DYSENTERY OF CATTLE.
Definition. Attacks ox mainly. Causes: accessory causes, chills, rain storms, night dews, hoar frost, foul or iced water, alimentary irritants, spoiled fodder, over exertion, hot damp weather, odors of carrion, crowding, swamps, foul stables, germs or pathogenic ferment, in man catarrhal, diphtheritic and amœbic, amœba dysenterica, other microbes, effect of better hygiene. Symptoms: attack sudden, languor, trembling, weakness, weeping eyes, fever, buccal epithelial softening, erosions, tenesmus, fœtid, liquid stools, involuntary defecation, hemorrhoidal congestion, open anus, colics, tender right flank, splashing on handling, anorexia, salivation, unthrifty skin, hide-bound, cracked muzzle, later prostration, low temperature, sunken glazed eyes, drooping head, ears, eyelids, weakness, emaciation, alkaline, fœtid, frothy, bloody, mucous stools, with sloughs, saliva acid, gastric liquids alkaline, bile suppressed. Duration: three days to three weeks or chronic. Mortality 50 to 80 per cent. Complications: mostly septic, abscess, gangrene of other organs, lungs, joints, glands, etc. Lesions: rapid sepsis, blood deep red, coagulum loose, venous congestion, large intestines congested, tumefied, softened, desquamated, eroded, sloughing, necrotic, folds perforated, cicatrizing, contents mucopurulent, bloody, putrid, microbes, glandular lesions, implication of small intestines, stomach mouth, liver, spleen, hepatic abscess. Diagnosis: from rinderpest by tardiness and comparative weakness of contagion, absence of general mucous congestion and epithelial concretions, from toxic enteritis by same. Prevention: avoidance of causes, separation of sick, disinfection, careful feeding. Treatment: Demulcents, antiseptics, astringent tonics, opiates, ipecacuan, calomel, sodium sulphate with antiseptics, antiseptic enemata of glycerine, phenol, creolin, iron sulphate, silver nitrate, salicylic and boric acids, rest, gravitation, careful dieting.
Definition. An infective, ulcerative inflammation of the large intestine but especially of the colic and rectal mucosæ.
It is well recognized as a disease of the ox, and the older writers allege its existence also in horses, swine and dogs, though this is not admitted in all modern veterinary works.
Causes. It was formerly ascribed to improper hygiene, chills, cold rain storms, night dews, hoar frost, malarious emanations, putrid, stagnant or iced water, irritants in food, green, fermented or musty food, a too liberal diet after starvation, overtaxation in very hot weather, and bad odors from decomposing carcasses. These can only be accepted as predisposing causes begetting a general debility, or debility of the alimentary canal and laying that open to the attacks of specific microbes. The close aggregation of cattle on ship-board, in besieged cities, and in the parks of armies in the field, has apparently contributed to the propagation of the dysentery. The removal of a victim to a herd with free healthy range seldom starts a new center of the disease. In all infected herds huddled in small compass there is every facility for the propagation of a germ already present, and especially in the commissariat of a belligerent army there are enough privations, over-exertions and other trying conditions to favor predisposition. Faulty food like stale bread, musty hay, have been supposed to cause it. For man and beast alike dysentery is preëminently a disease of the tropics, and of hot seasons, and will often subside on the advent of cold weather.
Its propagation on given (swampy) soils, and in particular (foul) stables strongly suggests a special germ, though for the cow this has not been perfectly identified. Gerlach vainly attempted to inoculate it, and it does not often propagate itself beyond the foul and infected localities or stables, yet its persistence in them for years bespeaks unequivocally the operation of a special pathogenic ferment.
It may also be fairly assumed that it is not necessary that the same factor should be present in all cases alike, but that one operates predominantly in one case and another in another. In other words dysentery must be recognized as not one disease, but several, of which the true pathogenic microbes have not yet been fully demonstrated, but which are classed together because of the similarity of the attendant lesions.
