McEachran compares the disease to what occurs in the human being during famines, from the ingestion of innutritious and unsuitable agents especially deficient in albuminoids. The Pictou farmers, being nearly all fishermen, neglect the farms during the summer season, so that hay is only cut after the seeds have been shed, and when little nutritive matter is left in the stalks. Almost all the cases he saw were on such neglected farms. Wyatt Johnston, however, found it equally prevalent in overfed animals, so that hepatic disorder from either extreme seems to conduce to it. Again, if caused by lack of nutrition in the hay, winter, rather than summer, ought to be the season of attack and prevalence. Starvation and excess may both favor the attack, but the gradual extension from farm to farm, is strongly suggestive of the presence of a specific cause—probably a living organism.
The limitation of the disease to certain farms and even fields, and the cirrhotic condition of the liver remind one of the Schweinsberg disease of horses, and the lupinosis of sheep, in which the poison is evidently the product of cryptogamic or bacterial growth. With the damp, foggy climate of Nova Scotia, it would not be surprising if it should be ultimately shown that the source of the trouble is in a cryptogam which has as yet only invaded a given limited area. The winter immunity would be explainable on this basis. So also would be the statement of Wyatt Johnston that “When it attacks a new farm it affects chiefly animals that have been on the farm for two or three years. By the end of the second year it kills or attacks 10 per cent., and by the end of the third season it has practically involved all the old cattle which have been allowed to remain on the farm.” The hepatic disorder being a progressive one and probably due to the toxic products of fermentations carried on outside the animal body, a few only would show the morbid results at first, while later, with advancing structural changes in the liver, and an increase of the toxins that cause it, the number of sick animals would steadily increase.
Symptoms. The animal is at first dull and sluggish, with drooping head, lusterless eyes, staring coat, normal respiration and temperature, pulse often about 60 per minute, relaxed bowels and marked diminution of the milk secretion. The milk acquires a bitter taste and unpleasant odor. The pulse is usually full and soft, and the eyeballs may bulge visibly out of the sockets. The diarrhœa tends to encrease, the stools becoming liquid and black, yet in exceptional cases the bowels are confined for the first four or five days, or even permanently, appearing to be completely paretic. By the end of a week the abdomen becomes full and pendent with hollow flanks (pot bellied), or even rounded and tense, while manipulation and percussion show an abundant exudation into the peritoneal cavity. The pulse encreases in frequency (80) but the temperature is not elevated unless there is concurrent sepsis (Johnston). Thayer quotes an advanced case with a temperature of 105° F. He also notes obstinate standing, trembling of the muscles of the hind limbs, and complete suppression of appetite and milk secretion.
The disease is essentially chronic, often lasting a number of months. Many cases are doubtless slightly affected before external symptoms are manifested.
Lesions. If the disease has resulted in death there is usually marked emaciation, yet the abdomen is distended by accumulation of a clear yellowish fluid. From six to nine or more gallons may be present. The fat of the omentum, mesentery and sublumbar region has disappeared and the connective tissue is distended by a clear, amber-colored, watery fluid. The liver is the seat of marked changes. In the early stages it is congested and the gall ducts and bladder are filled to repletion with a thick, dark colored bile, which is further present in abundance in the intestines. In these early stages Johnston found cloudy swelling and opacity of the hepatic cells; somewhat later they had undergone distinct fatty degeneration. In the advanced stages, however, in animals that had been ill for two or three months, there was distinct fibrous degeneration, and compression and disappearance of the normal liver cells, in other words, a condition of marked cirrhosis, the result doubtless of the early congestion.
Johnston further notes the distension of the submucosa of the fourth stomach at intervals by a clear, viscid, liquid exudate, so that rounded swellings appear on the surface, and in some instances, after a month’s illness, distinct ulcers are shown upon the mucosa.
The lungs, pleuræ, pericardium and nervous system, are usually normal, unless in case of septic complication when petechiæ and circumscribed blood extravasations may be seen.
Prevention. The Canadian government has gone to great expense in buying and slaughtering the diseased cattle with no very evident good result. McEachran suggested the feeding of oil cake and other albuminoid and oleaginous food to counteract the alleged malnutrition, but Johnston’s cases in over fed animals show that something more is demanded. Another suggestion has been made to the effect that cattle should be exterminated in the affected counties to remove the material necessary for the maintenance of the poison. But, if the poison is produced by a cryptogam growing on the vegetation, as seems not improbable, it would be likely to extend all the same in the absence of cattle. In such a case the true course is to study the nature of the organism, and the phanerogam on which it grows, when it might become possible either to exterminate the flowering plant which acts as a host for the offending organism, or to spray it with an effective fungicide and thus reach the object in another way.
INFECTIVE GASTRO-ENTERITIS AND PNEUMONIA IN THE NEW BORN; WHITE SCOUR.
In treating of this disease in Vol. II, page 141–2, the work of Jensen, Perroncito and Nikolski is quoted, with the remark that “it is premature to specify any particular microbe as the sole cause of the affection.” Since the publication of that volume, Nocard, investigating in Ireland a very prevalent and fatal affection of new born calves, which proved fatal by “white scour” a few days after birth, or by pneumonia one or two weeks later, identified as the pathogenic agent a small, nonmotile, ovoid bacterium, taking the polar aniline stain, bleaching in Gram’s solution, failing to liquefy gelatine, or to form indol or to grow on potato. In other words it shows the general characters of the colon group of bacteria, causative of hæmorrhagic septicæmia, and classed as pasteurellas by Trevisan and Lignieres. This is not found in blood and lesions in all subjects, but is usually present in pure culture in the most acute, fatal cases. Its occasional absence later in the disease is explained, according to Lignieres, by the power possessed by these germs of robbing the healthy tissues of their power of resistance and laying them open to the attacks of other microörganisms which are usually present in abundance, but are harmless to the healthy tissues in the absence of the Pasteurella. As the disease advances, therefore, the primary pathogenic agent (the Pasteurella) is crowded out by the active growth of other bacteria, which accordingly are found in complex cultures and in great variety. In his first observations on the victims of the white scour, Nocard found only these complex cultures, of which no one variety, isolated in pure cultures in vitro, and inoculated, proved capable of causing the disease. Later he found the Pasteurella (cocco-bacillus) in impure cultures from the diseased femoro-tibial joint of one of the subjects of the affection, and the pure cultures obtained from this were virulently infective.