As predisposing causes, must be named a weak constitution and damp, dark, filthy, or otherwise unwholesome buildings. Buildings with no drainage nor ventilation beneath the floors, standing on filth-saturated soil, and those with double walls holding dead rats and chickens are especially to be dreaded. In breeds of inconstant color the lighter colored calves (light yellow, light brown) are more subject to such attacks than the darker shades (dark browns, reds, blacks). The weak constitution may be a result of close breeding, without due consideration of the strength and vigor of the parents. Then young animals kept indoors in impure air, damp and darkness are more susceptible than those that are kept in pasture and are invigorated by exercise, pure air and sunshine.
Aside from the general run of causes, predisposing and exciting, we must recognize the contagious element. Jensen has sought to identify the microbe as a small ovoid bacillus united in pairs, or in long chains. This was present not only in the ingesta, but in the lesions of the mucosa, and in the lymph glands. Its cultures ingested in milk, or injected into the rectum sometimes produced the affection. Microscopically it resembled the bacillus fœtidus lactis, but the latter failed to produce the disease. He looks upon it as a sport of the bacillus coli communis.
Perroncito found micrococci, usually arranged in pairs and comparable to the cultures of those obtained from the blood in the pneumonia of calves. The injection of the cultures into the thorax of a Guinea-pig caused pleuro-pneumonia with or without dysentery. The rabbit proved immune. At the necropsy the Guinea-pig like the calf showed the diplococci in the blood. Nikolski who studied the affection in lambs seeks to incriminate both micrococci and bacilli.
It is premature to specify any particular microbe as the sole cause of the affection. It seems not improbable that bacterial ferments of one or more specific kinds, which in a healthy animal have no injurious effect, may by special combination, or by growth in a mucosa in a given morbid condition, acquire properties which render them not only violently irritating, but may retain such properties so as to render them actively contagious. In this condition they may overcome the resistance of the most healthy stomach and bowels and attack all young animals into which they may secure an entrance. Certain it is that the infection may persist in the same stable for years, will enter a new herd with a newly purchased cow or calf bought out of a previously infected lot, and will follow the watershed and affect in succession the different herds drinking from a stream as it flows downward.
The similarity of the germ found by Jensen to the bacillus coli communis, suggests that in this as in a number of other contagious affections a pathogenic sport from this common saprophyte is at least one of the microbian factors in this disease.
Symptoms. These may set in just after birth but usually the disease occurs within the two first weeks of life. When delayed for a few days after birth it may be preceded by some constipation, the fæces appearing hard, moulded, and covered with mucus. This is especially the case when the meconium has been retained and has proved a cause of irritation. The young animal is careless of the teat or refuses it (or the pail if brought up by hand), yawns and seems weary. The abdominal muscles are tense and the belly may be swollen if fermentation has already set in but this is rarely excessive. Straining to defecate usually causes eructations of an acid odor, and sometimes vomiting of solid soursmelling clots. Abdominal pain may be manifested by uneasy movements of the tail and hind limbs, by looking toward the flank and even by plaintive cries. This is followed within six hours by liquid dejections, at first merely soft, slimy and sour but soon complicated by a peculiar odor of rotten cheese which becomes increasingly offensive as the malady advances. The tail and hips become soaked with the discharges and as the putrid fermentation goes on after their discharge of the fæcal matters, the air becomes more and more repulsive. The same odor pervades the mouth and the breath and the tongue is coated with a whitish, grayish or yellowish fur.
The fæces become more watery and slimy, with much casein in course of putrefaction, and the patient is rapidly run down by the profuse discharge and the general poisoning by absorbed putrid products. In the worst cases this may prove fatal in one or two days.
When the illness is more prolonged the alvine passages which at first number five or six per day, increase to fifteen or twenty and are passed with more effort, usually leaving the anus in a liquid stream. The color of the stools changes from a yellow to a grayish yellow or dirty white, hence the common name of white scour, and the fœtor is intensified.
Appetite may be in part preserved for a time but is gradually lost, and the subject becomes dull, listless and weak, indisposed to rise and walking unsteadily when raised. A general appearance of unthriftiness, staring coat, scurfy, unhealthy skin, pallor of the mucous membranes, arching of the back, tucking up and tenderness of the abdomen, excoriation of the margins of the anus, and congestion of the rectum as seen everted during defecation, mark the advance of the disease. Emaciation becomes very marked, and weakness and prostration extreme.
Fever usually sets in as the disease advances, as marked by hyperthermia, hot dry muzzle, hot ears, accelerated pulse and breathing.