In man three distinct forms are recognized. 1. Catarrhal dysentery, with frequent small stools of rosy mucus, and blood; and later pus, scybala, passed with tenesmus, but no sloughs and little odor; 2. Diphtheritic dysentery, with thin watery bloody discharges having a pronounced cadaveric odor; also tenesmus, sloughs, and increasingly offensive smell; 3. Amœbic dysentery with frequent bloody mucus stools, tenesmus sloughs and fœtor, but with distinct remissions or intermissions. With the latter, amœbæ are found abundantly and more so in the more acute cases with alkaline stools. They are found in the fresh warm stools, 5 to 8 times the size of a red blood globule and oval, pyriform or irregular in form, with nucleus and nucleolus. Kartulis and Hlava succeeded in inducing dysentery in cats and dogs by injecting pure culture of the amœba, and the former testifies that dogs in Egypt take the disease spontaneously, and their stools contain the same amœba coli as is found in man.
Cunningham who investigated the subject in India found amœba in the bowels of healthy men, and also abundantly in the fæces of horses and cows, which have naturally the requisite alkaline reaction.
The mere presence of the amœba therefore may not be sufficient to cause the disease, but with the requisite predisposition and an alkaline condition of the intestinal contents, it is manifestly an important factor in the disease.
The causative microbes in other forms of dysentery have not been identified, but under the requisite irritation and local debility one can easily conceive of the ordinary bacterial ferments of the intestine, concurring with others introduced from without, in determining the morbid condition. With better hygiene the disease is steadily diminishing in man and beast, though violent epizootics (in cattle) still appear in connection with wars (siege of Belfort, 1870, Zundel), and carriage by sea in hot climates (Mediterranean trade, Bouley).
Symptoms. The disease sets in suddenly, yet prodromata may occasionally be observed, such as dullness, langor, trembling over the flanks and elbows, weakness, prominent, weeping, congested eyes, and low moans when moved. Then follow hyperthermia, at first slight, heat of the mouth without injection, epithelial concretions or erosions and diarrhœa (sometimes there is straining without passage at first). Then follows a period of profuse and fœtid discharge, with relaxed or open anus, the liquids escaping involuntarily and smearing the tail, perineum, thighs and hocks, and the protruded mucosa showing dark red congestions and even commencing erosions. Colicy pains, slight at first, have now become intense, and the right side of the abdomen is very tender to the touch and fluctuates noisily when manipulated. Appetite and rumination are lost. Salivation may be present, the saliva falling in films to the ground. The buccal epithelium is softened, loosened and easily detached by the finger, leaving raw sores. The temperature which has risen slowly (not as in rinderpest abruptly) may reach 106°. The hair becomes dry, the skin harsh, rigid, and firmly adherent to the deeper parts, and often cold, while the muzzle is hot, dry and even cracked.
At a still more advanced stage, the pulse is small, the temperature lowered, the animal very weak and unsteady and inclined to lie, great emaciation, sunken glazed eye, drooping head, ears and eyelids, and a general fœtor from the skin as well as the dejections, which attracts crowds of flies. By this time there may be passed only bloody mucus mixed with eschars, and having a most repulsive odor.
It is a noticeable fact that the fæces are alkaline, and in man the saliva is acid and destitute of its glycogenic properties, the stomach secretions are alkaline and no longer peptogenic, and the secretion of bile is arrested until improvement sets in.
Course. Duration. Some mild cases recover in two or three days, and in violent cases death may occur at this early date. More commonly the disease continues for two or three weeks before ending in death or recovery. Some merge into the chronic form and may last for months and die in a condition of marasmus. These last cases become mere walking skeletons, with pallid mucosæ, sunken eyes, scurfy hide-bound skins covered with vermin, and the frequently everted rectum is congested and covered with ulcers and eschars. Mortality is from 50 to 80 per cent.
Complications. Most complications are in the direct line of septic infection. Among the most common are hepatic abscess, gangrenous pneumonia, and extensive gangrene of the intestinal walls. In man arthritis, paralysis, parotitis and other secondary affections are seen. In the animal as well we may expect necrotic centres in any organ, from the supervention of a general septicæmia.
Lesions. The carcasses putrefy with extraordinary rapidity being as a rule pervaded by septic microbes and their toxins. The blood is of a deep red, loosely and imperfectly coagulated, and accumulated in the veins and subcutaneous connective tissue.
