot.
EFFECTS.
Rate of outflow.
Location.
Secondary change of extravasate.
Hemorrhage is the escape of blood from a vessel, (capillary,
vein, artery or heart.)
Etiology. — Some animals are predisposed to hemorrhage
(hemophilia). Hemorrhagic diathesis or hemophiha is an ^in-
herited condition in which there is little or no tendency for co-
112 VETERINARY PATHOLOGY.
aguiation of blood. The cause of this condition is the absence
of some blood constituent essential to coagulation.
This type of hemorrhage sometimes occurs in colts, usually
appearing at the time or within a few days after foaling. In
those cases that occur at the time of foaling the hemorrhage is
usually from the umbilical vessels although there may be some
cutaneous capillary hemorrhage, (hematidrosis). In some cases
there may be no evidence of hemorrhage at the time of foaling,
but wuthin from 24 hours to three or four days, oozing of blood
on to the skin surface may be noticed, the extent of which varies
and may or may not be fatal. Gough, of Benton, Ky., reported a
case of hemophilia in a mule colt in the American Journal of
Veterinary Medicine, July, 1911.
A case of hemophilia in a medium sized 17 months old Ger-
man sheep dog was reported by L. & E. Lepmay. This dog
first showed tendency to hemophilia at 15 months of age, by per-
sisted hemorrhage from the mucous membrane of the gums. A
little later a subcutaneous hemorrhagic extravasate was observed
in the thoraco-axillary region and the dog died of acute intesti-
nal hemorrhage when about 17 months of age.
Hemorrhage may be caused by degeneration or ulceration of the
vessel wall — thus hemorrhage by diahrosis is produced ; it may be
caused by rupture of the vessel wall due to increased intravascular
or diminished extravascular pressure and trauma of the vessel wall
— 'thus hemorrhage by rliexjs is produced; or it may be increased
permeability of the vessel walls due to increased intravascular press-
ure or disease of the vessel wall — thus hemorrhage by diapcdcsis is
produced.
Diabrotic hemorrhage is observed in tumors as a result of the
destruction of the vessel wall by the neoplasm ; gastric ulcers
particularly in dogs ; glanders, especially the acute type in which
the mucous membrane of the respiratory tract becomes necrotic ;
in septic wounds, etc.
Hemorrhage by rhcxis is the type most common, it is the type
observed in traumatisms, and is sometimes observed in apoplexy
resulting from vascular occlusion (apoplectiform anthrax), this
type has also been observed in some cases of canine vascular
strongylosis due to infestation of the strongvdus vasorum.
Diapedetic hemorrhage is rather uncommon, being observed
occasionally in such disease as purpura hemorrhagica and in
some septicaemias.
The escaped blood, i. e., the extravasate, may flow upon the
surface of the skin, serous or mucous membranes, or into the
tissues.
CIRCULATORY DISTURBANCES.
113
TISSUE HEMORRHAGES may vary greatly in amount and are
designated by the following terms, petechia, ecchymosis, sug-
gilation, effusion, infarction and hematoma.
Petechiae are small sharply defined hemorrhagic points and are
probably caused by bacterial products in the blood.
Ecchymoscs are hemorrhagic spots larger than petechiae and
less sharply defined caused by rupture of capillaries or precapil-
laries. Ecchmymotic hemorrhages are of common occurrence in
the nasal and ocular mucous membrane of horses affected with
purpura hemorrhagia and equine infectious anemia.
FipT. fi4. — Petechial hemorrhage. Kidney hog cholera lesion.
a. Hemorrhagic area. c. Glomerulus engorged with blood.
b. Normal kidney tubule.
Siiggillations and effusions are large indefinable hemorrhagic
areas, caused by bruising which ruptures the small vessels.
Hemorrhagic infarction is a hemorrhage into an anemic area.
This is not a hemorrhage as ordinarily understood, for the blood
is within the vessels and escapes into the anemic area because of
the diminished pressure.
A hcinatonia is a circumscribed collection of extravasated blood
in the tissues and is usually the result of hemorrhage from an
artery.
114
VETERINARY PATHOLOGY.
SURFACE HEMORRHAGE is designated according to its origin, thus :
Epista.vis is hemorrhage from the nasal mucous membrane and
is quite common in acute nasal glanders.
Hematemesis is hemorrhage from the stomach and is observed
in anmials poisoned with arsenic and those afflicted with gastric
ulcer or gastric carcinoma. The hemorrhagic extravasate is act-
ed upon by the acid gastric content and converted into coffee
bean like masses. These masses, which are dark in color, char-
acterize gastric hemorrhage.
Fig. Go. — liematoiria, caused li>' luiiture of spur vein.
Hemoptysis is hemorrhage from the lungs. It may be the result
of excessive exertion, abscess formation, tuberculosis,.
Pulmonary hemorrhage is characterized clinically by the dis-
charge from the nose or mouth of a frothy sanguinous extra-
vasate.
Hematuria is hemorrhage into the urinary tract or bloody urine.
The blood may escape from the kidne3^ and if so there will be
tubular casts discernible on microscopic examination of the
urine ; it may come from the ureter or bladder, and would then
CIRCULATORY DISTURBANCES. 115
be thoroughly mixed with the urine; or it may have its origin
from the urethra and would not be mixed with the urine but
w'ould usually precede it.
Heinatidrosis is hemorrhage from the surface of the skin and is
the so-called sweating of the blood and is caused by increased
permeability of cutaneous capillaries.
Entcrorrliagia is hemorrhage from the intestinal mucosa and
may be differentiated from hematemesis by the appearance of
the extravasate in the feces. The extravasate in hematemesis
has the appearance of coffee bean grains in the feces while the
enterorrhagia extravasate retains the hemoglobin color and is
not broken up into granules. (The coffee bean appearance of
blood extravasated into the stomach is due to the action of the
hydrochloric acid of the gastric juice.) Enterorrhagia is caused
by infection as in anthrax and by caustics.
Heuiatomctra is hemorrhage from the uterine mucosa, the extra-
vasate being almost entirely retained in the uterus. This is
usually caused by improper removal of retained placenta.
Metorrhagia is hemorrhage from the uterine mucosa and the
extravasate passes out of the uterus. Menstruation in the hu-
man is an illustration of metrorrhagia.
Hemococlia is hemorrhage into the peritoneal cavity and is
caused by rupture of the peritoneaum or some abdominal organ.
Hemothorax is hemorrhage in the pleural cavity, and is caused
by ruptured pleura as a result of fracture of a rib, etc.
Hematocele is hemorrhage into the tunica vaginalis cavity. This
may be the result of laceration or rupture of the tunica vaginalis
testis.
Effects. — The effects of a hemorrhage depend upon the quan-
tity of blood lost and the location and secondary changes of the
extravasate. In health the vascular system practically maintains
a constant blood pressure by accomodating the capacity of the
blood channels to the volume of the blood.
The quantity of blood that an animal may loose without be-
ing seriously affected varies according to its age and health.
The blood tissue of the horse has been estimated at from
1-16 to 1-12 of the total body w^eight. One-tenth of the esti-
mated total amount of blood in the body has been withdrawn
from horses used in the production of anti-toxin once every two
weeks for from six to eight months without injurious results.
From one-third to one-half of the volume of the blood in the
body may be withdrawn at once and the animal recover. Hem-
orrhage from a small vessel has little effect upon the w^elfare.of
the body for the quantity lost is immediately restored from the
116 VETERINARY PATHOLOGY.
lymph and other fluids of the body. Thus there may be a con-
stant hemorrhage from the digital artery of the horse for twen-
ty-four hours without injurious consequences.
A sudden large loss of blood diminishes blood pressure and
this results in imperfect action of the heart valves. The blood
is churned back and forth, becomes mixed with air and this
frothy mass accumulates beneath the valves and prevents their
closure.
Hemorrhage is serious when it occurs in the more delicate
or the more highly organized tissues. Thus the amount of ex-
travasate into the cerebrum may be very small and yet produce
sufficient disturbance to destroy life, while the same amount of
extravasate into the muscles of the thigh, forearm, etc., would
probably not be observed.
The extravasation of blood into one of the body cavities, as
the pleural or peritoneal cavity, will be partially absorbed as
entire blood before it becomes coagulated, the remaining un-
absorbed portion will be in part disintegrated and carried out
by the leucocytes and the remaining portion will finally become
organized and remain as a mass of fibrous tissue. If the loss of
blood is not sufificiently large to materially diminish the blood
pressure and the extravasate remains free from infection there
will be very little inconvenience from the hemorrhage ; but if
the extravasate becomes infected the outcome will be more
serious. If the extravasate is into some important tissue the
secondary changes will be of more consequence than when in
the body cavities.
There is a natural tendency for self-arrest of hemorrhage,
because, 1st, blood pressure is diminished during hemorrhage
and thus coagulation is favored ; 2nd, the endothelium of the
injured vessels becomes roughened and thus thrombic formation
is favored ; and 3rd, fibrinogen is liberated from vascular endo-
thelium and thus the coagulation of the blood is favored.
CIRCULATORY DISTURBANCES. 117
LYMPHORRHAGIA.
DEFINITION.
(Extent of lymphatic system).
(Lymph transudate qiiantitv determined bv blood pressure).
ETIOLOGY.
Ruptured vessel or space.
LOCATION.
Surface, because of lymph spaces and lozu pressure.
Thoracic duct.
APPEARANCE.
Macroscopic.
Microscopic.
EFFECTS.
Lymphorrhagia is the escape of lymph from injured lymph-
atic vessels. The lymphatic system in general is the connecting
system between the blood capillaries and the jugular vein.
Lymph, the fluid in the lymphatic vessels, is that portion of the
blood which passes through (or is secreted by), the capillary
walls into the perivascular spaces and consists of plasma diluted,
leucocytes, and usually contains considerable waste material.
Lymph varies in its composition, depending upon the source,
location and condition of the surrounding tissue. The lymph of
the lacteal system depends upon the kind of food-material
digested and the length of time since its ingestion.
Etiology. — Lymphorrhagia is as a rule the result of laceration
or rupture of the lymphatic channels. In rare instances it may
be caused by an increased permeability of the lymphatic vessels
or spaces. Because of the low pressure within the lymphatic
vessels, lymphorrhagia takes place only upon surfaces or into
the body cavities. Lymphorrhagia onto a surface, if long con-
tinued, results in the so-called lymphatic fistula. Rupture of
the abdominal portion of the thoracic duct accompanied by the
escape of its contents into the peritoneal cavity produces the
condition known as chylous ascites.
Chylous ascites is differentiated from abdominal dropsy or
ascites proper by examination of the accumulated fluid. The
fluid of chylous ascites and lacteal fluid are practically identical
in composition. Ascitic fluid proper is diluted lymph and con-
tains no evidence of chyle or lacteal fluid. Lymphorrhagia may
also occur into the pleural cavity as a result of the rupture of
the thoracic portion of the thoracic duct.
The effects of lymphorrhagia depend upon the extent, loca-
tion and length of duration of the process. Extensive lymph-
orrhagia from a large lymphatic vessel depletes the body .be-
cause of the loss of food substances, albumin, etc., in the lymph.
118 VETERINARY PATHOLOGY.
Lymphorrhagia from the thoracic duct, especially into the peri-
toneal cavity, is serious because of the loss of food.
OEDEMA, DROPSY OR HYDROPS.
DEFINITION.
ETIOLOGY.
Increased production.
Increased permeability (Cohnheim).
Increased pressure.
OBSTRUCTED OUTFLOW.
Valvular insufficiency or stenosis (cardiac).
Gravid uterus.
Tumor, Abscess, Ligature, etc.
LOCATION.
Peritoneal cavity (ascites).
Thoracic cavity (hydrothora.v).
Pericardial cavity (liydropericardium).
Arachnoid space (hydrocephalus e.vteriial).
Lateral ventricles (hydrocephalus internal).
Tunica vaginalis cavity (hydrocele).
Subcutaneous Ivtnph spaces (aimsarca), (in legs OJilv, stocking).
APPEARANCE.
Macroscopic.
Microscopic.
EFFECTS.
Oedema, dropsy or hydrops is the accumulation and reten-
tion of an excessive quantity of lymph in the lymph vessels and
spaces. Lymph is the conveyor of metabolic substances to and
from all tissues of the body except those directly supplied by
the blood capillaries. The quantity of lymph in the lymphatic
channels is determined by the permeability of the capillary walls
and the rapidity of lymphatic absorption. In health there is a
balance between the transudation of lymph from the blood ves-
sels and its absorption into the lymph vessels. In oedema there
is either a larger amount of lymph transuded or a smaller
amount absorbed.
Etiology. — The causes of oedema may be :
1. Increased transudation which may be caused by (A) In-
creased permeability (or secretory function) of the capillary
walls, thus allowing an increased amount of fluid to escape from
the blood (Cohnheim theory). (B) Hyperemia: which pro-
duces an increased intracapillary pressure resulting in sufficient
injury to the endothelial lining to allow an increased outflow of
plasma. Passive hyperemia is more frequently associated with
oedema than active hyperemia. Thus, tricuspid stenosis or tri-
cuspid insufficiency is usually associated with general dropsy.
"Stocking" is an oedema usually resulting from venous hyper-
emia.
CIRCULATORY DISTURBANCES.
119
2. Obstructed outflow of lymph. Swollen lymphatic glands,
the result of inflammatory disturbances or neoplasms, and
external pressure hinder the passage of lymph and hence favor
its accumulation. As the anastomoses of lymph channels is
quite complete the obstruction of the outflow of lymph is a
minor cause.
Varieties of oedema according to location are as follows : —
AsciteSi: an abnormal accumulation of an oedematous fluid in the
peritoneal cavity usually resulting from obstructed portal cir-
Fijf. tin. — Dog with Ascites, a rt'teulU of tiii hepatic tumor.
culation. Chylous ascites is a condition resulting from obstruc-
tion of some of the lacteal lymphatic vessels or the abdominal
portion of the thoracic duct, or it may be the result of leakage
of the abdominal thoracic duct.
Hydrothorax: an abnormal accumulation of oedematous fluid
in the pleural cavity or cavities. It is usually bilateral in the
horse and is caused by obstruction of the internal thoracic vein.
Hydropericardiiiiii : an abnormal accumulation of oedematous
fluid in the pericardial sac. This variety is very rare as a pri-
mary condition. It is caused from venous obstruction of cardiac
vessels or vessels of the cardiac sac.
Hydrocele: an abnormal accumulation of an oedematous fluid
within the vaginal tunic, e. g., the so-called "water seed," caused
by adhesion of the vaginal tunic in the inguinal canal, which is
usually the result of improper castration.
120
VETERINARY PATHOLOGY.
Hydrocephalus: an abnormal accumulation of oedematous fluid
in the serous cavities of the brain or its meninges, caused by
venous hyperemia. Thus external hydrocephalus is an affection
of the subarachnoidean spaces, and internal hydrocephalus an
affection of the ventricles of the brain.
Fig.
Mil)(u*;iiu'^:;P^-"'' '■■■'•V-v,-v';\'--^:-^ ^,' ■■i}'vV',V' ■':..-'■ " : ■■-■J:.
■ ^^^rf*^"!" ' ■
T^,-!;-;;'>'<^- :.Av,--^.,v-;V:\ X - ' "■ ' ^^'''ir'^'''^:'- — -/-.\ ■ '■'V;:^a;:;.-,
^-;^'^
Fig. 71. — Aneniio infarcts in tlie .spleen.
a. Infarcted areas due to emboli in capillaries supplying them.
Effect. — The results of embolism depend upon the composi-
tion of the embolus, and the vessel obstructed.
Composition of the embolus. — Emboli composed of cells having
the power to multiply, at the point of impaction (embolism) be-
come secondary foci or metastases of the primary pathological
condition, as metastatic sarcomata, leukemic infarctions, etc.
Pathogenic bacterial emboli not only obstruct circulation, but
also produce metastases of that disease as in necrobacillosis,
anthrax, etc. Filarial emboli and emboli composed of fatty cells
CIRCULATORY DISTURBANCES. 131
produce a mechanical effect only. Air emboli in small vessels
mechanically obstruct the vessels but are absorbed after a time.
Obstructed circulation. — Obstructed circulation when produced
by non-infective emboli will have the same effects and termina-
tions as the non-infective obstructive thrombi.
Infarction. — Infarction is the process of obstructing a vessel
with an embolus. The area supplied by the obstructed vessel
is called an infarcted area. The area of infarction is determined
by the region supplied by the occluded vessel and is usually
wedge-shaped. An area supplied by an artery that has been in-
farcted does not become bloodless at once because some of the
blood remains in the vessels of the infarcted area and some' may
enter the periphery of the infarct through anastamosing capil-
laries and venules of adjacent regions.
Infarcts may be anemic or hemorrhagic.
An anemic infarct is one in which there is limited anasta-
moses of venules and capillaries of contiguous areas. The blood
remaining in the vessels of an anemic infarct soon becomes de-
colorized and the area appears pale in color. Anemic infarcts
usually undergo necrosis early because of the lack of nutrition.
The type of necrosis is largely dependent upon the nature of
the embolus. Infarcts produced by infectious emboli usually
suppurate or putrefy and infarcts produced by non-infective em-
boli may become liquified, absorbed and replaced with fibrous
tissue or it may become caseated or calcified and surrounded by
a fibrous capsule and persist for a long time.
A hemorrhagic infarcted area is one in which there are anas-
tamoses of the vessels of the infarcted area and the venules and
capillaries of contiguous areas through which blood passes and
becomes stagnated in the affected area. Hemorrhagic infarcts
may become decolorized, there may be inflammation established
around their periphery, or the blood and the involved tissue may
be disintegrated and absorbed.
Infarcted areas may become cystic, caseous, calcareous, ab-
sorbed and substituted wath fibrous tissue, or they may become
infected and there may be abscess formation or gangrene.
Infarction occurs most frequently in the kidney, spleen, brain,
lung and less frequently in the heart, liver, retina, etc.
Typical terminal arteries are common in the kidney and spleen
and hence infarction most frequently occurs in these organs. In the
kidney anemic infarcts are most common, hemorrhagic and ane-
mic infarcts occur in the spleen. Cardiac infarction is not com-
mon and is usually caused by thrombosis of the coronary vessels.
Cerebral anemic infarction occurs occasionally and the infarct
132 VETERINARY PATHOLOGY.
usually undergoes simple softening, hemorrhagic cerebral in-
farction is rare.
ISCHEMIA.
DEFINITION.
ETIOLOGY.
Diminished calibre of supplying arteries.
Stimulation of vaso constrictor nerves.
Inhibition of vaso dilator nerves.
Tonic spasms of vessel musculature.
Occiilsion of supplying arteries.
Mechanical.
Tumors.
Thrombi, etc.
Collateral hxperemia.
APPEARANCE.
Macroscopic, pale, flabby, lower temperature.
Microscopic, cell degeneration, atrophy or necrosis.
EFFECTS.
Depend upon extent and duration and may be atrophy or necrosis.
Anemia, as usually considered, is a condition in which there is
either a deficiency in the quality or in the quantity of blood.
The discussion of this theme will be found in special pathology.
Ischemia is a condition in which there is insufficient or total
absence of blood in a part of the body.
Etiology. — Ischemia may be caused by influences that dimin-
ish the calibre or occlude the vessels supplying blood to a part
or by collateral hyperemia. The calibre of arteries may be
diminished by contraction of the vessel musculature induced by
low temperature, high temperature, drugs, etc., which stimulate
the vaso-constrictor nerves, or inhibit the vaso-dilator nerves
or cause tonic spasms of the vascular musculature. The supply-
ing arteries may be occluded b)^ mechanical pressure produced by
bandages, ligatures, harness, collar, thrombi, emboli, neoplasms,
tissue proliferations and tissue infiltrations. Ischemia in one
juirt may be caused by hyperemia in a related part, because the
blood of the entire body is easily contained in the vessels main-
tained at the normal calibre, blood pressure causing an equal
distribution of it ; and if the vessels of one area are increased in
calibre, followed by an increased inflow of blood, the quantity of
blood will be diminished in some part, thus a marked hyperemia
of the spleen is usually accompanied by ischemia of the stomach.
It is possible for sufficient blood to collect in the vessels of the
liver to drain the system to a sufficient extent that the animal would
die of ischemia of the brain.
Appearance. — Macroscopic. — An ischemic tissue appears
bloodless and is pale, flabby and of a lower temperature than the
CIRCULATORY DISTURBANCES. 133
same tissue with a normal blood supply. If incised the tissue ap-
pears dry and there will be limited or no hemorrhage.
Microscopic, the blood vessels are practically empty and the
tissue cells are more or less shriveled as a result of insufficient
moisture.
Effects. — The outcome of ischemia is determined by the
length of time it exists and the degree of completeness of the
condition. Temporary, partial ischemia usually terminates in
complete recovery. Continued partial ischemia is a frequent
cause of atrophy. Complete absence of blood for a considerable
time results in necrosis.
HYPEREMIA.
Hyperemia is a condition in which there is an increased
quantity of blood in a part. The condition is practically local
for an increased total amount of blood could not be retained in
the general circulation without increasing the general blood
pressure which would result in an increased production of lymph
and hence diminish the volume of blood. Psysiologic hyperemia
is evident whenever an organ or part is active. Local patho-
logic hyperemia may be passive (venous) or active (arterial).
Passive or Venous Hyperemia.
DEFINITION.
ETIOLOGY.
Enfeebled circulation.
Mechanical interferoice.
APPEARANCE.
Macroscopic, bliiisli. cold clanniiy.
Microscopic, engorged veins, degeneration.
EFFECTS.
Depend upon cause, duration, degree and location, and may be varicose
veins, fibrosis, oedema, thrombosis, necrosis and recovery.
Passive or venous hyperemia is a condition in which there
is a normal quantity of blood constantly flowing into an organ
or part, but a diminished quantity flowing out. An excess of
venous blood consequently accumulates in the part.
Etiology. — Passive hyperemia is caused by enfeebled circu-
lation due to weak heart, biscuspid and tricuspid insufficiency or
stenosis, or diseased vessels and by pressure upon the outgoing
vessels by ligatures, bandages, neoplasms, dislocations, fractures,
etc.
Appearance. — Macroscopic. — The affected tissues are bluish
in color and usually feel spongy, cold and moist when palpated.
134 VETERINARY PATHOLOGY.
Microscopic. — A tissue affected with venous hyperemia has dis-
tended capillaries and venules, the lymph spaces are engorged
with lymph and the cells are swollen and their protoplasm cloudy.
Effects. — The outcome of venous hyperemia depends upon
the cause, degree, duration and organs affected. Thus venous
hyperemia resulting from infective phlebitis is more serious than
if caused by noninfective agencies. A venous hyperemia caused
by complete obstruction of a vein is more likely to be fatal than
one resulting from partial obstruction. Venous hyperemia of
short duration is usually of little consequence but, if long con-
tinued, it results in necrosis or fibrosis depending upon the de-
gree of obstruction. Venous hyperemia of vital organs, as the
brain or lungs, is more likely to have a fatal termination than if
some less important structure as a muscle were involved.
Therapeutic Venous Hyperetnia properly produced results in
(a), diminution of pain, probably because of the dilution of the
irritating substances (b), destruction of bacteria, the accumu-
lated blood serum, possessing strong bactericidal properties (c),
increased nutrition because of the increased amount of blood.
Bier's hyperemic treatment of open joints by producing venous
hyperemia illustrates this type.
Pathologic Venous Hyperemia may result in fibrosis, oedema,
thrombosis, necrosis, or recovery. A long continued slight ven-
ous hyperemia usually results in fibrosis and is noted in the liver
of animals affected with a slight tricuspid insufficiency or steno-
sis. A marked venous hyperemia, but not caused by complete
venous obstruction usually results in oedema, and is noted in the
peritoneal cavity (ascites), in animals in which the portal circu-
lation is partially obstructed. Venous hyperemia caused by com-
plete obstruction results in thrombosis and is observed in intus-
susception of the intestines. If other venous channels are unable
to conve}^ the blood from a part in which there is a complete
venous thrombus, necrosis occurs as in strangulated herniae.
Venous hyperemia of short duration, even though it is quite
extensive, results in complete recovery if the cause is removed and
the tissues are repaired.
CIRCULATORY DISTURBANCES.
135
ACTIVE OR ARTERIAL HYPEREMIA.
ETIOLOGY.
Increased calibre of arteries.
Stimulation of vaso-dilator nerves.
Inhibition of vaso-constrictor nerves.
Paralysis of vessel musculature.
Collateral ischemia.
Diminished external (pressure.
APPEARANCE.
Macroscopic, red, hot, szvollen.
Microscopic, engorged arteries and capillaries.
EFFECTS.
Hypertrophy, hyperplasia, inflammation, recovery.
Active or arterial hyperemia is a condition in which there
is an increased inflow of blood to a part or organ without an
equally increased outflow.
d—
— .b
Fig. 11. — Hyperemia, hemorrhage and oedema of intestine of a horse.
a. Surface exudate. c. Area of oedema.
b. Engor.?ed vesHels. d. Subsurface hemorrhage.
Etiology. — Arterial hyperemia is caused by an increase in the
calibre of the supplying arteries, by collateral ischemia and by
diminished external pressure. The calibre of the supplying
artery may be increased by stimulation of the vaso-dilator nerves,
by heat, chemicals, etc., by inhibition of the vaso-constrictor
nerves, and by paralysis of the muscular tunic of the artery.
The calibre of the surface vessels is in part of the result of- ex-
ternal pressure. If the external pressure is materially dimin-
136
VETERINARY PATHOLOGY.
ished, there will be arterial hyperemia of the cutaneous arteries
as is evidenced in hyperemia produced by cupping. Collateral
ischemia may cause hyperemia of the related parts for the same
reason that collateral hyperemia may cause ischemia.
Appearance. — Macroscopic. -^Kn arterial hyperemic part is
scarlet red in color, usually feels dense, dry and has an increased
temperature. If the tissues are incised, blood escapes freely.
Fig 73. — Hyperemia of Kidney, showing engorged capillaries.
Microscopic. — Tissues affected with arterial hyperemia contain
dilated arteries and capillaries, the lymph spaces are engorged
with lymph, the tissue cells may be considerably swollen and
diapedesis may be noted.
Effects. — The effects of arterial hyperemia depend upon the
cause, degree, and duration and organs affected. Arterial hyper-
emia caused by infective agencies is more serious than if caused
by other means. Arterial hyperemia of a sthenic type is usually
succeeded by inflammation and asthenic hyperemia may terminate
in recovery.
CIRCULATORY DISTURBANCES. 137
Arterial hyperemia of short duration is less serious than it
would be if long continued, thus, active pulmonary hyperemia is
occasionally aborted in the horse and such animals are usually
ready for service in 24 to 48 hours, but if active pulmonary
hyperemia continues for 24 hours it is succeeded by inflamma-
tion (pneumonia).
Arterial hyperemia varies in different organs. Affections of
the more highly organized structures are usually more serious.
Physiologic arterial hyperemia is a condition in which there is
an increased amount of blood flowing into a tissue because of
increased physiologic demand, thus during gastric digestion an
excess of blood passes to the stomach through the gastric
arteries.
Therapeutic arterial hyperemia, when properly produced in a
diseased part, results in (a), diminished pain, (b), resorption of
inflammatory exudate, hemorrhagic extravasate, and oedematous
transudate, (c) increased nutrition, thus by the alternate use of
cold and hot applications an arterial hyperemia is produced and
is of value in strained tendons, bruises, etc.
Pathologic arterial hyperemia may produce hypertrophy, hyper-
plasia and permanent arterial dilatation. Excessive development
of a part (hypertrophy or hyperplasia) may result from a long
continued active hyperemia as in thickening of the skin as a
result of continued application of blistering agents, but arterial
hyperemia is as a rule of short duration for it usually terminates
in recovery or is succeeded by inflammation.
CHAPTER VI.
INFLAMMATION.
DEFINITION.
GENERAL CONSIDERATION OF STIMULI AND REACTIONS.
ETIOLOGY.
Non-infective.
Mechanic.
Physic.
C hemic.
Infective.
Nonsuppurative.
Suppurative.
FACTORS CONCERNED IN INFLAMMATION. (Phenomena).
I'ascular.
Constriction of vessels.
Dilatation of vessels.
Acceleration of rate of blood iioiv.
Retardation of rate of blood Hoiv and leucocytic margination.
Oscillation of blood in the vessels and diapedesis.
Stasis.
Exudation.
E.Yudate.
Composition.
Physic.
C hemic.
Histologic.
Varieties.
Serous.
Fibrinous.
Hemorrhagic.
Factors determining quality and quantity.
Cause of iniiamniation.
Condition of animal.
Location of process and of tissue affected.
Significance of the exudate.
Increased amount of nutrition to the affected part.
Dilutes, counteracts, neutralizes or destroys the irritant.
Circumscribes the inffanimatory process, protects in. in.
Spread infection., occludes air cells, produces adhesions.
Cheniotaxis.
Phagocytosis.
THE SIGNS OF INFLAMMATION.
Redness.
Sivelling.
Increased temperature.
Pain.
Impaired function.
EFFECTS UPON THE TISSUE INVOLVED.
Degeneration.
Parenchymatous.
Fatty.
Mucoid.
Serous.
Amyloid.
Hyaline.
Necrosis.
Regeneration or proliferation.
138
INFLAMMATION. 139
THE KINDS OF INFLAMMATION.
Etiology.
Simple.
Infective.
Non-siippiirative.
SuppiiratiTc.
Surface.
Sub-surface.
Exudate.
Serous.
Fibrinous.
HemorrJiagic.
Tissue.
Parenchymatous.
Interstitial.
Time, activity and results.
Acute.
Chronic.
Miscellaneous.
Catarrhal.
Purulent.
Ulcerative.
Vesicular.-
Pustular.
Proliferative.
Specific.
TERMINATION.
Resolution.
Tissue proliferation.
Dissolution.
CONCLUSIONS.
Inflammation is a name applied to a group of pathologic
processes including circulatory disturbances, retrogressive and
progressive tissue changes. The term inflammation is difficult
to define because of the several factors entering into the process
and of the variation of each factor. It may be defined as the
reaction of a living animal tissue to an irritant.
A stimulus is anything that produces action in a living tis-
sue. An irritant is anything that produces excessive stimulation
in a responsive tissue. Stimuli and irritants dififer only in
degree. Mild friction of the skin is a stimulus to that structure.
When the friction is intensified and the cutaneous function is
overstimulated the friction becomes an irritant. All living tis-
sues respond to stimuli and likewise to irritants. The response
or reaction of a living tissue to an irritant, i. e. excessive tissue
stimulation, accompanied by destructive or proliferative tissue
changes, and by circulatory disturbances constitutes the pro-
cess known as inflammation. The general phenomena of in-
flammation will be better understood if some preliminary con-
siderations of the reaction to stimuli are first discussed.
General Consideration of Stimuli and Reactions. — It is a
1-40 VETERINARY PATHOLOGY. "
well known fact that all living things (organisms) respond tO
stimuli. A stimulus is that which excites or produces a tem-
porary increased vital action, or it is any substance or agent
capable of producing activity in a living tissue or producing
an impression upon a sensory organ. The extent or degree
of response to a stimulus is directly proportional to the organi-
zation and complexity of the tissue and especially those tissues
which are: (a) capable of being stimulated; (b) capable of trans-
mitting an impulse; and (c) capable of interpreting the impres-
sions produced by the impulse. The following discussion of
response to stimuli is confined to animal tissues because inflam-
mation affects animals only.
Protozoa, although of the simpliest structure, consisting of
a single cell, respond to the various stimuli. They respond to
light. Thus, if a portion of a cover glass preparation of living
amoebae be exposed to intense light, the amoebae in the
lighted area will, in a short time, become restless and begin
to move about and will finallv move away from the area of
light. By a specially arranged hot stage, so that there are areas
of different temperature, amoebae will be observed to ac-
cumulate in the areas of favorable temperature and emigrate
from those of unfavorable temperature. That is. they respond
to or are responsive to thermic stimuli. In a similar way
amoebae respond to various chemical stimuli. If a drop of acid
be so placed that it will slowly diffuse into the water or fluid
in which the amoebae are being studied, they will move away
from the acid. If an amoeba be divided by mechanical means
so that one segment contains the entire nucleus and the other
segment has no nucleus, it will be observed that the nucleated
segment responds to the stimulus by regenerating tissus to re-
place the nonnucleated segment which was removed. On the
other hand, the nonnucleated segment of the amoeba may
survive the shock of separation, but soon begins to degenerate
and finally dies. Thus is shown the response of living struc-
ture to photic, thermic, chemic and mechanic stimuli.
If more complex animals be considered there will be ob-
served a similar response to stimuli. Thus, the hydra responds
to the various kinds of stimuli and has a remarkable power of
regeneration of tissues. Vermes are very responsive to stimuli
and all observers have noticed that when an angle-worm is
cut in two both ends will crawl away. Vermes are among the
lowest forms of animals that possess cells corresponding to
white corpuscles or leucocytes of higher animals. These cells
are observed to emigrate to the point of injury or to surround
INFLAMMATION. 141
tlie foreign bodies or substances that are experimentally in-
troduced into the bodies of vermes. This reaction is analogous
to the reaction of the mammalian leucocytes.
The discussion so far, has been with reference to animals
that possess no blood or vascular systems, or at least only in
a rudimentary form.
Vertebrates are m.ore highly organized and are consequently
more responsive to stimuli than invertebrates. Mammalia arc
the most complex in structure of all animals and thev are like-
wise most responsive to stimuli.
The mammalian cornea is a nonvascular structure being
composed of fused layers of fibres arranged parallel to the sur-
face. Between the layers of fibres connective tissue cells and
lymph spaces are found but no nerves. The cornea is covered
externally by the conjunctiva. If the cornea be irritated there
will be a reaction, the extent of which depends upon the in-
tensity of the irritant. A puncture of the cornea with a sterile
needle produces the following reaction or tissue changes ; (a)
within a few hours after the injury the affected area appears
swollen and the cells that were punctured begin to degenerate
while the uninjured cells immediately surrounding the needle
puncture become tumefied and vacuolated ; (b) from twenty to
thirty hours after the puncture, wandering cells appear in and
around the injured area, and as the cornea is nonvascular they
must be migratory connective tissue cells ; (c) by the third
or fourth day the punctured cells will have been removed, by
solution or otherwise, from the affected areas. Those cells sur-
rounding the injury will have divided by mitosis, the newly
formed cells replacing those that were destroyed and the
wandering cells will have migrated from the injured focus.
(The destroyed epithelial cells of the conjunctiva are replaced
by those next to the injury).
If sterile iron dust, or other insoluble granular material is
aseptically introduced into the cornea, a reaction, as described
above, will take place, and, in addition, the migratory connec-
tive tissue cells will ingest or incorporate the introduced par-
ticles and carry them out of the injured focus.
When the cornea is injured more severely, as by the ap-
plication of a caustic solution (irritant), in addition to the
above reaction, a migration of leucocytes from the marginal
corneal vessels usually occurs within thirty hours. Some of
the invading leucocytes become destroyed and some of them
may multiply, but they usually all disappear from the point of
mjury within from forty to fifty hours. The length of time
142 Veterinary pathology.
necessary for repair of such an injury is variable according to
the extent of the injury and the readiness of response of the
tissue.
In vascular tissue the following- reaction occurs. An asep-
tic cutaneous incision unites almost immediately if the wound
margins are placed and maintained in exact apposition. The
tumefaction is slight because of the limited extravasate from
the severed vessels. There is a slight exudate which coagu-
lates and cements the margins or lips of the wound. In a
microscopic section through such a wound some cells are found
destroyed and others injured. The cells bordering such an in-
jury sometimes increase in size to such an extent that they
project into the cement between the two incised surfaces. Wan-
dering cells and leucocytes in varying numbers appear through-
out the entire injured area. The cement (exudate) and the de-
generated and necrotic marginal cells are later absorbed. The
cells bordering the incision multiply by direct cell division, the
newly formed cells replacing those destroyed. New capillaries
extend through the newly formed tissue. Finally the leucocytes
emigrate and disappear from the injured area.
In a more extensive injury, such as a gaping wound that
later becomes infected, a more complex reaction is observed.
The following changes take place during the first twenty-four
hours after an injury of this nature is inflicted. There is hem-
orrhage, the extent of which depends upon the size of the ves-
sels severed and the gaping of the wound. The extravasated
blood accumulates in the wound and also infiltrates the ad-
jacent tissues. The injury (irritation) causes hyperemia, es-
pecially of the arterioles, resulting in engorgement of the capil-
laries. From the engorged and dilated capillaries there is
marked exudation. The exudate escapes upon the wound sur-
face and infiltrates the tissues of the injured area. The ac-
cumulation of the hemorrhagic extravasate and the inflam-
matory exudate plus the increased size of the vessels (hyper-
emia) tumefies or swells the injured area. There is an ac-
cumulation of mononuclear leucocytes or wandering connec-
tive tissue cells in the injured tissue and an immigration of
polymorphonuclear leucocytes. Many cells are destroyed out-
right by the injurv or bv the action of infectious bacteria.
Those cells bordering the destroyed cells are injured and be-
come tumefied and may later undergo necrosis. The cells, es-
pecially the connective tissue cells located peripherally to the
injured cells, become enlarged and multiply by indirect cell di-
vision. The injured cells are repaired and the newly formed
INFLAMMATION. 143
cells are massed together and project outward thus replacing
the destroyed cells.
The discharge from such a wound after twenty hours con-
sists of serum, shreds and fragments of necrotic tissue, dead
cells (especially leucocytes) and a variety of microorganisms.
The reaction in the above case consists of circulatory dis-
turbances, degeneration, necrosis, and regeneration of tissues.
Etiology. — The exciting causes of inflammation may act
from within the body, hematogenous or lymphogenous, or from
without, i. e., extraneous as burning, etc. They may produce their
action by direct contact upon surfaces of the body as from a
blistering agent externally applied, or, by contact internally, as
from arsenic. They may produce their effect while being ex-
creted, as in the production of nephritis by cantharides or tur-
pentine. Some harmless agents may become irritants as the
result of chemic change produced by some of the body juices
or fluids (lysins).
The causes of inflammation mav be divided into two gen-
eral classes, non-infectious and infectious.
NoN-iNFECTious. — The non-infectious causative factors are not
as active in producing inflammatory disturbances as the in-
fectious agencies, but they are of some importance and should
not be overlooked. Some have positively stated that "There
is no inflammation without infection." Reasonable interpreta-
tions of clinical and experimental observations supply suffi-
cient evidence that there is inflammation without infection.
The following are the principal non-infectious causes of in-
flammation.
Mechanic or traumatic. — Surgical wounds which heal by
primary union are undisputed examples of mechanically pro-
duced inflammation. The reaction taking place in an aseptic
incision consists in cell-destruction, slight circulatorv disturb-
ances, leucocytic immigration and regeneration of tissue. Such
a reaction is typical of inflammation and the affected area is
devoid of any infection. A sterile needle introduced into a
tissue, the surface of which is aseptic, produces a reaction
identical to the reaction observed in primarv union of tissue.
Mechanic or traumatic causes of inflammation mav produce, or
cause to be produced in the injured cells, chemic substances
that are responsible for the reaction.
Thermic. — A temporary exposure to a high or low tem-
perature is sufficiently irritating to produce a marked inflam-
mation. Let those doubting this statement take the chimney
from a lighted lamp and hold it in the hand for one minute and
144 VETERINARY r\\TIIOLOGY.
they will acknowledge that heat produces all the symptomatic
evidences of inflammation and there is no infection. The prin-
ciple object in the use of the thermo-cautery is to produce or
establish inflammation. A thermo-cautery, or any severe burn,
produces tissue necrosis, as well as the destruction of bacteria
in that area (sterilization), and an inflammatory zone is im-
mediately established around the necrotic tissue wdiich is sterile
and may remain free from infection.
A short exposure to an extremely low temperature produces
an inflammation. If the exposure is of long duration necrosis
is likely to occur. "Chilblains" is an inflammation resulting
from temporary exposure to a low temperature. Sloughing
following freezing of calves' ears, pigs' tails and cocks' combs
are familiar examples of necrosis resulting from long exposure
to extremely low temperature. An inflammatory zone is es-
tablished around necrotic areas produced bv freezing similar
to the inflammatory zone observed around necrotic areas pro-
duced by burning. Thermic variations may produce chemic
substances in injured tissues which are sufficiently irritating to
establish inflammation.
Electric. — 'It is common knowledge that electricity causes
inflammation. Animals injured by lightning usually show evi-
dences of cutaneous inflammation. In cities animals as well as
men frequently contact wires charged with powerful electric
currents and receive local injuries that are usually inflammatory
in their nature.
Chcinic. — There are ma^ny chemicals that are irritants. A
number of them are used as therapeutic agents w'hen irritants
are indicated. Mineral acids, caustic alkalies, mercury salts
and arsenic are some examples of chemic agents that produce
inflammation when applied in dilute solutions, and necrosis
when applied in more concentrated form. A 10 per cent solu-
tion of nitric acid applied to the skin for a very short time pro-
duces inflammation. Inflammatory symptoms following the
nitric acid application appear immediately ; and, as the acid is
a disinfectant, the inflammation cannot be the result of infec-
tion. In animals poisoned by any of the mineral poisons there
may always be observed an inflammation in the mucosa of the
alimentary tract more extensive than could have been produced
by infection in the limited time of action.
Many reptiles, bees, wasps, and ants introduce chemic sub-
stances into animal tissues that are extremely injurious and es-
tablish inflammation of verv rapid evolution.
Infectious or vital agencies are the most important etiologic
INFLAMMATION. 145
factors in the production of inflammation because they are the
most frequent offenders. Infection usuaMy produce inflam-
matory disturbances through the action of chemic substances
elaborated by the infecting micro-organisms, as metabolic pro-
ducts. The infection may be local and produce localized in-
flammation as in a superficial abscess and in coccidiosis. The
elaborated chemic substances may be absorbed from the local-
ized infection and produce inflammation elsewhere in the body.
Infection may be general and produce conditions similar to in-
flammation in practically all the tissues of the body as in gen-
eralized anthrax. However, the term inflammation is usually
confined to local disturbances. The extent of irritation pro-
duced by any infecting organism is dependent upon the virul-
ency of the given organism, and the resistance of the infected
animal. Thus, infection with Streptococcus pyogenes equi may
produce pyemia in one animal and only a local abscess in an-
other. Again, some bacteria, as the anthrax bacilli, may pro-
duce septicaemia in one animal and localized inflammation in
another. A concise etiological classification of inflammation
produced by living organisms is impossible because of variations
both in the virulency of the organisms and in the resistance of
the tissues. Animal parasites are of considerable consequence
in the production of inflammation. They may produce inflam-
mation by mechanical interference, as the Echinorychus gigas
which inserts its barbed proboscis into the intestinal mucosa
thus injuring the tissue as well as opening an avenue for the
entrance of various bacteria. The Trichina spiralis by perfor-
ating the intestinal wall and by burrowing in the muscular
tissue produces sufificient irritation to establish inflammation,
the results of which are evidenced on microscopic examina-
tion of a lesion. It has been suggested that the etiological
factor of rabies is an animal parasite ; the round-celled infil-
tration of the ganglionic nerve cells and perivascular spaces
having marked characteristics of the lesions of inflammation.
Psorospermosis, a condition resulting from psorospermic in-
festation, is inflammatory in its character.
In a general way infective inflammations mav be discussed
as non-suppurative and suppurative.
The non-suppurative infective inflammations are those in-
flammatory disturbances in which there is no purulent fluid or
pus produced. As examples the following may be cited — septic
infection succeeding nail pricks in horses feet ; blackleg in
calves caused hy the Bacillus anthracis s^mptomaticus, (Sar-
146 VETERINARY PATHOLOGY.
cophysematous bovis) ; malignant oedema caused by the Bacil-
lus of malignant oedema.
Suppurative infective inflammation is characterized by the
formation of pus. The causative bacterial agents of suppura-
tion are designated as pyogenic bacteria or pyobacteria. The
following are the most important bacteria of this class :
Micrococcus pyogenes aureus.
Micrococcus pyogenes albus.
Micrococcus pyogenes citreus,
Strepto-coccus pyogenes.
Bacillus pyocyaneus.
Factors Concerned in Inflammation. — The animal body is
an intricate mechanism composed of different tissues in various
combinations. The phenomena of inflammation are the changes
that take place in the tissues plus the conditions resulting from
those tissue clianges, thus including all the changes taking place
in the inflammatory focus. The following are the most impor-
tant.
Vascular disturbances. — These are universally present in
animals possessing a vascular system, but inflammation, or a
condition analagous to it, occurs in the tissues of animals that
have no vascular system, and in nonvascular tissues of animals
that have a vascular system. Hence vascular changes are not
essential in the process. The vascular changes are dependent
upon nervams influence, because the calibre of blood vessels,
especially arteries, is controlled by vasomotor nerves. Inflam-
matory areas become necrotic when dilatation of the supplying
arteries and arterioles is inhibited. In experiments in which
dilatation of the arterioles takes place mild inflammatory pro-
cesses are limited and usually terminate in recovery in a short
time. Necrosis usually succeeds inflammation in tissues in
which continuity of the vasomotor nerves have been de-
stroyed. For example, the cubital nerve in the horse probably
contains the vasomotor fibres that innervate the vessels of the
foot and the median nerve the sensitive fibres that innervate
the pedal structures. ]\Tedian neurectomy is not succeeded b}'-
vascular disturbances, but cubital neurectomy is frequently
succeeded by vascular disturbances and excessive exudation
that terminates in necrosis followed by sloughing of the hoof.
The following vascular changes occur in an inflammatory
focus and in the order designated:
Decreased ealibre of the supplying arteries and arterioles.
INFLAMMATION. 147
Temporary contraction of arteries is the first result of the applica-
tion of an irritant. The cause of the constriction of the arteries is a
spasmodic contractioii, which is of vaso-motor origin, of the muscu-
lature of the vessels. This is succeeded by a marked arterial dilatation.
Dilatation of the arteries and arterioles. The response to stimuH
on the arteries is rapid and always active, in veins slow and usually
passive, in capillaries either rapid or slow but always passive. Dila-
tation of vessels in an inflamed area is also of vaso-motor origin and
is said to be caused by stimulation of the vaso-dilators or inhibition
Fig-. 74. — Blood ve.ssel, showing Corpuscles occupying central portion of stream,
typical of normal circulation.
of the vaso-constrictor nerves. An increase in the calibre of the
arteries results in an increased amount of blood flowing through
them and into the capillaries. The increased amount of blood in
the capillaries mechanically increases their calibre and also in-
creases the amount of blood which enters the related veins and
results in a dilatation of them. By increasing the lumen of a
vessel the resistance to the flowing contents is correspondingly
diminished and this results in a temporary acceleration of the
rate of l)lood flov/.
Acceleration of the rate of flow of the blood. The cor-
puscles occupy the axial, or central part of the stream as in
the normal circulating blood. The arterial dilatation plus the
acceleration of the blood flow constitute the essential factors in
active hyperemia.
148 VETERINARY PATHOLOGY.
Retardation of the rate of flozv. — A long continued dilata-
tion of a vessel results in injury especially to the endothelial
lining. The injured endothelial cells become swollen, rough-
ened and sticky. The leucocytes begin to appear in the peri-
pheral portion of the stream, probably because of the libera-
tion of some chemic substance by the endothelium that exerts
a limited chemotactic action upon the leucocytes. They roll,
Fig. 75. — Dilated blood vessel sliowing corpuscles spread throughout tlie entire
lumen typical of first stages of hyperemia.
tumble, and creep along over the swollen endothelial cells and
finally adhere to their roughened surfaces. The continued at-
tachment of leucocytes to the endothelium diminishes the cali-
bre of the vessel and increases the resistance thus retarding
the rate of blood flow.
Oscillation.— The resistance of the flowing blood, due to the
roughened endothelium of the vessels and accumulation of
leucocytes becomes so increased that the propelling force is
momentarily overcome. The blood in the engorged capillaries
and arteries may temporarily cease flowing or it may flow
toward the heart, i. e. in the reverse direction during the dias-
tolic periods. This to and fro movement is termed oscillation.
INFLAMMATION. 149
Stasis. — The resistance may become greater than the pro-
pelling force and the circulation cease for a varying period of
time. This condition is denominated stasis.
Exudation. — Varying quantities of the fluid and of the cell-
ular constituents of the blood pass through the vessels nor-
mally and an increased quantity escapes through during in-
flammation. The portion of the blood that escapes through the
blood vessels is called exudate. The passing of the exudate
^^^^- "^-"^ ^ '^ ^ -^ "^ .
'«■' :& .-«■ «■ fe.. <^- i. t- »
Fig. 76. — Blood vessel showing margination of leucocytes typical of the first stage.s
of inflammation.
through the vessel wall is termed exudation. It is a muted
question whether the normal tissue lymph is a secretory pro-
duct of the capillary endothelium or is produced Ijy such physi-
cal processes as diffusion or filtration. The source of the in-
flammatory exudate is no doubt, the same as the source of nor-
mal tissue lymph. Exudation is a result of the vascular dis-
turbances.
It has been previously stated that in normal circulatory
blood the corpuscles occupy the axial stream and the plasma the
150 VETERINARY PATHOLOGY,
peripheral stream. The corpuscles occupy the axial stream
because they have a greater specific gravity than the plasma.
The leucocytes enter the peripheral or plasmatic stream in inflam-
mation, that is margination is a result of chemotactic influences.
After the leucocytes become marginated they pass through the
vessel wall as follows : Small protoplasmic processes extend
and project through the vessel wall. These processes gradually
increase in size until the entire leucocyte has, by protoplasmic
extension, passed through. The leucocytes usually pass be-
tween the endothelial cells but they may pass directly through
p'jo 77_ — Blood vessel showing diapedesis of leucocytes typical of the exudative
stage of inflammation.
them. The exudation of erythrocytes is passive, the cells being
forced through the vessel wall by pressure. To recapitulate:
fluid exudation is either a physical process, such as filtration, or
a physiologic process, a secretion ; leucocytic exudation is a
physiologic process depending largely upon the chemic influ-
ences of the adjacent tissues, i. e., chemotaxis ; exudation of
erythrocytes is a physical process resulting from intravascular
pressure plus diminished resistance of the vessel wall.
Exudate. 1. Composition. — Inflammatory exudate contains
varying quantities of cells suspended in a fluid (plasma, tissue
juice, etc). The fluid part of the exudate contains proteids
(serum albumin and serum globulin) in excess of normal plasma.
It has a specific gravity of 1018 or more. The quantity of pro-
teid is directly proportional to the severity of the process and
INFLAMMATION,
151
is never less than 4 per cent and frequently as much as 6 per
cent. It usually coagulates readily if withdrawn from the in-
flammatory tissues. The coagulability of inflammatory exudate
is so constant that it may be used in differentiating inflamma-
tion from oedema. The exudate is usually acid in reaction.
The fluid portion of the exudate is similar to the blood plasma
with the exception of the varying percentage of proteids, and
the presence of some other soluble substances. Leucocytes are
the principal cellular elements found in the exudate, erythrocytes
occurring only in certain inflammatory conditions, such as
croupus pneumonia.
The following types of leucocytes are especially concerned in
inflammation : polymorphonuclear leucocytes, lymphocytes small and
large. Polymorphonuclear leucocytes with neutrophile gran-
ules are the type most frequently found in an area afitected
with acute inflammation, providing the causative irritant w^as
not too severe. About 70 per cent of the leucocytes present are
of this type. These cells appear in the affected area in the be-
gining of the process. They have the power of amoeboid
movement and may emigrate from the blood and lymph vessels
independently of the fluid exudate. These cells possess phago-
cytic properties and n:ry produce and liberate antitoxic and
bactericidal substances. They are the pus cells and constitute
the bulk of the exudate in suppuration. These cells may be
destroyed and disintegrated in the field of action or when the
inflammatory process ceases they may migrate from the in-
jured area and reenter the lymph or blood vessels. They do
not become formative cells and never produce new tissue.
Eosinophylic leucocytes, (polymorphonuclear leucocytes hav-
Fig'. 78. — Types of cells in innammatory e.xiidales.
1. Lymphocyte. 4 — 5. Polymorphonuclear leucocytes.
2. Mononuclear leucocyte. 6. Endothelial cells from lining of an artery.
3. Transitional leucocyte.
152 Veterinary Pathology.
ing acidophile granules), appear early in an inflamed area.
They are usually quite limited in number except in localized
inflammation induced by animal parasites. Foci, composed of
a mass of eosinophiles, are frequently observed in the liver,
kidney, and other tissues, and appear as inflammatory centers.
These eosinophilic inflammatory foci are probably the result
of invasion of animal parasites. Eosinophiles are abundant in
the lesions of bursattae and in epizootic lymphangitis. Their
origin is, so far as has been determined, from the blood, the
lymph and tissue spaces indirectly, and the bone marrow di-
rectly. The specific action of these cells in inflammation is
not known. They do not aid in the formation of new tissues.
Mast cells or polymorphonuclear leucocytes with basophile
granules are observed in subacute inflammation (Adami).
Their origin is from bone marrow. Their nuclei apparently
become disintegrated in inflamed tissue. The significance of
these cells has not been determined.
Lymphocytic invasion of the afl:'ected areas and an excess of
them in the blood characterize some of the slow .cooing or
chronic inflammatory processes such as tuberculosis and ac-
tinomycosis. These cells also appear in afi'ected tissues in the
later stage of acute inflammation but are never very abundant.
They may have their origin from the blood, the lymph and
from adjacent lymphoid tissue. The large lymphocytes may
have their origin from the small lymphocytes. Lymphocytes
have a very limited power of amoeboid movement. They have
never been observed to ingest bacteria although they may in-
corporate fragments of destroyed tissue cells or other inert sub-
stances. These cells may partake in the formation of new tis-
sue but this has not yet been positivelv determined.
Cells other than leucocytes are sometimes observed in in-
flammatory foci. Endothelial cells, wandering connective tis-
sue cells, giant cells, and red blood corpuscles may be present in
inflamed areas.
Endothelial or mesothelial cells are especially evident in the
exudate of a serous membrane afl'eoted with inflammation. They
appear later in the process than either polymorphonuclear leucocytes
or lymphocytes. Their origin is probably from pre-existing, like
cells of the serous membrane. They usually have a sluggish move-
ment, are slightly phagocytic and also ingest fragments or particles
of inert substances. These cells may be destroyed or they may
emigrate from the afifected area.
Wandering connective tissue cells are usually present in
inflamed tissues. These cells do not appear until some time
I^fFLAMMAtrON.
153
a^ter the injury is inflicted because of their slow movement.
Their source is from tissue spaces, and they are the preexist-
ing wandering- connective tissue cells that occur in practically
all tissues of the immature animal. They may be phagocytic
but this property is not usually well developed. They are es-
pecially active in the process of repair.
Giant cells, so-called, are of common occurrence in some in-
flammatory processes especially tuberculosis and actinomvcosis.
It is probable that endothelial cells are the progenitors of
» fv.
■f^'v-'-fis
Fig. 79. — Gastritis, hog', induced by a caustic, showing- destruction of gastric
mucosa.
giant cells. Wandering connective tissue cells may produce giant
cells. The giant cells may be formed either by a multiplication of
nuclei without division of the cell body or by a fusion of several
independent cells (Syncytium). The latter view is the one most
accepted at the present time. The function of the giant cell has
not been specifically determined, but those in tubercular lesions
frequently contain many tubercle bacilli indicating that they are
phagocytic.
Red blood corpuscles or erythrocytes occur in the inflam-
matory exudate as a result of intense engorgement of the ves-
sels. They begin passing through the vessel wall after the
leucocytic migration. Increased intravascular pressure is the
principal cause of their escape from the vessel, their passage
through the vessel wall being entirely passive.
154
Veterinary pathology.
2. Varieties. — Inflammatory exudates mfiy be serous, fibrin-
ous, or hemorrhagic.
a. A serous exudate continues in the fluid state as long as it
remains in the tissues or tissue spaces. It is composed ahiiost
entirely of fluid, having very few cells. This variety of ex-
udate is characteristic of mild inflammatory conditions. The
constancy of the fluidity of the serous exudate is the result of
the action of enzyms that continually convert the albuminous
substances into soluble compounds as proteoses and peptones.
b. Inflammatory fibrinous exudate contains two enzyms, one
of which (leucoprotase) is active in an alkaline medium and
the other in an acid medium. "These enzyms probably exert
their greatest activity in a neutral medium, slight changes in
reaction increasing digestion by the one, and suspending di-
Fig. 80. — Acute Pleurisy.
Engorged vessels.
gestion by the other." In suppuration the acid digesting enzym
probably disappears (Barker). A fibrinous exudate is one
that coagulates within the tissues or tissue spaces. The coagu-
lation of the exudate is identical with the coagulation of blood
and is probably due to the liberation of fibrin forming enzyms
from disintegrated leucocytes. Fibrinous exudate is the variety
observed in inflammation resulting from severe irritation. The
exudate usually contains many cells and a large amount of.
proteids.
c. Hemorrhagic exudates are those in which the red blood cells
as well as leucocytes and plasma have passed through the ves-
sel wall. This exudate coagulates the same as the fibrinous
INFLAMMATION. ISS
exudate. Intense irritants are usually the causative agents <>i
hemorrhagic inflammation. Croupous pneumonia is character-
ized by a hemorrhagic exudate.
A so-called purulent exudate has been described but pus is
not purely exudative for some of its constituents are not derived
from the blood. Pus is composed of altered leucocytes, tissue
shreds, and usually pyo-microorganisms, suspended in a fluid-liquor-
puris. Liquor puris is blood plasma and dissolved tissue. Pus
contains no fibrin, the proteid constituents being converted into
soluble compounds by cellular enzymes and bacterial ferments.
3. The following are probably the determining factors of the
quality and quantity of inflammatory exudate.
(7. Cause of inflammation: — Generally speaking a mild irritant
or injury produces a serous inflammation, and an intense ir-
ritant produces fibrinous inflammation. Mechanical injuries,
when there are no surface abrasions, produce an inflammation
of a mild degree and the exudate is limited m quantity and is
usually of a serous nature. Such injuries, however, usually
produce abrasions which favor the invasion of nncro organisms.
Thermal disturbances of mild degree, produce a serous ex-
udate, if more severe the exudate is extensive and of a fibrin-
ous or hemorrhagic character. The use of a thermo-cautery is
an excellent example of thermal production of inflammation and
the severity of its use demonstrates the intensity of inflamma-
tion and the variations of the exudate. An irritating chemical
substance injected into a tissue produces inflammation char-
acterized by excessive exudation especially of a serous fluid.
The more irritating the chemical, the greater the quantity of
exudate and the greater the percentage of proteids. External
application of chemical irritants produces inflammation char-
acterized by a serous or by a fibrinous exudate. This latter
mav be observed in the application of blistering agents. In-
fective inflammation is usuallv accompanied by a marked exu-
date from the beginning of the infection. The quantity and
quality of the exudate varies with the virulency of the organ-
ism. There are some exceptions however, e. g., tetanus infec-
tion causes a verv limited exudate regardless of the virulency
of the tetanus bacillus. In some infections, as malignant
oedema, the exudate is largely fluid. In suppuration the ex-
udate is almost entirely leucocytic.
b. Condition of the animal effected. The exudate is usually
limited in animals having normal vessels, heart action, and
blood. In those animals in which the vessels are diseased, and
especially if the endothelium has been injured there is a ten-
1S6
Veterinary i'ATHoLoGY.
I
dency to excessive exudation. A weak heart is conducive to
excessive exudation, e. g., inflammatory oedema. Animals pos-
sessing dilute blood (hydremia) are predisposed to excessive
fluid exudation. The leucocytic amoeboid movement may be tem-
porarily suspended, or it may be increased during inflamma-
tion, resulting in an absence or in an excessive number of
leucocytes in the exudate. In animals having a clean close
build the exudate is not so extensive as it is in those animals
of a loose flabby make-up.
c. The location and tissue affected. Exudation is in direct pro-
portion to the vascularity and density of the tissue. Inflam-
mation in compact bony tissue or beneath dense fascia, liga-
Fig. 81 — Acute Meningitis.
Exudate. b. Engorged vessels.
ments or tendons is accompanied by a limited exudate. In-
flammation of the cutaneous structure is usually associated
with excessive exudation, which accumulates in the subcutane-
ous areolar tissue. Inflammation of serous and mucous mem-
branes is accompanied with exudation which may in part be
discharged upon the surface but is usually accumulated in the
substructures.
4. Significance of the exudate. — The significance of the exu-
date has had various interpretations. Virchow considered that
the irritation producing the inflammation resulted in increased
cellular activity in the injured area and that the exudate sup-
plied increased nourishment to the area in which there was
an excessive metabolism. Others, have attributed to the exudate
the "flushing out" of the injured area thus mechanically carrying
INFLAMMATION.
157
away the irritant. The exudate dilutes the irritant, especially
chemical irritants, thus reducing- the activity of the causative
agent and mitigating the inflammatory process.
It has been determined that serum possesses some sub-
stances, as opsonins, antitoxins, bacteriolysins and bactericides,
that are detrimental to infectious agents either by their bacter-
icidal action or by chemical union with bacterial products. Thus
the exudate has a ten-
dency to reduce the ir-
ritation of infection by
rendering bacteria in-
active or less active,
or by neutralizing
their products. Phago-
cytes are very import-
ant factors in the exu-
date as they ingest and
destroy infectious mi-
cro-organisms.
