Etiology, Anatomical Changes. 1041 



develops in association with diseases of neighboring organs or 

 in the course of a generalized acute infectious disease. Aside 

 from inflammations of the heart muscle or the endocardium 

 which easily pass over into the pericardium which is connected 

 with the intramuscular connective tissue, pericarditis occurs 

 preferably as a sequel to pleurisy, pneumonia, pulmonary or 

 pleural tuberculosis and is produced in these cases by the virus 

 of the related diseases. Pericarditis may also develop directly, 

 by continuity, after perforation of the gullet and in consequence 

 of the mediastinitis due to it, also after suppuration of the 

 peribronchial lymph glands, etc. Of the acute infectious dis- 

 eases it is especially hemorrhagic septicemia, pyosepticemia 

 neonatorum, less often strangles, variola, articular rheumatism, 

 etc., which lead to pericarditis. 



The bacillus bipolaris, the pyogenic bacteria and the tuber- 

 cle bacillus do not necessarily exert their inflammatory action 

 only after a previous affection of other organs or after a 

 generalized infection (secondary or consecutive pericarditis) 

 but may in many cases do so independently (primary peri- 

 carditis). 



The pericarditis observed in epizootic extension in sheep by Trasbot, Anacker 

 and Kowalewsky was evidently not primary, but a partial manifestation of 

 hemorrhagic septicemia, and as a matter of fact Kowalewsky found, on autopsy, 

 endocarditis and pneumonia in addition to pericarditis. 



It is only exceptionally that chemical substances or me- 

 chanical irritants give rise to chronic pericarditis, the former 

 in bacterial diseases of other organs, in nephritis, etc., the latter 

 by new-growths, parasites, sterile foreign bodies. (Borchardt 

 saw serous-hemorrhagic pericarditis with nephritis and hepa- 

 titis in two horses which suffered from lysol poisoning.) 



In infectious non-traumatic pericarditis certain predispos- 

 ing causes like cold, over-exertion, railroad transportation, etc., 

 are of importance although they are not capable, of them- 

 selves, of giving rise to an inflammation. 



Anatomical Chang^es. In acute pericarditis delicate or thick 

 fibrinous membranes are deposited on one or both layers of 

 the pericardium which may, in larger animals, attain a thick- 

 ness of 2-3 cm., and a fluid exudate accumulates in varying 

 amounts in the pericardial cavity, which may be clear or very 

 cloudy; it may contain floccules of fibrin and in traumatic 

 pericarditis it has usually a foul odor. If fibrin is secreted 

 copiously, the surface of the heart becomes uneven, villous 

 (villous heart, cor villosum), and the fibrin masses may divide 

 the pericardial cavity into irregular compartments (which are 

 especially well marked in cattle). In many cases the exudation 

 assumes a purulent character and if the inflammation is pro- 

 longed a proliferation of connective tissue is more manifest. 

 The latter form of inflammation, and also pericarditis in its 



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