^^ w^S 
 
 CORNELL UNIVERSITY 
 
 THE 
 
 Stlomcr Hetennatg Hibtary 
 
 FOUNDED BY 
 
 ROSWELL P. FLOWER 
 
 for the use of the 
 N. Y. STATE VETERINARY COLLEGE 
 
 1897 
 
Cornell University Library 
 RB 123.B96 
 Outline of lectures in special pathology 
 
 3 1924 000 343 933 
 
I Cornell University 
 fj Library 
 
 The original of tiiis book is in 
 tine Cornell University Library. 
 
 There are no known copyright restrictions in 
 the United States on the use of the text. 
 
 http://www.archive.org/details/cu31924000343933 
 
OUTLINE OF LECTURES 
 
 IN 
 
 SPECIAL PATHOLOGY 
 
 DEPARTMENT OF 
 
 Comparative Pathology, Bacteriology 
 and Meat Inspection 
 
 ■O-a NEW YORK STATE VETERINARY COLLEGE 
 
 , ^-, AT CORNELL UNIVERSITY, ITHACA, N. Y. 
 
 6'\t 
 
 1912—1913 
 
^^/^-t^ 
 
 CORNELL UNIVERSITY 
 
 THE 
 
 Jlam^r Uptprtnarn library 
 
 FOUNDED BY 
 
 ROSWELL p. FLOWER 
 
 for the use of the 
 
 N. Y. State Veterinary College 
 
 1897 
 
 4675 
 
INFLAMMATION. Bf^ 
 
 Adami's conception of inflammation. 
 
 " It is the series of changes constituting the local manifestation 
 of the attempt at repair of actual or referred injury to a part, or, 
 briefly, as the local attempt at repair of actual or referred injury." 
 
 Reaction to injury in lower animals (Invertebrates). 
 
 In Amoeba (unicellular organisms) the reactive process is twofold 
 
 (a) destruction or removal of irritant, — destruction by in- 
 tracellular digestion, removal by extrusion of irritant. 
 
 (b) new growth of the organism. 
 This response is essentially reparative. 
 
 In multicellular organisms there is a separation of functions. 
 Twofold reaction is clearly marked. 
 
 (a) destruction or removal of irritant is in the main accom- 
 plished by the wandering. cells of mesoblastic origin. 
 
 (b) the new growth of. tissue to replace that destroyed by 
 the irritant proceeds in the main from the fixed cells of the 
 tissue. 
 
 In higher forms of Metazoa, further differentiation of function 
 among wandering cells, — more than one kind of leucocyte, some 
 phagocytes, others not. Certain fixed cells especially endothel- 
 ial cells of vessels have power of removing harmful matter. 
 
 In those in which a closed vascular system is not present, at first 
 the attraction of leucocytes is the only recognizable reaction, 
 proliferation of fixed cells later. 
 
 In higher metazoa with well developed vascular system, leucocytes 
 collect at region of irritation. 
 
 Vascular phenomenon serves a twofold purpose : 
 
 (a) pouring out of increased fluid into injured area and 
 
 (b) collection and diapedesis of leucocytes. 
 
 Even in highest metazoa response to injury in a non vascular 
 area, as cornea, may be with no change in neighboring blood ves- 
 sels, but consist of a collection of leucocytes that were already 
 in the injured area. 
 
 Determination of leucocytes to area of irritation is most constant 
 early response to injury — proliferation is the prominent char- 
 acteristic of later stages of the process. 
 
 Vascular changes as second and important adjuvant factor of 
 later development (not in early metazoa). 
 
Inflammatory reaction in non vascular tissue; — 
 
 mild irritants on cornea — destruction of cells followed by 
 swelling and multiplication to make good the loss. No vas- 
 cular changes. This is not common. 
 
 more intense irritation, e.g. corneal vaccinia, many wandering 
 cells gather, remove foreign matter and protect proliferating 
 corneal cells. 
 Phenomena, inflammatory reaction in non-vascular tissue. 
 
 (1) irritation and degeneration or death of cells, 
 
 (2) accumulation of wandering cells and 
 
 (3) regeneration of fixed tissue cells. 
 Inflammation in vascular tissues. 
 
 (1) Primary union of incised wounds, very slight vascular dis- 
 turbance, hemorrhage slight, ends of vessels promptly closed 
 by clots, very few tissue cells destroyed, slight fibrinous coa- 
 gula glues edges together, at end of an hobr wound appears 
 closed and only slight reddening about incision, moderate 
 hyperemia, conn, tissue cells send long processes into coag- 
 ulum. 
 
 (2) Secondary union. Marked vascular reaction, exudative in- 
 flammation, 
 
 (3) Intense vascular reaction, suppurative inflammation, healing 
 by granulation. 
 
 (4) Inflam. reaction with local death of tissue ; necrotic inflam- 
 mation. 
 
 (5) Inflam. reaction with diffuse death of tissue ; diphtheritic in- 
 flammation. 
 
 (6) gangrenous inflammation. 
 
 (7) Invasion of blood stream by bacteria. 
 Inflammatory process. 
 
 Degeneration or death of tissues (initial injury). 
 Changes in the circulation. 
 Active hyperemia, 
 Exudation of blood plasma, 
 Diapedesis of red corpuscles. 
 Emigration of leucocytes, 
 I^eucocytosis. 
 
 Poly nuclear leucocytosis,. 
 Mononucleosis — (typhoid, tuberculosis), 
 Eosinophilia — (parasites, skin diseases), 
 I<ymphocytosis. 
 
Changes in tissue cells in inflammation 
 degeneration 
 
 disturbance of nutrition of cell, accumulation of intracellular 
 secretion products (bile, glycogen), disturbance of specific cell 
 ferments, autolysis, 
 action of exogenous ferments, 
 varieties : granular, hydropic, fatty, 
 mucous, glycogenic, hyaline, amyloid, 
 necrosis coagulation, 
 
 liquefaction, 
 caseous, 
 regeneration of cells. 
 
 Variation in appearances in inflammation. 
 
 A. Nature of tissue affected 
 
 vascular and non vascular, loose and dense tissue. 
 e. g. cutaneous surfaces, exudation marked, vesicles and 
 blisters. 
 
 mucous and cutaneous surfaces, tendency to remain local- 
 ized, does not spread from surface so much, 
 serous surfaces, tendency to spread superficially because 
 irritant carried into cavity affects other parts of serosa, 
 excretory organs suffer in removing irritating material — 
 parenchymatous inflammation. 
 
 B. Position of tissues. 
 
 e. g. suppuration in deep and superficial tissue^ — abscess 
 and ulcer, though process same, may be more serous exu- 
 date in ulcer ; more exudate near surface as a rule. 
 Peyer's patches become infiltrated and necrotic, but are 
 cast off leaving an ulcer ; but the mesenteric glands, though 
 similarly affected generally recover. 
 
 C. The relative intensity of the irritant is a greater cause of var- 
 
 iation. 
 The ratio between virulence or intensity of irritant and re- 
 sisting powers of the body, 
 e. g. heat slight produces redness, congestion 
 heat moderate " blisters 
 heat greater ' ' death of tissue, etc. 
 
 strong chemical, death of few cells, prompt repair to 
 deep necrosis, swelling about edges, pain, granulation 
 tissue — scar. 
 
with pathogenic bacteria e. g. anthrax 
 
 very much attenuated — no recognizable effect ; 
 not so much attenuated — some hyperemia, some infil- 
 tration of leucocytes, little fluid exudate, in day or 
 two all trace gone ; 
 
 slightly more virulent — migration of leucocytes — ne- 
 crosis of tissue with abscess formation ; 
 more virulent — no migration of leucocytes, exudation 
 extends, leads to bacteremia. 
 Same kind of change with same virus but using animals 
 more and more susceptible. 
 D. The nature of the irritant. 
 
 Can not classify inflams. according to nature of the irritant, 
 no sharp line between those caused by heat and chemicals 
 from those caused by bacteria for example. 
 Suppuration may be produced not only by micro-organisms 
 but also by chemicals — turpentine, croton oil, copper, 
 silver nitrate, may produce suppuration. 
 Under ordinary conditions suppuration indicates presence 
 
 and growth of microbes. 
 Is not common to all microbes. 
 Pyogenic bacteria. 
 Same microbe may produce different effects under different 
 
 conditions. 
 Classification of bacterial irritants (Adami, p. 210) 
 Other factors 
 
 Duration of action, in general mechanical injury sets up 
 simplest forms of inflammation. 
 Classification of inflammation. Nomenclature (Ewing) p. 50 sq. 
 
 1 . Degeneration 
 
 2. Exudative inflammation 
 
 serous 
 
 fibrinous or croupous 
 
 hemorrhagic 
 
 purulent 
 
 3. Necrotic inflammation 
 
 Simple abscess formation 
 
 ulceration 
 
 Diphtheritic exudative process with rapid and diffuse ne- 
 crosis of superficial tissues. 
 
 Gangrenous Large masses of tissue destroyed with decom- 
 position. 
 
4. Productive inflammation 
 
 (a) simple acute productive inflam. 
 
 (cellular inflam.) (serous membrane) 
 
 (b) productive inflam. with exudation (granulation tissue 
 
 (c) chronic productive inflam. 
 
 Principles of treatment, read Adami Chap. 27, pp. 216-220. 
 References 
 
 Adami. Gen. Path. pp. 375-450 
 
 Adami. Inflammation. Ch. I-VII, XV. XVI, XVIII-XXVII. 
 
 (May omit 8, 9, 10, 11, 12, 13, 14, 17). 
 or Albutt's System of Medicine, article Inflammation. 
 Ziegler. Gen. Path. pp. 319-370. 
 
 Ewing. Syllabus of lectures on inflammation and associated con- 
 ditions, 1905. 
 
CARDIO-VASCULAR SYSTEM. 
 
 HEART. 
 Function of the heart. 
 
 Hypertrophy — is not primary, is preceded by distension. 
 distension 
 dilatation 
 
 simple hypertrophy 
 excentric- hypertrophy 
 Incompetence — insufficiency 
 
 relative — especially likely to happen in right heart. 
 actual 
 Distension of right ventricle outcome of (l) incompetence or sten- 
 osis of pulmonary valves ; (2) obstructive disease of the lungs 
 and pulmonary circulation oi: (3) obstruction of flow of blood 
 through left heart. 
 Results of incompetence. 
 
 Regurgitation— overloading of chambers into which blood regur- 
 gitates — distension of same — followed by compensatory hyper- 
 trophy — sooner or later damming of blood on the venous side 
 of the heart. 
 Incompetence frequently associated with stenosis. 
 
 PERICARDIUM. 
 
 Pericardial sac normally contains more fluid than other body 
 
 cavities. 
 Hydropericardium — due to obstruction of flow of blood in right 
 
 heart ; slow dissolution, incompetence, lung disease and 
 
 other diseases which lead to distension of the right heart. 
 Pneumopericardium — puncture or bacteria 
 Hemorrhages — petechiae, ecchymoses 
 Pericarditis. Hematogenic or by extension ; may be extension from 
 pneumonia, or endocarditis, by traumatic pericarditis (in cattle). 
 Acute pericarditis 
 
 fibrinous, the ordinary form 
 
 sero-fibrinous 
 
 purulent, usually fibrino -purulent. 
 Chronic productive pericarditis, arises from the acute or insidiously. 
 
 thickening of membrane by increase of fibrous connective 
 
 tissue. 
 
May be adhesions between two layers of pericardium, com- 
 plete or partial synechia, 
 villous heart, especially frequent in dogs. 
 Tuberculous pericarditis. 
 Actinomycotic pericarditis. 
 
 Traumatic pericarditis common in cattle— swallowing foreign 
 bodies. 
 Melanosis maculosus in calves. 
 
 Tumors, not common, primary are rare ; secondary by metastasis 
 and by extension from mediastium. 
 
