This curious affection is recorded as having prevailed in the winter of
1897–8 in different localities in Iowa, Missouri, Kansas and Nebraska.
In 1900 and 1901 it was again reported in different parts of Iowa.
_Causation._ No bacteriology of the disease has been given, and its
appearance in isolated herds which had no known communication with other
herds, and even in the young cattle on a farm to the exclusion of the
older ones, seems to suggest an enzoötic origin, perhaps in food or
water, or in some toxin determined by a fermentation of organic matter
out of the body.
On the Rodkey farm at Blue Rapids, Marshall county, Kan., eight heifers
from ten to fourteen months old, suffered, while the seventeen steers of
the same age and the milch cows escaped. (Steddom). Near Shelby, Ia., a
bull, from a healthy herd, broke into an affected herd and served cows
there, and was afterward returned to his own herd and served cows there,
but did not communicate the disease. (S. T. Miller). No case is recorded
to show that any bull serving affected cows or heifers contracted ulcer
or other disease of sheath or penis.
In one herd near Shelby, Ia., nineteen head of cows and heifers
suffered, while the four steers in the herd escaped. In another herd of
twenty-six head, in the same district, the four cows and eight of the
twenty-two steers suffered. It is not, therefore, confined to the
females. (S. T. Miller).
In all cases the disease appeared in the cooler months, from October to
April inclusive, and while the cattle were secluded in muddy yards.
In different cases they occupied the yards in common with swine which
were charged with wounding the vulva, until the general character of the
outbreak forbade this conclusion. At Blue Rapids it was sixty-two days
after they had been yarded with the hogs before the disease was
observed.
In this case the lot was small, poorly drained and very muddy most of
the time. Calves and hogs drank from the same troughs until the disease
appeared. The water supplied to the calves and hogs was from a well
sixteen feet deep. The cows, which escaped, were supplied with water
from the Blue River.
Cows, heifers and steers were fed on a ration of shelled corn 6 parts,
rye 1 part, oats 1 part, and had an abundance of fodder, consisting of
prairie hay and millet in equal parts. They were in good condition, some
of them fat, and nearly all dehorned. A second herd had shelled corn,
kafir corn and cane, with water from a shallow well, and all (cows and
heifers) suffered.
As showing the localized nature of the cause, C. Muller adduces the case
near Ottumwa, Ia., in which a herd of 30 calves were attacked, and sold
out, the owner filling the same yard a few days later with 30 more
bought in the surrounding country, and which he put on the same rations.
In about 10 days the disease appeared in the second lot.
On the Rice farm, Blue Rapids, were 60 yearling heifers, bought in
Kansas City, and two home cows. In the first week after arrival 5
heifers suffered, in the second week 20, in the third week 40, and in
the fourth week all the 60. The two cows mingling with them were only
slightly affected.
In the Rodkey farm, Blue Rapids, cases, all of the young cattle (which
alone suffered) had been raised on the farm and had not been exposed to
outside cattle.
_Symptoms._ “The ulcer, in almost every case, started as a mere
abrasion, the size of a pinhead, usually on the inner surface of the
labia, near the border of the inferior commissure, gradually eating its
way through until it appeared as a much larger denuded surface on the
outside” (C. Miller). S. T. Miller says: “The first noticeable symptom
was serous exudate, rapidly forming into a brown scab, under which was
very fœtid pus, with extensive inflammation. The affection usually
occurred on the lower portion of the lips of the vulva, in heifers and
cows, and in steers around the anus or root of the tail. The scabs which
formed seemed to spread very rapidly, destroying more and more of the
underlying tissue and forming a thicker and thicker scab. The scab, if
pulled off, would expose a raw surface which would bleed very readily.
In a short time a new scab would be formed.”
Steddom says: “The vulvar lips thickened and continued to discharge for
four or five days. In the meantime certain pustules appeared, 0.1 to 2.5
centimeters in diameter. About the fifth day these ruptured and
discharged yellowish pus.” The mucous membranes of the vulva and vagina
were dry and slightly congested. The ulcers were covered with brown
leathery scabs, which adhered tenaciously and when detached left an
angry, red, purulent, granular, elevated and pitted surface. In some of
the more severe cases, one or both lips of the vulva had sloughed off,
and the sore had extended 10 to 15 centimeters on the skin of the
escutcheon. The pus from this sore did not corrode the adjacent skin.
The more severe cases showed loss of appetite, constipation, hurried
breathing, tucking up of the abdomen, with general dulness and
dejection, and great tenderness of the affected skin with stiff,
straddling gait.
_Pathology._ This is very obscure. The primary cause of the sores is not
evident, though their occurrence on the anus and vulva only, and
especially on the latter would suggest an elective affinity of the
poison (microbian or chemical) for these structures and their products.
If we assume a pathogenic microbe in the fæces, the question arises as
to the cause of the habitual immunity of the steer, and of the margin of
the anus in the majority of the affected heifers. The susceptibility of
heifers rather than cows may imply a previous exposure and acquired
immunity on the part of the mature animal.
Again if we suspect the existence of a necrobiotic agent of organic
origin (like ergotin, secalin, sphacelin) we must assume a superadded
microbian infection, implanted in the primary sore and rapidly extending
it. The prompt recovery under antiseptic treatment shows that no mere
chemical poison maintains the destructive process, for it is manifestly
the microbicide which puts a prompt limit to the disease, and under such
treatment no sphacelating agent in the blood or tissues keeps up the
advance of the ulceration or prevents healing.
_Treatment._ The ulcers healed rapidly under cleanliness and antiseptic
applications. The tail, anus, and vulva were washed with tepid water,
and then dressed with a solution of creolin (5:100), or carbolic acid
(3:100), or mercuric chloride (1:500 or 1000). The ulcers were touched
with a pencil of silver nitrate. S. T. Miller followed the sublimate
lotion by the subjoined ointment: iodoform 20 grains, eucalyptol 40
minims, phenic acid 20 minims, petrolatum enough to make 2 oz. C. Miller
in addition to the carbolic acid lotion applied the common white lotion
(zinc sulphate 1 oz., lead acetate 1 oz., water 1 qt.) and used silver
nitrate on the ulcers. Four dressings on four successive days were given
and in the milder cases healing was completed in 10 or 12 days.