230 DISEASES OF THE HORSE. 



and often gives rise to symptoms Avhich. at first, are obscure and 

 unnoticed. 



In influenza we may find the heart becoming- involved in the dis- 

 ease, in consequence of the morbid material conveyed through the 

 heart in the blood stream. In view of the fact that many affections, 

 in even remote portions of the body, may be traced directly to a 

 primary endocardial disease, we shall feel justified in inviting special 

 attention to this disease. 



Endocarditis may be acute, subacute, or chronic. In acute inflam- 

 mation we find a thickening and a roughened appearance of the endo- 

 cardium throughout the cavities of the heart. This condition may be 

 followed by a coagulation of fibrin upon the inflamed surface, which 

 adheres to it, and by attrition soon becomes worked up into shreddy- 

 like granular elevations: this may lead to a formation of fibrinous 

 clots in the heart and sudden death early in the disease, the second or 

 third day. 



Subacute endocarditis, which is the most common form, may not 

 become appreciable for several days after its commencement. It is 

 characterized by being confined to one or more anatomical divisions 

 of the heart, and all the successive morbid changes follow each other 

 in a comparatively slow j^rocess. Often we would not be led to sus- 

 pect heart aifection were it not for the distress in breathing, which 

 it generally occasions when the animal is exercised, especially if the 

 valves are much involved. When coagula or vegetations form upon 

 the inflamed membrane, either in minute shreds or patches, or when 

 formation of fibrinous clots occurs in the cavity affected, some of theso 

 materials may be carried from the cavity of the heart by the blood 

 current into remote organs, constituting emboli that are liable to sud- 

 denly plug vessels and thereby interrupt important functions. In 

 the great majority of either acute or subacute grades of endocarditis, 

 whatever the exciting cause, the most alarming symptoms disappear 

 in a week or ten days, often leaving, however, such changes in the 

 interior lining or valvular structures as to cause impairment in the 

 circulation for a much longer period of time. These changes usually 

 consist of thickening or induration of the inflamed structures. But 

 while the effects of the inflammation in the membrane lining the 

 walls of the ventricles may subside to such a degree as to cause little 

 ox no inconvenience, or even wholly disappear, yet after the valvular 

 structures have been involved, causing them to be thicker, less flexible 

 than normal, they usually remain, obstructing the free passage of the 

 blood through the openings of the heart, thereby inducing secondary 

 changes, which take place slowly at first, but ultimately seriously hn- 

 pair the animaFs usefulness. A\^iat was but a slight obstruction to 

 the circulation during the first few weeks after the subsidence of the 

 cardiac inflammatory attack becomes in process of time so much in- 