 MYOCARDIUM 
 
 anemia — may be partial or general, pericardial exudate or hydro- 
 pericardium, blocking of coronary vessels. 
 
 hyperemia. 
 
 hemorrhage, infectious diseases, e. g, anthrax, septicemia hemor- 
 rhagica, rinderpest, fowl cholera, morbus maculosus, mercur- 
 ial poisoning, sometimes agonal ; blocking of arteries, etc. 
 
 degenerations, from arterial anemia, cloudy swelling, fatty degen- 
 eration, fatty infiltration. 
 
 necrosis, in small areas, as in livers of cattle, frequent in heart 
 muscle, due to B. Necrosis (Bang) 
 
 Calcification and ossification, of right auricle in horses. 
 Myocarditis. 
 
 (1) acute, from infection or intoxication 
 
 (a) parenchymatous or diffuse, may produce incompetence 
 by relaxation of muscles. 
 
 (b) fibrino- purulent, traumatic, the most frequent in cattle, 
 (e) purulent, disseminated by metastasis through blood, 
 
 e. g. after parturition in cow and bitch, strangles, 
 navel ill and similar wound infections. 
 
 (2) chronic productive (interstitial), ordinarily accompanies endo- 
 carditis, eventually the sequel of the cellular infiltration in 
 parenchymatous myocarditis. 
 
 Rupture of heart — muscle weakened by disease. 
 Hypertrophy — due to 
 
 (1) obstruction to outflow of blood 
 
 (a) endocardial, stenosis of valvular orifice, 
 
 (b) arterial, diminution of lumen, sclerosis, etc., 
 
 (c) pericardial, from complete synechia. 
 
(2) increase in volumne of blood to be propelled 
 
 (a) plethora, 
 
 (b) from regurgitation. 
 
 (3) increase in rate of flow of blood 
 
 (a) in tachycardia (in exophthalmic goiter) 
 
 (b) in athletes. 
 Tumors, mostly secondary. 
 
 primary fibroma rhabdo myoma rare 
 
 myxo-fibroma 
 
 lipoma (man) 
 secondary — carcinoma, sarcoma, lympho-sarcoma, osteoid sarcoma, 
 mel ano-sarcoma . 
 
 Animal parasites 
 
 Sclerostoma equinum. 
 
 Filaria immitis, in dogs. 
 
 Echinococcus, in cattle 
 
 Cysticercus cellulosus, in swine 
 
 C. inermis, in cattle. 
 
 larvae of other nematodes then Filaria 
 
 ENDOCARDIUM 
 
 valves are formed by reduplication of endocardium with an in- 
 creased amount of supporting connective tissue. 
 In aortic and pulmonary values there are no blood vessels. 
 Hemorrhages. 
 
 Thrombosis, with ulceration of endocardium, stenosis of openings; 
 thrombi are apt to form in cavities in dilatation of the heart, 
 in slowing of blood stream, changes in composition of the 
 blood. 
 Endocarditis. Acute from intoxication or infection. 
 
 lesions often ulcerations with vegetations (thrombi), valves 
 more often affected. 
 Acute. Swelling and coagulation necrosis of affected region, be- 
 gins on closing surface of valve, greyish appearance there, 
 shedding of endothelium and thrombus formation, leading to 
 warty or granular nodular formation as villous or polypoid 
 outgrowths (vegetations) . 
 
 part of valve may be destroyed while rest shows fresh inflam- 
 mation, first a small opaque yellowish patch, surface uneven. 
 
 8 
 
Chronic endocarditis. Very frequent in dogs, occasionally in 
 horses. Fibrous thickening of valves and inner surface in 
 heart. A vascularization of cusps of valves with growth of 
 cicatricial connective tissue, where was earlier an ulcer, the 
 cusp is weakened by the contraction in scar and has in- 
 creased strain, thickened valves, edges may grow together. 
 
 Fatty degeneration. 
 
 Fatty infiltration. 
 
 Auriculo-ventricular defects occur in all kinds of domesticated 
 animals, about as often on one side of the heart as the other, 
 rarely double sided in same heart. Dog affected with valvu- 
 lar defects following verrucous and contracting endocarditis. 
 Horse frequently has defective semilunar valves, but often 
 without sequlee if they remain small. In swine and sheep 
 the valvular vegetations are especially voluminous. 
 Melanosis maculosus in calves, sub-endocardial as well as sub-epi- 
 
 cardial. 
 Tumors of the heart in domesticated animals are mostly in sub- 
 endo — and sub-epicardial connective tissue. 
 
 BLOOD VESSFIvS. 
 
 vascular function, normal. 
 
 thrombo-arteritis , phlebitis, 
 
 verminous arteritis in horses. 
 
 suppurative arteritis, phlebitis most often through naval infection 
 
 in calves and foals. 
 Arteriosclerosis most frequent in aorta, first greyish semi-trans- 
 lucent patches in intima, may have gelatinous appearance 
 (mucoid degen.), later patches become harder, have more 
 cartilaginous appearance, fibrous connective tissue formed, 
 degenerates becoming a structureless mass, with this may be 
 fatty degen. of cells, and production of granular, shreddy 
 detritus {atheroma^ resulting in necrosis, often is deposition 
 of calcium salts in this in advanced stages (calcified plaques), 
 may break down into a shallow ulcer; on such ulcers throm- 
 bi may be formed. 
 Experimental arterio-sclerosis, due to strain hypertrophy and over- 
 strain atrophy. 
 Fatty degeneration 
 Fatty infiltration 
 Calcification in arteries in horses, in cattle sometimes. 
 
 Aneurisms. 
 
 9 
 
CAPII.LARIES. 
 
 Thrombosis 
 aneurisms 
 degenerations 
 References : 
 
 Read Krehl 2d. ed., pp. 35-44 
 
 Adami and Nicholls, pp. 115-203 
 
 Kitt S. 334-411. 
 
 BLOOD. 
 
 The blood ^s a tissue 
 formed elements 
 red corpuscles 
 leucocytes 
 blood plates 
 plasma 
 
 water, inorganic salts — phosphates^ chlorides, carbonates and 
 sulphates, ijon, serum albumin and small quantities of urea, 
 uric acid, glucose, glycogen, fat, acetone, ferments — oxidase, 
 lipase, proteolytic, glycolytic, diastatic. 
 Knowledge of the changes in chemical composition is of un- 
 doubted importance ; but substances are present in small amounts 
 and are of complicated structure. Importance of these, for example, 
 specific agglutinating or precipitating substances in certain infectious 
 diseases, e. g. glanders, typhoid, etc., substances producing im- 
 munity. 
 
 Main reliance in examining blood is on changes in the formed 
 elements and in amount of hemoglobin, changes in red corpuscles, 
 changes in Hb., changes in leucoc5rtes, presence of parasites. 
 Changes in quantity and quality of blood, 
 affecting red corpuscles and hemoglobin, 
 plethora — test too complicated for clinical use ; 
 amount of blood is increased by proper hygienic measures, 
 polycythemia increased no. per cmm. 
 
 produced in anhydremia, by withholding water, profuse 
 sweating, watery diarrhea (infectious diseases or by pur- 
 gative), rapid exudation ; in venous stasis, with increased 
 exudation, e. g. cardiac insufficiency, pneumonia, emphy- 
 sema and thrombosis of lungs, asphyxia, chloroform anes- 
 thesia (3 mill, in horses in 1/^ — 2 hrs.). 
 
 10 
 
cold baths, massage, muscular exercise and electricity. 
 
 lyocal polycythemia by ligature, pressure of tumor, partial 
 paralysis, after certain drugs, — pilocarpin, eserin, Glauber's 
 salt, phosphorus. 
 Age, sex, pregnancy, parturition, high altitude. 
 
 Anemia. Tallquist's Hb. scale. 
 
 Oligemia 
 
 oligocythemia 
 
 oligochromemia 
 
 Anemia occurs in * variety of conditions, the most important 
 
 of which are : — after hemorrhage, after marked exudation, 
 
 in diminished nutrition, in diminished activity of the blood 
 
 forming organs, in increased destruction of red corpuscles. 
 
 Changes in blood in anemia 
 
 obligochromemia 
 
 r megalocyte 
 anisocytosis ) 
 
 y. microcyte 
 
 poikilocytosis — poikilocyte 
 
 polychromasia 
 
 punctate bosophilia 
 
 r normoblast 
 „ J megaloblast 
 nucleated red cells i gigantoblast 
 
 Lmicroblast 
 Varieties of red corpuscles 
 
 r normocytes — small, medium, large 
 non-nucleated < microc5rtes 
 I, megalocytes 
 
 r normoblasts 
 
 nucleated^ microblasts , 
 
 r megaloblasts 
 [ gigantoblasts 
 
 11 
 
The blood in normal domesticated animals 
 
 Species 
 
 Red 
 
 corpuscles 
 
 leucocytes 
 
 hemoglobin 
 
 
 million per cmm. 
 
 per cmm. 
 
 per cent. 
 
 Horse 
 
 
 6j^-9 
 
 4000-9000 
 
 
 Avera 
 
 ge 
 
 7.215 
 
 
 94 
 
 Cow 
 
 
 4.8-7.9 
 
 2300-10,600 
 
 45-85 
 
 
 
 6.15 
 
 6000 
 
 60 
 
 Sheep 
 
 
 8 
 
 8000 
 
 
 Goat 
 
 
 9-10 
 9.976 
 
 9200 
 
 
 Dog 
 
 
 5.6-6.5 
 
 6000-10,000 
 
 
 
 
 6 
 
 8200 
 
 90 
 
 Cat 
 
 
 6.6 
 
 13,300 
 
 
 Swine 
 
 
 
 
 
 
 
 7.9 
 
 19,000 
 
 88 
 
 Rabbit 
 
 
 5-8 
 
 
 
 
 
 6 
 
 10,000 
 
 96 
 
 Guinea Pig 
 
 
 4.25-6 
 
 5550-21,000 
 
 85-100 
 
 5.276 
 
 10,000 
 
 94 
 
 normal 
 lymphocytes 
 
 , . , J large mon. 
 
 varieties of leucocytes^ , 
 
 polymorphs 
 
 pathological 
 myelocytes 
 eos. my el. 
 plasma cells. 
 
 eosms 
 .mast cells 
 Leucocytosis 
 
 polynuclear leucocytosis, lymphocytosis, eosinophilia, basophilia 
 Inflammatory leucocytosis 
 characterization 
 
 occurrence in stranges, pyogenic infections, abscesses, fistu- 
 lous withers, quittor, suppurations, wound infections, pneu- 
 monia (croupous, pleuro— , gangrenous, broncho—)', pleu- 
 ritis, tetanus, muscular rheumatism. 
 Course observed in patients; best seen in experimental cases, 
 initial stage (leucopenia) 
 increase (in from J^ to 4 hours usually) 
 
 polymorphs increase 85-95% ; eosins decrease ; eosins re- 
 appear at time of crisis. 
 
 12 
 
Measures the relation of severity of infection to resisting 
 powers of individual. 
 
 Infection mild, resistance good, small leucocytosis. 
 Infection less mild, resistance less good, moderate 
 
 leucocytosis. 
 Infection severe, resistance good, very marked leucocytosis. 
 Infection severe, resistance poor, no leucocytosis. 
 
 Post hemorrhagic leucocytosis 
 
 Ante mortem 
 
 lyeucocytosis of digestion 
 new born 
 
 post parturition and pregnancy 
 exercise and massage 
 cold baths 
 
 Bxperimental leucocytosis after administration of : 
 quinine, salicylate, mercurials and antimomials, 
 oil of mustard and vesicants, tuberculin, mallein, thyroid 
 extract, nuclein, antitoxin, lysol injections. 
 
 Lymphocytosis in young, after digestion, after administra- 
 tion of thyroid extract, pilocarpin, tuberculin, quinine, after 
 splenectomy, anemia (relative), with most splenic tumors, 
 during the initial stage of inflam. leucocytosis, in infec- 
 tious diseases with acute hyperplasia of lymph tissue, in 
 lymphatic leukemia 
 
 Eosinophilia. 
 
 high in young in man and dogs. 
 
 helminthiasis, Scherostoma equinum, Trichinella spiralis, 
 mange (Sarcoptic, Psoroptic), chronic skin diseases, de- 
 pends on intensity of dermatitis more than on extent or 
 duration of the disease. See Welch's art. Abstracts of 
 work done in laboratory of Veterinary physiology. No. 7, 
 1910, p. 17, 
 Basophilia 
 I<eucopenia 
 
 fasting, malnutrition, after short hot baths or long cold baths, 
 during initial stage of inflam. leucocytosis, in anemia (many 
 cases), in tuberculosis (often in non-septic), after injections 
 of ergot, tannic acid, sulphonal, atropin, agaricin, picro- 
 toxin, peptone, diastase. 
 
