Definition. Causes: presence of sclerostoma in arteries, form, habit,
nature, immature, biology, life in bowel, in submucosa, in arteries,
outside the mammal, pathogenesis, blood-sucking, verminous cysts,
verminous aneurisms, seats of latter, coagula, embolism, stagnation of
blood, œdema and thickening of intestine, mesentery, fermentations,
tympany, infective inflammations, blood extravasations, infection of
liver and spleen. Symptoms: sudden attack, violent colics, reckless
movements, frequent defecation followed by its arrest, palsy of
peristaltic movement, of pain, prostration. Course: two to twenty-four
hours, death from indigestion, tympany, obstruction, hemorrhage,
poisoning, recovery, sequelæ, laminitis, intestinal catarrh or atony,
debility. Treatment: aneurism worms beyond reach, treat lesions,
venesection, anodynes, stimulants of peristalsis, antiseptics,
compresses, sinapisms. Prevention: expel intestinal worms, exclude
embryos, tartar emetic, iron sulphate, arsenic, phenol, pure water,
occasional vermifuges.
_Definition._ Congestion and spasms of the intestines in connection with
blocking (thrombus or embolism) of the mesenteric arteries, and
verminous aneurism.
_Causes._ The essential cause is the migration of the sclerostoma
equinum (strongylus armatus, Rud.) into the mesenteric arteries in its
agamous condition. It seems appropriate therefore to here notice the
life history of this parasite.
The =sclerostoma equinum= (_strongylus armatus_) is one of the common
pin worms of the horse. It is distinguished by its dull gray or reddish
brown body, thickest at the cephalic end and tapering off toward the
caudal, but ending in a blunt point; by the round, open mouth furnished
with several firm chitinous rings, of which the _outer_ bears six short
symmetrically arranged papillæ, an _intermediate_ row of rounded blunt
tooth-like projections, and the _innermost_ a row of fine, closely
aggregated and very sharply pointed teeth for penetration of the mucosa.
Male ¾ to 1½ inches long, with caudal membranous alæ in two lateral
lobes, joined by a rudimentary central lobe: two delicate spicula.
Female ¾ to 2 inches long, blunt pointed tail, vulva in posterior half
of the body. Eggs ovoid with slightly raised ring around the centre:
oviparous.
_Habitats._ They are found in solipeds in two stages of existence, the
_mature worms_ in the cæcum and colon, and the _immature_ in the same
organs encapsuled in little pellets of manure, and in cysts in the
mucosa but also apart in the arterial system especially in the anterior
mesenteric artery and other gastric or intestinal trunks.
The =mature sclerostomata= are found attached to the mucosa of the large
intestine into which the head is sunk for the purpose of sucking the
blood, and they may be gray, brown or red according to the quantity of
blood which they have imbibed. The author has found them in little
hernial sacs of the mucosa hanging from the peritoneal surface.
The =sexually immature sclerostomata= are found in little pill-like
masses of ingesta in the large intestines and from which they project
part of the body through a narrow opening. Another habitat is in cysts
of the mucosa of the cæcum and colon and less frequently of the small
intestine, individual cysts varying in size from a pin’s head to a hazel
nut, and containing the young worm rolled upon itself, and varying in
size but always less than the intestinal worm and always asexual. In
some cases the cyst is found empty but with a small opening toward the
lumen of the bowel showing the means of escape of the parasite. A third
habitat of the immature worm is in the blood-vessels, especially the
posterior aorta and its divisions, and still more constantly the
anterior and other mesenteric arteries.
=Biology.= The ova of the sclerostoma are segmented in the oviduct but
are hatched out after they have been laid. The hatching may be effected
in the intestine or in manure or water external to the body. When
hatched out in the intestine they may pass out at once with the manure
or they may envelop themselves in pellets of the finer ingesta and
remain for a time in the bowel and finally pass out in this condition.
Baillet has traced their development out of the body. In a watery or
damp medium they are hatched out in a few days as a cylindroid worm ¼ to
⅓ mm. long, thick in front and with a filiform tail. In moist
environment but especially in damp manure they grow to 1 mm. or 1.5 mm.
and continue for months in this condition, but remain small and asexual,
until taken in, in the drink or green food of the soliped. Reaching the
intestine and especially the cæcum and colon they bore their way into
the mucosa and encyst themselves, or if they happen to perforate a
blood-vessel they make a habitat of that. In the cyst, development
proceeds and when it has reached a certain stage the worm once more
bores its way through the mucosa and reaching the intestine becomes
sexually mature.
In this last migration the young worm is liable to perforate a
blood-vessel in which case it is destined to a period of existence in
the blood. It may, however, have blundered upon a blood-vessel at an
earlier stage when seeking a temporary home in the mucous membrane, so
that the sclerostomata of aneurisms may be derived from two separate
sources. In the blood-vessels the parasite attains a length of 1 to 8
lines, whereas in the mucous cysts it does not exceed 3½ lines. Yet
Neumann holds that after leaving the blood-vessels they may again encyst
themselves in the mucosa before escaping into the intestine.
