Synonyms. Definition: Acute protozoan remittent fever, of rainy season
or after, with destruction of red globules, anæmia, emaciation,
dropsy, icterus and cutaneous or mucous eruption or discharge.
Distribution: India, Burma, Cochin China, Persia, Phillipines, etc.
Trypanosoma Evansi: a fusiform flagellate infusorian with undulating
membrane, attacking the red globules: agency of flies as carriers,
infection of dogs; of crows; feeding, licking; rats; open sores;
stables; yards; pastures; pickets; stagnant water; manure or rubbish
heaps; abattoirs. Lesions: anæmia; trypanosoma swarms during relapses;
leucocytosis; œdemas; effusions; blood extravasations; splenic
enlargement; emaciation; gastric and intestinal congestions; gastric
ulcers; kidneys petechiated, swollen; brain effusion. Incubation, 2 to
8 days. Symptoms: local swelling, 2 to 4 inches by 4th day; decreases
to 14th day; the general symptoms; hyperthermia 102° to 104° F., night
highest; dulness; sluggishness; inappetence; icterus; cutaneous
eruption; remission in 1 or 2 days; exacerbation after 3 to 10 days;
catarrhs; petechiæ; stocked legs; pectoral swelling; encreasing anæmia
and emaciation; ulcers on mucosa or skin; generative excitement; fœtid
diarrhœa; urine profuse, bilious, albuminous or with casts; thirst;
intestinal rumbling; debility; marasmus; hair erect; skin dry, rigid.
Duration variable. Diagnosis: based on above, confirmed by finding
blood parasites, constantly fatal in horses. Surra in camel, ox,
buffalo, rabbits, rats, mice, dogs, cats, apes. Treatment:
unpromising; mercurials, iodides, chromates, arsenates,
terebinthinate, phenic acid, santonin. Dry, clean, airy stable, dry
grain, tonics. Prevention: keep horse and mule from infecting
locality; use oxen rather: stables, pickets, etc., apart from marshes,
pools, manure and rubbish heaps; disinfectants, insecticides, seclude
all surra-affected animals: smudges. Sanitary police.
_Synonyms._ Sar, Zahrbad, Gumzahrbad, Kushkzaharbad, Sokra, Sokhra, Tap,
Tapdik (Punjab): Phitgya, Purana (Meerut): Berbag (Bombay): Tarai,
Tebersa, Wabai-ki-bokhar, Pernicious Anæmia, Trypanosomosis, Relapsing
Fever, etc.
_Definition._ An acute, relapsing, protozoan fever of equines, camels
and elephants, inoculable on other animals, occurring during or after
the rainy season, and characterized by hyperthermia which is liable to
be intermittent, remittent or relapsing, anasarcous swellings, petechiæ
of the mucosæ, icterus, cutaneous eruption, nasal, ophthalmic, vaginal
and other mucous discharges, rapidly advancing anæmia, emaciation and
debility, and above all, by the presence in the blood, at intervals from
one to six days, of swarms of protozoa, analogous to those found in
dourine or nagana.
_Geographical Distribution._ Surra has long been known to the English
veterinarians in India, occurring during or just after the rainy season,
and especially on the low flooded lands, along canals, rivers, lakes,
etc., and later in Burma, Cochin China, the Persian Gulf, Persia.
Lingard claims its existence in East Africa, North and South America,
Australia and Southern Europe, but he has evidently confounded it with
nagana and other affections. The discovery of the disease by Dr. Slee in
1901, among American, Australian and Chinese ponies in the Philippines
is suggestive of a very wide diffusion of the infection in Southern Asia
and adjacent islands, with which an American work on veterinary medicine
must deal.