 13 
 
Iveukemia 
 
 characterization 
 
 (1) lymphatic 
 
 (2) mixed- celled (myelogenic) 
 
 Changes in the blood; red corpuscles diminished, may be 
 
 erythroblasts present. 
 Lym-phatic 
 
 Leucocytes much increased 100,000-1,000,000 per cmm., 
 lymphocytes 92-99%, other varieties scarce. 
 Mixed-celled (myelogenic) 
 
 leucocytes much increased 100,000-1,000,000, finely gran- 
 lar myelocytes, polymorphs, small lymphocytes, large 
 lymphocytes, eosins, eosinophilic myelocytes, mast cells 
 Pathological anatomy 
 
 Bone marrow — red marrow of ribs, vertebra, etc., lighter 
 colored and of firmer consistency, cellular hyperplasia of 
 lymphocytes or myelocytes, extension of lymphoid mar- 
 row in shafts of long bones and an atrophy of fat marrow. 
 Spleen enlarged, rich in cells, sometimes pulp cords, some- 
 times follicles or both, usually distinction not so clear as 
 in normal, sometimes boundaries indistinguishable, stro- 
 ma may be much increased. 
 Liver usually enlarged, capillaries widened and contain 
 many leucocytes (lymphocytes) , cellular infiltration be- 
 tween lobules, may be collection of cells in the lobules. 
 Lymph glands enlarged, cellular hyperplasia, boundaries of 
 follicles and medullary cords are commonly apparent 
 though sometimes indistinct, lymph sinuses and blood 
 vessels contain many leucocytes, reticulum sometimes 
 thickened making gland more firm. 
 May be masses of lymphocytes (in lymphatic variety) in 
 other organs, kidney, skin, serous membranes, central 
 nervous system, etc., appearing as grayish nodules. 
 Pseudo-leukemia group. 
 
 Marked enlargement of lymph glands and usually of the spleen. 
 Group 1. hyperplasia of lymph cells. Lymphocytomatosis. 
 Group 2. chronic productive inflam. changes, increased conn, 
 tissue and endothelial cells ; occurs in tuberculosis, syphilis, 
 and in cases with cause unknown. 
 Relation of leukemia to pseudo-leukemia and lympho-sarcoma. 
 See Report of Director of N. Y. State Veterinary College for 
 1910, p. 130. 
 
 14 
 
Pernicious anemia. 
 References. 
 
 Adami and Nicholls, pp. 19-32, 83-102. 
 
 Burnett, Clinical Path, of Blood of Domestic Animals. 
 
 Ewing, Clin. Path, of Blood. 
 
 Kitt, pp. 412-459. 
 
 SPI.EEN 
 
 Shape in different animals. 
 
 Physiological variations in size. 
 
 Hyperemia — active from intoxication or infection. 
 
 passive enlarged firmer, dark red color, capsule tense, 
 opaque ; often extensive pigmentation from disinte- 
 gration of red corpuscles. 
 Infarction from emboli, generally first white, later may become 
 
 hemorrhagic. 
 Acute hyperplastic splenitis. 
 
 enlarged in infectious diseases to Vi to 2-6x, capsule distended, 
 tissue at first firm and dark red (hyperemic), becomes soft or 
 even diffluent, color paler ; extensive hemorrhagic extravasa- 
 tions not uncommon. 
 Microscopically overdistension of vessels, proliferation of cells both 
 in pulp, or in Malphigian bodies, or in both ; degeneration of 
 cells — fragmentation of nuclei, lack of nuclear staining, cellular 
 detritus, fatty degeneration ; usually terminates in resolution. May 
 proceed to rupture, to suppuration or fibrous hyperplasia. 
 Suppurative splenitis. In septic processes. Usually embolic, ab- 
 scesses usually multiple, or by extension from adjacent suppuration. 
 Chronic indurative splenitis. 
 diffuse hyperplasia of conn, tissue, from repeated attacks of acute 
 splenitis or from long continued venous stasis (cirrhosis of liver). 
 Capsule thickened, consistency of organ usually increased, asso- 
 ciated with parenchymatous changes. May be adhesions, great 
 increase in trabecular tissue. 
 
 Tumors. 
 
 Sarcoma sometimes primary, Melanosarcoma usually secondary, 
 lymphosarcoma. Carcinoma (metastatic). 
 
 15 
 
LYMPH GIvANDS 
 
 Structure — cortical nodes, medulla, trabeculse and capsule, lymph 
 
 sinuses. 
 Function — filter for lymph, on guard at all orifices and channels of 
 body, to form leucocytes (Var. I). 
 
 Lymphatic tissue more prominent in young, becomes less in old. 
 Hyperemia practically only inflammatory. Normally contain 
 
 little blood. Glands reddened, enlarged, juicy. 
 Hemorrhages, in inflammations, occur readily. 
 Edema inflammatory or part of general anasarca. 
 Pigmentation. 
 Simple atrophy in old age. 
 Amyloid and hyaline degeneration. 
 Calcification — common in tuberculosis of cattle. 
 Lymphadenitis, due to infection somewhere, a common condition 
 (one of the most common) . 
 
 Acute lymphadenitis — glands swollen, injected and soft, on section, 
 surface smooth, reddish grey, in severe cases studded with yel- 
 lowish grey foci (areas of necrosis). 
 
 Microscopically — normal structure often unrecognizable, blood 
 vessels distended, hemorrhagic extravasations; lymph sinuses 
 filled with desquamated endothelial cells, red corpuscles and 
 leucocytes ; round cell proliferation in nodes, degeneration of 
 lymph cells, nuclei disintegrated, cells swollen. Ends in se- 
 vere cases in necrosis, may end in suppuration, or in indura- 
 tion where irritation is not severe but long continued. 
 Supptirative lymph- adenitis — from pyogenic infection, gland 
 
 softens, suppuration. 
 Chronic indurative lymph-adenitis — from acute or may start insidi- 
 ously. Gland enlarged, firm and dense ; hyperplasia of conn, 
 tissue of capsule, trabeculae and may also be of recticulum, de- 
 crease of lymph cells from encroachment of conn, tissue. 
 Pseudoleukemia group. Hodgkin's disease. Enlarged lymph glands 
 without increase of leucocytes in circulating blood. 
 
 Sub-group I. enlarged glands chronic productive in flammatory 
 process. 
 
 Sub-group II. Enlarged glands are growths of lymphocytes with 
 more or less framework of conn, tissue. Aleu- 
 kemic lymphocytoma. Hodgkin's disease. 
 Tumors— lympho-sarcoma, sarcoma, fibro-sarcoma, enchondroma 
 
 and carcinoma (metastatic). 
 
 16 
 
RESPIRATORY SYSTEM. 
 
 Primary function 
 
 Exchange of Oj and COj 
 
 internal respiration, the more important takes place in all the tis- 
 sues. Some of symptoms of anemia are like those of interfer- 
 ence with breathing. 
 
 external respiration 
 
 (1) disturbances in mechanism by which air reaches lungs and 
 and effects of these, 
 
 (2) disturbances in the air sacs and their effects, 
 
 (3) changes in composition of air entering lungs. 
 I. The respiratory mechanism. 
 
 (a) air passages. They are long, so air is warmed and made 
 moist before entering the air cells and is freed from dust and 
 foreign particles and so is sterile. 
 
 Complete obstruction leads to -death in a few minutes ; in- 
 complete to inspiratory or expiratory dyspnea or both, followed 
 according to amount by death by slow suffocation, by asphyxia 
 or by adaptation of respiration and needs of body to the lessened 
 supply of oxygen. With obstruction to inspiration, respiration 
 becomes slow and labored, diaphragmatic contractiorJs deeper 
 and other accessory respir. muscles into action to make thorax 
 as large as possible. The expirations are short and labored. 
 Inspiratory stridor. The reverse occurs in expiratory obstruc- 
 tion. Expiration slow and labored ; the accessory muscles 
 called into action are those which most lessen the size of the 
 thoracic cavity, especially the abdominal muscles and those 
 bringing the ribs closer together. With one bronchus affected a 
 period of rapid respiration followed by indications of adaptation, 
 the one lung being able to perform the function of both. Rapid 
 period due probably to different periods at which vagus inspir- 
 atory and expiratory stimuli are started in the two lungs. 
 
 (b) The muscles of respiration. — In ordinary quiet breathing in- 
 spiration is active, expiration passive. 
 
 (c) 7 he pleural cavities h-cK^Z about uniform expansion. When 
 lungs are attached to pleura, as in adhesions, there would be 
 unequal expansion. There is negative pressure in pleural 
 cavities. 
 
 Pneumothorax — deeper respiration 
 
 open, pressure positive, lung collapses. 
 closed, some slowing of rate, 
 
 17 
 
Pleural effusions — lessen space that may be occupied by lung, 
 may bring about complete collapse. With any quantity of 
 fluid, elasticity of lung is not effective. Fluid is under 
 positive pressure till amount becomes very small, 
 (d) The nervous mechanism. — Several separate factors, several 
 muscles, which must be regulated by center. Pulmonary 
 branches of vagus the main afferent nerves of respiration. 
 Center stimulated by increased carbon dioxide and depressed 
 not by increased oxygen but by decreased carbon dioxide ten- 
 sion. Over ventilation of the lungs may bring about arrest 
 of breathing due to lack of carbon dioxide, e. g. in surgical 
 " shock," painful injuries, to revive do not need more air, 
 but less or rather more carbon dioxide. 
 
 Coughhig. — Reflex due to irritation in the larynx (usuully), 
 in the lungs, or of the pleural surfaces. Deep inspiration 
 followed by closure of glottis during the first part ; with 
 sudden opening of glottis, air under pressure is freed car- 
 rying with it mucus, etc., in bronchi, trachea, or larynx. 
 Dyspnea is manifested under the following conditions : 
 
 (1) conditions of severe hindrance to entrance of normal 
 amount of air (a) in the air passages (leading to dimin- 
 ished ingress and egress of air (foreign bodies, imflam- 
 matory or other narrowings of larynx, trachea or 
 bronchi or compression from without ; (b) in the lungs 
 themselves — collapse, diminution of ventilating sur- 
 face by exudates into the alveoli, tuberculous and other 
 growths in lung substance, destruction of lung sub- 
 stance (gangrene, cavitation, etc.), fibroid inflamma- 
 tion, atrophy, emphysema. 
 
 (2) conditions affecting the muscular mechanism of respir- 
 ation (a) diseased conditions, inflam. etc., of the dia- 
 phragm or other respiratory muscles ; (b) pathological 
 condition of the main and secondary centers and of 
 the nerves forming the respiratory arc, paralysis or 
 irritation of the centers, trauma or destruction of the 
 afferent nerves (vagus) or again of the efferent nerves 
 (more particularly of the phrenics.) 
 
 (3) conditions affecting the circulation of the blood ; (a) 
 through the lungs (obstructive heart disease emphy- 
 sema) ; (b) through the medulla. 
 
 . (4) conditions modifying the constitution of the inspired 
 air— rarefaction of the air at high altitudes, reduction 
 
 1§ 
 
of the amount of contained oxygen, increased carbon 
 dioxide content, presence of carbon monoxide which 
 unites with hemoglobin preventing the taking up of 
 oxygen. 
 
 Asphyxia. Three stages. 
 
 1st. of increased amplitude as well as rate of the respira- 
 tory movements. 
 
 2nd. with increase of the expiratory movement out of all 
 proportion to the inspiratory, the expiration becoming 
 prolonged, the inspiration short and convulsive. 
 Whole musculature of the body may be called into 
 action to produce the.se violent expirations. 
 
