Il8 CLINICAL VETERINARY i\IEDICINE AND SURGERY. 



and the more intense strain and rubbing to which the serous mem- 

 brane is subject. Others declare that, as endocarditis is usually 

 caused by aerobic microbes, the superior richness in oxygen of the left 

 heart blood constitutes a predisposing factor. In the horse the pre- 

 dominance of left endocarditis is probably a result of the frequence of 

 pulmonary inflammation, during which the endocardium of the left 

 side is particularly exposed to infection. 



Acute endocarditis may be produced by different microbes. In 

 man, where the subject has been much better studied than in animals, 

 the lesions most commonly contain micrococci, staphylo- and strepto- 

 cocci, pneumococci, gonococci, and less commonly Eberth's bacillus, 

 the Bacillits colt communis, and the Bacillus tuberculosis. MM. Gilbert 

 and Lyon have noted a paracoli bacillus. Weichselbaum discovered a 

 microbe never before seen in other diseases. The same species of 

 microbes have been found in the principal anatomical forms of endo- 

 carditis — the vegetating and the ulcerating. The characters of the 

 lesions seem, then, to depend especially on the degree of virulence 

 of the infectious agents. In addition to these, one sees so-called 

 cryptogenic endocarditis, from which pathological agents have not 

 yet been isolated. In endocarditis lesions in the horse Penberthy and 

 Fuchs found micrococci. In a case of tuberculosis I detected the 

 specific bacillus. 



Inflammation of the endocardium frequently complicates rheu- 

 matism, and is due to the same cause as the arthritis, synovitis, 

 pleurisy, and pericarditis. Apart, however, from the pseudo-rheu- 

 matism which follows pneumonia, acute rheumatism is rare in the 

 horse, and endocarditis arising from this cause is much less common 

 than the forms of which I have just spoken. 



At the present day we are all agreed as to the extreme rarity of 

 acute primary endocarditis — what has been called endocarditis a 

 frigore. Cold alone can no more produce it than can an aseptic 

 injury ; its action must be preceded, or accompanied, by some other 

 pathological influence which plays the principal part, that is to say, 

 the entrance of some microbe. Cold here acts as in pneumonia a 

 frigore, by diminishing the resistance of the organism, thus favouring 

 infection, the latent centres of which are numerous. Infection may 

 occur through the uninjured membrane of the respiratory tract ; ex- 

 periments seem to have established that various microbes can traverse 

 the pulmonary epithelium without any preliminary lesion, and pass 

 into the circulation by way of the lymphatic channels. 



It has been suggested that certain therapeutic or toxic materials, 

 internally administered, are capable of producing acute inflammation 