_Cause. Parasite. Trypanosoma Evansi._ The essential cause of the
disease, Trypanosoma Evansi, discovered by Dr. Griffith Evans,
Inspecting Veterinary Surgeon, British Army, in 1880, is a flagellate
infusorian, pointed at one end, near which is a dark centrosome, and
from this a flagellum running along the free border of the broad
undulating membrane to the extreme opposite end of the parasite and
extended beyond this as a waving lash. The length of the Trypanosoma
Evansi is 20 to 50μ, (10 to 14μ, Smith and Kinyoun, Manila), its breadth
1 to 1.5μ. By reason of its large size and active motion it is easily
detected in a film of fresh blood under ⅙th inch objective, and no less
easily when dried and stained on a cover glass. It must be borne in mind
that the mature parasite appears in the blood at intervals in swarms, so
that examination at one time of day, or on a particular day, may fail to
detect it, while examinations made earlier or later are successful. The
general structure and successive stages of growth of the parasite appear
to be the same as described for the Trypanosoma Equiperdum of Dourine,
to which accordingly the reader may turn for description. The
distinction from that parasite is to be found mainly in the
pathogenesis. In this respect it should be noted that the parasites are
strongly attracted by the red globules, upon which they fasten
themselves by the blunt ends, shaking the cell in the most vigorous
manner and even breaking pieces off and carrying them away. They are
most strongly attracted by the concave part of the disc, and when there
are rouleaux they will bore between the globules and even push them
apart (Evans).
The appearance of the disease at the conclusion of the rainy season when
the waters dry up and become foul, has led to the idea that the parasite
lives in waters, but as this is also the time of the great swarming and
activity of flies, and as the trypanosoma is found in the bodies of
tabanidæ and hippoboscidæ that have bitten affected animals (Lingard),
and as horses crowded together so that the fly with piercing apparatus
still wet can pass from horse to horse (Evans), the opinion has grown
that it is a compulsory parasite which is transmitted through the bites
of insects. In 1880, Griffith Evans found that the native Hindoos
attributed the disease to the bites of a very large brown fly which was
active in July (probably a tabanus), in 1897, Pease identified the
incriminated fly as the tabanus tropicus. Finally, Rodgers, in 1901,
took flies that had been on surra horses, kept them 4 days or longer and
found that their bites failed to produce surra; whereas those that were
allowed to go directly from the sick to the healthy animal produced the
disease in the latter. The direct experimental inoculation from horse to
horse infallibly conveys the disease so that the flies are not needed to
pass the parasite through an intermediate stage of its existence, but
merely to carry it. It follows that no particular fly is the bearer but
any insect may carry the infection from a bite or sore to inoculate it
on a sore or by a bite on a fresh animal. Different observers have
noticed the tendency to the infection of dogs and other animals that fed
from rubbish heaps, or upon the carcasses of animals dead of surra,
suggesting at once the intervention of the swarms of flies that
congregate at such places. This is probably another example of the
shrewd insight of the common mind, as in the case of the tick-borne
Texas fever.
Lingard finds another bearer in the crow which sits on the backs of
affected horses, pecking at the wounds, and passes at once to other
healthy horses to peck their sores.
Experiments in feeding the infested blood to sound animals, have
apparently succeeded, and the observation that dogs and cats suffer from
eating the carcasses is in favor of this view. Horses that lick the
infested sores, or the blood drawn by the flies may readily infect
themselves, and especially if the mouth bears scratches caused by
fibrous food, leech bites, or sores from bits, or if the pharynx or
stomach has been wounded by bots or spiroptera.
The water and food are blamed by the natives in some quarters, but
Pease’s observations on the Bombay tramway horses, which all perished
though kept on boiled water and carefully picked fodder from sound
regions, would suggest that this if a channel of infection at all, is
not the main one.
The bowel excretions of rats harboring trypanosoma, when mixed
experimentally with the food of the horse, have been charged with
causing surra, but there are objections to the acceptance of this as a
common cause. The alleged period of incubation in the horse in such
cases was 40 days in place of the usual 7 or 8 days, when inoculated
from a horse first affected in this experiment on a second the usual
incubation of 7 or 8 days was shown, and though the horse fed on rat’s
dung in the infected region of Bombay contracted the disease, the
experiment failed when the same dung was fed in a high dry region
unaffected by surra. The natural inference is that Bombay experimental
horses contracted the affection in the usual way, probably through
insects.
In the rainy season the Indian rats swarm with the Trypanosoma Lewisi,
an entirely different species, and though they can be successfully
inoculated with the T. Evansi of Surra, the T. Equiperdum of Dourine,
the T. Brucii of Nagana, and it is alleged the T. Equinum of Mal de
Caderas, yet these are not their common parasite. The presumption is
that the rat affected with Trypanosoma Evansi could transmit the disease
to the horse through one of the many possible insect channels or
otherwise.
Neither condition, sex nor age appears to affect receptivity. Open sores
especially open the way for infection.