 3rd. violent expirations cease almost suddenly and slow, 
 deep inspirations manifest themselves ; mouth widely 
 open, head back to give most free entrance of air into 
 trachea, body stretched, complete insensibility. In- 
 spiratory movements further and further apart, weaker 
 and weaker ; in few minutes last gasp. These changes 
 accompanied by changes in circulation most marked a 
 rise of blood pressure, in third stage heart begins to 
 fail, poisoned by venous blood. 
 II. Disturbances in the air sacs and their effects. 
 
 (a) those in which more particularly the entrance into and egress 
 from the air sacs of the proper amount of air is prevented. 
 
 by want of distension, as in atelectasis and collapse ; 
 
 by collection within them of fluid or solid matter, 
 
 (1) by serous fluid as in cases of acute or chronic con- 
 gestion, 
 
 (2) by blood as in rupture of an aneurism in branch of 
 pulmonary artery or of aorta into trachea, 
 
 (3) by water or other fluid from without, 
 
 (4) by inflam. exudates and migrated cells, as in pneu- 
 monia. Effects depend on extent of lung tissue in- 
 volved and on the cause. May not be noticeable, 
 may be rapid respiration, dyspnea and finally adapta- 
 tion or asphyxia and death. 
 
 Diffusion of products of coagulation and of death 
 of red corpuscles in cases of hemorrhage, of toxins 
 and cytolytic products in cases of pneumonia sets up 
 febrile state, and among other things affects the re- 
 spiratory centers, inducing an increased rate of 
 
 19 
 
breathing out of proportion to the extent of tissue 
 involved. 
 
 In a lobar pneumonia the pleura is involved. The 
 pleural surfaces painful — inhibits thoracic move- 
 ments — another cause of rapid and shallow breath- 
 ing. May fill air sacs of entire lung or lower parts 
 of both without fatal result. 
 
 Fluid agents tend to accumulate to lower portion — 
 vary with position of patient and may set up dis- 
 turbances in respiration during change. 
 
 Greater interference with circulation with disten- 
 tion of air sacs by solid contents. In collapse and 
 atelectasis no air pressure in air cells, blood flows 
 unhindered, vessels become dilated. 
 
 When serous fluid in sacs, in active or passive 
 congestion. When passive not in lung but obstruc- 
 tion in left heart, mitral or other disease. Dilation 
 of capillaries which continues, however great the 
 accumulation of serous fluid. 
 
 With coagulation, pneumonia and hemorrhagic 
 infarcts, passage of more and more substance into 
 air sacs, these become over-distended and pass from 
 state of congestion to narrowing and compression of 
 capillaries between air cells. If much lung affected 
 increases work of right heart, dilatation of right 
 heart, and some incompetence. Local necrosis and 
 gangrene are comparatively rare as a result of the 
 anemia. Do show sometimes, 
 (b) changes in walls of air sacs hindering aeration, 
 atropic — in vesicular emphysema, 
 interstitial deposits. 
 Emphysema overdistension 
 
 (1) increased difficulty of expiration leading to raised in- 
 traalveolar pressure. 
 
 (2) diminished elasticity of walls. 
 
 Bronchiectasis, dilatation, result is diminished aeration of 
 blood. 
 
 Interstitial deposits, fibrous conn, tissue as in chronic inter- 
 stitial pneumonia, actinomycosis or neoplastic • leads to 
 compression and diminution or even occlusion of air spaces. 
 Also obstructs circulation — double effect. 
 
 20 
 
MORBID ANATOMY OF THE I.UNGS 
 
 Blood supply — two sources. 
 Anemia 
 
 local — hindrance to flow of blood to lungs, as pressure of tumors, 
 
 emphysema, etc. 
 general — general oligemia, color clear, yellowish rose tint, in high 
 grade may be white yellowish tint. That is the case with 
 emphysema. 
 Edema. 
 
 Of common occurrence. The most frequent cause is relaxa- 
 tion at time of death. May be of entire lung or one or more 
 lobes. lyUngs become heavier and firmer than normal, pit on 
 • pressure, on section tissue filled with thin, watery fluid, shown 
 easily by pressing lungs with hands. When fluid removed lung 
 regains normal crepitant state. 
 Hyperemia, 
 passive — with cardiac lesions stenosis, insufficiency, most with 
 mitral insufficiency ; in chronic cases there is an increase of 
 fibrous tissue in walls of lung {cyanotic induration^ in brown 
 induration is also hemorrhage by dispedesis, blood pigment 
 freed and taken by large clear mononulcear cells ( ' ' heart fail- 
 ure cells") 
 active — functional, over exercise 
 
 lessening of air by obstruction or narrowing of upper air 
 
 passages 
 irritating gases 
 collateral 
 inflammatory 
 hypostatic — with obstruction to free outflow of blood from the 
 lung or lack of power in right heart, lower part affected. In 
 some infectious diseases, fatty heart; cloudy swelling of heart. 
 Hemorrhage. 
 
 Hemorrhagic spots in suffocation or asphyxia are dark red 
 punctiform sharply circumscribed hemorrhages, may be size of 
 small coin, on sub pleura over lungs, are numerous on costal 
 pleura, especially at greater angle of ribs. Occur in cases of 
 death with appearance of high grade difficulty of breathing. 
 Called by Kitt " haemorrhagia per suffocationem sive as- 
 phyxiam", 
 
 Hemorrhagic infarcts. 
 
 Embolism and thrombosis, fat, air, tumors, 
 
 21 
 
atelectasis 
 
 congenital 
 
 obstructive — bronchial obstruction 
 
 compressive, external pressure by fluids, air, elevated dia- 
 phragm, aneurisms, tumors, etc. 
 eviphysenia 
 
 interstitial, interlobular and bullous. 
 
 vesicular or alveolar — simple, ectatic, atropic. 
 
 An acute vesicular form of emphysema occurs in last stages 
 
 of all diseases where death occurs with marked difficulty of 
 
 breathing. 
 
 Chronic form is frequent in horses. The entire lung enlarged. 
 Effect of emphysema. In beginning enlargement of alveoli 
 
 may assist in exchange of gases. But as they become more en-* 
 
 larged, the walls press on the blood vessels and hinder flow of 
 
 blood, so hinders respiratory function. Blood cannot enter lung 
 
 so well, is held back in right heart — enlargement of rt. heart. 
 
 Passive hyperemia there and in venous system. 
 Inflammation of lungs from three sources — through blood, lymph, 
 bronchioles 
 
 In inflammation in lungs find exudate in alveoli as a rule in- 
 stead of in walls which are thin and permeable. 
 
 croupoits, fibrinous, lobar pneumonia, e. g. principal appearance 
 in contagious pleuropneumonia of horses, contagious pleuropneu- 
 monia of cattle, hemorrhagic septicemia of various animals, often 
 in swine plague, occurs in glanders in carnivora (cats, lions) 
 
 Is due to germs (specific ?) 
 
 Characterized by exudate, fibrinous in alveoli, affects alveoli and 
 bronchioles ; usually unilateral, 
 several stages. 
 
 1. congestion — engorgement of blood vessels, alveoli may contain 
 some serum, a few corpuscles and few leucocytes. 
 
 2. stag-e of red hepatization — lung dense, tumefied (larger than 
 normal) of consistency of liver, alveoli filled with fibrinous 
 exudate, more or less red corpuscles and leucocytes. I^euco- 
 cytes in walls of alveoli. Reaches its height at 5-6 days. 
 Pieces sink in water. 
 
 3. stage of grey hepatization. Affected lobes dirty greyish in 
 color, alveoli filled with leucoc5tes and fibrin. May scrape 
 off graular material ; pleura with fibrinous exudate. 
 
 4. stage of resolution. Fibrin granular, absorbed. Alveoli 
 filled with leucocytes ; on scraping surface of section con- 
 
 22 
 
tents of alveoli come out as plugs. Resembles pus. Fatty 
 degeneration of leucocytes. Exudate absorbed or partly ex- 
 pectorated. L,ymph glands swollen (softer than normal). 
 May be gangrenous areas, small usually, may be large in 
 affected part. Heart often fatty, also liver and kidneys. 
 Catarrhal or broncho-pneumonia. 
 
 Cause — irritants as dust, " cold ", in other diseases, often ter- 
 minal, hypostatic. Staphylococci and streptococci. Most fre- 
 quent in dogs (Kitt), in sheep and goats somewhat common — due 
 to lung worms. Is lobular, extends to alveoli from bronchioles. 
 First bronchitis, peribronchitis, then pneumonia. 
 Differentiation. 
 
 Catarrhal begins with bronchitis, has irregular course, ends by 
 atelectiasis (in young pigs) and induration, is lobular — limited 
 area. 
 Gangrene of the lungs. 
 
 Most often in horses following hemorrhagic croupous pneu- 
 monia, in cattle following introduction of foreign bodies from 
 rumen, and as metastatic (embolic) may be one area or several. 
 More rarely gangrenous pneumonia occurs in dogs. 
 Suppurative pneumonia. 
 Abscesses. 
 
 PLEURA. 
 
 Hydrothorax 
 Hematothorax 
 Emphysema of mediastinum 
 Pleuritis 
 
 serous and serofibrinous 
 
 hemorrhagic ' ' 
 
 purulent, suppurative 
 
 empyema of the thorax 
 chronic productive 
 Tumors 
 Parasites 
 
 RESPIRATORY PASSAGES. 
 
 Stenosis of trachea 
 Bronchiectasis and bronchi stenosis 
 Hyperemia 
 Hemorrhages tracheo 
 broncho 
 
 23 
 
edema of the glottis 
 laryngitis, tracheitis, bronchitis, 
 
 croupous, diphtheritic, necrotic 
 catarrhal 
 
 serous, desquamative, purulent 
 chronic productive 
 suppurative 
 tumors. 
 References. 
 
 Adami and Nicholls, p. 237-338. 
 
 Kitt, p. 146-333. 
 
 Henderson, Bui. Johns Hopkins Hosp., XXI, Aug. 1910. 
 
 24 
 
DISEASES OF THE STOMACH AND INTESTINES. 
 
 STOMACH. 
 
 Function 
 
 Blood supply, affected by disease of liver, directly and indirectly. 
 
 Volvulus in dogs 
 
 Bezoars 
 
 Dilation of stomach in dogs 
 
 Rupture 
 
 Autodigestion of mucosa — post mortem maceration, 
 
 Hyperemia — functional, active, passive 
 
 Anemia 
 
 Hemorrhage 
 
 Acute catarrhal gasrtitis . 
 
 morbid changes may be so slight as to pass unnoticed without 
 anamnesis. 
 
 Mucosa of pyloric part of stomach shows swelling with redness, 
 congestion in patches or diffuse. Small hemorrhages, punctiform 
 or larger, give mucosa a dotted or spotted appearance. Mucus 
 incresed glairy or sometimes purulent, may be blood stained. 
 Microscopically, secreting cells show cloudy swelling, goblet cells 
 numerous (mucous degeneration), cellular infiltration (round 
 cells?) of conn, tissue between glands and in the submucosa. 
 Interstitial blood vessels hyperemic, swelling and desquamation 
 of endothelium of lymph vessels ; on surface stringy mucus con- 
 taining clumps of epithelial cells, red corpuscles and leucocytes. 
 
 Chronic catarrhal gastritis. 
 
 Mucosa covered by greyish, thick, tenacious mucus, may be more 
 purulent, sometimes streaked with blood, more or less thickened, 
 forming ridges or folds, color dark brownish red, in advanced 
 cases slate grey. Discoloration due to blood pigment from hem- 
 orrhage. Mucosa may be increased to x 5 normal thickness. 
 Rarely mucosa thinner than normal. Mucosa may have warty 
 appearance due to proliferation of fibrous conn, tissue between the 
 glands. May be outgrowth of glands giving an adenomatous ap- 
 pearance. These two sometimes called hypertropic gastritis. 
 Other coats may show hyperplasia, so stomach wall may be much 
 thicker. Sometimes stomach, dilated by relaxation of muscles, is 
 thinner. 
 Mic. most striking feature is cellular infiltration in interstitial 
 
 25 
 
areolar tissue, especially in outer layers of mucosa, leading to 
 more or less separation of glands. Ducts are catarrhal, often tor- 
 tuous, dilated, cystic, secreting cells enlarged and more numerous. 
 Other forms of gastritis 
 
 hemorrhagic leading to erosions in mucosa, 
 phlegmonous , 
 
 tuberculosis occurs, but is rare, 
 poisoning 
 Gastrophilus "erosions" shallow not of importance in ordinary 
 
 cases 
 Parasites, long list. (See text books). 
 Tumors. 
 
