PROTOZOAN ICTERO HÆMATURIA IN SHEEP. PALUDISM OF SHEEP. CARCEAG.
This is described by Babes and Starcovici as prevailing among sheep in the delta of the Danube, and held by them to be identical with the Roumanian Hæmoglobinuria of cattle (compt. rend. de l’Acad. des Sciences, 1892). Its essential cause is a piroplasma affecting the red blood globules, and very analogous to that of the protozoön of Texas fever, but its especial election for the sheep shows a specific difference, inasmuch as the Texas cattle fever does not attack sheep. Not only the parasite, but the symptoms and lesions as well, furnish a close counterpart to those of the cattle infection. It remains to be seen whether the pathogenic difference is due to a distinction in the piroplasma or to the absence from the Southern States of America of the particular tick or other insect which attacks the Danubian sheep.
Bonome (1895, Virchow’s Archives) describes the same disease as prevailing in Italy, describing the parasite and lesions at great length.
Finally my colleague Dr. W. L. Williams, and later Dr. Knowles, have identified the disease in the upper part of Deer Lodge Valley and the lower part of Silver Bow Valley in Montana, prevailing among sheep only, extending year by year, and proving disastrous to the sheep husbandry. Sheep were introduced into these valleys as early as 1875, but it was only in 1891 that the flock masters recognized the existence of this disease. By 1895 it prevailed over an area of 300 square miles. It made its advent in 1891 in four or five large flocks (2,000 to 10,000 head each) on land which they had occupied for nine years, and so disastrously that several sheep ranchers, after an experience of a year or two, sold out to the butcher and abandoned the sheep industry.
All or nearly all cases seen in 1896 were in parturient ewes, (4 to 6 days after parturition), the constitutional condition attending on lambing proving a most potent factor in causation.
The protozoön repeated the characters of that found in the sick sheep in Italy and the Danubian delta, and the conditions of the blood and the structural lesions supported the idea of identity.
Altitude seems to have little or no effect as a causative factor, as the disease is domiciled alike on the low alluvium of the Danube and the Deer Lodge Valley of Montana over 5,000 feet above the ocean. In both regions there is the common condition of inundation or its equivalent irrigation, for the Montana range is dry and arid, interspersed with alkaline bogs inimical to vegetation, but prolific and fruitful under irrigation. The Montana disease has been attributed to mineral poisons carried on the winds from the extensive copper smelters in Butte and Anaconda, but the smelters had been in existence for eight or ten years before this disease was observed, and from its appearance the infection has gradually extended, attacking sheep only, and sparing other domestic animals, which would have suffered as well from a mere mineral poison on the vegetation. The doctrine of a mineral poison is equally contradicted by the habitual prevalence of the disease in spring and autumn, while it is dormant in winter and summer. In winter the flocks eat hay cut from the richer valley lands and meadows, while in summer they are pastured on the foothills and mountains, and drink from the mountain springs surrounded by alkaline bogs. The autumn outbreak occurs long after the mountain grasses have dried up, when the flocks are thrown back on the supplies obtained from the alkaline bogs and the valley pastures. In late winter and early spring the growth naturally starts first in the same boggy and valley areas, and both facts suggest a microbian infection—protozoan or bacteridian. If an intermediate host or bearer—insect or other invertebrate—is to be assumed it implies two generations of these, a spring and an autumn one, in the same season, or otherwise a restriction of such invertebrate to the low valley pastures and the alkaline bogs on the higher levels, and that they disappear from the drier, arid areas in summer. It cannot be an obligate parasite like a louse or melophagus which would be constantly present, nor a musquito absent in early spring. But up to the present no invertebrate host or intermediate bearer has been identified. Cases were at first reported in the Angora goat, but this animal is now known to be immune.
Microbiology. The parasite is formed in the red globules and blood serum of the affected sheep and closely resembles the microbe of Texas fever. In the blood globules the parasite is seen in different forms, round, oval, oblong or curved and from one tenth to one sixth the diameter of the red globule. A single red globule may show from one to four of the microörganisms. They may at times show indications of division, and at others, automatic amœboid movements, from one portion of the blood globule to another, or from the periphery toward the centre. The affected blood globules are usually enlarged, having lost their biconcave outline, and become biconvex or spherical, with irregular crenated surface, and a dull, lustreless appearance instead of a clear red or yellow aspect. The protozoön stains readily in anilin red or methylene blue.
Lesions. The condition of the carcass was good or even high, in sheep attacked when in good flesh, and in which the affection ran a rapid and fatal course. In sheep attacked while in low condition on the other hand, the case tended to be milder and more prolonged, and the body was emaciated and anæmic. Dropsical swellings were common on the ears and sides of the head and neck.
The skin, connective tissue, fat, and other normally white tissues were usually of a yellow color, varying from sulphur to lemon color. The muscles were pale and soft with a yellowish tinge.
The blood was pale, thin and watery, especially in protracted cases, formed a loose coagulum, or remained fluid with a grayish red color. There was marked leucocytosis (1:4 or 5).
The stomach and intestines were more or less icteric, and contained little ingesta.
The liver was congested, softened, shrunken in protracted cases, colored of a deep yellow especially in the interior, and with gorged biliary radicles so that the acini stood out very prominently. The gall bladder was usually well filled with a thick, flocculent bile, yellowish green, blackish green or chocolate color.
The spleen appeared shrunken, somewhat spherical, 2 to 3 ozs., firm, and with a dark, reddish brown pulp.
The kidneys were greatly enlarged, weighing 12 to 16 ozs., dark red or bluish black, friable, and on section exuding freely a bloody or chocolate-colored liquid. The capsule was easily detached. The bladder contained a bloody or chocolate-colored urine, but was sometimes empty.
The heart cavities were empty or contained small diffluent blood clots. Petechiæ were common on pericardium and endocardium.
Yellowish or yellowish green gelatinoid effusion was often present, not only on the head and neck, but also on the inner side of the thighs, and in one or other of the serous cavities.
Symptoms. The first indications noticed are dulness, listlessness, a dragging behind the flock, ceasing to graze, arched back, and stiff or unsteady movements. There is moderate fever, yellowness of the visible mucosæ and skin, and rosy, bloody, or reddish brown urine.
Puffy dropsical swellings are noticed, especially on the ears, sides of the face, on the neck or thighs, and the patient lies down most of the time.
The patient usually dies in a state of collapse which has lasted for several hours, yet in certain cases it is preceded by a convulsive agony.
It is certain that the affection may appear in a mild form, as sheep slaughtered in apparent health are found to show the general icterus, the congested liver, and the leucocytosis with crenation of the red globules which characterize the disease. The icteric carcasses are said to be recognized and condemned at Kansas City and Omaha.
The duration of the affection is from 1 to 5 days, though it may last longer, and severe attacks usually end in death.
The prevention of this disease can, as yet, be based only on the same principles that guide us in the case of Texas fever. Search should be made for an invertebrate host of the protozoön, by the extinction of which infection may be stopped. The spring outbreak could be opposed by feeding hay on safe ground until the higher pastures furnish sufficient vegetation. To counteract the autumn attack, the sheep might be fenced out from the alkaline bogs, and the forage supplied in the form of hay or soiling crops. If it should appear that any wild animals harbor or transmit the parasite, a campaign of extermination upon them would be in order. If, as seems to have been the case in the early nineties, the movement of sheep from the infected flocks and pastures tends to cause the disease, this should be legally interdicted. Finally, the complete extermination of the sheep on infected areas could be practiced, and their place supplied by the immune Angora goat.