Chapter 55

_Immunization by vaccination._--Three French veterinarians, Arloing, Cornevin, and Thomas, were the first to discover that cattle may be protected against blackleg by inoculation with virulent material obtained from animals which have died of this disease. Later they devised a method of inoculation with the attenuated or weakened blackleg spores which produced immunity from natural or artificial inoculation of virulent blackleg germs. Their method has undergone various modifications both in regard to the manufacture of the vaccine and in the mode of its application. Kitt, a German scientist, modified the method so that but one inoculation of the vaccine was required instead of two, as was the case with that made by the French investigators. The vaccine formerly prepared and distributed by the Bureau of Animal Industry combined the principle of Arloing, Cornevin, and Thomas, and the modification of Kitt.

By vaccination we understand the injection of a minute amount of attenuated--that is, artificially weakened--blackleg virus into the system. This virus is obtained from animals which have died from blackleg, by securing the affected muscles, cutting them into strips, and drying them in the air. When they are perfectly dry they are pulverized and mixed with water to form a paste, smeared in a thin layer on flat dishes, placed in an oven, and heated for six hours at a temperature close to that of boiling water. The paste is then transformed into a hard crust, which is pulverized and sifted and distributed in packages containing either 10 or 25 doses. This constitutes the vaccine, the strength of which is thoroughly tested on experiment animals before it is distributed among the cattle owners. This vaccine, which is in the form of a brownish, dry powder, is mixed with definite quantities of sterile water, filtered, and by means of a hypodermic syringe the filtrate injected under the skin in front of the shoulder of the animal. The inoculation is usually followed by insignificant symptoms. In a few cases there is a slight rise of temperature, and by close observation a minute swelling may be noted at the point of inoculation. The immunity conferred in this way may last for 18 months, but animals vaccinated before they are 6 months old and those in badly infected districts should be revaccinated before the following blackleg season.

The effect of the vaccine prepared by this bureau in preventing outbreaks of the disease and in immediately abating outbreaks already in progress was highly satisfactory, and it is not to be doubted that thousands of young cattle were saved to the stock owners during the 25 years in which the vaccine was distributed.[6] More than 47,000,000 doses were sent out during this period, and from reports received it is safe to conclude that more than 40,000,000 were actually injected, whereby the percentage of loss from blackleg has been reduced from 10 per cent, which annually occurred before using, to less than one-half of 1 per cent per annum. With these figures before us it is plain that the general introduction of preventive vaccination must be of material benefit to the cattle raisers in the infected districts. Moreover, there is every reason to believe that with the continued use of blackleg vaccine in all districts where the disease is known to occur, and an earnest effort on the part of the stock owners to prevent the reinfection of their pastures by following the directions given, blackleg may be kept in check and gradually eradicated.

Immunization against blackleg is now frequently accomplished by the use of the so-called blackleg aggressin and blackleg filtrates.

NECROTIC STOMATITIS (CALF DIPHTHERIA).

[Pl. XLIII.]

Necrotic stomatitis is an acute, specific, highly contagious inflammation of the mouth occurring in young cattle, and characterized locally by the formation of ulcers and caseo-necrotic patches and by constitutional symptoms, chiefly toxic.

This disease has also been termed calf diphtheria, gangrenous stomatitis, ulcerative stomatitis, malignant stomatitis, tubercular stomatitis, and diphtheritic patches of the oral mucous membrane.

_History._--During the last few years farmers and cattlemen in this country, especially in Colorado, Texas, and South Dakota, have increasingly noted the occurrence of enzootics of "sore mouth" among the young animals of their herds. Instead of healing, like the usual forms, of themselves, these cases, if untreated, die. Careful study of some of them has resulted in their identification with cases reported in 1877 by Dammann, from the shore of the Baltic; in 1878 by Blazekowic, in Slavonia; in 1879 by Vollers, in Holstein; in 1880 by Lenglen, in France; in 1881 by Macgillivray, in England; and in 1884 by Lˆffler, who isolated and described the microorganism which produces the disease. Bang obtained this organism from the diphtheritic lesions of calves in 1890, and Kitt likewise recovered the bacillus from similar lesions of the larynx and pharynx of calves and pigs in 1893.

_Etiology._--The cause of necrotic stomatitis, as demonstrated by Lˆffler and since confirmed by other investigators, is _Bacillus necrophorus_, often spoken of as the bacillus of necrosis. This organism varies in form from a coccoid rod to long, wavy filaments, which may reach a length of 100µ; the width varies from 0.75µ to 1µ. Hence it is described as polymorphic. It does not stain by Gram, but takes the ordinary anilin dyes, often presenting, especially the longer forms, a beaded appearance. A characteristic of the organism, of great moment when we come to treatment, is that it grows only in the absence of oxygen, from which fact it is described as an obligate anÊrobe.

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.

The disease frequently extends to the nasal cavities, producing a thin, yellowish, or greenish-yellow, sticky discharge which adheres closely to the borders of the nostrils. Their edges also show caseous patches similar to those in the mouth. Sometimes the nasal passage is obstructed by great masses of the necrosed exudate, thus causing extreme difficulty in breathing. When the caseous process involves the larynx and trachea there result cough, wheezing, and dyspnea, together with a yellowish mucopurulent expectoration.

When life is prolonged three or four weeks, caseous foci may be established in the lung, giving rise to all the signs of a bronchopneumonia. Many of these cases are associated with a fibrinous pleurisy. The invasion of the gastrointestinal tract is announced by diarrheal symptoms. This disease principally attacks sucklings not more than 6 weeks of age, but calves 8 and 10 months old are frequently affected, and several cases in adult cattle have been reported to this office.