The position of stables, yards, pastures or picket grounds near stagnant
water, manure or rubbish heaps, abattoirs or other places that breed or
attract flies, is a much more important consideration. Foul stables, or
those having light from both sides are more exposed to flies.
_Pathology and Lesions._ The pathology of the disease consists in the
rapid destruction of the red blood globules by the trypanosomata. It is
a form of rapidly advancing pernicious anæmia due to the great and
active voracity of the trypanosoma. The swarming of the trypanosoma in
the blood at the period of the relapse and the absence of the mature
form in the intervals is remarkable. The trembling movement in the blood
at the period of swarming results from their prodigiously active
movements. The red globules may assume various forms, crenate,
echinated, (Ranking), and more or less broken up or disintegrated, their
numbers steadily decrease, leaving the blood thin and watery with rusty
serum and yellow (icteric) staining of the white tissues, even the
bones. Encrease of white globules, actual or relative, has been a marked
feature (always present in typical cases, Burke).
Petechiæ are especially common on the conjunctiva, vaginal mucosa,
endocardium, and less marked in the nose, mouth, and serosæ.
Œdemas are common, yellowish, gelatinoid exudate at the base of the
heart, subcutem, between the muscles of the limbs or elsewhere, and as
effusions into the pleuræ, pericardium or peritoneum.
Distinct blood extravasations have been noted beneath the endocardium.
The spleen is often enlarged, excessively so if death occurred during a
paroxysm. The lymph glands are swollen and appear dropsical.
The whole body is emaciated and shrunken, the visible (unpetechiated)
mucosæ are pale and bloodless, often yellow, yet rigor mortis is well
marked.
Gastric ulcers are common (Steel, Burke, G. W. Evans) apparently
preceded in many cases by capillary embolism, congestion and
degeneration. Intestinal congestions are frequent (Steel, Burke), but
ulcers are rare (Geo. H. Evans).
The liver may be normal (Griffith Evans), or especially during a
paroxysm (Lingard) congested, inflamed and enlarged. The pancreas is
usually normal.
The kidneys are petechiated, congested, œdematous, or the seat of blood
extravasations.
Instances have been noted of cerebral and meningeal œdema (Steel,
Lingard), encrease of fluid in the arachnoid or lateral ventricles, or
in the spinal cord, with gelatinoid exudation in the lumbar portion
(Lingard). Like other tissues, in advanced stages the nerve centres are
usually anæmic (Geo. H. Evans).
_Incubation._ As made out by inoculation cases this extends from two to
eight days, according to the dose—five to seven days being the most
common. Infection by inoculation subcutem in mules showed a hyperthermia
on the fifth day; or by ingestion (feeding the virus) on the sixth day
(Steel). Longer (alleged) incubation depends mainly on the first slight
paroxysms having been overlooked, or set down for the frequent bilious
and icteric condition which is common in mules and horses in India
(Steel), or to a later infection by insects or otherwise.
_Symptoms._ In experimental cases a small raised swelling in the seat of
the inoculation, appears in 24 hours, encreasing to 2 to 4 inches in
diameter, and 1 to 1½ inch high by the 4th day, and loosely connected
with the parts beneath. From the 4th to the 14th day it decreases in
size and softens and general symptoms set in.
In casual cases these general symptoms are the first to be observed.