 INTESTINES. 
 Hernia 
 
 strangulation (by lipoma) 
 volvulus 
 prolapse 
 invagination 
 
 intusseption, happens sometimes at death, 
 dilatation (sometimes is distended by gas after death), 
 phytoconcrementa, pili concrementa, bezoars, hair, wool, bristles, sab- 
 
 bura coli, mixture of sand, silt, hay and straw and other portions 
 
 of fodder, enteroliths 
 hyperemia 
 hemorrhage diffuse, capillary, punctiform, hemorrhagic erosions, 
 
 diffuse stasis. 
 
 necrosis 
 
 
 
 gangrene 
 
 
 
 Inflammation 
 
 
 
 duodenitis 
 
 typhlitis 
 
 gastro-enteritis 
 
 jejunitis 
 
 coliti 
 
 
 ileitis 
 
 proctitis 
 
 
 Acute catrrrhal enteritis. 
 
 one of the most frequent affections. May accompany many dis- 
 eases. Mucosa appears in places or throughout its entire extent 
 reddened, (hyperemia), sometimes confined to villi, sometimes 
 about Peyer's patches which are swollen and project as nodules 
 follicular catarrh" . May lead to small crateriform ulcers. In- 
 creased amount of secretion, mucus may be blood stained. Sub- 
 mucosa infiltrated with fluid. Intestinal contents in large intes- 
 tines thin. 
 
 26 
 
Chronic catarrhal enteritis. 
 
 Mucosa dark red in streaks and spots, sometimes slate grey, 
 vessels dilated and tortuous, surface covered by glairy mucus. 
 Follicles are at first swollen, later atrophy and disappear when 
 mucosa has an areolated appearance, contents watery. Mucosa 
 generally thickened, may be thinned, compact and wrinkled by 
 proliferation of interglandular and submucous conn, tissue. 
 In large intestine follicles frequently prominent as nodular swell- 
 ings, may form ulcers. 
 
 Hemorrhagic enteritis, colitis,, etc. 
 
 diphtheritic, superficial necrosis. 
 
 croupous or membranous 
 
 ulcerative hog cholera, i. e. B, necrosis, tuberculosis 
 
 Tuberculosis 
 
 Actinomycosis (rare) 
 
 Glanders 
 
 Parasites, very many kinds and many individuals. 
 
 See I,aw, Kitt, Neumann. 
 Tumors 
 
 Lipoma in serosa containing adipose tissue, in mesentery, 
 omentum, diaphragm, sarcoma, lymphosarcoma, melanoma, 
 leiomyoma, adenoma, adenocarcinoma, carcinoma, 
 Sequelae of diseases of the intestines. 
 
 Many complications, in general all diseases of the intestines tend 
 to interrupt the digestive function, destroying absorption, hin- 
 dering excretion, shown both as diarrhea and constipation. 
 Law of vicarious ftinction. When one organ or system fails to per- 
 form its function, others will attempt to take up the work and do 
 it as well as they can, e. g. elimination of urea from skin in 
 chronic Bright's disease, stomatitis and diarrhea not an uncom- 
 mon result; ulcer of the lower bowel sometimes. Exposure to 
 heat and cold frequently followed by diarrhea. 
 Number of serious disturbances may arise from resorption of se- 
 cretions. A certain amount is normal. Water in intestines, 
 feces more solid in large than in small. A considerable amount 
 of bile salts and pigments are resorbed from the intestines. Under 
 ordinary circumstances resorption is followed by no ill effects, 
 when excessive there is. 
 
 Bile is absorbed into the circulation when there is obstruction to 
 its flow into the intestines. By calculi, catarrh of fine ducts, 
 tumors of bile ducts or head of pancreas, enlarged glands or ab- 
 scesses at hilus of liver and tumors of liver. Jaundice (icterus), 
 
 27 
 
digestive processes interfered with, feces clay colored, pulse slowed 
 dullness, itcininess of skin, lessened coagulability of the blood. 
 Resorption of bile depends on degree of obstruction and viscidity 
 of bile. With thicker bile less obstruction produces jaundice. 
 Thick viscid bile may be absorbed in cases of catarrh of the finer 
 bile ducts. 
 
 Obstruction to free outflow of pancreatic juice may be followed by 
 serious results. May lead to fibrosis, if of a lateral branch — cyst 
 formation — may be very large cysts. If large areas of secreting 
 cells are destroyed may be interference with the internal secretion — 
 glycosuria, obsruction may be by tumors in head of pancreas or cal- 
 culi. If it allows bile to enter pancreas ; hem. pancreatitis follows 
 with fat necrosis. Fat necrosis occurs in other conditions of dis- 
 ease of the pancreas, rarely in cases of suppuration. 
 (Read in Adami and Nicholls, pp. 372-380.) 
 
 PERITONEUM, OMENTUM AND MESENTERY. 
 
 Hydrocoecle, 
 
 hematocoele, 
 
 pyocoele, 
 
 pneumatosis peritonii, 
 
 emphysema of the intestines, peritoneum, 
 
 some cases due to B. coli, gas cysts always on small intestine; 
 gas cysts come from lymph vessels, often in healthy slaughtered 
 swine, 
 ascites. 
 
 serous peritonitis 
 
 chronic productive peritonitis, may be adhesions between intestine 
 and body wall, intestine and sometimes 'liver, different loops or 
 part. 
 Omentitis, mesenteritis, perihepatitis, perisplenitis, 
 perimetritis, perigastritis perityphlitis, 
 tuberculosis 
 actinomycosis 
 Parasites. 
 
 Filaria, Sclerostoma bidentatum, 
 Stephanurus denticulus, lyingulatula denticulata, 
 Cyysticercus tenuicoUis, Echinococcus. 
 Tumors 
 
 Carcinoma, primary once reported in horse ? 
 melanoma, sarcoma, lipoma. 
 
 28 
 
IvIVER. 
 
 Appearance of liver in cadavers, 
 color cold 
 horse chocolate brown 
 
 normal weight 
 
 3-4 Kg. in old ; 6-8 in younger 
 
 during digestion. 
 
 cattle 
 
 chocolate brown 
 
 4.5 Kg. average 
 
 
 (in steer and ox- 
 
 
 
 en, red brown) 
 
 
 sheep 
 
 clear chocolate 
 brown. 
 
 370-870 gm. 
 
 goat 
 
 
 370-870 gm. 
 
 swine 
 
 clear chocolate 
 
 1-2 J^ Kg. (in fasting fattened 
 
 
 brown 
 
 swine 500 gm. difference). 
 
 dog 
 cat 
 
 bright red brown 
 
 small 90-250 gm. ; large 500 gm.— 
 \% Kg. 
 80-120 gm. 
 
 still with body heat livers are clear brown to greyish yellow. 
 Hemocysts serosa hepatis. In sound slaughtered calves peculiar large 
 
 cysts, congenital blood cysts in the liver. Besides these cysts 
 
 liver otherwise normal. 
 Anemia. Part of a general anemia or due to local disturbance as 
 
 pressure on the liver or swelling of parenchyma. 
 Hyperemia. 
 
 Active. Physiological after a meal. Patholog, in early stages of 
 acute hepatitis and in all cases of congestion of the gastro-in- 
 testinal vascular system. 
 
 Passive. Brought about by anything that raises the pressure in 
 the hepatic vein and vena cava. Among others stenosis or in- 
 sufficiency of mitral or tricuspid valves, cardiac weakness, em- 
 physema of lungs, indurative pneumonia, right sided pleural 
 effusions, aneurisms, tumors, or enlarged glands pressing on 
 the post cava. 
 
 In early stages liver is enlarged, soft, full of blood, which drips 
 out on section. Color dark, purplish red ; after blood has been 
 drained out, liver will be found to be somewhat shrunken {red 
 atrophy). I,ater liver is smaller, firm, with finely granular sur- 
 face. On section, appearance like that of a nutmeg (nutmeg 
 liver) due to central congested part of lobule being depressed 
 below general surface, the periphery being pale yellow or yel- 
 
 29 
 
lowish brown and swollen, due to fat in secreting cells. May- 
 be redder patches — regenerated lobules. In most advanced 
 stage liver small and hard, due to conn, tissue formation 
 (cyanotic induration). 
 Hemorrhage, rupture, infarction (rare), acute yellow atrophy, 
 
 infections. 
 Cloudy swelling. 
 
 Fatty liver, common sequel of cloudy swelling, occurs in severe 
 anemias, acute yellow atrophy, congestion, intoxication (phos- 
 phorus and arsenic). 
 Amyloid, occurs in horses, dogs, cattle, sheep, rabbits and poultry. 
 In cachectic conditions, suppuration. 
 
 Liver generally enlarged, rounded edges, consistency increased 
 somewhat, amyloid centers sometimes evenly spread, some- 
 times irregularly. Liver contains but little blood. In hens are 
 scattered nodules. Gross appearance gelatinous, semi-translu- 
 cent. Liver cells atrophied and fatty. 
 reaction Lugol's sol. mahogany red 
 
 H2SO4 dilute grey to violet blue 
 
 methyl violet aniline red. 
 
 Necrosis. As multiple nodules, often in livers of cattle and sheep 
 and pigs due to B. necrophorus. Liver enlarged, foci from size 
 of pea to walnut, round, hard, dry, yellowish and often sur- 
 rounded by capsule of conn, tissue. 
 
 Chalky nodtiles in horse livers. M.2cy be glanders, more likely to 
 be parasites. 
 
 In sheep Oesophagostoma columbianum. 
 Atrophy. In dog and cat can lose Yi of volume in starvation. 
 
 Compression atrophy. Of some part of liver not infrequent ; most 
 common is the atrophy of right lobe in old horses, sometimes 
 also the left, from pressure of the colon. 
 Acute parenchymatous hepatitis. 
 
 Causes — damaged fodder, mechanical, excessive heat, poison, in- 
 fectious diseases. 
 
 Appearance very closely resembling that of cloudy swelling. 
 Liver slightly enlarged, edges blunt, soft and friable ; pale yel- 
 low, clayey color ; lobes may be adherent, perihepatitis, may 
 be adherent to diaphragm. 
 
 Mic. appearance ; cells swollen and granular, nuclei pale ; fatty 
 degeneratiion, hyperemia interlobular ; may be collections of 
 leucocytes in portal sheaths. 
 May be considerable necrosis, pigment in cells, liver becoming 
 
 30 
 
smaller. Acute yellow atrophy (most frequently seen in lupino- 
 sis in sheep and horses) a very acute form of parenchymatous 
 hepatitis Diminution in size of organ ; softeaing and yellowish 
 discoloration of parenchyma, liver cells show granular and fatty 
 degeneration, contain pigment, necrosis extensive, 
 extensive icterus acute yellow atrophy, considerable hyperemia 
 acute red atrophy (commonly fatal termination). 
 Suppurative hepatitis. 
 
 (1) from infection of bowels or metastasis from hepatic arteries, 
 e. g. in pyemia, glanders and acute infections. 
 
 (2) from thrombosis of portal or umbilical veins e. g. omphalo- 
 phlebitis. 
 
 (3) foreign particles from stomach, bowels or blood — fodder, bar- 
 ley awns, parasites. 
 
 (4) mechanical injuries, from inflam. of bowels, gall stones, etc.; 
 sometimes minute multiple abscesses, sometimes larger ; 
 may be few or many, sometimes confluent, sometimes single. 
 
 Chronic productive hepatitis. 
 Hyperplasia of conn, tissue which in time becomes sufficient to 
 interfere much with function of liver. Due to irritation of 
 toxic substance reaching liver through portal circulation (hep- 
 atic artery?) or bile passages. In horses, swamp fever or in- 
 fectious anemia of horses, in dogs with valvular disease of 
 heart. More than one cause. Cause is ordinarily not severe 
 but is mild and long continued e. g. alkali in swill for pigs. 
 Surface granular, nodular or even lobulated in much protracted 
 cases, capsule thickened, color at first brownish, later light 
 yellow, organ bloodless. 
 
