The real cause is to be sought in the manner of preserving the pulp in simple earth silos or in cemented silos, where it undergoes fermentation and putrefaction. The contained liquid is then extremely toxic. Filtered through porcelain and injected under the skin, it produces vaso-motor and vaso-paralytic disorder, identical with that seen in acute forms of the disease; in other cases it excites abnormal secretion, and leads to permanent diarrhœa and chronic gastro-enteritis.
This liquid, if injected intravenously, may prove toxic in doses of 2 to 3 cubic centimètres per kilogram of bodily weight. Its injurious effect is due to toxins secreted by special bacilli, which were isolated and studied by Arloing. The toxicity diminishes as the pulp becomes older, and can be avoided by adding antiseptics like common salt, which prevent fermentation. These experiments of the Lyons professor are certainly very interesting, and, although perhaps not identical with what occurs in practice, sufficiently indicate the way in which poisoning occurs.
Pathological disturbance only follows the use of decomposed pulp.
Animals reared on farms where distillery and sugar factory pulp is regularly given become accustomed to it, and are rarely affected. The chief sufferers are those recently imported, or recently placed on such food; in them the disease may assume either the acute, nervous, subacute, or chronic form.
Acute form: Symptoms. This form is exceptional in the ox, but is more frequent in the sheep. In oxen the earlier symptoms point to digestive disturbance, and consist of dulness, loss of appetite, colic, sensibility of the abdomen, cessation of rumination (without tympanites), and constipation. The excreta are hard, coated, and blackish in colour, but not blood-stained.
Diarrhœa follows, is accompanied by aggravation of the general symptoms, the temperature rises to 104° or 106° Fahr. (40° or 41° C.), and exhaustion is pronounced. Other, less characteristic, symptoms, such as grinding of the teeth and mastication without food being present in the mouth may accompany the above and arouse fears of peritonitis. In sheep the dulness and prostration shown at first suggest the existence of anthrax—a view strengthened by the fact that the respiration becomes very frequent and the fever intense, whilst death may be rapid, and may sometimes occur with startling suddenness.
Lesions. Bacteriological examination, or even a naked-eye examination, made immediately after death enables one easily to differentiate between the two conditions. When the animals have died very rapidly—in one night—lesions of enteritis alone are present. More marked cases exhibit thickening and intense congestion of the mucous membrane of the abomasum, which may be of a deep mahogany colour.
The intestine itself is affected, and even though the glandular epithelium is little changed, the intercellular spaces show ecchymoses and multiple hæmorrhages, which give the contents of the digestive tract the appearance of wine lees.
The abdominal viscera scarcely present any characteristic lesions. The liver has the appearance of having been boiled, as in many forms of poisoning. The kidney is congested and blackish; the spleen only appears hypertrophied when post-mortem examination has been delayed and microorganisms from the intestine have invaded the circulatory system. After death the kidneys and spleen very rapidly undergo softening.
Nervous form: Symptoms. Whilst in the first form the symptoms appear especially due to diastatic ferments present in the pulp liquid, in the nervous form they appear rather to result from the convulsing and paralysing action of ptomaines.