In aseptic incised
wounds the exudate is
of value in cementing
the incised surfaces to-
gether, although new
tissue formation is re-
tarded by an exudate. The exudate mechanically protects the in-
jured surfaces in gaping wounds and possesses bactericidal proper-
ties for a short time after the injury has been inflicted. After
the exudate becomes inactive in its protecting properties it is a
favorable medium for infection and is then probably detrimental.
Injurious chemic substances may result from the aseptic
dissolution of an inflammatory exudate. Thus the exudate
that fills the air cells in croupous pneumonia may become putrefied
by the infection and activity of putrefying bacteria and the absorp-
tion of the putrid material would be detrimental to the animal
economy. The extent of which would depend upon the condition
of the animal body and the quantity of putrid material absorbed.
Fibrinous exudates may be injurious or beneficial depending
upon the location and the changes taking place in the exu-
date. The fibrinous exudate in croupous pneumonia is injuri-
ous because it coagulates in the alveoli of the lung thus pre-
venting the respiratory function of that area. The fibrinous
Fig. 82. — Inflammation. Gray Hepatization.
a. Air cell.s enydrged with leucocytes.
b. Hyperemia of capillaries.
15g
VEFERIXARY I>ATHOLOGY.
exudate in serous cavities is beneficial, especially in localized
inflammation, because it limits or circumscribes the inflamma-
tory irritant or process by coagulating thus producing adhe-
sions of the two serous membranes. Many horses upon which
paracentesis abdominis or paracentesis thoracis is performed
might succumb to generalized peritonitis or pleurisy if the
inflammatory process established at the point of the puncture
was not circumscribed by adhesions the result of organization
Fig. 83. — Fibrinous Pleurisj-, showing an extensive exudate upon surface,
of fibrinous exudate. The immediate efifect of a fibrinous exu-
date in a serous cavity is beneficial but the adhesions are fre-
quently permanent thus interfering with the normal function-
ing of the part afifected. The fibrinous exudate is also benefi-
cial in croupous enteritis because of the protection of the dis-
eased mucosa from mechanical injuries by food stufifs. It is
on the other hand injurious in croupous enteritis for the exu-
date is a favorable nidus for bacteria and they may produce
substances that are irritating to the injured mucosa. The
coagulated exudate may also hinder intestinal secretion. The
INFLAMMATION. 159
fibrinous exudate of diphtheritic inflammation is very injurious
because of its coagulation and pressure upon the tissues.
Inflammatory exudate is usually beneficial in inflamed areas until
opsonins, antibodies, and bacteriacidal substances become neutral-
ized or inert and the phagocytic cells impaired or destroyed, after
which the exudate is usually injurious as it is a mass of foreign
dead nitrogenous substances that serves as an excellent food for
various bacteria.
Chemotaxis. — It has been determined by experiment that
chemic substances exert a definite influence upon motile cells.
There is always a leucocytic migration into capillary glass tubes
previously charged with turpentine or croton oil and tlien in'^ert-
ed into living animal tissues. The same migration is obsCi-ved
when the capillary tubes are charged with bacteria or their
products. Negative results are obtained when the tubes are
charged with quinine or chloroform. This attraction of leuco-
cytes toward chemic substances is positive chemotaxis. The
repulsion of leucocytes from chemic substances is negative chem-
otaxis. The term "Chemotaxis" unmodified includes positive
and negative. Leucocytic migration into an inflammatory area
is a result of chemic influence or chemotaxis.
Phagocytosis. — This is the incorporation and destruction of
pathogenic bacteria and other foreign substances by phagocytes.
Phagocytes are cells having the power of ingesting and destroy-
ing microorganisms and other foreign particles. Polymorpho-
nuclear leucocytes having neutrophile granules are the most ac-
tive cells concerned in phagocytosis. Endothelial cells and wan-
dering connective tissue cells may under some conditions be
phagocytic. The phagocytic property of cells is variable depending
upon the virulency of the micro-organisms or strength of the
chemic substance and upon the resistance of the phagocyte. Bac-
teria are enveloped by protoplasmic extensions from the cell
body until they are entirely included in the aggressive phago-
cyte. After the enveloping process there may be observed diges-
tion vacuoles surrounding the bacteria. The included bacteria
are destroyed bv ferments produced by the phagocyte. It is an
intracellular digestion. The length of time necessary for the
phagocyte to destroy the bacteria is variable. The bacterial
destruction may be instantaneous or the bacteria may possess
sufficient vitality to destroy the phagocyte. There is consider-
able evidence that infection is frequently generalized in the ani-
mal body by leucocytes that have enveloped bacteria and wan-
dered to another portion of the body. The included bacteria
destroy the leucocyte and, thus liberated, establish a new ten-
ter of infection.
160
VETERINARY PATHOLOGY.
Phagocytosis is a very important factor in inflammation.
No doubt many localized inflammatory conditions are aborted
and the intensity of the attack of other infective inflamma-
tory conditions reduced by the process of phao^ocytosis. There
is a peculiar variation of phagocytosis occasionally observed,
e. g., leucocytes becoming phagocytic toward other leucocytes.
Fixed tissue cells may under some conditions become phago-
cytic towards leucocytes ; this perhaps is for the purpose of
obtaining nutrition for the fixed tissue cells.
The Signs of Inflam-
mation. — Inflamma-
mation may be recog-
nized in exposed tis-
sues by the so-called
"Cardinal signs :" red-
ness, swelling, increas-
ed temperature, pain
and impaired function.
These signs are usual-
ly perceptible in the
early stages of acute
inflammation, but they
may not be evident
throughout the entire
process. Mild, chronic
inflammation may not
be accompanied by any
of the above signs.
These signj> are very
variable in their acute or chronic inflammation of internal or-
gans.
Rcdticss ( Ru1)or ) is a constant sign in the early stages of
acute inflammation. It is the result of an excessive amount of
blood in the vessels of the affected area.
SiveHiiifj (Tumor) is characteristic of acute inflammation.
It is the result of the accumulation and retention of the inflam-
matory exudate plus the increased amount of blood in the part.
The extent of the swelling is in a direct ratio to the density of
the tissue. Thus the swelling resulting from subperiosteal in-
flammation may not be detected because of its limited extent.
On the other hand, the swelling succeeding inflammation of
loose areolar tissue may be very extensive, as in cellulitis. The
swelling resulting from inflammation is usually firm, dense and
quite resistant in contradistinction to swelling resulting from
Fig. 84. — Acute Myositis.
a. LeUfoo>'tis exudate. Musole fibres disinte-
grated and vessels engorged.
INFLAMMATION. 161
oedema, e. g., the tumefaction accompanying tendonitis is dense,
while the swelling accompanying "stocking" is soft and doughy.
TJie temperature (Calor) of tissue affected with active in-
flammation is invariably increased. This is the result of the
excessive cellular action in the inflamed area and the increased
amount of blood flowing into the part.
Pain (Dolor) is a common symptom of inflammation. This
may be the result of pressure upon nerve endings by the accu-
mulated exudate. However, oedema is accompanied by an ex-
cessive accumulation of fluid in the tissues, and oedematous
tissues are not hypersensitive. It seems more probable that in-
flammatory pain is the result of the injurious action of the chemic
irritants or soluble products of the exudate upon the sensory
nerve endings. The inflammatory pain is often referred to some
other part of the body, e. g., in pleurisy the pain frequently
appears abdominal.
luipuired function (Functio laeso) is a constant feature ob-
served in inflammation. In the beginning of the process the
function of the affected tissues (especially secretory) is in ex-
cess of the normal, but this is succeeded in the later stages by
depression of the function. The increased function is a result
of increased nourishment, increased stimulation, and probably
increased pressure is also a factor ; the depressed or diminished
function is the result of the injurious action of katabolic prod-
ucts, produced by excessive cellular action, and of the irritant
producing the inflammatory process. Thus, in the beginning
of acute nephritis there is an excessive amount of fluid (urine)
excreted, this is succeeded by diminution or complete suppres-
sion of the excretion (urine).
Effects upon the Tissue Involved. — As a result of
the inflammatory process the tissues involved may un-
dergo various changes. These changes may be degenerative,
necrotic, regenerative or proliferatii'e in character. Degenera-
tion usually precedes regeneration, but the two conditions may
be independent of each other; thus in ulceration, degeneration
and necrosis may alone be evident, and in the formation of a
tubercle of tuberculosis proliferation is the principal process.
Both conditions mav exist at the same time in different parts
of an affected area, degeneration taking place in the center of
the diseased area and regeneration or proliferation in the peri-
phery. Inflammation not accompanied by either degeneration
or regeneration is rare. The injuries or irritants establishing
inflammation may and frequently do produce death of some of
the tissue cells; necrotic tissue is sufficiently irritating to pro-
162
VETERINARY PATHOLOGY,
duce inflammation, and necrotic areas are usually surrounded
by an inflammatory zone. Inflanunation is confined to the
reactive process of the injured cells and should not be confused
with the death of the cells or necrosis.
Degeneration and regeneration are distinctly opposite pro-
cesses. The former is destructive, resulting in impairment and
death, while the latter is constructive, resulting in overgrowth
and proliferation. Degeneration is caused by insufficient food,
by the chemic action of certain poisons, or excessive and frequently
perverted functional activity. Regeneration occurs when there
is an adequate supply of nutrition, and depends upon the rever-
Fig. 85. — Chronic Pneumonia.
Alveolus. c. Wandering leucocytes.
Fibrous proliferation.
sion of the cells to the embryonic type or stimulation of the
reproductive properties of the cells, the latter usually at the
expense of the normal functional activity. Both processes affect
the cellular elements of the tissues, primarily and actively, and
the intercellular substances secondarily and passively. Some
exceptions will be mentioned later. The leucocytes and wander-
ing cells may also undergo changes similar to those which the
fixed tissue cells are subject. In general, degeneration character-
izes acute inflammation and regeneration characterizes chronic
inflammation. The importance of either of the above processes
depends upon their extent The general consideration of the two
processes has been combined for the sake of comparison ; but
they will now be considered separately.
Degeneration. — Practically all degenerations, to which tis-
INFLAMMATION. 163
sues in general arc subject, are common in inflamed tissues.
The following are the principal ones that have been described.
1. Parenchymatous degeneration (cloudy swelling), is the most
common type in acute inflammatory tissues. It is indeed rare
to examine sections of tissue afl:'ected with acute inflammation
and not find this degeneration. The presence of parenchymatous
degeneration is an additional factor frequently resorted to in diff-
erential diagnosis of inflammation. This type of degeneration
occurs in all tissues, but more especially in glandular structures.
2. Fatty degeneration does not occur as frequently as paren-
chymatous degeneration. Like parenchymatous degeneration,
it occurs in tissues afl^ected with acute inflammation. It in-
variably occurs in combination with parenchymatous degenera-
tion and is usuallv a sequel of the latter. The presence of fatty
degeneration in inflammatory tissue may cause confusion in
microscopic diagnosis, especially if the degeneration is exten-
sive. The degeneration is common in epithelium (glandular),
muscular tissue and connective tissue.
3. LIucoid degeneration is quite common in inflamed tissues.
It is characteristic of catarrhal inflammation. This degenera-
tion afifects the intercellular substance as well as the cells.
Mucus is bactericidal, therefore it is protectant and beneficial,
unless produced in sufficient quantity to induce mechanical in-
jury. Epithelium and connective tissue are most frequently
affected by this degeneration.
4. Serous degeneration, or more properly infiltration, is char-
acteristic of tissues affected with inflammatory oedema or other
inflammations in which there is excessive serous exudation.
This con.dition results from the passage into the cells of extra-
cellular serous fluid. The infiltrated fluid mechanically inter-
feres with the activity of the cell. It occurs most frequently
in muscular and connective tissue and occasionally in epi-
thelium.
5. Hyaline degeneration is of common occurrence in tissues
affected with chronic inflammation. It is the conversion of the
tissue into a clear, waxy substance. It is common in the mus-
cular tissue of blood vessels in chronic inflammator)^ foci as
well as in fibrous tissue resulting from proliferative inflamma-
tion.
6. Amvloid degeneration has been observed in chronic inflam-
matory tissues (Adami), although this is not a common sequel
of inflammation.
An intercellular degeneration specifically affecting the ce-
ment substances between the myocardial cells has frequently
164 VETERINARY PATHOLOGY.
been observed in myocarditis. This causes a separation of the
heart muscle cells, i. e., fragmentation, which seriously inter-
feres with their function. The striations of muscle cells fre-
quently disappear as a result of inflammation.
Necrosis (local death). — All degenerations produce impair-
ment of function and frequently end in necrosis of the afifected
cells. Destruction of tissue is a common result of inflammation
because of the various degenerations that accompany the in-
flammatory process. Suppuration is a type of inflammation and
is a liquifying necrosis. Necrosis of inflammatory tissue often
occurs independently of suppuration, though both conditions
result from the same cause. Destroyed tissue constitutes a fac-
tor in the future changes that occur in the affected tissue.
Superficial necrotic tissue is usually cast off. Ulceration is the
condition resulting from a continuous and sometimes a pro-
gressive cellular necrosis. An ulcer is a denuded surface result-
ing from continuous and sometimes a progressive cellular
necrosis.
Subsurface necrotic tissue may be disintegrated or dissolved,
and pass out of the affected area in the exudate or be carried
out by phagocytes ; necrotic tissue may become surrounded and
permeated by large numbers of leucocytes which liberate dis-
solving ferments, thus forming an abscess ; this liquefied necro-
tic mass may become inspissated, a condition termed caseation;
the necrotic tissue may become impregnated with calcium salts,
denominated calcification ; finally, the necrotic tissue may be-
come dissolved and encapsulated, thus forming a cyst.
Regeneration. — This process usually begins when degenera-
tion ceases, although it may be evident from the first. Cells
concerned in regeneration undergo a reversionary change, be-
coming similar to embryonic cells. Reproduction is an active,
vital property of embryonic cells, and this is ialso the principal
function of regenerating cells. The appearance of a tissue con-
taining an exudate with the succeeding degeneration has been
previously discussed. A concise comprehension of such tissue
is essential to a clear conception of the appearance of regenera-
tion in an inflammatory zone. Whether degenerated cells are
capable of regeneration depends upon the kind of cells and the
extent of the injury to them. Regeneration of tissues impaired
or destroyed bv acute inflammation consists in the enlargement
and proliferation of the contiguous uninjured cells. The exu-
date is usually diminished in quantity at this stage. Prolifera-
tion in tissues affected with chronic inflammation is, in reality,
a fibrous hyperplasia. Cirrhosis of any structure is usually the
INFLAMMATION.
165
result of chronic intiammation. The lowest types of tissues, i. e.,
those passive in function, are most easily and most frequently
regenerated, e. g., connective tissue. Surface epithelium is fre-
quently regenerated — muscular and nervous tissues are rarely
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'"■•• * '*.,, '"■> . ' ■ 4' - & ,, ' ,. ■f '•' " •«'
^ ■'. '..
Fig. 86. — Cliroiiic Hepatitis, showing intralobular fibrous formation, which results
in h.vpertropliic eirrhcsis.
regenerated. The age of the individual is an important factor in
the regeneration of injured tissues. Tissues in young animals
regenerate more readily than like tissues in old animals.
The origin or source of the cells that regenerate connective
tissue is still a disputed point. It is certain that fixed and wander-
ing connective tissue cells are capable of this function. Endothelial
cells are a type of fixed connective tissue cells which are active in
regeneration of connective tissue. IMononuclear leucocytes as well
as lymphocytes may be capable of producing connective tissue. The
regenerating connective tissue cells (fibroblasts) are either oval or
166 VETERINARY PATHOLOGY.
spindle snaped, the latter predominating, especially during the active
regeneration period.
Endothelial cells are active in the production of new vessels.
Inflammatory tissue is usually more vascular than normal tissue.
In the vascularization of an inflammatory area the endothelial cells
produce long protoplasmic projections. Several of these projec-
tions of different adjacent cells may fuse, thus forming an anasto-
motic channel, or a single projection may separate in a longitudinal
direction, thus producing an extension of the old channel. As the
protoplasmic projections become larger and longer there is an
activity in the cell nucleus indicative of mitosis, and cell division
soon follows. This process of protoplasmic projections and mitosis
continues as long as the inflammatory process is active. The irreg-
ular blood channels (capillaries) so formed become surrounded by
a layer of involuntary muscle tissues and yellow elastic tissue as a
result of extension of muscle fibres and connective tissue cells from
the adjacent vessel, the whole structure being surrounded by a
loosely arranged layer of white fibrous connective tissue. Thus the
capillary becomes an arteriole. These cells that are active in vas-
cularization are designated angioblasts. They are the progeny of
endothelium.
Inflammatory injuries to surface epithelium, as epidermis or
mucous membrane, are usually repaired by multiplication of the
cells bordering the injury.
Irregular masses of nucleated protoplasm have been observed
in myositis and may represent regenerating muscle cells.
Lesions. — The principal lesions of acute inflammation usually
consist of arterial hyperaemia, cloudy swelling of parenchymatous
cells and the presence of varying quantities of exudate. These
lesions are evidenced by redness due to an increased amount of
blood, by swelling or tumefaction of the part, and the loss of luster,
sheen or gloss of the tissue, the latter change occurs especiall}' in
inflamed serous membranes.
Chronic inflammation is characterized by a relatively mild hyper-
aemia and by an increased amount of fibrous tissue. The newly
formed fibrous tissue may or may not displace normal tissue.
Kinds or Types of Infllammation. — It is difficult to classify
inflammation because of the numerous variable factors that com-
pose it. The following classification is based upon etiology, exudate,
tissue involved, and time or severity of attack.
Etiology. — Etiology, inflammation may be classified as simple
and infective.
1. Simple inflammation is non-infective and results from me-
chanic, physic or chemic interference,
INFLAMMATION, 167
Fractures, sprains, bruises and surgical-procedure wounds are
types of mechanic inflammation.
As types of thermic inflammation, burns and frozen tissues may
be mentioned. Local inflammatory disturbances resulting from
lightning or contact with electric currents are types of electrically
established inflammation. The following may be mentioned as
chemic inflammations: formalin dermatitis, arsenical enteritis,
chlorine pneumonitis, turpentine nephritis, and those induced by the
bites of poisonous reptiles, scorpions, bees, wasps and ants; also
those caused by the products of bacteria and animal parasites. The
inflammatory processes established by mechanical interference may
and usually do become infected either by external contamination or
by the deposition of infectious agents from the blood or lymph.
2. Infective inflammation is of more frequent occurrence than
non-infective. It is the kind of inflammation that concerns the
practitioner, veterinary inspector and sanitarian because of its
tendency to become generalized in the infected animal, and is fre-
quently transmissible to other animals. All tissues are susceptible
to infective inflammation except hair, wool, feathers, and the
insensitive, nonvascular portions of the teeth, hoofs, claws and
horns. Infective inflammation may be either non-suppurative or
suppurative.
(a) Non-suppurative infective inflammation is typified in mal-
ignant oedema, blackleg, localized anthrax and the earlier stages of
tuberculosis and actinomycosis, and is characterized by the general
phenomena of inflammation previously discussed. Infective inflam-
mation may be nonsuppurative in the earlier stages and in the later
stages be complicated by typical suppuration, as in tuberculosis.
IMore rarely non-suppurative inflammation continues throughout the
entire process, as in blackleg.
(b) Suppurative infective inflammation or suppuration. — Sup-
puration is inflammation characterized by liquefying necrosis, and
may be surface or subsurface, circumscribed or dift'use. The
liquefied necrotic tissue produced by suppuration is pus. Pus is a
fluid, varying from a thin watery substance to a thick, sticky tena-
cious mass, and is usually alkaline in reaction. The color of pus is
determined by the infective agent, and it may be white, lemon
yellow, golden yellow, greenish yellow, green or black, and is fre-
quently tinted red with blood. Pus obtained from solipeds is usually
white or grayish white ; from cattle, creamy yellow ; from sheep,
greenish yellow, and from hogs, green or greenish yellow. Pus is
usually odorless, although it may undergo putrefaction with the
evolution of ill-smelling gases. Actinomycotic pus has a nutty odor
(Mayo). Pus may have a greasy, smooth, sticky or granular feel
16S
Veterinary pathology.
when rubbed between the fingers, depending upon its composition.
Histologically, pus is composed of pus cells, i. e., leucocytes (the
most of which are necrotic, though some of them may possess vital-
ity), shreds of necrotic tissue and tissue cells (the type of which
depends upon the tissue afifected). usually pyo-microorganism in
varying numbers (many of them being included in the pus cells)
and liquor puris (the plasma or fluid portion of the exudate and the
fluid resulting from the solvent action of the various ferments).
Animal microparasites are found in the pus resulting from their
activity. Practically all of the pus cells are derived from polymor-
phonuclear leucocytes, and are usually the neutrophile variety, there
being only an occasional .mononuclear leucocyte. Extensive nuclear
fragmentation and parenchymatous and fatty degeneration of the
cell protoplasm are evident in most pus cells, indicating that they
have undergone necrosis. Degeneration or necrosis are also present
in the fixed tissues of the suppurative areas. The pus found in acute
abscesses or discharging from granulating wounds is usually a
creamy fluid, yellowish in color. Sanious pus is a reddish fluid result-
ing from an admixture with blood. Ichorous pus is an acrid, corro-
sive fluid that excoriates the tissues it contacts. J\Iuco-pus and sero-
Fig. 87. — Drawing of a pus smear from a case of strangles, showing the organism
arranged in chains — the Streptococcus pyogenes equi.
INFLAMMATION. 169
pus are mixtures of mucous and pus, and of serum and pus,
respectively. Putrid pus is a thin, ill-smelling fluid, the result
of putrefaction.
Infection is the usual cause of suppuration. The following
is a brief description of the process. Pyogenic micro-organisms
gain entrance either by deposition upon or into a wound by
passing through the tissue or are carried and deposited by the
blood or lymph, and, finding conditions favorable, develop and
multiply. In their development, pyobacteria produce chemic
substances that are sufiiciently irritating to establish an active
hyperemia and also to exert a positive chemotactic influence,
the latter attracting at first mononuclear leucocytes and later
causing the migration of neutrophilic polymorphonuclear leuco-
cytes to the focus of infection. Alultiplication of the pyobac-
teria and leucocytic immigration continue. Phagocytosis be-
comes evident in leucocytes and some other cells, e. g., endo-
thelial cells. Liberated ferments, produced by the pyobacteria,
leucocytes and other cells, cause degeneration, necrosis and,
finally, solution of the tissue involved. Continued pyobacteria!
multiplication stimulates an increased leucocytic immigration,
and the tissues are thus densely packed with cells. There is a
marked accumulation of leucocytes around the suppurative focus
apparently attempting to circumscribe the affected area. Thus
the process continues, there being a progressive liquefying cen-
tral necrosis within and a marginal leucocytic accumulation
without. The condition is repeated until the resistant influences
of the animal body destroy the pyobacteria, or until the pyo-
bacteria have destroyed the involved tissue, or the entire ani-
mal. (Suppurative osteitis may occur subperiosteal or in the
osseous tissue proper. Leucocytes invade the lacunae and pro-
duce solution of the mineral matter, and thus the bone becomes
porous. If this process continues the bone ultimately liquefies ;
this is termed caries.)
Surface suppuration (purulent inflammation) is suppuration
of a surface tissue. Pas produced in surface suppuration con-
stitutes a purulent discharge, and a persistent purulent discharge
is termed pyorrhoea. Inflammation of a mucous membrane ac-
companied by a purulent discharge is purulent catarrh. In puru-
lent catarrh the surface epithelium is infiltrated with leucocytes
frequently to such an extent that the epithelial cells are disin-
tegrated, become loosened and exfoliate. The surface cells of
serous membranes and the skin are similarlv afifected in purulent
inflammation. In any purulent inflammation there is always
170
VETERINARY PATHOLOGY.
an engorgement of the subsurface vessels and the related areo-
lar tissue is infiltrated with inflammatory exudate.
Subsurface suppuration may be circumscribed or diffuse.
Suppurative centers become circumscribed first by a dense wall
of leucocytes and later by a fibrous capsule. The capsule is in
nearly all cases denser on the side next to the more important
tissue. Fibroblasts that form the circumscribing fibrous capsule
are probably the wandering connective tissue cells or their
progeny. The collection of pus in tissues, or lymph spaces, and
as considered bv some in body cavities, constitutes an abscess.
The circumscribed pus may, by solvent action of its ferments,
a. Normal kidney tubule.
88. — Suppurative Nepliritis.
b. Suppurative focus surrounded by kidney tissue.
dissolve or erode the limiting structure (cells or capsule), and be
liberated; the erosive action being in the direction of the least
resistance. In this way a surface discharge is effected. The
channel of exit of tlie pus may persist and become circumscribed
by a fibrous wall, thus forming a fistulous tract. If the pus
cavity is completely evacuated by surgical interference or other-
wise, and the cause removed, the surrounding tissue will, by
proliferation, fill the space previously occupied hv the pus. The
pus in an abscess may be absorbed and the destroyed tissue be
replaced by regeneration. If the capsule is exceedingly dense
the contained pus may become caseated and calcified.
Abscesses may be classified as superficial and deep ; primary
or metastatic (metastatic abscesses may or may not be embolic),
simple or multiple, subfascial and intermuscular. A hot abscess
INFLAMMATION. 171
results from rapid, active suppuration, as submaxillary abscesses
in strangles, while the so-called cold abscess results from a slow
suppurative process, as in tuberculosis. Accumulations of pus
in body cavities as the peritoneal, pleural, pericardial, synovial
and the facial sinuses constitute empyema. Vesicles may be-
come infiltrated with leucocytes, which become pus cells, and
thus the vesicle becomes a pustule.
Diffuse suppuration is not limited by any definite border line.
It is the result of agencies possessing sufficient strength or
virulency to continuously and progressively destroy and licpiefy
tissue or it occurs at a time when the resistance of the animal
or its tissues is so greatly diminished that there is inability to
successfully antagonize the causative agent. Purulent infiltra-
tion is the permeation of tissues with pus. Phlegmonous in-
flammation is the rapid and usually extensive infiltration of
tissues with leucocytes (pus cells), and occurs most frequently
in the subcutem and submucosa.
Exudate. — According to the nature of the exudate inflammation
tion may be classified as serous, fibrinous, and hemorrhagic.
The physical properties, chemic and histologic composition of
inflammatory exudate has been previously discussed.
(a) Serous inflammation is characterized by a serous exudate.
Inflammation of serous membranes and inflammatory disturb-
ances of other tissues than serous membranes, caused. by mild
irritation, may be of this type. Occasionallv serous inflamma-
tion is the result of intense irritation as in malignant oedema.
The terms serous inflammation and inflammation of serous
membranes should not be used interchangeably, because in-
flammation of serous membranes may be characterized bv
fibrinous or hemorrhagic exudate. A circumscribed accumula-
tion of inflammatory serous fluid (exudate) in the deeper lay-
ers of the epidermis or mucosa constitute a vesicle. Inflam-
matory oedema, a serous inflammation, is the condition result-
ing from the diffusion of an excessive amount of inflammatory
serous exudate into tissues as in cellulitis (inflammation of
sub-cutem).
(b) Fibrinous inflammation designates that type of inflammatory
disturbances in which there is produced a coagulable exudate.
The exudate may coagulate within the tissues or upon the tis-
sue surface. Croupous inflammation is the term applied to the
condition resulting from the coagulation of the exudate upon a
tissue surface. Diphtheritic inflammation is the condition pro-
duced by coagulation of the exudate within the tissue- and
upon its surface. Croupous inflammation and diphtheritic in
172 VETERINARY PATHOLOGV.
flammation are not distinctly separable although the former is
usually milder than the latter. Typical croupous exudate may
be detached without serious injury to the surface tissue but
the diphtheritic exudate cannot be removed without detaching
or extensively lacerating the surface tissue. Croupous pneu-
monia and croupous enteritis are examples of croupous inflam-
mation, the former being the most frequent type of pneumonia
in horses and the latter occurring occasionally in cattle. Roup
or avian diphtheria, and diphtheritic stomatitis and enteritis are
examples of diphtheritic inflammation, the former being com-
mon in fowls the latter in pigs. Fibrinous exudate may be
present in inflammation of serous membranes, constituting
fibrinous pleurisy, peritonitis, etc.
(c) Hemorrhagic inflammation is significant of the action of
an extreme irritant. Hemorrhagic exudate coagulates, especially
upon surfaces, though it may coagulate within a tissue. Inflam-
mation of tissues in which the blood vessels are of meager struc-
trure (capillaries), and hence easily permeated or ruptured, is fre-
quently of this type. Croupous pneumonia is a hemorrhagic in-
flammation. Nephritis and hepatitis are frequently accom-
panied by a hemorrhagic exudate.
(Mucus and pus have been described as inflammatory exu-
dates by some and as inflammatory products by others.) They
Fig. 89.— Hemorrhagic Exudate (Red Hepatization.)
INFLAMMATION. 173'
are not inflammiatory exudates. Inflammation of mucous mem-
branes in which there is an excessive production of mucus is
catarrh or catarrhal inflammation. (Suppuration is inflammation
accompanied by the formation of pus and may be surface or sub-
surface. Purulent inflammation is surface suppuration.)
Tissue. — Histologically a gland or organ is composed of
parenchymatous and interstitial tissue. Parenchymatous tissue
is the essential or functioning portion of a structure, as hepatic
cells. Interstitial tissue or stroma is the supporting framework
of an organ or part as the stroma of a lymph node. The pro-
cess of inflammation may occur in either the parenchyma or
stroma. Classifying upon the basis of tissue affected then, there
are the two forms, namely, parenchymatous and interstitial in-
flammation.
(a) Parenchymatous inflammation is usually the result of
severe, active irritation, the interstitial type results from the
long, continued action of mild arritants. The tw^o types may be
present simultaneously in the same structure or they may occur
independently.
(b) Interstitial inflammation is often the sequence of paren-
chymatous, although it may be the initial process. Inflammation
of the hepatic cells is parenchymatous hepatitis, of the hepatic
interlobular tissue, interstitial hepatitis, etc.
Time, Activity and Results of the Process. — It is questionable
if the length of time an inflammatory process continues should
constitute a factor in its classification. By common usage, inflam-
mation would be classified according to the time basis, as acute
and chronic. Formerly this classification was based upon the
time element alone, but the duration of inflammation is so vari-
able that it is now recognized as an insignificant factor. The
activity and results of the process are the basic essentials relied
upon in differentiating acute and chronic inflammation.
(a) Acute inflammation is characterized by a sudden onset, by
a vigorous action and by production of retrogressive changes in
or destruction to the tissue affected.
(b) Chronic inflammation is characterized usually by an
insiduous onset, by a mild action, and by resutling in prolifera-
tion of tissue. The proliferated tissue may induce retrogressive
changes, as atrophy, but this is only an indirect result of the pro-
cess.
Either acute or chronic inflammation may occur throughout
the entire reaction or they may both prevail at the same time in
different parts of the same structure. The causative agents .may
become less active as the process continues, thus acute inflam-
174 VETERINARY PATHOLOGY,
mation is often succeeded by chronic inflammation. Injuries of
tendons are usually accompanied by acute inflammation, but
this usually subsides early and is succeeded by chronic inflam-
mation. Chronic inflammation may be succeeded by acute in-
flammation provided that the irritating factor be sufficiently in-
creased or the resistance of the animal diminished.
Miscellaneous. — a. Catarrhal inflammation is inflammation of a
mucous membrane, accompanied by an excessive production and
discharge of mucus.
b. Purulent inflammation is characterized by the production
of pus. This term is confined, by some, to surface suppuration.
c. Ulcerative inflammation is one in which there is erosion
of surfaces, i. e., the production of ulcers.
d. Vesicular inflammation is one characterized by the pres-
ence of vesicles.
e. Pustular inflammation is one characterized by the pres-
ence of pustules.
f. Proliferative inflammation is practically the same as
chronic inflammation. It signifies the production of new tissue.
g. Specific inflammation is one resulting from a specific in-
fection, as glanders.
Termination. — The tendency of the reaction produced by
an injury is always favorable, but the reaction may be so sud-
den and extensive or continued so long that its results may
be harmful. The termination of inflammation depends upon the
extent, intensity, and duration of the irritant and the resistance
of the tissues. Inflammation may terminate in resolution, tissue
proliferation or dissolution.
Resolution embraces the processes of repair and these may
be summarized as follows:
a. Removal of the cause.
b. Re-establishment of circulation. This may be accom-
plished in a few hours or perhaps not for several days depend-
ing upon the extent of the injury and the kind of tissue injured.
c. Restoration of vessels to their normal condition. The
length of time required for restoration and the completeness of
the process depends upon the severity of the injury and the re-
establishment of the circulation.
d. Removal of the inflammatorv exudate. The time re-
quired to remove the exudate depends upon its nature. Serous
exudates are usually removed by resorption, i. e., by the lymph
channels. Fibrinous and hemorrhagic exudates are usually dis-
solved and absorbed, or they may be carried away by phagocy-
INFLAMMATION. 175
tes. Exudates may in part be consumed as nutrition by local
cells.
e. Disposal of necrotic tissue. Necrotic tissue is disposed of
by sloughing, absorption, phagocytosis, or sequestration. Small
areas of necrotic tissue are usually promptly absorbed or dis-
posed of by phagocytic action. Considerable time is usually re-
quired in disposing of large areas or masses of necrotic tissue,
unless it is superficially located and separates from the surround-
ing tissue and sloughs. Subsurface necrotic tissue may be gradu-
ally liquefied and absorbed, discharged through a fistulous tract
(submaxillary abscess of Strangles), collected and carried out
by phagocytes, encapsulated, or sequestrated, and remain per-
manently in the tissue. Encapsulated necrotic tissue may be-
come infiltrated with calcium salts.
f. Regeneration of degenerated tissue and replacement of
necrotic tissue. The regeneration of degenerated tissue consists
in replacing the injured or destroyed cell protoplasm by normal
protoplasm. If only a fe\y cells are destroyed the adjacent cells
reproduce and thus renewal is usually rapid. Connectiye tissue
cells and surface epithelium are easily and efficientl}^ regenerated,
but cardiac muscle, ganglionic nerve and cartilage cells are
rarely perfectly regenerated. Large areas of necrotic tissue are
usually substituted by fibrous tissue. This proliferated tissue is
termed granulation tissue in the beginning and cicatricial tissue
after it has become dense and more or less contracted. Granu-
lation tissue consists of capillary loops surrounded by masses
of cells. These cells are largely fibroblasts and produce fibro-
connective tissue. After the fibro-connectiye tissue has been
formed it contracts, thus becoming cicatricial tissue. Cicatriza-
tion is of yalue in closing gaping wounds, but is injurious when
it occurs in internal organs as the liyer, because the pressure
produces atrophy and obstructs circulation. The capsule sur-
rounding pus cayities, after the purulent fluid has been evacuated,
becomes a granulating membrane which soon fills the gap with
fibrous connective tissue. Exuberant granulation results from
excessive multiplication of cells, undue extension of capillary
loops, and failure of contraction of the fibrous tissue.
Tissue Proliferation. — The tissue proliferated in inflammatory
resolution takes the place of tissues that pre-existed and had be-
come necrotic, while that occurring in inflammation resulting
from long continued mild irritation is not a substitution but an
addition to the tissue already existing. In this latter phase
tissue proliferation may begin in a very short time after the. in-
flammation is established or it may not appear for two, three,
176 VETERINARY PATHOLOGY.
or several days. Fibro-connective tissue is invariably the pro-
duct of tissue proliferation. Fibro-connective tissue prolifera-
tion is closely associated with chronic inflammation, in fact it is
almost inseparable from it. The proliferated tissue appears first
in the frame-work of the tissue involved and may later extend
into the parenchymatous tissue. If the proliferated tissue is
excessive it may, by pressure, produce atrophy of the parenchy-
matous tissue. Cicatrization of the proliferated tissue causes an
irregular lobulation and constriction of the involved organ, as
in cirrhosis of the kidney. Strictures of hollow organs are pro-
duced in the same way. Adhesions of serous membranes are
produced by fibrous tissue formed during inflammation.
Dissolution or destruction is a result of intense irritation.
Necrosis of tissue is frequently a sequence of inflammation. A
single cell or only a few cells may be destroyed or large areas
of tissue may undergo necrosis. Ulceration results from con-
stant cellular necrosis. Circulation may be obstructed by an
inflammatory exudate and cause necrosis in large masses of
tissue. It may terminate fatally, in partial recovery, or in reso-
lution, depending upon the importance of the tissue involved in
the affected animal.
Conclusion. — Inflammation is the reaction of a living tissue
to an irritant.
Inflammation is a complex process, the result of many fac-
tors.
It is not always a result of infection.
It is an adaptive, reparative and protective process.
It may produce sufficient reaction to cause destruction of
the portion involved and occasionally of the entire organism.
CHAPTER VII.
PROGRESSIVE TISSUE CHANGES.
REGENERATION.
DEFINITION.
EXTENT — Depends upon age and tissue involved.
Blood.
Connective tissue.
Fibrous.
White.
Vellozv.
Cartilage — Rarely regenerated perfectly.
Bone.
Epithelium.
Surface — Complete and perfect.
Glandular — Irregular and incomplete.
Muscle — Perfect regeneration rare.
Nerve — Cells do not regenerate, fibres do.
Regeneration is the process by means of which destroyed
tissues are replaced. Tissue destruction is the result of necro-
sis, primarily, and inflammation and degeneration, secondarily.
Regeneration is accomplished by multiplication of pre-existing
adjacent cells or by invasion and multiplication of wandering
connective tissue cells. The proliferating cells assume the-charac-
teristics of embryonal cells, that is, their reproductive property
is over-developed and their other vital functions depressed. The
power of regeneration of a tissue is inversely proportional to its
specialization. Regeneration of the tissues of the less complex
animals is more nearly perfect than that of the tissues of highly
organized animals ; thus invertebrates regenerate entire organs
or parts. Spallanzani cut off the legs and tail of a salamander
and observed in the course of three months six crops of these
members. In the entire three months 687 perfect bones were re-
produced and the regeneration was perfect regardless of the
point of amputation. The tissues of young growing animals are
more easily regenerated than those of mature animals. Single
cells or small areas of tissue are more perfectlv regenerated than
large areas. In some cases destroyed tissues are not regenerated
but are replaced by fibrous tissue. The functions of some de-
stroyed tissues and organs may be performed by other struc-
tures. Thus, if the tibia of a dog is destroyed, the fibula in-
creases in size and assumes its function. Destruction of one
kidney is succeeded by a compensatory hypertrophy of the other
l?7
178
VETERINARY PATHOLOGY,
kidney. The law of specificity, i. e.. cells beget like cells, is
the same in regeneration and in physiologic processes. Regen-
eration is the outcome of the unhindered multiplication of cells.
Blood is continually regenerated during the natural life of an
animal. The normal maintenance of blood is a physiologic pro-
cess, but regeneration of blood or some of its constituents may,
under certain conditions, be abnormal, as in leukemia. Leuco-
cytes are produced in lymphoid tissue of the lymph nodes, spleen
and bone marrow, and it is possible that they may multiply in
the tissue spaces. Erythrocytes probably have their origin in the
red marrow of bones in adult animals. The red blood corpuscles
are nucleated in the beginning but the nucleus vanishes by so-
lution or extrusion before the cells reach the general circulation
except in case of severe hemorrhage or other conditions in
which there has been rapid, extensive loss or destruction of
blood.
Blood vessels are usually the first tissue regenerated in the
repair of wounds. Blood vessels are formed in the embryo by
canalization of large mesodermal cells, many of which fuse, thus
forming; continuous canals that later become blood vessels. This
Fig. 90. — Vasrular Regeneration, showing v-ascular buds.
type of vascular formation is not common in repair of injured
.vessels or regeneration of destroyed vessels. The usual manner
of vascular regeneration is by the growth and development of
endothelial buds from adjacent vessels. These buds are solid,
conical processes which extend outward from the capillary en-
dothelium. The buds or processes increase in size and become
hollow at their base, the cavity being thus continuous with the
'umen of the pre-existing vessel. As the buds increase in size
PROGRESSIVE TISSUE CHANGES.
179
there is an increase in the number of cells composing them.
Union or fusion of buds or processes from different vessels re-
sults in anastomosis or inosculation. These processes are thus
the forerunners of capillaries and by a dilatation and an increase
in the thickness of their walls due to formation of fibrous and
muscular tissue, arteries and veins are formed. The new vessels
produced in the repair of an injury are invariably in excess of
the normal vascular recjuirements of the part. The excess ves-
sels in an injured area are obliterated by cicatrization.
Connective tissue is usually completely regenerated. Con-
nective tissue is regenerated from pre-existing connective tissue
cells, wandering cells and endothelial cells.
Mucoid connective tissue is not normally found in the adult
animal except in a modified form in the vitreous chamber of the
eye. Mucoid tissue is not regenerated, although it is possible
that other types of regenerated connective tissue are mucoid in
the beginning.
Fibrous comicctivc tissue is rapidly and completely regen-
erated. White fibrous connective tissue is frequently substi-
tuted for other tissues. The fibres in regenerated fibrous con-
Fig. 91. — Fibrous Regeneration.
nective tissue have the same origin as those in normal fibrous
tissue. Regeneration of white fibrous tissue may be studied in
the union of the ends of a tendon after tenotomy. The space
between the ends of the tendon is filled with blood and lymph
which escaped from the severed vessels. The pre-existing con-
nective tissue cells bordering the wound in the tendon, together
with wandering cells, begin proliferating within forty-eight
hours, their progeny being fibroblasts. The fibroblasts produce
a tangled mass of fibrous connective tissue, and at the same time
there is vascularization of the extravasate which occupies the
space between the severed ends of the tendon. After the ends
180 VETERINARY PATHOLOGY. "^
of the tendon are firmly united by the mass of newly formed
fibrous tissue the extravasate and the fibres, excepting those ex-
tending in a longitudinal direction, are absorbed. Finally the
repair is so complete that the defect is not visible to the unaided
eye and is difficult to detect microscopically. Scars are bands,
sheets or masses of white fibrous tissue and indicate imperfect
regeneration, the fibrous tissue in scars being largely a substitu-
tion tissue.
YcUow clastic tissue is not as perfectly regenerated as white
fibrous tissue. White fibrous tissue usually is substituted for
yellow elastic tissue when the latter has been destroyed.
Regeneration of cartilage is very imperfect probably because
of its irregular supply of nourishment. Destroyed cartilage is
usually replaced by fibrous tissue. In some instances injuries
to cartilage are succeeded by excessive cartilaginous prolifera-
tion. A case was observed in which the arytenoid cartilage was
severed in an operation to relieve roaring; six months later there
had developed at the point of operation a cartilaginous mass as
large as a goose Qgg- Perfect regeneration of cartilage does
occur, although it is rare. Regenerating cartilage cells are de-
rived from the inner portion of the perichondrium. Fibrous
tissue formation usuallv precedes the regeneration of cartilage,
althr-'t^gh it may be formed from the beginning.
Osseous tissue is usually perfectly regenerated . The cells
that produce osseous tissue are called osteoblasts. Osteoblasts
are usually derived from the osteogenetic layer of the perios-
teum, although they may have their origin from undifferentiated
connective tissue cells. The formation of osseous tissue is usu-
ally preceded by mucoid, fibrous or cartilaginous tissue. The
various stages of osseous regeneration are very similar to those
of normal bone formation. Osseous regeneration may be illus-
trated by the imion of a fracture as follows: Blood and lymph
vessels are ruptured when the fracture is produced. Blood and
lymph escapes into the surrounding tissues and the interstice
between the two ends of the fractured bone. The injury pro-
duces necrosis and establishes inflammation. Vascularization of
the injured area initiates the process, after which there is solu-
tion of the extravasate, exudate and necrotic tissue. Osteo-
blasts accompany the newly formed vessels and produce irregu-
lar masses of fibrous tissue which later calcify. The calcareous
tissue is infiltrated with osteoclasts derived from the blood which
dissolve out regular canals in the regeneration of long bones,
and irregular cavities in the regeneration of flat or irregular
bones. Osteoblasts appear in the canals ^nd cavities, formed
PROGRESSIVE TISSUE CHANGES. 181
by the osteoclasts, and produce fibrous lamellae which are later
calcified. This process continues until the canals or cavities are
filled with lamellae excepting a small central cavity which con-
tains blood vessels, thus Haversian systems are frequently com-
pletely regenerated. Excess of osseous tissue formed over and
around bones at the line of fracture (provisional callous), is
usually later reabsorbed.
Adipose tissue is not a tyjiical primary tissue. It is derived
from the undifferentiated connective tissue cells by the conver-
sion of their protoplasm into fat. Adipose tissue is consumed
when the food supply is deficient, and the cells become typical
connective tissue cells or are destroyed. Adipose tissue is also
formed when the food supply exceeds the demand as a result of
production and accumulation of fat in the connective tissue cells.
Dentine is not replaced except in some of the lower animals.
Epithelium of surfaces is constantly destroyed and regen-
erated. The outgrowth and shedding of the superficial epi-
dermal cells is a physiologic process. Epithelization of small
abrasions of the epidermis and mucous membranes is rapid and
complete, the regenerating cells having their origin from the
epithelium bordering the injury. If the denuded surface is large
regeneration may proceed from the cells of the sweat glands
of the skin, or mucous glands of mucous membranes as well as
the epithelium bordering the injury.
Squamous epithclinni is more completely regenerated than
columnar. Constant destruction of columnar cells may cause
the production of short columnar cells and finally squamous
cells. This, however, is rare, as the law of specifi.city is practi-
cally without exception. Glandular epithelium of large glands as
the kidney liver pancreas and salivary glands is not regenerated
as perfectly as surface epithelium. The eoithelium of sweat
glands, oil glands, mucous glands, gastric glands, Brunner's
glands, crypts of Lieberkuhn and uterine glands, is generally
quite perfectly regenerated even after destruction of practically
all of the glandular epithelium. Any of the latter will regener-
ate from small islands of cells either in the duct or body
of the gland. The epithelium of the mammary gland in
creases in amount during lactation and diminishes when lacta-
tion ceases. By observation it has been determined that mam-
mary epithelium regenerates after it has been destroyed bv ab-
scess formation or other destructive processes, provided newly
formed fibrous tissue is not substituted. By analogy it might
be supposed that the destroyed epithelium of salivary glands
18f VETERINARY PATHOLOGY.
and of the pancreas may be regenerated, but this has not been
clinically or experimentally demonstrated. The liyer is a tul)U-
lar gland and regeneration of a single cell or a few cells is not
uncommon, but large areas of liver tissue are probably never
regenerated, although some pathologists claim that they have
observed the regeneration of the major portion of a liver lobe
in the dog, cat and rabl)it. Kidney cells, especially of the tubules,
are constantly regenerated, although the regeneration of an
entire tubule has never been observed. The testicular and ovar-
ian tissues are probably never regenerated except m the physio-
logic maintainance of spermatogenesis and oogenesis.
Muscular tissue is imperfectly regenerated. Injuries of invol-
untary muscular tissue are usually repaired by the substitution
of fibrous tissue which may later be replaced bv involuntary mus-
cular tissue, the latter l)eing derived from the adjacent muscle
cells. Two or three days after an injury to a voluntary muscle
fibre, the nuclei near the injury divide and a multinucleated
protoplasmic mass is formed on the damaged fibre. These pro
toplasmic masses extend into the substituted fibrous tissue and
may split longtitudinally into regular fibres but more frequently
they die and disintegrate. Destroyed heart muscle cells are
invariably replaced by fibrous tissue.
Nerve cells are not regenerated, at least in adult animals,
although their processes, axones and dendrites, are regenerated in
peripheral nerves. After a nerve fibre is injured the axone
degenerates to the distal end and to the first or second node of
Ranvier proximally. A few days after the injury the axone, if
its continuity has not been destroyed, begins to elongate, ex-
tending peripherally, in the direction of least resistance, which
is in the old sheath. If the axone extends in the original sheath
the tissue deprived of its nerve supply may become perfectly
innervated. The rate of growth of an axone has been variously
estimated at from .1 nun. to 1mm. in twenty-four hours. Foot
lameness in horses that has been completely relieved by meta-
carpal and metatarsal neurectomies, sometimes reappear, in
from eighteen months to three years after the operation, thus
indicating that there has been reinnervation. If the proliferating
axone does not continue in the original nerve sheath it may
become entangled and coiled up in the scar tissue, of the wound,
thus producing sensitive scars and amputation neuromata.
TRANSPLANTATION AND GRAFTING.
Transplantation is the process of partial severing a piece of
tissue from its connection and moving it so that it occupies a
new position. Such transplantation usually grows and this
PROGRESSIVE TISSUE CHANGES. l83
method is resorted to in the surgical rehef of wounds and in plas-
tic operations.
Grafting is the process in which a piece of tissue is removed
and transferred to some other part of the body or a piece of tissue
may be obtained from one individual and grafted into another.
Grafts are not as likely to grow as are transplantations, how-
ever, it has been found that grafts of the same kind of tissue in
the same individual, if properly placed, usually take and grow
and become a part of the individual. In some instances the
graft is rapidly absorbed, while in still other instances the graft
persists for a while, ultimately dies but has served the purpose
for some little time.
Grafting is much more successful in the lower animals,
although it has reached rather a high state of efficiency in the
higher animals, even the body of man. The success of a graft
depends somewhat upon its size and upon the length of time that
the graft has been kept out of the tissue.
Alexis Carrell perfected a method of patching an abdom-
inal vessel with a flap of peritoneum, subperitoneal tissue and vol-
untary muscle, and by a series of experiments has demonstrated
that an artery can regenerate itself by using heterogeneous
anatomical elements. The regeneration was so perfect that in
less than two years after the operation on the aorta it was nor-
mal, although the wall was composed of tissue dififerent than the
normal but the shape and lumen had not been changed. '
184 VETERINARY PATHOLOGY.
WOUND HEALING.
DEFINITION.
CLASSIFICATION.
Etiology.
Traumatic.
Thermic.
Clicniic.
Location.
Surface.
Subsurface, {Cephalic, cervical, thoracic, etc.)
Character.
Incised.
Punctured.
Lacerated.
Contused.
Stab.
Gun shot.
Bites.
Condition.
Aseptic.
Septic.
HEALING.
Primary union. (First Intention.)
Hemorrhage arrested.
Appro.vimation of zi'ound margins.
Adhesion of ivonnd lips zcith c.rndate.
Multiplication of related cell:.
I 'ascitlarization.
Epithelicalion.
Cicatrication.
Substitution.
Secondary union, (Second Intention.)
Hemorrhage arrested.
Immigration of leucocytes to wound margins.
Infection.
Suppuration.
Granulation.
Cicatrication.
Epithelization.
Substitution.
The reo^eneration of the individual tissues has been discussed.
The simultaneous regeneration of the tissue-complex of an area
in which there has been previous tissue destruction constitutes
wound healing. A wound is the result of sudden interruption of
the continuity of tissue or tissues. Some have restricted the
term 'wound' to those conditions resulting from traumatisms ;
others confine it to injuries of soft tissue, and again some main-
tain that wounds occur onlv upon a surface. There is no good
reason for restricting the term, because both thermic and
chemic influences produce tissue destruction not distinguish-
able from wounds mechanically inflicted. A fracture is a break
in the continuity of osseous tissue and is repaired in the same
way as wounds of soft tissue. Rupture of the liver or spleen is
PROGRESSIVE TISSUE CHANGES. 185
characterized by tissue destruction and regeneration, the entire
process being identical with that in surface wounds. Wounds
result from sudden and violent action. Thus ulcers or necrotic
tubercular centers are not wounds. A bruise may or may not be a
wound, depending upon the nature of the lesion, i. e., whether or
not the interruption of tissue has been affected.
Wounds may be classified as to cause, location, character, and
condition.
1. Etiologically wounds may be traumatic, thermic or chemic.
2. According to location wounds may be, surface or subsur-
face, abdominal, cervical, thoracic, etc.
3. As to their character, wounds may be incised, punctured,
lacerated, contused, stab, shot, or bullet and from bites.
4. Wounds may be noninfectious and infectious.
Traumatic wounds usually heal more readily than wounds re-
sulting from thermic or chemic causes because traumatisms arc
caused by mechanical force only and the destructive influence
ceases immediately upon removal of the cause ; whereas the in-
fluence of thermic and especially chemic causes are more lasting
as their action continues after the wound has been produced.
Cell reproduction is probably the result of physiologic auxetics as
kreatin, globulin, and xanthin, which stimulates cell multiplication.
In persistent ulcers cell proliferation succeeds the local application
of a solution of 5 parts globulin and 2 parts kreatin. The more
rapid healing of an ulcer succeeding scarification is probably
because of auxetics liberated from cells destroyed by the
curette.
Wound healing n^ay be of one of two types, healing by pri-
mary union (first intention), and healing by granulation (sec-
ond intention or secondary union). These two modes of heal-
ing differ only in the extent of tissue reaction. Other methods of
healing have been described as immediate union, healing by third
intention, and healing under a scab. Immediate union, signifies
union of parts of a cell or the cut ends of fibres, etc., and is now-
thought to be impossible ; healing under a scab and healing by
third intention are properly discussed under the caption of prim-
ary union or granuation.
Healing by Priimiry Union. — This is the most desirable
method of wound healing and is usually obtained in veterinary
practice only in surgical wounds and recently inflicted, clean cut
wounds. This mode of healing is of short duration and is ac-
186 VETERINARY PATHOLOGY.
companied by little if anv infection and limited inflammation.
Healing by primary union takes place only in clean cut wounds,
i. e., when the tissues are smoothly and evenly divided and in
which hemorrhage is limited and easily controlled. After hem-
orrhage ceases or has been arrested the extravasate coagulates
thus agglutinating and drawing the wound margins together.
If the incised surfaces or severed tissues be approximated by
surgical procedure the coagulated extravasate and exudate as-
sists in maintaining them in that position. In surface wounds
varying quantities of serum and lymph discharge and coagulate
upon the surface thus forming a scab. An injury producing
a wound and the extravasate are sufficiently irritating to es--
tablish hyperemia and in some cases slight inflammation ac-
companied by a serous exudation and a leucocytic immigration.
The hemorrhagic extravasate is graduall)- disintegrated and re-
moved by phagocytes and at the same time, there is enlarge-
ment and extension by multiplication of the marginal tissue
cells of the wound into the coagulum which serves as a support
for the regenerating tissue.
Vascularization accompanied by fibrous formation initiates
the process of regeneration in the healing of a wound
by primary union. Vascularization is usually limited because
of the small size of the wounds. The newly formed vessels
are capillaries and supply the regenerating tissue. Fibrous
tissue is produced in sufficient quantities to replace all tissues
destroyed.
Disintegration of the coagulum and regeneration of new tis-
sue thus proceed until the newly formed tissue has entirely re-
placed the extravasate. The scab which is hemorrhagic extravas-
ate and inflammatory exudate is firmly held upon the wound
surface by fibrils continuous with the subsurface coagulated ex-
travasate and exudate and as the latter is absorbed the scab grad-
ually becomes loosened and finally drops off leaving a shining
surface. The regenerated tissue formed in the extravasate is
embryonic fibrous tissue the amount of wdiich depends upon the
quantity of coagulum. Upon the embryonic tissue thus formed,
in surface wounds, epithelization is usually rapid and complete.
The scar appears pale pink and is tender until cicatrization takes
place and then appears white, dense, firm and hard. Whether
the fibrous tissue produced in wound healing is substituted later
by the normal tissues of the part involved depends upon the gen-
erative power of the tissues destroyed.
PROGRESSIVE TISSUE CHANGES.
187
To recapitulate, healing by primary union embraces, coagula-
tion of the hemorrhagic extravasate, agglutination of the wound
margins, hyperemia, inflammation, vascularization, fibrous form-
ation, disintegration of the hemorrhagic extravasate and in-
flammatory exudate, cicatrization, epithelization and substitu-
tion.
Fig. 92. — Wound Healing- by first intention.
a. Fibrinous exudate with proliferation of vessels. c.
b. Regeneration of epithelium. d.
Bottom of wound.
Leucocytes.
Healing by granulation. — This is the usual mode of wound
healing in domestic animals. It dififers from the healing by
primary union in that there is invariably infection and suppur-
ative inflammation, degeneration and necrosis preceding regen-
eration. This mode of healing takes place in irregular wounds
having lacerated margins and in which there is considerable de-
struction of tissue and extensive hemorrhage and in wounds
the margins of which are not approximated. The extravasated
blood may coagulate in the wound, especially in subsurface
wounds, and also in surface wounds in which the margins are
188
VETERINARY PATHOLOGY,
approximated and retained by mechanical means, such as su-
tures, adhesive tape, etc. In lacerated or gaping surface
wounds, as wire cuts, the coagulum becomes detached and
drops out leaving the wound margins covered by a thin layer
of coagulated serum. Within a short time after the injury is
inflicted there is extensive leucocytic immigration into the tis-
sues bordering the wound. The infective micro-organisms cause
destruction and solution of the marginal cells until the tissue re-
sistance or local immunity checks their activity. Upon the ex-
posed wound surfaces there appears velvet like projections
(granulations), which are capillary loops regenerated from ad-
jacent vessels.
Kxiiberant Graiuilation, resulting from wire cut.
Between and intermingled with the granulations, regenera-
tion of connective tissue takes place. Constant exposure of the
PROGRESSIVE TISSUE CHANGES. 189
wound insures continued infection which retards tlie j^ranula-
tiou more or less, depending upon the extent of the infection,
the degree of activity of the micro-organisms and the resistance
of the tissue. The destroyed tissue in the wound is ultimately
replaced with granulation tissue and, if the wound is upon the
surface, epithelization proceeds as in healing by primary union.
The embryonic granulating connective tissue contracts i. e.,
cicatrizes about the time that epithelization occurs. Cicatriza-
tion constricts and obstructs the capillary vessels, that are in
excess of the normal, thus diminishing the blood supply. If ci-
catrization does not occur new capillary loops (granulations)
are rapidly extended producing a fungoid bloody growth, called
excessive or exuberant granulation (proud flesh).
The efficient regeneration and substitution of the destroyed
tissues in wounds that heal by granulation is possible only in
very young animals and in tissues not highly organized.
To recapitulate, healing by second intention embraces sup-
puration, granulation, cicatrization, epithelization and substi-
tution.
In some individuals the formation of fibrous connective tis-
sue is continuous and there is formed large masses of cicatrical
tissue known as keloids. Keloids are classified with neoplasms
by some authors.
HYPERTROPHY.
ETIOLOGY.
Inherited.
Antenatal.
Unequal pressure..
Amniotic adhesions.
Post-natal.
Increased )iittrition.
Increased function.
Internal secretion.
Diminished pressure.
APPEARANCE.
Macroscopic.
Microscopic.
TISSUE AFFECTED.
EFFECTS.
Hypertrophy literally means excessive nutrition. By usage
the term has come to mean, an abnormal increase in the size of
an organ or part. In a more restricted and definite sense, hy-
pertrophy is a term applied to that condition resulting from an
abnormal increase in the size of the essential cells of the part.
Thus an increase in the size of the liver as a result of an. in-
creased amount of the interstitial tissue or an increase in the
size of a kidney due to an accumulation of an inflammatorv ex-
190 VETERINARY PATHOLOGY.
udate or oedematous transudate is not an hypertrophy, al-
though such conditions have been called false or pseudo-hyper-
trophy. Tumors produce an increase in the size of the struc-
ture affected, but this should not be confused with hypertrophy.
Hyperplasia is a condition resulting from abnormal increase in
the number of the cells though it is difficult to dififerentiate
from hypertrophy.
Compensatory uvrERiROPirY is the name applied to that type
of hypertrophy caused by increased functional activity. Thus
an increased blood pressure m.aintained for some time induces
compensatory hypertrophy of the heart.
Concentric hypertrophy is a term denoting an hypertrophy of
the tissues of a hollow organ, accompanied by a diminution in
the lumen of the hollow organ, e. g., hypertrophy of the heart,
oesophagus, intestine, or an3' other hollow organ in which the
hypertrophied tissues occupy a portion and thus diminish the
lumen of the organ.
In some instances hypertrophy represents a normal, physio-
logic process. The increased size of the pregnant uterus, and
the enlargement of the mammae during the gestation period are
examples of physiologic hypertrophy. Increased size of the
heart and voluntary muscles in horses trained for racing rep-
resents a physiologic hypertrophy. After the destruction of one
kidney b}^ disease or the removal of one by operation, the re-
maining kidney increases in size and ultimatelv performs the
function of both, this is functional or physiologic hypertrophy
and also compensator}^ hypertrophy. In fact practically all hy-
pertrophies are physiologic, however, the hypertrophied struc-
tures are abnormal, therefore the condition is pathologic.
Excessive development of an entire animal i. e., giantism is
designated by some as general hypertrophy.
Excessive development of a part as one foot is designated
local hypertrophy. Local hypertrophy is much more common
than general hypertropliy.
Hypertrophy may be inherited, (natural) or acquired. Ac-
quired hypertrophy may be antenatal or postnatal.
Etiology.
Ii\HER!TED HYPERTROPHY. — Thc causc of inherited hypertrophy
is unknown except that there is an inherited impulse to grow
large. This type of hypertrophy is noted in giants.
Antenatal hypertrophy is usually the result of unequal pres-
sure and amniotic adhesions.