 On section shows whitish narrow bands of conn, tissue sur- 
 rounding the yellowish lobules. 
 
 Microscopically first infiltration of small cells in periportal tis- 
 sue, later development of conn, tissue. 
 
 Usually is an interstitial productive hepatitis. Sometimes dif- 
 fuse, e. g. " Pictou disease" in cattle. Also in other cases 
 besides "Pictou disease." In diffuse form proliferation of 
 conn, tissue within lobules isolating small groups of liver cells. 
 Changes in other organs, hyperemia and chronic catarrh of 
 stomach and intestines, enlarged spleen, ascites, anasarca, hem- 
 rhages in various organs. 
 
 Parasites. 
 
 Coccidosis in rabbits. Distoma hepaticum. 
 
 31 
 
Cysticercus tenuicollis, C. pisiformis, Echinococcus, more often 
 
 in cattle and swine, only once reported in liver of ass and horse. 
 Regeneration, in experimental cases can lose X. J^ or even }i 
 
 of liver and loss made good by regeneration of remainder. 
 Tumors. Adenoma in cow, Adeno carcinoma, and carcinoma 
 
 not so often as in man, sarcoma, (primary is rare), lipoma, tel- 
 
 angiescasis, hemangioma. 
 
 (melanosis maculosa of calves, spots on surface of liver and in 
 
 section). 
 Effects of disease of the liver on other organs. 
 References. 
 
 Ad ami and Nicholls. 
 Kitt, pp. 612-708. 
 Ivaw, Vol. V, pp. 332-364. 
 Neumann, pp. 421-464. 
 
 32 
 
URINARY SYSTEM. 
 
 Structure of the kidneys. 
 Function of the kidneys. 
 
 external excretion seems to be the function, are chief eliminative 
 organs of the body. Other eliminative organs for toxic sub- 
 stances are intestines, liver, lungs and skin. Most of water in 
 urine passes out through glomeruli, discharge of urine influenced 
 largely by circulatory conditions. Blood pressure reduced to 40 
 mm. Hg or lower secretion ceases ; with increase of amount of 
 blood passing through kidneys the amount of urine is increased. 
 But with renal vein ligated blood pressure in kidney is very much 
 increased but no urine is secreted. 
 
 Water of urine is mostly discharged from glomeruli, nature of 
 selective discharge, not a mere filtration, also some simple salts, 
 e. g. peptone, glucose. 
 
 In tubules may be some absorption but resorption is secondary, 
 main function of this part is to excrete urea, uric acids and ex- 
 tractive bodies of the nature of toxins. Formation of hippuric 
 acid. 
 
 Nerve supply. Form a fine plexus around renal artery, largely vaso- 
 motor ; network of filaments in cortex and medulla with ends on 
 Bowman's capsule and in membrana propria of convoluted tu- 
 bules, probably secretory in function. 
 
 Amount of urine seems to depend on glomerular blood supply 
 which in turn depends on the tone of the interlobular arteries. 
 Glomeruli themselves probably passive, no nerves have been 
 demonstrated in them. Constituents may exert some influence 
 indirectly on walls of glomeruli. 
 
 Contraction and expansion of arterioles may be due to central 
 nervous influence or directly by action of substances diffusing out 
 from the circulating blood. 
 Relationship of vascular disturbances and chronic interstitial 
 nephritis. 
 
 Continued rise in blood pressure — muscular coat of cortical arter- 
 ies hypertrophied — degeneration of glomeruli— others undergo 
 compensatory hypertrophy and become more pervious than 
 usual — more fluid passes through. 
 
 When glomeruli atrophy or become impervious it cuts off sup- 
 ply from tubules in cortex, especially convoluted, they undergo 
 
 33 
 
degeneration. No urine from glomeruli or from the tubules. 
 In both cases the trouble is with blood supply. 
 Conclusions. 
 
 Quantity of urine discharged depends on quantity of blood pass- 
 ing through the glomeruli. Flow depends on difference in pres- 
 sure between renal artery and vein. Greater arterial pressure 
 without increase in venous then greater amount of blood passing 
 through glomeruli and greater urine excreted. 
 Pressure in vein increased without increase in artery then urine 
 diminished. 
 Polyuria. 
 
 Brought about (l) by increase in the general arterial pressure 
 without renal change (2) dilatation of cortical arteries without 
 of necessity any rise in general blood pressure (diabetes insipidus). 
 
 Perhaps another group. 
 Two groups of diuretics (l) those, inducing increased blood. pres- 
 sure with better circulation through the kidneys e. g. digitalis. 
 (2) those having little or no effect on general blood pressure, 
 e. g. dextrose, urea, sodium chlorid and other saline diuretics. 
 Question whether they dilate renal vessels or stimulate the 
 renal cells. 
 Oliguria and Anuria. 
 
 Brought about (l) by direct contraction of afferent arteries (as 
 through action of adrenalin), (2) by lowering arterial pressure, 
 (3) by rise in venous pressure e. g. valvular disease) may be a 
 fourth, obstruction to outflow if it affects both kidneys (either in 
 tubules or in ureters, etc.) 
 Hydronephrosis . 
 Hemoglobinuria. 
 Chyluria. 
 
 Aplasia. One may be absent 
 Cysts. Common. Supposed to be due to retention due to imperfect 
 
 fusion of collecting tubules with secreting portion. 
 Oliguria. General 
 
 local (anemic infact.) 
 Hyperemia. * 
 
 Active, in acute inflam., various intoxications, forcibly acting left 
 heart, and so on. 
 
 Passive, usually due to obstruction in general circulation as val- 
 vular heart disease, or pulmonary trouble. 
 Kidney enlarged, firmer than normal, capsule peels off easily. 
 
 34 
 
Stellate veins are injected, surface has dark purple red, or cya- 
 notic appearance. On section organ very firm, drips blood and 
 has uniform dark red appearance. 
 
 Microscopically vessels all enlarged and congested. Bowman's 
 capsule contains albumen and may be red cells and tubules con- 
 taining a few hyaline casts. Some of epithelial cells (those of 
 descending loops especially) contain pigment (from blood). In 
 long standing cases capillary and venous walls are thickened. 
 There is increase in interstitial conn, tissue and sometimes a round 
 celled infiltration in interstitial tissue — "cyanotic induration." 
 In some cases epithelium of tubules is fatty. 
 Infarction. Usually anemic, due to plugging of one of branches of 
 
 renal artery. 
 Arteriosclerotic contracted kidney. 
 
 A form of granular kidney due to narrowing and finally ob- 
 struction of afferent blood vessels. May be restricted to renal 
 artery and its branches or may be part of a general arteriosclerotic 
 process. Chronic proliferation of intima or media leads to col- 
 lapse of glomerular capillaries and atrophy of glomerular tufts. 
 Tufts become rounded hyaline masses, glomeruli atrophy. Tu- 
 bules become collapsed and atrophied. As the various structures 
 atrophy they are replaced by conn, tissue which shrinks forming 
 scar. Surface of kidney becomes granular. Capsule somewhat 
 adherent. Color bright red or greyish red, or may be streaked 
 with yellow, due to fatty degeneration. Organ smaller in size and 
 firmer than normal. Cortex narrowed and distorted. Glomeruli 
 appear as whitish dots. The smaller arterioles are easily recog- 
 nisable, due to the increased thickness of their walls. Pelvis 
 relatively large and filled with fatty tissue. Narrowing of cortex 
 and medulla. May not be easy to distinguish from inflammatory 
 contracted kidney. Cause different, though. 
 Senile atrophy, 
 parenchymatous degeneration. Sometimes difficult to draw the line 
 
 between this and inflammation, 
 amyloid, not so common in domesticated animals as in man : 
 mostly after chronic suppurative process, not after every suppura- 
 tive process so must be some other condition. In walls of arteries 
 and arterioles. After tuberculosis in birds, in man after tubercu- 
 losis. 
 Nephritis. Besides kidneys, organs that eliminate toxins are intes- 
 tines, liver, lungs and skin. Troubles of these organs interfering 
 with their functions add to work of kidney e. g. water from kid- 
 
 35 
 
ney during cold weather, sweat lessened ; urea excreted from the 
 skin when kidneys fail to perform their function. Infection most 
 important cause of acute nephritis. Sometimes follows gastro- 
 enteritis. May occur after sudden chilling of body. With cer- 
 tain drugs Hg, Pb, cantharides, KCIO3, salicylic acid, phosphorus. 
 In course of acute infectious diseases, hog cholera, pneumonia, etc. 
 Acute parenchymatous nephritis. 
 
 Characterized by marked degeneration of epithelium of secreting 
 tubules with congestion and exudation of serum and desquama- 
 tion of epithelial cells. Degeneration is cloudy swelling and 
 fatty degeneration. In early stage may be difficult to determine 
 whether it is cloudy swelling or actual nephritis. With conges- 
 tion, exudation and desquamation inflam. shown. Changes in 
 urine. Kidneys usually more or less swollen and edematous. 
 Capsule peels off easily, bulging of kidney through cut. Surface 
 of kidney pale, veins injected; cortex pale, swollen, cloudy, in 
 contrast to the dark red, or bluish red medulla. Sometimes cor- 
 tex somewhat congested. Oftentimes can see petechiae on sur- 
 face and in cortex. 
 
 Microscopically. Convoluted tubules most affected. Cells swollen, 
 granular, often vascuolated, nuclei stain poorly or not at all. 
 Hyaline or granular casts in tubules, especially in collecting. 
 Desquamated cells often found. Sometimes blood in tubules. 
 Glomeruli show signs of degeneration. Epithelium lining Bow- 
 man's capsule swollen and often desquamated. Hemorrhage in 
 capsule sometimes. Sometimes blood and blood casts may appear 
 in the urine. This may be called Acute hemorrhagic nephritis. 
 Interstitial tissue swollen and edematous and sometimes a round 
 celled infiltration between tubules, and may be some fibrin between 
 tubules. In some cases glomeruli affected. It is then an Acute 
 glomerulo -nephritis. Kidney doesn't show much gross change 
 somewhat cloudy and hyperemic, glomeruli swollen and show as 
 reddish or pale greyish dots. Microscopically may be (l) degen- 
 erative or (2) proliferative changes in glomeruli. 
 
 (1) capillaries congested or hyaline degeneration, epithelium 
 lining Bowman's capsule degenerated and desquamating. 
 Space in capsule is filled with degenerated epithelium, red 
 corpuscles, leucocytes, albumen and granular material. 
 
 (2) lining cells show proliferation. 
 
 Desquamative papillary nephritis a form of acute parenchymatous 
 nephritis. 
 
 36 
 
Acute diffuse nephritis. With parenchymatous changes find also 
 exudation into interstitial tissue and edema and purulent exudate- 
 Parenchyma and supporting tissue about equally affected. Lesions 
 most marked in cortex, as that is the most acive functionally. 
 
 Chronic diffuse nephritis. Chronic nephritis, non-indurative, large 
 white kidney. 
 
 Combination of interstitial inflam. with degeneration of parenchy- 
 matous cells, slow course. Changes like those found in acute and 
 sub-acute stages, but more extreme. Chronic parenchymatous, 
 chronic hemorrhagic and chronic glomerulo-nephritis. Gross. 
 Kidney is enlarged, soft and doughy, capsule peels readily, sur- 
 face smooth and greyish yellow or greyish white. Sometimes in- 
 jected veins or minute hemorrhages. Color due to degenerative 
 changes, necrosis and fatty degen., partly to anemia. Color may 
 be uniform or blotchJ^ patches of congestion alternating with pale 
 areas. Cortex pale uniformly or patchy with occasional areas of 
 congestion. Medulla dull red, congested, in marked contrast 
 with pale cortex. With much hemorrhage is chronic hem. 
 nephritis. Microscopically varies somewhat. Fat or soaps in 
 epithelium of glomeruli and tubules and even in endothelium of 
 blood vessels. With this is infiam. edema, leucocyte infrltration 
 in interstitial tissue. In more advanced cases indications of 
 atropy of glomeruli and secreting epithelium of tubules and a 
 little secondary fibrosis. 
 
