DISEASES OF. CATTLE 309 



pigeon, and chicken appear to be absolutely immune. It is not 

 pathogenic for man. 



The importance of this bacillus is far beyond even its relation 

 to necrotic stomatitis. Besides this disease it has been demonstrated 

 as the causative factor in foot rot, multiple liver abscesses, dissemin- 

 ated liver necrosis, embolic necrosis of the lungs, necrosis of the 

 heart, in cattle ; gangrenous pox of the teats, diphtheria of the uterus 

 and vagina, in cows; diphtheritic inflammation of the small intes- 

 tine of calves. Among horses it is the agent in the production of 

 necrotic malanders, quittor, and diphtheritic inflammation of the 

 large intestine. In hogs it has caused necrotic or diphtheritic pro- 

 cesses in the mucous membrane of the mouth, necrosis of the ante- 

 rior wall of the nasal septum, and pulmonary and intestinal necro- 

 sis, accompanying hog cholera. Abscesses of the liver, gangrenous 

 processes of the lips and nose, and gangrenous affections of the hoof 

 have all been caused in sheep by this organism. 



Pathology. The principal lesions in necrotic stomatitis occur 

 in the mucous membrane of the mouth and pharynx. The altera- 

 tions may extend to the nasal cavities, the larynx, the trachea, the 

 lung, the esophagus, the intestines, and to the hoof. The oral sur- 

 faces affected are, in the order of frequency, tongue, cheeks, hard 

 palate, gums, lips, and pharynx. In the majority of cases the 

 primary infection seems to occur in the tongue. 



Infection takes place by inoculation. Some abrasion or break 

 in the continuity of the mucous membrane of the mouth occurs. 

 Very likely the origin may be connected with the eruption of the 

 first teeth after birth, or, in animals somewhat older, the entrance 

 of a sharp-pointed particle of food. Gaining an entrance at this 

 point, the bacilli begin to multiply. During their development 

 they elaborate a toxin, or poisonous substance, which causes the 

 death, or necrosis, of the epithelial, or superficial, layer of the mu- 

 cous membrane and also of the white blood cells which have sallied 

 forth through the vessel walls to the defense of the tissues against 

 the bacillary attack. This destruction of the surface epithelium 

 seems to be the essential factor in the production of the caseous 

 patch, often called the false membrane. From the connective tissue 

 framework below is poured forth an inflammatory exudate highly 

 albuminous or rich in fibrin-forming elements. When this exudate 

 and the necrosed cellular elements come in contact, the latter fur- 

 nish a fibrin ferment which transforms the exudate into a fibrinous 

 mass. This process is known as coagulation necrosis, and the result- 

 ing fibroid mass, containing in its meshes the necrosed and degen- 

 erated epithelium and leucocytes, constitutes the diphtheric or false 

 membrane. Did the process cease at this point it would be properly 

 called a diphtheric inflammation. But it does not. A caseating fer- 

 ment is supplied by the bacilli, and this, acting upon the fibroid 

 patch, transforms it into a dry, finely granular, yellowish mass of 

 tissue detritus resembling cheese. 



Frequently this caseous inflammation results in the formation 

 of one or more ulcers with thickened, slightly reddened borders, 