The large intestines are the special seat of the disease, the walls being found hyperæmic, with concentration especially on the mucous surface which is red, congested, infiltrated, tumefied so that it is easily detached under pressure by the finger, or broken down into a putrid pulp. At other points the epithelium or the whole mucosa has been detached leaving ulcers, varying from mere erosions to the deep and even perforating sores, through which the putrid contents escape into the abdominal cavity. At other points the surface is covered by necrotic masses surrounded by a swollen margin of living mucosa. Elsewhere the eschars have been detached and the granulating base and margin have contracted into more or less perfect cicatrices. The contents of the affected bowel may be largely mucopurulent, or it may be mixed with blood, with eschars and putrilage from the sores and at times with small packed masses of food, but in all cases it is very putrid and repulsive. It always contains the elements of blood and exudation, together with many microbes, the predominance of individual species suggesting the main factors in the pathogenesis. Peyers’ patches and the solitary glands are often the seat of infiltration and ulceration. Virchow points out that in man the lesions are largely concentrated in the flexures of the colon in which the ingesta is longer delayed, and the very convoluted arrangement of the viscus in cattle may be one reason of their special predisposition to the disease.
The small intestines are exceptionally implicated, and the abomasum red, congested, ecchymosed and even ulcerated. The mouth and pharynx are often congested, with erosions and ulcerations on the gums and tongue.
The mesenteric glands are red and swollen or pigmented of a dark gray color, and these or the adjacent connective tissue may be the seat of abscess. The liver is enlarged congested, of a yellowish red color, with granular degeneration and softening. Hepatic abscess is rare in cattle. The spleen is engorged with black blood and distinctly enlarged.
Diagnosis. Dysentery is distinguished from rinderpest by the slower advance of the hyperthermia, by the absence of buccal concretions of epithelium, and of vaginal congestion, and above all by the absence of the virulent contagion by which the rinderpest spreads widely and rapidly, irrespective of special unwholesome environment. The lesions of dysentery are concentrated on the large intestines, while in rinderpest they are extended over the whole alimentary canal, and do not spare other mucosæ.
From toxic gastro-enteritis it is distinguished by the absence of any history or lesions showing the ingestion of a poison and by the concentration of the lesions on the large intestines whereas in poisoning with irritants, the stomach and small intestines are the most liable to suffer.
Prevention. Precautions against overcrowding on board ship in hot seasons, and the maintenance of cleanliness are prime considerations. In commissariat herds close crowding must be avoided, feeding should be done at different points for six or eight cattle at each, the yards should be frequently changed, or carefully cleared of manure and sprinkled with a solution of 3 per cent. sulphuric acid. In case an animal is attacked it should at once be removed and killed, and its offal and the yard where it has been, disinfected. Food and drinking water should be specially wholesome.
Treatment. Mild cases may be successfully treated by the use of mucilaginous draughts, (boiled flaxseed, mallow, slippery elm, gum arabic) with antiseptics (salicylic acid or salicylate of soda 2 to 3 drs., salol 1 dr., creosote 1 dr., sulphate or chloride of iron 1 dr.) every three hours.
In the more severe cases the most varied treatment has been resorted to. Formerly opiates and astringents were largely employed, practically shutting up the poison in the intestine. Ipecacuan in large and frequently repeated doses had the advantage of soliciting the action of both liver and bowels, but however useful, it has gradually declined in public confidence.
An eliminating and antiseptic treatment has at present the most general acceptance. Seven grains of calomel has been given every two hours for two or three days in succession. Still more recently 2 to 4 ozs. sulphate of soda every three hours with hot water and antiseptics (salicylates, sulphites, salol, boric acid, creolin, naphthol) have been substituted. Even more important is the washing out of the large intestine by antiseptic enemata. These should be very copious and frequently repeated so as not only to render the contents of the rectum and colon antiseptic but to secure the discharge of the offensive matters as they are produced. The agents may be glycerine, carbolic acid, creolin, sulphate of iron, nitrate of silver, salicylic or boric acid. If the animal can be made to stand on an inclined plane with its hind parts elevated it will favor the penetration and retention of the liquid. Perfect rest is a most important accessory.
In case of recovery the return to ordinary diet should be gradual.