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.