 White spotted kidney of calves — Nephritis fibro-plastica not infrequent. 
 Rare in adult cattle so probably is transitory. Kitt thinks this 
 becomes multiple and diffuse sclerosis which is frequent in adult 
 cattle. 
 
 Chronic indurative nephritis — chronic productive nephritis. 
 
 Purulent nephritis, infection from blood or bladder. 
 
 Diffuse suppurative infect, from blood, micrococcus chiefly. 
 
 Capsule contains many small abscesses, many also in cortex, oc- 
 curs chiefly in pigs and calves. 
 
 abscess, chiefly from emboli, as in horses during strangles, in cattle 
 due to purulent pyelo- nephritis, single or several abscesses. En- 
 tire kidney may be a fluctuating abscess. 
 
 Pyelonephritis from bacteria 
 
 Pyelitis 
 
 Nephrolithiasis 
 
 Parasites Eustrongylus gigas, Cysticercus cellulosus, 
 
 larvae of sclerostomes, Echinococcus, 
 
 Stephanurus dentatus, Coccidia 
 Tumors adenoma, adeno-carcinoma. 
 
 37 
 
OSSEOUS SYSTEM 
 
 Rickets. Doubtful as to its nature ; by some thought to be due to 
 infection or intoxication and so to some extent inflammatory ; 
 but it is closely dependent on malnutrition. It may be regarded 
 at present as a disorder of growth. Occurs in the young. 
 Pathological changes. There is excessive absorption of bone 
 with impairment of the process of calcification. Normal process 
 of lacunar bone absorption is much increased, so solidity of 
 greater part of the skeleton is more or less destroyed. External 
 denser layers become porotic and the trabeculae of the spongy 
 part are attenuated and may even disappear. There is early a 
 formation of new bone that is deficient in lime salts (osteoid 
 tissue), derived from periosteum and marrow, which are ex- 
 tremely vascular. When arising from the marrow the new sub- 
 stance is like the internal callus. The trabeculae from the perios- 
 teum are formed in much the same way as the outer callus, are 
 composed of cellular or cellulo-fibrous tissue. 
 
 In the periosteum of the long bones cartilage is often laid 
 down, which later is transformed. So bones are covered with a 
 vascular spongy layer, especially at junction with the epiphyses. 
 In extreme cases the original bone becomes porotic. Enchondral 
 ossification is interfered with ; spicules or none at all in zone of 
 calcification. There is always an enlargement of the proliferation 
 zone of cartilage, the columns of cartilage cells longer. Vascu- 
 lar marrow spaces, which gradually encroach on the solid carti- 
 lage, are formed. As the disease heals lime salts are deposited. 
 Bones may become harder and denser than normally. 
 Hyperemia active ; passive, chronic passive hyperemia appears to 
 favor growth of bone, e'. g. clubbed fingers and toes in man in 
 chronic pulmonary and cardiac affections. 
 Hemorrhage is not very uncommon. As a rule blood is readily ab- 
 sorbed in bone 
 
 Hemomel anosis of the bones in slaughtered cattle. 
 Embolism. There are abundant anastomoses in bone, except at the 
 
 ends of diaphyses. 
 Thrombosis — not of practical importance. 
 
 Retrogressive metamorphoses . The structure of the bones in health 
 is constantly changing. In the young production predominates, 
 the bones increase in size ; in the old resorption is in excess so 
 
 38 
 
bones become smaller and lighter. I^acunar resorption takes 
 place, both in normal and pathological conditions, by means of 
 osteoclasts, situated in the periosteum and bone marrow. These 
 take position on the bony trabeculae and erode their way into the 
 bone forming excavations called Howship's lacunae. 
 Atrophy. In rapid resorption of bone osteoclasts are increased 
 and lie close together. Surface of bone eroded and rough. 
 When it begins at center excentric atrophy, in outside concentric 
 atrophy. 
 
 In some cases compact bone becomes porous, due to widening 
 of Haversian canals. This known as osteoporosis. Atropied 
 bones are light and easily broken. Marrow varies in appearance. 
 Sometimes hyperplastic, resembling lymphoid marrow ; fatty or 
 fat may be replaced by semitranslucent, gelatinous material 
 serous atrophy. 
 
 Atrophy of bone may arise as senile, marantic, from pressure, 
 from disuse or neuropathic disorders. Inflammatory atrophy 
 may follow inflammation. 
 
 Death of bone. Caries is slow death, in fine particles, is analogous 
 to suppuration of soft tissues ; due practically always to inflam- 
 mation. Necrosis may be due to inflammation, interference with 
 circulation, traumatism or chemical or thermal agents. Ordina- 
 rily the necrotic part of bone becomes separated from the healthy 
 part by zone of inflammation where resorption and exfoliation 
 are actively going on. Such a piece is called a sequestrum. 
 Halisteresis. Organic substances remain unalte'red, but lime 
 salts are diminished, so bone becomes soft and yielding. May 
 be in restricted area or may be general. When more extended is 
 known as osteomalacia. In general there is decalcification of 
 old bone with a tendency to form new which remains imperfectly 
 calcified. Decalcification begins at the periphery of bone trabe- 
 culae and gradually goes deeper. It occurs in adults, may be in 
 young. It is not an anomaly of growth. 
 Inflammation affects the vascular structures chiefly i. e., the perios- 
 teum and bone marrow, periostitis and osteomyelitis . Compact 
 bone may be involved secondarily in either condition, ostitis 
 usually in the form of erosion and disintegration. 
 Periostitis is the most frequent in the domesticated animals. 
 Due to local or systematic causes, usually traumatic, may be in- 
 fectious or toxic. Results vary. Mild inflammations that are 
 treated early and efficiently may heal without noticable effect. 
 
 39 
 
Often there are serious results (a) disintegration, (b) prolifera- 
 tion ; may be both processes together. 
 
 (a) necrosis is a marked feature in many acute and chronic in- 
 flammations. It may be slow eroding {caries), or exfoliation of 
 larger masses {sequestration) . Bone may h&come. parotic, owing to 
 lacunar resorption, resulting from action of granulation tissue in 
 the medullary spaces, {rarefying' ostitis). 
 
 (b) Bone formation may be stimulated, e. g. near abscesses, se- 
 questra, injuries, etc. The bone becomes harder and denser by 
 deposit of more bone on the trabeculae {osteosclerosis)). 
 
 Acute simple periostitis, a simple aseptic inflam. Cellular in- 
 filtration, tissue swollen, reddened, with scattered hemorrhagic 
 spots ; may be hemorrhagic periostitis when hemorrhage is 
 marked feature. Acute simple periostitis is present in fractures. 
 Chronic fibro-plastic periostitis . In this form the tissue of the 
 periosteum is increased. Is longer continued than the above. 
 With repeated trauma ; may be chronic from the beginning. 
 Usually passes into the next form. 
 
 Chronic ossifying periostitis. Frequent in the horse and cow. 
 There is an increase of the inner layer, osteoblasts. May be 
 diffuse or local. 
 
 Exostoses or osteophytes , hyperostosis , paraostoses in connective 
 tissue near bone not joined to bone. 
 
 Suppurative periostitis, due to infection usually from external 
 injury ; may be hematogenous, then belong to group of septi- 
 cemic affections ; may extend from marrow or from neighbor- 
 ing tissues (skin). Is severe, involves neighboring parts. 
 Characterized by suppuration and necrosis. In the acute form 
 the affected region swollen, tense, reddened and intensely 
 painful. May extend to bone marrow {osteomyelitis) Some- 
 times epiphyses and joints involved. In mild cases may ter- 
 minate without much disturbance ; but owing to interference 
 to the circulation by pressure of exudates, larger or smaller 
 portions of bone necrose. May be in center or on surface. 
 Surface where periosteum has been lifted from bone. When 
 bone has been splintered, fractured or crushed, it is inflamed ; 
 may readily heal. If microorganisms are circulating they may 
 localize in the injured part and condition similar to infective 
 osteomyelitis and periostitis be produced. In a compound 
 fracture may be infection from without. 
 
 40 
 
Ostitis and osteomyelitis, inflammation of bone and marrow. 
 Rarefying; ostitis, bone becomes spongy, due to action of granu- 
 lation tissue in the medullary spaces ; absorption in lacunae and 
 Haversian canals. 
 Osteosclerosis. 
 Spavin and ringbone. 
 
 Suppurative ostitis and osteomyelitis. 
 
 A ciinomycosis . 
 
 Tuberculosis. 
 
 Echinococcus , the only parasite found in the bones. 
 
 Progressive metamorphoses. In adults waste and repair are bal- 
 anced. Sometimes waste may exceed. 
 Hyperplasia, cause sometimes obscure. 
 
 a. congenital and primary e. g. gigantism. 
 
 b. acquired and secondary e. g. after fracture and in some 
 cases of inflammation ; experimentally by driving ivory 
 pegs into growing ends. 
 
 c. In some cases due to chemical substances circulating in the 
 blood e. g. P, As. stimulate bone production experimentally. 
 
 d. associated with disorders of internal secretion e. g. acrome- 
 galy. 
 
 Prolonged passive congestion seems to favor overgrowth 
 e. g. clubbed fingers of those with chronic pulmonary and 
 cardiac affections. 
 
 It may be compensatory e. g. after fracture of tibia, fibula 
 increases in size. 
 
 Overproduction may occur in several ways — 
 
 hyperostosis , when bone is enlarged in whole or part, 
 osteosclerosis , when density is increased, 
 osteophytes or exostoses, local outgrowths, 
 enostoses, local growths within spongiosa. 
 Fracture, simple or uncomplicated ; compound or complicated. 
 Callus, after fracture repair begins in periosteum and marrow. 
 ' With injury is tearing and bruising of soft tissues with effusion 
 of blood ; moderate inflammation with exudation of fluid and 
 infiltration of leucocytes. This subsides in 5-6 days. About 
 the second day cells of periosteum and marrow show signs of 
 proliferation. This increases greatly in next few days and 
 endothelium of blood vessels joins in, so about 4th day the 
 osteoblastic layer of periosteum is changed into a vascular ger- 
 minal tissue. After 4th day germinal layer begins to difEeren- 
 
 41 
 
tiate into" chondroid and osteoid tissue which is rapidly con- 
 verted into bone. After a week ends of fractured bone are 
 embedded in large number of young osteophytes and bone 
 spicules. So about the ebiternal injury is produced a spindle 
 shaped sheath, the external callus. A continuation of this be- 
 tween the broken ends is the intermediary callus. 
 
 A callus is formed within the cavity of the bone (if a hollow 
 bone) constituting the internal callus. This is produced by 
 osteoblasts grouped in masses and are transformed into osteoid 
 and finally into osseous tissue. 
 
 In two or three weeks the ends of bone are united. Amount 
 of callus differs much depending on individual, condition of 
 bone, nature of fracture and amount of deformity. With forma- 
 tion of new tissue, is resorption. Broken ends become round- 
 ed, splinters are resorbed. Callus at end of 6th or 7th week is 
 rather soft and porous. The bony tissue becomes harder, so 
 the permanent or definitive callus is formed. After months or 
 years the permanent callus is modified further. 
 Tumors. They primarily belong to the connective tissue group. 
 They arise from the periosteum, marrow or cartilage. Fibroma, 
 chondroma, myeloma, osteoma, sarcoma, osteoid sarcoma, mel- 
 anosarcoma. 
 
 JOINTS 
 Structure and function. 
 Hyperemia, active in early stages of inflammation, passive under 
 
 same conditions as elsewhere. 
 Hemorrhage, usually due to traumatism. Small effusions are rap- 
 idly absorbed ; larger ones may be partly absorbed, the remain- 
 der replaced by fibrous connective tissue. 
 Degeneration, may affect articular surface or synovial membranes. 
 
 Fatty, hyaline, amyloid and mucoid. 
 Necrosis and caries. 
 Pigmentation. 
 