PROGRESSIVE TISSUE CHANGES. 191
The causative factors of postnatal hypertrophy are, 1st. in-
creased nutrition, 2nd, increased function, 3d, a stimulus, prob-
ably an internal secretion, that causes the affected tissue to con-
sume excessive quantities of food. Two or more of these etio-
logic factors are usually evident in all cases of hypertrophy.
Increased ntitrition. — A long continued, mild arterial hypere-
mia in a tissue insures increase of the nutritive supply to the
affected part and such parts usually become hypertrophic.
Increased function, is the prime causative factor of physiologic
or functional hypertrophy. Increased function is intimately
associated with increased nutrition, in fact long continued in-
creased function without increased nutrition is not possible. In
tiie production of functional hypertrophy the part must be
accustomed to the extra work gradually. An excessive amount
of work, assumed at once, by any structure will produce atrophy
or degeneration. Cardiac hypertrophy is invariably functional
as it usually is the result of valvular defects. Hypertrophy of
the involuntary' muscle anterior to a stricture is also functional
as it results from increased muscular action to force the contents
of the intestine past the stricture. A'oluntary muscular hyper-
trophy is also functional.
Some unknown cause is active in the production of certain
hypertrophic conditions. This unknown cause is probably an
internal secretion, at least this would appear to be the cause of
hypertrophv of the mammae and uterus in pregnant animals.
That certain internal secretions are required to sustain the nor-
mal balance in the growth of tissues is evident in disease of the
pituitary body wdiich frequently results in excessive develop-
ment of certain parts (acromegaly).
By diminishing the external pressure, experimentally, some
parts have l)een noted to become hypertrophic. This is because
of arterial liyperemia produced bv diminished pressure.
Appearance.
Macroseo(^ica!ly, Inpertrophied organs or parts are larger
and hea-vier than normal and may be regular or irregular in
shape. The general appearance of hypertrophied parts other
than size is not usually sufficiently distinct to differentiate them
from normal.
Microscopic. — Renal compensatory hypertrophy is charac-
terized bv increased length and size of the uriniferous tubules.
Hypertrophy of muscular tissue is characterized bv increase in
the size of muscle cells. In general hypertrophied organs or
parts contain an excess of parenchymatous tissue.
192
VETERINARY PATHOLOGY.
Effects. — The effect of hypertrophy varies according to the
tissue affected. There is usually an increased functional capac-
ity in an hypertrophied structure. The heart musculature may
become hypertrophied to such an extent that its force ruptures
some important blood vessel and causes death. Increased func-
tion of hypertrophied suprarenal bodies tends to increase
blood pressure by the production and elimination of large quan-
tities of adrenaline which causes constriction of arteries and
cardiac dilation or rupture.
HYPERPLASIA.
DEFINITION.
VARIETIES.
Parenchymatoits.
Interstitial.
ETIOLOGY.
APPEARANCE.
Macroscopic.
Microscopic.
TISSUE AFFECTED.
EFFECTS.
Hyperplasia, according to the derivation of the word, is ex-
cessive formation. Hyperplasia and hypertrophy are incorrectly
used interchangeably by some. Hyperplasia should be used to
Fiff 94. — H.vperplasia Interstitial Testieiilar Cells.
a. Interstitial hyperplastic tissue. b. Seminiferous tubules not fully developed
designate the condition resulting from an abnormal increased
size of a part due to an increase in the number of cells of the
part. Accepting the last definition, hyperplasia may be due to
an increased number of parenchymatous cells, or an increased
PROGRESSn'E TISSUE CHANGES.
193
number of interstitial cells the two types being called parenchy-
matous hyperplasia and interstitial hyperplasia respectively.
Parenchymatous hyperplasia and numerical hypertrophy are
sometimes used synonymously. Interstitial hyperplasia is prac-
tically the same as fibrous hyperplasia.
ParciicJiynialous hyperplasia is not of common occurrence
It is usually either inherited or congenital.
Interstitial hyperplasia is quite common as it is usually evident
in chronic infiammatory tissues and it is also occasionally
observed in structures affected with functional fibrosis as is evi-
dent in the liver of animals afflicted wnth disturbances of the
cardiac valves. The descended or scrotal testicle of single cryp-
torchids is usually enlarged because of an increased amount of
parenchyma and hence is an example of interstitial hyperplasia.
Etiology.
The cause of parenchymatous hyperplasia is unknown. Inter-
stitial hyperplasia is produced by the long continued action of
mild irritants or other substances that produce over stimulation.
-Pen drawing of an Hjperi)lastic Ureter, ox, natural size.
Appearance.
Macroscopic. — Parenchymatous hyperplastic structures are
regularly or irregularly enlarged and are heavier than normal.
Interstitial hyperplastic parts vary in appearance according
to the lamount of hyperplastic fibrous tissue. The part may vary
194
VETERINARY PATHOLOGY.
from normal to dense, hard, pale irregularly lobulated masses of
fibrous tissue.
Microscopic. — Parenchymatous hyperplastic structures have
the same appearance microscopically as sections of normal tissue.
Sections of tissue afifected with interstitial hyperplasia con-
tain an increased quantity of fibrous tissue which may be readily
recognized microscopically especially if the section is stained
with hematoxylin and picro-fuchsin.
Effects.
A part afifected with parenchymatous hyperplasia will have
an increased functional capacity. The effects of an increased
functional capacity of a structure depends upon the part in-
volved, and may or may not be injurious to the animal in which
it occurs.
Interstitial hyperplastic structures have an increased quantity
of fibrous tissue and usually a diminished amount of parenchy-
matous tissue and a diminished function. Interstitial hyper-
,<^
c- CJ^ -., *■ _ ^ ^ ^ -^
. ^« j^: '..^ ^"^-b^/ .' ■-^^..-:.t
Fig. 9 6. — Fibrous Tissue Ossification.
a. Fibrous tissue. b. Osteoblasts.
plasia of the walls of hollow organs may cause irregularity of
the lumen (intestine) and hinder passage of the organ's con-
tents.
PROG^CSSIVE TISSUE CHANGES. 195
METAPLASIA.
Metaplasia is the name applied to the conversion of a devel-
oped or matured tissue into another closely related. Under
normal conditions a matured tissue has specific cells and a char-
acteristic structure. The character of a tissue may be changed
by certain pathologic conditions. Metaplasia should not be con-
fused with degenerative or infective tissue changes which are
observed in functional or inflammatory fibrous formation. Meta-
plasia is usually concerned in the conversion of one variety of a
primary tissue into another variety of the same tissue as fibrous
tissue into bone and occurs in physiologic processes as well as
in disease.
Metaplasia occurs in scars, the conditions consisting of the
replacement of fibrous tissue by osseous tissue. This type of
metaplasia is also evident in bone spavin, ringbone, sidebone, as
well as in scars resulting from fistulous withers, poll evil, etc,
Metaplastic osseous formation was recently noted in the omen-
tum of a sheep. The conversion of lymphoid tissue into adi-
pose tissue is metaplasia. The replacement or substitution ol
sqtiamus epithelium for cubic or columnar epithelium repre-
sents a type of metaplasia.
Metaplasia is of little significance except as a pathologic con-
dition.
CHAPTER VIII.
RETROGRESSIVE TISSUE CHANGES.
DEFINITION.
ETIOLOGY.
Variations in nutrition.
Chemic poisons.
Cheniic reaction of tissue.
Variations of temperature.
Variations of function.
VARIETIES.
Atrophy.
Degeneration.
Infiltration.
Pigmentation.
Physiologic cell growth and function are dependent upon nor-
mal metabolism. Retrogressive processes are those conditions in
which normal cell growth and function are diminished or sus-
pended. Retrogressive tissue changes are caused primarily by
abnormal cell metabolism or abnormal functioning, and are
accompanied by structural or chemic alteration of the cell proto-
plasm or diminution in the size of the cells.
Metabolic disturbances may be caused by the following:
Diminished nutritive supply caused by (a) occlusion or di-
minution of the calibre of nutrient vessels ; (b) insufficient
supply of food to the animal; (c) incomplete or lack of digestion
of the ingested food ; (d) failure of absorption of digested food ;
(e) inability of the cells to utilize digested food that has been
carried to them. Nutrition may be supplied in excess of the
normal requirements, thus disturbing the metabolic equilibrium.
Excess nutrients may be stored within the cells or they may be
converted into energy by oxidation. In the former the stored
food is a mechanical hindrance to cell action and in the latter
the cell is overworked in converting the food into energy. With-
holding of nutrient substances from cells produces destructive
metabolism and ultimately cell death.
Chemieal substances, i. e.. poisons exert their action on cells
by combining with some of the protoplasmic constituents or by
accelerating, inhibiting or suspending the action of the cell
enzyms, thus interfering with metabolism.
Chemic reaction of a tissue influences the action of cell
196
RETROGRESSIVE TISSUE CHANGES. 197
enzyms, and hence is a factor in metabolism and in bringing
about retrogressive tissue changes.
J^ aviations in tcmpcratitrs. — The various albumens of protop-
lasm are coagulated at different temperatures. An increase of 3.6°
F. is sufficient to coagulate one group of albumins and an increase
of 9° F. is usually fatal because of the coagulation of other impor-
tant albumin constituents of the cell protoplasm. Fever is invariably
accompanied by coagulation of some albuminous constituents
of protoplasm although it is possible that chemic substances as
well as the high temperature may have some influence in this
coagulation. Diminished temperature retards metabolic process-
es and if tissues are exposed for a sufficient time to a low tem-
perature the protoplasm dies and metabolism ceases.
Diminished or increased cell functioning are factors in the
causation of retrogressive changes. Diminished functioning for
a considerable length of time results in atrophy and if function-
ing of a specific part is decreased progressively through several
generations there will be failure of development of that part
(aplasia). Excessive functioning, to a limited extent, in a
part supplied with an excess of food, produces hypertrophy.
Fimctioning beyond the nutritive supply produces degeneration
and finally destruction of the cells.
Retrogressive tissue changes include atrophy, degeneration,
infiltration and pigmentation.
ATROPHY.
DEFINITION.
DIFFERENTIA TION.
KINDS.
Physiologic.
Patliologic.
ETIOLOGY.
Physiologic.
Senility.
Pathologic.
Disfurhed nutrition.
Disturbed function.
Undue pressure.
APPEARANCE.
Macroscopic.
Microscot'ic.
TISSUE AFFECTED.
EFFECTS.
Atrophy is that condition in which there is a decrease in the
size of an organ or tissue caused bv a decreased size or a dimin-
ished number of the composing cells. In some instance the
interstitial tissue increases and replaces the atrophied cells ,and
the affected organ does not diminish in size. The term atrophy
198 VETERINARY PATHOLOGY.
is usually restricted to a local diminution in size, as, of an organ
or part, although it has been applied to the condition resulting
from a general wasting away of all the tissues of the body, i. e.,
emaciation.
Atrophy is differentiated from degeneration by the fact that
the former is purely a diminution in the size of the part, (a result
of decreased size or diminished number of the cells and without
any alterations in the cell protoplasm) while the latter consists
of chemical changes of the cell protoplasm and may result in in-
creased or diminished size of the cells. Atrophy and degenera-
tion may occur simultaneously in the same structure, the result-
ing condition being known as atrophic-degeneration or degenera-
tive-atrophy. Hypoplasia is an underdevelopment in contradis-
tinction to atrophy, which is diminution in the size after the
part has been developed.
Atrophy may be physiologic or pathologic.
PHYSIOLOGIC ATROPHY is a term used to designate the normal
diminution in the size of an organ or part. This occurs in the
thymus gland which is well developed at the time of birth. Soon
after this it begins to diminish in size and is practically extinct
by the time the animal matures. The mammary gland atrophies
after lactation ceases. Testicles and ovaries atrophy after the
period of reproduction or sexual activity. Senile atrophy is a
term employed to designate all atrophic conditions occurring in
the tissues of old or aged animals. Senile atrophy is a physio-
logic process.
PATHOLOGIC ATROPHY is a term used to designate abnormal
diminution in the size of an organ or part. Pathologic atrophic
disturbances involve muscular, glandular and nervous tissue
although no tissue is exempt. This type of atrophy is of fre-
quent occurrence, viz., diminution of muscle cells and the size of the
muscle in lameness and sweeney, and the diminution in the size of
the liver in hepatic atrophy.
Etiology. — Pathologic atrophy may be the result of either
disturbed nutrition or disturbed function.
Disturbed Nutrition. — Atrophic disturbances resulting from
mal-nutrition are most frequently the result of insufificient food.
Cells receiving insufficient food gradually shrink in size, possi-
bly because of auto-digestion. Insufficient nutritive supply may
be due to a diminished quantity of blood or an impoverished
blood. Diminished quantity of blood, i. e., a local anemia, is a
result of diminishing the calibre or obstructing the supplying
vessels.
Thrombic formation, aneurisms, etc., rnay cause partial or even
RETROGRESSIVE TISSUE CHANGES. 199
complete obstruction of nutritive vessels and thus be a causative
factor in atrophy. Starvation, or failure, of assimilation of food
is a cause of atrophy (general). However, in such cases atro-
phic degeneration of the cells is usually evident by the time the
body weight has diminished ^/^o of the total weight. Certain
chemic substances may indirectly be of significance in the pro-
duction of atrophy, but they influence either the cell nutrition or
function.
Excess nutrition ma}^ induce metabolic disturbances of suffi-
cient gravity to cause the cells to become sluggish and more or
less inactive to such an extent that they Avill become atrophied.
However, excess food is a much less frequent cause of atrophy
than insufficient food.
Disturbed function. — Diminished or excessive functioning are
causative factors in producing atrophy, the former being the
most frequent cause. Tissues deprived of function usually be-
come more or less atrophied. When an aiTerent nerve fibre is
disconnected from its end organ, (the mechanism by which it
picks up impressions), it begins to atrophy at once, probably
because of its failure to function. Muscles not functioning
atrophy. Thus there is muscular atrophy during most cases of
lameness. Diminished cardiac function resulting from dimin-
ished blood pressure, is succeeded by atrophy of the heart muscle.
Glandular structures become atrophied because of disuse..
Excessive functioning, long continued, causes fatigue and in
some instances paralysis, the latter usually being succeeded by
atrophy. Atrophy from excess function is sometimes observed in
race horses, show animals and is not uncommon in musicians,
acrobats, trapeze operators, etc.
Pressure. — Aside from the influence of the vaso-motor mech-
anism there may be sufficient pressure from tumors, hyperplas-
tic formations, mechanical contrivances, as harness, etc., to dim-
inish or obstruct vessels and cause atrophy. Pressure may also
exert influence other than diminishing the blood supply, for con-
stant pressure alone causes atrophy, e. g. pressure atrophy of
osseous tissue. Pressure atrophy, accompanying cirrhosis of
glandular structures as the liver or kidney, is usually caused by
pressure of the newly formed fibrous tissue which partially ob-
structs the nutrient vessels. However, the compression of the
parenchymatous cells disturbs their metabolic equilibrium and
is also a factor of some importance.
Appearance. Macroscopic. Atrophied organs are usually di-
minished in size, are irregular or regular in shape, have a dry
shrunken anemic appearance and are usually pigmented. The
200 VETERINARY PATHOLOGY.
parenchymatous tissue is most frequently involved, interstitial
tissue rarely becoming atrophied. The diminution in size may
be uniform throughout, the atrophied part thus retaining its nor-
mal shape, or the diminution may be unequal in different parts,
thus producing a lobulation of the aft'ected portion. Atrophied
bone usually maintains its normal external shape, as the process
is essentially a rarefication in which the Haversian and medul-
lary canals are increased in size . Pulmonary atrophy may con-
sist of diminution of the alveolar membranes to such an extent
that they rupture, thus produciing large cavities. Atrophic mus-
cular tissue is usually more intensely pigmented than normal
muscle. The source of the excess pigment in atrophic muscles
may be from the atrophied muscle cells or it may have its origin
from the blood.
Microscopic. — The cell body and nucleus shrink in size in
simple atrophy without previous alteration in the cell structure.
In numerical atrophy the cells first diminish in size and then dis-
integrate and die. Thus atrophy, disintegration and necrosis are
evident in numerical atrophy. The appearance of atrophic tis-
sues vary according to the structures involved. Atrophic kidney
tissue is characterized by the diminution in the size or in the
number of the glomerular and tubular cells. The tubules and
glomeruli may collapse the supplying capillaries becoming oblit-
erated by pressure of the hyperplastic fibrous tissue. In muscu-
lar atrophy, the muscle cells diminish in size probably because
some of the fibrillae disappear.
Effects. — The eff'ect of atrophy depends upon the structure
involved the extent of the condition and the age of the animal.
If the involved structure is not vital and the atrophy is of only
slight extent and in a young animal, in which the regenerative
power is good, the part will recover if the cause is removed.
Extensive atrophy of vital structures in old animals is usually
fatal or at least predisposes to other conditions that are fatal.
Again, a part may partially recover after atrophic disturbances.
RETROGRESSIVE TISSUE CHANGES. 201
CLOUDY SWELLING.
DEFINITION.
OCCURRENCE.
ETIOLOGY.
C hemic.
Bacterial products.
Phosphorous, Arsenic, etc.
Thermic.
APPEARANCE.
Macroscopic.
Microscopic.
TISSUE AFFECTED.
Epithelium.
Muscle.
Nerve.
EFFECTS.
Cloudy swelling-, albuminous, granular or parenchymatous
degeneration is a retrograde metamorphosis in which the proto-
plasm of the cell becomes granular. The granules in cells afifected
with cloudy swelling are albuminous, at any rate they are solu-
ble in an excess of a 2% solution of acetic acid or a 1% solution
of potassium hydroxide, and give the typical albumin reaction
to the xanthoprotein test. Active glandular cells, especially those
that produce ferments, are normally granular ; but the granules
in these cells do not respond to the foregoing tests and hence are
not albuminous. Cells in the earlier stage of fatty degeneration
are granular but the granules are not dissolved by solution of
acetic acid or potassium hydroxide, and they are dissolved by
ether or chloroform and are stained red with Sudan III. There-
fore they are fat granules.
Cloudy swelling probably occurs more frequently than any
other retrogressive change. It invariably afifects parenchymatous
cells in areas afflicted with acute inflammation and is usually
associated with infective diseases.
Etiology. — The causes of cloudy swelling may be divided in-
to two groups, Chemic and Thermic.
Chciiiic substances produce cloudy swelling either by influ-
encing the action of cell enzyms, thus causing the separation
(coagulation) of the cell albumins, or by combination with the
albumins of the cell protoplasm thus forming new compounds
(albuminate of mercury, etc.) that are of no value to the cell.
Excessive quantities of albuminous substances may be assimi-
lated by the cells, the unused portion becoming coagulated or
rendered insoluble as it accummulates, thus producing cloudy
swelling. The chemic substances that produce cloudy swelling
are usually soluble and are in solution in the blood or lymph
from which they readilv diffuse into the cell body wher^ they
exert their action.
202
VETERIN^r^- PATHC^-"";'^ \
Of the chemic substances capable. of produeiiig cloudy swell-
ing bacterial products are the most important. The diphtheria
toxin is probabl)' the most active of all bacterial products in the
production of cloudy swelling. Other organic substances as leu-
comains and phenol are capable of producing this degeneration
as well as many inorganic substances as arsenic, mercury, phos-
phorous and the mineral acids.
Thcnnic disturbances, c ially high temperature, is prob-
ably a cause of cloudy swelling. Halliburton has demonstrated
that certain high temperatures produce turbidity or granular
degeneration of cells. From experimental evidence it is appar-
ent that different groups of the albumins of the cell protoplasm
are separated (coagulated) at different temperatures. The high-
er the temperature the more fixed the coagula and the more
difficult they are of solution. From the present known facts,
although the chemistry is not determined, it is evident that high
Of"-
\«>
Vcs e-
V^!
3 « ■■ <
r/'^^^^^^^^
"ti^ - ^'^
,.A\.' ^v-/t^>
i', I^Qi^EUc ^:
Fig. 97. — Cloudy Swelling, sho.wing granular degeneration of kidney cells
RETROGRESSIVE TISSUE CHANGES. 203
temperature is at least a predisposing if not an exciting cause
of cloudy swelling.
Appearance. — Macroscopic. — An organ or part affected with
cloudy swelling, has a parboiled appearance, it is lusterless and
lighter in color, softer in consistency, and is slightly enlarged.
Microscopic. — An organ or part affected with cloudy swelling
appear cloudy, because of the presence of many small albuminous
granules, and the cells are slightly enlarged, hence the name
cloudy swelling. The increased size of the cell results from co-
agulation, the coagula occupying more space than the non-coag-
ulated protoplasm. If the tissues of an organ are examined with
the high power microscope the cell may appear slightly swollen
and its limiting membrane quite distinct ; it may be considerably
swollen and have an indistinct membrane ; or, finally, it may have
ruptured and the space it previously occupied may contain a mass
of granular debris. The protoplasm of the cell body may con-
tain small, irregular granules, the nucleus may be almost normal,
slightly degenerated, or it may even be entirely disintegrated.
Tissues Affected. — Epithelium, muscular, nervous, and con-
nective tissue are aft"ected with cloudy swelling, the frequency
being in the order mentioned. Cells of excretory organs are
especially affected because of their eliminative function.
Effects. — The eft'ects of cloudy swelling depend upon the
structure involved, the extent of the involvment, and the age of
the affected animal. Affected muscular tissue has a diminished
contractile power. Renal tubules ma}^ be occluded because of
the swollen tubular cells and the affected cells may also have
a diminished functional capacity. The function of any structure
is decreased and in extreme cases inhibited by cloudy swelling
of its component cells.
Cloudy swelling is usually a repairable process, providing the
cause is removed before the cells are destroyed.
204 Veterinary pathology.
FATTY CHANGES.
PHYSIOLOGIC (Fatfv Infiltration^.
DEFINITION.
ETIOLOGY.
Excess food.
Insufficient exercise.
Heredity.
Infiiiciice of disease.
Uiisexiiig.
Lactation.
Venesection.
APPEARANCE.
Macroscopic — Greasy, pale color.
Microscopic — Droplets of fat between cells.
TISSUE AFFECTED.
Normal depositions.
Epithelium, muscle.
EFFECTS.
PATHOLOGIC (Fatty Degeneration).
DEFINITION.
ETIOLOGY.
Insufficient food.
Inability of cells to utilize food.
Excessii'e activity.
APPEARANCE.
Macroscopic — Greasy, pale, light.
Microscopic — Droplets of fat in cells.
TISSUE AFFECTED.
Epithelium.
Muscle.
Nerve.
EFFECTS.
Adipose tissue is not a specific tissue, but represents a modi-
fied connective tissue. Tlie cells that later become fat cells, are
originally flat or spindle shaped and usually occur in clusters or
groups. There are certain locations, called fat depositories,
where fat usually occurs. Normally the principal fat depositories
are located in relation to the kidney capsule, subserosa (parietal,
visceral and omental peritoneum), subcutem, intermuscular areo-
lar tissue, and in the orbital fossa. A well fattened animal has
accumulations of fat in all the fat depositories. In an emaciated
animal limited quantities of fat occur only around the kidney
in the omentum, and orbital fossa.
Normal adipose tissue varies in color and consistency in the
dififerent animals. In general it is white or yellow and appears
lobulated when cut across. The consistency depends upon the
melting point of the fat.
Olein is the principal kind of fat in the hog, stearin and pal-
Hiitin in the ox, and stearin in the sheep. It has been demon-
RETROGRESSIVE TISSUE CHANGES,
205
strated, however, by Prof. Hopkins, of the University of Illi-
nois, that the body fat is the same as the ingested fat. (Hogs
were fed on cotton seed oil and the presence of the same kind
of fat was demonstrated in the hog tissue.) It has also been
found that butter fat in cow's milk is the same as ingested fat.
Opinions are at variance in reference to the digestion and assim-
ilation of fat. The fat splitting enzyms convert the fats into
fatty acids and glycerine. The alkali present in the intestines
unites with a part of the fatty acid, forming soap, the latter and
the glycerine pass by osmosis into the intestinal epithelium or
through the mucous membrane where the glycerine is substituted
for the alkali, the alkali passing back into the intestinal lumen
to form more soap (Hammersten). Some of the fat may be so
finely emulsified that it passes directly into and through the in-
testinal epithelium, and some of it may be incorporated by leu-
cocytes, and thus carried from the lumen of the intestine to the
lacteals (Howell). Fat droplets are present in the circulating
blood. The exact manner of the production of fat cells in normal
adipose tissue has not been determined.
All normal animal tissues contain varying quantities of neu-
tral fat. As much as 23 per cent of fat has been extracted from
kidney tissue (Adami). The proportion of neutral fat in the
same kind of tissue varies in the same animal under different
conditions and in animals of dift'erent species under the same
conditions. Thus the quantity of fat in the muscular tissue of
an emaciated animal is less than in an animal in good flesh. The
muscular tissue of the hog contains more fat than the muscular
tissue of the ox, sheep, horse or dog. In fact the presence of fat
droplets betwen the muscle cells is a distinguishing characteris-
tic of porcine muscular tissue. There is no definite limit to the
quantity of fat normallv contained in the tissues of any animal.
Certain abnormal fatty changes occurring in the various tis-
sues have been described as fatty infiltration and fatty degen-
eration. These changes, although originally thought to be en-
tirely distinct, are closely related and may represent different
stages of the same process. These fatty changes may be dis-
cussed as physiologic fatty changes (fatty infiltration), and path-
ologic fatty changes (fatty degeneration), although there is no
good reason for the division of the subject other than to recog-
nize the previous classification and prevent undue confusion.
206 VETERINARY PATHOLOGY.
Physiologic Fatty Changes.
(Fatty Infiltration.)
Physiologic fatty changes is a condition in which there is an
excessive accumulation of fat, but the function of the affected
part is not materially changed.
Etiology. E.vccss Food. — House dogs and cats and many family
horses are usually fed to excess, resulting in the deposition of exces-
sive quantities of fat in practically all tissues, thus producing general
obesity. The "Strassburg goose" is force-fed with dough balls
in excessive quantities until excessive obesity is produced, the
liver especially becoming the seat of marked fatty accumulations.
In fact all prime "butcher stuff" is affected with physiologic fatty
changes or dietary obesity.
Insufficient Exercise. — Animals kept in tie stalls or in close
quarters have a tendency to become excessively fat, especially if
they are fed a full ration, because there is diminished oxidation
on account of lack of exercise and the bulk of the consumed food
is stored as fat.
J^cnescction. — Frequent bleeding diminishes the percentage of
red 1)lood corpuscles and thus indu-ectly diminished oxidation
and favors fat accumulation.
Disease. — Some diseases appear to influence the physiologic
deposition of fat. The early stages of tuberculosis in cattle and
hogs and distomatosis in sheep is accompanied by physiologic
fatty deposition. During convalescence from some diseases there
is an increased deposition of fat.
Lactation. — The early period of lactation is accompanied by
fatty accumulation especially in the liver. (Possibly the liver
may act as a distributing center of fat.) The fatty accumulation
in the liver is evident regardless of any variations in the composi-
tion of food stuff.
Heredity. — Some animals, especially hogs, except the Tamworths
and Yorkshires, appear to have an inherent tendency to become
excessively fat.
Castration. — Removal of the genital glands favors fat accumula-
tion in the tissues. Castrated dogs and cats, especially if cas-
trated when mature, become obese.
In general the exciting causes of physiologic fatty changes
are excess of food or diminished oxidation, heredity being a pre-
disposing factor.
RETROGRESSIVE TISSUE CHANGES.
207
Appearance. — Macroscopic. — Tissues affected with fatty infil-
tration are greasy or oily, more friable than normal, and paler in
color, the color being uniform throughout or mottled. The quan-
tity of blood in the fat varies, there being more, in general, in
the fat of young animals. Muscular tissue in which there is a
fatty accumulation contains areas or strata of fat and strata of
muscular tissue. Tlie deposition of fat may be so extensive in
muscular tissue of hogs that there is little evidence of muscle.
Subserous accumulations of fat may be localized, giving the ap-
pearance of masses of fat, or it may be accumulated diffusely
as thick layers of fat. In dogs and cats the excess fat is usually
deposited around the kidneys.
Microscopic. — In the early stages of physiologic fatty changes,
small droplets of fat are observed between and within the cells.
The intracellular fat gradually increases and assumes the space
within the cell, the nucleus being crowded to the margin of the
cell and may ultimately disappear.
Fig. 9S. — Fatty InfiltratioH, liver, hog. showing infiltration of globules from
periphery of lobule toward its center.
Tissue Affected. — All tissues are subject to fatty accumula-
tions, excepting the normal depositories, the liver being most
prone to the affection.
Effects. — The influence of physiologic fatty changes is, de-
pendent upon the extent of the condition and the duration of
208 VETERINARY PATHOLOGY.
the process. If the nuclei of the cells are not injured and the
process is discontinued the infiltrated fat is disposed of and the
part recovers. If non-regenerative cells, such as heart muscle,
are destroyed, they will not be regenerated, even though the
fat is reabsorbed. The destroyed heart muscle cells may be
replaced with fibrous tissue.
Pathologic Fatty Changes,
(Fatty Degeneration.)
Pathologic fatty change, or fattv degeneration, is a condition
in which the protoplasm of the affected cells diminishes liecause
of an increase of the intracellular fat. Fat or some of its cleav-
age constituents is probably constantly present in varying cjuan-
titles in all active cells.
Pathologic fatty changes are of frecpient occurrence, being
associated with diseases of malnutrition, and occurring in acute
fel)rile diseases and many of the infective diseases, ft is espe-
cially evident in chronic phosphorous poisoning and some other
chemically induced diseases.
Pathologic fatty change is differentiated from cloudy swelling
as follows : The droplets of fat are soluble in ether and chloro-
form and are not dissolved with dilute acetic acid or potassium
hydroxide ; while the granules in cloudy swelling are insoluble in
ether and chloroform, but are soluble in dilute acetic add or po-
tassium hydroxide. Again the fat droplets are stained red by
Sudan III, while the granules of cloudy swelling are not.
Fatty degeneration is difificult to differentiate from fatty infil-
tration, and in some instances it is impossible to differentiate
them ; in fact, future investigation may confirm the identity of
the two processes. In rhe early stages the fat droplets are usu-
ally intracellular in fatty degeneration, and intercellular in fatty
infiltration.
Etiology. — In general, fatty degeneration is the result of the
disturbance of cell metabolism. The production of energy, be-
ing intimately associated with the metabolism of fat, becomes
a factor in the causation of fatty degeneration. Specifically,
disturbed nutrition is the principal cause of fatty degeneration.
Disturbed nutrition may be the result of, 1st, variation in the
composition of the blood, 2nd. diminished quantity of blood, ord,
diminished oxygen supply, and 4th, changed environments of the
cells. Insufificient supply of cell nutriment is the principal in-
RETROGRESSIVE TISSUE CHANGES. 209
fluence resulting from circulatory disturbances or altered com-
position of blood. Diminished oxygen supply results in incom-
plete oxidation of the available intracellular fat which is then
accumulated within the cell. Changed environments include the
variation of the chemic reaction of a tissue, the tissue tempera-
ture, amount of fluid, etc. Disturbance of the environments in-
fluences the cell metabolism and may cause the union of cleav-
age products of fat that exist within the cell, or the infiltration
and intracellular accumulation of fat may be favored. Changed
environments may also render the cells unable to utilize the food
brought to them.
The causes of cloudy swelling are also etiological factors in
the production of fatty degeneration, in fact, fatty degenera-
tion is frequently associated with cloudy sweUing. Disturbed
metabolism is produced by insufficient or improper food, dimin-
ished supply of oxygen, or inability of the cells to utilize the
food or oxygen supplied, the inability of utilization being a re-
sult of the damaging influence of chemic or thermic variation
of the environments of the cells.
Appearance.— il/orro?ro/'zc. — A tissue afifected with fatty de-
generation varies in appearance according to the extent of the
process. In general, affected tissues are paler in color (change
in color is frequentlv in patches which appear yellowish), lighter
in weight (in extreme case, liver tissue afifected with fatty de-
generation, floats in water), greasv or oily in appearance, (a
knife blade that had been used in sectioning a fatty tissue is
usuallv smeared with drops of oil or fat), and usually swollen
or enlarged in the early stages, succeeded by diminution in size
as the fat is resorbed. Tissues afifected with fatty degeneration
are less elastic, and more friable.
Microscopic. — In the very early stages the cells contain small
granules that are dilTerentiated from the granules of cloudy
swelling only by the chemic test referred to above or by special
stains, as Sudan III. As the degeneration progresses, the minute
fat droplets coalesce, forming drops sufficiently large to be rec-
ognized microscopically, as small, clear spots or holes in the
cell protoplasm in sections of tissue fixed in fluids that are sol-
vents for fats and as fat drops in fresh tissues. The affected
cells are swollen to an extent which is proportional to the degree
of the degeneration. Ultimately the cell membrane ruptures
and the enclosed fat is liberated, thus producing a condition not
210
VETERINARY PATHOLOGY.
differentiable from fatty infiltration. The nucleus is usually not
involved in the beginning, but as the degeneration progresses
in the cytoplasm, the chromatin network disappears and the
entire nuclear structure finally becomes disintegrated, producing
the so-called granule cell. The degeneration may be continuous
throughout a tissue or it may be more or less patchy. The ex-
tent of involvement of the cells in an affected area is usually
unequal, some cells being only slightly affected, others contain-
ing considerable fat, and still others being entirely converted
into fat.
Fis'. 99.
-Fatty Degeneration of the Liver, showing the early stage of the process
around the central vein.
Tissue Affected — Glandular tissue, particularly the liver,
is probably most prone to become affected with pathologic fatty
changes, or fatty degeneration. Muscular tissue is quite subject
to fatty degeneration, especially heart muscle. Epithelium other
than glandular, nervous and connective tissues, are not exempt
from this process. Tumors are occasionally observed to be
affected with pathologic fatty changes. Necrotic tissue fre-
quently becomes a fatty mass or an entire cadaver may be con-
RETROCKKSSIVK TISSUE CHANGES. 211
verted into a fatty mass termed adipocere, which is no doubt
the result of ferments liberated from the dead tissue.
Effects.- — The conversion of the cell protoplasm into fat im-
pairs the cell function. At least diminished cell action, as well
as disturbed cell metabolism is evident in cells affected with
pathologic fatty change. In cells slightly affected, the droplets
are either oxidized or are extruded from the cell (absorbed when
the cause is removed). Cells more extensively aft'ected may be
destroyed, leaving a meshwork of vessels and fibrous tissue.
The area may later be filled with the new parenchymatous cells
arising from the surrounding less aff'ected zones, and, like those
destroyed, it may persist as a mass of fibrous tissue, i. e., a scar.
If regeneration occurs there must be an adequate blood supply.
The degenerated cells may become caseated as a result of
the conversion of the fatty material into a cheese like mass.
The usual cause of caseation of fatty debris is diminished or
obstructed blood supply resulting in gradual absorption of the
fluids, saponification of the fats and in some instances the forma-
tion of cholesterin. Caseated material derived from the fatty
debris may later be liquified or calcified.
AMYLOID CHANGES.
DEFINITION.
ETIOLOGY.
APPEARANCE.
Macroscopic.
Microscopic.
TISSUE AFFECTED—Siibcudothclimn.
EFFECTS.
Some masses mav be found in the acini of the prostate gland,
especially in old dogs and aged humans, that respond to the iodine
test and are considered by some authorities as amyloid bodies.
Physiologic amyloid fc^-mations have not l^een observed other
than in the pros late gland and they probably have a pathologic
origin. Thus a physiologic prototype of amyloid formation is
unknown.
Amyloid substance (amylin) is an albuminoid, insoluble in
water, alcohol, ether, chloroform, xylol, dilute acids or alkalies
and is not acted upon by pepsin. W'hen tissue containing amy-
loid substances is immersed in Lugol's solution the amyloid
areas assume a mahoganv brown color and the normal tissue is
stained a vellowish brown. (To make this test wash the affected
tissue thoroughly until all blood has been removed, apply a lib-
212
VETERIXAR\- PATHOLOGY.
eral quantity of Lugol's solution for one or two minutes, wash
the excess of the reagent off and the above color reaction will
be observed). The test is equally applicable to macroscopic and
microscopic sections. If the sections, macroscopic or micro-
scopic, are immersed in dilute sulphuric acid, after the application
of Lugol's solution, the amyloid area will assume a blue color,
the normal tissue a brown color. The analine dyes usually stain
amyloid substances some shade of red.
The source of amylin is not definitely known. It may be
derived from the blood or from tissue cells. The formation of
amylin may depend upon variations in the percentage of some
chemic substance in the blood or tissue juices.
Amyloid formation is not common in the domestic animals.
Occasionally a dog is observed that is affected with amyloid ac-
cumulations in the prostate gland. One case has been observed
n a hog in which the liver was affected, and, excepting this, the
carcass showed evidence of no other lesions.
Etiology. — The cause of amyloid change is not known, al-
though it has been assumed by some pathologists to be associ-
ated with chronic suppurative conditions, as, tuberculosis, and
other chronic debilitating diseases, as carcinomatosis. The
tissues from several animals affected with chronic suppurative
processes, as fistulous withers, poll e^dl, quittor, tuberculosis,
glanders, caseous-lymphadenitis, as well as tissue from animals
affected with tumors have been examined, but amyloid changes
have not been found. Increased or diminished quantity of some
of the salts of the blood may be found to be an etiologic factor
in amyloid changes.
Appearance. — Macroscopic. — Affected tissues or organs are
larger, paler, and firmer than normal. The amyloid areas are
homogeneous and translucent in appearance. The entire organ
or tissue appears homogeneous when the amylaceous material
is dift'use.
Microscopic. — Amyloid substance is deposited in the frame-
work beneath the endothelial cells lining the blood vessels. It
appears as an annular homogeneous mass encircling the vessel.
The amyloid substance may accumulate to such an extent that
the vessel is obstructed. After the capillaries have been gorged
beyond their resistance thev rupture, thus allowing the amyloid
substance to permeate the interstitial spaces where it appears
microscopically as irregular homogeneous masses.
Tissue Affected. — The blood-vascular subendothelial con-
nective tissue is the principal location of amyloid formation,
although it may occur in lymph vessels and even the perimysium
RETROGRESSIVE TISSUE CHANGES. . 213
and endomysiuin may be affected as well as the stroma of the
mucous membranes. The liver, spleen, and kidney are the
most frequent locations of the process, probably because of the
large number of capillaries in those organs.
Fig. 100. Amjldid Denegeration, Liver.
a. Livtr cells. b. Amyloid matei-ial.
Effects. — The condition is so rare that it is not possible to
generalize upon the effects of the process. The amylaceous ma-
terial is insoluble in the body fluids and it is quite probable that
if a part becomes aft'ected. it remains so permanently.
HYALINE CHANGES.
DEFINITION.
ETIOLOGY.
APPEARANCE.
Macroscopic.
Microscopic.
TISSUE AFFECTED.
J'cssels, Muscles.
EFFECTS.
This is a pathologic condition characterized by the conversion
of the cell substance into a homogeneous material called hyaline.
In the phenomena accompanying the physiologic changes of the
corpus luteum of pregnancy, a hyaline sul)stance is produced.
The physiologic formation of hyalin, aside from that produced
in the corpus luteum of pregnancy, has not been recorded.
The formation of hyalin is quite common in the muscular
214
VETERINARY PATHOLOGY.
portion of the l)lood vessels of tissues affected with clironic in-
flammation and in the blood vessels of sarcomata. It has also
been observed in voluntary and heart muscle in certain diseased
processes.
Hyalin, an albuminous substance very similar to amylin, does
not respond to the iodine test, and is not acted upon by alcohol,
ether, chloroform, acids, ammonia, or water. Acid stains, as
eosin and acid fuchsin. have an affinity for hyalin and stain it
quite intensely.
Etiology. — The specific cause of hyaline fijrmation is not
definitely known. Certain predisposing- factors, however, are of
interest. Wells found that lactic acid injected into voluntary
muscle was succeeded 1)v hyaline formation, and it may be as-
sumed that the cause of hyaline changes in voluntary muscle is in
some instances at least is due to an excess of sarcolatic acid. Some
diseased processes, as chronic inflammation, tuberculosis, and sarco-
matosis appear to produce conditions that favor hyaline formation.
I* * f
%f r )>■
('
<^ ~ 'f /•■
Fig. 101. — H.valine Uenegration. Vessels.
a. Hyaline around arteries in maxilla of colt,
Appearance. — Macroscopic. — Rarely does this condition l)e-
come sufficiently marked to be recognized with the unaided
eye. The hyaline substance appears as a translucent, homogen-
eous, firm mass, intermingled with the normal tissue.
Microscopic. — The hyaline substance appears as glassy areas,
and the adjacent tissue frequently becomes less distinct. Except
for the affinity of hyaline substances for acid stains and its fail-
RETROGRESSIVE TISSUE CHAXGES. 215
ure to react to iodine it is difficult to differentiate from amyloid
change.
Tissues Affected. — Muscular tissue, involuntary muscle,
especially of the blood vessels, voluntary muscle and heart mus-
cle are subject to hyaline changes. Connective tissue is less fre-
quently involved and epithelium rarely, if ever.
Effects. — When hyaline has been formed in small quanti-
ties ana che cause is removed the hyaline substance is probably
resorbed and the affected cells repaired. If the production of hyalin
has replaced the protoplasm of large cell masses, especially of mus-
cular cells, the area will probably not be repaired with muscular
tissue, but it may be substituted with fibrous tissue, provided the
cause is removed.
MUCOID CHANGES.
Physiologic.
DEFINITION.
ETIOLOGY — Physiologic, pathologic.
APPEARANCE. '
Macroscopic.
Microscopic.
TISSUE AFFECTED— Connective, epithelium.
EFFECTS.
The transformation of cell protoplasm into mucus is evident
in the physiologic production of mucus in the surface epithelium
of mucous membranes as well as in mucous glands. The physi-
ologic conversion of protoplasm into mucus is the result of in-
tracellular enzyms, or at least depends upon protoplasmic activ-
ity. As the mucus is produced the cell becomes enlarged and
ultimately ruptures, discharging the mucus. The mucus may be
formed only in the distal end of the cell or it may entirely re-
place the protoplasm of the cell. In the former the remaining
protoplasm of the cell regenerates the portion destroyed. In the
latter the adjacent cell multiplies, thus filling the gap.
Mucus is a viscid, glairy stringy nitrogenous fluid. The
principal ingredient of mucus is mucin, a glucoproteid, although
there mav also be present pseudomucins. Mucin imbibes water,
thus becoming swollen, and from this swollen mass there is pre-
cipitated a stringy material bv addition of alcohol or dilute acetic
acid. Pseudomucin forms a gelatinous mass when dissolved
in water, but by the addition of alcohol to this gelatinous mass
a stringy precipitate is formed which is redissolved in excess' of
water, differino- in this respect from nuicm.
216 VETERINARY PATHOLOGY.
Pathologic.
Pathologic mucoid formation ^affects cells and intercellular
substance. Cellular pathologic mucoid change is identical to
normal mucus formation except that it is in abnormal locations
or is in excess in those locations in which mucus is normally
produced. Intercellular mucoid formation is a condition result-
ing from the conversion of fibres, matrix of cartilage and bone,
or other intercellular substances, into mucus. Pathologic mucoid
changes occur rather frequently. It is evident in catarrhal in-
flammation, in cyst formations and as a retrogressive process in
many tumors.
Etiology. — The cause of pathologic mucoid changes is not
known. Excessive cellular mucoid formation accompanies mild
inflammatory disturbances of mucous membranes — so called
catarrh. The increased production of mucus in catarrhal inflam-
mation may be the expression resulting from the exaggerated
function of the mucous membrane induced by the excessive
quantity of blood supplied.
Intercellular mucus formation may result from improper
nutrition or injurious influences induced by chemic substances.
It has long been thought, although it has never been proven,
that some product is evolved when the thyroid gland is dis-
eased that causes a mucus degeneration of all fibrous tissue in
the body (myxoedema). Some sarcomata and carcinomata are
afifected with mucoid changes, probablv the result of chemic sub-
stances elaborated bv the tumor cells.
Appearance. — Macroscopic- — .Mucus of pathologic origin is not
dififerentiable from physiologic mucus. In pathologic conditions
accompanied by mucus formation the mucus is frequently mixed
with other substances, as blood, pus and food stufif. Thus the
mixture assumes various appearances. A discharge composed
of mucus and pus (muco-purulent) is common in practically all
catarrhal inflammation, being the characteristic discharge of
catarrhal pneumonia and is the usual discharge from the respira-
tory tract and conjunctiva, in dogs afifected with distemper, in
horses afiflicted with "stock yard fever," etc.
The appearance of a tissue afifected with pathologic mucus
changes, regardless of whether the cells or intercellular sub-
stance is involved, depends upon the quantity of mucus pro-
duced. If there is a limited quantity of mucus and it is equally
distributed throughout, the afifected tissue will appear swollen
and soft. If more extensive and dififuse the afifected tissue will
be soft, spongy, and slimy. If the entire structure has practically
been converted into a mass of mucus, it will appear as a slimy,
RETROGRESSIVE TISSUE CHANGES.
217
stringy, pulpy substance from which varying quantities of mucus
may be expressed.
The mucoid changes mav afifect circumscribed local areas that
appear moist and soft, spongy, or even cystic in contradistmction
to the surrounding normal tissue.
Microscopic. — Mucus appears as a stringy substance containing
varying quantities of detritus. Fixing agents coagulate mucin
in which case it api:)ears as a more or less homogeneous mass
containino- manv fibrillae or threads of coagulated material.
c.
b
*p
X
^
-tSf - -
-
' ■ ', ^
O----
Ss--^
^ ^ ^ ^
-"
as-
c.
Fis. 102. — Mucoid Degeneration.
Fibrous tissue. c. Mucoid cells.
Mucous substance.
Microscopic appearance of a tissue affected with pathologic
mucoid changes is variable according to the extent of the pro-
cess but in general the picture observed is the same as that of
the normal tissue plus the mucus.
Tissue Affected. — Epithelium and the cells and intercellular
substance of connective tissue as well as some tumors are sub-
ject to mucoid changes.
Effects. — The eft'ects depend upon the extent, duration, and
regenerative ability of the affected tissue.
218 VETERINARY PATHOLOGY.
COLLOID CHANGES.
DEFINITION.
ETIOLOGY— Unknozun.
APPEARANCE.
Macroscopic.
Microscopic.
TISSUE AFFECTED.
Tlivroid, prostate, tumors.
EFFECTS,
The term "Colloid" has rather an indefinite meaning and by
present day writers is used to indicate a variety of substances.
"The word colloid is merely morphologically and macroscop-
ically descriptive of certain products of cell activity or disinte-
gration, which have nothing in common except the fact that they
form a thick glue like or gelatinous, often brownish or yellow-
ish substance" (Wells). One type of colloid substance is a
physiologic product of the thyroid gland, it is in part a secre-
tion of the thyroid cells and in part a conversion of those cells
into colloid material. This product is normally absorbed as it
is produced though it may accummulate in small quantities in
the gland acini, especially in aged animals.
Chemically the physiologic thyroid colloid is composed of
iodo-thyreoglobulin (a compound of globulin and thyroidin).
Thyroid colloid is glue like in consistency and varies in color
from brown to yellow. Colloid and mucous are closely related.
Colloid does not increase in bulk when it is suspended in water,
neither is it precipitated by alcohol or acetic acid — two tests that
are usuallv sufficient for difTerentiation of mucus and colloid.
Pseudo-mucin is more difficult to dififerentiate from colloid. The
latter, however, contains iodine and the former does not.
Pathologic colloid changes are conditions resulting from the
excessive production and retention of collagenous material. The
disturbance induced by excessive colloid accummulation is usu-
ally not serious although it may cause fatal termination. This
condition occurs more frequently in old dogs than in other ani-
mals. Sheep occasionally show lesions of this condition, in
some instances the entire flock becoming afifected. Pathologic
colloid accummulation is a constant lesion in the thyroid gland
of animals suffering from exophthalmic goitre. Colloid changes
have been observed in cattle, sheep, horses, mules and one case
has been recentlv noted in a calf.
Etiology. — The specific exciting cause of pathologic colloid
changes is not known but undue exposure to inclement weather
is a predisposing cause of considerable moment. Exposure, in
some instances, appears to become an exciting cause of thyroid
RETROGRESSIVE TISSUE CHANGES.
219
colloid accummulation. A flock of 128 h«althy, yearling- sheep
shipped from south central New Mexico to the Kansas City stock
yards, were all found to Iiave enlarged thyroid giands at the
time of slaughter, which was about 2-t hours after their arrival
at the stock yards. The thyreoid glands were found on micro-
scropic examination to be affected with pathologic colloid accum-
ulation. This occurred in April, the sheep, having been sheared
just previous to shipment, and the weather having been very
inclement during the entire time that they were in transit. Other
entire flocks of sheep that have been undul_y exposed have been
aft'ected in a like manner.
Fig. 103. — Photograph uL a lh.\ mid ylaiul aftictta with Colloid DeKeneralion.
Endemic goitre in the human is indicative of an infectious
cause though the individual cases in non-aft'ected areas dispels
the infection theory.
The absence or diminished quantity of iodine in the food,
water or air, may be a causative factor in the production of
goitre and other colloid accunuiiulations in the thyroid glands.
Appearance. — Macroscopic. — -Colloid most frequently oc-
curs in masses, varying in size from mere microscopic pqints
to bodies as large as a lead pencil rubber or even cyst like bod-
220 VETERINARY PATHOLOGY.
ies as large as a black walnut. More rarely the colloid material
may have infiltrated the tissue spaces and become dilYuse. Col-
loid varies in consistency from a watery to a jelly like mass, is
usually of a clear amber color, although it may be translucent
or of a deep mahogany tint.
An afifected tissue contains variable sized areas of hyaline,
rather firm, amber or mahogany colored masses deposited ir-
regularly throughout the entire structure.
Microscopic. — The cells are noted to contain small droplets
of colloid material which is constantly produced and passed out
of the cells and accumulated in the acini, tubules, or intercellu-
'ar spaces. Other entire cells are converted into a colloid
Fig. 104. — Colloid Degreneration. Thyroid Gland.
a. Colloid material completely filling the acini of gland.
mass. The conversion of a large number of cells into colloid
material in one vicinity produces colloid masses or the so-called
colloid cysts. Colloid substance is homogeneous or slightly gran-
ular and is stained, by acid stains. It assumes an orange color
when stained according to Van Giesen's method.
Tissue Affected. — Epithelium is probably the only tissue
in which colloid formation occurs. The thyroid gland is most
commonly affected. There is a degenerative change occurring
in carcinomata that is similar to the colloid formation although
it may be pseudomucin formation. McFarland states that col-
loid casts occur in the uriniferous tubules, in kidneys affected
with chronic inflammation. Ziegler regards the prostatic con-
cretions, of the human, that do not react to iodine, as colloid.
RRTROGRESSIVE TISSUE CHANGES. 221
Effects. — The effects of colloid accumulation depend upon
the extent of it. The exact function of the thyroid gland has not
been determined but it is quite certain that the iodine compound,
iodothyrein or thyroiodin is the active principle of the thyroid
secretion. It is not known whether the thyroid secretion has
some action tTon cell metabolism or neutralizes various poison-
ous substances that result from metabolism or poisons intro-
duced into the body from without. The colloid accummulations
in goitre contain less iodine per given volume than the normal
secretion, but the total quantity of iodine is materially increased
resulting in circulatory disturbances, as rapid weak pulse, in-
creased metabolic activity especially of proteids, increased secre-
tions, irritability, etc. Diminished iodine production, as ob-
served in my::oedema, is not common in colloid accummulation.
SEROUS INFILTRATION.
DEFINITION.
ETIOLOGY— (Oedema).
APPEARANCE.
Macroscopic.
Microscopic.
TISSUE AFFECTED.
EFFECTS.
Serous infiltration is a condition in which excessive quantities
of lymph or serous fluid infiltrates the cells.
In the anatomo-physiologic discussion of the cell, the nutri-
ents were said to be obtained by specific selective action of the
cells and by osmosis. Osmosis is probably the most important
mode of passage of extracellular substances into the cell.
In hydremia or other conditions in which cells are bathed by
excessive quantities of fluid, there is a tendency for them to
become hydropic.
Serous fluid that enters the cells in serous infiltration is thin,
watery and contains small quantities of proteids and salts.
Etiology. — The cause of serous infiltration is an excess of
serous fluids in the tissues. Serous infiltration is, therefore, an
accompanying condition of oedema and the causes of oedema
would likewise be the primary cause of serous infiltration. A
second cause may be the impairment of the cells in which they
are stimulated to imbibe more fluid.
Appearance. — Macroscof^is. — Because of the simultaneous
occurrence of oedema and cellular serous infiltration and in
view of the fact that oedema is so conspicuous, the serous i\ifil-
tration is not recognizable in gross examination.
222 vkti-:rtxary PATiinr.nr.Y.
Microscopic. — When examined in the fresh state the cells
are enlarged, the extent of which depends upon the quantity of
fluid imbibed. The infiltrated fluid accumulated in the cells
appears as clear spaces or vacuoles. The vacuoles occur either
in the CAto-]:lasm or the nucleus and in extreme cases, they
occupy the entire cell and mav even cause its rupture.
Tissues Affected. — Practically all tissues are subject to
serous infiltration. Those tissues in which oedema occurs are
most frecjucntl}' afl:'ected. Epithelium is quite frequently in-
volved in serous infiltration because this tissue forms the sur-
face of those structures affected with oedema.
Effects. — The effects depend upon the extent and duration
of the condition. Some vegetable cells are capable of imbibing
fluid to a sufficient extent that they increase their size one hun-
dred times.
Animal cells cannot imbibe fluids to such an extent as vege-
table cells without being rent asunder. After the cells have
been subjected to serous infiltration for sometime, the nuclear
chromatin appears to dissolve and dift'use through the cell body.
This necessitates an impairment of the cell activities.
GLYCOGENIC IXEIETRATION.
DEFINITION.
ETIOLOGY— ( Disfiirhcd cnrbohxdratc JiicUibnlisni) .
APPEARANCE.
Macroscopic.
Microscot^ic.
TISSUE AFFECTED.
EFFECTS.
This is a condition characterized l)v the infiltration of exces-
sive quantities of glycogen into cells that normally contain a
limited amount of it or the infiltration of glycogen into cells
normally glycogen free.
The source of glycogen is not definitely known. Accord-
ing to some phvsiologists, glycogen may be formed from either
carbohydrates or proteids. The digested carbohydrates are
probablv stored up in the form of glycogen, at least glycogen
is readily converted into dextrose whenever carbohydrates are
needed. Glycogen can be demonstrated in the normal liver cells,
kidney cells, and in muscle cells, although it occurs iu limited
quantities.
Glvcogen is soluble in water and insoluble in alcohol, chloro-
form and ether. Its presence in tissue may be demonstrated by
smearino- the tissue on a slide and allowing it to dry inverted.
ri:tr()c;ressive tissue CHA^■GES. 223
over crystals of iodine. The glyco^-en appears as l^rownish areas
in the cells. It may also be demonstrated by immersing in a
mixture of four parts of alcohol and one part of tincture of iodine,
sections that have been hardened in absolute alcohol, the glyco-
gen assuming a port wine color.
Pathologic glycogenic infiltration occurs in pus cells of suppu-
rating processes. The blood cells, especially leucocytes, contain
some glycogen in those animals affected with septic infection or
sapremia. Thus horses afflicted with sapremia induced by punct-
ure wounds of the foot show glycogenic infiltration, of the blood
cells. In diabetes mellitus the liver and kidney cells are infil-
trated \vith excessive quantities of glyct)gen.
Etiology. — Disturbed carbohydrate metabolism is insepar-
ably associated with glycogenic infiltration although the specific
relation of disturbed carlDohydrate metabolism and glycogenic
infiltration is not known. Glycogenic infiltration has some asso-
ciation also with certain infectious and inflammatory disturban-
ces as well as tumor formations.
Appearance. — Macroscopic. — Glycogenic infiltration does not
produce lesions sufficiently characteristic to be recognized with-
out the aid of a microscope.
Alicroscopic. — The affected cells contain transparent colorless
areas near the nucleus. If the specimen has been hardened in
absolute alcohol, the areas of glycogen may be stained port
wine color b_v four parts of alcohol and one part tincture of
iodine. The areas are \ariable in size depending u])on the ex-
tent of the condition. In extreme cases the glycogen may be
observed in the intercellular spaces.
Tissues Affected. — Liver, kidney, muscle, and blood cells are
most subject to glvcogenic infiltration, the frequencv in the order
named.
Effects.- — The glycogen is readily reabsorbed provided the
cause be rem.oved. The condition being associated with other
pathologic conditions, their removal becomes essential before
the sflvcogenic infiltration can be overcome.
224 VETKRINARV PATHOLOGY.
URATIC INFILTRATION.
GENERAL DISCUSSION.
DEFINITION.
ETIOLOGY — Deficient uric acid secretion.
APPEARANCE.
Macroscopic.
Microscopic — Needle like crvstals.
TISSUE AFFECTED— Articulations.
EFFECTS.
Uric acid is formed by the kidneys from urea and passes out
normally with the urine. If not promptly eliminated, it com-
bines with sodium carbonate of the blood to form sodium urate
(quadriurate and biurate). The quadriurates are unstable but
the biurates are quite stable. Uric acid and urates do not nor-
mally exist as such in the blood of birds or mammals. The urin-
ary excrement of birds is composed of urates but no urea. In
birds the ureter terminates in the cloacum ; the kidney excretion,
which is almost solid in consistency, is thus mixed with the feces
before it is eliminated from the body. This anatomic arrange-
ment probably favors the resorption of uric acid. At any rate
uratic infiltration is more common in birds than in any other
domestic animal.
Sodium urate is the usual compound found in uratic infiltra-
tions and when examined miscroscopically appears as a feltwork
of radiating clusters of needle like crystals. If urate of sodium be
treated with a few drops of nitric acid, and then evaporated to
dryness, and to the amorphous residue a few drops of ammo-
nium hydrate be applied, the entire mass assumes a purple-red
color, or if potassium hydroxide be applied, the mass becomes
bluish-purple.
Etiology.— L'ratic infiltration is due to deficient excretion
of uric acid bv the kidneys. It may be caused bv ligation of the
ureters or by any obstruction to these ducts. An exclusive
meat or other nitrogenous diet, sometimes produces uratic infil-
tration in fowls. Old age is a predisposing factor.
Appearance. — Macroscopic. — The phalangeal, metatarsal and
tarsal joints are most frequentlv afifected in fowls. In the begin-
ning the condition is evidenced by a soft, painful, diiTuse swell-
ing becoming more circumscribed as it becomes lareer. The skin
over the afl:"ected area becomes thickened and scales of¥ as the
swelling increases in size. The nodular swellings ultimately
rupture, the contents lacing luiff colored and crumbling as it is
discharged. Sometin.ies masses of the urates accumulate as
small stones (tophi) under tendons, etc. The articular surfaces
are frequently eroded.
retr()(;ki:ssivk tissue changes. 225
Microscopic. — The needle like crystals of sodium urate, in
addition to more or less detritus from necrosis of the tissue, is
characteristic of sections or smears of tissues atTected with uratic
infiltration.
Tissue Affected. — Articulations arc the usual location of
uratic intiltration, especially those in the metatarsal region. The
skin and visceral organs may be affected.
Effects. — The accumulation of the urate crystals in the artic-
ulation, produces erosion of the articular surfaces, and thus
interferes with luovement. Tophi beneath tendons also produce
disturbance of mobility.
KERATOSIS.
DEFINITION.
GENERAL DISCUSSION.
ETIOLOGY.
Dessicalioii of surface epithelium.
Excess of intercellular cement.
APPEARANCE.
Macroscopic— LI amy grozvfhs.
Microscopic.
TISSUE AFFECTED— EpitJieliiim.
EFFECTS.
Epithelium becomes cornified thus forming the hard horny
hoofs, horns and claws. The conversion of epithelium into horn-
like substance (characteristic of the hoof) consists of a dehy-
dration of the cells and the production of a glue like inaterial
that cements the dessicated cells together. The ergots and
chestnuts in the skin of the horse are produced by the accumu-
lation of dessicated cells cemented together.
The cornified epithelium that characterizes keratosis varies
from dried scales to dense horn tissue.
Pathologic cornification is of rather common occurrence in
the domestic aninrals. The skin covering the carpus of oxen fre-
quently becomes materially thickened and cornified, one case
having been observed in which the cornified mass accumulated
until a projecting horn like structure some ten inches long and
six inches in diameter at its base, was present. As a general
condition it is observed in the skin of animals affected with ich-
thyosis.
Etiology. — Irritation appears to be a causative agent in
keratosis. The condition mav be a sequel of inflammation and
sometimes occurs in scars. Whatever increases dessication' of
226
VETERINARY PATHOT.or.V.
epithelium and stimulates the formation of excessive quantities
of cellular cement favors keratosis.
Appearance. — Macroscopic. — Keratotic accumulations appear
like so much irregularly formed horn tissue. The resistance
of the cornified epithelium varies according to the completeness
of cornification.
Fig. 105.— Fhotograph of a Keratotio, horn-liku grovvlh removed from
region of withers of an ox.