In its very acute form many of the cases run their course in from five to eight days. In these the local lesions are not strongly marked, and death seems due to acute intoxication. In other enzootics the majority of the affected animals live from three to five weeks. These are cases that occasionally present the pulmonary and intestinal symptoms, and sometimes develop also caseo-necrotic lesions in the liver.

Ordinarily cases show no tendency to spontaneous cure. Left to themselves they die. On the contrary, if taken in hand early, the disease is readily amenable to treatment. In the latter event the prospects of recovery are excellent.

_Differential diagnosis._--Necrotic stomatitis may be differentiated from foot-and-mouth disease by the fact that in the latter there is a rapid infection of the entire herd, including the adult cattle, as well as the infection of hogs and sheep. The characteristic lesion of foot-and-mouth disease is the appearance of vesicles containing a serous fluid upon the mucous membrane of the mouth and upon the udder, teats, and feet of the affected animals. In necrotic stomatitis vesicles are never formed, necrosis occurring from the beginning and followed by the formation of yellowish, cheesy patches, principally found in the mouth. Mycotic stomatitis occurs in only a few animals of the herd, chiefly the adult cattle, and the lesions produced consist of an inflammation of the mouth and lips and of the skin between the toes, followed in a few days by small irregular ulcers in the mouth. This disease appears sporadically, usually in the early fall after a dry summer, does not run a regular course, and can not be inoculated.

_Prevention._--Prophylaxis should be carried out along three lines:

(1) Separation of the sick from the healthy animals.

(2) Close scrutiny and thorough disinfection once or twice daily for five days of the mouths and nasal passages of those animals that have been exposed.

(3) Complete disinfection of all stalls and sheds.

The disease appears to break out in winter and hold over to spring. It is conceivable that exposure to cold might so disturb the normal circulation of the oral tissues as to make the mucous membrane an excellent location for the causative factor of the disease. There is another possibility, however, which bears on the third line of prophylaxis. The so-called diphtheritic inflammations of the vagina and uterus in cows are caused by the same organism that induces necrotic stomatitis. A European writer has recently pointed out the almost constant relation of such attacks to previous occurrences of foul foot or foot rot in the same or other cattle on the place.

In all likelihood, in such cases, the stalls and sheds are the harborers of this germ. It is possible that many of these outbreaks have some relation to preceding cases of the above-mentioned diseases and the greater use in winter of the stalls and sheds, thus harboring the _Bacillus necrophorus._

_Treatment._--The treatment consists almost solely in careful and extensive cleansing and disinfection of the mouth and other affected surfaces. The mucous membrane of the mouth should be copiously irrigated with a 4 per cent solution of boracic acid in warm water at least twice daily. As exposure to oxygen kills the bacilli, one need have no fear about disturbing or tearing off the caseous patches or necrotic tissue during irrigation. The irrigation of the sores should then be followed by the application with a brush or rag on a stick of a paste made with 1 part of salicylic acid and 10 parts of water, or the affected areas may be painted with Lugol's solution of iodin (iodin, 1; potassium iodid, 5; water, 200). Frequent injections of 1 per cent carbolic-acid solution into the mouth make an excellent treatment. The internal administration of 2 grams of salicylic acid and 3 grams of chlorate of potassium three times a day has also proved to be very beneficial when accompanied with local antiseptic treatment.

MALIGNANT CATARRH.

Malignant catarrh, or infectious catarrhal fever, is an acute infectious disease of cattle preeminently involving the respiratory and digestive tracts, although the sinuses of the head, the eyes, and the urinary and sexual organs are very frequently affected. It is relatively rare in this country, being more common on the continent of Europe. Outbreaks have occurred, however, in Minnesota, New York, and New Jersey. So far the causal agent of the disease has never been isolated, and inoculation experiments with the view of artificially reproducing the disease have proved negative in every case. In spite of the foregoing statements the consensus of opinion of eminent investigators points to malignant catarrh as being of specific origin; that is, due to some form of microorganism the contagious character of which is poorly developed. This accounts for the slow transmissibility of the disease from one animal to another. In fact, malignant catarrh is a type of that class of affections scientifically known as miasmatic diseases; that is, they remain stationary in stables with damp floors, low ceilings, poor ventilation, and bad sanitary conditions in general. Such places furnish a favorable seat of propagation for the infective material, and it will remain active for a long time, causing the loss of a few animals each year. One European veterinarian reports an instance in which the disease remained for 25 years on the same farm, attacking in all 225 animals, with a mortality of about 98 per cent.

The disease is most common in late winter and early spring, at all altitudes, and has a special preference for young, well-nourished cattle, although older animals are not immune. The time between the entrance of the infective principle into the body of the animal and the appearance of the first symptoms is relatively very long, averaging, according to German investigators, from 20 to 30 days. Fortunately, it is not a disease which spreads to any great extent or which causes severe losses, and hence legislative enactments do not seem to be necessary for its restriction.

_Symptoms._--These are extremely variable according to the point of localization of the lesions. It is usually ushered in with a chill, followed by a marked rise of temperature (104∞ to 107∞ F.). The head droops, the skin is hot and dry, and the coat staring. Quivering of the muscles in various parts of the body is frequently observed. Marked dullness of the animal, passing, according to some observers, into an almost stupefied condition later on, is quite common. The secretion of milk stops in the beginning of the disease, and loss of flesh, invariably associated with the disease, is extremely marked and rapid. The lesions of the eyes may best be likened to moon blindness (periodic ophthalmia) in horses.