 Uric acid deposit, especially occuring in birds. 
 Distortion. 
 
 Luxation and subluxation. 
 Deformities of vertebral column,— lordosis, kyphosis, scoliosis, 
 
 wry neck. 
 Inflammation, acute inflammation may involve first the lining 
 membrane [acute synovitis'), the cartilage {chondritis'); with severe 
 inflammation bones and soft tissues are usually also involved 
 {ostitis and periarthritis) . 
 
 42 
 
Acute arthritis and synovitis arise from traumatism or by exten- 
 sion from neighboring tissues ; some cases are hematogenic e. g. 
 navel ill, acute articular rheumatism. In early stages of severe 
 and in milder forms the synovial membrane is hyperemic and 
 swollen, especially about the folds. There may be small hemor- 
 rhages and exudation of thin yellowish fluid containing a few 
 floculi of fibrin {^serous synovitis). In more severe cases the exu- 
 date contains more fibrin {^serofibrinous synovitis) ; in some cases 
 exudate may be mostly fibrin with a little fluid {fibrinous synovi- 
 tis) . Exudate may become purulent or may be purulent from 
 the beginning {purulent synovitis, empyema articuli). In this 
 case the synovial membrane is swollen, infiltrated and covered 
 with fibrinopurulent or purulent exudate, the cavity containing 
 turbid fluid. In the most severe forms the synovial mem- 
 brane may be partly destroyed and cartilage may undergo fatty 
 degeneration, fibrillation and finally necrosis. The joint may 
 become disorganized. Process frequently extends to bones. 
 
 Acute synovitis and arthritis often heal leaving little or no 
 trace, or may pass into a chronic condition. More or less fibrous 
 proliferation often occurs during repair. Osteophytes forming 
 about the joint, ankylosis sometimes results. 
 Chronic arthritis 
 
 Chronic serous arthritis arises from the acute or may be chronic 
 
 from the beginning. This form is common in horses and cattle 
 
 in fetlock, tarsal and knee joints. " Galls " 
 
 Chronic suppurative, empyema of the joint. 
 
 Chronic arthritis 
 
 (a) chronic serous proliferating synovitis ; 
 
 (b) arthritis ankylopoetica, ankylotica ; 
 
 (c) arthritis deformans, two forms the proliferative and the 
 degenerative. Osteoarthritis intertarsalis ankylopoettca 
 ossificans (spavin) and ringbone. A disease primarily 
 of bone, a rarefying ostitis, which may extend to in- 
 volve articular cartilage, or may extend to periosteum or 
 may involve both. Destruction of cartilage, ulcerative 
 arthritis, with proliferation of cartilage and other tissue, 
 formation of exostoses, ossifying periostitis, ankylosis, 
 osteosclerosis, etc. 
 
 Arthritis uratica s.urica, gout, occurs in birds and man, some- 
 times in dogs. 
 
 43 
 
SKIN. 
 
 ucture and function. 
 
 Anomalies 
 
 hypotrichosis in swine 
 
 Hyperemia shows best in unpigmented areas. Active in inflamma- 
 tion, erythema, in vasomotor disturbances, excessive heat and cold, 
 mechanical and chemical irritants, /'awzz/^ in conditions favoring 
 stasis, may be diffuse, cyanosis, or in areas, livido (^lividity), after 
 death, postmortem lividity, local passive hyperemia may be due 
 to pressure of tumors or of inflammatory products on veins. 
 
 Edema 
 
 Hemorrhage, generally traumatic, also in infectious diseases, pete- 
 chiae, ecchymoses, vibices, purpura papulosa, hematoma, hema- 
 tidrosis, suggilation. 
 
 Emphysema 
 
 Anemia, may be general or local. 
 
 Atrophy 
 
 Necrosis, ulceration, gangrene. 
 
 Abnormal pigmentation 
 
 Melanosis maculosa in calves. 
 
 Inflammation dermatitis. Inflammations of the skin present much- 
 varied appearances according to cause, course and anatomical 
 changes. Different causes produce similar changes. No satisfac- 
 tory classification yet made. Is generally due to external causes, 
 mechanical injuries, chemicals, heat, cold, light, local infections, 
 vegetable and animal parasites. Sometimes dermatitis seems to be 
 neuropathic (e. g. urticaria prurigo) and some forms are of 
 unknown or doubtful origin. Some inflammations of the skin are 
 secondary, accompanying general infectious diseases, or are due 
 to the action of toxic substances taken internally. These hema- 
 togenic affections of the skin are commonly called exanthemata. 
 Diffuse redness and swelling is called erythema. Color is bright, 
 not the dull livitidity of passive hyperemia ; disappears momen- 
 tarily on pressure. lyocally raised areas from minute to size of 
 pea due to infiltration in the skin <i2X\q.A. papules ; larger elevations 
 to size of hazelnut called nodules or nodes. Wheals are broad, 
 flattened, fairly well-defined elevations which appear and disap- 
 pear rapidly, color dull reddish, larger ones may have whitish 
 center. Microscopically in these mild forms of dermatitis, one 
 finds infiltration with serum and leucocytes, sometimes red cor- 
 
 44 
 
piiscles also in tissue. Epithelium is but little changed, may be 
 swollen. There may be slight proliferation. With greater 
 amount of serous exudation, local collections of fluid occur, blis- 
 ters, blebs or vesicles. Fluid clear, without cells. May be some- 
 what turbid from leucocytes or reddish from blood {blood blisters). 
 Exudate turbid, whitish (purulent) , pustule. When pustule dries 
 forms scab or crust. 
 
 A mild acute dermatitis, may pass quickly, leaving little or no 
 trace. Frequently even after erythema superficial epithelium des- 
 quamates. Pigmentation also common sequel. If papilary layer 
 or corium is damaged, scar results. In chronic dermatitis atrophy 
 and hypertrophy may be combined. Superficial dermatitis which 
 resembles catarrhal inflammation of mucous membrane is ordin- 
 arily called eczema. 
 
 One of the simplest forms of dermatitis is due to exposure to 
 sun {sunburn). Blood vessels relaxed, active hyperemia and 
 slight exudation. After process has subsided there is desquama- 
 tion and more or less pigmentation. Inflammation due to burn- 
 ing in mildest form is similar {burn of the first degree) . With 
 higher temperature or more prolonged exposure, injury is more 
 severe. There is considerable exudation, epidermis is raised into 
 vesicles {burn of the second degree) . With loss of substance of 
 cutis {burn of the third degree) . If charred {burn of the fourth de- 
 gree). Burns of the second degree heal by simple regeneration of 
 the epithelium if there is no infection. With loss of substance 
 healing takes places by granulation with formation of scar. Der- 
 matitis of frost bite is very similar. There may be different de- 
 grees, erythema with swelling and later desquamation or forma- 
 tion of vesicles or gangrene. 
 
 Exudative dermatitis is a common form and exhibits a great 
 variety of appearances. Sometimes the lesions are restricted, 
 sometimes diffuse. The skin is reddened and swollen. It may 
 be covered with papules, vesicles, pustules or crusts. The affected 
 part may itch . It may desquamate. In chronic cases the skin 
 becomes thickened. A number of names are in use to distinguish 
 different stages of exudative dermatitis and differences in the kind 
 of exudate. One of the mildest dermatitis papulosa, characterized 
 by small nodular swellings in the skin. In somewhat more severe 
 cases vesicules are produced, dermatitis vesiculosa. With consid- 
 erable areas of skin painful, red and swollen, dermatitis erythema- 
 tosa. If blisters formed in this inflamed area, later becoming 
 pustules, dermatitis pustulosa. When considerable patches of 
 
 45 
 
epidermis are lost, the underlying surface presents a dusky red 
 appearance, dermatitis rubra. Often the serous or purulent exu- 
 date dries up on the surface into yellowish crusts, dermatitis crus- 
 tosa. Under the crusts pus may accumulate, dermatitis inpeti- 
 ginosa. In other cases the epithelium may proliferate beneath 
 the scabs so that the surface appears reddened, thickened and 
 scurfy, dermatitis squamosa. When somewhat larger pustules 
 covered with crusts occur, it is often called impetigo. Histolog- 
 in acute inflammation, congestion of blood and lymph vessels in 
 corium, exudation of plasma and diapedesis of leucocytes. Con- 
 nective tissue fibers are swollen and compressed and there is some 
 proliferation of the connective tissue cells. In the milder form 
 process confined mainly to papillary regions and upper layers of 
 corium, but in more severe cases extends to subcutem. Cells of 
 rete swollen, effusion of fluid with wandering cells. Rete cells may 
 undergo liquefacation necrosis with formation of cavities. When 
 exudation marked, vesicles or bullae may form between rete and 
 horny layer. In pustular variety many leucocytes. Desquama- 
 tion of superficial epidermis takes place often and is a character- 
 istic change in dermtitis squamosa and rubra. 
 Dermatitis phlegmonosa, phlegmon of the skin ; panaritium. 
 Suppurative dermatitis, abscesses of the skin, ulcers, fistulae. 
 Dermatitis gangraenosa, gangrene of the skin. 
 Chronic productive, dermatitis, restricted as on lower part of foot 
 of horse, or diffuse. 
 
 Tuberculosis 
 
 Glanders 
 
 Epizootic lymphangitis 
 
 Vaccinia and Variola 
 
 Epithelioma contagiosum 
 
 Actinomycosis 
 
 Botryomycosis 
 
 Parasites, long list 
 
 flies, lice, ticks, acari, worms. 
 
 Herpes tonsurans, favus. (See parasitologies). 
 
 Progressive changes, hypertrophy, cornu cutaneum, callus, elephan- 
 tiasis. 
 
 Tumors. Fibroma, papilloma, lipoma, chondroma, angioma, aden- 
 oma, adenocystoma, carcinoma, sarcoma (rare), Hodgkin's dis- 
 ease, melanoma (frequent in horse). 
 
 References. 
 
 Adami and Nicholls, pp. 907-977. 
 Kitt, pp. 134-243. 
 
 46 
 
MAMMARY GLANDS 
 
 Structureand function. 
 
 Hyperemia, physiological, ante partum and post partum. 
 
 Hemorrhage, suggillation, hematoma. 
 
 Edema, congestive, stagnation, collateral and inflammatory. 
 
 Concretions, in cow and goat. 
 
 Cysts. 
 
 Inflammations that arise naturally are due to infection. Several 
 
 species of bacteria culpable. Enter through milk ducts (teat). 
 
 May enter through the blood. 
 
 Acute catarrhal galactophoritis , inflammation of the milk ducts, 
 due to infection through teats ; may be manifest only on exami- 
 nation of sediment or microscopic examination of the organ. 
 Acute parenchymatous mastitis. Inflammatory edema often over 
 the entire gland, gland sometimes swollen to double its normal 
 size. On section, color red, red gray or even dark wine red ; 
 milk ducts filled with flocculent whey, may have fibrin adhering 
 to walls, fluid may be serous, bloody. 
 
 Suppurative mastitis. Purulent exudate into ducts, the secretion 
 may be rich in leucocytes. Process may go on to abcess for- 
 mation. 
 Gangrenous mastitis, more frequent in sheep, fatal in twenty-four 
 
 hours to five days. 
 Chronic productive mastitis, increase in connective tissue, usually 
 
 follows acute inflammation. 
 Thelitis, inflammation of the teat, nipple, superficial is inflam- 
 mation of the skin. 
 Thelitis moriificans, in cow. 
 
 Chronic productive thelitis, in inside, production of connective 
 tissue leading to obstruction. 
 Infectious mastitis. 
 Glanders. 
 Tuberculosis. 
 Actinomycosis . 
 Botry omycosis . 
 Animal parasites. 
 
 Echinococcus in cow. 
 Tumors. Fibroma, adenofibroma, enchondroma, osteoma, angio- 
 ma, sarcoma, and carcinoma. 
 
 47 
 
References : 
 
 Adami and NichoUs, pp. 882-905. 
 Kitt, pp. 244-282. 
 
 I/cBlanc, " The Diseases of the Mammary Glands of the Domes- 
 ticated Animals", translated by Nunn, 1904. 
 
 48