Microscopic. — The cornified epithelium usually appears as
a mass of debris, although in some instances there may still be
evidence of cellular elements. The epithelial pearls of epitheli-
omata probably represent a type of keratosis, — the pearls appear-
ing as whirls of scale like elements suggesting the gross appear-
ance of a section of an onion.
Tissue Affected. — Epithelium is particularly affected. Some
tumors are affected, especially epitheliomata.
Effects. — The area involved is inconvenienced. If the en-
■tire skin is involved there may be secondary constitutional les-
ions.
RliTROGRESSIVE TISSUE CHANGES. 227
OSSIFICATION.
PHYSIOLOGIC.
PATHOLOGIC.
ETIOLOGY.
Irritation.
Improper iiiitritioii.
APPEARANCE.
Macroscopic — Osseous masses.
Microscopic — Osseous plates.
TISSUE AFFECTED.
Muscle.
Arteries.
Tumors.
EFFECTS.
Ossification, as in the formation of bone, is a normal process.
The process consists in the formation of fibrous lamellae that
are later calcified. Osseous bodies are sometimes formed in such
structures as the falx cerebri and tentorium cerebelli. These
osseous formations assume the shape of the original structures,
and are called osteophytes.
Pathologic ossification consists in the formation of a bone
like substance in abnormal locations, as muscles, arteries, tum-
ors, etc.
Etiology. — Ossification probably results from chronic irrita-
tion, improper circulation, or impoverished nutrition.
Appearance. — Macroscopic. — Ossified muscle appears as a
porous osseous mass. In an autopsy of a horse the flexor bra-
chii muscle, was found to be a porous osseus mass, and appeared
like cancellated bone. Muscle ossification is usually designated
myositis ossificans. An ossified falx cerebral or tentorium cere-
bellar osteophyte appears as an irregular bony mass.
Microscopic. — The porous osseous tissue formed in pathologic
ossification is found on microscopic examination to consist of
osseous plates surrounding irregular cavities.
Tissue affected. — Muscle, arteries, connective tissue and tum-
ors.
Effects. — Ossification occurs only when the normal struct-
ures have been practically destroyed. It represer/ts a condition
that is not reparable.
For dififerentiation of this condition and osteomata see discu?-
sion of the latter.
228 VETERINARY PATHOLOGY.
CALCAREOUS INFILTRATION.
DEFINITION.
ETIOLOGY.
Impaired circulation.
Rickets.
Iiito-vication, Mcrctirv, etc.
VARIETIES.
Tissue Spaces — Calculi.
Tissue.
TISSUE AFFECTED.
EFFECTS.
Calcareous infiltration is a condition in which lime salts are
deposited in abnormal locations or excessive quantities are
deposited in those tissues in which calcareous depositions nor-
mally occur.
In the formation of osseous tissue, certain definite quantities
of lime salts impregnate the softer formative tissue, thus produc-
ing typical bone. Considerable quantities of lime salts normally
occur in the blood and lymph of the various animals. The urine
of the horse, donkey, and mule frequently contains such large
amounts of calcium phosphate that it is quite turbid when ex-
creted. Excessive quantities of lime salt in solution predispose
to calcareous infiltration as well as to calculus formation.
The lime salt most frequently found in tissues affected with
calcareous infiltration is the carbonate, though other salts of
lime mav be present as the phosphate and rarely, the sulphate.
These salts are all insoluble in water, alcohol, ether and chloro-
form, as well as most other solvents. The application of dilute
acids usually cause excessive effervescence because of tlie lib-
eration of carbon-dioxide.
Pathologic calcareous infiltration sometimes occurs in dense
scar or cicatricial tissue as in extreme cases of poll evil, fistu-
lous withers or quittors ; in necrotic areas as tul^ercles of tuber-
culosis in cattle and hogs ; in necrotic areas of arteries affected
with atheromatous degeneration; in inspissated pus; in the sup-
porting framework of the lungs producing pneumono-koniosis ;
in the kidney ; and in other organs in chronic bichloride of mer-
cury poisoning; in parasitic cysts, as the trichina cysts in hogs,
and psorosperm cysts ; and in dead foetuses.
Etiology. — Imperfect circulation.— Tuhercu\ar lesions (tubercles)
are nonvascular and invariably become calcified sooner or later. Al-
though tubercles are nonvascular, there is more or less enzy-
motic action taking place resulting in the liberation of carbon
dioxide; there are variable quantities of fluid containing lime
RETROGRESSIVE TISSUE CHANGES. 220
salts in solution filtering into the tubercles ; the liberated car-
bon-dioxide combines with the soluble lime salts forming insolu-
ble calcium carbonate which is deposited in the tissue thus pro-
ducing calcification. Enzymotic action is also present in local
areas of tissue, other than tubercular, that have recently become
necrotic, as inspissated pus, thrombi, infarcts, necrotic areas in
arteries, and there is also sufficient soluble lime salts present
to combine with the carbon-dioxide liberated by the enzyms to
form insoluble calcium carbonate, thus necrotic tissue becomes
calcareous.
Dense fibrous masses are frequently poorly nourished because
of the obliterated vessels and occasionally become calcareous.
Thus it is not rare to find calcareous centers in the dense fib-
rous tissue of fistulous withers.
Improper Food. — Food or water containing excessive quanti-
ties of certain lime salts predispose to calculus formation and in
some instances to the deposition of lime salts in tissues as the
kidney and lung.
Inhalation of air containing large quantities of lime or clay dust
in suspension, results in their deposition in the alveoli of the
lung, and infiltration into the framework of the lung producing
the condition known as chalicosis. Horses and mules worked
in and around cement plants, stone crushers, rock quarries, etc.,
are afifected with pulmonary chalicosis and are more subject to
pulmonarv diseases than animals not so afifected.
There are probably some chemic substances, resident in the
body which when increased or diminished favor the deposition
of lime salts. It may be that the chemic reactions of a tissue is
a factor of considerable moment in calcareous infiltration.
Appearance. — Macroscopic. — Tissue afifected with calcareous
infiltration is hard, granular and gritty. When palpated, it is
quite resistant and may be massive, but is more likely to be com-
posed of small calcareous masses held together by variable quan-
tities of soft tissue. It is gritty when incised or sawed and in
some instances the tissue is so densely infiltrated that it is impos-
sible to either cut it with a knife or saw, a chisel being required
to break it asunder. Calcareous tissues are heavier than normal
tissues. Tissue may be equally afifected throughout or the calcar-
eous material may be concentrated in small areas arranged con-
centrically around a central mass or in lines radiating from a cen-
tral point. The calcareous material may appear in spherical
masses as in the tubercular lesions or in scales as in arteries
afifected with athermatous degeneration. The air cells and bron-
chioles in the lungs of horses afifected with chalicosis contain
230
VETERINARY PATHOLOGY.
incrustation of scales of lime and the framework of the lung may
be infiltrated with small gritty calcareous masses.
Microscopic. — The calcareous material may be amorplious or
crystalline and it may occur in the cells or between the cells.
Cellular calcareous infiltration normallv occurs in the cells of
the pineal body and pathologically in kidney cells, nerve cells,
etc. The calcareous granules or crystals are usually stained
dark with hematoxylin and give the general impression that
chromatolysis (fragmentation of the nucleus) had occurred.
Fig. 106. — Atlieromatoiis Degeneration, Aorta.
a. Calcarious deposit in the tunica media.
Calcareous material infiltrated between the cells may be amor-
phous or crystalline and assumes the same stains and appears
similar to the intracellular infiltrated lime salts. The calcareous
material is soluble in dilute acids, except calcium sulphate, with
more or less effervescence.
Tissue Affected. — Necrotic tissues are most subject to cal-
careous infiltration. Blood vessels, lung tissue, kidney tissue,
dense fibrous tissue, are also subject to calcareous infiltration.
Effects. — Calcareous infiltration is a means of converting
necrotic tissue into a noninjurious mass. Calcified tissue is prob-
ably never regenerated because calcareous deposits are not ab-
sorbed.
RRTROGRESSIVE TISSUE CHANGES. 231
CALCULI.
DEFINITION.
ETIOLOGY.
STRUCTURE.
SHAPE.
SIZE.
NUMBER.
COLOR.
COMPOSITION.
VARIETIES.
Urinary.
Salivary.
Gastric.
Intestinal.
Biliary.
Lacteal.
Venous.
Arterial.
Calculi are accumulation in the body cavities, of min-
eral matter precipitated from the body fluids, or they miay
be mineral incrustations upon foreign substances in the body
cavities. The mineral deposits formed within the tissues of
the animal body, as calcified tubercules, etc., are calcareous in-
filtration or tissue petrification. Calculi, however, may and
frequently do, become attached to the tissue, surrounding them
(phleboliths), .and a calcified tissue may become separated from
the surrounding structures (calcified necrotic tissue in fistula).
Hence the two conditions, calculus formation and calcification,
approximate each other closely and at times are not separable.
Etiology. — The causes of calculus formation are not thor-
oughly understood. The most probable cause is the supersatur-
ation of the body fluids with salines. The fluids may become
super-saturated either by an excessive production of the salines
or diminished excretion of them. The lack of oxygen or an
excess of carbon dioxide mav cause the precipitation in body
fluids, especially of calcium and magnesium carbonates. Fer-
mentation of various juices may result in precipitation of a vari-
ety of compounds. Btit why the precipitate should accumulate as
a calculus is unexplained. It is a phenomenon not understood.
There are many predisposing causes that aid in the formation of
calculi. The retention or delay in the excretion of fluids, especi-
ally if they undergo any chemical change, are principal factors in
calcular formation. Intoxication from mercury predisposes to the
formation of urinary calculi. The presence of any foreign body,
as particles of sand, desquamated cells, coagulated albumen,
parasites, etc., upon which a precipitate may accumulate, is a
predisposing- cause. According to Ziegler all calculi have an
232 VETERINARY PATHOLOGY.
organic nucleus. But it seems possible and quite probable that
particles of inorganic matter may be deposited upon an inorganic
nucleus in the formation of calculi.
Structure. — The structure of calculi varies. Homogeneous
calculi are composed of layer upon layer of the same material
and have the same appearance throughout. Heterogeneous cal-
culi are laminated, i. e., thev are composed of layers of different
material and appear different in the succeeding layers. Calculi
vary from finely granular masses (appearing as though many
grains of sand had been fused into a mass) to lobulated masses
(mulberry calculi) ; or they appear smooth as though they were
molten mineral run into forms.
Shape. — Calculi assume all conceivable shapes. Cystic calculi
vary in form from spheres to jack straws, and even coral like
bodies or stalactite calculi have been observed. Their form may
be determined by their location. Thus renal calculi may assume
the shape of renal tubules, renal pelvic calculi the shape of the
renal pelvis. Intestinal calculi are usually more or less spherical
in shape. Salivary calculi are ovoid. Calculi mav be faceted
when occurring" in large numbers.
Size. — The size of calculi varies from the finest sand-like
grains to enormous accumulations. A 22S-gram (7 oz.) cystic
calculus was removed from a Jack, by Dr. McCasey, Concordia,
Kansas. A 260-gram (8 oz.) cystic calculus was removed from a
five-year-old Jack at the Missouri Valley Veterinary Association
clinic in February, 1907. Dr. Z. C. Boyd, in 1906, removed from
Steno's duct, in a horse, a salivary calculus weighing 125 grams (4
oz.). Enteroliths weighing 20 lbs. or more are occasionally observed.
Number. — The number of calculi occurring in one animal is
quite variable. There has been a case reported in which there
were over 300 cystic calculi in one dog, although that is an un-
usual number.
Color. — The color of calculi is determined by their composi-
tion. Thus biliary calculi are highly colored because of the bile
pigment, bilirubin and biliverdin, that they contain. Enteroliths
are usuallv colored from the intestinal contents. Arterioliths
and phleboliths are colored with hemoglobin or some of its
derivatives. Urinary calculi may be gray, brown, yellow, or
even red, depending upon their composition. Salivary calculi
may be chalk white or tinged with various colors.
Composition. — A varietv of chemical compounds are found
in the various calculi. Urinary calculi mav contain cystin, xan-
thin, urates, oxalates, carbonates, phosphates, calcium, magnes-
ium, etc. Cystin and xanthin urinary calculi are quite rare.
RETROGRESSIVE TISSUE CHANGES.
233
Urates are common in renal tubular calculi, also in cystic calculi
of dogs and cats. Carbonates predominate in cystic calculi of
the horse and ox. Ammonium-magnesium-phosphate is the prin-
cipal compound in cystic calculi of the sheep and hog. Urethral
calculi are of the same composition as cystic calculi of the
Fig. 107. — Group of Calculi, showing a variety of shape.
same animal. Preputial calculi are usually composed of car-
bonates in the horse and of phosphates in the ox and sheep.
Biliary calculi may be composed of carbonates or phosphates, but
are more frequently composed of calcium biliverdin. Enteroliths
may contain a large nucleus of fecal matter or hair which be-
comes permeated and incrusted with calcium or magnesium car-
bonates, phosphates, sulphates, or oxalates. Salivary calculi,
234
VETERINARY TATHOLOGY.
arterioliths, and phleboliths are usually composed of the carbon-
ates and phosphates of calcium and magnesium. Lacteal calculi
are composed chiefly of phosphates.
Varieties.
UrUiar\ Calculi are of frequent occurrence and may be con-
veniently classified according to the location in which they
occur.
1. Renal tubular calculi are most common in dogs and cats,
but may occur in horses, cattle and hogs. After formation they
frequently pass into the pelvis of the kidney and the urine may
wash them down through the ureter into the bladder and some-
Fig-. lOS.— Photograph of a 7 ounce Cystic Calculus successfully removed from the
bladder of a jack.
times on out of the animal body. Thev may ol)struct the tubule
causing retention of urine with distension of the tubule and thus
occasion cyst formation.
2. Renal pelvic calculi are not rare, the pelvis of the kidney
sometimes being completely filled with a calculus. This variety
has been observed in the hog, dog, cat, horse, and sheep, the
frequency in the difi^erent animals being in the order named.
A 7-gram (J4 oz.) renal pelvic calculus was obtained in 1906
from a horse used for dissection purposes at the Kansas City
Veterinary College. G. H. Woolridge, of Dublin, describes a
case of calculus formation in the renal pelvis of a liorse (Veter-
inary Journal for Jnne, 1907) in which the entire kidney was
practicallv replaced bv the calculus. The results of calculi in
the renal pelvis depend upon their extent. Complete obstruc-
tion necessarilv results in the retention of urine followed either
by its resorption (producing uremia) or its accumulation (form-
RETROGRESSIVE TISSUE CHANGES.
235
ing a cystic kidney). The former condition has been observed in
dogs, the latter in hogs.
3. Ureter calculi have been observed but are rare.
4. Cystic or vesical calculi are the most common of all urin-
ary calculi. Dogs and cats are quite subject to them, occurring
more frequently in the older animals, but the puppy and kitten
are not exempt. Bitches and castrated male cats are especially
subject to cystic calculi. Jacks are frequently affected with
cystic calculi, horses, goats, sheep and cattle less frequently.
A cystic calculus 18 x 20 cm. (7x8 inches) was successfully
removed from a 2-year-old colt by Dr. E. S. Fry, of
.^
Preputial calculus.
Fig. 109. — Irinary Calculi
Renal pelvic calculi
Naperville, 111. Cystic calculi may cause no inconvenience or
they may produce sufficient irritation to estalDlish a severe cys-
titis. They may obstruct the urethral opening resulting in reten-
tion of urine and rupture of the bladder. Frequentlv they become
imbedded in the walls of the bladder, and may cause dilatation
or pouching of its walls. Sometimes the calculi pass out of the
bladder and become lodged in the urethra, resulting in retention
of urine, difficult micturition, and usually urethritis.
0. Urethral calculi are common in old dogs, also in the bull
and ram. and have been observed in the horse. They occur in the
urethra, in the beginning of the gutter of the os penis in the
dog, usuallv in the first curve of the penis in the bull, just pos-
terior to the meatus urinaris in the ram and at the ischial arch
236 VETERINARY PATHOLOGY.
in the horse. The}' usually cause difficulty in micturating and
may completely obstruct the urethra with the same results that
are produced by occluding the uretliral opening of the bladder.
Urethral calculi may produce erosions of the urethra and sur-
rounding tissues and thus, produce an artificial urinary canal
through which the urine will be discharged, this is probably
more common in male bovines, than in other animals.
About 200 urethral calculi were observed in the urethra of one
steer by Dr. B. F. Kaupp.
6. Preputial calculi sometimes occur in geldings, although these
are more frequently accumulations of the secretion from the ad-
jacent sebaceous glands. W. Williams reported cases in which
there was formation of stalactite bodies in the prepuce of oxen
and sheep that had been fed food material containing a large per
cent of phosphates. A preputial calculus weighing 11 grams
(Yg oz.) and another weighing 10 grams were obtained from a
hog" by a veterinary inspector.
Salk'arv calculi occur most freciuently in the horse, although
they do occur in the ass, ox and sheep. Their formation depends
upon the ingested water containing a large quantity of car-
bonates of potassium, sodium and magnesium and the presence
of calcium salts in the saliva. (Dr. J. M. Lawrence, Veterinarian
U. S. Army, Fort Wingate, N. M., operated upon two horses,
removing from Steno's duct in each a salivary calculus. In
the center of one of these calculi an oat grain (nucleus) was
J
Fig. 110.— Photograiih of a Salivary Calculus removed from Steno's Duct, horse.
found upon which the deposit had taken place. This calculus
weighed 19 grams {-/. oz.) The result of salivary calculi is
to obstruct the outflow of saliva, the retention of which in the
smaller ducts may cause inflammatory, degenerative or atrophic
changes in the gland, and if the calculi are not removed the des-
truction of the gland or the rupture of the duct and a salivary
fistula. Tartar on dogs' teeth has an origin similar to that of
salivary calculi.
RETROGRESSIVE TISSUE CHANGES. 23/
Gastric Colculi (gastrolitlis) occur in the paunches or reticula
of cattle, sheep and goats. They are exceptionally ra^e in the horse
and hog, and prohahly never occur in dogs and cats.
Intestinal Caicnli or enteroliths are found in the large intes-
tine of the horse, especially those fed upon bran. These cal-
culi are composed primarily of ammonio-magnesium phosphate,
the magnesium phosphate being dissolved out of the bran by the
acid of'the gastric juice and uniting with nascent ammonia form-
ing an almost insoluble phosphate. Enteroliths may be of enor-
mous size, in some cases, weighing as much as ten kilograms
(22 lbs.). These calculi are likely to cause erosions of the mucous
Fig. 111.— Photograph cii an Intestinal Calculus having a circumference
of 12 inches and weighing 3 pounds.
membrane as well as obstruction of the lumen of the intestine.
Linch, of Albany, N. Y., reported a case in the Review, 1906, in
which a calculus weighing 3.4 kilograms (7><^ lbs.) was found.
Gage reported a case in which a calculus weighing .9 kilo-
grams produced fatal results. Hodgkins and Son of Hanley, Eng-
land, recently obtained three enteroliths, each weighing 1.6 kilo-
grams {oy2 lbs.) from the intestine of a horse.
Biliarv Calculi (Choleliths) are not rare in the domestic ani-
mals. They vary from the size of a pea to a baseball, are tinted
yellow, brown, red, green, or may be chalk white in color. Fre-
quently they occur in large numbers, are variable in shape, and
structure. They are usually composed of biliary pigments in
2ZS,
VETERINARY PATHOLOGY.
combination with calcium, although carlxmates and phosphates
are common ingredients. Biliary calculi may form in the biliary
collecting tubules of the liver in the bile duct or in the gall blad-
der. The results of their presence depend upon their location
and size. If they are small and cause no obstruction there will
be no inconvenience from them. If they are of a size that they
can be forced through the bile ducts they wall produce severe
colickv pains at the time of passage. They may be sufficiently
large to obstruct the bile duct of some principal collecting tubule
and produce a stagnation and resorption of bile, resulting in
Fig. 112. — Biliary Calculi, Ox.
Showing- Facets. ". Showing Crevice.
Showing' Facets and Lamination.
various disturbances because of the presence of the bile in the
blood.
Pancreatic calculi, or calculi in the ducts of the pancreas, have
been observed particularly by veterinary inspectors. These calculi
produce obstruction of the ducts and there may be reabsorp-
tion of some of the pancreatic secretion. Fatty necrosis sometimes
succeeds obstruction bv pancreatic calculi.
Lacteal Calculi ( galactoliths ) may be formed in the galacto-
phorus sinuses, particularly of the ox. They are usually com-
posed of calcium phosohate.
RKTROGRKSSIVE TISSUE CHANGES. 239
P/ilcbolitl's or calculi in veins have been observed by Spoon-
er in abdominal veins and by Simmonds in the jugular vein.
They are probably the result of calcification of thrombi which
have later become detached from the vessel walls and are true
calculi. They produce an obstruction in the vessels in which
they occur. They may be of slight significance or may cause a
fatal termination, depending upon the importance of the vessel
and extent of the collateral circulation or anastomoses. These
calculi are usually composed of calcium compounds.
Artci'ioHUis are calculi formed in arteries. Their cause, for-
mation, composition and termination being practically the same
as that of phleboliths.
Lithopcdia are calcified foetuses. In extra-uterine foetation the
foetus occasionally lives only for a short time. Dead extrauter-
ine foetuses frequently become impregnated with lime salts,
producing the so-called lithopedia. Lithopedia may also occur
within the uterus. This class of calculi is quite common in
swine and some cases have been observed in cattle and sheep.
CONCREMENTS.
DEFINITION.
ETIOLOGY.
VARIETIES.
Hair balls.
Fecal matter.
Bile.
Pus.
Milk.
Cerumen,
Concrements are abnormal accumulations of organic material
in the cavities of hollow organs. Their effects are practically the
same as the effects of calculi. Their formation depends upon the
collection and massing together of organic substances derived
either from the body in which the concrements occur or from
some extraneous source. They may be homogeneous or hetero-
geneous in structure ; oval, spherical, or angular and faceted in
shape, variable in size, color and number, (873 oat hair concre-
ments were found in the great colon of a horse by C. Roberts,
M. R. C. V. S.). They may be composed of hair, mucus, fecal
matter, casein, inspissated pus or bile, ingesta of various kinds,
etc.
240
VETERINARY PATHOLOGY.
Hair Balls (Egagaropiles or Trichobezoars) are accumulations
of hair into masses. They occur most frequently in animals that lick
themselves as the ox and deer. Other animals are affected as the
hog, dog and cat, also man, espe-
cially barbers, hair-sorters, hair-
dressers, etc. Dr. A. Trickett
observed a Persian, cat that
womited a mass of hair ^}4-inch
in diameter and 3 inches long.
Egagaropiles vary in size from a
pigeon's egg to a basket ball.
They are in some cases simply
masses of hair in others they
are impregnated and incrusted
with mineral substances, giving
them the appearance of calculi.
Hair balls incrusted with min-
eral salts taken from the deer by
someone's grandfather or great-
grandfather is the ordinary
"mad-stone" in use at the pre-
sent time. Recently a hair ball
(bristles) completely filling the
stomach was obtained from a
hog slaughtered in a packing
house. Hair balls are usually
found in the abomasum or large
intestines of the ox and in the
stomach or large intestine of the
hog. The presence of a hair
ball produces the same effects
that would be produced by any
other indigestible body of the
same size in the same location.
Fecal Concrements. — The
intestinal contents may accumu-
late into compact masses. These
Pis. 113- — Hair Balls. i • j. r "j-l 4-1
(Egagaropiles.) coiicremcnts interfere witli the
tlETROGRESSIVE TISSUE CHANGES.
241
movement of food-stiifif through the canal and may completely
obstruct it. Appendicitis in the human is frequently a result of a
fecal concrement in the vermiform appendix. These concrements
occur most frequently in the horse, dog and cat. They are usu-
ally composed of cellulose in the horse, of bones and bone frag-
ments in the dog and cat. The large intestine is the usual loca-
tion of them in the horse and the small intestine in the dog or
:at. Maxwell reported a case in which alfalfa accumulated in
the large intestine of a horse, the concrements being irom 17^
to 22y2 cm. (7 to 9 inches) in diameter. The fine hair of
clover or oats (phytobezoars) frequently accumulates and forms
concrements. The results of fecal concrements depend upon either
mechanical interference in the passage of intestinal contents, erosion
of the intestinal mucous membrane or perforation of the intestinal
wall, or a combination of two or more of the above.
Inspissated Bile. — If the outflow of bile is obstructed it will
become condensed or inspissated to a degree depending upon
the length of time of obstruction. Inspissation of bile frequently
occurs. The animals most frequently afTected are the ox and
hog. An ox liver, containing several concrements composed of
inspissated bile in the interlobular ducts has been observed. Bile
in this condition may form masses which in general appearance
resemble biliary calculi. It is sometimes impossible to differen-
tiate biliary calculi from inspissated bile, and, in fact calculi are
Fig. 114.
X. inspissated pus from lung abscess. 2, Inspissated pus, guttural pouth, horpe,
242 VICTFRrXARV PATTIOr.OGY.
frequently of secondary origin, the thickened bile forming the
nucleus. The results of inspissated bile depend first upon the
resorption of bile into the system and, second, upon the absence
of bile in the intestine.
Inspissated Pus. — Empyema sometimes terminates, when
there is no surgical interference, in resorption of the liquor puris,
after which the solid constituents frequently mass together,
forming concrements. These concrements may form in any cav-
ity in which the suppuration is slow going or chronic, provided
the movement of the part is limited. Their formation has been
noted in the guttural pouch. After formation they may become
calcified. They are of little importance except as pathologic
phenomena.
Lacteal concrements result from the coagulation of the casein
of milk and its accumulation in the galactophorous sinuses.
These concrements occur in the cow and can usually be expelled
through the lacteal duct by manipulation.
Cerumincus concrements" occur in animals in which the hair
or wool extends far into the external auditory meatus. They
are composed of cerumen and are the result of an excessive pro-
duction or limited excretion of it. They may form into sufficient
masses to completely occlude the external auditory canal and
thus interfere with hearing. Concrements have been found iB
the bronchial tubes. Their formation depends upon the accu-
mulation and condensation of mucus or purulent fluid. They
may obstruct l^ronchioles and produce atalectasis.
Prostatic concrements frequently occur in old dogs. They
are present in inanv of the enlarged prostate glands. They con-
sist of masses of accumulated colloid-like material. The results
depend ujion the pressure that they may exert. Thus there may
be an obstruction to the outflow of urine.
PIGMENTARY CHANGES.
Physiologic pigmentation is variable. The color and extent
of pigment varies in dift'erent animals and in the same animal
under different conditions. All physiologic pigmentation is the
result of deposition of hemoglobin or some of its derivatives.
The skin of animals is usuallv extensively pigmented, with
the exception of albinos and some white skinned animals not
albinos. The production of the cutaneous pigment is not well
understood but probablv results from metabolic activity of the
deeper layers of epidermal cells. Because of the intense cutan-
RETROGRESSIVE TISSUE CHANGES. 243
eous pigmentation of animals, erythema, hemangiomata and other
pathologic processes are not as evident as like conditions in the
human. The excessive cutaneous pigmentation protects the skin
from the injurious influences of sunlight.
Hair, wool, fleece, fur and feathers are variously colored, the
color depending upon the soluble pigment in the cortical portion
of the cutaneous appendages. The color of the skin is usually
an index to the color of the hair or similar epidermal appendages.
The color of hoofs, horns, and claws is probably dependent upon
cutaneous pigment.
Voluntary muscle tissue is pigmented with varying quanti-
ties of hemoglobin, excepting the so-called white meat of fowls
(the sternal muscles and muscles of the pectoral arch). The
pigmentation of the voluntary muscles varies in the different
animals. The equine muscles are the most intensely red, the
intensity of pigmentation in the muscles of other animals being
in the following order: bovines, ovines, porcines, canines, felines.
The flesh of duck and quail and the dark meat of other fowls is
darker even than equine muscle. Heart muscle is very dark in
color because of the excessive quantities of pigment. Gizzard
muscle is intensely pigmented. Involuntary muscle of all ani-
mals is very light in color, because of the limited quantity of
pigment contained. The significance of the pigmentation of
muscle is not known, possibly the hemoglobin of the muscle cell
has some important metabolic function.
The mucous membrane, particularly of the mouth, is fre-
quently pigmented. The buccal mucous meml^rane of the sheep
and dog is often black. The uterine mucous membrance of
the bitch is occasionally quite black as a result of pigmentation,
this pigment being derived from the uterine glands, and no doubt
is indirectly a derivative of hemoglobin.
Bones, especially the internal portion of the articular extremi-
ties, are frequently pigmented from the red marrow that occupies
the spaces in the cancellous bone.
The liver and spleen are naturally deeply pigmented because
of the excess of free hemoglobin in those organs. The kidney
also appears pigmented, probably because of the excess quantity
of blood contained in it. The choroid tunic of the eye is deeply
pigmented with a substance not unlike melanin, the purpose of
which is to absorb rays of light.
244 VETERINARY PATHOLOGY.
EXCESSIVE PIGMENTATION.
(Hyperchromatosis.)
DEFINITION.
ETIOLOGY OR SOURCE.
Hematogenous.
Hemoglobin.
Hemosiderin.
Heinatoidin.
Hepatogenous.
Bilirubin.
Biliveridin.
Cellular.
Suprarenal — Addison s disease.
Tumor — Melanin.
Pregnancy.
Freckles.
Extraneous.
Pneumonokoniosis.
.Anthracosis — Carbon.
Siderosis — Iron.
Argyriasis — Sik'cr.
Plnnibosis.
Hvdrargiriasis..
TATTOO.'
EFFECTS.
Excessive pigmentation, also known as pigmentary infiltra-
tion, is a pathologic condition characterized by the presence of
an excess of pigment in the tissues. Pathologic pigmentation is
quite common. Icterus, melanosis, and anthracosis are types
of pathologic pigmentation. This condition may be congenital
as melanosis maculosa of calves, or it ma^^ be acquired as in
icterus.
Etiology. — In pathologic pigmentation the coloring matter
may be derived from internal sources, as blood, bile and cells, or
from external sources as coal dust, silz'cr, lead and various pig-
ments.
Blood. — Pigmentation as a result of deposition of hemoglobin
of the blood is designated hematogenous pigmentation. Hemo-
globin is the principal hematogenous pigment, although hemo-
siderin and hematoidin, both derivatives of hemoglobin, are of
some importance.
Hemoglobin is the normal coloring matter of the red blood
cells and muscle. It constitutes about 90 per cent of the solids
of red blood cells. It is a compound proteid and exists only in
combination with lechithin. Hemoglobin splits up readily into
RETROGRESSIVE TISSUE CHANGES.
245
globin and hemochromogen, the latter combines with oxygen no
form hematin.
Hemoglobin is liberated from the red blood cells and in all con-
ditions in which there is rapid destruction of these cells, as in tick
fever, anthrax, hemorrhagic septicemia, toxic doses of chlorate of
potassium, lead poisoning, and other hemolytic agents, excessive
quantities of hemoglobin is set free. A portion of the liberated pig-
ment is eliminated by the liver and kidneys, thus excessive quan-
tities of bile and Ijloody urine (hemaglobinuria) are a feature of
tick fever, lead poisoning, etc. The liberated hemoglobin not
eliminated from the body is deposited, especially in the vessel
walls, but ultimately diffuses into the lymph and infiltrates prac-
tically all tissues. Post-mortem staining is the result of hemo-
globin deposition into the dependent tissues. Hemoglobin is
also liberated from muscle tissue in azoturia and other diseased
.^_...
<^
p
SQWVjfeTjj
Fig. 115. — Hemosiderin Pigmentation.
a. Tubules containing rteposits of liemosidtrin in the cells.
b. Normal kidney tubules.
246 VETERINARY PATHOLOGY.
conditions of muscle. The hemoglobin liberated from muscular
tissue is disposed of in the same way as that derived from red
blood cells. Hemoglobin pigmentation, the results of bruising, is
common in the superficial tissues of animals bruised in transporta-
tion and slaughtered immediately after shipping.
Hemosiderin is a derivative of hemoglobin. It is yellowish
brown in color, is insoluble in water, alcohol, ether, chloroform,
dilute acids and alkalies. It contains iron and gives the typical
iron reaction with potassium ferrocyanid. Hemosiderin is the
common pigment observed in tissues that have been previously
stained with hemoglobin. Extravasated blood observed in pete-
chiae and hematomata appear as typical hemoglobin pigmenta-
tion for a few days, after which the hemoglobin is converted into
hemosiderin and the alTected parts become a yellowish brown.
Hemosiderin pigmentation is observed in tissues of animals that
have been bruised three or four days prior to slaughter. It is
also observed in post-mortem examinations of animals that have
been afYected with diseases accompanied by hemorrhages for a
period of three to five days, as purpura hemorrhagica, acute tick
fever, anthrax, etc. Hemosiderin pigmentation is of common
occurrence in tumors.
Hcmatoidin is an iron free pigment, probably derived from
hemosiderin. It is soluble in chloroform, but is insoluble in
water, alcohol and ether. It occurs in rhombic crystals and is
occasionally observed in old hemorrhagic foci.
Blood pigments, hemoglobin, hemosiderin, and hemacoidin
are deposited in the cells and intercellular substances. The pig-
ments are removed by solution and resorption of the dissolved
pigment or by leucocytes which incorporate the insoluble pig-
ment granules and carry them out.
Blood pigmentation has little eiifect upon the tissue in which
deposition occurs, but the flesh of food producing animals is
usually condemned when pigmented because of its unsightly
appearance.
The deposition of a brownish or blackish pigment in tendons,
ligaments, cartilage and bones (ochronosis) is occasionally observed
in the carcasses of cattle which were apparently in good health.
The cause of this pigmentation is unknown. It probably does not
injure the tissues or the meat for food, but such meats are usually
condemned because of their unsightly appearance. Another brown-
ish pigmentation of muscular tissue (xanthosis) is associated with
muscular atrophy or disease of the suprarenal bodies. This con-
RETROGRESSIVE TISSUE CHANGES.
247
dition is of no consequence except public sentiment prevents the
sale of such meat.
Bile pigmentation results from the resorption of bile and its
deposition in the tissue. Bile pigmentation is designated hepa-
togenous pigmentation and the condition produced is commonly
known as icterus or jaundice. Obstruction of the bile duct or
any of its radicles by pressure, duodenitis, calculi, etc., will result
in retention of the generated bile which is later resorbed into
the blood. In some instances it is possible that extensive destruc-
tion of red blood cells and the chemic change of the hemoglobin into
bilirubin or biliveriden may produce bile in the blood vessel and
thus cause the so-called hematogenous icterus, again destruction
of considerable numbers of liver cells or diminution of their func-
tion may possibly result in the retention in the blood of those
products that are normally converted into bile, and thus produce a
hematogenous icterus. Excessive production of bile, as in acute tick
fever, is frequently accompanied by resorption of some of the bile
and its deposition throughout the body, thus producing a generalized
icterus.
Bile staining is most evident in the conjunctiva and ocular
sclera of the living animal where it produces a lemon or greenish
yellow discolorization. If resorption of bile is very extensive
— Ok
Fig. 116. — Icterus affecting lymphatic tissue.
Normal tissue. b. Deposit of bile pigment.
248 VETERINARY PATHOLOGY.
it may appear in the urine. In carcasses, biliary pigmentation
is most evident in the adipose tissue, especially the subcutaneous
fat, although it is usually well marked in the subserous fat and
may be detected in the lymph nodes, spleen, kidney and muscu-
lar structures.
The bile may be deposited in the cells or between the cells
as greenish-yellow amorphous granules. The granules are read-
ily soluble in alcohol, hence they are best detected in frozen sec-
tions.
The effects of resorption of bile are variable. The tissues are
discolored ; there may be pruritus, as the bile appears to act as
an irritant on nerve endings ; putrefactive changes may occur in
the intestine, and the heart may be depressed. Other inconstant
symptoms may appear, especially if the quantity of resorbed
bile is large.
Cells. — Aside from hematogenous and hepatogenous pigmenta-
tion the products of certain body cells become a factor in hyper-
chromatosis.
The principal pigment produced bv cellular activitv is mel-
anin. Melanosis maculosa is a congenital, cutaneous, pathologic
pigmentation of calves resulting from the excessive production
of melanin bv cutaneous cells in certain areas.
Melanotic deposits are of common occurrence in the various
glandular tissues, especially the liver, kidney, and suprarenal
glands. The deposits in the glandular tissue may occur in the
cells or intercellular spaces, and may appear as irregular yellow-
ish-brown or black masses. Melanin may occur in the form of
fine granules or be flocculent. Black kidneys are occasionally
observed, in abattoirs, especially in hogs. These usually result
from deposition of delicate, flocculent masses of melanin in the
kidney cells.
Melanosis is of most frequent occurrence in white animals,
although it has been observed in Aberdeen angus cattle, red
short horns, black and bay horses, and black and red hogs.
Melanotic tumors are pigmented with melanin. The melanin
may be a product of the tumor cells or of the adjacent tissue
cells. The principal melanotic tumors are the melano-sarcomata,
although there may be a benign melanotic tumor called a mel-
anoma.
Melanotic deposits occur in practically all tissues. The author
observed the heart muscle of an ox, that was slaughtered in an
abattoir, in which there was extensive melanotic deposits. F. G.
Retrogressive tissue changes. 249
Edwards reported an interesting case of melanotic pigmentation in
the cerebellar meninges and lymph nodes in a horse.
In a disease of the suprarenal capsule in the human (Addi-
son's disease) there is a peculiar bronzing of the skin. This con-
dition has not been noted in the domestic animal, probably be-
cause of the dense pigmentation of the skin. It is thought to be
a form of melanosis.
A pigmentation has been noted in atrophic tissues, especially
atrophied muscles. The pigment of atrophic muscles may be
the result of disturbed cell metabolism or it may result from con-
centration of the pigment, because of the diminution in the size
of the cells. Brown atrophy of the heart is a condition in which
pigmentation is prominent.
Freckles are pigmented areas of the skin in the human, the
result of cutaneous cellular action. Because of the intense pig-
mentation of the skin in domestic animals, freckles are not easily
observed, except in white animals.
Pregnancy in the human is frequently accompanied by local-
ized pigmented cutaneous areas. Such areas have not been re-
corded in domestic animals.
Aside from the blood, bile and cellular activities, pigments
may be introduced into the body from without.
The most common external substance that produces pigmen-
tation is carbon. The most extensive pigmentation by carbon
is in the lung, producing the condition known as anth'racosis.
Anthracosis is a common condition in the lungs of animals used
in and around coal mines, in cities in which there is large cjuan-
tities of coal smoke, in cats and other pet animals confined in
coal bins, engine houses, etc. The inhaled carbon is largely ex-
creted in the mucus discharged from the respiratory tract, al-
though some of it is deposited in the epithelium of the air cells,
and ultimately may be found in the interstitial tissue of the lung,
Anthracosis apparently produces little harm unless it is exces-
sive, when it predisposes to inflammatory disturbances. When
examined in gross the lungs vary in color from a gray to a deep
black. Microscopically small particles of carbon may be observed
in the cells and intercellular substances of the lung tissue.
Argyriasis is a condition in which silver is deposited in a tissue.
After the silver is deposited it is combined with sulphur, thus
forming silver sulphid, which is brownish black and imparts a
similar color to the tissue. Argyriasis is not common in animals
except those used in and around silver smelters or as a result of
the application of some silver preparation to the tissues.
250 VETERINARY PATITOEOGV.
Sidcrosis is a condition in which iron is deposited in a tissnc.
Iron, like silver, usually combines with sulphur, forming the
sulphid, which is brown or black in color. Siderosis is not
common in domestic animals, except in the intestinal epithelium
of animals that have been medicated with iron preparations.
Hydrargirosis is a condition resulting from the deposition of
mercury in a tissue. This condition is present in the intestinal
mucosa after medication with calomel or other mercury prepara-
tions. The mercury sulphid, which is brown or black in color,
is the usual pigment in hydrargirosis.
Phimbosis is a term applied to pigmentation with lead. This
form of pigmentation may be evident in the intestine in chronic
lead poisoning. It appears as a bluish black pigment.
Tattooing is the introduction of insoluble pigments into tissues.
In tattooing, the tissues are first punctured or injured, after
which some insoluble pigment is introduced into the wounds.
Some of the pigment is carried out by leucocytes and some of it
is entangled in the cicatrix of tlie healing wound, where it re-
mains permanently. Tattooing is a very valuable means of
marking stock, as it gives a positive means of identification.
Registered cattle, horses, sheep, hogs, dogs, etc., are tattooed in
the ear, and fowls on the legs. The wound is made with an instru-
ment similar to a hog ringer, in which slugs containing needle
points arranged in the form of figures or letters are used. This
instrument is used to punch holes into the inner surface of the
external ear, immediately after which carbon is rubbed into the
v^ound. When the wounds are healed, the tattoo may be easily
observed.
Effects. — Excessive pigmentation of a tissue or tissues is of
little pathologic significance. Pigmented tissues are probably
not hindered in their physiologic activities, excepting in so far
as the cause of the pigmentation is an etiologic factor in the dis-
turbance of the functioning of a part. Icteric pigmentation may be
of consequence because of the action of the bile upon nerve cells.
Pigmentation, especially when excessive, is a basis for the
condemnation of meat and meat products because of public sen-
timent.
ABSENCE OF, OR DIMINISHED PIGMENTATION.
(Hypochromatosis.)
Visible pigmentation mav be less than normal, and in some
instances there is a complete absence of pienient. Areas con-
RETROGRESSIVE TISSUE CHANGES. 251
taining less pigment than normal and depig'mented areas are
permanently white in color, as they are not affected with sun-
light or any other conditions that tend to produce pigmentation.
This condition mav be of antenatal or postnatal origin.
Etiology. — Antenatal absence of, or diminished pigmentation
may be inherited or it may be caused by disturbances of the
embryonic cells that produce normal pigmentation. Postnatal
absence of, or diminished pigmentation is usually the result of
disease in which areas of tissue have been destroyed and later
substituted by cicatricial tissue.
The total absence of pigment (achromatosis) is not of com-
mon occurrence, being most frequent in rabbits, birds and rats
(albinos). An albino is an animal devoid of cutaneous and chor-
oid pigment, the condition being inherited or congenital. The
animals thus have white skin and usually white hair and their
eyes are pink or red because of the absence of choroid pigment,
the blood being observed through the transparent ocular struc-
ture. The so-called "Wall-eyed" horses have little if any pig-
ment in the choroid tunic, and frequently they have depigmented
localized cutaneous areas.
Depigmentation is probably never generalized. Permanent
localized depigmentation, leucoderma or vitiligo, is a character-
istic symptom affecting the external genitals of horses afflicted
with dourine. It is also observed in cicatrices resulting from
burns or extensive operative procedure. Surgeons usually make
incisions in an oblique direction in order that the hair in the ad-
jacent skin may cover the scar. Scars are usually devoid of hair,
and when hair is present it may lack pigment. The application
of some medicaments on the skin of some animals causes the
hair to lose its pigment.
Temporary depigmentation is evident after an attack of coi-
tal exanthema, vaginitis accompanied by an ichorous discharge,
and by many other conditions characterized by erosion or necro-
sis of cutaneous tissue.
Effects. — The absence of pigment is of no serious conse-
quence except in some animals. Hogs that are white skinned
cannot be raised in some localities because of the effects of the
sunlight. Depigmentation of the choroid is also of some conse-
quence, because the eye is exposed to the effects of excessive
light.
CHAPTER IX.
NECROSIS AND DEATH.
NECROSIS.
DEFINITION.
ETIOLOGY.
Suspended nutrition.
Thermic.
Burning.
Freezing.
Chemic.
VARIETIES.
According to cause.
Inanition.
Thermic.
Chemic.
According to character of necrotic tissue.
Coagulation.
Colliquation.
Caseation.
Gangrene.
Mummification.
Miscellaneous.
Senile.
Fatty.
Focal.
Jack-sores.
TISSUES AFFECTED.
DISPOSITION OF NECROTIC TISSUE.
Absorption.
Exfoliation.
Encapsulation.
Sequestration.
EFFECTS.
Necrosis is local death. It is death of a part of a living body.
The term necrosis is applicable to the death of any kind of tissue,
glandular, muscular, osseous, etc. Necrosis is usually a rapid
process, that is, it is sudden death of a part. Death of a cell or
a group of cells that have been previously afifected with degen-
eration, i. e., a slow or lingering death, is termed necrobiosis.
Caries is a term used to designate necrosis of dentinal or osseus
tissue.
Cells are constantly worn out and destroyed in physiologic
active tissues. The physiologic destruction of cells is not usu-
ally thought of as necrosis although tlie cause and manner of
death may be similar, and there mav be no difference in the ap-
pearance of cells destroyed by physiologic and pathologic pro-
cesses.
253
NECROSIS AND DEATH. 253
The term necrosis is applicable to the pathologic death of a
single cell, although such a limited necrosis is rarely recognized.
Clinically necrosis is usually not noted except when the area is
sufficiently large to observe with the unaided eye.
All tissues of aH animals are subject to necrosis, and it may
occur u])on a su'^^ace or in subsurface structures. Bursattae is
a disease characterized by necrosis of the skin. Necrotic stoma-
titis, a disease in puppies, calves and pigs, is accompanied by
necrosis of the buccal mucous membrane. Tuberculosis, glan-
ders, actinomycosis, and caseous-lymph-adenitis are diseases in
which there is surface or subsurface tissue necrosis.
Etiology. — Necrosis may be primary but it is more fre-
quent h' secondary. Secondary necrosis is a seciuel or result of
some other pathologic process, as hemorrhage, oedema, throm-
bosis, anemia, hyperemia, inflammation, degeneration, infiltra-
tion and infection.
Primary necrosis is the result of; (T) obstructed nutrition;
(2) chemic substances; (o) temperature variations.
Obstructed nutrition. — A tissue or part, from which nutri-
tion is entirely obstructed, will die after all the available nutri-
ents have been consumed.
Nutrition may be obstructed from a part by some mechanical
means. An occasional result of mechanically obstructed nutri-
tion is observed in dogs in which a rubber band has been placed
upon a leg, an ear, the tongue, or the tail, the circulation being
thus obstructed the part distal to the rubber band soon becomes
necrotic. The improper adjustment of bandages, especially when
used to support fractures, is frequently a cause of necrosis.
Tumors, cysts, abscesses and other pathologic enlargements
may exert sufftcient pressure to obstruct circulation and produce
necrosis. Fractures and herniae may mechanically occlude blood
vessels and result in necrosis. The seriousness of omental
hernia or, in fact, any hernia, is due to the fact that the vessels
supplying the hernied structures are occluded, resulting in ne-
crosis and the absorption of the products of the necrotic tissue.
The plugging of a terminal vessel by a thrombus or an em-
bolus (infarction) produces necrosis if collateral circulation is
not established. Thrombo-embolic colic is a condition usually
caused primarily by the larvae of the Strongylus armatus enter-
ing and producing a parietal thrombus in the anterior mesen-
teric artery, fragments of the thrombus become detached, pass
down to and occlude the terminal mesenteric arteries, resulting
in ischemia of the walls of the intestine, and if the circulation
is not soon established the ischemic area becomes necrotic.^
254
VETERINARY PATHOLOGY.
A part or organ separated from the remainder of the body
undergoes necrosis sooner or later, the time depending- upon the
condition of the tissue and the temperature in which the sep-
arated portion is kept. Maceration and bruising produces ne-
crosis to a varying degree, depending upon the extent of the in-
jury.
S ig. 117. — Photograph showing Necrosis above the loot of a horse.
Chcmic substances. — Certain cliemic substances as phenol,
arsenic, mercury bichloride, strong solutions of the caustic alka-
lies and mineral acids, as well as the products of a large number
of bacteria, are tissue destroyers. Phenol abstracts water from
all cells to a sufficient extent to destroy their vitality, and it pro-
duces a rapid disintegration of red blood cells. Arsenious tri-
oxide is frequently applied on tumors because of its erosive
action. Bichloride of mercury combines with the cell albumins,
forming albuminate of mercury, thus inhibiting the cell action,
and when all of the cell albumin is combined the cell is de-
stroyed. The caustic alkalies and mineral acids coagulate the
cell albumin or abstract the cell water, thus destroying them.
The Bacillus necrophorous produces chemic substances that
cause coagulation of the cell protoplasm (coagulation necrosis).
NECROSIS AND DEATH.
25:
De Schweinitz has described a chemic substance produced by
the Tubercle bacillus, as necrotic acid, which is thought to pro-
duce necrosis in tubercular lesions. The toxin of the diphtheria
bacillus produces focal necrosis in practically all tissue in an
individual afflicted with diphtheria. The products of pyogenic
bacteria produce marked tissue destruction.
Chemic substances produce necrosis by coagulation of the
Fig. 118. — Bacillus Necroplionis — Pleomorphic form.
albumin by dehydration or by the formation of new cell com-
pounds, thus inducing metabolic disturbance and cell death.
Tcuipcratiin- z'ariatioiis. — All active cells have a maximum
and a minimum temperature. Thermic variations beyond these
means are injurious and destructive if the variation is extensive.
The high temperature causes coagulation of the cell protoplasm
(cloudy swelling), which, if extensive, destroys the cells.
Necrosis resulting from burning is of common occurrence. Low
temperature is not as rapidly destructive as high temperature.
Freezing produces necrosis of the tissues of warm blooded ani-
mals, probably because of cell disintegration induced by the for
mation of ice in the cells.
Types or Varieties of Necrosis. — Several factors may be used
as the basis for the classification of necrosis.
Etiology. — According to the cause, necrosis may be: a. In-
anition necrosis, b. Thermic necrosis, c Chemic necrosis.^
256
Vi;Ti:RIX.\RV I'ATPIOLOGY.
Inanition necrosis is that type resulting from obstructed
nutrition. As an example of this type may be mentioned the
necrosis of the scrotum and its contents in rams induced by
placing a rubber band moderately taut around its upper portion.
Fig. 119. — Photograph of the Eri^dt <.f K.ve.
This is a method frccjuently resorted to in the castration of old
rams. Bed sores observed in the superficial structures in ani-
mals afflicted with diseases that cause them to constantly assume
the decubital position, are the result of obstructed nutrition in-
duced by pressure upon the nutrient vessels or thrombic forma-
tion secondary to bruising.
Thermic necrosis results from exposure to extreme tempera-
tures. Thus necrosis of cutaneous tissues is of common occur-
rence in animals as a result of conflagrations or undue exposure
NECROSIS AND DEATH.
257
to the solar heat rays or thermo-cautery. Necrosis induced by-
freezing is very common in calves, pigs, and chickens, in the
temperate and frigid zones.
Chemic necrosis is represented by the extensive destruction
of the buccal, oesophageal, gastric, and intestinal tissues induced
by the ingestion of lye. Corrosive sublimate and arsenious tri-
oxide destroy the mucous membrane and frequently the deeper
tissues of the alimentary tract in animals poisoned with these
agents.
Location. — Necrosis may be surface or subsurface. Surface
m
^
m
■
p
w
JJjJH J
w
A
tf
%
\rm^*^
' . J' i
li
1^
b'^
L^..^.'-JW
:^ ^^ -- m tmr^
■'"■;^
\
V:-
Fig. 120.
1. Sloughing
-Ergot Poisoning in Cattle. Photograph by Dr. W. T. Spencer.
above the fet-t. 2. Sloughing of the ends of the tails.
necrosis may be of the skin, mucous or serous membranes. Sub-
surface necrosis may be of any tissue, muscle, bone, glandular,
etc.
Nature or condition of the necrotic tissue.
1. Coagulation necrosis. — This type of necrosis is character-
ized by the coagulation of the necrotic tissue. It is the result of
the presence of some enzym that produces the formation of fibrin
or some allied substance. Coagulation necrosis is evident in the
coagulation of blood and inflammatory exudates. The exudate
in fibrinous inflammation (croupous and diphtheritic) usually
becomes firmly coagulated. On the other hand, coagulation is
rarely observed in collections of lymph, as in ascites, etc. The
necrotic tissue in anemic infarcts, especially in the kidney, is
sometimes coagulated.
2. Colliquation necrosis. — The condition resulting froin solu-
258 VETERINARY PATHOLOGY.
tion of a substance or surface area of necrotic tissue is colliqua-
tion. Solution of the necrotic tissue is the result of enzyms
that dissolve or digest the dead tissue. Suppurative processes
(as abscess formation, etc.), are examples of this type of necro-
sis. Liquefication of anemic infarcts, inflammatory exudates
and thrombi, with or without the formation of cysts, is colliqua-
tion necrosis. In the brain of horses that have died of the so-
called blind staggers areas are found containing liquefied nerve
tissue.
3. Caseation necrosis. — When the fluid is absorbed from li-
quefied necrotic tissue, the remaining solids may become cheese-
like, thus producing the condition known as caseation. Caseation
may be primary, but it is more frequently secondary to liciuefying
necrosis. Caseous material is granular, soft or crumbly in con-
sistency. Caseation is characteristic of the typical lesion of cas-
eous-lymph-adenitis in sheep and goats. Liquefaction precedes
caseation in this disease. Tubercular lesions, especially in the
bovine, is characterized by caseation, although they later become
calcified. Necrotic centers of a caseous nature are observed in
the lesions of bursattae.
■i. Mummifying necrosis (mummification, dry gangrene). —
Necrotic tissues superficially located may becom.e dessicated, thus
producing the condition known as mummifying necrosis. This
type of necrosis occurs upon a surface that is freely exposed to
air and of tissues in which there is little moisture. The ear, tail
and hoof lesions, characteristic of ergotism, are the most typical
examples of mummifying necrosis. In ergotism, the lesions are
produced by constriction of the arterioles. This in turn in-
creases blood pressure, and, consequently, the work of the heart.
This ultimately results in the diminution or complete absence of
blood from the extremities, and the latter sooner or later become
necrotic. The necrotic tissue, as ears, tails, etc., in animals
afifected with ergotism become mummified because blood is prac-
tically shut ofif from the afifected parts and the contained moist-
ure soon evaporates, for they are freely exposed to the air on
two or more surfaces. Frozen tissues may become mummified.
The umbilical cord in new born animals undergoes mummifica-
tion.
5. Gangrene. — By the laity, the term "gangrene" is used to
designate any type of necrosis, and by some medical men it is
used to signify death of soft tissue en masse. Gangrene is that
type of necrosis characterized bv putrefaction of the necrotic tis-
sue. Gangrene invariably occurs in tissues in which there is a
good supply of moisture, as in a tissue affected with venous con-
NECROSIS AND DEATH.
259
gestion. and usually occurs upon a surface because infection is
more likely to occur there. Parenchymatous mammitis of the
bovine is frequently succeeded by necrosis and putrefaction of
the necrotic tissue (gangrene). Gangrenous pneumonia is not
uncommon and may be the result of embolic metastasis of organ-
isms from septic metritis, etc., or it may be induced by medica-
ments introduced into the lung.
Alisccllancoiis.
1. Senile Necrosis. — This is a type of necrosis occurring in
old age. It is not uncommon in old dogs and aged horses, and
is usually the result of inelasticity of the arteries and an insuffi-
cient supply of nutrition.
3. Fatty Necrosis. — This is a condition characterized by the
Fig, 121. — Multiple Fatty Necrosis.
Fat cells undergoing disintegration, because of Saponiflcation.
conversion of fat into fatty acid and glycerine, that is, saponifica-
tion of fat. The name fatty necrosis is a misnomer, as the condi-
tion is not necrosis. It should be called saponification of fat. In
fact, a fully developed fat cell represents that amount of stored,
available food, and tliere is in reality no vitality in the cell, and
necrosis in dead tissue is not conceivable. Again, the real exist-
ing condition is saponification of the fat, not necrosis. The prob-
able cause of fatty necrosis is resorption of steapsin induced by
pancreatic disturbances, although steapsin may be absorbed from
the intestine. Some four or five cases have been observed in the
dog, several cases in the sheep, and one horse was examined
that was afifected with fatty necrosis. In each of the abovfe cases
260 VETERINARY PATHOLOGY.
there was evidence of pancreatic lesions, as inflammation, hem-
orrhage and atrophy was noted in one case. Recently it has
been suggested that this condition is caused by disturbances of
the islands of Langerhan.
The areas afifected are at first soft and spongy, but later be-
come more or less calcareous as a result of combination of lime
salts with the free fatty acid.
Fatty necrosis usually involves the omental fat, and espe-
cially that in close proximity to the pancreas, though all fatty
tissue is subject to this condition.
In gross appearance the involved portions are dull, lusterless,
opaque, slightly raised, usually circumscribed areas, of a yellow-
ish white color. If the lesions are advanced, calcareous granules
may be observed by palpation. In microscopic section the cells
of the affected areas may contain needle-like crystals, or the cell
substance may appear as a granular mass.
3. Focal necrosis. — In certain infective diseases it has been
noted that small foci of the various parenchymatous tissues un-
^«%%-e t «> f «.V:^«*l-:.%%^<*«^%^^ .;Scv\s-ber.j^ «•
Fis. 122. — A necrotic tubercle; lung. x250. Showing necrotic center surroundta
tiy small round cells, cpitheloid cells, and leucocytes.
NECROSIS AND DEATH.
261
dergo necrosis. In many instances, this occurs in the absence of
any circulatory disturbance, indicating that the exciting cause,
chemic substance, is carried by the blood and appears to have
a selective action for certain tissue. This type of necrosis is com-
mon in diphtheria and typhoid fever in the human and in hog
cholera, glanders, generalized tuberculosis and probably some
other infective and chemically induced diseases of the lower ani-
mals.
The areas affected are frequently not sufficiently large to
observe with the unaided eye. Microscopic sections show the
cells in various stages of necrosis. The nucleus may be appar-
ently normal or entirely disintegrated, the cell body may be
granular or hyaline, it mav be intact or appear fragmented. Leu-
cocytic invasion of the necrotic area is of frequent occurrence,
and may at first give the impression of an infected focus. Necro-
tic tissue in focal necrosis may be absorbed and the destroyed
tissue regenerated; it may become liquefied, thus forming a cyst;
it may become infected and be succeeded by abscess formation,
or it may be substituted with scar tissue.
4. Jack-Sores. — This is a name applied to a very prevalent
condition in jacks in which there is necrosis of the skin and sub-
cutaneous tissue. Perhaps jack-sores should not be classed as
a separate or distinct type of necrosis, but it is so common that
it merits a special mention. The skin and subcutaneous struc-
tures of the legs, venter surface of the abdomen and thorax, and
maxillary region are most frequently affected. The necrotic
areas may be very extensive, in some instances involving the
entire metatarsal or metacarpal region.
The etiology of "Jack-Sores" is not known, but no doubt it
is the result of malnutrition and probably an irregular, indefinite
lymphatic circulation is the primiary cause.
Tissue Affected, — No tissue is exempt from necrosis. The
tissue affected depends upon the cause, the animal and geog-
raphical location.
Disposition of Necrotic Tissue. — Necrotic tissue or products
derived from it are more or less irritating and may produce an
inflammation in the living tissue around the necrotic mass.
The perinecrotic inflammation insures an increased number of
leucocytes around and in the necrotic area. The necrotic tissue,
leucocytes and other living cells may produce enzyms that
will u'ltimatelv dissolve the necrotic tissue. There may be
a contraction of the necrotic tissue and later it may separate
from the surrounding normal tissue. The reaction of the adja-
cent living tissue may be limited and cause the production
262 VETERINARY PATHOLOGY.
around the necrotic area of a fibrous or osseous capsule, cr evei'.
cause a fibrous formation throughout the entire necrotic m?ss.
From the foregoing it is apparent that necrotic tissue may be
disposed of as follows: 1. Absorption. 2. Exfoliation. 3. En-
capsulation. 4. Sequestration.
Absorption. — The necrotic mass is more readily absorbed
when it is in a liquid state (colliquation), although leucocytes,
and various other cells may produce enzyms that are capable of
dissolving coagulated necrotic tissue. Absorption of fluid ne-
crotic tissue is in part accomplished by means of the lymphatic
tissues, and in part by means of leucocytes that incorporate and
convey fragments of necrotic cells to the various organs that
dispose of waste materials. Necrotic infarcts are occasionally
entirely absorbed.
Exfoliation. — Necrotic surface tissue is frequently disposed
of by separation of the dead from the living tissue as a result oi
inflammation or contraction of the necrotic mass. The separated
necrotic mass is the sphacelus. The process of separation and
sloughing is exfoliation. Exfoliation is the usual disposition of
necrotic extremities induced bv freezing and by ergot poisoning.
Encapsulation. — The irritation produced by subsurface ne-
crotic tissue may be insufficient to cause an acute inflammation,
but it may stimulate fibrous hyperplasia. Thus a fibrous capsule
or wall is built around the necrotic mass, i. e., it becomes encap-
sulated. In some instances the encapsulated necrotic tissue later
becomes calcified, or it may become liquefied, the capsule retain-
ing the liquid, thus a cyst is formed.
Fibroblasts may extend into the necrotic area and form
fibrous tissue throughout the entire mass, thus there would be
a mass of cicatrizing fibrous tissue permeating the necrotic
mass.
Sequestration. — This is a term applied to the separation of
subsurface necrotic tissue, more especially necrotic bone, from
the surrounding healthy tissue. The separate necrotic portion
is termed the sequestrum, and the process of its separation
sequestration. Afi osseous sequestrum may be encapsulated, the
capsule later becoming osseous, thus forming an involucre.
