Very few organisms exhibit a wider range of pathogenesis. According to clinical observation to the present time, Bacillus necrophorus is pathogenic for cattle, horses, hogs, sheep, reindeer, kangaroos, antelope, and rabbits. Experimentally it has been proved pathogenic for rabbits and white mice. The dog, cat, guinea pig, 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, disseminated 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 intestine 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 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, 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 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. ([Pl. XLIII].)
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 feed. 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. When this exudate and the necrosed cellular elements come in contact, the latter furnish a fibrin ferment which transforms the exduate into a fibrinous mass. This process is known as coagulation necrosis, and the resulting fibroid mass, containing in its meshes the necrosed and degenerated epithelium and leucocytes, constitutes the diphtheritic or false membrane. Did the process cease at this point it would be properly called a diphtheritic 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, surmounted by several layers of this necrosed tissue. The floor of the ulcer is formed by a grayish-yellow, corroded surface, under which the tissue is transformed into a dry, friable, or firm cheesy mass. In the tongue this may progress to two fingers' thickness into the muscular portion; in the cheek it may form an external opening, permitting fluids to escape from the mouth; upon the palate it frequently reaches and includes the bone in its destructive course; upon the gums it has produced necrosis of the tooth sockets, causing loss of the teeth. In the advanced forms, caseous foci may be seen in the lung and in the liver and necrotic patches observed on the mucous membrane of the gastrointestinal tract.
Symptoms.—Necrotic stomatitis is both a local and a systemic affection. Primarily it is local. The local lesion is the caseo-necrotic patch or ulcer developed as a result of the multiplication of the bacilli at the point of inoculation. The general affection is an intoxication, or poisoning, of the whole system produced by a soluble toxin elaborated by the bacilli.
The stage of incubation is from three to five days. The first symptoms noted are a disinclination to take nourishment, some drooling from the mouth, and an examination of the mouth will show on some portion of its mucous membrane a circumscribed area of infiltration and redness, possibly an erosion. The latter gradually extends in size and depth, forming a sharply circumscribed area of necrotic inflammation. It may measure anywhere from the size of a 5-cent piece to that of a silver dollar or even larger. It has the appearance of a corroded surface, under which the mucous membrane or muscular tissue seems transformed into a dry, friable, or firm cheesy mass. It is grayish yellow in color and is bordered by a zone of thickened tissue slightly reddened and somewhat granulated. The necrotic tissue is very adherent and can be only partially peeled off. It is homogeneous, cheesy, and may extend two fingers' depth into the tissues beneath. The general symptoms are languor, weakness, and slight fever. In spite of plenty of good feed the calf is seen to be failing. It stops sucking, or, if older, altogether refuses to eat. The temperature at this time may be from 104° to 107° F. The slobber becomes profuse, swallowing very difficult, opening of the mouth quite painful, and a most offensive odor is exhaled. The tongue is swollen and its motion greatly impaired. Sometimes the mouth is kept open, permitting the tumefied tongue to protrude. One or more of the above symptoms direct the attention to the mouth as the seat of disease; or, having noticed the debility and disinclination to eat, an examination of the animal may show a lump under the neck or swelling of the throat or head. The following extract from a letter is characteristic:
I noticed my calves beginning to fail about the first week in December, but could not account for it, as they were getting plenty of grain and hay. My attention was first attracted by a swelling under the neck of one of the calves. I cast the animal and found that it was feed that had collected and the animal couldn't swallow it. I removed it, and in so doing noticed a large ulcer on the tongue and a very offensive odor. This was the first knowledge I had of anything being wrong with the calves' mouths. They may have been sick for some time before this.
Out of a herd of 100 belonging to this man, 70 were affected, and the letter emphasizes the insidious character of the onset.
The general affection at this time manifests itself by dejectedness, extreme weakness, and emaciation, constant lying down, with stiffness and marked difficulty in standing.