INTECTIOUS DISEASES OF CATTLE. 471 



vagina, in cows; diphtheritic inflammation of the small intestine of 

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

 malanders, quittor, and diphtheritic inflammation of the large intes- 

 tine. In hogs it has caused necrotic or diphtheritic processes in the 

 mucous membrane of the mouth, necrosis of the anterior wall of the 

 nasal septum, and pulmonary and intestinal necrosis, accompanying 

 hog cholera. Abscesses of the liver, gangi-enous 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 alterations 

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

 esophagus, the intestines, and to the hoof. The oral surfaces 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. (PI. XLV.) 



Infection takes place by inoculation. Some abrasion or break in 

 the continuity of the mucous membrane of the mouth occure. 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 mucous 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. AATien this exudate and the necrosed cellular 

 elements come in contact, the latter furnish a fibrin ferment which 

 transforms the exudate into a fibrinous mass. This process is known 

 as coagulation necrosis, and the resulting fibroid mass, containing in 

 its meshes the necrosed and degenerated epitheliiun 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 ferment 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, sur- 

 mounted by several layers of this necrosed tissue. The floor of the 

 ulcer is formed by a gi-ayish yellow, corroded surface, under which 

 the tissue is transformed into a dry friable or firm cheesy mass. 