Effects. — Necrosis is the condition resulting from tissue des-
truction. The effects of tissue destruction depend upon the
variety of tissue, the extent and location of the condition, and
the age and condition of the animal in which it occurs. If th*^?
tissue destroyed is capable of regeneration, or if it is limited in
extent, and the animal is otherwise in good 'condition, the effects
will be insignificant. If the tissue destroyed cannot be regener-
NECROSIS AND DEATH, 263
ated and is extensive, the animal will be deprived of that quan-
tity of tissue and if the function of the destroyed tissue is of
prime importance, the animal will die.
Necrosis is invariably associated with inflammation, which is
especially active around the necrotic area, and the results of
this inflammatory reaction must also be considered in estimat-
ing: the sum total of the effects of necrosis.
DEATH.
DEFINITION.
ETIOLOGY.
Suspended heart action.
Respiratory arrest.
Suspended brain action.
SIGNS.
Post Mortem Staining.
Temperature change.
Muscular rigidity.
Decomposition.
TESTS.
Mirror.
Blister.
Incision.
Rcla.vation of sphincter muscles.
Death is the condition resulting from the permanent arrest
of all functions. Death should not be confused with necrosis.
The former refers to somatic death and the latter to -the death
of a part. It is diflficult and in fact impossible to determine the
exact time when life ceases in a body. The various body tis-
sues do not all become lifeless when the individual as a whole
dies. The length of time that vitality is retained in the tissues
of a dead animal depends upon the variety of tissue, the age of
the animal and the cause of death. The less highly organized,
the tissue, the longer its vitality is retained. The tissue of young
animals possess their vitality for a longer time than the same
tissues of an aged animal. Death results from disturbance of
certain vital centers and these tissues, as well as all others speci-
fically acted upon by the agency that causes death, lose their
vitality earlier than tissues not acted upon.
Death may be physiologic or pathologic.
Physiologic Death.
This is that type of death observed in old animals. During em-
bryonic life the principal function of all tissue cells is reproduc-
tion. As the tissue becomes more matured, the reproductive prop-
erty of its cells gradually diminishes and has practically disap-
2G4 VETERINARY PATHOLOGY.
peared in old age. Cell repair is complete in early life, but gradu-
ally diminishes as the animal becomes aged. The activity of cells
and their life cycle is limited as is that of all active structures
either animate or inanimate. Therefore, if new cells are not pro-
duced and the old cells are not repaired their energy or vital
forces are finally exhausted and they degenerate and die. If large
numbers of cells of all tissues die the animal involved is incapaci-
tated and ultimately sufftcient cells die to diminish the function of
the vital organs to such an extent that there is collapse and som-
atic death.
Physiologic deatli is initiated bv a gradual decline which
may continue until the individual dies. Or after a long per-
iod of slow decline, death may be sudden as a result of a sudden-
I3' diminished function of a vital organ. Physiologic death is sim-
ilar in a way to the collapse of the one horse chaise which, as the
story runs, was used until it literally fell to pieces. Very few
domestic animals die a physiologic death. Those animals whose
flesh is used for food are butchered long before physiologic death
would intervene, and those animals used as beasts of burden are
usually destroyed when their earning capacity is monetarily less
than the food they consume.
Pathologic Death.
Pathologic death signifies the ending of life prior to the time
that the vital forces have been exhausted.
Etiology. — Pathologic death is that type caused by accident
or disease process. Death is primarily the result of permanent
suspension of heart action, respiration or brain functioning.
Suspended heart action may be caused by influences acting upon
the cardiac nerve centers in the medulla or upon the heart mus-
culature direct. The significance of suspended heart action is
self evident. There being no blood circulating the tissue would
soon consume all available nutriment and then succumb. Tem-
porary arrest of heart action is called syncope.
Respiratory arrest is usually the result of nervous influences
though clonic spams of the respiratorv muscles would produce
a similar effect. The absence of respiration implies the absence
of oxygen to oxidize the blood and the tissues and the absence
of oxygen for a considerable length of time results in carbon-
dioxide poisoning and death. Apnoea is a condition in which
respiration is arrested.
Permanent arrest of all brain fnnetioning even for a brief period
results in cessation of all the principal functions and death.
iSTECROSIS AND DEATH. 265
Thus, suspended brain function results in arrest of heart action
and respiration either of which results in somatic death. Coma
is a term used to designate a condition in which all conscious-
ness or recognition of environments is suspended but the con-
trol of vital functions is still maintained.
Signs of death. — The changes that occur in dead tissue are of
considerable importance especially to inspectors of carcasses of ani-
mals, the flesh of which is intended for human consumption. The most
important post mortem changes in tissues are as follows ; post mor-
tem staining (livores mortis) ; temperature change (algor mortis) ;
death stiffening (rigor mortis) ; and decomposition or putrefaction.
Post Mortem Staining. — The blood usually undergoes changes
immediately after death. The disintegration of red blood cells
allows of the liberation of hemoglobin which is deposited more
or less extensively upon the inner lining of the blood vessels and
heart and also filters through the vessels and stains the peri-
vascular tissues. The length of time after death that post mor-
tem staining becomes evident depends upon the cause of death.
In fact the purplish staining along the cutaneous vessels evident
in dead bodies may be evident in the living body of animals. Thus
liberation of hemoglobin takes place during life in the blood of
animals affected with septicemic diseases.
Temperature changes. — The carcasses of all dead animals assume
the temperature of the environment sooner or later. The length
of time necessary for the body heat to pass out of a dead body
depends largely upon the cause of death. In some diseases,
those in which tissue change is limited, the temperature is sub-
normal at the time of death and rapidly assumes the environmen-
tal temperature after death. In other diseases, those in which
tissue changes are extensive, the temperature may vary from
normal to considerably above normal at the time of death and
may increase for several hours after death. Temperature changes
may be extremel}^ variable in a carcass. Also a remarkably low
subnormal temperature has been observed in many living ani-
mals, especially those in a comatose state and yet the animals
recover. The thermic variations should never be relied upon in
determining whether or not life is extinct, at least not within
48 hours after the animal is supposed to be dead.
Rigor Mortis. — That the body of an animal becomes rigid after
death is common knowledge to all observers. Rigor mortis re-
presents a condition of the muscle fibre in which it becomes rigid
as if in a tonic contraction. The length of time after death that
rigor mortis appears and the length of time that it persists de-
pends upon the condition of the animal at the time of ^ death.
266 VETERINARY PATHOLOGY.
Thus muscular rigor appears usually in a few minutes after
death and is of brief duration in animals, that have died as a
result of a long continued exhaustive disease, as chronic tuber-
culosis. On the other hand rigor mortis may not become evi-
dent until 24 hours after death in animals that have been killed
while in a perfect state of health and it may continue for from
two to four days. In catalepsy, muscular rigidity is a charac-
teristic symptom. Other conditions, however are sufficient to
differentiate this from rigor mortis.
Dccouiposition or putrefaction is caused by the action of putre-
fying bacteria.
The decomposition of a tissue is sufficient evidence of the fact
that it is lifeless. Decomposition or putrefaction is not easily
detected in the early stages. The evolved odor is usually the
accepted sign of decomposition and during some seasons of the
year, decomposition may not become evident for several days
after death. The carcasses of animals dead of septic infections
usually decompose immediately after death, e. g. carcasses dead
of anthrax, hog cholera, etc.
Tests. — Because of the uncertainty of the above signs espe-
cially, during the first 24 or 48 hours after death, certain tests
are recommended to determine the presence or absence of life
in a certain body. They, like the above signs, are not absolute.
The mirror test. — .Respired air contains more or less water
vapor. Respiration is not always perceptible. Water vapor is
condensed upon a cold surface. The procedure of this test con-
sists in holding a mirror over the nostril and if any air is ex-
pired the watery vapor from the expired air will be condensed
and rendered visible upon the surface of a mirror. This test is
not infallible for the respiratory functions may be so diminished
that the moisture (watery vapor) of the expired air is insufficient
for condensation upon the mirror.
Blister Test. — Blisters or vesicles can usually be produced by
heat or chemic vesicants applied to the skin of a body in which
life still exists. The formation of vesicles is not possible in dead
tissue because the production of a blister represents the response
of a living tissue to an irritant and only living tissues are cap-
able of reacting. Vesicle productions varies in living animals
and in some cases they are not produced.
Incision. — Because of the elasticity of living tissues, all incised
wounds gap in the living body. Tissue elasticity disappears
when the tissue dies, consequently incised wounds in dead tis-
sues do not gap.
NECROSIS AND DEATH. 267
Certain post mortem changes are rather constant in the eye.
These changes consist of a cloudiness of the lens and the aque-
ous humor, the condition gradually becoming more intense.
The surface of the eye, i. e., the conjunctiva, becomes dry and
scaly in appearance.
All sphincter muscles are usually relaxed at the time of death
and remain so permanently.
Still Birth. — The expulsion of a dead matured foetus from the
uterus is denominated a still birth. A variety of conditions may
cause the death of a foetus, as: ruptured umbilical vessels, stran-
gulation of the umbilicus and various diseases of the foetus. Veter-
inarians are frequently asked to determine whether a foetus has
been dead or alive at the time of its expulsion from the uterus. The
principal evidence is found in the lung, which in the case of a still
birth is solid as it has never been inflated.
CHAPTER X.
TUMORS.
(Neoplasms li
DEFINITION.
FREQUENCY.
STRUCTURE.
Cells.
Intercelhilar.
Vessels.
Nerve tissue.
SIZE.
SHAPE.
COLOR.
CONSISTENCY.
NUMBER.
GROWTH.
EXTENSION.
NATURAL RESISTANCE.
RETROGRESSU'E CHANGES.
CLINICAL CONSIDERATION.
ETILOLOGY.
VARIETIES.
Occurrence.
Primary.
Secondary.
Recurrent.
Structure.
Histoid.
Organoid.
Teratoid.-
Clinically.
Benign.
Malign.
Tissue.
Adult.
Epithelial and connective — Papilloma,
Connectiz'e.
Fibrous — Fibroma.
Mucous — My.Yonui.
Cartilage — Chondroma.
Osseous — Osteoma.
Dentine — Odontoma.
Adipose — Lipoma.
Glia — Glioma.
Muscular.
Involuntary — Leiomyoma.
J'olunfary — Rhabdomyoma.
Vascular.
Blood 2'esscl — Hemangioma.
Lymph z'cssel — Lymphangioma.
Nervous.
Neuroma.
268
TUMORS. 269
Embryonic.
Connective.
Sarcoma.
Endothelioma.
Hypernephroma.
Placentoma,
Epithelial.
Carcinoma.
Epithelioma.
Adenotna.
Hypernephroma.
Plancentotna.
Adult and Embryonic.
Any and all tissues.
Teratoma.
The term "tumor" was formerly used to indicate any swelling
in animal tissues. They, more than any other pathologic entit}'',
have been studied and investigated by scientists, and yet little
is known of their pathology. With the present limited knowledge
it is impossible by definition to clearly differentiate them from
some other pathologic conditions. They have been defined as
new growths of tissue developing independently in any tissue
of the animal body and atypical in structure and function. Also
they are non-inflammatory growths of new tissue, persistent,
independent of the surrounding structures, atypical in structure
and function. A more concise idea can be formulated by think-
ing of them as parasites, that is, they are new^ growths of tissue
that develop in or upon the animal body at the expense of the
animal, and are subject to the same pathologic conditions that
the normal tissues are, as degeneration, necrosis, etc.
Frequency. — Tumors are of frequent occurrence. They
are more common in dogs particularly aged ones than in other
animals. Of 127 animals presented in the daily clinic at the
Kansas City Veterinary college during one college session, 12
were affected with tumors.
The frequencv of tumors in animals treated in the Berlin,
Dresden, and Munich veterinarv colleges for an average period
of seven years is shown by the following:
Of 86,613 diseased horses, 1,113 suffered from tumors, or 1.3 per cent.
0^85,537 diseased dogs, 4.020 suffered from tumors, or 4.7 per cent.
Of 4,972 diseased cattle, 102 suffered from tumors, or 2 per cent.
The following statistics from the annual report of the Sanitarv
Veterinary Service of Paris is of interest. Of 39,800 animals exam-
ined, of which 20,000 were mares, 16,200 were geldings, and 3,600
were stallions, 184 were affected with malignant tumors. Of the
affected animals 86 were mares, 43 were geldings and 55 were stal-
lions. Of the 184 cases the kidneys were involved, in 62, the tes-
270 VETERINARY PATHOLOGY,
tides in 50, the mammae in 45. the intestine in 9, the bladder in 6,
the ovary in 2, the hmgs in 2, the uterns in 1. the sheath in 1, the
jaw in 1 ; the origin of 5 being undetermined. Practically all of the
184 cases occurred in aged animals.
Structure. — Tumors are composed of cells and usually, an
intercellular substance. The cells ma\ be similar to normal em-
bryonic cells or to adult cells. The embryonic tumor cells differ
from normal embryonic cells in tliat the former have no ten-
dency to become matured while the latter have. The accom-
panying' cut shows a section of a sarcoma composed of embry-
onic cells that are similar to embryonic connective-tissue cells.
Papillomata are composed of cells that are very similar, if not
identical, to adult epithelial cells, and are supported by an adult
connective-tissue framework.
Tumor cells are very similar to the cells of normal animal
tissues. They have practically the same structure and require
the same kind of nutriment. However, they do differ from the
normal tissue cells in their power of growth and reproduction.
Tumor cells are usually more susceptible to changed environ-
ments than normal tissue cells. The nuclei of the cells of a rap-
idly growing tumor are usuallv larger probably because of in-
creased functional activity.
The intercellular substance of tumors is as variable as the
intercellular substance of normal tissues. Tumors having a
mesodermal origin usually have an intercellular substance closely
resembling that of normal connective tissue and hence may be
mucus, fibrous, cartilaginous, or osseous. Tumors of an ectoder-
mal or an entodermal origin may appropriate the pre-existing
tissue framework for their stroma. Some tumors, like some
normal tissues, are practicalh^ devoid of intercellular substance.
Again, in some tumors the blood-vessels are the only intercellular
substance. Anatomicallv the intercellular substance or stroma
is an integral part of a tumor and its function corresponds to
the function of intercellular sul^stance of normal tissue. The
cells and intercellular substance of tumors may be so arranged
that the resulting structure, approximates that of normal tissue
(histoid tumors), but is never identical to a normal tissue. The
different parts of a tumor may be assembled so that the resulting
organization appears as an atypical gland or organ (organoid
tumor), or tumors may be composed of structures derived
from all three germ layers grouped indiscriminately but having
some resemblance to an embryo (teratoid tumors.)
Like normal tissue, tumors are usually nourished, by blood
and lymph. The blood and Ivm.ph vessels may be structurally
TUMORS.
271
the same as normal vessels, or they may be composed entirely of
tumor cells. The vessels have their origin from pre-existing ves-
sels in the tissue from which tlie tumors are developed. They
may be telangiectatic, cavernous, or plexiform, and their
course is usuallv along the tumor stroma. Blood and lymph may
also permeate the tumor through intercellular spaces, frequently
resulting in hemorrhage or lymphorrhage. Some tumors have
no blood or lymph supply, their nourishment probably being
derived from consumption of normal tissue.
Nerve cells and axones have been demonstrated in some
tumors. They are, in some cases at least, a result of peripheral
extension and development of the tumor tissue around normal
nerve tissue, thus entangling it in the tumor. It is an open
question whether nerve tissue exists in tumors except in those
derived from normal nerve tissue or those in which normal
nerve tissue is entangled.
Fig. 123. — Section of Sarconia. showing sarcomatous cells and blood vessels.
Leucocytes are common in tumors. Lymphocytes and poly-
morphonuclear leucocytes have been demonstrated in the blood
and lymph channels, perivascular and intercellular spaces, and
272
VETERINARY PATHOLOGY.
within the tumor cells. The cells and the manner in which they
are assembled, the structure and arrangement of the intercellu-
lar substance, and the presence of the blood and lymph vessels
indicate a common origin of tumor tissue and normal tissue.
Size. — Tumors are quite variable in size. They mav become
so large that they mechanically destroy life. An abdominal sub-
serous lipoma, about the size of a wash-tub and weighing thirty-
eight kilograms, (83^ lbs.) was observed in an ox. A six-
kilogram (13 ^/, lbs.) fibroma was removed from the inferior
cervical region of an eighteen kilogram (40 lbs.) dog. A twelve
kilogram (26 2/5 lbs.) chondroma was obtained from the ster-
num of a fifty kilogram (110 lbs.) sheep. All of the above tum-
ors were of sufficient size to mechanically inconvenience the
animals afflicted, and in one case resulted fatally. From the
enormously large tumors there are all gradations tO' those
miscroscopic in size, miliary tumors. The size of tumors is
determined to some extent bv the amount of nourishment sup-
plied, the kind of tissue of which they are composed, and their
location.
Shape. — The form of tumors is largely determined by the loca-
tion and the kind of tissue in which they occur. They may be
spherical, ovoid, elliptoid, nodular, miliary, tubercular, fungoid,
polypoid, tabular, elongated, cylindrical, etc. Where there is no
resistance or only a slight resistance there is a tendency to
sphericity. In outline they may be regular or irregular, smooth,
nodular or even granular and in some oases the exact outline
cannot be determined. Large tumors that in shape approach a
sphere are designated as spherical, ovoid, elliptoid, etc. Those
that vary in size from a pigeon egg to a small pea are spoken
of as nodular tumors. Miliary tumors are small spherical
growths varying from a small pea to those microscopic in size.
Spherical or oval tumors causing an elevation in the tissue in
which they grow are known as tubercular tumors. Fungoid or
projecting tumors are those that develop from the surface
or sub-surface tissue, being attached to the normal tissue by a
wide base. Polypoid tumors or polypi have the same origin and
project as fungoid tumors, but are attached by means of a
small pedicle. Tabular tumors are flat and usually develop be-
neath the surface and especially beneath fasciae, tendons or liga-
ments.
Color. — llie color of tumors is dependent upon ; first, the
kind of tissue composing them ; second, pigmentation ; third,
degeneration ; and fourth, the amount of blood they contain. A
rhabdomyoma is more intensely colored than a fibroma, provided
TUMORS.
273
that the blood supply is the same in both, because of the hemo-
globin in the muscular tissue. Melanomata and chloromata are
so classified because of the deposition of pigment in them. Tum-
ors, like normal tissues, become changed in color as a result of
the various degenerations. Those having a limited blood supply
are pale in color, while those having a large blood supply are
highly colored. Hemorrhages may result in a deposition oi
hemoglobin or some of its derivatives, thus giving the tumor
a mottled appearance. Mottling may also result from an un-
equal blood supply.
Consistency. — Some tumors are soft and spongy, jelly-like,
and from this type there are all variations up to those that
are hard and resistant, bone-like. Their consistency is determined
largely by the kind of tissue composing them and the secondary
changes (degenerations) that affect them. Myxomata being
largely composed of mucus are soft, fibromata are more resistant
and osteomata are bone-like. Chondromata are usually quite firm
and resistant, but they may undergo mucoid degeneration and
become soft and spongy. Colloid degeneration is rather common
in carcinomata, rendering them glue-like in consistency. Occa-
sionally a tumor becomes calcified as a result of calcareous infil-
tration.
Number. — Tumors may be single, that is, a single one only
occurring in the animal body. Single tumors are usually benign
although thev may be malign. An animal may be afflicted with
a great many tumors at the same time (multiple tumors). Tum-
ors may become multiple by metastasis. Tumors resulting from
metastasis are designated secondary and the original tumor pri-
mary. Multiple tumors may be malign, as sarcomata, carcino-
mata, etc., or they may be benign, as multiple fibromata. Tum-
ors that recur after they have been removed are designated recur-
rent tumors.
Growth. — The growth of tumors is the result of the inherent
proliferative property of the tumor cells. Some tumors grow like
an onion, there being a multiplication and accumulation of the
central or internal cells, resulting in an interstitial expansion and
an increase in the size of the tumor. Practically all benign tum-
ors grow by interstitial expansion. Malign tumors grow by mul-
tiplication of the peripheral cells and their infiltration as well as
by interstitial expansion. The extent of growth of all tumors is
proportional to the amount of nourishment they receive and to
the adjacent tissue resistance. The relative amount of nourish-
ment to tumor tissue and to normal tissue in the same body may
be very unequal. Thus a tumor fretiuently receives an excessive
274
VETERINARY PATPIOLOGY.
amount of nourishment and grows rapidly, while the normal tis-
sue in the same bodv is deprived of nourishment, resultmg in its
atrophy or deg^eneration and emaciation. As a rule, the rate of
growth is indefinite. Malign tumors grow^ more rapidly than be-
nign. A. tumor that is growing rapidly may cease growth, dim-
inish in size, grow again and diminish again. Diminution in
size may be succeeded by absorption and disappearance.
Ejctension. — The manner of extension of the various tumors
depends upon the migratory properties of the tumor cells and
the relation and structure of the blood and lymph vessels. Tum-
Fig. 124. — Photograph of a section of a horse's lung, showing Metastatic Sarcomata.
ors composed of embryonic cells extend more repidly than those
composed of adult cells because embryonic cells are plastic and
are to some extent capable of amoeboid movement. Adult cells
are fixed in their form and none of them, excepting leucocytes
and endothelial cells are migratory. The nutrient vessels of
tumors are sometimes formed of tumor cells that are easily de-
tachable, a structural peculiarity predisposing to tumor metas-
tasis.
Benign tumors usually extend only by growth in continuity
TUMORS. 275
or contigufty. In fact, practically all tumors composed of adult
tissues extend by pushing aside the normal tissue. Malign tum-
ors are extended by blood, as sarcoma; by lymph, as carcin-
oma ; or they pass from one point to another through natural
channels as the digestive and respiratory tracts.
Summary. — Tumors may be extended (1) by growth in con-
tinuity, (2) by growth in contiguity, (3) by blood, (4) by lymph,
(5) by natural channels other than the blood and lymph vessels.
Natural Resistance. — Normal tissues have a natural resist-
ance to any injurious influence as the formation of tumors, in-
flammation, degeneration, etc. Tissue resistance to the devel-
opment of neoplasms varies in different animals, in the same
animal at different times, and possibly also in the different tis-
sues of the same animal. The resistance of the surrounding
tissue is made evident in some cases by the formation of a fibrous
wall or capsule that limits and separates the tumor and the nor-
mal tissue. Degeneration and necrosis may also be interpreted
to be a result of opposed action by the invaded tissue.
The body fluids may contain chemic substances that neutralize
the substances that produce cell reproduction ; in this way an
immunity may be established. Blood serum from non-tumorous
animals inhibits the growth of tumors according to recent experi-
ments.
Retrogressive Changes. — Tumors are subject to the same
degenerative processes that normal tissues are. Hemorrhages,
necrosis and degenerations are frequent in tumors 'because
of the imperfectly formed and irregular distribution of the
supplying vessels. The results of hemorrhage into tumors
depend upon the amount of extravasted blood and the secondary
changes therein. A tumor the size of a cocoanut would likely
become necrotic if a vessel ruptured and a half a liter of blood
escaped into the tumor tissue. A small quantity of extravasate
when infected with putrefactive microorganisms as a rule results
in necrosis of the tumor tissue. Necrosis is a sequel of ob-
structed circulation or results from the solvent action of meta-
bolic products. Thus, necrosis may be the result of thrombosis
or embolism. Thrombic formation is especially prevalent be-
cause of the irregularities of the lining of the tumor vessels.
Emboli are common, as they are frecjuently detached tumor cells.
Circulation may also be interfered with by pressure of the tumor
tissues, thus obstructing the efferent or afferent blood vessels.
Some metabolic products of tumors constantly dissolve the sur-
face cells, resulting in ulceration, a common necrotic condition
276 VETERlXAin' PATHOLOGY.
observed in tumors. Tumors may be invaded with pyogenic
bacteria, resulting- in suppuration.
Of the degenerations, mucoid and colloid are the most com-
mon. Fatty degeneration arid calcareous infiltration occur less
frequentl}-. Mucoid degeneration affects connective tissue and
epithelial tissue tumors, occurring more frequently in the former.
Colloid degeneration is found in epithelial tissue tumors.
A four-kilogram (iJ-lb.) renal hypernephroma undergoing
colloid degeneration was obtained on post-mortem examination
of a three-year-old steer. Fatty degeneration usually succeeds
necrosis in tumor tissue. Calcification, especially of small centers,
is occasionally observed in tumors. Pigmentation is more common
in tumors than in normal tissue. Melanomata are tumors contain-
ing melanin that has been deposited in the tumor cells. Chloromata
are tumors containing a green pigment. Hemoglobin, hematoidin
and hemosiderin are frequently found in tumors after hemorrhage
into the tumor tissue.
Clinical Consideration. — Tumors are benign or malign. Benign
tumors are usually encapsulated, i. e., they grow slowly and only by
interstitial expansion; are composed of adult or matured tissue;
haye little or no tendency to recur when removed, and have only a
mechanical eft'ect upon the body in which they occur. Malign tumors
are usualh' not encapsulated : they grow relatively rapid by peri-
pheral infiltration; are usually composed of embryonic tissue; fre-
quently recur when removed, and have a tendencv to kill by
absorption of the metabolic products which arc deleterious to
the body. Malign lunujrs of domestic animals are not as fatal
as they are in the human. ^lany horses aft'ected with sarcomata
have been permanently relieved by operation.
Etiology. — There are some predisposing factors as heredity
and breed peculiarities that are frequently involved in the devel-
opment of tumors. Cadiot refers to a family of dogs in which
the females were aft'ected with carcinomata of the mammae for
two successive generations. Murray has demonstrated bv the
breeding of mice that there is an inherited tendency to mammary
tumors. Hereford cattle are more frequently affected with ocular
tumors than any other breed. Injuries in which there is a destruc-
tion of the tissue surfaces predisposes to tumor formation, and, in
many instances, in the human, subsurface wounds are a causative
factor in the production of epithelial embryonic tumors. A few
cases of epitheliomata have been studied in the horse and ox that
were secondary to injuries.
TI'MORS.
277
The exciting causes of tumor formation have not been defin-
itely determined, and this accounts for their undetermined char-
acteristics, ^lanv theories have been advanced. Cohnheim ad-
vanced the idea that tumors were developed from misplaced
embryonic cells (cell rests). This theory has received the sup-
port of many pathologists. It is in accord with the general
.J^i
Fig. 125.— Photograph of a horse affected with an ocular Epithelioma.
Tliis was a sequel of a wiro cut.
iMologic law that every cell produces a cell like itself or '"like
begets like." The supporters of this theory have not proved it.
but the opponents have not disproved it. All biologists recog-
nize the complexity of embryonic development and are aware
of the possibility of cells becoming entangled or misplaced dur-
ing the formation period. Experiments have demonstrated the
possibility of successfully transplanting tissue, both embryonic
and adult, into a foreign location in the body. Transplanted em-
bryonic tissue, however, does not remain as such, but soon be-
comes mature tissue, whereas malignant tumor cells have no
tendenc)- to become matured. Transplanted tissue cells do not
infiltrate the surrounding tissue nor form metastases, but remain
as distinct islands of cells.
278
VETERINARY PATHOLOGY.
The parasitic theory has been supported bv a large number
of scientists. No doubt malignant tumors resemble infectious
diseases in that they extend hv metastasis and produce similar
effects. However, the uncertain transmission of tumors from
one animal to another is certainly antagonistic to the parasitic
theory.
Bashford, superintendent of the Imperial Cancer Research
Fund, London, England, successfully transplanted (36 per cent
of sporadic tumors. On the other hand, Ehrlich has successfully
transplanted only about 14 per cent of sporadic tumors. No one
has produced a satisfactory proof of the isolation of any causa-
tive parasite. By some authorities bacteria were thought to be
the active agent in tumor production, and by others protozoa
were claimed as the causative factor, and, more recently, many
radical observers have proclaimed that yeast were the cause.
Some have even claimed that the tumor cells are parasites.
Chemic disturbances, particularly changed chemic reaction in
a tissue, is responsible for tumor formation according to some.
An alkaline secretion at points where exposure and irritation occurs
stimulates the production of carcinomas (Hertzler). Following
this thought an acid reaction in a normally alkaline tissue would
tend to produce sarcomatous tissue.
Harmone theory is upheld by some as the causative agent of
tumors. The specific causative factor of tumor formation is not
known, but it is something that excessively stimulates the repro-
ductive power of cells. In fact, all other functions practically cease,
the entire cell energy 'being expended in reproduction. That is,
tumors are the result of a disturbance in the cell metabolism in
which reproduction is far in excess of the physiologic limit and is
exercised at the expense of all other functions. As before stated, it
is probable that maiotic division is the usual form of cell reproduc-
tion in tumors, and although normal serum inhibits auxetic action
other conditions are sufficient to ofifset the inhibitory action. Thus
the combination of the physiologic auxetic and the pathologic putre-
factive alkaloids are sufficient.
Varieties. — There is no satisfactory method of classifying
tumors. Some authors have attempted methods of classifying,
but until more is known concerning them a classification is un-
wise. The following is an attempt at grouping them, but is in
no way complete. They may be grouped as to :
TtJMORS.
21^
OCCURRENCE. ^ ^ ^
Primary — The original or first fumor.
Secoiidar\ — Metastatic tumor. .
^^^„,.,.^„}_^^ nezvly developed tumor at the point from ivJuch
one has been recently removed.
STRUCTURE.
Histoid — Simple tissue tumor.
Orqanoid — Organ-like tumor. _ . , , „^
Teratoid-Mixture of various tissues resulting m a structure re-
sembling an embryo.
CLINICALLY.
Benign — No tendency to kill.
Malign— Having a tendency to kill.
The following scheme shows the general structure and rela-
tion of the various tumors:
f Adult Tissue
I umorsn
Connective
Epithelium
i Myxoma, Chondroma
Osteoma, odontoma.
Lipoma, Glioma ■ • • •
Fibroma ) papjUoma
fLeiomvoma . •
Muscular-myoma | Ri^abdomyoma
,, , . f Lymphangioma
Vascular-angioma ^ Hemangioma • •
Nervous-neuroma
Connective-Sarcoma
Embryonic Tissue-;
( Round Cell ■
\ Spindle Cell
\ Mveloid Cell
( Enc
Epithelium
Endothelioma
Carcinoma
Adenoma
Epithelioma J
Placentoma . ■ •
Hypernephroma
3
FIBROMA.
Fibromata are tumors composed of adult fibrous connective
tissue. They occur in all animals. The skin and subcutaneous
areolar tissue is their most frequent location, but no tissue is
exempt. They are frequently found in the region of the sternum
of the horse and ox, in the ovary and uterus of the cow, and in
the perineal and elbow regions of the dog. In the skin and sub-
cutaneous tissue thev usuallv appear as loose, circumscribed,
nodular growths. Some fibromata have no well defined border
or line of demarcation but are apparently diffused through the
tissue. This type, however, is somewhat rare, and possibly they
are not fibromata. Thev may become so large that their pres-
sure produces atrophy, degeneration or necrosis of the skm cov-
ering them, or the surface epithelium may produce sufficient
new tissue to compensate for the increased surface. These tu-
280 VF.TKRTXARY PATITOLOGY.
mors are nsnally sint^le. that is, onlv one tumor occnrino- in the
individual; but they may be multiple. Multiple fibromatosis is
occasionally observed in the subcutaneous tissue of horses.
They are variable in size, being so small in many instances that
they are not observed in an ordinary examination. A fibroma
may be so large that the diagnostician would mistake it for a
malignant tumor, a hernia, cold abscess, etc. Their shape is as
variable as their size. Thev ma}' be oval, tabular, tubercular,
nodular, and, in fact, they may have any conceivable shape and
contour.
If the skin or covering tissue is incised or dissected away the
tumor is usually found to be surrounded by a fibrous capsule or.
in rare instances, it may blend imperceptibly with the surround-
ing normal tissue. They are not difficult to remove in their
entirety because of their encapsulation. When they are excised
their blood supply is found to be disproportionate to their size.
With the small or limited blood supply there is a tendency to
a slow growth and degeneration and necrosis. "With an exces-
sive blood supply tliere may be rapid growth and perhaps fre-
quent hemorrhages into the tumor tissue. If the excised tumor
is sectioned and the cut surface examined with the unaided eye,
it appears to be composed of compact bundles of fibrous connec-
tive tissue atypically arranged (hard fibroma) or of loosely ar-
ranged bands of fibrous connective tissue inclosing areolar spaces
(soft fibroma). In color the section appears pearly white with
grayish-white, yellowish-white or dull pink areas, depending
upon the compactness of the tissue, whether the fibre bundles
are ctit longitudinally or transversely, and the amount of blood
contained. A fibroma is firm, dense and resistant, and when cut
mto there may be a creaking sound similar to that produced in
cutting a tendon. They have little or no tendency to peripheral
infiltration but grow by central or interstitial expansion, mechan-
ically pushing the contacting tissue aside.
It the tumor has degenerated or become necrotic quite a dif-
ferent picture than the above v.ill be seen. It may be a mass of
mucus as a result of mucoid degeneration. It may contain
necrotic areas or the entire tumor may imdergo necrosis, the
necrotic tissue becom.ing liquified, coagulated, caseated or calci-
fied. Hemorrhage into the tumor tissue may give it a mottled
appearance. The hemorrhagic spots may be red, yellowish-red
or greenisli-red, depending upon the changes in tire hemoglobin.
Microscopically, the tumor tissue appears as white fibrous
connective tissue, being composed of cells and a white fibrous
intercellular substance.
TUMORS.
281
The cells are usually few in number, are flat and have a flat,
oval nucleus. Cells are more prevalent in the rapidly growing
tumors. The arrangement of the fibres varies and is the deter-
mining factor of the denseness of the tumor.
A hard fibroma is made up of bundles of fibres extending in
Fig-, 126. — Si otion of a hard Fibroma showing: 1. Transverse section of
bundles of Fibres; 2. Longitudinal section of bundles.
various directions and occupying practically the entire space,
there being no interfunicular spaces. The bundles are compact
masses of parallel, wavy fibres, with here and there a cell. The
fibres are of two varieties, viz. : glia fibres and collagen fibres.
Glia fibres are found along the surface of the cell and are parallel
to its long axis. They are straight or slightly curved and prob-
ably extend from one cell to another. Collagen fibres are out-
side but lie close lo the cell and appear slightly wavy. Collagen
fibres predominate in fibromata. Ijlood vessels are few in num-
ber and may be absent.
A soft fibroma is composed of small bundles or bands of
fibrous tissue loosely arranged. Cells and blood vessels are more
numerous than in hard fibromata. The general appearance of a
loose fibroma magnified one hundred diameter'-; is very similar
282
VETERINARY PATHOLOGY.
to areolar tissue, except that in the former yellow elastic tissue
is absent, wliile in the latter it is present. All variations in the
compactness of the fibrous tissue is found from the soft to the
hard fibroma. In fact some sections indicate that a soft fibroma
becomes a hard fibroma by an increase in the intercellular fibres.
Clinically, fibromata are innocent or benign tumors. Their
rate of growth is relatively slow. They may cause a fatal termin-
ation by mechanically obstructing tlie lumen of a hollow organ,
as the intestine, by pressure upon vital organs, as the brain, or
they may become so large that the afifected animal is unable to
move about in search of its food. Thus Kitt mentions a fibroma
Fig 137. — Soft Fibroma, showing wavy loosely arranged fibrea.
that weighed 178 kilograms (391 Vo lbs.) They do not extend
by metastasis, neither do they recur when removed.
Fibromata can usually be dififerentiated from inflammatory
new growths by the history of the case, fibromata having no
defined cause and inflammatory new growths resulting from irri-
tation. Microscopically, inflammatory new growths contain mi-
totic plasma cells and fixed connective tissue cells, while mitosis
is rarely observed in fibromata. There is also an extensive blood
supply in inflammatory growths, but a limited supply in fibroma-
tous tissue. Actinomycotic and botryomycotic tissues are recog-
nized by the presence of the causative fungi. Spindle-cell sar-
comata may be confounded with fibromata and are sometimes
difficult to differentiate. Sarcoma cells usually contain more
TUMORS. 283
protoplasm than fibroma cells, and this may be used as a basis
for differentiation. By a gross examination a leiomyoma may
be mistaken for a fibroma, but the microscopic appearance of the
nuclei is characteristic. The nuclei of fibroma cells are oval
while those of leiomyoma cells are rod-shaped. If the fibroma
contains degenerated or necrotic centers the differentiation may
be more difficult in gross section but microscopic examination
of the unchanged tumor tissue will be sufficient. \\'hen the en-
tire tumor has degenerated or become necrotic diagnosis may
be impossible. Fibromatous tissue may be found in other tu-
mors or fibromata may become contaminated by permeation or
infiltration of other tumor tissue as mucoid, sarcomatous, etc.,
resulting in a fibro-myxoma, fibro-sarcoma, etc. The first por-
tion of the compound word denoting that the mixed tumor con-
tains more of that tumor tissue. Thus a fibro-myxoma is a
tumor composed of fibroma tissue (fibrous connective) and myx-
oma tissue (mucoid connective), the former predominating.
Mixed tumors will be discussed after consideration of the simple
tumors.
A keloid is a dense overgrowth of white fibrous connective
tissues in a cicatrix. These growths are quite common in the
negro, especially at the point of an injury, as a razor cut or ear
puncture for an ear-ring, etc. Because of their frequency and
extent they have been considered as tumors by some authors.
They are not true tumors but rather an inflammatory new
growth resulting from improper cicatrization in wounds. They
are not common in the lower animals.
284 VF.TF.RIXARY PATHOLOGY.
MYXOAIA.
Myxomata are tumors composed of mucoid connective tissue
These tumors may be a sul:)variety of tibroma. Purely myxo'
matous tumors are not very common, occurring more frecjuentlv
in combination with other tumor tissue. They are usually found
in connective tissue, but in no special location. They have been
found in the heart, along- nerve trunks, in the nostril, and a case
has been reported of a pure myxoma involving the entire orbital
structures in a horse. These tumors are usually about the size
of a hen's egg, rarely becoming very large, probably because of
their destruction by degeneration. They are invariably single.
They appear as semi-solid masses, surrounded by fibrous cap-
sules and are usually dirty-white or gray in color. After they
are removed and an incision made into them a mucus or gela-
tinous, ropy fluid escapes. The cut section appears as a glassy,
semi-transparent, semi-solid mass and is very similar to Whar-
ton's jelly. The escaped fluid will be found by chemical test to
contain considerable mucin. Their blood supply is usually very
meager,- in fact some authors regard myxomata as a mucoid
degeneration because of their limited blood supply.
Microscopically, a myxoma is composed of stellate cells, in
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^Microscopic sections of lipomatous tissue closely resemble
normal adipose tissue, except that the cells may be larger and
perhaps more irregular in shape. As in normal adipose tissue
the adipose cells are supported by connective tissue cells and
fibres. The application of Sudan III and osmic acid gives
further proof of the composition of the cells.
Lipomata may be multiple but they are typical benign tumors,
though death mav result from the mechanical effects produced
131. — Section ul a Liiu.iiia fiom omentum of
of adipose cells,
au o.\, showing framework.
by them. They do not form metastases. Subserous lipomata pro-
duce volvuli which terminate fatally in horses. Large periton-
eal or omental lipomata of the ox and dog frequently cause suffi-
cient displacement of the abdominal organs to materially de-
range their function. Subcutaneous carpal lipomata in the horse
mav become so large that they mechanically interfere with loco-
motion. Lipomata may have a fibrinous infiltration and organ-
ization resulting in lipomatous elephantiasis.
290 VETERINARY PATHOLOGY.
OSTEOMA.
An osteoma is a tumor composed of osseous tissue. Pure
osteomata are not common. They occur most frequently in re-
lation to bones and usually at the union of osseous tissue devel-
oped from different ossif}-ing centres. These tumors are quite
common in mules, appearing as projecting pedunculated masses
attached to the inferior maxilla. More rarely they are found in
other organs, as the lung, parotid gland, mammary gland, etc.
Fig. 182. — rediiiiculated Osseous Tumor .Maxilla. Horse.
These tumors are usually small, rarely becoming as large as
a cocoanut. They are hard, nodular masses that are frequently
lobulated and usually firmly attached to the surrounding tissue.
It is possil)le that they are developed from osseous cells which
have been misplaced in bone formation or from the osteogenetic
layer of the periosteum. WHien they develop adjacent to pre-
existing bone the periosteum or endosteum surrounds them.
Those osteomata developing in other structure than bone are
surrounded by a distinct membrane which is usually very sim-
ilar to periosteum. Osteomata may be classified as: (1) hard,
ivory or eburnated, and (2) soft, spongy or cancellated. Either
of the foregoing classes may be homologous or heterologous.
Homologous osteomata occur in bony structures and may be an
exostosis or an enostosis. Heterologous osteomata occur in other
tissue than bone.
Hard, ivory or eburnated osteomata are structurally very
similar to the compact osseous tissue of a long bone. Haversian
systems may be present or they may be absent. If the Haversian
systems are present they are irregularly arranged and are ap-
proximately perpendicular to the surface of the related bone. If
TUMORS. 291
the Haversian systems are absent the tumor is composed of
superimposed lamellae like the outer circumferential lamellae of
the shaft of a long bone.
Soft, spongy or cancellous osteomata are surrounded by a
periostoid membrane. In structure they are similar to cancellous
osseous tissue. The marrow spaces may be occupied by tissue
that is structurally identical to red marrow or they may be filled
with sarcomatous tissue, fibrous connective tisssue, etc. The
blood vessels are usually normal in structure and their distribu-
tion is through Haversian canals in the hard osteoma or the
spaces in the soft osteoma.
Osteomata are invariably single; do not recur when removed;
have no tendency to form metastases ; and hence are benign.
They should be differentiated from (1) ossification of inflam-
matory new growths as ringbone, spavin, myositis ossificans,
etc. ; (2) hyperplasia of osseous tissue ; (3) ossification of tumor
tissue as fibromata, chondromata, etc. ; (4) metaplasia in which
osseous tissue is the end product; (5) calcification.
GLIOMA.
A glioma is a tumor composed of supporting cells (neuroglia
cells) of the tissue of the central nervous system. Neuroglia
tissue occurs in two forms, as ependymal cells lining the neural
canal and the ventricles and as glia cells whichare derived from
the ependymal cells and act as a supporting framework of the
central nervous system. Gliomata are of two types, depending
upon the type of cells composing them, viz., spider cell glioma
and mossy cell glioma. Gliomata have been observed only two or
three times jn the domestic animals. They usually have their
origin in the gray matter near the central canal of the spinal
cord or in the gray matter of the cerebrum. They do not become
large and they are usuall}^ not encapsulated. They are composed
of cells that are very similar to normal neuroglia cells. The
glioma cells mav be slightly larger than neuroglia cells but they
have the fibre-like processes characteristic of them.
These tumors do not form metastases but are likely to produce
a fatal termination by pressure upon nerve centers.
ODONTOMA.
Odontomata are tumors composed of dental tissue and usu-
ally occur in connection with teeth, particularly the superior
molars. Odontomata are of frequent occurrence, the majority
of dental diseases in two to five-vear-old horses being due to
292
VETERINARY PATHOLOGY.
them (Williams). Facial bulging is a common symptom of
them and there may be an excessive mucus discharge from the
nostrils. Cystic odontomata may produce super-resonance, which
is useful in differentiating them from empyema of the facial
sinuses.
These tumors are derived from the enamel organ, dentine
papilla, or the tooth follicle. Their derivation to some extent
determines their structure. Those derived from the enamel
organ are composed of an enamel covering and in some cases
the entire odontoma is enamel. Dentine is usually the pre-
dominating tissue in those derived from the dentine papilla.
From the tooth follicle there are usually formed cystic odonto-
mata, although they may be fibrous or may contain ossified cen-
tres and cementum. Their structure varies considerably and it is
not rare that all of the above structures are represented in one
odontoma.
In size, odontomata vary from microscopic masses to irregu-
Fig. 133. — Photograph of an Odontoma of the interior maxilla of a horse.
TUMORS. 293
lar bodies. Their shape and color are as variable as their size.
Epithelial or enamel odontomata are the highest in the scale of
hardness of all tumors. Other types of odontomata are soft.
Cystic odontomata may be single or multiple, as many as three
hundred having been observed in a single follicular tumor of
this type. They may grow very rapidly but more frequently
they develop slowly. They have no tendency to form metastases.
Degeneration is common in those developing from the tooth
follicle. Clinically they are benign but may cause fatal termina-
tion mechanically or from infection.
According to the derivation Sutton describes four classes of
odontomata as follows :
1. Those derived from the enamel organ or epithelial odonto-
mata. They usually appear as irregular masses covered with
enaniel. They may contain cystic cavities separated by enamel
partitions. Epithelial odontomata are usually surrounded by a
firm capsule, and in some instances appear to have had their
origin from a mucous membrane. Miscroscopically they are found
to be composed of enamel cells and irregular columns of epithe-
lial cells forming alveoli. The epithelial cells vary in shape from
columnar to the stellate or typical progenitors of enamel. These
tumors occur in most of the domestic animals and usually in
early life. Two epithelial odontomata were obtained from the
left maxillary sinus of an aged horse used for dissecting pur-
poses. These odontomata were completely enclosed in an osse-
ous mass, the maxillary sinus being completely filled by the new
growth. The facial bones were slightly bulged. The osseous
formation surrounding the odontomata and the thickening of the
facial bones indicated that considerable time had elapsed since
their formation.
2. Those derived from the tooth follicle. Depending upon the
nature of the neoplasm this group may be further subdivided
into follicular and fibrous odontomata, cementomata and com-
pound follicular odontomata.
Follicular odontomata result from hyperplasia of the tooth
follicle tissues which thus prevents the normal eruption of the
tooth. They may appear as simple or multiple cysts. Their
walls may be calcareous or osseous but thev are more frequently
membranous. The cysts are usually subdivided into many com-
partments, the cavities of which are lined with epithelium. This
lining epithelium secretes a viscid fluid, the accumulation of
which is responsible for the enlargement of the cysts. They
occur in sheep, hogs and horses.
Fibrous odontomata are produced by a marked increase of
294
VETERINARY PATHOLOGY,
the enveloping fibrous capsule of the follicle. The hyperplastic
fibrous tissue usually fuses with the cementum, and the entire
mass may later become calcified or ossified. These odontomata
are most common in ruminants, goats especially being affected.
They are prone to occur in animals afflicted with rickets.
Cementomas (Osteocystoma capsulare dentiferum) are
formed by ossification of excess tissue developed around the
tooth follicle. The hvperplastic cementum may include several
tooth germs. They appear as masses of cancellous or spongy
bone and are structurally very similar to cementum, being com-
posed of irregular spaces surrounded by osseous tissue contain-
ing branched lacunae. They are most common in horses, occur-
ing most frequently in connection with the incisor teeth.
Fig. 134. — Epithelial Odontoma.
Compound follicular odontomata result from the ossification
of irregularly located areas of the tooth follicle tissues, thus
leaving intervening areas of fibrous tissue. The ossified masses
are designated denticles and they may be very numerous, as
many as three hundred having been observed in a single tumor.
The intervening tissue usually degenerates and becomes of a
liquid consistency. Thus the tumor appears as a cyst containing
many cavities. The denticles vary in size and consistency. These
tumors have been observed in the goat, sheep, ox, and horse,
TUMORS. 295
3. Radicular odontomata are those derived from the dental
papilla, developing from the roots of a tooth after the crown
has formed. They appear as bony masses and are frequently
enclosed within the maxilla. Structurally, they consist of den-
tine and cementum, the dentine usually being surrounded by a
cemental capsule. They are occasionally observed in domestic
animals, being most common in boars.
4. Composite odontomata are composed of varying amounts
of irregularly arranged enamel, dentine and cementum. A single
tumor may contain several teeth fused into one mass. Their
structure varies with the amount of each of the above named
constituents they contain. Thus they may be almost entirely
enamel or contain a very little enamel. They may be solid and
massive or cystic. They are very likely to cause suppuration
and necrosis of the adjacent tissues. This type of odontomes
occurs more frequently in the horse.
Dentigerous cysts are more properly classified as a type of
teratomata and will be discussed with that group of tumors.
NEUROMA.
Neuromata are tamors composed of nerve tissue. They are
exceedingly rare. They occur in connection with ganglionic
cells and most frequently those of the sympathetic ganglia, al-
though they may occur in the brain. They appear as. nodular
growths varying from the size of a pin head to that of an apple
They are gray or white in color, rather firm, and usually sur-
rounded by a capsule. Irregularly shaped ganglionic cells inter-
posed with some nerve fibres constitute their minute structure.
These tumors should be dififerentiated first from the so-called
"amputation neuromata," which are simply an entangled mass
of regenerated axones and are not tumors ; second from fibromata
that develop from the perineurium or endoneurium of a nerve
trunk.
Neuromata may be multiple but they are usually benign.
ANGIOMA.
These are vessel tumors that are developed independently of
pre-existing vessels. But it is frequently impossible to deter-
mine whether the mass of vessels is a result of excessive growth
of the pre-existing vessels (hyperplasia) or whether they are
newly-formed vessels.
Possibly angiomata should be discussed under the caption of
296 VF.TKRIXARV PATHOLOGY.
endotheliomata as it has been thought by some that the endothe-
lium is the only neoplastic portion of an angioma.
This group is composed of (1) hemangiomata. (2) lymphan-
giomata.
Hemangiomata are blood-vessel tumors. In the human they
are found most frequently in the skin and may occur in the skin
in domestic animals, but are not often observed there because
of the pigmentation of the skin. They are found most frequently
in the liver and the spleen of the ox, dog, horse and sheep. An
occasional case is observed in the subcutaneous tissue of the
horse. Hemangiomata may be subdivided into four varieties.
Hemangioma simplex (Capillary telangiectases, nevus, birth
mark) is a tumor in which there is an excess of capillary vessels
that are considerably enlarged or dilated. The vessel wall is usu-
ally altered in structure, the endothelial cells being larger and
the perivascular tissue more dense. These are quite common
in the liver of the ox where they appear as irregular blood spots,
red or purplish in color.
Fig. 135. — Haemangioma Simplex.
a. Large capillaries engorged with blood. b. Liver colls.
Cavernous hemangioma (hemangioma cavernosum) is a tumor
composed of spongy tissue similar to erectile tissue. The caver-
nous spaces are filled with blood, thus coloring the tumor red or
bluish-red. These tumors are found most frequently in the liver
and spleen. An ox liver containing cavernous spaces, each as
large as a hen's egg and containing parietal thrombi, has been
observed. A lobulated enlargement in the spleen of a dog was
TUMORS.
297
found to be a cavernous hemangioma. The spaces in cavernous
hemangiomata are lined by endothelium that is supported by a
very limited amount of white fibrous connective tissue, yellow
elastic tissue being practically absent.
FiK. 136. —Photograph of spleen of dogr affected with an Hemangioma Carvernosum.
Heman>gioma hypertrophicum is a blood-vessel tumor composed
of masses of relatively small vessels, in which the vessel walls
are hypertrophied. One of these tumors occurring in the subcu-
taneous tissue of the metacarpal region of a horse has been
observed. It appeared as a mass beneath the skin and was
about the size of a hen's egg. Pulsations could be observed and
by palpation they were quite distinct. The tumor when removed
was a tangled mass of blood-vessels with comparatively small
openings. Microscopically, the vessel walls were found to be
hypertrophied. The vessels were held together by fibrous con-
aective tissue.
Cirsoid aneurisms are tumors composed of dilated and enlarged
298 VETERINARY PATHOLOGY.
tortuous arteries. This variety of hemangiomata is not common
in the domestic animals.
Lymphangiomata are tumors composed of newly-formed lym-
phatic vessels. These tumors are not common ; in fact, only one
•#4 'v,-'\ ' ','1 » ■ n^\' ^,'.
'-.-> '
Fig. 137. — Section of Hemangionia H.vi)ertrophiciiin, showing an increase in
the number of the vessels and an hyjjertrophy of their walls.
or two cases have been reported by veterinarians. The tumors
may be conveniently divided into capillary and cavernous.
Angiomata are usually benign tumors, although by rupture
they may produce fatal hemorrhage or lymphorrhage.
MYOMA.
Myomata are muscle tumors. They are divided into two
classes : 1. Leiomyomata or the smooth muscle tumors. 2.
Rhabdomyomata or the striated voluntary muscle tumors. My-
omata, found occasionally in the human, are rare in the lower
animals.
TUMORS.
299
Leiomyomata are found most frequently in those locations in
which involuntary muscle tissue normally exists, as the uterus,
bladder, intestine, etc. They are nodular or diffuse, dense, pale
pink masses appearing very similar to fibromata. Microscopic-
ally they are composed of miscellaneously arranged involuntary
muscle cells. They dififer from fibromata in that the muscle cells
are thicker and usually not as long as the fibres of fibromata.
Frequently they are combined with fibromata forming a leiomyo-
fibroma, making the diagnosis more difficult. Leiomyoma cells
may be very similar to the cells of a spindle-celled sarcoma, but
Fig. 138. — Leiomyoma, small intestine, mule.
the nuclei of the former are long and rod-shaped while those
of the latter are oval in shape, a ch^iracteristic usually sufficient
for diagnosis. The cytoplasm of .the leiomyoma cells stains
densely with acid stains.
Rhabdomyomata have been found in the kidney, ovary and
testicle. They are probably the result of the development of
misplaced embryonic myoblasts. These tumors are usually pale
in color. In microscopic section the cells are irregularly striated,
300
VETERINARY PATHOLOGY.
and are variable in shape and arrangement. These tumors are
benign.
Fig. 139. — Leiom.vonia.
a. Smooth nucleus cell, showing nucleus.
SARCOMA.
A sarcoma is a tumor composed of embryonic connective tissue
cells. Sarcoma occasionally succeed an injury and are common
where globin is prevalent, as in muscle, bone, etc. The cells have
no tendency to become mature but constanly appear as undiffer-
entiated mesoblastic embryonic cells. Sarcomata are of frequent
occurrence in all domestic animals. They have no predilection for
tissue or location, and are variable in size and shape. They may be
circumscribed but are more frequently diffuse. Metastases are
frequent in the lungs, liver and kidney. Metastatic sarcomata are
usuallv circumscribed.
TUMORS.
301
Sub-surface sarcomata may produce necrosis of the surface tis-
sue, the tumor projecting as a red, granular mass, which appears
very similar to exuberant granulation. The surface tissue may not
be destroyed, in which case the tumor appears as a sub-surface
nodule or dififuse mass. Some sarcomata are encapsulated and
are easily enucleated, but the malignant varieties have no cap-
sule and it is impossible to differentiate the surrounding tissue
from that of the tumor. Sarcomatous tissue may be soft and
spongy or hard and dense, depending upon the extent of the
intercellular substance and the kind of cells composing it. In
color they vary from gray or white to pink and they may be
mottled, depending upon an excessive amount of blood or hemorrh-
agic extravasate, pigmentation, or necrosis.
The microscopic appearance varies with the different varieties,
but in general they are found to be composed of embrxonic cells-
Fig. 140. — Photograph of a horse affected with Sarc<>itia of the Mediastinum result-
ing in obstructed circulation.
(a) Oedema inferior thoracic region.
ib) Jugular vein engorged with blood.
(c) Subcutaneous veins.
302
VETERINARY PATHOLOGY.
having a limited amount of intercellular substance. The cells may
be round, spindle, or myeloid, and the intercellular substance may
be mucoid, fibrous, cartilaginous or osseous. The cells contain a
large centrally located ovoid nucleus, which occupies practically the
entire cell body. Mitotic figures are common in rapidly growing
sarcomata. Frequently there are multipolar mitotic figures indi-
cating the possible division of a cell into three or more daughter
cells. Karyolysis or nuclear fragmentation is well marked in those
cells that are centrally located in the tumor, and especially in
degenerating centres, and in the cells of sarcomas that are not
vie. 141. — Ppction of tumor, showing mottled appearance, a result of Necrotic centred
TUMORS.
303
growing rapidly. The portion of the cell body not occupied by
the nucleus is composed of undifferentiated protoplasm. In
appearance the intercellular substance varies according to its
composition. An abundance of capillaries and small blood
vessels are found in sarcomata. These may be normal in struc-
ture or they may be infiltrated with sarcomatous tissue, and,
in some cases, the blood flows through channels formed by sar-
coma cells. Hemorrhage is of frequent occurrence in sarcomata.
The blood vessels have no regularity in their distribution, a
structural peculiarity frequently resulting in degeneration and
necrosis. Lymphatic spaces and vessels are absent in sarcomata,
excepting lympho-sarcomata, unless they are entangled during
the development of the tumor. Nervous tissue has not been
demonstrated as a distinct new growth in sarcomas. There are
usually many leucocytes and frequently some plasma cells in sar-
comatous tissue. The plasma cells may produce the intercellular
structures of sarcomas or they may become adult connective cells
and produce fibrous connective tissue.
Fig. 142. — Round cell Sarcoma.
The rapid development and the irregular distribution of blood
vessels predispose sarcomas to destructive processes. Mucoid
degeneration frequently occurs and may result in the complete
destruction of the tumor. Necrosis is also quite common, and
suppurative conditions are not rare. If the normal tissues are
eroded, exposing the tumor tissue, septic infection is common
and sometimes results fatally.
This group of tumors may be (classified, according to their
304
VETERINARY PATHOLOGY,
cellular elements, as (1) round-celled sarcomata, (2) spindle-
celled sarcoii;ata, and (3) myeloid-celled sarcomata.
Round-cell sarcoma. This tumor is composed primarily of
round cells (spherical cells) and is rather common. They de-
velop in any tissue and are, as a rule, the most malignant tu-
mors of this entire group. They are soft, spongy, and usually
quite vascular, and, as a rule, are not encapsulated.
Structurally the cells of this variety approximate the embry-
onic epithelial cells more closely than do those of any of the
other types. According to the size of the cells two classes may
be recognized, viz. : small and large. There is, however, no dis-
tinct line between the two classes. The small, round cells are
about the size of lymphocytes while the large, round cells are
as large and sometimes much larger than mononuclear leuco-
cytes. The nuclei of this type of sarcoma cells are, relatively,
much larger than the nuclei of lymphocytes or leucocytes. In
fact, the nucleus occupies practically the entire cell body. The
intercellular substance is very limited and is usually mucoid or
reticular. Blood vessels are usually numerous, and their walls
are frequently formed by sarcomatous cells. Metastatic growths
are frequently of this type. The cut on page 274 is from a pho-
tograph of the lung of a horse, showing metastatic round-celled
pig. 143. — Photograph of sheep's heart, showing a l.vmpho sarcoma of the
pericardium.
TUMORS.
305
Fig. 144. — Section of a Ljmpho Sarcoma of a dog's omentum, showMng tht
lymph VLSsels and sarcomatous tissue.
sarcomata. The primary tumor involved the eye-ball and finally
destroyed the soft structures of the entire orbit. In this case
two or three metastatic tumors were observed in the liver also.
The cut on page "SOI is a photograph of a horse in
which there was an extensive sarcomatous formation in the
thoracic cavitv involving the mediastinum, pericardium, pleura
and some smaller nodules in the lung. (The lung nodules were,
no doubt, metastatic formations.) Because of their tendency to
form metastases and the rapid peripheral infiltration these tu-
mors usually cause a fatal termination.
Lympho-sarcomata are a variety of round-celled sarcoma, and
are called lymphomata by some authors. They are quite com-
mon in all domestic animals. These tumors have their origin
in lymphoid tissue and are extended by the lymph. Two cases
have been studied in the ox in which the primary lesion was in
the wall of the abomasum. One case of generalized lymphosar-
comatosis has been observed in a chicken. A pericardial^ lyirj-
306
VETIiRINARV PATHOLOGY.
phosarcoma was found in a post-mortem examination of a sheep.
An omental lymphosarcoma in a dog was reported in the Ameri-
can Veterinary Review, December, 1905. The color, consistency
and size of lymphosarcomata is quite variable.
Microscopically these tumors are found to be composed of
lymphoid cells, the tumor cells being supported by stellate cells.
Lymph vessels are usuallv quite numerous and their structure is
similar, if not identical, to that of normal lymph vessels. The
stellate supporting cells and the presence of lymph vessels are
the distinguishing characteristics of lymphosarcomata. There
is no leucocytosis in animals affected with lymphosarcomata,
while in those affected with leukemia leucocytosis is well marked.
These tumors are malignant. They form metastases through
the lymph and blood channels. They are usually surrounded by
a very thin capsule.
1— .