There is a transient fever 102° to 104°, highest toward night and
without preliminary chill, hot mouth and skin, dulness, sluggishness,
inappetence, yellowness of the mucosæ, petechiæ on conjunctiva or vulva,
and sometimes nodules like those of urticaria on the skin. After a day
or two these symptoms subside, the temperature is 101° F., or below, the
mucosæ clear and pale, and spirit and appetite nearly normal. These
slight first paroxysms are rarely seen by the veterinarian, having been
looked upon as one of the oft-recurring bilious attacks of a hot
climate. The remission lasts for 3 to 10 days when the second paroxysm
sets in, like the first but often more marked: temperature 102° to 104°,
eyes especially the membrana nictitans petechiated, epiphora, slight
catarrh from nose or vulva, it may be stocking of the legs, or pitting
swelling under the breast bone, or abdomen, or in the sheath. Like the
first, the second paroxysm subsides, and after another interval a third
sets in, to be followed in like manner by a fourth, a fifth and so on,
if the patient survives. With each the symptoms become more pronounced,
the mucosæ are left more pale and bloodless, debility and weakness are
greater, emaciation is more marked, œdema of the limbs or body more
extensive, hyperthermia may reach 105° or more, the pulse is weaker and
the heart more liable to palpitation, and the respirations may reach 50
or 60 per minute. Yet in sparely built animals dropsy may be entirely
absent (Steel). Steel often found superficial, circumscribed ulcers on
the tongue, inner sides of the lips, nose, eye, or vulva, beginning as
epithelial degeneration, followed by superficial erosion and early
healing. Sometimes, similar erosions appeared on the skin. Generative
excitement may be present, the mare appears to be in heat, while the
horse has erections, which are supposed to depend directly on the
implication of the generative centre in the lumbar myelon. The
submaxillary glands sometimes swell and even suppurate and discharge a
gluey pus (Griffith Evans). The bowels are usually costive at first, the
fæces may be glazed, but in advanced stages they become soft, pultaceous
and fœtid. The urine at first normal in amount, becomes later abundant
or even profuse (Griffith Evans, Ranking, Nariman and Vaz, Lingard). It
is at first yellow and turbid, later of a dingy green or greenish
yellow. Sometimes it diminishes as the disease advances. It may contain
bile, albumen, or even casts (G. H. Evans), though the latter appear to
be exceptional. The reaction varies, sugar is absent, and the parasite
has not been found in it. Appetite though interfered with during the
paroxysms, remains fair or even voracious in the intervals and the
animals may eat to the last (Burke). Thirst usually encreases with the
advance of the disease, in keeping with the free urinary secretion.
Rumbling and gurgling of the bowels are common and even tympany at times
(Lingard).
In the advanced stages the picture is one of great anæmia, marasmus and
general debility. When moved the animal will stumble over the slightest
obstacle, even the litter, recovering himself with effort and
difficulty. If he should fall he is liable to remain down indefinitely,
the side next the ground becoming drenched with sweat though there is no
general perspiration. The hair becomes encreasingly dry, withered and
erect, the skin dry, powdery, rigid and more and more firmly adherent to
the bones and muscles, losing all its natural pliancy and mellowness,
and becoming like that of a dead animal. It is bloodless, and sloughs
readily over the prominent bones, where compressed or bruised in lying,
owing to the lack of nutritive and reparatory action. The visible mucosæ
are absolutely bloodless. The muscles as a whole are wasted to an
extreme degree, but this atrophy is most marked in the back and loins,
along the longissimus dorsi and in the quarter in the gluteal muscles.
The patient may remain recumbent, from sheer weakness, for a length of
time at the last, or he may get up after a long recumbency and stand to
the end.
Death may occur early with general anasarca and extreme hyperthermia
(110° F.). In the great majority it appears to result largely from
perforation of the stomach, clots in the heart, or general debility and
heart failure.
_Diagnosis._ With symptoms such as are above described the discovery of
the trypanosoma in the blood completes the diagnosis. Trypanosoma is
found in dourine, nagana and other affections so that the discovery of
it alone would not be conclusive as to the existence of surra. Nor can
the discovery of the parasite always be made at the first or second
attempt. The swarm of mature trypanosomata is found with the advent of a
paroxysm, and as the veterinarian is often called during the decline of
the attack the parasites have already retired and elude his
investigation. It becomes needful to take the temperature and examine
the blood daily sometimes for eight or ten days, and when with a sudden
rise of temperature he finds also a swarming of the mature
trypanosomata, the diagnosis is perfect. A drop of blood placed on a
cover glass, pressed down upon the slide, and placed under the
microscope, will show the parasite with eel-like movements among the
blood globules. There may be very few during the first or second
paroxysm, but they become numerous and very obvious as the disease gains
its height. Evans recommends to use defibrinated blood.
They may be dried rapidly on a cover glass, fixed in absolute alcohol
one or two minutes, then stained ten minutes in a mixture of the two
following liquids united just before using:
A.—ONE PART OF THE
MIXTURE.
Methylene blue 1 Grams.
Borax 2.5 „
Distilled water 100 „
B.—FOUR PARTS OF THE
MIXTURE.
Eosin .1 Grams.
Water 100 „
The plasma of the trypanosoma appears blue, the flagellum red and the
chromatin of a different shade of red. It may be permanently mounted in
balsam.
_Mortality._ The disease is constantly fatal in horses, though the
animal may survive for months.