Fi^. 146.— Photograph of a muie affected with a spindle cell Sarcoma of ttte eyelids,
I. Granular denuded tumorous surface. i. Granular fungoid tumorous mass.
TUMORS. 307
Spindle-Cell Sarcoma. — Tumors of this variety are composed
of spindle-shaped cells. They are more firm and dense than the
round-cell sarcomata. These tumors are not rare, occurring
most frequently in connection with the skin or sulicutaneous
tissue. Some of the resistant and incurable cases of fistulous
withers are spindle-celled sarcomata. A collar boil that did not
respond to treatment was found to be a spindle-cell sarcoma. These
tumors are common in the eyelids of horses and mules and are
sometimes quite persistent regardless of surgical interference. The
Fig. 146. — Section from spindle cell Sarcoma of a mule's eyelid.
and are sometimes quite persistent regardless of surgical inter-
ference. The cells vary from short, thick fusiform cells to elong-
ated fibre-like cells. Spindle cells are more matured than the
cells of round-cell sarcoma. Round cells have no tendency to
become spindle cells, neither do spindle cells become either round
cells or matured connective tissue cells. The cells in spindle-
cell sarcomata have no definite arrangement but extend in all
directions. In microscopic section some cells are cut trans-
versely, others obliquely, and still others longitudinally. The
nucleus is centrally located, is usually spherical or oval in shape,
and is not as large in proportion to the size of the cell as that
of the round cells. Some have suggested a classification oi this
308 VETERINARY PATHOLOGY.
group into large and small-celled varieties. The cells are usu-
ally held together by reticular connective tissue. This may be
demonstrated in sections in which the sarcoma cells have been
dissolved out by acetic acid. The density of the tumor depends
upon the relative quantity of protoplasm the cells contain and
the amount of intercellular material. A tumor composed of
short, thick spindles is less dense than one composed of fibre-
like cells. Blood vessels usually have normal vessel walls and
are not as numerous as thev are in round-cell sarcomata.
Fig. 147. — M.veloid «r Giant cell Sarcoma of the Humerus.
a. Giant cl'IIs. b. Sarcoma cells.
These tumors are usuallv encapsulated, rarely form metas-
tases and are, in general, not as malignant as the round-cell
variety. They may be mistaken for fibromata, but a careful
study of a microscopic section is usually sufficient for differen-
tiation. Fibromata contain no elements that appear like trans-
verse sections of spindle cells. Leiomyoma may be differen-
tiated by the shape of the nucleus and the selective action of
stain as picrofuchsin.
Myeloid-Cell Sarcoma (Giant-Cell Sarcoma). — This is a
variety of sarcoma characterized by the presence of myeloid or
large multinucleated giant cells (myeloplaxes). Giant cells of at
least two types occur in tumors, one of which results from multi-
ple mitosis and usually indicates rapid growth and may occur in a
variety of different tumors. The second type of giant cells is due to
TUMORS.
309
the fusion of invading endothelial leucocytes and occur most fre-
quently in bone tumors. The latter are therefore not true tumor
cells, although they usually receive the name. Surgeons and patho-
logists frequently find myeloid sarcomata in man, but they are rare
in domesticated animals. They are invariably found in relation to,
or in connection with, bone-marrow, or more rarely in relation
with periosteum. They frequently contain cartilaginous, osseous
or calcareous centres. Ball in "Jo'-^^^'^l cle Med. \^et., et de Zoo-
techny de Lyon." reported a case of giant celled sarcoma affected
the right front foot of a 6 year old cat.
Microscopically, they are composed of myeloid cells and
round or spindle cells. The myeloid cells are the distinguishing
elements of this
variety of sarcoma.
The size of the
myeloid cells is
variable, frequent-
ly being 80 to 100
microns in diam-
eter and with an
irregular outline,
varying in shape
from a sphere to
an elongated mass.
Their protoplasm
may be quite gran-
ular or almost
clear. They have
many nuclei — 150
being observed in
one cell. These
nuclei have no de-
finite arrangement
but occur miscel-
laneously through-
out the entire cell
body. The round
and spindle cells
are like those
occurring in round
and spindle-cell
sarcoma. There may be an excess of one or the other or they
may be equal in number. The intercellular substance varies
from mucoid to calcareous in nature. There is usually an exces-
sive blood supply, the blood vessel walls being usually normal
Fig. 14 8. — Photograph of horse's head affected with
mixed cell Sarcoma.
310 VETERINARY PATHOLOGY.
in structure. Degeneration as well as necrosis and calcification
are of frequent occurrence in myeloid sarcomata.
These tumors may not be completely encapsulated, though
there is always a tendency for them to be circumscribed. They
are the least malignant of all sarcomata. They rarely form me-
tastases.
Mixed-Cell Sarcoma. — This is a variety of sarcoma charac-
terized by the presence of variously shaped cells, as round, spin-
dle and even stellate cells. This variety is not as common as
either the round-cell or spindle-cell varieties. They have been
observed in the horse, hog and ox, but they doubtless occur in
all domestic animals. They aiTect bone, glandular tissue, and
meninges of the brain, in fact, no tissue is exempt. An inter-
esting case of mixed-cell sarcoma of the inferior maxilla of a
horse was described in the December Veterinary Review, 1905.
The tumcjrs frequently degenerate and become necrotic. Mi-
croscopically they are composed of round cells and spindle
cells that are identical in structure with those described in the
discussion of round-cell and spindle-cell sarcomata. Stellate
cells may be present, and are very similar in structure to mucoid
connective tissue cells. The cellular elements are supported bv
reticular tissue or by fibrous connective tissue. The number of
blood vessels is variable. There is an excess of vessels in those
Fig. 149. — Photograph of 3Ia\illa of horse shown in Fig. 162, showing S bony points;
the remainder of the maxilla being completely destroyed by the sarcomatous tissue.
TUMORS.
311
made up principally of round cells and in those that have a lim-
ited amount of intercellular substance. The vessel walls may
be normal or thev may be composed of sarcomatous tissue. De-
generate or necrotic changes in the tissue necessarily alter the
microscopic appearance.
.^::ii)^'W\
^
Fig. 150. — Section of a mixed cell Sarcoma of tlie inferior maxilla of a horse.
These tumors are usually dififuse ; that is, they are not encap-
sulated. They form metastases, and hence are malignant.
Alveolar Sarcoma. — This is a sarcoma characterized by the
arrangement of the sarcoma cells into groups or nests, and is
occasionally found in domestic animals, especially in the ox and
hog. The reproductive glands, ovary and testicle, are the struc-
tures most frequently invaded by them. They may become
quite large. An alveolar sarcoma obtained from the ovary of a
heifer weighed 1'^ kilograms ('^'^ lbs.) and was about 20 cm. (8
in.) in diameter.
Microscopically the cells are usually round, although they
\na_y be spindle-shaped. The stroma of the tumor is made^ up oi
312
V FjT e r 1 X a r y pa t h o log y .
two portions. One portion is usually composed of spindle cells
which are connected into dense bands extending in various direc-
tions and forming alveoli ; hence the name alveolar. The other
portion of the stroma is intercellular and corresponds to that of
the round-cell sarcoma. The arrangement of the cells into nests
is suggestive of a carcinoma, but the differentiation is not diffi-
cult and depends upon ; first, the presence of intercellular sub-
stance between the cells which is present in sarcomata but is
absent in carcinomata ; second, sarcomatous cells are embryonic
connective tissue cells and hence contain nuclei relatively large
in proportion to the size of the cell, while carcinomatous cells are
embryonic epithelial cells and contain nuclei relativel}- small in
proportion to the size of the cell.
-Section of Alveolar Sarcoma from ovary of heifer sliowin^
with sarcomatous cells.
alveoli filled
These tumors grow slowly. They are usually encapsulated
and have no tendency to form metastases. They are very mildly
malignant.
Endothelioma is a tumor composed of endothelium. This is
a tumor that is not specifically a sarcoma, but mr.y be so classed.
Endothelium has the same origin as connective tissue, i. e., the
TUMORS. 313
mesoderm. Embryonic endothelial cells are structurally iden-
tical with embryonic connective tissue cells. These tumors are
not very common in domestic animals. An endothelioma was
observed in the lung of a dog, another in the testicle of a bull.
These tumors may have their origin fromx the endothelium lining
blood or lymph channels, peritoneum, pleura, pericardium, arach-
noid membrane, any organs developed from mesothelium, or
deflections from anv of them. They are variable in shape, size,
color and consistency.
Microscopically they are composed of cells that most fre-
.(^■^
ia> & 'J> ■ "^CI» re, ^ ,,
Qi.
^
'i^ol//r lV'C~
Fig. ]52. — Section of Endothelioma from a bull's testicle. Note the bands of
connective tissue and arrangement of cells.
quently resemble sarcoma cells, although they may approximate
the structure of carcinoma cells. The cells mav be arranged
in tubules, transverse or oblique sections appearing as sections
of gland tubules or acini. If arranged in columns transverse or
oblique sections appear as cell nests. The cells are usually
cubical or spherical in shape, although thev may be spindle or
even squamous. The stroma varies according to the tissue in-
vaded and may be dense fibrous or mucoid. Blood vessels are.
usually quite numerous, and if the endothelium is derived from
314 VETERINARY PATHOLOGY.
the endothelium of a vessel, the vessel may be very irregular in
calibre and structure. If the cells occur in columns or nests it will
be necessary to differentiate them from carcinomata. This differ-
entiation involves the comparison of cells derived from mesoderm
and those derived from entoderm or ectoderm. The only essential
difference, and that is not constant, is the size of the nucleus. The
differentiation may also be governed to some extent by the distribu-
tion of the blood vessels. If the cells occur in tubules, their differ-
entiation from the adenoma will be necessary. Adenomata may be
Fig:. 153. — From drawing of a Nodule of a IMediastinal endothelioma.
1. Column of endothelial cells. 2. Diffuse mass of endothelial cells.
differentiated by observing the same factors that are used in differ-
entiating endotheliomata from carcinomata. Alveolar sarcomata are
very difficult to differentiate from endotheliomata, in fact it is some-
times impossible, and they may be considered in one class or group.
These tumors are not encapsulated and usually form metastases.
They usually occur in internal organs and hence surgical relief is
impossible. Fatal termination is the usual outcome.
Psammo-Sarcoma. — The existence of this type of tumor is
questioned by some authorities. They are composed of sarcomatous
tissue and have calcified masses or cells within. They are rather
TUMORS.
315
rare One case was observed by Harvey, an army veterinarian, and
another case was reported as a cholesteatoma in the Journal of
Comparative Pathology and Therapeutics These tumors occur
most frequently in relation to the brain and particularly the lateral
ventricles, in which they are intimately associated with the choroid
plexus. Because of their location they invariably produce symp-
toms evidencing brain disturbances.
Microscopically modified sarcoma or endothelioma cells vari-
ously arranged constitute the minute structure of psammo-sarcoma.
There is usually evidence of calcification of small centers and there
may be cholesterin crystals present
Fibrosarcoma. — This is a tumor composed of both adult and
embryonic connective tissue. They are quite common, espe-
cially in the eyelids and in labial commissures of horses and
Fig. 154. — Photograph showing location of tumor in ventricle.
Cerebrum.
Left lateral ventricle.
Cerebellum.
Medulla.
Psammoma.
316
Veterinary pathology.
mules. Several cases of dense tissue growths in the withers
of horses have been observed. These animals when presented ap-
peared to be affected with chronic inflammation of the subcutan-
eous tissue or deeper structures. Alost of the above cases were
clinically diagnosed as fistulous withers and an operation recom-
mended. The operation usually consisted of dissecting away
the dense masses of tissue. The cases were usually returned in
Fiff 155 —Photomicrograph showing nature of connective tissue, leucocytes, n^o-
big. 1D3. ^j^^j^;; cells, lime deposits and one blood vessel surrounded by
hyaline like substance.
Fig. 156. — Higher magnification of No. 2.
from four to six weeks after the operation with growths larger
than those present before the operation. The operation was
usually repeated two or three times with the same results.
On microscopic examination these growths were found to be
fibrosarcomata, being composed principally of fibrous connective
TUMORS.
317
tissue in which there were some spindle cells and occasionally a
few round cells. The presence of both fibrous and sarcomatous
tissue is the principal characteristic of these tumors. The num-
ber, size and distribution of blood vessels are very irregular.
These tumors are not distinctly encapsulated, but they do not
form metastases. They are prone to recur after ablation. They
may destroy life after a considerable time, as their growth is
Fig. 157. — A so called giiiut* sarcoma from uterus of a cow.
318
VETERINAT^Y P ATTTOT.OGY.
relatively slow. Operation usually stimulates them to grow
more rapidly.
Melanosarcoma. — A melanosarcoma is any variety of sarcoma
in which melanin is deposited in the tumor cells. These tumors
are quite prevalent. Gray horses seem to have a special predis-
position to them, but they are also found in bay and black horses,
black or red cattle, black hogs, and, in fact, all varieties of do-
Fig. 158. — Melano Sarcoma of hog skin.
mestic animals regardless of color. On microscopic examination,
melanin is found deposited in the tumor cells. The melaiiin may
be in masses or granular and occasionally it may be found out-
side of che cells. Excepting the deposit of melanin, these tumors
have the same microscopical appearance as the round or spi-idle-
cell sarcomata described before.
TUMORS.
319
Melanotic sarcomata are frequently malignant. In an autopsy
of a gray mare metastases of melanosarcomata were found in the
liver, lung, spleen and kidney, the primary growth being located
in the subcutaneous tissue on the right superior portion of the
anus. Another case was observed in which there was general-
ized melanosarcomatosis in a short-horn cow.
Myxosarcoma. — Phis is a tumor composed of myxomatous
and sarcomatous tissue. The existence of this group of tumors
o
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Fig. 170. — Section of a Cvstadenoina of the mammary gland of a sheep, showing:
1. Coagulated cystic contents surrounded by an atrophied acinous wall.
thus appear similar to carcinomatous nests of cells. The epithe-
lial cells are small and usually contain finely granular chromatin.
The connective tissue cells are usually fusiform although they
may be nearly spherical in shape. They contain relatively large
nuclei in which granules may be observed.
Cystadenoma is also common, especially in those adenomata
that produce secretion. They are found in the adenomata of the
mammary and sebaceous glands.
Hypernephroma are tumors which may be classed either with
TUMORS.
333
sarcomas or carcinomas and is composed of tissue similar to adrenal
tissue. They occur most frequently in the kidney, ovary or ad-
renal body itself. Fingle reported case a hypernephroma in a
23 years old mare. Bloody urine was the first evidence of disease
in Fingle's case. On autopsy a renal tumor about one foot in
diameter was observed. Hypernephromas are rarely diagnosed
as such in living domestic animals. They are variable in size, fre-
quently weighing as much as five kilograms (11 lbs.) Usually
gray in color and invariably containing hemorrhagic areas they
thus appear mottled. There is usually an encapsulating mem-
brane present. Blood-vessels are numerous, especially in the
stroma. Dee'eneration and necrosis is of common occurrence.
'If ^''V.-^^ V'*'"^ "^^ /
m
V#*^l';
\ '^'
_^ « « V
Pig. 171. — Hypernephroma of the kidney of an ox, showing large typical hypertie-
phromatous cells containing fat droplets.
Microscopically, these tumors are found to be made up of large
cells similar to epithelial cells and usually containing fat droplets.
These cells are arranged in rows or columns, the columns being
separated from each other by a small amount of stroma. The
columns of cells may be quite variable in their diameter, appearing
at times as long, slender columns and again as rather long nests of
cells. The stroma is composed of fibrous connective tissue and
contains many blood-vessels.
Clinically, these tumors are very malignant, and, although
334 VETERINARY PATHOLOGY.
they are encapsulated, they form metastases through the blood.
They frequently result fatally in the human, even after operation,
probably because of the liberation of considerable af th« adrena-
lin substance which increases blood pressure to nich an extent
that heart failure supervenes.
PLACEXTOMA.
(Syncytioma.)
A placentoma is a tumor composed of tissue similar to the
chorionic villi.
These tumors have been described under a variety of names
as syncytioma malignum. deciduoma malignum, chorio-epithel-
ioma, epithelioma seritonale, chorio-carcinoma. Only recently
have placentomata been recognized as distinct tumors.
A placentoma is essentially a tumor of the uterus. They are
not common in domestic animals but this may be because of fail-
ure to recognize them. The uterus or fallopian tube is their
most frequent location. They occur more frequently after spur-
ious or mole-pregnancy and usually appear a sliort time after
parturition. Abortion is a predisposing cause. The primary
tumor almost invariably occurs in the uterus though a few cases
have been reported in women in which the primary tumor was
in the kidney. They are very malignant.
These tumors appear as soft, spongy, villous, bleeding masses
and are variable in size. Thev have the general appearance of
placenta or foetal membranes in both the primary and the metas-
tatic tumors. They begin to develop at the cotyledons or zone
of placental attachment and rapidly extend into the uterine mus-
cular tissue and invade l)lood vessels, thus metastases occur
in a short time after the tumor appears. Because of their struct-
ure (embrvonic cells and rich vascular supplv) thev grow rap-
idly.
The presence of a placentoma is indicated by uterine hem-
orrhage occurring a few days after normal parturition or abor-
tion. The uterus is enlarged and the afifected individual rapidly
becomes anemic and emaciated. The uterine discharge usually
contains shreds of the tumor and the cavity of the uterus is
occupied witli a soft bleeding mass.
Microscopically, these tumors are composed of a protoplasmic
ground-substance, which is arranged in an irregular network
forming alveoli. The protoplasmic mass is usually continuous,
there being no evidence of cell partitions, and it contains many
nuclei thus forming a syncytium. Within the alveoli of the pro-
TUMORS.
335
toplasmic mass occur many small variously shaped cells. Blood
cavities and canals are abundant and hemorrhaq-ic areas are not
uncommon.
TERATOMA.
These tumors are composed of the different kinds of tissues that
approximate the structure and arran,<;ement of normal tissue so
closely that it is difficult in some instances to differentiate them
macroscopically or microscopically from normal tissues and organs.
Teratomas are also so closely related pathologically to malfor-
mations, that in some cases it is impossible to determine which
condition exists. Structurally they are found to be composed
of either embryonic or adult tissues. Cutaneous structures are
the most frequent tissues observed in this class of tumors,
although tissues of bone, muscle, intestine, rudimentary eyes,
brain, etc., have been found in them as well as sarcomatous and
carcinomatous tissue.
Fig. 172 and Fig. 173. — Dermoid Cysts, natural size.
These tumors are tjuite variable in size, shape and color. In
consistency, they vary from a viscid inass to dentine and enamel.
Tliey are usually single, grow slowly and rarely form metasta-
ses, although a few have been observed that grew rapidly, metas-
tasized and recurred when removed. They frequently undergo
degeneration tending to cystic formation. Clinically, teratomata
are benign, onlv rarely terminating fatal!\\
336
VETERINARY PATHOLOGY,
Etiologically, they are as mysterious as the other types of
tumors. They may have their origin from tissue inckisions. Some
teratomata may succeed imperfect tissue union. The theory of
partlienogenesis may
be apphcable in the
explanation of some
of the m, but the
specific cause or
causes of teratoma-
ta has not yet been
determined.
Teratomata are of
frequent occurrence
in all domestic ani-
mals but are more
prevalent in equines.
They are found in
any tissue and in all
parts of the body
although they are
more frequent in the
skin, ovaries, testi-
cles, kidneys and
parotid glands. Be-
cause of the hetero-
genous structure of
teratomasa they are
difficult to classify.
Dermoid cyst are
teratomata com-
posed primarily of
skin and its appen-
dages (hair, sebace-
ous glands, horns,
teeth, etc.) These
cysts are due to the dislocation of epithelium during development.
The most common location is in the connective tissue of the head
and neck. They may be solid, but are more frequently cystic. In
size they vary from a pea to a basket ball. There is usually sur-
rounding them a dense capsule from which a villous mass may be
Fig. 174. — Dermoid Cyst from eye of a steer,
showing tuft of hair, growing upon cornea.
TUMORS.
337
observed projecting into the cyst cavity. Extending from the vil-
lous projection are tufts of hair or teeth. The villous is, in struc-
ture, very similar to skin. In some teratomasa hair and teeth are
produced directly from the inner portion of the cyst wall. Cys-
tic dermoids usually contain hair and a pultaceous material de-
rived from the sebaceous glands or they contain teeth and a vi']-
cid fluid. Dermoid cysts without any capsule are occasionally
observed. The accompanying cut illustrates hair extending
from the anterior surface of the eve. Those found in the ovaries
1
k'^kO
tvacUDumi^r
Fig. 175. — Dentigeroiis Cyst on left inferior maxillary of 3 years old colt
containing 431 teeth. Removed Dec. 11. 1905,
by H. M. Stevenson. Perry. Iowa.
usualh^ contain elements of all three germ layers. Those of the
testicles may contain vestiges of all the germ layers, but are
usually cystadenomatous or cystocarcinomatous in type although
they may contain cartilage, teeth, osseous tissue, etc. Solid der-
moid cysts are a heterologous mass, of embryonic or adult tissue.
Dentigerous cyst is the name applied to those dermoid cysts
containing teeth. These are the most important to the veterin-
arian because they are of the most frequent occurrence. They
are invariably encapsulated and may or may not cc.itair^ a villus
338 VETERINARY PATHOLOGY.
projection. The teeth vary from an irregular conglomerated mass
of dental tissue to those perfect in form and structure. The con-
stant production and accumulation of the containing viscid fluid
results in enlargement of the cyst and frequently rupture of the
capsule and the production of a fistula. The most frequent lo-
cation of dentigerous cysts is near the base of the ear in the
region of the parotid gland although they may occur in any
other place especially in the ovary and testicle. They are most
common in horses.
Cholesteatoma is a teratoma composed of pearl like masses
of endothelium in which there is more or less cholesterin. They
are not common but have been observed in the brain, (choroid
plexus and tuber cinereum) and urinary organs.
CYSTS.
DEFINITION.
ETIOLOGY.
Retained secretion.
Obstructed outHozu.
Excessive production in ductless glands.
Retention of hemorrhagic extravasate.
CoUiquation necrosis.
False bursae.
Parasites.
STRUCTURE.
VARIETIES.
Retention; Atheroma.
Exudation; Hygroma, Slioe boil. Capped hock, Meningocele.
Extravasation; Hematocele, Hematoma.
Degeneration; CoUiquation necrosis, Hydatiforni
.Pai-asitic; E chinoccosis, Measley pork.
Dermoid; Cutaneous, Dentigerous
SECONDARY CHANGES.
EFFECTS.
A cyst is a bladder like growth surrounded by a capsule
and containing a liquid, semiliquid or gelatinous material. Cysts
are not true tumors. However, a tumor ma}' become cystic,
(Cystoma,) and the capsule surrounding. a cyst may proliferate
and become a true tumor. Collections of inflammatory and oede-
matous fluids, are not usually considered as cysts. Cysts may
be single or multiple. The latter are designated multilocular
cysts.
Cause. — Cysts mav be caused by, 1. obstruction of gland ducts,
thus favoring- accumulation and retention of a normal secretion
TUMORS.
339
or excretion, e. g., renal cysts ; 2. By excessive secretion into duct-
less structures, e. g., distension of bursae ; 3. By extravasation
into the tunica vaginalis sac, e. g., hematocele ; 4. Liquefying
necrosis, e. g., formulation of cysts in the cerebrum of horses
affected with "blind staggers." 5. Parasites, e. g., Cysticercus
cellulosae.
Structure. — The cystic wall varies according to the age of
the cyst. In the beginning it may represent the original gland
structure or a condensation of the normal tissue of the part.
Later the cystic walls may be lined with epithelium or endothel-
ium, which actively secretes as long as the cyst grows. The cys-
tic capsule may be composed entirely of fibrous connective tissue.
In some instances the primary capsule is fibrous and later an
endothelial lining develops. The cyst wall or capsule may be
firmly adherent to the adjacent tissue or it mav be looselv at-
tached.
Fig. 176. — Cyst on Abdomen of Mule.
(Courtesy of American Veterinary Review)
340
VETERINARY PATHOLOGY,
The cystic contents varies according to the nature of the cyst.
Urine, milk, saliva, mucus, semen, liquor folliculi and other secre-
tions and excretions are represented in cystic contents. Blood
i. e., hemorrhagic extravasates and various tissues that have
undergone colliquation necrosis may represent the contents of
cysts. The various secretions, excretions, extravasates, exudates
and necrotic tissue usually undergo some modification when re-
tained within a cyst.
Varieties. — Retention c\sts. those resultingr from the accumu-
Fig. 177. — Uterine Cyst the capsule of which had become osseous.
lation and retention of normal secretions, e. g., renal cysts, mam-
mary cysts, testicular cysts, ranulae, mucus cysts, sebaceous cysts
(Atheromata).
Of 3,000 kidneys from swine 108 were found to be cystic.
An ovarian cyst in the ovary of a goat was reported by Hebrant
& Antonie. The ovary in this case was about the size of a three
gallon pail.
Exudation cysts\, those resulting from excessive secretion into
ductless glands or cavities, e. g., ovarian cysts, hygroma, capped
hock, meningocele.
Extravasation cysis, those resulting from hemorrhage into tis-
sues or closed body cavities, e. g., hematocele, hematoma.
Degeneration cysts, those resulting from liquefaction of ne-
crotic tisstie ,e. g. colliquation cerebral cysts.
Parasitic cysts, those resulting from the development of para-
sites in the tissue, e. g.. cysticercus cellulosae, cysticercus bovis,
cysticercus echinococcus, etc.
TUMORS. 341
Dermoid cysts, those resulting from inclusion of cutaneous tis-
sue. These have been discussed under the head of teratomasa.
Implantation cysts, those resulting from transplantation of epi-
dermal cells into the sub-epithelial connective tissue. When such
transplanted cells continue to multiply and form a continuous epi-
thelial mass the central part of which sooner or later undergoes
necrosis and become of a semisohd consistency, thus forming a
pultaceous mass.
Secondary Changes. — The cystic wall may become the seat of
inflammatory disturbances, neoplastic formation or necrosis. In
some instances cysts are destroyed because of the disintegration
of their capsule, by disease.
The cystic contents may undergo degeneration, become in-
spissated or calcified.
Effects. — The effects of cyst formation depend upon the
tissue involved and the size and nature of the cyst. The cysts
frequently become so large that the entire organ is destroyed,
e. g., ovarian and renal cysts. In some cases the cysts may
destroy life, especially if a vital organ, e. g., the brain is in-
volved. Cysts may persist for years and be of no serious con-
sequence, on the other hand they may seriously inconvenience
the functional activity of the part involved and impair the health
of the animal from the beginning.
CHAPTER XI.
FEVER
(Pyrexia ).
DEFINITION.
ETIOLOGY. — Toxins; ptuiinuns; katcibolic tissue products; drugs.
PERIODS OR STAGES (Course).
Onset {Stadium Incrementi).
Acme {Stadium Fastigium).
Decline {Stadium Decremenli).
Convalescence.
J'ARIETIES, according to
Course.
Regular.
Irregular.
Duration and temperature z'ariation.
Eplicincral.
Continuous.
Remittent.
Intermittent.
Severity.
Sthenic.
Asthenic.
SYMPTOMS.
Chill, diminished secretions, increased heart c:!io>i aiul respire tic n,
nervousness and restlessness.
LESIONS.
Parenchymatous degeneration, hemolysis, hyaline degeneration, loss
of fat.
Body lieat is a product of metabolism. The body heat or
temperature of warm blooded animals is practically constant,
although changed environment, diet and use or occupation pro-
duce some variations. Thus a horse confined in a barn has a
temperature .5 to 1° F. higher than when not so confined, pro-
vided the diet is the same in both conditions. A narrow ration
is conducive to increased oxidation and consequently a higher
temperature. Animals in action have a higher temperature than
when at rest. Thus a dog's temperature is from 1 to 1" F. higher
immediately after than it is before a chase.
The accurate regulation of body temperature is accomplished
by the action of the thermo-regulating center or centers. Tissue
action is always accompanied by increased heat production, and
frequently different parts of the same animal may vary 1 to 6° F.
in temperature. The equalization of body heat and the distribu-
tion of heat to the different parts of the body is accomplished
by means of the circulating blood. Heat is continually produced
in the animal body and is constantly eliminated from the body
342
FEVER.
343
in the excretions (air, perspiration, urine and feces), as well as
by direct radiation. The relative amount of heat dissipation by
the excrementation and by radiation varies in different animals.
Normal temperature is the balance of equilibrium maintained
between thermogenesis (generation of heat) and thermolysis
(dissipation of heat). The normal temperature of an animal
used during the day is about 1° F. higher in the evening than in
the morning.
Fever is a condition in which the equilibrium between ther-
mogenesis and thermolysis has been overthrown, i. e., there is
a disturbance of metabolism accompanied by increased tempera-
ture. It is not a disease but a symptom complex, common to
several different pathologic conditions. Fever should be dif-
ferentiated from heat stroke and sunstroke. In heat stroke there
is no disturbance of thermogenesis or thermolysis, but the ther-
molytic centers are unable to cope with the existing external
conditions, and there is accumulation of heat in the body, whereas
fever is a result of disturbed equilibrium between thermogene-
sis and thermolysis. Sunstroke is a condition produced by the
action of actinic or chemic rays of the sun upon the nerve cen-
ters, temperature variations being only a predisposing factor.
Etiology. — Fever is usually caused by bacterial products
as toxins, endotoxins and bacterial proteids. Tissue products
as leucomains, peptones and various albumins are also capable
of producing fever. Certain therapeutic agents may be causative
factors of fever.
Course. — The course of a fever may be divided into four per-
iods or stages, as follows:
Onset (stadium incrementi) is the period of increase between
the time of normal temperature and the time that the tempera-
t
f
3
4
r
f,
g
5
la
1,
It
-l
y
y^
— '
t-
X7
^
-f^
_
Fig. 179. — Continuous fever chart showing morning and evening variations, but a continuous
higii temperature.
Symptoms. — Fever is usually ushered in by a chill because
of the constriction of cutaneous vessels which thus diminishes
the temperature of the skin and produces the sensation of chill-
ing. There are diminished secretions, as perspiration, saliva and
urine. In long continued fever there is constipation because of
absorption of fluid from the intestines. The pulse rate is usually
1 _
.«.
t
r
t
7
8
?
IC
1,
,1
,5
It
IS
n
'7
'1
1^
to
il
s«
i.\
Sf
55
tl
«7
tt
%1
3o
»i
IX
lej
'
r
N
/
\
-"1
y
^-"<
^''■^
N
/
\
^^■
y
'^
^'
^
^^
,/■'
_.
v^-
.y
V,
^
/
■vv
';i
->.'
/
f
z^-
~"
V
/
—
Fig. 180. — Keniittent fever chart, siiowing variations
always above normal.
in whicli the temperature
increased and its character is changed because of the action of
katabolic products on the nerve centers. Respiration is increased
probably because of an efifort to eliminate large quantities of air
and waste material, and thus there is a tendency for the tem-
perature to be diminished. The afifected animal is more or less
nervous and restless.
346
VETERINARY PATHOLOGY.
-^
pL.
3
pi-q
f
t.
—
—
p-^
-^
-^
i>
>T
f»
IS
-ii_
—
r^
r-'"^ 1
Jo
1/
at
2S
gl
tf
at
i7
»»
j»
»j
»i
M
r
A
^^
>-
,
/
V
/
/
^
/
\
/
""
/
V
I
\
'
I
\^
/
\
J
\
/
'
1
/"
^-
N
/
/
\
V-
•>-
'""
'''■
'
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Kti
_»'
rs<
~^-<
—
Fig. 181. — Intermittent fever chart in \vliicl\ tlicre are periods of normal tempera-
ture.
Lesions.^ — All parenchymat(jus structures are affected with
cloudy swelling-, the extent of which depends upon the degree
of temperature and its duration. Hemolysis is more or less ex-
tensive. Chronic or long continued fever usually causes hyaline
degeneration, especially of the vessel walls. The affected animal
rapidly diminishes in w^eight because of the consumption of fat.
CHAPTER XII.
INFECTIVE GRANULOMATA.
Infective granulomata embraces a group of specific inflam-
matory conditions characterized by the proliferation of endothe-
lial cells, fibroblasts and other cells. Though the consideration
of the following diseases belongs more properly to a discussion
of infective diseases, their description will be of value to the stu-
dent of general pathology.
TUBERCULOSIS.
Tuberculosis is a specific, infective disease, caused by the
bacterium of tuberculosis affecting practically all of the higher
animals and also some of the lower forms of animal kind.
Extent. — McFarland states that 14% of the deaths in the hu-
man familv are from tuberculosis. It is probable that 25% of
all humans have or have had tuberculosis.
The prevalence of animal tuberculosis is variable in different
communities, the percentage depending upon methods employed
for control and eradication under different sanitary laws, upon
transportation rules and regulations and upon the conditions un-
der which the animals are maintained. The exact percentage of
tubercular animals in any country is not known, but the relative
number has been determined by tuberculin testing and by post-
mortem examination at abattoirs. In the United States the
percentage, generally speaking, is low in comparison with other
countries. According to the post-mortem findings of 7,621,717
cattle slaughtered in United States establishments having official
inspection during the fiscal year beginning July 1st, 1906, and
ending June 30th, 1907, 29,835, i. e.. .4% were tubercular.
This percentage is probably below the actual percentage, as
dairy cattle are more extensively affected than beef cattle. The
Secretary of Agriculture in his report for 1908 holds that 1%
of beef cattle and 10% of dairy cattle are tuberculous.
According to the above report 2% is the estimated prevalence
in the United States of tuberculosis among swine.
Porcine tuberculosis is apparently on the increase in the
United States. In Germany it varies from 1-7%. Equine tuber-
347
348 VETERINARY PATHOLOGV.
culosis is not common in the United States, or at least only a
few cases have been reported. Tuberculosis is usually found in
those horses and mules that have been fed on tubercular cows'
milk.
Tuberculosis of goats is rather rare and the disease is still less
common in sheep.
Dog and cat tuberculosis is not uncommon and is usually
observed in pets of tubercular humans, although barn cats, espe-
cially those fed milk from' tubercular cows, frequently become
tubercular. (A dairy was recently inspected in which 68% of
the cows were tubercular and on autopsy three barn cats also
were found to be affected in a like manner.)
Tuberculosis of fowls is more prevalent in the United States
Fig. 182. — Bacterium Tuberculosis Bovine. Pus showing leucocytes and bacterium
tuberculosis.
than is ordinarily suspected, although the percentage of affected
birds is difficult of determination because there is at present no
official inspection of fowls.
Etiology — Tuberculosis is caused by the Bacterium tuberculo-
sis. This bacterium has rounded ends and is frequently slightly
ment. It varies from 2 to 5 microns in length and from .3 to .5
in width. (These bacteria may appear as long, delicate, mycelial
threads, branching forms, or even as a ray like fungoid growth,
the form depending upon the environment. The pleomorphism
of this micro-organism has caused some doubt as to its classifica-
tion as a bacterium.) The Bacterium tuberculosis may occur
singly or in pairs, and it is not uncommon to find several lying
INFECTIVE GRANULOMATA. 349
side by side. They do not form spores, but they may contain
granules and vacuoles, and they may have a beaded appearance
because of fragmentation of their cytoplasm.
The Bacterium tuberculosis is extremely resistant to external
injurious influences, probably because of a wax-like substance
that constitutes about one-third of the body weight and forms
the principal part of the external covering or capsule. (These
bacteria are stained with difficulty but when once stained retain
their stain even though subjected to the action of alcohol and
acids.) The staining peculiarities are probably due to a fatty
substance they contain.
Source of infection. — The bacterium tuberculosis may be
transmitted direct from tubercular to healthy animals, but infec-
tion is more frequently obtained from foodstuffs, or barns, feed
racks, watering troughs, posts, soil, etc. Tubercular animals
are almost constantly eliminating the bacterium which contam-
inates everything that the tubercular discharges contact. The
cadavers of tuberculous animals are usually deposited in the soil,
and, in many instances, the proper precautions are not taken to
destroy the infecting micro-organism. Infected manure is
spread upon the soil and thus it becomes infected. The various
crops, including hay, grown upon a tubercular infected soil, may
be contaminated with the Bacterium tuberculosis and infect sus-
ceptible animals that consume such food. Sometimes the car-
casses of animals dead of tuberculosis are thrown into rivers or
creeks, thus infecting the w^ater. The waste products of many
small slaughter houses are fed to hogs and this affords oppor-
tunity for them to become infected. Skimmed milk and whey
from creameries and cheese factories are also sources of tuber-
cular infection.
Channel or avenue of entrance of the infection. — The Bacter-
ium tuberculosis may gain entrance into the tissues of a healthy,
susceptible animal through the mucous membranes or through
abrasions of the skin, though the latter mode of infection is not
of common occurrence in domestic animals. Cutaneous infec-
tion is occasionally observed in the mammae of sows and in the
castration wounds of barrows.
From clinical and experimental evidence and autopsy lesions
observed in abattoirs, it seems evident that the digestive tract
is the principal channel of entrance of the Bacterium tubercu-
losis in hogs, cattle and fowls. It was originally erroneously
concluded that the presence of pulmonary tubercular lesions was
positive evidence that the infection had gained entrance through
the respiratory tract. Tubercular free experimental animals fed
350 VETERINARY PATHOLOGY.
foodstuff contaminated with the Bacterium tuberculosis have
frequently become affected ;vith primary pulmonary tubercular
lesions. (The possibility of inhalation of the infection was care-
fully guarded against in these experiments.) It is presumed that
the Bacterium tuberculosis is incorporated by leucocytes in the
digestive tube and that the leucocytes then pass through the
intestinal wall into the lacteals and thence to the thoracic duct
to the right heart and on to the lung, the first capillary system
encountered, where they may lodge and establish tubercular foci.
No doubt the respiratory tract is the channel of entrance in some
cases of tuberculosis, but the number of animals infected through
this channel is very small.
An occasional case of tuberculosis may be the result of infec-
tion through the genito-urinary organs. Thus the penis of a
bull may become infected by serving a cow afflicted with uterine
or vaginal tuberculosis, and this same bull by copulation may
infect other cows. Tubercular lesions are occasionally observed
in the superficial inguinal glands of steers, and this may be the
result of infection in the castration wounds.
Conjunctival infection may occur as a result of forcible dis-
charge of infection from the respiratory tube of an affected
animal.
In summarizing, the digestive, respiratory, cutaneous abra-
sions, and genito-urinary organs are the principal channels of
entrance of the Bacterium tuberculosis, the frequency being in
the order mentioned.
Lesions. — The characteristic lesion of tuberculosis is the
tubercle. A tubercle is a nonvascular nodule, composed of leu-
cocytes, endothelial, giant and connective tissue cells, with a
tendency for the central part of the nodule to undergo necrosis.
The lesion may vary in animals of different genera and in differ-
ent animals of the same genus. Thus tubercular lesions in hogs
may differ in some particular from those in cattle because of
variations in the resistance of the hog and ox. Variations of the
tubercular lesions in different individuals of the same genus occyr
because of variation of individual resistance of the infected ani-
mal and variation of the virulency of the infecting organisms
Tubercular lesions may be modified or obscured by lesions re-
sulting from secondary infections. The initial or primary lesion
may occur in any tissue or organ. Lymphoid tissue however, is
more frequently affected than any other.
The Bacterium tuberculosis and its products are the etiologic
factors in the formation of a tubercle. The bacterium having
lodged in a tissue favorable for its growth and development, be-
INFFXTIVE GRANULOMATA.
351
gins to multiply and to eliminate those products that stimulate
the surrounding connective tissue and endothelial cells to in-
crease in number, and, at the same time, exerts a positive chemo-
tactic action upon leucocytes. If the influence of the bacterial
products is exerted upon the connective tissue and endothelium,
the resulting tubercle will be composed of connective tissue cells
and endothelial cells, and if the influence of the bacterial pro-
ducts is of a chemotactic nature, the tubercle will contain leu-
cocytes.
Structurally, a young tubercle consists of a cellular focus in-
fected with varying numbers of the Bacterium tuberculosis. As
Fig. 183. — Small oellular tubercle; liver, xoOO. Showing small louml cells with tu-
bercle bacilli scattered here and there, also a few partially destroyed
hepatic cella.
352 VETERINARY PATHOLOGY.
fhe bacteria multiply the quantity of their products is increased,
and these stimulate cellular multiplication and accumulation, and
thus the tubercle grows. The formation of a tubercle constitutes
a tissue reaction, but there is no vascularization ; that is, no
new blood vessels are formed, and the existing capillaries in the
invaded tissues are finally obliterated. A tubercle is, therefore,
strictly non-vascular, although in the very beginning the afifected
zone may be hyperemic. Cells constituting a tubercle obtain
nutriment from adjacent tissues by absorption. Tubercles grow
by multiplication of the peripheral cells, the central cells becom-
ing degenerated after they have consumed all available nutrition.
The structure and appearance of a tubercle varies according to
its age, thus : a tubercle in the very early stages is a cellular mass,
a little later the central portion of the cellular mass becomes
necrotic, and at about the same time a median zone, consist-
ing of bacteria, endothelial, and, in some cases, giant cells,
becomes evident ; the outer zone is the active zone and is com-
posed of bacteria, connective tissue cells and leucocytes. As
the tubercle becomes larger the necrotic zone extends to the
median and outer zones toward the periphery. Necrosis is
usually evident in tubercles that have attained the size of a pea.
The central necrosis is primarily of the coagulation type, but
the coagulated necrotic tissue may become liquefied, always be-
comes caseous and usually calcified according to the quantity of
fluid contained. The calcification may be limited in extent, the
necrotic tissue containing small calcareous particles that cause
the necrotic tissue to have a "gritty feel," or it may be so ex-
tensive that the tubercle cannot be dissociated except by the use
of a sledge. Liquefied tubercular necrotic tissue (pus) is yellow-
ish in color in the ox, dirty white in hogs and yellowish in fowls.
It is not sticky, although it becomes quite thick and is finally
caseated.v
Tubercles may vary in size from a microscopic point to large
masses. All tubercles are small in the beginning and are usually
entirely cellular. Small cellular tubercles in which there is no
necrosis are designated miliary tubercles. Miliary tubercles ap-
pear as minute, grayish, translucent, pearl-like specks or nodules.
If all the lesions in an affected animal are miliary in character,
the disease is termed miliary tuberculosis. Miliary tuberculosis
is common in hogs.
The appearance of a tubercle changes when central necrosis
begins. The color of caseous and calcareous tubercles varies
from a dirty white to a yellow color. The tubercles may or may
not be encapsulated. The capsule of a tubercular lesion is rela-
INFECTIVE GRANULOMATA.
353
tively thin, though it is tough. Secondary tubercles may develop
from a primary tubercle, and daughter tubercles may develop
from a secondary tubercle, thus are produced the irregular nodu-
lar tubercular masses. The tissues contiguous to a tubercle are
ischemic, probably because of the enfringement of the affected
areas with lymphoid cells. '
Little diflference is noted in tubercular lesions in the various
C--
^^e*«^''©®^
pig. 184 — A Lesion of Tuberculosis from tlie Post-pliaryngeal I>ynipli Gland of an
Ox. A — giant-cells; b — caseous center within the tubercle; c — fibrous capsule.
tissues except possibly osseous tissue and serous membranes.
Tubercular lesions of osseous tissue are usually associated with
extensive suppuration of the osseous structures, while tubercular
lesions of serous membranes are frequently entirely cellular in
structure and do not undergo central necrosis.
Boiinc tiiberatlar lesions are usually encapsulated and become
quite extensively calcified. The age of the lesions is sometimes
important in medico-legal cases. Calcification usually^ begino
154
VETERINARY PATHOLOGY.
when the tubercle is from six to eight months of age and is ex-
tensive by the time the lesion is one year old. Tubercular masses
are occasionally observed in the lung, bronchial or mediastinal
glands, and in the liver. These masses may contain all stages of
tubercular formation or the entire mass may all be in the same
stage of development, as liquefying necrosis, caseation or calcifi-
cation. Tuberculosis of serous membranes of bovines should
receive special mention because of the characteristic appearance
of the lesions. Bovine serous membrane lesions vary in size from
a millet seed to a walnut, but are usually about the size of a pea.
These lesions are frequently thickly studded over large areas of
a serous membrane. The nodules are surrounded by a firm cap-
sule which causes them to appear as pearl-like bodies, and lience
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Fig. 185. — Photograph of a tuberi-nlar nianiniary Kland. Ox.
the name, "pearly disease.' Sometimes serous membrane tuber-
cular lesions are very extensive ; this type m^ay be called "mass
tuberculosis."
Porcine Tubercular lesions are characterized by enlargement of
lymphatic glands, the formation of tubercles of variable sizes in
or upon serous membranes and within the substance of glandular
organs, bones and other connective tissues. The tubercles pro-
duce increased density of invaded soft tissues and are, therefore-,
easily detected except in very recent infection. The tubercular
nodules in the eiarly stages present about the same color as tlie
surface of the tissue invaded. In sectioning the tubercle the cen-
tral portion is caseous and slightly yellow or fibrous and white.
INFECTIVE GRANULOMATA. 355
Sometimes there is a combination of both conditions and occa-
sionally the tubercles contain calcareous granules. The central
portion of porcine tubercles rarely contains liquefied necrotic
tissue.) J
]\licroscopically porcine tubercular lesions are always cellular
in the beginning. The cellular tubercles are fairly constant in
structure regardless of the tissue in which they occur. The
center is at first represented by a mass of lymphoid cells, the
other cellular elements occurring as the tubercle develops.
Necrosis, or fibrosis, succeeds the cellular stage in the por-
cine tubercular lesion. Necrosis of tubercles is probably the
result of the activity of very virulent bacteria or the low resis-
tance, of the infected animal. The necrotic center may be sur-
rounded by a cellular zone (lymphoid and endothelial cells), or
it may be surrounded by fibroblasts. The necrotic material is
invariably caseated and later becomes calcified.
Fibrous lesions vary from the formation of small quantities
of fibrous tissue to dense fibrous centers. Fibrous lesions are
probably produced by bacteria of low virulence, or occur in ani-
mals having a marked resistance. The central portion of the
fibrous lesion may become calcified.
The so-called arbor vitae gland is a fibrous center in which
the fibrous tissue is arranged similar to the trunk and branches
of a tree, hence the name. This lesion is observed in the hog
in the cervical lymph nodes. The bacterium tuberculosis has
been demonstrated in about 30 per cent of arbor vitae glands.
The lesions of porcine tuberculosis are in brief either cellu-
lar, necrotic and calcified tubercles, or cellular, fibrous and calci-
fied tubercles. The lesion is always non-vascular as in other
animals. '
Avian tubercular lesions are very similar to mammalian tubercles,
and may occur in practically any tissue. Microscopically, avian
tubercules are found to contain giant cells, endothelioid cells,
small round cells and connective tissue cells, the arrangement of
whTch is the same as described in mammalian tubercles. Avian
tubercular lesions have been found in the liver, spleen, intestine,
mesentery, kidney, lung, skin, and bones, the frequency being
in the order mentioned.
Avian tubercles in glandular tissue, i. e., in the liver, kidney,
spleen, etc., begin as small, dirty, white cellular foci. They usu-
ally occur singly, though they may occasionally become conflu-
ent, thus producing nodules a quarter of an inch in diameter.
As the tubercles in glandular tissue undergo necrosis, they as-
sume a yellowish color. Intestinal tubercles are about the same
356 VETERINARY PATHOLOGY.
size as those in glandular tissue. The intestinal lesions are usu-
ally quite hard and dense and present a glistening appearance.
Necrosis frequently destroys the intestinal wall and thus a tuber-
cular intestinal ulcer is produced. Mesenteric tubercles are fre-
quently pedunculated and they invariably present a pearl like
appearance.
Extension. — Tuberculosis, except in some cases of the acute
form, is essentially a localized disease. However, the disease,
even in the chronic form, has a tendency to extend and involve
new tissue. The extension may be accomplished by means of,
first, the lymphatic system, second, the digestive, respiratory
and genito-urinary tubes, third, the blood vascular system and
fourth, by continuity and contiguity.
Tuberculosis is usuall)- extended by the Ivmphatic circulation.
Thus the first group of lymph nodes through which the lymph
passes from a tubercular lesion is almost invariably involved. In
fact this is a characteristic of the disease. The large per cent of
lymphatic lesions is also evidence of extension bv means of the
lymph. It has been previously stated that hogs are invariably
infected by ingestion of tubercular material and in 93 per cent of
tubercular hogs the submaxillary lymph nodes are afifected, which
is further evidence of lymphatic extension. The fact that infec-
tion may extend along the digestive, respiratory or genito-urin-
ary tracts, has been demonstrated. Thus the discharges, con-
taining the Bacterium tuberculosis from a pharyngeal tubercle
may pass through the oesophagus and stomach and find a nidus
favorable for its development in the intestine. In a like manner
the lung tissue may become afifected bv extension from laryngeal,
tracheal or bronchial tuberculosis and prostatic tuberculosis may
result from extension of renal tubercular lesions. In extensive
or generalized tuberculosis the tubercles not infrequently in-
volve and produce necrosis of the blood vessel walls and the
virulently contaminated necrotic material being discharged into
the blood resulting in tubercular metastasis. Thus tuberculosis
is extended by means of the blood. Extension by the blood in-
variably results in generalized tuberculosis which is usually
acute.
In the discussion of tubercular lesions, the formation of sec-
ondary and daughter tubercles was mentioned. The production
of secondary and daughter tubercles is a means of extension.
If the newly formed tubercles are in the same kind of tissue as
the primary tubercle then the extension is by continuity. If the
secondary or daughter tubercles are in tissues dissimilar to that
INFECTIVE GRANULOMATA. 357
in which the primary tubercle occurs the extension is by con-
tiguity.
In the majority of the cases of lymphatic extension and in
some of the cases of blood extension the Bacterium tuberculosis
is incorporated in and transported by leucocytes. The leucocytes
usually have sufficient vitality to destroy the incorporated bac-
teria but occasionally the leucocytes may be destroyed after
having transported the bacteria a considerable distance. Thus a
Bacterium tuberculosis from a pulmonary tubercle may be incor-
porated by a leucocyte and carried to the kidney and the leuco-
cyte being destroyed the liberated bacterium may establish a tub-
ercular focus in the renal tissue. The occurrence of Bacterium tub-
erculosis in the milk of cows having no mammary tubercular
lesions as well as the fact that ingestion of tubercular material
frequently causes pulmonary tuberculosis, may be due to leuco-
cytic incorporation and transportation of the infecting micro-
organism.
Elimination. — From the sanitary point of view it is always of
considerable importance to know the channels or avenues
through which infectious agents are discharged in order that they
may be destroyed. Tuberculosis afifects all tissues and the Bac-
terium tuberculosis may not be eliminated from the affected ani-
mal or it may be discharged in one or more of the secretins or
excretions. It has been determined by the Department of Agri-
culture that about 40 per cent of tubercular cattle elim'inate the
Bacterium tuberculosis in their feces. The same investigators
also found, in a lim.ited number of dairies, that about 25 per
cent of tubercular cows, regardless of location of the lesions,
eliminated the Bacterium tuberculosis in their milk. These are
facts of prime importance in adopting means for checking the
progress or for suppression of the disease. The discharges from
the respiratory tract of tubercular animals frequently contain the
Bacterium tuberculosis, especially if they have pulmonary lesions
of the disease. The urine and discharges from the female genital
organs may be contaminated w^ith the infection. Renal tuber-
culosis, hovs^ever, is not of frequent occurrence and it is not
probable that the Bacterium tuberculosis is eliminated in the
urine of tubercular animals in which there are no renal lesions.
In general the channel of elimination of the bacterium tuber-
culosis depends largely upon the location of the lesion.
Tuberculin and Tuberculin Test. — Tuberculin is a bio-chemic
material containing the products and the disintegrated bodies
of the Bacterium tuberculosis. It is prepared bv growing the
Bacterium tuberculosis in glycerine bouillon for a certain lengtll
358 VETERINARY PATHOLOGY.
of time. The glycerine bouillon culture is filtered and the fil-
trate sterilized by heat and concentrated to the desired strength
by evaporation over a water-bath. The active principle of tuber-
culin is probably a nucleo-proteid or its chemic derivatives.
Tuberculin is a very reliable diagnostic agent. Its chief use
in veterinary medicine has been in the diagnosis of tuberculosis
in cattle. It is practically as reliable in the detection of human,
porcine and probably avian tuberculosis as in the detection of
bovine tuberculosis. A tuberculin reaction consists of a local, focal
and general or systematic reaction. The local reaction is manifested
at the point of injection of the tuberculin and is the reaction
evidenced in intradermal and ophthalmic tuberculin testing. The
focal reaction consists of a hyperaemia and increased tissue action
around the tubercular centers and is probably responsible for the
systematic disturbances evidenced in the ordinary thermal or sub-
cutaneous tuberculin test. The principal method of application has
been by subcutaneous injections and noting the temperature
changes in the suspected animal. The normal temperature of the
animal is ascertained previous to the injection and the tempera-
ture is taken every two hours, beginning eight hours after tuber-
culination. On the day succeeding the injection a rise of from two
to three degrees Fahrenheit is considered a reaction and this sig-
nifies that the patient is tuberculous. This reaction is probably
due to the specific irritating action of the injected tuberculin
upon the tubercular foci producing intense hyperemia around
and disintegration of the tubercle. Thus there is a sudden dis-
charge of tubercular products into the system and the intense re-
action, thermic and constitutional follows.
A purified tuberculin used directly in the conjunctival sac
is now on the market. The ophthalmic reaction consists of the
production of a marked hyperemia of the conjunctiva in from six
to ten hours after tuberculination. The intradermal tuberculin test
is the official test in the state of Missouri.
ACTINOMYCOSIS.
Actinomycosis is a specific, inflammatory granuloma, caused by
the Cladothrix actinomyces and characterized by the formation of
tumorous masses of fibrous tissue in which there usually develops
suppurating centers and fistulous tracts.
Distribution and extent. — Actinomycosis is prevalent in Eu-
rope, Australia, Africa. North and South America. The extent
of the disease varies in different countries. According to the 24th
Annual Report of the Bureau of Animal Industrv there were
slaughtered in establishments having federal inspection 7,621,717
cattle, of which 22,7^2 were found to be affected with actinomy-
cosis, or one in about each 340. The actual per cent is even
INFECTIVE GRANULOMATA.
359
larger, for many animals afflicted with actinomycosis are slaugh-
tered where there is no official inspection maintained.
Susceptible Animals. — Cattle are more frequently affected
with this disease than other animals, though actinomycosis of
sheep, goats and hogs is occasionally reported. A few cases
have also been observed in the horse, mule, dog and wild ani-
mals.
Etiology. — A fungus, the Cladothrix actinomyces or actino-
myces bovis, is the specific cause of actinomycosis. The life his-
tory of this organism is not known, but it is thought that it
passes a part of its life cycle upon some of the grasses. Each
matured fungus is composed of a central body 10 to 40 microns
in diameter, from which the radiating filaments (mycelia) extend
outward for a distance of from 5 to 20 microns, then becoming
enlarged, terminate in club-shaped bodies from 10 to 50 microns
in length. Thus the matured fungus has the appearance of a
rosette and is commonly called the "ray fungus." Detached clubs
are capable of reproducing the entire rosettes as described. The
fungus can be cultivated in artificial media where it develops
a tangled mass of mycelia.
Source. — The Cladothrix actinomyces is probably most fre-
* €
®^^ # ©^^
_iiiSMij^hL(!^
Fig. 186. — Drawing of Actinomyces (Ray fungu.s) in section of tongue,
360 VETERINARY PATHOLOGY.
quently obtained from vegetation, especially wild rye (Hor-
dium murinum) consumed by the animal. Infection occurs most
frequently in animals fed on dry feed as fodder, stover, straw or
hay. During January and February, 1908 .86% or 376 cattle of
41,405 slaughtered had actinomycosis of the tongue or submax-
illary lymph nodes, and of 12,484 cattle slaughtered in July, 1908,
44 or .34% were affected with actinomycosis. Some rather exten-
sive outbreaks have been investigated in which it seems highly
probable that infection has been direct from one animal to an-
other, or indirect by means of the discharge of actinomycotic ani-
mals that had been smeared on rubbing posts, feed racks and feed
troughs. (Of 98 head of cattle, three of which were actinomycotic
when placed in the feed lot in November, 42 head were affected
with actinomycosis when inspected 2^/ months later.)
Channel of Entrance. — The causative fungus may gain en-
trance into the system by way of the digestive tract, the respira-
tory tract or through the skin. Abraded surfaces appear to be
essential for infection, though it has not been proven that the
fungus cannot penetrate uninjured surfaces. The digestive tract
is the most frequent channel of entrance in cattle. The tongue,
especially the dorsal surface at the junction of the base and apex,
is subject to injury by the rough, harsh food consumed by cattle.
Tongue injuries may also be inflicted by licking boards, posts,
etc., containing nails and splinters. Awns of wheat, barley and
rye, chaff, splinters and hair accumulate in the erosions or wounds
of the tongue, producing the so-called "hair sores." More than
12% of 48,000 cattle slaughtered during the winter months in one
of the Kansas City packing houses had "hair sores" upon their
tongues. The "hair sore" is intimately associated with lingual
actinomycosis ; indeed it is rare to find actinomycosis of the
tongue or submaxillary lymph glands when there is no "hair
sore." Diseased teeth, especiallv if the gingival mucous mem-
brane is involved, also provide an entry for the ray fungus. The
possibility of the infection passing through the intestinal or
gastric wall explains the cases of peritoneal actinomycosis that
are occasionally observed
Respiratory infection is not of common occurrence. This type
of infection probably occurs by inhalation of chaff or awns con-
taminated with the Cladothrix actinomyces.
The skin is probably the most frequent channel of entrance
in hogs. Actinomycotic scirrhus cords are quite common, the in-
fection taking place in the castration w^ound. Mammary acti-
nomycosis is sometimes observed in sows, especially those run-
nmg in stubble fields, the infection taking place through abra-
INFECTIVE GRANULOMATA, 36l
sions produced by the stubble. Abrasions resulting from rub-
bing on stanchions and feed boxes may be a source of infection in
dairy cattle.
Lesions. — Macroscopic. — Actinomycotic lesions may be sur-
face or subsurface. The fungus may invade and produce the
lesion in a^ny tissue.
Surface} lesions begin as small inflammatory centers which
usually thicken and become elevated above the general surface.
The lesion gradually increases in size, and in some cases assumes
a fungoid appearance. At this stage the lesions vary in size from
a small pea to a walnut. The surface tissue may become eroded
as a result of the extension of necrosis from the lesion and the
typical actinomycotic pus discharged or more frequently the
lesion becomes encapsulated by the formation of a dense fibrous
capsule. The capsule usually limits the development of the lesion
and it may be diminished in size by the contraction of the fibrous
tissue constituting the capsule.
Subsurface lesions, though beginning as inflammatorv centers,
are invariably Circumscribed by. a dense, fibrous wall. As
the disease progresses the center of the lesion undergoes lique-
fying necrosis. The necrosis extends, producing irregular, tor-
tuous sinuses that may extend through the capsule and into the
surrounding normal tissue. Ultimately the liquified necrotic
tissue (pus) would ordinarily be discharged upon a surface, or
the fungus contained in the necrotic tissue (pus) would perfor-
ate the primary capsule and cause the production of a. secondary
fibrous capsule. Thus the lesion is frequently composed of sev-
eral communicating cavities (multilocular) containing actinomy-
cotic pus. If such a lesion is incised and pressure applied the
typical beads of actinomycotic pus will appear in various
places upon the cut surface. Actinomycotic pus is creamy,
sticky, tenacious, yellowish-white and contains small, vellow,
gritty granules. The pus has a greasy feel and may have a
slight odor. If the pus is permanently maintained within the
capsule, its fluid content is absorbed and becomes cas$ous.
Osseous actinomycosis is of common occurrence. The fungus
having gained entrance produces inflammation, which is suc-
ceeded by disintegration of the osseous tissue and the formation
of cavities or pockets. By growth and extension of the infect-
ing fungus, inflammation and disintegration is favored, and thus
tommunicating cavities are formed in the afifected bone. As the
process of rarefaction continues within there is new osseous tis-
sue deposited without. Thus bone affected with actinomycosis
362
VETERINARY PATHOLOGY.
becomes enlarged and cancellous and has a honeycombed ap-
pearance.
Microscopic. — The presence of the Cladothrix actinomyces in
a tissue produces an irritation resultino- in an accumulation oi
INFECTIVE GRANULOMATA.
363
small round cells, the production of endotheloid and giant cells by
the invaded tissue, and finally the development of a fibrous cap-
sule around the entire mass. The fungus may appear in the be-
ginning as mycelial elements, but later it has the typical rayed
appearance. In old lesions the central portion or body of the
fungus becomes calcified.
Surrounding the clubs or mycelium in the early stages are
varying numbers of small, round cells (lymphocytes).
As the disease progresses, the matured fungus is more or
less surrounded by giant cells that actually contact the fungus.
The actinomycotic giant cell is very irregular in shape and size
and has varying numbers of nuclei scattered indiscriminately
throughout the cell body.
Endotheloid cells appear marginally to the giant cells. These
cells are similar in appearance to the endotheloid cell of tuber-
culosis, having a relatively large cell body and a small, single
nucleus.
The small, round cells are first noticed immediately around
the fungus, but later they infiltrate the surrounding tissue also,
and are in excess of all other cells in the lesion.
Fibroblasts appear in the margin of the early lesion, and
through their activity a thick fibrous capsule is produced.
Actinomycotic pus is found to be composed of tissue shreds
and fragments, lymphoid cells and some polymorphonuclear
leucocytes, an occasional endotheloid cell and the Cladothrix
actinomyces.
Extension. — The extension of actinomycosis has usually been
described as taking place only by growth in continuity or contig-
uity, or by passing along the respiratory, digestive or genito-
urinar}' tubes. By a careful observation of over 72,000 cattle
slaughtered, it has been found that many cases, in which there
were "hair sores" but no actinomycotic tongue lesions, showed
actinomycosis of the submaxillary lymph nodes. The majority
of cases of lingual actinomycosis are accompanied by involve-
ment of the submaxillary lymph nodes. That practically all
cases of actinomycosis of the submaxillary lymph nodes occurred
in animals having "hair sores" is indicative of lymphatic exten-
sion. It is therefore quite probable that actinomycosis may be
extended in the animal body by means of the lymph.
Differential Diagnosis. — Bovine actinomycosis may be con-
founded with tuberculosis, nodular disease, abscess formation
and various tumors.
Tubercular lesions calcify, actinomycotic lesions rarely be-
come cakified. Tubercular pus is usually quite different from
364 VETERINARY PATHOLOGY.
actinomycotic pus. The former is not sticky or tenacious, and
does not contain the small, yellow, gritty granules found
in the latter. The capsule of an actinomycotic growth is
thicker and denser than the capsule of a tubercular growth. The
two diseases can be differentiated positively by microscopic ex-
amination of the pus and the lesion. The Bacterium of tuber-
culosis would be found in tubercular pus and the Cladothrix
actinomyces in the actinomycotic pus. Tubercular lesions are
characterized by the presence of the horse shoe giant cell, the
actinomycotic giant cell is irregular in outline and size, is poly-
nuclear, the nuclei being scattered indiscriminately through the
the cell body.
Nodular disease, though not very prevalent in cattle may be
mistaken for actinomycosis. The nodules of nodular disease
are in the intestinal wall. The pus in the nodule is greenish yel-
low in color, and though fluid in the early stages, it later be-
comes caseous but never contains the calcareous granules.
Microscopically the finding of the Cladothrix actinomyces in
actinomycotic lesions or pus and the absence of this fungus in
the lesions of nodular disease is sufficient for differentiation.
From abscesses the differentiation may be made by the pecul-
iarity of the pus, and the capsule, which is usually much more
dense in actinomycotic lesions than in abscesses.
Osteosarcomata may produce lesions in bone similar to actin-
omycotic lesions. A microscopic examination is always suffi-
cient for dift'erentiation of these diseases.
Ovine actinomycosis may be confounded with ovine caseous
lymphadenitis and nodular disease. Ovine caseous lymphaden-
itis is essentially a disease of lymphoid tissue characterized by
the formation of greenish yellow pus that later caseates in con-
centric layers, but never contains gritty granules. The color of
the pus and the arrangement of the caseated necrotic tissue is
usually sufficient for differentiation of ovine caseous lymphaden-
itis from actinomycosis.
The remarks on the differentiation of nodular disease in
bovines is equally applicable to ovines.
GLANDERS.
Glanders is a specific, infective disease, especially affecting
equines, caused by the bacterium mallei.
Glanders is prevalent in all countries with the possible ex-
ception of Iceland, Australia, and some isolated islands. The
disease is found in practically all parts of the United States. It is
INFECTIVE GRANULOMATA.
365
more prevalent in those portions of a country in which there is
extensive horse traffic. The invasion of a province or a country
by an army is usually succeeded by the appearance of glanders.
Etiology. — Glanders is caused by the Bacterium mallei. This
organism was described by several dififerent investigators in
1882. It is similar in appearance to the Bacterium tuberculosis,
has rounded ends, is from 2 to 3.5 microns in length and .3 to
.5 microns in width. This bacterium occurs singly except that
w^hen grown upon potato medium, pairs or even long filaments
are not rare. Like, the Bacterium tuberculosis, it produces ple-
omorphic forms when cultivated in different media or under
varying conditions. In old cultures it frequently becomes
short and is sometime coccoid in appearance. Branching forms
are not uncommon. It does not form spores.
The Bacterium mallei is stained by aqueous solutions of ana-
Fig. 188.— Bacterium Mallei, xlOOO.
line dyes that are slightly alkaline in reaction, such as Loef-
fler's methylene blue. It is so-called "Gram negative," i. e.,
it is decolorized by Gram's solution.
Source of Infection. — Infection probably occurs most fre-
fluently in an indirect manner, i. e., the infection is obtained
from some surrounding object or thing that has been contamin-
ated with the infected discharges of a glandered animal.
The Bacterium mallei is strictly parasitic and the source of
the micro-organism is either the discharges from an infected
animal or the carcasses of animals that have died of
glanders. Fortunately this bacterium possesses little re-
366 VETERINARY PATHOLOGY.
sistance to light, dessication and other external influ-
ences and consequently the infection in discharges is as a rule,
promptly destroyed. The length of time that the Bacterium
mallei may exist outside of the animal body and retain its viru-
lency has never been absolutely determined. Authentic cases
of glanders have appeared in horses that had been pkced in
stalls that had been vacant for one year, but prior to that time
occupied by glanderous horses. A few reports are indicative of
the fact that ihe Bacterium mallei may retain its virulence in
infected buildings for two or even three years, but these re-
ports need further substantiation. It seems probable from clin-
ical and experimental evidence that, except in the animal body,
the virulence of Bacterium mallei is rarel^^ retained longer than
one year.
In cities, public drinking fountains, hitching posts and feeding
troughs are probably the greatest sources of infection. The
purchase of second hand harness, wagons, and other equipment
should be regulated by ordinances or laws to prevent the
spread of such infections as glanders.
The Channels of Entrance of the Infection. — All exposed
surfaces and natural openings of the body may permit the Bac-
terium mallei to gain entrance to the tissues. In glanders, as
in tuberculosis it has been quite conclusively demonstrated
experimentally that the majority of the cases of glanders results
from the ingestion of the Bacterium mallei. No doubt infection
may occur by inhalation of the infectious agent, the discharges con-
taining the Bacterium mallei becoming pulverized and carried by
air currents, and an occasional case may be the results of cutaneous
inoculation. Farcy may or may not result from cutaneous infec-
tion. Such inoculations are easily accomplished by bridles,
harness, saddles, curry combs, etc. More rarely the conjunc-
tival membrane may be the channel of entrance. For example
a horse, afifected with nasal glanders may sneeze or cough and
thus infection be forcibly introduced onto the mucous mem-
brane of the eye of another horse.
Lesions. — Macroscopic. — The lesions of glanders are found
especially in the mucous membrane of the anterior respiratory
passages, lymph nodes, lung and skin, the frequency being in
the order mentioned. It is probable that the Bacterium mallei
primarily affects lymphoid tissue. The gross lesions may be
diffuse or circumscribed, depending upon the virulency of the
infecting organisms and the resistance of the afifected animal.
Diffuse glander lesions are usuallv found in animals having*
INFECTIVE GRANULOMATA. Z67
little resistance and in which the disease assumes an acute
form. In the nasal mucous membrane, diffuse, glanderous les-
ions appear as severe inflammation in which the submucosa is
extensively infiltrated. The engorgement of the tissue may be
sufficient to obstruct circulation and result in necrosis of the
mucous membrane thus producing ulcers variable in size and ir-
regular in contour. The submaxillary lymph nodes are invari-
ably hard and enlarged and may or may not be adherent to the
maxilla.
Pulmonary, diffuse glander lesions vary in size from a hazel
nut to a basket ball and are irregular in shape. These lesions
are grayish or dirty white in color. The lesions may undergo
a central necrosis or they may become fibrous in nature. The
necrotic material may be of a semi-solid or caseous consis-
tency and in the smaller foci there may be calcification. In
practically all cases of pulmonary glanders the bronchial and
mediastinal lymph nodes are enlarged and contain cellular necro-
tic or fibrous centers.
Diffuse cutaneous lesions are not of common occurrence.
They may be present in acute general glanders, the manifesta-
tion in the skin being of the nature of a diffuse gangrenous der-
matitis. Cutaneous nodular lesions may become diffuse as a
result of rapid and extensive necrosis. Diffuse lesions occur
in lymphoid tissue. Splenic lesions are usually nodular though
a few cases have been reported in which there were diffuse
lesions of the spleen. Osseous lesions are usually diffuse land
appear as a suppt rativc osteitis.
Circumscribed or nodular lesions are common in animals that
have a marked resistance or in those cases infected with mildly viru-
lent bacteria. In chronic glanders the lesions are usually nodular.
The appe^irance of nodular lesions in the nasal, pharj'-ngeal
and tracheal mucous membranes as well as in the mucous lin-
ing of the facial sinus varies according to the age of the lesion.
In the beginning the lymphoid tissue of the mucosa or submu-
cosa becomes swollen and the tumefaction is surrounded by a
hyperemic zone. As the disease progresses there is necrosis
which not only involves the lesion but also the surface tissue.
thus producing an ulcer. The size depth and contour of the
ulcer necessarily depend upon the extent of the necrosis. In
some instances the nasal septum and facial bones mav be per-
forated. The ulcers vary in size from mere points to areas a?
large as a silver dollar. The large ulcers are usually the result
of two or more necrotic centers becoming confluent. The de-
nuded surface is usually limited or surrounded by a 'raised
368
VETERINARY PATHOLOGY.
border, the latter being the result of cellular infiltration. The
tissue adjacent to the denuded surface may finally produce
sufficient new tissue or granulation tissue to repair the injury.
If the necrosis involves only the superficial epithelium the re-
pair will be complete and there will be no scar, but if the
necrosis has involved the mucosa and portions of the submucosa.
Fig-. 189. — Nasal septa, showing glanderous ulcers.
A A nasal septum from glandered horse.
1. A crateriform ulcer having a thick raised border with a depressed granulating
center.
2. Shows characteristic outline of an ulcer, also fusion of two or more
primary ulcers.
3. Thumb tacks.
B. A nasal septum from a second glandered horse.
1. Typical crateriform ulcers and large necrotic area the result of fusion ot several
ulcers.
2. Cicatrices shown as irregular white spots.
8. Thumb tacks.
INFECTIVE GRANULOMATA.
369
there will be large quantities of cicatricial tissue produced and
consequently a scar. In nodular glanders of the anterior air
passages, the submaxillary lymph nodes are invariably enlarged
and contain fibrous, caseous or calcified necrotic foci.
Pulmonary nodular lesions are usually dirty white in cok-r
and vary in size from pin point centers to masses as large as a
man's head. These nodules in the beginning are entirely cellu-
lar and are surrounded by an hyperemic zone. As they become
larger the central portion usually becomes necrotic and the
hyperemic zone becomes infiltrated with fibroblasts that pro-
duce a fibrous capsule. The small nodular lesions may be small
and thickly distributed throughout the entire lung. The large
Fig. 190. —Cutaneous Glanders — Farcy.
1. A U'.rge erosion or ulcer (farcy bud) on the internal surface of fetlock.
i: 5 and 4. Other ulcers appearing- along the course of the lymphatics,
370
VETERINARY PATHOLOGY,
lesions are usually few in number and they may be formed by
two or more nodules becoming- confluent. The central caseous
necrotic tissue in the small foci frequently becomes calcified.
Calcification is usually not evident in the large pulmonary les-
ions. The bronchial and mediastinal glands are invariably in-
volved and they may be caseous, calcified or indurated.
Nodular lesions of the skin are found in the superficial por-
tion of the dermis or in the subcutaneous tissue. The nodules
in the skin rarely become larger than a pea but those of the
subcutaneous tissue may become as large as a hen's egg. The
central portion of the cutaneous and subcutaneous nodules and
Fig. 191. — Micros<*opio Section through a glandtrous ulcer.
1. Margin of ulcer-necrotic tissue.
2. Normal nasal mucous membrane.
2. Showing depth of erosion.
4. Small round cells.
5. Epitheloid cells.
6. Fibrous tissue.
the superficial tissue covering them become necrotic and a
sticky, tenacious, semi-fluid luaterial is discharged on1o the
surface. The related lymphatic vessels are all engorged anc?
the lymph nodes are enlarged and later become indurated.
The tissue destroyed in the lesions of cutaneous glanders
may be partially regenerated, but are more frequently repaired
by the substitution of fibrous tissue thus pi-oducing a thickened
fibrous skin.
Small nodular lesions have been noted in the spleen, liver
and kidney. The splenic lesions may be caseous or calcified.
Hepatic lesion'; are usually caseous. The portal lymph nodes
gire usuallv involved when lesions are present in the liver and
INFECTIVE GRANULOMATA. 371
the lymph nodes along the hilus of the spleen are invaded in splenic
lesions.
Microscopic. — The bacterium Mallei multiply in the invaded
tissues and their metaholic products produce a progressive cell
necrosis indicated first by karyolysis and later by a complete dis-
integration of cells. Smaller lesions are the result of a diffuse
proliferation of lymphoid and endotheloid cells and migration of
polymorph leucocytes. The proliferated cells may accumulate in
groups, thus producing nodules. In the beginning there is usu-
ally a well marked hyperemic zone around the cellular center
The cells constituting the central portion of the lesion later un-
dergo necrosis and about the same time the hyperemic zone
becomes less evident. A fibrous capsule may or may not en-
close the lesion, depending upon whether it is diffuse or nodular.
In the nodular form of the disease there is a proliferation of
fibroblasts in the tissue that was previously hyperemic. The
fibroblasts produce the capsule that characterizes nodular gland-
ers. In the older subsurface centers there is formed caseous
material and in the small centers calcareous particles. In sur-
face lesions, necrosis or fibrosis is evident.
Diagnosis. — Mallcin is a filtrate obtained from a glycerinated
bouillon culture of the Bacterium mallei. Mallein is of diagnostic
value only. Reaction to mallein consists of a local, focal and
systematic disturbance. The cause of the reaction of glandered
horses to mallein is due to increased tissue action. The reaction
noted in glanders after the subcutaneous injection of mallein con-
sists in a thermic disturbance, a swelling at the point of inocu-
lation, stiffness in gait, general depression and there is usually
frequent urination. The temperature variations in glanders range
from 2° F. to 5° F. The maximum rise of temperature usually
occurs in from ten to twelve hours after malleination, though it
may not appear until the eighteenth hour after injection of the
mallein. The high temperature evidenced in a mallein reaction
is maintained for a period of from 24: to 60 hours. The swelling
is usually quite large and is very sensitive. The lymphatic ves-
sels that are related to the swollen area become engorged and
present a knotted appearancee. The swelling characterizing a
mallein reaction persists for several days. Stiffness of gait may
be due largely to the disturbance induced bv the swelling at
the point of injection, but at least in some cases it is evident that
the stift'ness of gait is not proportional to the size of the sw^ell-
ing. Aside from stiffness the reacting animal has a dejected
appearance. The cause of frequent urination is not known.
372 VETERINARY PATHOLOGY.
The ophthalmic mallein test is now the recognized test by the
United States government. The test is made by applying specially
prepared mallein into the conjunctival sac. The reaction consists
of an intense hyperaemia within 16-18 hours after the application
of the mallein.
'Agglutination. — The bacterium mallei produces an agglutinogen
which causes the animal body to produce an agglutinin. A spe-
cific agglutinin is found in small quantities in the blood serum
of normal horses and in larger quantities in horses with gland-
ers. The agglutination test for glanders depends upon the
same principle, as that upon which the typhoid agglutination
depends. The agglutinin appears to cause the bacterial cell
membrane to become sticky and thus the bacteria acted upon
adhere to each other when they are brought into contact and
clumps or clumping of the bacteria results ; this constitutes
the agglutination reaction. Blood serum is obtained from the
suspected animal and placed in a normal salt solution in which
are suspended dead Bacteria mallei. A series of four tubes is
usually used in order that different dilutions may be made. In
the 1st tube the dilution is made 1 to 200, i. e. one part of serum
is taken to 200 parts of salt solution in which the Bacterium
mallei is suspended. In the 2nd tube, the dilution is made 1 to
500, the 3rd tube 1 to 800 and in the 4th tube, 1 to 1200. These
tubes are placed in an incubator. The reaction consists in a
deposit of clumped or agglutinated Bacteria mallei in the bot-
tom of the tube. Normal horse serum usually contains suffi-
cient agglutinin to produce a reaction in tube number one, that
is in a dilution of 1 to 200. A deposition in tube number two is
considered suspicious and deposits in tubes three and four is
positive evidence of glanders. The reaction time is from 24
to 60 hours.
The agglutination test is an accurate means of diagnosis if
the test fluid is properly prepared and has been properly pre-
served and if the operator uses care in making the test. The
time required is much less than the time necessary in making
the mallein test. Another advantage is that the blood serum of
an animal dead of suspected glanders can be as readily tested as
the serum from a living animal — hence it is useful in medico-
legal cases.
The complement fixation test has been used in the identification
of glandered horses. This test is very reliable if properly con-
ducted. It is a technical laboratory test in which many variable
factors enter in and amateurs are likely to encounter more or less
difficulty should they attempt this test.
INFECTIVE GRANULOMATA.
373
EPITHELIOMA CONTAGIOSUM.
Epithelioma Contagiosum is a specific infective disease of
fowls and it may be transmissible to pigeons. The disease is
widespread in the United States. It is, according to Gary the
most serious drawback to the poultry industry of the south. It
is quite prevalent in Hawaii, and has been described in many
different localities in Europe.
Etiology. — The cause of contagious epithelioma is unknown.
The evidence obtainable at the present time indicates that the
eiologic factor is either a protozoon, (coccidium), or an ultra
microscopic or filterable virus.
Lesions. — Macroscopic. — The disease is initiated by a catarrhal
inflammation of the mucous membrane of the head and neck.
The disturbance may be localized in the eye, nose or mouth, or
may Involve all those parts. The inflammatory disturbance stim-
ulates or is accompanied by a proliferation of epithelial cells in
the eye, nose, mouth or even on the wattles and comb. These
epithelial new growths are at first grayish, have a smooth, glis-
tening appearance and are surrounded by a hyperaemic zone.
Later the growths, which become nodular, undergo degenera-
tion, especially upon the surface. The necrotic tissue may re-
main and form a scab or it may slough leaving a ragged, brown-
Fig. 192.
Left side of head, showing eye with extensive accumulation of caseous necrotis
material.
ish or grayish indurated surface. These nodules may become
as large as a pigeon's egg. They frequently entirely obstruct
vision and in some cases destroy the eye ; those appearing in
374
VF^.TERINARY PATHOLOGY.
the nostril may seriously interfere with respiration or even
obstruct the air passages ; and nodules in the buccal cavity may
prevent eating or the prehension of food ; while those that occur
in or upon the wattles and comb may be so extensive that
these structures are practically destroyed. These nodules may
entirely undergo necrosis, the necrotic tissue becoming dry
and scaly or necrosis may begin in the center of the
nodule and be of a liquefying character and when the entire
nodule has undergone necrosis the mass is discharged as a
thick, -vatery fluid containing flakes of coagulated necrotic tis-
sue. Again the discharge may be thick and creamv or li :i.^' ..ven
be of a caseous nature.
"^^^^ '^ TuS.
1^ "l.*^
Fig. 193.
Kight side, showing growth from eye, nasal cleft, and mouth.
INFFXTTVE GRANULOMATA,
375
Microscopic. — These nodules are found to be composed largely
of epithelial cells supported by irregular bands of connective
tissue in which there is a limited blood supply. The majority of
cells are very large. Some of these cells contain oval re-
fractile bodies that have been considered as protozoa by some.
These bodies are also observed between the cells. The epithelial
cells, especially those in the center of the nodule, usually show
more or less of a nuclear disintegration. The marginal cells in
the nodules are usually more or less flattened. The cell nests
Fig. 194.— Microscopic section of Eiiithelioma contaginsuni.
1. Surface of growth from nasal mucous menibi-ane.
2. Area of epithelial cells, cells large in center, becoming smaller and finally
blending with the connective tissue.
'. Apparently connective tissue undergoing mucoid degeneration.
4. Probably blood vessels, but the cells are smaller than normal red blood cells
of the chicken. The cells are also quite irregular in shape.
5. Degeneration of central cells. The nucleus of the cell first degenerates and
finally the cell body.
may develop from glandular or surface epithelium, which, in
the attempt to repair the eroded surface, becomes entangled in
the ragged edges of the ulcers and develop as an epithelioma.
The cell nests increase in size by a multiplication of the peri-
pheral epithelial cells. The rapidly multiplying marginal cells
consume practicallv all of the central cells and there is central
necrosis of the cell nests.
The nests are irregular in size and outline and Ihey are
grouped to form the nodules. The nodules may or may not
have bands of clear, hyaline substance that represents fibrous
tissue undergoing hyaline or mucoid degeneration.
GLOSSARY
Ablated (L.Ab, from and Ferre, to bear).
Removal of a part as by cutting off.
Abnormalities (L.Ab, from and Norma,
rule). Conditions not in accord with
the usual.
Aborted (L.Ab, from and Oriri, to arise).
Prevented from full development.
Abraded (L.Ab, from and Radere, to
rub). Having: the surface tissue
rubbed off.
Abscess (L.Ab, from and Ceder, to de-
part). A circumscribed, molecular
disintegration of sub-surface tissue.
Absorption (L.Ab, from and Sorbere, to
suck in). The process of taking up
substances into the tissues.
Accesor.v (L. Accessorius, additional).
In addition to.
Acliromatosis (Gr.A, without. Chroma,
color and osis, a condition of). A
condition of absence of color.
Acidopliile (L. A Cere, to be sour and Gr.
Phileein, to love). Readily stain-
able with acid dyes.
Acini (L.Acinus, a grape). The small-
est lobules or parts of a compound
structure.
Acromegaly (Gr. Okros, end and Megalos,
large. A condition characterized by
overgrowth of the extremities and
face.
Actinomycosis (Gr. Aktis, a ray, Mukes,
fungus and osis, a condition og). A
disease caused by the "ray fungus."
Cladothrix actinomyces.
Adenoma (Gr.Aden, gland and Oma.
tumor). An epithelial tumor re-
sembling a gland in structure.
Adipocere (L.Adeps, fat and Cera, wax).
A wax-like substance formed by
exposure of tissue of a cadaver to
moisture with air excluded.
Aerobic (Gr.Aer, air and Bios, life).
Requiring free oxygen (air) in or-
der to live and multiply.
Agglutinin (L.Agglutinare, to stick to-
gether). An adaptation product of
the body cells produced by immu-
nization with corresponding cells
which causes a clumping or coales-
cing of the kinds of cells used in
immunization.
Agglutinogen (L.Agglutinare, to stick
together). A substance present in
bacteria! immunization which gives
rise to the production of agglutin-
ins by the body cells.
Alveolar (L.Alveolus, a small lobe).
Pertaining to an alveolus, (A small
cavity for a tooth or histologic di-
vision in a lung, gland, etc.)
Amboceptor (Gr.Ambo, both and L. Ca-
pere, to take). One of the types of
receptors or intermediary bodies in
Ehrlich's lateral side-chain theory.
Amitosis (Gr.A, without and Mitos,
thread.) Direct division of cells
without formation of thread-like
structures.
Amniotic (Gr.Amnion, a foetal mem-
brane.) Pertaining to the amnion,
one of the foetal membranes.
Amoeba (Gr.Amoibe, a change.) A co-
lorless, single-celled, animal organ-
ism that constantly undergoes
changes of form.
Amylaceous (Gr.Amulon, starch.) Of
the nature of, or containing starch.
Amylin (Gx. Amnios, starch.) The in-
soluble wall of a starch grain.
Starch cellulose.
Amyloid (Gr. Amnios, starch and Eidos,
form.) Like starch.
Anabolism (Gr.Ana, up and Ballein, to
throw.) The transformation of food-
stuffs into complex tissue-elements.
Anaerobic (Gr.A, without, Aer, air and
Bios, life.) Able to live in the ab-
sence of free oxygen or air.
Anaphase (Gr.Ana, up and Phasis,
Phase.) The third stage in mitotic
cell division.
Anasarca (Gr. Ana, up and Sarx, flesh.
An accumulation of non-inflamma-
tory serum in the sub-cutaneous
areolar tissue.
Anastomosis (Gr.Ana up and Stomoein,
to bring to a mouth.) The establish-
ment of a communication between
two distinct portions of the same
organ (Usually vessels).
Anemia (Gr.A, without and Haima,
blood.) A deficiency of blood or of
any of its constituents.
Angioldast (Gr.Aggeion, a vessel and
Blastos, germ.) One of the cells of
angioblastic origin concerned in the
formation of vessels.
S76
GLOSSARY.
37^
An&ionia (Gr.Aggeion, vessel and Oma,
tumor.) A tumor composed of ves-
sels independently of pre-existing
blood or lymph vessels.
Anhydremia (Gr.A, without. Hudor, wa-
ter and Haima, blood.) A diminu-
tion of the watery constituents of
the blood.
Ankylosis (Gr.Agkulos, stiffened, and
osis, a condition of.) A union of
bones in an articulation.
Anlagen (Ger.Anlagen.) The founda-
tion or design of a structure, the
beginning.
Anomaly fGr.A, without and Homalos,
average.) A marked deviation from
the normal.
Antenatal (L.Ante, before and Natus.
born.) Existing before birth.
Anthracosis (Gr.Anthrax, black and
osis, a condition of.) A lung disease
characterized by deposition of coal
dust.
Antitoxin (Gr.Anti, against and Toxi-
kon, poison.) A substance elabo-
rated by the body-cells to counter-
act the toxins of other cells.
Aplasia (Gr.A, without and Plasis, for-
mation.) A condition of failure of
development.
Apnoea (Gr.A, without and Pheein, to
breathe.) A transient cessation of
respiration.
Argyrosis (L.Argentum, silver and osis,
a condition of.) A condition of pig-
mentation by deposition of silver.
Arteriolith (Gr.Arteria, to keep air,
trachea and Lithos, stone.) A cal-
culus or stone in an artery.
Arteriosclerosis (Gr.Arteria, trachea,
Skleros, hard and osis, a condition
of.) A chronic inflammation of ar-
teries with hardening of the walls,
especially of the intima.
Arthropoda (Gr.Arthron. a joint and
Pous, foot.) A class of animals hav-
ing jointed legs.
Ascites (Gr.Askos, a bag.) An abnor-
mal collection of non-inflammatory
fluid in the peritoneal cavity.
Assimilation (L.Ad. to and Similare, to
make like.) The process of taking up
food-stuffs by the tissues and mak-
ing them a part of themselves.
Asthenic (Gr.A, without and Sthenos,
strength.) Characterized by absence
of strength or violence.
Asymmetrical (Gr.A, without. Sun. to-
gether and Metron, measure.) Be-
ing unlike in corresponding organs
or parts of opposite sides of a body
that are normally of the same size.
Atavismal (Gr.Atavus. grandfather.) A
condition of reappearance in an in-
dividual ot a peculiarity possessed
by a more or less remote progeni-
tor.
Atelectasis (Gr.A, without, Telos, form
and Ektasis. expansion.) Imperfect
expansion or collapse of the air ves-
icles of the lung.
Atheromatous (Gr.Athere, gruel, Oma,
tumor and ous, of the nature of.)
Of the nature of an aethroma. (A
sebaceous cyst containing a grumous
material.)
Atresia (Gr.A, without and Tretos, per-
forated.) Failure of a normal open-
ing or canal to develop.
Atrophy (Gr.A, without and Trophe.
nourishment.) A condition in which
there is a decrease in size or num-
ber of the composing cells of an
organ or tissue.
Atypical (Gr.A, without and Tupos.
type.) Not conforming to type, ir-
regular.
Autosite (Gr. Autos, self and Sitos, food.)
A monster capable of independent
existence after birth.
Avidae (L.Avis, bird.) A family of ver-
tebrates.
Bactericidal (Gr.Bakterion, a little stick
and L.Coedere, to kill.) Destructive
to bacteria.
Basophile (Gr.Basis, foundation and
Pheleein, to love.) A substance that
readily combines with basic dyes.
Benign (L.Benignus, kind.) Not danger-
ous to health or life.
Bifida (L.Bis, twice and Findere, to
cleave.) Divided into two parts.
Biologic (Gr.Bios, life and Logos, stu-
dy.) Pertaining to Biology. (The
study of the structure, function and
organization of living forms.)
Buccal (L.Bucca, cheek.) Pertaining to
the cheeks.
Bursattae (L.Bursa, purse.) Small bur-
sae or vessels. A disease of the skin
characterized by necrosis.
Calcified (L.Calx, lime and Fiere, to be-
come.) A condition of deposition of
calcareous matter in tissues.
Canalization (L.Canalis, a canal.) The
process of formation of canals.
Caries (L.Caries, rotten.) The molecular
necrosis of bone, enamel, dentine,
etc., corresponding to necrosis in
soft tissue.
Carcinoma (Gr.Karkinos, crab and Oma,
tumor.) A malignant epithelial
newgrowth.
Catarrh (Gr.Katarrhein, to flow down.)
An inflammatory condition of a
mucous membrane in which there is
an excessive production of mucu.s.
Caustic (Gr.Kaiein, to burn.) A sub-
stance that destroys tissue. More
violent than corrosive.
378
GLOSSARY.
Cellulose (L.Cellula, a small cell anrl
osis, a condition of.) The principal
constituent of cell-membranes.
Cementum (L.Caementum, a rough
stone.) A plastic material capable
of becoming hard and of binding
together contiguous materials.
Centrosome (Gr.Kentron, center and
Soma, body.) A structural part of
a cell in active mitotic cell-divi-
sion.
Ceraminoiis (L.Cera, wax and osis, a
condition of.) Of the nature of cer-
umen. (The wax of the ear.)
Chalicosis (Gr.Chalix, gravel and osis,
a condition of.) A disease of the
lungs caused by the inhalation of
dust.
Chemotaxis (Gr.Chemia, chemistry and
Tassein, to arrange.) The property
of cell attraction or repulsion due
to chemlc substances.
Chlamydo (Ger.Chemus, a cloak.) A
cloak or mantle. (Used as a limit-
ing prefix.)
CholelUliiasis (Gr.Chole. bile, Lithos,
stone and osis, a condition of.) The
condition in which there are cal-
culi in the gall-bladder or ducts.
Cholesteatoma (Gr.Chole, bile, Stear,
fat and Oma, tumor.) A tumor
composed of pearl-like masses of
epithelial tissue mingled with
more or less cholesterin.
Choroid (Gr.Chorion, chorion and Eidos,
like.) The vascular tunic of the eye
continuous with iris and between
the sclerotic coat and retina.
Chromatin (Gr.Chroma, color.) The part
of the protoplasm of a cell that
takes up stains.
Chromatolysis (Gr.Chroma, color and
Luein, to loose.) The destruction of
coloring matter.
Chromosome (Gr.Chroma, color and
Soma, body.) One of the minute
bodies into which the chromatin of
the cell is resolved in indirect cell-
division (Mitosis.)
Cicatricial (L.Cicatrix, a scar.) Of or
pertaining to a cicatrix.
Cicatrix (L.Cicatrix, scar.) The con-
nective tissue that rep^aces a local
loss of tissue.
Circumscribed (L.Circum, around and
Scribere to write.) Of limited or
defined extent.
Cirrhosis (Gr.Kirrhos. reddish -yellow. 1
An overgrowth of connective tissue
In an organ usually the result of
chronic inflammation.
Cirsoid (Gr.Kirsos, a varix and Eidos.
form.) Resembling a varix. (A di-
lated and tortuous vessel.
Clonic (Gr.Klonos, commotion.) Char-
acterized by spasmodic and convuls-
ive muscular contractions alternat-
ing with relaxations.
Clot (A.S.Clate, a burr.) A special soli-
dification of the blood outside of a
vessel.
Coag-ulated (L.Coagulare, to curdle.) A
condition in which there is a coag-
ulum.
Coagulum (Coagulare, to curdle.) A
solidification of the blood occurring
in a dead vessel.
Coagulation (L.Coagulare. to curdle.)
The process of forming a coagu-
lum.
Coalesce (L.Coalescere, to grow to-
gether. ) The union of two or more
parts of things.
Coccidiosis (Gr.Kokkos, a berry and
osis, a condition of.) The condition
of being affected with Coccidia, a
genus of unicellular protozoa.
Collagen (Gr.Kolla, glue and Gennaein,
to produce.) A substance of the
Ijody, especially of cartilage, that is
converted into a gelatin by boiling.
Collagenous (Gr.Kolla, glue and Gen-
naein, to produce.) of the nature
of Collagen.
Collateral (L.Con, together and Latus
side. ) Of tlie nature of an acces-
sory, not direct.
Colliquation i L.Con, together and Li-
quare, to melt.) The liquefaction
or breaking down of a tissue or
organ.
Coma (Gr.Koma, a deep sleep.) A
state of unconsciousness not influ-
enced by external stimuli, control
of vital functions still persisting.
Compensatory (L.Compensare, to equal-
ize.) Restoring a balance or defi-
ciency of a part by means of some
other part or organ.
Complement (L.Cum, together and Pie-
re, to fill.) That which supplies a
deficiency.
Complex (L.Cum, together and Plere,
to fill.) The totality of a thing. A
thing taken as a whole with consi-
deration of its make-up of parts.
Component (L.Cum, together and Po-
nere, to place.) One of the parts
that make up a body.
Concentric (L. Cum, together and Cen-
trum, center.) Arranged in an
equidistant manner about a common
point.
Congenital (L.Cum, together and Gr.
Gennaein, to produce.) Existing or
occurring at birth.
GLOSSARY.
379
Congestion (L.Con. together and Ce-
rere, to bring.) An abnormal col-
lection and retention of blood in
the vessels of a part.
Conglomerate (L.Cum, together and
Glonierare, to heap up.) Arranged
in a mass together indiscriminately.
Conidia (Gr.Konis, dust and diminutive
term.) The deciduous, axial spores
of certain fungi.
Conjugation (L.Cum, together and Ju-
gare, to yoke.) A condition of being
.ioined.
Contiguity (L.Cum, together and Tan-
gere, to touch.) A condition of being
in contact. (Spoken of two different
kinds of tissue.)
Continuity (L.Cum, together and T.'\n-
gere, to touch.) A condition of being
without interruption of part. (With-
in the same tissue.)
Conventionall.v (L.Con, together and Ve-
nire, to come.) According to agree-
ment.
Cornifled (L.Cornu, horn and Facere, to
make.) The condition of having
been made or having become horny.
Cori>oration (L. Corpus, a body.) A col-
lective body considered as one or
taken as a whole.
Corpuscle (L.Corpus, body and diminu-
tive term.) A small body or struc-
ture. LTsually the cell-content of the
blood.
Correlated (L. Con, together and Rela-
tio, relation.) Related to.
Corrosive (L.Con, together and Rodere,
to gnaw.) A substance that destroys
tissue (less violent than a caustic.)
Cortical (L.Cortex, bark.) Of or per-
taining to the cortex, the surface
layer.
Cotyledons (Gr.Kotuledon, a socket.)
An enlarged vascular organ of the
chorion.
Croupous (A.S.Kropan, to cry aloud.)
Of the nature of croup. Character-
ized by a development of a mem-
branous deposit or exudate on the
surface of a mucous membrane.
Cutaneous (L.Cutis, skin.) Pertaining
to the skin.
Cycle (Gr.Kuklos, a circle.) A round of
years. A period of time.
Cystadenoma (Gr.Kustis, bladder, Aden,
gland and Oma, tumor.) An aden-
oma containing cysts.
Cystic (Gr.Kustis, a bladder.) Pertain-
ing to or resembling a cyst.
Cytoplasm (Gr.Kutos, cell and Plessein,
to mold.) The essential, viscid sub-
stance of a living cell. — proto-
plasm.
Cytosis (Gr.Kutos, cell and osis, a con-
dition of.) Cell proliferation.
Dearth (A.S. Death.) The total cessation
of life.
Debris CL.Dis. apart and Briser, to
break.) The material resulting from
the destruction of anything.
Decubital (L. Decubitus, a lying down.)
The position of lying down.
Degeneration (L.De, away from and
Gerere, to become.) A morbid con-
version of the elements of a tissue
into new substance.
Deleterius (L.Delere, to destroy.) Char-
acterized by a hurtful or destruc-
tive tendency.
Denticle (L.Dens, tooth and diminutive
term.) A small tooth or projecting
point.
Depleted (L.De, from and Plere, to
fill.) Condition of diminished amount
or fluid In a body or part.
Dermatologic (Gr.Derma, skin and Lo-
gos, study.) Pertaining to derma-
tology. The study of the skin.
Dessicant (L.Dessicare, to dry up.) A
substance that has the property of
drying up other substances.
Dessicated (L.Dessicare, to dry up.) A
condition of being dried up.
Detritus (L.De, away from and Terere,
to rub.) Finely divided material worn
off from substances by rubbing.
Diabrosis (Gr.Dia, through and Bibros-
kein, to eat.) A. condition of having
been broken through corrosive ac-
tion.
Diapedesis (Gr.Dia, through and Pedae-
In, to leap.) The passage of blood
through an unruptured vessel-wall.
Diaster (Gr.Dis, two and Aster, star.)
The so-called double star or wreath
in the mitoic cell division.
Diastole (Gr.Dia, through and Stole, a
drawing.) The period of dilatation
of the chamber of the heart.
Dicliotomous (Gr.Dicha, asunder and
Temnein, to cut.) Regularly divid-
ing into pairs from bottom to top.
Diffuse (L.Dis, apart and Fundere. to
pour.) Not limited in extent.
Digestion (L.Dis, apart and Gerere to
carry.) The preparation of food-
stuffs for absorption and assimila-
tion.
Diphtheritic (Gr.Diphtheria, skin or
membrane.) Pertaining to dipthe-
ria, or characterized by formation
of false membrane in and upon a
mucous membrane.
Disintegrated (L.Dis, apart and Integer,
a whole.) Broken up or decomposed.
DissimUation (L.Dis, apart and Simu-
380
CjLOSSAfiY,
lare, to make like.) To cause to
appear different.
Dissociated (L. Dis, apart and Sociare, to
associate.) A condition of being- se-
parated or broken up.
Dropsy (Gr.Hudrops, dropsy.) The col-
lection and retention of a non-in-
flammatory lymph transudate with-
in a tissue or body-cavity.
Ebumated (L.Ebur, ivory.) An increased
density of bone, similar to ivory.
Ecchymosis (Gr.Ek. out and Chumoma.
a flowing out.) An extravasation of
blood into the subcutaneous tissues.
Ectropia (Gr.Ek, out and Trepein, to
turn.) Eversion or turning out of
the edga of a part, especially of the
eyelid.
Effervescence (L.Effervescere, to boil
up.) Giving off bubbles of gas.
Effusion (L.Effundcre. to pour out.) The
escape of a liquid exudate into a
tissue or part, especially of serum
or blood.
Elimination (L.Ex, out and Limen,
threshold.) The expulsion of any-
thing from the body, especially of
waste products.
Emaciation (L.Emaciare, to become
lean.) A condition resulting from
a general wasting away of all tis-
sues of the body.
Embolus (Gr.En, in and Ballein, to
throw.) An obstruction in a vessel
by matter from another point.
Embryonal (Gr.En, in and Bruein, to
grow.) Pertaining to an embyro. The
foetus in the early stages of its de-
velopment.
Emphysema (Gr.Emphusaein, to inflate.)
A condition in which there is an
accumulation of gas in the inter-
stices of the connective tissue.
Empyema (Gr.En, in and Puon, pus.)
Pus in a body cavity.
Enceplialoid (Gr.Egkephalos, brain.) Of
the nature of brain tissue.
Endemic (Gr.En, in and Demos, people.)
A disease found in a certain place
more or less constantly.
Endomysium (Gr. Endon, within and
Mus, muscle.) The connective tissue
structure separating muscle-fibre
bundles.
Endotlielioma (Gr.Endo, within and
Thele nipple and Oma, tumor.) A
tumor composed of endothelial cells.
Endothelium (Gr.Endo, within and The-
le, nipple.) Cells covering the inner
surface of vessels not communicat-
ing with the outer air.
Endotoxin (Gr.Endon, within and Toxi-
kon, poison.) A poisonous substance
found within the cell body of a
bacterium.
Enterolitli (Gr.Enteron, bowel and Lith-
os, stone.) A concretion found in
the intestines: An intestinal calcu-
lus.
Enterorrhagia (Gr.Enteron, bowel and
Hregnunai, to burst forth.) He-
morrhage into the intestines.
Enucleated (Ij.Ex, out of and Nucleus,
kernel.) Removed in such a way
that the body comes out clean and
whole from its capsule (as of a tu-
mor.)
Enzootic (Gr.En, in and Zoon, animal.)
Pertaining to a disease of lower
animals and found in a certain place
more or less constantly.
Enzym (Gr.En in and Zume, leaven.)
A ferment formed within the body.
Enzymotic (Gr.En. in and Zume. leaven.)
Pertaining to leaven, (Enzym.)
Eosinopliile (Gr. Eos, dawn and Philee-
in to love.) Showing a peculiar af-
finity for eosin or acid stains in
general.
Ependymal (Gr.Epi. upon and Enduma,
a garment.) Pertaining to the Epen-
dyma. The lining membrane of the
cerebral ventricles and of the cen-
tral canal.
Ephemeral (Gr.Epi, upon and Hemera,
day.) Lasting but a day; tempo-
rary.
Epidermal (Gr.Epi, upon and Derma,
skin.) Pertaining to the epidermis,
the outer layer of the skin.
Epilepsy (Gr.Epi, upon and Lepsis, sei-
zure.) Paroxysmal loss of con-
sciousness with convulsions lasting
but a short time.
Epistaxis (Gr.Epi, upon and Stazein, to
cause to drop.) Hemorrhage from
the nose.
Epitlielium (Gr.Epi, upon and Thele, nip-
ple.) Cells forming the epidermis
and lining vessels that communicate
with the external air.
Etiology (Gr.Aitios, cause and Logos,
study.) The study of the causes of
disease.
Evolutionary (L.Ex. out of Volvere, to
roll.) Pertaining to evolution: The
process of development from simple
to complex form.
Exantliematous (Gr.Ex, out of and Ant-
hema, a breaking forth and ous,
pertaining to.) Of the character of
Exanthema: An eruption of the skin.
Exciting (L.Ex, out and Citare, to stir.)
Calling forth directly.
Excrement (L.Ex, out and Cernere, to
separate.) Matter cast out as waste
from the body (especially the feces.)
Excretion (L.Ex, out and Cernere, to
GLOSSARY.
38i
separate.) The discharge by the tis-
sues of waste products.
Exfoliate (L.Ex from and Foliare, to
give forth leaves.) To separate In-
to thin layers.
Exfoliation (L.Ex, from and Foliare to
give forth leaves.) The proces'i of
separating into thin layers
Exophthalmic (Gr. Ex, out and Oph-
thalmos eye.) Pertaining to abnor-
mal extrusion of the eye-ball.
Extirpation (L.Ex. out and Stlrps
stem.) Complete removal or eradi-
cation of a part.
Extravasation (L. Extra, outside, and
Vas, vessel.) The escape of fluid
from its containing cavity or ves-
sel (Especially applied to the
blood.)
Extra-uterine (L.Extra, outside of and
Uterus, uterus.) Outside of the ute-
rus.
Extrinsic (Extra, without and Secus,
otherwise.) Coming from the out-
side: Not directly belonging to a
part.
Exudate (Ex, out and Sudare, to
sweat.) A portion of the blood
that has passed into a tissue from
its vessels because of Inflammatory
disturbances.
Exudation (L.Ex, out and Sudare, to
sweat.) The production of an exu-
date.
raceted (Fr.Facette, a little face.)
Provided with many small plane
surfaces.
Facultative (L.Facultas capability.)
Capable of assuming a part or con-
dition (spoken of bacteria.)
Fever (L.Fibres. ) An abnormally high
temperature.
Fibrinopurulent (L.Fibra, fibre and Pus,
pus.) Composed of fibrin and pus.
Fibrinous (L.Fibra, fiber.) Of the na-
ture of or consisting of fibrin.
Fibroglia (L.Fibra, thread and Glia,
glue.) The glue-like fibres of some
tumors.
Filamentous (L.Fllum, a thread and
ous of the nature of.) Like a small
thread in structure.
Filaria (L.Filum, a thread.) A genus of
nematode worms, thread-like, endo-
parasitic.
Filum terniinale (L.Filum, a thread and
Terminale, terminal.) The long,
slender, thread-like termination of
the spinal cord.
Flagrella (L.Flagella, a whip.) A motile
whip-like process (usually applied
to some bacteria.)
Foci (L. Focus, a fire-place.) The prin-
cipal seats of a disease.
Foetus (L. Foetus, offspring.) Unborn
off-spring of viviparous animals In
later developmental stage.
Follicle (L.FoUis, a bellows and diminu-
tive term.) A small sac or gland.
Fractous (L.Frangere, to break.) Apt
to become difficult to control.
Fracture (L.Frangere, to break.) A
break in the continuity of osseous
tissue (bone.)
Function (L.Fungi, to perform.) The
normal action or work of a part.
Fusiform (L.Fusus, a spindle and For-
ma, form.) Like a spindle in form.
Galactopherous (Gr.Gala, milk and Fer-
ein, to bear.) Producing milk.
Gangrene (Gr.Gangraina, a sore.) That
type of necrosis characterized by
putrefaction of the necrotic tissue.
Gemmation (L.Gemma, bud.) The act
of budding or reproduction by bud-
ding.
Gestation (L.Gestare. to bear.) The
period from fertilization of the
ovum to its expulsion from the
uterus.
Glia cells (L.Glia, glue.) Neuroglia or
the supporting-structura cells of
nerve-tissue.
Glioma (Gr.Glia, glue and Oma, tumor.)
A tumor composed of neuroglia
cells.
Glycogen (Gr.Glukos, sweet and Gen-
naein to produce.) A substance
formed from carbohydrates In the
body and stored up in certain
structures: often called animal
starch.
Granulation (L.Granula, a little grain.)
The formation of new tissue in the
repair of local loss of tissue and
composed of capillary vessels en-
closed by groups of connective tis-
sue cells.
Haptophore (Gr.Haptein. to seize and
Phorein, to carry.) The stable,
nonpoisonou: element (of a toxin
which enables it to unite with a
antitoxin (Ehrlich's lateral side-
chain theory.)
Helminths (Gr.Helmins, a worm.) A
branch of Invertebrates known as
worms.
Hematemesis (Gr.Haima, blood and
Emesis, vomiting.) The vomiting
of blood. Gastric hemorrhage.
Hematidrosis (Gr.Haima. blood and Hl-
drosis, sweating.) The sweating of
blood or of a blood-like substance.
Hematin (Gr.Haima, blood.) A product
of decomposition of Hemoglobin.
Hematocele (Gr.Haima, blood and Kele,
tumor.) The extravasation of blood
into a cavity, especially the tunica
vaginalis testis.
Hematosrenous (Gr.Haima, blood and
382
GLOSSARY.
Gennaein, to produce.) Derived
from or having origin in the blood.
Hematoidin (Gr.Haima, blood and Ei-
dos, resemblance.) A yellowish-
brown, iron-free substance obtained
from hemoglobin of the blood.
Hematoma (Gr.Haima blood and Oma,
tumor.) A circumscribed collection
of extravasated blood.
Hematometra (Gr.Haima, blood and
Metra. uterus.) An accumulation
of blood in the uterine cavity, ex-
travasated from the mucosa.
Hematuria (Gr.Haima, blood and Du-
ron, urine.) Urine containing whole
blood. A condition of bloody urine.
Hemochromogen (Gr.Haima, blood.
Chroma, color and Gennaein, to pro-
duce.) A crystalline coloring mat-
ter derived from the hemoglobin
of the blood.
Hemocoelia (Gr.Haima, blood and Kol-
lia, belly.) An accumulation of
blood within the peritoneal cavity.
Hemogenous (Gr.Haima, blood and Gen-
naein.) Derived from the blood or
having origin in the blood.
Hemoglobin (Gr.Haima, blood and L..
Globus, globe.) The coloring matter
of the red blood corpuscles.
Hemoglobinuria (Gr.Haima, blood. L.-
Globus, a globe and Gr.Ouron,
urine.) A discharge of urine con-
tainitig hemoglobin. A condition
of hemoglobin in the urine.
Hemolysis (Gr.Haima, blood and Luein,
to loose.) Destruction of the blood
or of its corpuscles.
Hemoptysis (Gr.Haima, blood and Ptu-
ein, to spit.) Spitting blood from
the respiratory passages — pulmonary
hemorrhage.
Hemorrhage (Gr.Haima, blood and
Hragnuni, to burst forth). The es-
cape of blood through a vessel wall.
Hemosiderin (Gr.Haima, blood and SI-
deros. iron.) A golden-yellow pig-
ment containing iron and derived
from the hemoglobin of the blood.
Hemothorax (Gr.Haima. blood and
Thorax, thorax.) An accumulation
of blood in the thoracic cavity.
Hepatogenous (Gr.Hepa, liver and Gen-
naein, to produce.) Produced by or
in the liver.
Hermaphrodite (Hermes and Aphrodite.
Greek deities.) An individual that
possesses more or less completely
both male and female genital or-
gans.
Hernia (Gr.Hernos, a sprout.) The pro-
trusion of an organ through an ab-
normal opening in the wall of its
containing cavity.
Heterogeneous (Gr.Heteros, other and
Genos, kind.) Composed of different
substances.
Humor (L.Humor, moisture.) A fluid or
semi-fluid part of the body.
Hyalin (Gr.Hualos, glass.) A translu-
cent substance. The chief nitrogen
constitute of hydatid cysts.
Hyaloplasm (Gr.Hualos, glass and Plas-
sein, to mold.) The fluid portion
of the cell-protoplasm.
Hydrargyrosis (Gr.Hudor, water and
Arguros. silver (Mercury.) A de-
posit of mercury in the tissues.
Hydremia (Gr.Hudor, water and Hal-
ma, blood.) A condition in which
the fluid of the blood is in excess
of the normal proportion of cells.
Hydrocele (Gr.Hudor. water and Kele,
tumor.) A collection of oedematous
fluid within the tunica vaginalis.
Hydrocephalus (Gr.Hudor, water and
Kephale, head.) A collection of
oedematous fluid in the serous cav-
ities of the brain or its meninges.
Hydropericardium (Gr.Hudor, water.
Peri, around and Kardia, heart.)
A collection of oedematous fluid In
the pericardial sac.
Hydropic (Gr. Hudrops, dropsy.) Per-
taining to or affected with dropsy.
Hydrops (Gr.Hudrops, dropsy.) Dropsy.
An abnormal collection and reten-
tion of serum in the cellular tissue
or in a body cavity.
Hydrothorax (Gr.Hudor, water and Tho-
rax, thorax.) Abnormal accumula-
tion of an oedematous fluid in the
pleural cavity.
Hyperchromatosis (Gr.Huper, above.
Chroma, color and osis, a condition
of.) A condition of excessive depo-
sition of pigment in the tissues.
Hyperemia (Gr.Huper, above and Hal-
ma, blood.) An increase in the
blood supply to a part.
Hypernephroma (Gr.Huper, above, Ne-
phros, kidney and Oma, tumor.) A
tumor composed of tissue similar to
adrenal tissue.
HyperiJlasia (Gr.Huper, above and Plas-
is, formation.) An increase in the
number of cells in a part.
Hyperplastic (Gr.Huper, above and
Plasis, formation.) Pertaining to
hyperplasia.
Hypersensitive (Gr.Huper, above and
L.Sensue, feeling.) A condition of
increased or abnormal tendency to
reaction to a stimulus.
Hypertrophy (Gr.Huper, above and Tro-
phe, nourishment.) An excessive
GLOSSARY.
383
increase in the size of the cells of
a tissue.
Hypbae (Gr.Hupha, a web.) The fila-
ments composing the mycelium of a
fungus.
Hyphomycetes (Gr.Hupha, a web and
Mukes, a fungus.) A group of
fungi including the molds. Some
are pathogenic.
Hypoplasia (Gr.Hupo, under and Plas-
is, formation.) Defective or incom-
plete development of a tissue.
Hypothesis (Gr.Hupo, under and Tithe-
nai, to put.) A proposition taken
for granted in order to draw a con-
clusion to aid in explanation of
certain facts.
Ichorous (Gr. Ichor, serum or pus.) Of
the nature of ichor: An acrid, thin,
puriform discharge.
Ichthyosis (Gr.Ichthus, a fish and osis,
a condition of.) A condition like
the scales of a fish.
Icterus (Gr.Ikteros, yellow.) Jaundice,
a yellow pigmentation of the tis-
sues with the coloring matter of the
bile.
Immunity (L.In, not and Munis, serv-
ing.) A condition of exemption
from a disease.
Impacted (L.In., in and Pingere, to
drive.) Driven firmly in or dis-
lodged with difficulty.
Inanition (L.Inanis, empty.) A wasting
of the body from lack of food or
from inability to assimilate it.
Inbreeclingr (A.S. In, and Brodan, to
nourish.) The production of off-
spring by closely related parents.
Incorporated (L.In, and Corpus, body.)
Thoroughly united with a body in
a compact mass.
Indurated (L.In, and Durus, hard.)
Rendered hard.
Inert (L.in, not and Ars, art.) Without
action.
Infarct (L.In, in and Farcire, to stuff.)
A wedge-shaped area (hemorrhagic
or anemic) in an organ produced
by obstruction of a terminal vessel.
Infection (L.In, in and Facere, to
make.) The invasion of the body
by pathogenic micro-parasites and
the sum-total of the disturbances
produced by their presence therein.
Infectious (L. In, into and Facere, to
make.) Capable of communicating
a disease.
Inflammation (L.In, and Flamma,
flame.) The reaction of a living
animal tissue to an irritant accom-
panied by circulatory disturbances
and by destructive or proliferative
tissue changes.
Ingested (L.In, in and Gerere, to bring.)
Taken into the stomach or alimen-
tary tract.
Inherited (L.In, into and Haerere, to
cleave.) Born to or belonging to by
birth.
Inhibiting: (L.In, in and Habere, to
hold.) Holding in check or hinder-
ing from doing a thing.
Inimical (L.In, not and Amicus, friend.)
Having a hostile tendency. Liable
to injure.
Inoculating (L.In, into and Oculus, a
bud.) The introduction of a virus
of a disease into a wound or abra-
sion of the skin.
Inosculation (L.In, into, and Os, mouth.)
The joining of blood vessels by di-
rect communication.
Insidious (L.Insidioe, ambush.) Coming
on stealthily or imperceptibly.
Inspissated (L.In, intensive term and
Spissare, to thicken.) Thickens by
removal of fluid.
Insusceptibility (L.In, not and Suscl-
pere, to receive.) Not having a
liability to acquire a disease.
Intercellular (L. Inter, between and Cel-
la, cell.) Existing between the cells
of a tissue.
Interfunicular (L. Inter, between and
Funiculus, cord.) Existing between
the bundles of tissue.
Intermittent (L. Inter, between and
Mittere, to send.) Characterized by
intervals between.
Interstice (L.Inter, between and Stare,
to stand ) Spaces between or to
stand between.
Interstitial (L.Inter, between and Sis-
tere, to place.) Pertaining to struc-
tures between the cells of a part.
(Stroma.)
Intracellular (L. Intra, within and Cella,
cell.) Existing within the cells of
a tissue.
Intrinsic (L.Intra, within and Secus,
otherwise.) Situated entirely with-
in or pertaining exclusively to a
part.
Intussusception (L.Intus. within and
Suscipere, to receive.) A slipping
of one part of an organ (usually
intestine) into the parts beyond.
Invagination (L.In, within and Vagina.
a sheath.) The unsheathing of a
tissue.
Involucre (L.In, in and Volvere, to
wrap.) The covering or slieath con-
taining the sequestrum of necrosed
bone.
Irritant (L.Irritare, to excite.) Anything
that produces an excessive action or
functioning in a responsive^ tissue.
384
GLOSSARY.
Ischemia (Gr. Ischeln, to check and Hai-
ma, blood.) A local anemia.
tschiopagus (Gr.Ischion, hip and Pa-
ges, union.) A monster with two
heads and with bodies united at the
hips.
Karyokinesig (Gr.Karuon, nucleus and
Kinesis, motion.) Indirect cell-divi-
sion with formation of thread-lilte
structures. (Mitosis.)
Karyolysig (Gr.Karuon, nucleus and
Luein, to loose.) The morbid de-
struction of the cell nucleus.
Katabolism (Gr.Katam, down and Ball-
ein, to throw.) The transformation of
complex tissue-elements into simp-
ler ones in the production of energy.
Keratitis (Gr.Keras, horn or cornea and
Itis, inflammation.) Inflammation
of the cornea.
Keratosis (Gr.Keras, horn or cornea and
Qsls, a condition of.) A disease of
the skin characterized by an over-
growth of horny tissue.
Kinetic (Gr.Kineein, to move.) Pertain-
ing to motion.
Keloid (Gr.Kele, a claw and Eidos,
like.) A raised, cutaneous dense
overgrowth of white fibrous con-
nective tissue in a cicatrix, very
common in the negro.
Lacerated (L.Lacerare, to tear.) Condi-
tion of being torn apart leaving
ragged edges.
Lacunae (L. Lacuna, a small lake.)
Small pits or depressions: Hollow
spaces.
Laminated (L.Lamina, a plate or scale.)
Made up of laminae, of thin flat
plates.
Lecithin (Gr.Lekithos, the yolk of an
egg.) A complex nitrogenous sub-
stance found wi^eJy distributed in
the body tissues.
Leiomyoma (Gr.Leios , smooth Mus,
muscle and Oma, tumor.) A tumor
composed of unstriped muscle tis-
sue.
Lesion (L Laesio, to hurt.) A mor-
bid structural change.
Leucodernia (Gr. Leukos, white and Der-
ma, skin.) A condition of abnormal
whiteness of the skin — Albinism in
patches.
Leucomain (Gr.Leukos, white of egg and
Oma.) A product of metabolism
of the tissues of the body and nor-
mally present in them.
Leucocytosis (Gr.Leukos, white, Kutos,
cell and osis, a condition of.) An
increase in the relative number of
leucocytes in the b'o'^d.
Leucoprotase (Gr.Leukos, white and
Protos, first.) A ferment.
Leukemia (Gr.Leukos, white and Hal-
ma, blood.) A condition in which
there is a proportional increase of
leucocytes in the blood.
Lobulate (Gr.Lobus. a lobe and diminu-
tive term.) Containing small lobes
Lumen (L.Lumen, light.) The cavity
surrounded by walls of a tubular
vessel.
Lymph (L.Lympha, water.) That por-
tion of the blood which passes
through the capillary walls into the
perivascular spaces and consists of
diluted plasma, leucocytes and
usually waste materic^l.
Lymphogenous (L.Lympha, water and
Gr. Gennaein, to produce.) Pro-
ducing lymph.
Lymphocyte (L.Lympha, water and Gr.-
Kutos, cell.) A variety of leucocyte
found in lymph glands. They are
small, with very large nucleus.
Lympliorrhagia (L.Lympha, water and
Gr.Hragnunai, to burst forth.) The
flow of lymph from a ruptured
lymph-vessel.
Lysin (Gr.Luein, to loose.) A cell pro-
duct with power of cleavage of
other cells or substances.
Lysis (Gr.Luein, to loose.) A gradual
decline. Generally used in combina-
tion to signify destruction or break-
ing up.
Maceration (L.Macerere, to make soft.)
The softening of a solid by soaking
in a liciuid.
3Iacro8copic (Gr. Makros, long and Sko-
pein, to view.) Visible with the ui^-
aided eye or without the use of a
miscroscope.
3IaIformation (L.Malus, bad and For-
ma, form.) An abnormal develop-
ment of an organ or part.
Malign (L.Malus, bad.) Likely to kill
Mammalia (L. Mamma, breast.) A class
of vertebrates that suckle their
young.
Margination (L.Marginase, to furnish
with a border.) The act of furnish-
ing with a district border. (The
accumulation of leucocytes on the
interior of a vessel wall.)
Mast-cell (Ger. Mast-zellen, food-cell.)
A large type of leucocytes filled
with basophilic granules, highly
stainable.
Melanin (Gr.Melas, black.) A black pig-
ment, natural in some tissues, often
pathologic.
Melanosis (Gr Melas. blick. osis, a con-
(Specimen page from Kinsley's Pathology.)
GLOSSARY.
385
dition of.) A condition of abnor-
mal pigmentation witli melanin.
Metabolism (Gr.Meta, after and Ballein,
to throw.) The phenomena by
which foodstuffs are transformed
into complex tissue-elements or com-
plex tissue-elements are converted
into simpler ones in the production
of energy.
3Ietainorphosis (Gr.Meta, after and
Morphoein, to change, and osis, a
condition of.) A change of shape or
structure, usually a degeneration.
3Ietaphase (Gr. Meta, after and Phasis,
phase.) The second period in in-
direct cell-division. (Mitosis.)
Metaplasia (Gr. Meta, after and Plasis,
formation.) The conversion of a
developed or matured tissue into
another closely related tissue.
Metastatic (Gr.Meta, after and Stasis,
halt.) Pertaining to Metastasis.
The transfer of a disease process
from one organ to another by means
of blood or lymph.
Metrorrhagia (Gr. Metra, uterus and
Hregnunai, to burst forth.) Hemorr-
hage from the uterine mucosa, the
extravasate being almost wholly re-
tained in the uterus.
Rlicron (Gr.Mikros, small.) One one-
thousandtli of a millimeter (1-
25,000 of an inch). Represented by
the Greek letter mu.
Microparasite (Gr.Mikros, small. Para,
beside and Sitos food.) A parasite
requiring high magnification for ob-
servation.
Microph.vte (Gr.Mikros, small and Phu-
ton, plant.) A microscopic plant.
Microscopic (Gr.Mikros, small and Sko-
peein, to view.) Not visible with
the unaided eye.
Microzoa (Gr.Mikros, small and Zoon
animal.) A microscopic animal or-
ganism.
Micturition (L.Micturire, to urinate.)
The passage of urine. Staling.
MUiary (L.Milium, millet.) Consisting
of small tubercles or nodules of the
size of millet seed.
Mitosis (Gr.Mitos, thread and osis, a
condition of.) Indirect cell-division
with formation of thread-like struc-
tures. Karyokinesis.
Mole (L. Moles, a mass.) A mass formed
in the uterus by arrested develop-
ment or degeneration of a foetus.
Also a Nevus.
Monaster (Gr.Monos, single and Aster,
star.) The single star or wreath in
indirect cell-division (mitosis).
MonQchpripiiic (Gr.Monos, single and
Chorion, a foetal membrane.) Hav-
ing a single chorion.
Mononuclear (Gr.Monos, single and L.-
Nucleus, nucleus.) Having but one
nucleus.
Morbid (L. Morbus, disease.) Pertaining
to disease.
Moribund (L.Moriri, to die.) In a dying
condition.
Morphology (Gr.Morphe, form and Lo-
gos, study.) The study of the form
and structure of organized beings.
Mucus (L.Mucus.) The viscid fluid se-
creted by special glands of mucous
membranes.
Multiparous (L.Multus, many and Pare-
re, to produce.) Bringing forth
more than one offspring at a birth.
Mycelial (Gr.Mukes, a fungus and He-
los, an overgrowth.) Pertaining to
a mycelium.
Mycelium (Gr.Mukes, a fungus and He-
los, an overgrowth.) The vegetative
filaments of a fungus.
Mycosis (Gr. Mukes, fungus and osis, a
condition of.) A growth of fungus
in the tissue.
Myeloid (Gr.Muelos. marrow and Eidos,
like.) Resembling marrow.
Myoblast (Gr. Mus, muscle and Blastos,
germ.) A cell developing into a
muscle fibre.
Myoma (Gr.Mus, muscle and Oma. tu-
mor.) A tumor composed of muscle
tissue.
3Iyositis (Gr.Mus, muscle and It is. in-
flammation.) Inflammation of mus-
cle tissue.
Myxodema (Gr.Muxos, mucus and Oide-
ma, oedema.) A condition in which
tissues, especially the hands and
face, are infiltrated with a mucus-
like substance.
My.xoma (Gr. Muxos, mucus and Oma.
tumor.) A connective-tissue tumor
made up of mucin-containing inter-
cellular substance.
Nascent (L.Nanciscor, to arise.) Just
coming into existence. Just liberated
from a chemical compound.
Necrobiosis (Gr.Nekros, a corpse and
Bios, life.) Gradual and progressive
death of a cell or of a group of
cells.
Necrosis (Gr.Nekros, a corpse.) Death
of a tissue suddenly, in mass while
surrounded by living tissue.
Neofomiation (Gr.Neos, new and L.For-
nia, form.) A circumscribed new
growth of tissue of abnormal struc-
ture and location and functionless.
Tumor.
Neoplasm (Gr.Neos, new and Plasgein,
386
GLOSSARY.
to mold.) A neoformatlon, a tu-
mor.
^^eurilenima (Gr.Neuron, nerve and
Lemma, a husk.) The covering-
sheath of a nerve-fibre.
Neuroglia (Gr.Neuron, nerve and Glia,
glue.) The tissue forming the basis
of the supporting framework of the
central nervous tissue.
Neuroma (Gr.Neuron, nerve and Oma,
tumor.) A tumor composed of nerve
tissue.
Neuter (L. Neuter, neither.) Neither the
one nor the other. Inactive. Neither
acid nor alkaline.
Neutrophile (L. Neuter, neither and Gr.
Phileein, to love. ) A cell or struc-
ture stainable by neutral dyes.
Nevus (L. Nevus, a mole.) A mole. A
congenital angioma of the skin.
Birthmark.
Nidus (L.Nidus, a nest.) The original
point of a morbid process or focus
Of infection.
Noxious (L. Noxious, harmful.) Having
harmful properties.
Nucleolus (L.Nucleus, a small nut and
diminutive term.) A small body
within the nucleus of a cell.
Nucleoplasm (L.Nucleus, a small nut
and Gr.Plassein, to mold.) The pro-
toplasm of a nucleus.
Nucleus (L.Nucleus, a small nut.) The
essential part of a living cfll.
Obligatory (L.Obligare. to bind.) Bound
by conditions. Not facultative.
Odontoma (Gr.Odons, tooth and Oma.
tumor.) A tumor of tooth-like
structure.
Oedema (Gr.Oidema, a swelling.) The
accumulation and retention of lymph
in lymph vessels and spaces. Dropsy.
Oogenesis (Gr. Oon, egg and Gennaein,
to produce.) The origin and de-
velopment of the egg.
Oplitlialuiia (Gr.Ophthalmos, the eye.)
Inflammation of the structures of
the eye.
Opsonin (Gr.Opsono, a dainty food.) A
product of the body-cells that pre-
pares bacteria for phagocytosis.
Optimum (L.Optimus, best.) A condi-
tion characterized by the most fa-
vorable conditions.
Organized (Gr.Organon, organ.) Con-
verted into an organ or organ-like
structure.
Oscillation (L.Oscillare, to vibrate.) A
regular motion back and foith
within narrow limits.
Osmotic (Gr.Osmos, impulse.) Pertain-
ing to osmosis. The passage of li-
quids and substances in solution
through a menibrane.
Ossification (L.Ossa, bone and Facere,
to make.) The formation of bone.
Osteitis (Gr.Osteon. bone and Itis, in-
flammation.) Inflammation of bone.
Osteoblast (Gr.Osteon, bone and Blas-
tos, germ.) A cell of mesoblastic
origin concerned in the formation
of bone.
Osteoclast (Gr.Osteon, bone and Klatin,
to break.) A large multinuclear cell
concerned In the removal of bone.
Osteophyte (Gr.Osteon, bone and Phu-
lon, plant.) A bony outgrowth,
tree-like in character.
Otologic (Gr.Ous, ear and Logos, study.)
Pertaining to Otology: The study
of the ear.
O.xyplille (Gr. Oxus, sharp and Phileein,
to love.) Stainable with acid dyes.
Talpated (L.Palpare, to feel of.) Ex-
amined with the hand to determine
conditions beneath.
Paracentesis (Gr.Para, near and Kente-
sis, puncture.) Surgical puncture of
the walls of a cavity.
Paralysis (Gr.Para, near and Luein, to
loose.) Loss of sensation or motion
in a part.
Parasite (Gr.Para, near and Sitos, food.)
An organism that gains protection
or sustenance or both at the ex-
pense of another organism.
Parencliyma (Gr.Para, near. En, in and
Cheem, foundation, to pour in.) The
foundation, or essential or function-
ing portion of a structure.
Parencliyniatous (Gr.Para, near, En, in
and Cheem, foundation, to pour in.)
Pertaining to or affecting the paren-
chyma.
Parietes (L. Paries, wall.) The envelop-
ing or Investing structure of a body
cavity.
Parturition (L.Parturire, to bring forth.)
The act of giving birth to young.
Patliogenesis (Gr. Pathos, suffering and
Gennaein, to produce.) The origin of
disease.
Pathology (Gr.Pathos, suffering and
Logos, study.) The study of dis-
ease.
Peptons (Gr.Pepton, digesting.) Pro-
teids formed by the action of pep-
sin on albumins during digestion.
Pericliondriuni (Gr.Peri, around and
Chondros, cartilage.) The fibrous
connective-tissue covering of carti-
lage.
Perimysium (Gr.Peri around and Mus,
muscle.) The sheath of connective-
tissue around a fasciculus of mus-
cle fibres.
GLOSSARY.
387
Periostoid (Peri, around, Osteon, bone
and oid, of the nature of.) Of tin-
nature of periosteum: The slieath
of connective tissue around bones
excepting- on articular surfaces.
Peripheral (Gr.Peri, around and Pher-
ein, to carry.) Pertaining to the pe-
riphery: The external boundary.
Petrification (Gr.Petra, a stone and L.-
Fat-ere. to make.) Conversion into
a stone-like substance.
Pliagocytic (Gr.Phagein, to eat and Ku-
tos, cell.) Pertaining to a phago-
cyte.
Pliagrocytosis (Gr.Phagein, to eat. Ku-
tos, cell and osis, condition ol.i The
active functioning of phagocytes. (A
blood cell that ingests and destroys
harmful matter in the tissues.)
Plilebolitli (Gr.Phlebs, a vein and Li-
thos, a stone.) A calculus or con-
cretion in a vein.
Phlegmonous (Gr.Phlegmone. phleg-
mon.) Pertaining to phlegmon. An
inflammation characterized by the
spreading of purulent fluid in the
tissues.
Phospliorescence (Gr.Phosphoros, phos-
phorous.) The emission of light
without appreciable production of
heat.
Photogenic (Gr.Photos, light and Gen-
naein, to produce.) Causing or pro-
ducing light.
Physiology (Gr.Phusis, nature and Lo-
gos, study.) The study of the func-
tions of the organs of the living
body.
Phytoparasite (Gr.Phutos, plant, Para,
near and Sitos, food.) A parasite
vegetable organism.
Pigmented (L.Plngere, to paint.) A con-
dition to deposition of coloring
matter in the tissues.
Placental (Gr.Plakous, a cake.) Per-
taining to the placenta. The organ
of the uterine wall to -which the
foetus is attached and from which
it obtains its nourishment.
Placentoma (Gr.Plakous, a cake and
Oma, a tumor.) A tumor composed
of placental tissue.
Pleomorphism (.Gr.Pleon, more and
Orphe, form. ) The state of having
more than one form.
Plexiform (L.Plexus, braid and Porma.
form.) Having the appearance or
structure similar to a Plexu.s. (A
network of vessels. )
Plumbosis (L.Plumbum, lead and osis,
a condition of.) A condition of poi-
soning by or deposition of lead in
the tissues.
Pneumonolioniosis (Gr.Pneumon, lung
and Konia, dust, osis a condition
of.) A condition of chronic indura-
tion in the lung tissues due to the
deposition of inhaled dust.
Post-natal (L.Post, after and Nansisci,
to be born.) Occurring after birth.
Polar (Gr. Polos, pole.) Pertaining to a
pole. (Either extremity of an axis.)
Polydactylism (Gr.Polus, many and
Dektulos. finger.) The condition of
having many digits.
Polygonal (Gr.Polus, many and Gonos,
angle.) Having many angles or
sides. (Spoken of a surface.)
Polyhedral (Gr.Polus, many and Hedra,
side.) Having many sides or sur-
faces. (Spoken of a solid.)
Polymeric (Gr.Polus, many and Meros,
part.) Pertaining to the existence
of a large number of parts.
Pol.vmorphonuclear (Gr.Polus, many.
Morphe, form and L. Nucleus, nuc-
leus.) Having nuclei of i-nany forms.
Potential (UPotens. powerful.) Cap-
able of doing work or of acting.
Predisposition (L.Prae, before, Dis
apart and Ponere, to place.) The
condition of liability to acquire a
disease.
Primitive (L.Primus, first.) First in
point of time: Original.
Progeny (Gr.Pro, before and Gennaein,
to produce.) Offspring or descend-
ents.
Progressive (L.Pro, before and Gredi,
to step.) Gradually advancing or
moving forward.
Prolapse (L.Pro, forward and Labi, to
slip.) The falling downward or for-
ward of a part.
Proliferate (L.Pro. forward and Fere, to
bear.) To form new tissue of the
same kind (usually excessive.)
Prolific (L.Pro, forward and Labi, to
slip.) The quality of being able to
proliferate.
Prophase (Gr.Pro, before and Phasis.
phase.) The first stage in indirect
cell division. (Mitosis.)
Proteoses (Gr.Protos, first.) Substances
formed in gastric digestion and into
intermediate between a proteid and
a peptone.
Protoplasm (Gr.Protos, first and Plasse-
in, to mold.) The viscid, es.^ential
substance of a living cell.
Prototype (Gr.protos, first and Tupos,
type.) An original type, one after
which others are copied.
Protozoa (Gr.Protos, flrst and Zoon, ani-
mal.) A class of unicellular, animal
microorganisms.
Pseudo (L.Pseudo, false.) False.'
388
GLOSSARY.
I'sorospei-niic (Gr.Psora, itch and Sper-
ma, seed.) Of the nature of or like
a Psorosperum. A protozoon. A
coccidium.
Ptoniain (Gr.Ptoma, a corpse.) A pro-
duct formed in the decomposition of
dead animals tissues.
Purulent (L.Pus, pus.) Of the nature or
associated with pus. upon a sur-
face.
Pus (L.Pus, pus.) Liquefied, necrotic tis-
sue composed of altered leucocytes,
tissue shreds and usually micropar-
asites, suspended in a fluid (liquor
puris. )
Pustule (L.Pus. and diminutive term.)
A vesicle containing pus.
P.vogrenic (Gr.Puon, pus and Gennaein, to
produce.) Capable of producing pus.
P.vorrhoea (Gr.Puon, pus and Hroia, a
flow.) A persistent discharge of pus
upon a surface.
Pyrexia (Gr.Pur, fi. .' and Hexis, a ha-
bit.) An abnormal elevation of a
temperature. (Fever.)
Radicular (L. Radix, root and diminu-
tive term.) Pertaining to or like a
radicle or root.
Ranula (L.Rana, frog and diminutive
term.) A cystic tumor in the mouth
(especially on the tongue) due to
the obstruction of a gland-duct.
Receptors (L.Recipere, to receive.) The
"Side-chains" of a body cell (Ehr-
lich's side-chain theory.)
Regeneration (L.Re, again and Genar-
are, to beget.) The process by
which destroyed tissues are re-
placed.
Remittent (L.Re, back and Mittere, to
send.) Characterized by abatement
or subsidence or repetition.
Resorbed (L.Re, again and Sorbere, to
absorb.) Taken up again into the
system. Spoken of a substance that
has passed out and accumulated in
the tissues.
Reticular (L.Reticulum, a little net,
Rete). Resembling a net. Formed
by a net-work.
Retrogressive (L.Retro, backward and
Gradus, step.) Of the nature of re-
trogression. A going backward from
a pre-existing condition.
Rhabdomyoma (Gr.Rhabdos. a rod,
Mus, muscle and Oma, tumor.) A
form of muscle-tumor (Myoma),
characterized by the presence of
striated muscle fibres.
Rhexis (Gr.Rhexis, rupture.) The rup-
ture of an organ or vessel.
Bythm (Gr.Hruthmos, rythm.) The re-
currence of a motion or sound al
regular intervals.
Rupture (L.Rumpere, to break.) A con-
dition of being broken apart by vio-
lence.
Sacculate (L.Saccus, a sac and diminu
five term.) To form small sacs.
Sanies (L.Sanies. ) A thin, fetid, sero-
purulent fluid discharge from an ul-
cer, fistula, etc.
Sanious (L.Sanies.) Pertaining to or of
the nature of Sanies.
Sapremia (Gr.Sapros, rotten and Haima,
blood.) The entrance into the blood
of the products of putrefactive mi-
croorganisms.
Saprogenic (Gr.Sapros, putrid and Gen-
naein, to produce.) Causing or pro-
ducing putrefaction.
Saprophytic (Gr.Sapros, rotten and Phu-
tos, plant.) Pertaining to Sapro-
phytes: (Vegetable organisms aving
on decaying organic matter.)
Sarcolemma (Gr.Sarx, flesh and Lemma,
a sheath.) The delicate sheath en-
veloping a muscle fibre.
Sarcoma (Gr.Sarx, flesh and Oma, tu-
mor.) A tumor made up of embryo-
nal connective tissue cells.
Scbistosis (Gr. Schistos, a cleft and
osis, a condition of.) A condition of
being split or cleft.
Scirrhous (Gr.Skirrhos, hard.) Of the
nature of a Scirrhus. (A hard tu-
mor: A Carcinoma.)
Sclera (Gr.Skleros, hard.) The firm
outer coat of the eye-ball continuous
with the cornea and optic nerve.
Secretion (L.Secernere, to secrete.) The
process of separating out a substance
from the blood.
Segmentation-cells (L.Segmentum from
Secare, to cut.) One of the cells of
an ovum formed by dividing into
two equal parts.
Senile (L.Senex, old.) Pertaining to old
age.
Sequel (L.Sequi, to follow.) A follow-
ing upon or a resultant of.
Sequestration (L.Sequestrare, to separ-
ate.) The formation of a sequestrum.
Sequestrum (L.Sequestrare, to separate.)
A piece of dead bone that has be-
come separated from the sound bone
during necrosis.
Siderosis (Gr.Sideros, iron and osis, a
condition of.) A condition of pig-
mentation by the deposit, especially
in the lungs, of particles of iron.
Siluroid (Gr.Siluros, a species of fish.)
Pertaining to Siluroidei, an order
of fishes.
SlmultaiieouB (L.Slmul. at the same
GLOSSARY,
389
time.) Existing or happening at the
same time.
Sinusoid (L. Sinus, a cavity and old, of
the nature of.) Like a sinus: (A
hollow or cavity or tract.)
Slough (M.E.Slouh, the skin of a snake.)
A mass of soft tissue destroyed hy
necrosis.
Sloughing (M.E.Slouh, skin of a
snake.) The process of becoming a
slough.
Soliped (L. Solus, alone and Pes, foot.)
An animal with a single hoof or
digit.
Somatic (Gr.Soma, body.) Pertaining to
the body, especially to the frame-
work as distinguished from the vis-
cera.
Specific (L. Species, species.) Of or per-
taining to a species. Produced by a
particular kind of organism.
Specificity (L. Species, species and Face-
re, to make.) The quality of being
specific.
Spermatogenesis (Gr.Sperma, semen and
Gennaein, to produce.) The develop-
ment of Spermatozooa.
Sphacelus (Gr.sphakelos, dead.) A mass
of soft tissue destroyed by necro-
sis.
Spirem (L.Spira, a coil.) The close or
mother-skein of chromatin fibrils in
indirect cell division. (Mitosis.)
Spongioplasm (Gr.Spoggos, a sponge and
Plassein, to mold.) The fine proto-
plasmic threads forming the reti-
culum of a cell.
Spontaneous (L Spons, will.) Occuring
without external influence.
Spore (Gr. Sporos, seed.) A reproductive,
resting element of lower organisms.
Sporulation (Gr. Sporos, seed and L.Fer-
re, to mkke.) The production of
spores.
Stalactite (Gr.Stalazein, to drop.) A
pendant cone of calcium salts like
an icicle.
Stasis (L. Stare to stand.) A standing
still or stoppage of motion, espe-
cially of blood, in a part.
Stenosis (Gr.Stenos, narrow.) A narrow-
ing of the lumen of a vessel.
Sterile (L.Sterilis, barren.) Incapable of
reproducing.
Sthenic (Gr.Sthenos, strength.) Char-
acterized by strength or severity.
Strata (L. Stratum, stratum.) A series
of layers.
Stroma (Gr.Stroma. a bed.) The tissue
forming the ground substance or
framework for the essential part of
an organ. Interstitial tissue.
Suggillation (L.Suggillare, to beat black
and blue.) An extensive, capillary,
tissue-hemorrhage.
Suppuration fL.Sub, under and Pus,
pus.) The formation of pus. (Sur-
face or subsurface.)
Susceptible (L.Sub, under and Cipere,
to take.) Having a liability to ac-
quire a disease.
Swelling (A.S.Swellan, to grow larger.)
An elevation or elevated area (spe-
cially abnormal.)
Symptom (Gr.Sun, together and Ptoma,
a falling.) Sequential functional
disturbances due to disease.
Syncytium (Gr.Sun, together and Kutos,
cell.) A fusion of several cells into
a single cell.
Syncope (Gr.Sun, together and Kop-
tein, to strike.) A partial or com-
plete, temporary suspension of heart
action.
Synthesis (Gr.Sun, together and Tithe-
nai, to put.) The formation of a
compound by putting together its
constituents.
Systole (Gr.Sun, together and Stellein,
to place.) The period of the heart's
contraction especially of the ven-
tricles. — Opposed to Diastole.
Telophase (Gr.Telos, end and Phasis,
phase.) The fourth and last stage
in indirect cell division. (Mitosis.)
Telangiectatic (Gr.Telos, end Aggeion, a
vessel and Ektasis, a dilatation.) Of
or pertaining to Telangiectasis. (A
permanent dilatation of groups of
capillaries aid arterioles.
Tenable (L.Tenere, to hold.) Able to be
held or supported.
Teratoma (Gr.Teras, monster and Oma,
tumor.) A tumor composed of tis-
sues derived from all three germ-
?ayers.
Tetinic (Gr.Tetanos, tetanus) Pertain-
ing to or resembling tetanus. Char-
acterized by tonic muscular spasms.
Thermic (Gr.Therme, heat.) Of or per-
taining to heat.
Thermogenic (Gr.Thermos, heat and
Gennaein, to produce.) Pertaining to
causing or producing heat.
Thermogenesis (Gi'.Therme, heat and
Gennaein, to produce.) The genera-
tion or production of heat.
Thermolysis (Gr.Therme, heat and Lue-
In. to loose.) The loss of heat.
Thoracischiopagrus (Gr.Thorax. thorax.
Ischion, hip and Pagos, union.) A
monster with two heads but with
bodies and hips united.
Thrombosis (Gr.Thrombos, a clot and
osis, a condition of.) A condition of
the existence of a thrombus.
390
GLOSSARY.
Thrombus (Gr.Thrombos, a clot.) A coa-
gulum formed within a living blood-
vessel.
Tolerance (L.Tolerare, to endure.) Abil-
ity to endure the continuation of an
act.
Tonic (Gr.Tonikos, tone.) Pertaining to
tone. Characterized by contimuous
tension or contraction, or an agent
that tends to restore normal tone.
Tophi (Gr.Tophos, a stone.) Hard stone-
like deposits.
Torsion (L.Torquere, to twist.) A twist-
ing or the act of twisting.
Toxin (Gr.Toxikon, a poison.) A nitro-
genous product formed by cells.
Bacterial toxin.
Transudate (L.Trans, through and Su-
dare. to sweat.) A fluid that has
passed through a membrane. Espe-
cially non-inflammatory blood, serum
that has passed through vessel
walls.
Transudation (L.Trans, through and
Sudare, to sweat.) The production
of a transudate.
Traumatism (Gr.Trauma, a wound and
ism. a condition of.) A condition
due to an injury or wound.
Tricephalus (Gr.Trls, three and Kep-
hale, head.) A monster having three
heads.
Tropbic (Gr.Trophic, food.) Pertaining
to nutrition.
Tubercle (L.Tuber, a swelling and dim-
inutive term.j A small nodule.
Tomefled (L.Tumere, to swell and Fa-
cere, to make.) In a swollen condi-
tion.
Tumor (L. Tumere, to swell.) A morbid
enlargement. A growth of new tis-
sue non-inflammatory, .persistent and
independent of the surrounding
structures, atypical in structure and
function.
Ulcer (L. Ulcus.) A denuded surface re-
sulting from a continuous and some-
times progressive cellular necrosis.
Ulceration (L. Ulcus, an ulcer.) The for-
mation of an ulcer.
Ultramicroscopic (L. Ultra, beyond, Gr.-
Mikros, small and Skopeein, to look
at.) Too small to be seen with a
microscope.
ITniparous (L.Unus. one and Parere. to
produce.) Bringing forth one off-
spring at a birth.
Vaccine (L.Vacca, cow.) An attenuated
virus used for inoculation purposes.
Vacuolated (L. Vacuus, empty.) A condi
tion of the presence of vacuoles.
Vacuole (L. Vacuus, empty.) A space or
cavity in the protoplasm of a cell.
Vascularization (L.Vasculum, a small
vessel.) The process of becoming
vascular or of being supplied with
vessels.
Vehicle (L.Vehere, to carry.) A sub-
stance serving to carry or hold an-
other.
Vesicle (L. Vesica, a bladder and dimin-
utive term.) A circumscribed accu-
mulation of inflammatory serous
exudate in the deeper layers of the
epidermis or of the mucosa, usually
about pinhead size.
Villus (L. Villus, a tuft of hair.) One of
the minute projections of the mu-
cous membrane of the intestinal
.canal.
Virulency (L. Virus, a poison.) Pertain-
ing to extreme poisonousness, dis-
ease producing power or strength.
Virulent (L. Virus, a poison.) Very pow-
erful or Poisonous.
Vitiligo (L.Vitiligo, vitiligo.) A skin-
disease characterized by disappear-
ance of normal pigment in patches.
Volvulus (L.Volvere, to roll.) A Twist-
ing of an organ so as to occlude its
lumen.
Wound (A.SWund, wound.) The result
of the sudden interruption of the
Continuity of a tissue or tissues.
gymogenic (Zume, leaven and Genna-
ein, to produce.) Causing or per-
taining to fermentation.
INDEX
Abdomino-schisis, 95.
Abscess, cold, 170.
Abscess formation, 169.
Abscess, hot, 170.
Abscess, metastatic, 170.
Absorption of necrotic tissue, 262.
Acardia, 92.
Acaudia, 92.
Acephalus, 91.
Achorion Schoenleini, 5P.
Achromatosis, 251.
Acidophiles in inflammation, 152.
Acme, fever, 344.
Acquired diseases, 38.
Acquired immunity, 79.
Acromegaly, 191.
Actinomycosis, 358.
Avenue of entrance, 360.
Differential diagnosis, ^63.
Distribution, 358.
Etiology, 359.
Extension, 363.
Lesions, 361.
Source of infection, 359.
Susceptible animals, 359.
Active and acquired immunity, 83.
Acute inflammation, 173.
Addison's Disease, 249.
Adenoma, 329.
Adenoma, clinically, 330.
Adenoma, microscopic, 329.
Adeno-sarcoma, 331.
Adeno-sarcoma, microscopic, 332.
Adipose depositories, 204.
Adipose digestion, 205.
Adipose tissue, 204.
Adipose tissue regeneration, 181.
Aerobic bacteria, 60.
Agastria, 92.
Agglutination test, glanders, 272.
Agnathus, 92.
Albino, 251.
Alveolar-sarcoma, 311.
Amboceptor, 88.
Amelus, 92.
Amitosis, 24.
Amputation neuromata, 182, 295.
Amyelus, 91.
Amylin, 211.
Amyloid changes, 211.
Amyloid formation, 212.
Amyloid formation, appearance, 212.
Amyloid formation, cause, 212.
Amyloid formation, effects, 213.
Amyloid formation, tissue affected,
212.
Anaphase, 27.
Anasarca, 120.
Anemia, 132, 198.
Angioma, 295-298.
Anhydremia, no.
Animal parasites, 64.
Anomalies, 90.
Ante-natal diseases, 38.
Ante-natal hypertrophy, 190.
Antitoxins, 85.
Anthracosis, 249.
Aplasia, 91.
Apnoea, 74.
Apoplexy, 74.
Aprosopus, 92.
Apus, 93.
Argyriasis, 249.
Arrested development, 91.
Arteriolith, 239.
391
392
INDEX.
Arterioclerosis, no.
Arthropoda, 66.
Ascites, 119.
Aspergillus fumigatus, 51.
Aspergillus, niger, 52.
Asthenic fever, 345.
Atheroma, 340.
Atheromatous degeneration, 229.
Atresia, 97.
Atresia anus, 98.
Atresia iridis, 98.
Atresia oculi, 98.
Atresia oris, 98.
Atresia urethra, 98.
Atrichia, 91.
Atrophy, 197.
Atrophy, appearance, 199.
Atrophy, cause, 198.
Atrophy, effects, 200.
Atrophy, pathologic, 198.
Atrophy, physiologic, 198.
Atrophy, pulmonary, 200
Atrophy, senile, 198.
Autosite, 107.
Avian tubercular lesion, 355.
Axone, rate of growth, 182.
Axone regeneration, 182.
B
Bacilli, 54.
Bacillus necrophorus, 254-255.
Bacteria, 54-56.
Bacterial immunity, 88.
Bacterial pigmentation, 62.
Bacterial proteids, 64.
Bacterial respiration, 60.
Bacterial toxins, 63.
Bacterium mallei, 365.
Bacterium tuberculosis, 348.
Basophiles, 152.
Benign tumors, 276.
Bile concrement, 241.
Bile pigmentation, 247.
Biliary calculi, 237.
Birth mark, 296.
Blister, 43.
Blister test, 368.
Blood, 178.
Blood, exudation, 149.
Blood flow in inflammation, 147, i^
Blood oscillation, 148.
Blood pressure, no.
Blood quality, no.
Blood, quantity, no.
Blood regeneration, 178.
Blood stasis, 149.
Blood vessel regeneration, 178.
Bovine tubercular lesions, 363.
Bursattae, 252.
Calcareous infiltration, 228.
Calcareous infiltration, appearance,
229.
Calcareous infiltration, cause, 228.
Calcareous infiltration, effects, 230.
Calcareous infiltration, tissue affect-
ed, 230.
Calculi, 231.
Calculi in arteries, 239.
Calculi bile ducts, 237.
Calculi, cause, 231.
Calculi, color, 232.
Calculi, composition, 232.
Calculi, lithopedia, 239.
Calculi, gall bladder, 237.
Calculi, intestine, 237.
Calculi, kidney, pelvis, 234.
Calculi, mammary ducts and sinuses,
238.
Calculi, number, 231.
Calculi of prepuce, 236.
Calculi of salivary gland ducts, 236.
Calculi, shape, 232.
Calculi, size, 232.
Calculi, structure, 232.
CalcuH, stomach, 237.
Calculi, ureter, 235.
Calculi, urethra, 235.
Calculi, urinary bladder, 235.
Calculi, uriniferous tubules, 234.
Calculi, varieties, 234.
Calor, 161.
Canalization, 178.
INDEX.
393
Cancellated osteoma, 288.
Capillaries, 166.
Carcinoma, 324.
Carcinoma, clinically, 326.
Carcinoma, differentiation, 326.
Carcinoma, encephaloid, 324.
Carcinoma, metastasis, 326.
Carcinoma, irricroscopic, 325.
Carcinoma, scirrhus, 324.
Caries, 252.
Capillary telangiectasis, 296.
Cartilage regeneration, 180.
Cartilaginous tumor, 285.
Caseation necrosis, 258.
Castration, fatty changes, 206.
Catarrhal inflammation, 174.
Causes, exciting, 41.
Causes, predisposing, 39-41.
Cavernous hemangioma, 296.
Cell, definition, 20.
Cell division, maiotic, 28.
Cell growth, 23.
Cell motion, 29.
Cell reproduction, 24.
Cell rests, 277.
Cell shape, 22.
Cell size, 23. ,
Cell structure, 21.
Cell waste, 33.
Cells in inflammation, 151-152, 153.
Cementoma, 294.
Centrosome, 22.
Cerumenous concrements, 242.
Cervical ectopia cordis, 102.
Cheiloschisis, 94.
Chemical causes of disease, 45.
Chemical necrosis, 254.
Chemical,reaction, cloud}- swelling,
201.
Chemical reaction of tissue, 196.
Chemotaxis, 159.
Chilblains, 144.
Cholelith, 237.
Cholesteatoma, 338.
Chondroma; 285.
Chondroma, clinically, 287.
Chondroma, microscopic, 287.
Chondro-sarcoma, 320.
Chorio-carcinoma, 334.
Chorio-epithelioma, 334.
Chromosome, 27.
Chronic inflammation, 173.
Chylous ascites, 117.
Cicatrization, 186.
Cilia, 30.
Circulatory disturbances, 109.
Cirsoid aneurisms, 297.
Cladothrix actinomyces, 359.
Cloacal persistence, 102.
Cloudy swelling, 201.
Cloudy swelling, appearance, 203.
Cloudy swelling, cause, 201.
Cloudy swelling, effects, 203.
Cloudy swelling, tissue affected, 203.
Coagulation necrosis, 257.
Cobra, 49.
Coccidium, yjS-
Cocci, 54.
Colliquation necrosis, 257.
Colloid changes, 218.
Colloid formation, 218.
Colloid formation, appearance, 219.
Colloid formation, cause, 218.
Colloid formation, effects, 221.
Colloid tests, 218.
Color blending, 35.
Compensatory hypertrophy, 190.
Complement, 89.
Complement fixation, test, ^,72.
Complete duplicates, 105.
Composite odontoma, 295.
Compound follicular odontoma, 294.
Concentric hypertrophy, 190.
Concrements, 239.
Concrements, bile, 241.
Concrements, cerumen, 242.
Concrements, fecal matter, 240.
Concrements, hair, 240.
Concrements, milk, 242.
Concrements, prostatic, 242.
Concrements, pus, 242.
Concrements, source, 239.
Congenital diseases, 36.
Connective tissue regeneration, 179.
Contiguity, 69.
Continued fever, 345.
394
INDEX.
Continuity, 68.
Convalescence, fever, 344.
Corneal, reaction, 344.
Cornification, 225.
Corrosive poisoning, 45.
Craniopagi, 106.
Craniorrachischisis, 94.
Cranioschisis, 93.
Crisis, 344.
Cryptorchids, 102.
Cyclopia, 97.
Cysts, 338.
Cysts, degeneration, 340.
Cysts, dermoid, 341.
Cysts, extravasation, 340.
Cysts, exudation, 340.
Cysts, multilocular, 338.
Cysts, parasitic, 340.
Cystic, calculi, 235.
Cystoma, 338.
ID
Death, "j},, 263.
Death, pathologic, 264.
Death, physiologic, 263.
Death signs, 265.
Death tests, 266.
Decomposition, 266.
Deciduoma malignum, 334.
Decline, fever, 340.
Degeneration, 162.
Degeneration cysts, 337.
Dentigerous cysts, 2>?>7-
Dentine regeneration, 181.
Depigmentation, 251.
Dermoid cysts, 336.
Diabrosis, 112.
Diapedesis, T12.
Dicaudis, 99.
Dicephalus, 106, 107.
Diphtheritic inflammation, 171.
Diplo-coccus, 54.
Dipygusamelus, 92.
Dislocation, 41.
Dissolution, 176.
Direct cell division, 24,
Diseases, 34, 35, 38.
Disease extension, 67.
Disease termination, 69.
Dithoracisamelus, 92, 93.
Dithoracisapus, 93.
Dolor, 161.
Dropsy, 118.
Duplicities, assymetrical, 107.
Duplicities, complete, 105.
Duplicities, free, 105.
Duplicities, incomplete, 107.
Duplicities, monochorionic, 105.
Eburnated osteoma, 290.
Ectopia gastrium, 95.
Effusions, 113.
Egagaropile, 240.
Ehrlich's lateral chain theory, 83.
Electric causes of disease, 45.
Embolism, 128, 130.
Embolism, effects, 130.
Embolus, 128.
Embolus air, 129.
Embolus cells, 128.
Embolus, composition of, 130.
Embolus, location, 129.
Embolus, parasitic, 128.
Embolus, thrombic fragments, 128.
Embryonic epithelial tumors, 324.
Encapsulation of necrotic tissue, 262.
Encephaloid carcinoma, 324.
Endemic goitre, 219.
Endothelial cells in inflammation, 152.
Endothelioma, 312.
Endotoxins, (>2).
Enterolith, 339.
Enterorrhagia, 115.
Ephemeral fever, 345.
Epistaxis, 114.
Epithelial odontoma, 293.
Epithelial pearls, 226.
Epithelial regeneration, 181, 182.
Epithelioma, 327.
Epithelioma, clinically, 329.
Epithelioma, microscopic, 328.
Epithelioma, pearl, 328.
Epithelioma, seritonale, 334.
Epitheliorna contagiosum, cause, 373,
INDEX.
395
Epithelioma contagiosum, lesion, ;^73,
374-
Epithelium cornified, 225.
Epithelization, 187.
Ergot of rye, 256.
Erythrocytes in inflammation, 153.
Etiology of disease, 39.
Exciting causes of disease, 41 to 49.
Excess food, 206.
Exercise, insufficient, 206.
Exfoliation, 262.
Exhaustion theory of immunity, 82.
Exophthalmic goitre, 218.
Extension of disease, 69.
Extravasate, 186.
Extravasation cysts, 340.
Exuberant granulation, 189.
Exudate, 150, 171.
Exudate, cause, determining kind,
155-
Exudate, composition, 150.
Eudate, effects, 155, 157.
Exudate, fibrinous, 154.
Exudate, hemorrhagic, 154.
Exudate, purulent, 155.
Exudate, serous, 154.
Exudate, significance of, 156.
Exudation cyst, 340.
Fatty changes, 204.
Fatty changes, pathologic. 208.
Fatty changes, pathologic, appear-
ance, 209.
Fatty changes, pathologic, cause, 208.
Fatty changes, physiologic, 206.
Fatty changes, physiologic, appear-
ance, 207.
Fatty changes, physiologic, cause, 206.
Fatty changes, physiologic, effects
207.
Fatty degeneration, 208.
Fatty infiltration, 206.
Fatty necrosis, 259.
Favus, 50.
Fecal, concrements, 240.
Fever, 342,
Fever, acme, 344.
Fever, asthenic, 345.
Fever, continuous, 345.
Fever, convalescence, 344.
Fever, course, 343.
Fever, decline, 344.
Fever, ephemeral, 344.
Fever, intermittent, 345.
Fever, onset, 343.
Fever, sthenic, 345.
Fibrinous exudate, 154.
Fibroblasts, 165, 179.
Fibroma, 279.
Fibroma, clinically, 282.
Fibroma, differentiation, 282.
Fibroma, hard, 281.
Fibroma, soft, 281.
Fibro-sarcoma, 315.
Fibrous connective tissue regenera-
tion, 179.
Fibrous hyperplasia, 192.
Fibrous odontomata, 293.
Fission, 58.
Fistulous tracts, 170.
Flagella, 55.
Follicular odontoma, 293.
Focal necrosis, 260.
Foramen ovale, 102.
Fracture, repair, 180-184.
Freckles, 249.
Functio laeso, 161.
Galactoliths, 238.
Gangrene, 258.
Gastric calculi, 2^7.
Gastroliths, 237.
General diseases, 39.
Giant cells, 153.
Giant cell sarcoma, 308.
Giantism, 190.
Glanders, 364.
Glanders, agglutination test, 372.
Glanders, avenue of infection, 365.
Glanders, cause, 365.
Glanders, diagnosis, 371, 372.
Glanders, lesions, 366.
396
INDEX.
Glanders, mallein test, 371.
Glanders, course of infection, 365.
Glioma, 291.
Glycogen, 222.
Glycogen composition, 222.
Glycogen tests, 222.
Glycogenic infiltration, 222.
Glycogenic infiltration, appearance,
223.
Glycogenic infiltration, cause, 223.
Glycogenic infiltration, effects, 223.
Goitre, 218.
Grafting, 182.
Granulation, healing by, 187.
Granulation, exuberant, 189.
Growth of tumors, 273.
H
Hair balls, 240.
Hair lip, 94,
Hair sore, 360.
Haptophores, 88, 89.
Health, 35.
Healing by primary union, 185.
Healing by granulation, 187.
Heart anatomical changes, 109.
Heart diminished action, 109.
Heart increased action, 109.
Helminthes, 65.
Helminthes response to stimuli, 140.
Hemaglobinuria, 245.
Hemangioma, 296.
Hemangioma cavernosum, 296.
Hemangioma cirsoid, 297.
Hemangioma hypertrophicum, 297.
Hemangioma simplex, 296.
Hemangiosarcoma, 321.
Hematemesis, 114.
Hematidrosis, 112-115.
Hematocele, 115.
Hematogenous pigmentation, 244.
Hematoidin, 246.
Hefnatoma, 113.
Hematometra, 115.
Hematuria, 114.
Hemic, poisons, 46.
Hemocoelia, 115. •
Hemoglobin in pigmentation, 244.
Hemolysis, 346.
Hemophilia, iii.
Hemoptysis, 114.
Hemorrhage, 74, 112.
Hemorrhage, cause, iii.
Hemorrhage, diabrotic, 112.
Hemorrhage, diapedetic, 112.
Hemorrhage, ecchymotic, 114.
Hemorrhage, epistaxis, 114.
Hemorrhage, effects, 115.
Hemorrhage, petechial, 113.
Hemorrhage, rhexis, 112.
Hemorrhage, suggillation, 114.
Hemorrhagic infarction, 113.
Hemorrhagic exudate, 154.
Hemosiderin, 246.
Hemothorax, 115.
Heredity, 35.
Heredity in fatty changes, 206.
Hermaphroditism, 103.
Hermaphrodite, bilateral, 103.
Hermaphrodite, lateral, 103.
Hermaphrodite, pseudo or false, 103.
Hermaphrodite, true, 103.
Hermaphrodite, unilateral, 103.
Hernia, 41.
Histoid tumor, 270.
Holoschisis, 94.
Humoral theory of immunity, 83.
Hyalin, 213.
Hyalin, chemical composition, 214.
Hyaline formation, 213.
Hyaline formation, appearance, 214.
Hyaline formation, cause, 214.
Hyaline formation, effects, 215.
Hydrargirosis, 250.
Hydrops, 118.
Hydrothorax, 119.
Hydropericardium, 119.
Hydrocele, 119.
Hydrocephalus, 120.
Hymen persistence, 102.
Hyperchromatosis, 244.
Hyperemia, 133-142.
Hyperemia, active, 135.
Hyperemia, arterial, 135.
Hyperemia, arterial, appearance, T36.
INDEX.
397
Hyperemia, arterial, cause, 135.
Hyperemia, arterial, effects, 136.
Hyperemia, arterial, pathologic, 137.
Hyperemia, arterial, physiologic, 137.
Hyperemia, arterial therapeutic, 137.
Hyperemia, passive, 133.
Hyperemia, venous, 133.
Hyperemia, venous, pathologic, 134.
Hyperemia, venous, therapeutic, 134.
Hypernephroma, 3^2.
Hyperplasia, 190, 192.
Hyperplasia, appearance, 193.
Hyperplasia, cause, 192.
Hyperplasia, effects, 193.
Hyperplasia, fibrous, 192.
Hyperplasia, interstitial, 192.
Hyperplasia, parenchymatous, 192.
Hypertrophy, 189.
Hypertrophy, ante natal, 190.
Hypertrophy, appearance, 191.
Hypertrophy, cause, 191.
Hypertroph}', compensatory, 190.
Hypertrophy, concentric, 190.
Hypertrophy, effects, 192.
Hypertrophy, general, 190.
Hypertrophy, inherited, 190.
Hypertrophy, post natal, 190.
Hypertrophy, false, 190.
Hyphomycetes, 50.
Hypochromatosis, 250.
Hypoplasia, 93.
Hypospadias, 95.
Icterus, 249.
Immediate union, 185.
Immunity, 75.
Immunity, acquired, 79-81.
Immunity, bacterial, 81.
Immunity, inherited, 80.
Immunity, opsonic, 81.
Immunity, passive, 8r.
Immunity, natural, yy.
Immunity, toxic, 80.
Impaired function, 161.
Inanition, necrosis, 257.
Incision test, 266.
Increased transudation, 118.
Indirect cell division, 25.
Infarct, 131.
Infarct, anemic, 131.
Infarct, hemorrhagic, 131.
Infarction, 131.
Infective granulomata, 344.
Inflammation, 138.
Inflammation, acute, 173.
Inflammation, catarrhal, 174.
Inflammation, causes, 143-155.
Inflammation, chemic, 144.
Inflammation, chronic, 173.
Inflammation, croupous, 171.
Inflammation, diphtheritic, 171.
Inflammation, electric, 144.
Inflammation, effects, 161.
Inflammation, factors concerned in,
146.
Inflammation, hemorrhagic, 172.
Inflammation, infective, 167.
Inflammation, interstitial, 173.
Inflammation, mechanic, 143.
Inflammation, non-infectious, 143.
Inflammation, non-suppurative, 167.
Inflammation, parenchymatous, 173.
Inflammation, phlegmonous, 170.
Inflammation, proliferative, 174.
Inflammation, purulent, 169, 174.
Inflammation, pustular, 174.
Inflammation, signs, 160.
Inflammation, simple, 166.
Inflammation, specific. 174.
Inflammation, suppurative, 16".
Inflammation, termination, 174, 175.
Inflammation, thermic, 143.
Inflammation, traumatic, 143.
Inflammation, types of, 166.
Inflammation, ulcerative, 174.
Inflammation, vascular changes, 146,
,147, 148.
Inflammation, vesicular, 174.
Inflammatory esxudate, 150.
Inflammatory exudation, T40.
Inherited diseases, 35.
Inherited epilepsy, 37.
Inherited immunity, yy.
Inherited malformations, 37.
398
INDEX.
Inherited ophthalmia, 38.
Inherited tumors, 37.
Inspissated bile, 241.
Inspissated pus, 242.
Intermittent fever, 345.
Interstitial hyperplasia, 192, 193.
Interstitial inflammation, 173.
Interstitial expansion, tumor, 274.
Intestinal calculi, 237.
Involucre, 262.
lodothyreoglobulin, 218.
Irritability, ;iS-
Irritant, 139.
Ischemia, 132.
Ischiopagus, 106.
Ischiopagus parasiticus, 106.
Leucomains, 49.
Leucoprotase, 154.
Lipoma, 287.
Lipoma, clinically, 289.
Lipoma, microscopically, 289.
Liquor, puris, 155.
Lithopedia, 239.
Local disease, 38.
Loco, 48.
Luxation, 41.
Lymphangioma, 298.
Lymphorrhagia, 117.
Lymphorrhagia, cause, 117.
Lymphorrhagia, effects, 117.
Lymphosarcoma, 305.
Lysis, 344.
Jack sores, 261.
Karyolysis, 302.
Karyokinesis, 25.
Katabolism, 32.
Keloid, 283.
Keratosis, 225.
Keratosis, appearance, 226.
Keratosis, cause, 225.
Keratosis, effects, 226.
Lactation a factor in fatty changes,
206.
Lacteal calculi, 238.
Lacteal concrements, 242.
Lamellae formation, 181.
Larkspur, 46.
Leiomyoma, 299.
Lesion, 19.
Leucocytes in inflammation, 151.
Leucocytes in tumors, 271.
Leucocytes, basophilic, 152.
Leucocytes, eosinophylic, 151.
Leucocytes, neutrophylic, 151.
Leucocytes, polymorphonuclear, 151.
Leucocytic margination, 159,
Leucoderma, 251.
M
Malformations, 90.
Malformations, atypical, 91.
Malformations, multiple, 105.
Malformations, single, 91.
Malformations, typical, 91.
Malign tumor, 276.
Mallein, 371.
Mammalian cornea, 141.
Margination, leucocytic, 150.
Mechanic causes of diseases, 41.
Melanin, 248.
Melano-sarcoma, 318.
Melanosis, 248.
Membrane, cell, 22,
Meningocele, 93.
Meroschisis, 94.
Metabolism, 32.
Metaphase, 27.
Metaplasia, 194.
Metastases, carcinoma, 326.
Metastatic tumor, 273.
Metorrhagia, 115.
Microcardia, 93.
Microcephalus, 93.
Micrococcus, 54.
Micrognathy, 93.
Micromelus, 93.
Microophthalmia, 93.
Miliar tubercle, 352.
INDEX.
399
Miliary tumors, 272.
Mirror test, 266.
Mitosis, 25.
Mixed cell sarcoma, 310.
Mole, 91.
Monopygiisamelus, 93.
Monopygusapus, 93.
Monothoracisamelus, 93.
Monothoracisapus, 93.
Moribund stage fever, 344.
Mosaic coloring, 36.
Moulds, 50.
Movement, amoeboid, 29.
Movement, ciliary, 30.
Movement, intracellular, 29.
Mucoid changes, 215.
Mucoid changes, appearance, 216.
Mucoid changes, causes, 216.
Mucoid changes, effects, 217.
Mucoid changes, pathologic, 216.
Mucoid changes, physiologic, 215.
Mucoid tissue regeneration, 179.
Mucus, 215.
Multilocular cysts, 338.
Multiplicity, 99-108.
Mummifying necrosis, 258.
Muscular tissue regeneration, 182.
Mycelia, 359.
Myeloid sarcoma, 308.
Myelomeningocele, 94.
Myocarditis, 109.
Myoma, 298.
Myositis ossificans, 227.
Myxoedema, 216.
Myxoma, 284.
Myxoma clinically, 285.
Myxoma miscropically, 284.
Myxosarcoma, 319.
N
Necrobiosis, 252.
Necrosis, 164, 254.
Necrosis caseation, 258.
Necrosis chemical, 254.
Necrosis, coagulation, 257.
Necrosis colliquation, 257.
Necrosis fatty, 259.
Necrosis focal, 260.
Necrosis inanition, 255.
Necrosis mummifying, 258.
Necrosis putrefying, 258.
Necrosis senile, 259.
Necrosis subsurface, 257.
Necrosis surface, 257.
Necrosis thermic, 255.
Necrotic stomatitis, 251.
Necrotic tissue, disposal of, 175.
Nephritis, 172.
Neoplasms, 268.
Nerve cell regeneration, 182.
Neuroma, 295.
Neuromata amputation, 182-295.
Neurotoxic poison, 46.
Nevus, 296.
Nucleus, 22.
Numerical hypertrophy, 192.
Nutritive disturbances in atrophy,
iq8.
Obstructed nutrition, 253.
Obstructed outflow of Lymph, 119.
Ochronosis, 245.
Odontoma, 291.
Odontoma composite, 295.
Odontoma compound follicular, 294.
Odontoma, epithelial, 293.
Odontoma fibrous, 293.
Odontoma follicular, 293.
Odontoma, radicular, 295.
Oedema, 118, 221.
Oedema appearance, 120.
Oedema cause, 118.
Oedema effects, 121.
Oedema varieties, T19.
Olein, 204.
Onset fever, 343.
Ospora porrigines, 50.
Ophthalmic tubercular, 358.
Opsonins, 82.
Organoid tumor, 270.
Osseous regeneration, 180.
Ossification, 227.
Ossification appearance, 227.
Ossification cause, 227.
Ossification effects, 227.
400
INDEX.
Osteoblasts, i8o.
Osteoclasts, i8o.
Osteoma, 290.
Osteoma cancellated, 290.
Osteoma clinically, 291.
Osteoma eburnated, 290.
Osteo-cystoma capsular dentifcrum,
294.
Osteophytes, 227.
Osteo sarcoma, 321.
Palatoschisis, 94.
Palmatin, 204.
Pancreatic calculi, 238.
Papilloma, 321.
Parasites vegetable, 49.
Parasites in embolism, 128.
Parasitic causes of disease, 49.
Parasitic cysts, 340.
Parasitic theory of tumors, 278.
Parenchymatous degeneration, 201.
Parenchymatous hyperplasia, 192.
Parenchymatous inflammation, 173.
Parenchymatous poisons, 46.
Partial recovery, 69.
Pathogenesis, 19.
Pathology definition, 19.
Pathology comparative, 19.
Pathology general, 19.
Pathology human, 19.
Pathology special, 19.
Pathology veterinary, 19.
Pathologic anatomy, 19.
Pathologic atrophy, 198.
Pathologic death, 264.
Pathologic physiology, 19.
Pearl cell epithelioma, 328.
Persistent foetal structures, loi.
Phagocyte, 159.
Phagocytosis theory, 82.
Phlebolith, 239.
Phlegmonous inflammation, 170.
Phosphorescence, 62.
Photic cause of disease, 44.
Physic cause of disease, 43.
Phyto-bezoars, 241.
Phyto-parasites, 49.
Phyto-toxin, 79.
Pigmentary changes, 242.
Pigmentary infiltration, 244.
Pigmentation bile, 247.
Pigmentation carbon, 249.
Pigmentation cells, 248.
Pigmentation diminished, 250.
Pigmentation excessive, 244.
Pigmentation effects, 250.
Pigmentation hemoglobin, 244.
Pigmentation hemosiderin, 246.
Pigmentation hemotoidin, 246.
Pigmentation iron, 250.
Pigmentation lead, 250.
Pigmentation mercury, 250.
Pigmentation silver, 249.
Placentoma, 334.
Plumbosis, 250.
Pneumonia groupus, 172.
Pneumomycosis aspergillosis, 51.
Porcine tubercular lesion, 354.
PolydactyHsm, 98.
Polymeluspygus, 99.
Polymelusthoracicus, 98.
Poisons, 45.
Post mortem staining, 265.
Post natal diseases, 38.
Post natal hypertrophy, 191.
Predisposing causes of disease, 39-4^-
Predisposing causes of age, 39.
Predisposing causes of breed, 40.
Predisposing causes of climate, 40.
Predisposing causes of color, 40.
Predisposing causes of food and
water, 41.
Predisposing causes of genus, 40.
Predisposing causes of imitation, 40.
Predisposing causes of location, 40.
Predisposing causes of occupation,
41.
Predisposing causes of overwork, 41.
Predisposing causes of previous dis-
ease, 41.
Predisposing causes of season, 40.
Predisposing causes of sex, 40.
Preputial calculi, 236.
Pressure atrophy, 199.
Primary tumors, 273.
INDEX.
401
Prognathism, loo.
Progressive tissue changes, 177.
Proliferation tissue, 175.
Proliferative inflammation, 174.
Prophase, 26.
Prostatic concrements, 242.
Protoplasm, 20.
Protozoa, 64.
Protozoa response to stimuli, 140.
Proud flesh, 189.
Psammo sarcoma, 314.
Pseudo-hermaphrodite, 103.
Pseudo-hypertrophy, 190.
Ptomains, 63.
Purulent inflammation, 169-174.
Putrefaction, 62.
Pus, 155, 167-168.
Pus concrements, 242.
Pustule, 170.
Pustular inflammation, 174.
Pygopagus, 105.
Pyorrhoea, 169.
Pyrexia, 342.
Regeneration white fibrous tissue,
179.
Renegeration yellow elastic tissue,
180.
Regenerative inflammation, 175.
Regenerative power, 177.
Remittent fever, 345.
Reinnervation, 182.
Renal adeno-sarcoma, 331.
Renal tubular calculi, 234.
Renal pelvic calculi, 234.
Resistance to tumors, 275.
Resolution, 174.
Retention cyst, 340.
Retention theory of immunity, 82.
Retrogressive tissue changes, 196-197.
Retrogressive tissue in tumors, 275.
Rhabdomyoma, 299.
Rhexis, 112.
Rigor mortis, 265.
Ringworm, 51.
Round cell sarcoma, 304.
Rubor, 160.
Rupture, 41-184.
Rachischisis, 94.
Ranulae, 340.
Rattlesnake, 49.
Ray fungus, 359.
Reaction aseptic injury,, 142.
Reaction, septic injury, 142.
Receptor, 85-86-S7.
Recovery, 69.
Redness, 160.
Regeneration, 164-177.
Regeneration adipose tissue, 181.
Regeneration blood, 178.
Regeneration blood vessels, 178.
Regeneration cartilage, 180.
Regeneration connective tissue, ,179.
Regeneration degenerated tissue, 175.
Regeneration dentine, 181.
Regeneration epithelium, 181.
Regeneration mucoid tissue, 179.
Regeneration muscular tissue, 182.
Regeneration nerve cells, 182.
Regeneration osseous tissue, 180.
Saccharomyces, 52.
Saccharomyces cerevisiae, 52.
Saccharomyces farciminosus, 53.
Salivary calculi, 236.
Saponification of fat, 259.
Sarcinae, 54.
Sarcoma, 300.
Sarcoma alveolar, 311. .
Sarcoma cells, 302.
Sarcoma, chondro, 320.
Sarcoma, fibro, 315.
Sarcoma, grape, 317.
Sarcoma, hemangio, 321.
Sarcoma, melano, 318.
Sarcoma mixed cell, 310.
Sarcoma myeloid cell, 308.
Sarcoma, myxo, 319.
Sarcoma, psammo, 314.
Sarcoma round cell, 304.
Sarcoma structure, 303.
Scar, 211.
402
INDEX.
Schistosis, 93.
Schizomycetes, 54.
Scirrhous carcinoma, 324.
Sebaceous cyst, 340.
Secondary tumors, 273.
Senile atrophy, 198.
Senile necrosis, 259.
Sequestration, 262.
Sequestrum, 262.
Serous exudate, 154.
Serous infiltration, 221.
Serous infiltration appearance, 221.
Serous infiltration cause, 221.
Serous infiltration effects, 222.
Siderosis, 250.
Significance of inflammatory exudate,
156.
Signs of death, 265.
Signs of inflammation, 160.
Situs viscerum inversus, 100.
Sodium urate, 224.
Specific inflammation, 174.
Spina bifida, 94.
Spindle cell sarcoma, 307.
Spirilla, 55.
Sporotrichium audouini, 51.
Stadium decrementi, 344.
Stadium incrementi, 343.
Staining, post mortem, 265.
Stearin, 204.
Sternopagus, 106.
Sthenic fever, 345.
Still birth, 267.
Stimulus, 139.
Stocking, 161.
Substitution, 186.
Sub-surface necrosis, 257.
Suppuration, 167.
Suppuration sub-surface, 170.
Suppuration surface, 167-169.
Suppurative osteitis, 169.
Surface necrosis, 257.
Swelling, 160.
Symmetrical duplicity, 105.
Synactosis, 93-97.
Syncephali, 107.
Syncope, JZ-
Syncytium, 153.
Syncytioma malignum, 334.
Syndactylus, 97.
Synmelus, 97.
Synmelusapus, 97.
Synmelusdipus, 97.
Synmelusmonopus, 97.
Synorchism, 97.
Synophthalmia, 97.
Tattooing, 250.
Temperature, 161.
Temperature, cause of cloudy swell-
ing, 202.
Temperature, cause of degenerations,
197.
Telophase, 28.
Teratoid tumors, 270.
Teratoma, 335.
Termination of disease, 69, 174.
Tests for death, 266.
Thermic causes of disease, 43.
Thermic necrosis, 255.
Thermogenesis, 343.
Thermolysis, 343.
Thoracisischiopagus, 106.
Thoracopagus, 106.
Thoracoschisis, 95.
Thrombosis, 122.
Thrombosis, cause, 123.
Thrombosis, effects, 127.
Thrombus, 122.
Thrombus annular, 124.
Thrombus appearance, 124.
Thrombus calcification, 127.
Thrombus complete, 124.
Thrombus decolorization, 125.
Tlirombus, extension, T24.
Thormbus infective softening. 126.
Thrombus location, 124.
Thrombus, mixed, 124.
Thrombus organization, 126.
Thrombus partial, 124.
Thrombus red, 124.
Thrombus simple softening, 125.
Thrombus white, 124.
Tinea tonsurans, 51.
Tissue, 173.
INDEX.
403
Tophi, 224.
Toxic immunity, 80.
Toxophore, 88-89.
Transplantation, 182.
Transportation of visceral organs,
100.
Traumatic wounds, 185.
Tricephalus, 108.
Trichobezoars, 240.
Tricopli3ton tonsurans, 51.
Tubercle, 352.
Tuberculin, 357.
Tuberculin test, 357.
Tuberculosis, 347.
Tuberculosis extent, 347.
Tuberculosis etiology, 348.
Tuberculosis avenue of infection, 349.
Tuberculosis source of infection, 349.
Tuberculosis lesions, 350.
Tuberculosis extension, 356.
Tuberculosis elimination, 357.
Tumor, 160.
Tumors, 268.
Tumors benign, 2y^.
Tumors body resistance, 275.
Tumors cause, 276.
Tumors cells, 277.
Tumors clinically, 276.
Tumors color, 272.
Tumors consistency, 273.
Tumors extension, 274.
Tumors frequency', 269.
Tumors growth, 273.
Tumors histoid, 270.
Tumors intercellular sulistance, 270.
Tumors malign, ly^,.
Tumors metastasis, 2y^.
Tumors miliary, 2y2.
Tumors mottled, 273.
Tumors number, 2yT,.
Tumors organoid, 270.
Tumors primary, 2y;},.
Tumors retrogressive changes, 275.
Tumors secondary, 273.
Tumors shape, 2y2.
Tumors size, 272.
Tumors structure, 270.
Tumors teratoid, 270.
Tumors xarieties, 278.
Twins, 105.
Ulcer, 164.
Ulceration, 164.
Ulcerative inHamniation, 174.
Union dorsal, 105.
Union posterior, 105.
Union ventral, 105.
Urates, 224.
Uratic infiltration, 224.
Uratic infiltration appearance, 224.
Uratic infiltration cause, 224.
Uratic infiltration effects, 225.
Ureter calculi, 235.
Uretheral calculi, 235.
Uric acid, 224.
Valvular insufficiency, 109.
Valvular stenosis, 109.
Varieties of tumors, 278.
Vascular constriction, inflammation,
146.
Vascular disturbances, 146..
Vascular permeability, no.
Vascular regeneration, 178.
Vascular variations, no.
Vascularization, 178-186.
Vegetable parasites, 49.
Venesection in fatty changes, 206.
Venom, 49.
Vesicle, 43.
Vesicular inflanunation, 174.
Viper, 49.
Vitiligo, 251.
w
Wall-eyed horses, 251.
Wandering cells, 152.
Wart, 321.
White fibrous regeneration, 179'..
Wound, 41.
Wound cause, 185.
Wound healing, 185.
Wound sub-surface, 185.
404
^^^ INDEX.
Wound surface, 185. w
Wound traumatic, 185.
Yeast, 52.
X Yellow elastic regeneration, 180.
Xanthosis, 246. ^
Xiphopagi, 106.
Zootoxins, 75.