Several moultings take place in the asexual condition.
Other views have been advanced as to the development of the
sclerostomata. Colin believed that the ova deposited in the ducts of the
mucous glands and in the perforations made by the parasite in
blood-sucking, hatched in this situation and the embryo at once encysted
itself in the mucosa.
Leuckart imagines that the embryo found in the fæces or in water outside
the body of the soliped, should pass through an intermediate host before
it can return to gain sexual maturity in the horse. But no evidence of
the existence of such intermediate host is furnished, and the encysted
intestinal worms show no indication of a special development which would
have been accomplished in such host.
Willach holds to a hermaphrodite stage passed in the intestine of the
soliped. He found in the bowel small worms apparently related to the
sclerostomata by the appearance of the head and the caudal membrane, but
not exceeding three to five lines in length. Some were evidently females
and contained not only eggs with soft shells, but in one case embryos.
Others had the caudal membrane of the male, yet contained also a few
eggs. There is no vulva and the embryos escape by rupture of the
oviducts. These embryos he supposes are developed in the same host into
the familiar mature sclerostomata.
Whatever may be said of those alleged modes, the first described series
of changes and migrations may be taken as the usual and regular method
of development.
=Pathogenesis.= _Lesions._ These embrace perforations of the mucosa,
cysts, aneurisms, embolisms and congestions.
=Irritation of the mucosa.= The adult worms, like so many leeches are
continually biting and sucking blood from the mucosa and when present in
large numbers, hundreds, thousands, or a million create an aggregate of
irritation which may determine violent indigestions and congestions.
=Verminous Cysts.= These are like a pin’s head, a pea or hazel nut,
containing the asexual worm in a mass of purulent debris, or if empty,
presenting a small orifice where it made its exit.
=Verminous Aneurisms.= These are perhaps the most important lesions
caused by the sclerostome as they are the steppingstone to the dangerous
embolisms, and too often fatal colics and congestions of the intestines.
They are very common in some localities, and rare in others following
the distribution of the sclerostomata. Bollinger found them in 90 to 94
per cent. of adult horses, and Ellenberger in 84 out of 85 horses
dissected. They are found in all ages from six months up, and are nearly
always in the short, stubby trunk of the anterior mesenteric artery.
Often two or three exist in the same animal, the whole length of the
posterior aorta showing patches of disease, exudations, neoplastic
elevations alternating with depressions, and aneurisms and thrombosis in
its different branches. In 100 horses Bollinger found 168 aneurisms, 153
in the anterior mesenteric, and its divisions, 4 in the cœliac axis and
its divisions, 3 in the hepatic artery, 3 in the posterior mesenteric
artery, 3 in the renal arteries and 2 in the posterior aorta.
The special predisposition of the anterior mesenteric artery is
variously accounted for: 1st. There is the obvious fact that its
branches are distributed to the cæcum and double colon, the home of the
mature parasite, and to the small intestines which are first reached by
the young parasites that are taken in with the water and the food. These
are therefore most likely to get into the branches of this vessel and to
follow them up toward its origin. 2nd. The anterior mesenteric artery
distributes its branches to the small intestines the most motile portion
of the intestinal tract, and the cæcum and colon the most heavily loaded
with solid ingesta, it is therefore the most subject to traction, and
distensions, and the more so that the parent trunk is extremely short
and the divisions pass in all directions and to a large extent at right
angles, so that there is a dragging of the walls apart as well as an
obstruction to the blood flow and an increase of internal tension. The
distension, laceration, inflammation and softening of the internal coat
have accordingly been regarded as the starting point of an endarteritis
upon which the parasites have been implanted as a further cause of
trouble. We must not forget, however, that the sharp circle of teeth of
the parasite, by which it fixes itself on the intima of the vessel are
quite enough to produce initial endarteritis, without any assistance
from distension, traction or laceration.
The irritation of the intima from whatever cause determines here as
elsewhere exudation, and coagulation, and the inflamed walls losing
their tone yield more and more readily to the internal tension.
Sometimes the coagulum lines the aneurism or vessel all round, leaving a
narrow central passage through which the blood still flows; in other
cases the clot extends into the adjacent smaller vessels, completely
blocking them and disturbing circulation and innervation in the parts
which they supply. As a rule the parasites are found in galleries
hollowed out in the clot, and heads or tails may be seen to project into
the circulating blood. Sometimes they are found imbedded in the arterial
coat, or in an adjacent small abscess. The formation of aneurisms in the
other arterial trunks may follow the same method.
=Embolisms.= These come very naturally from the formation of thrombi in
the various arteries. The coagulum determined by the presence of the
worms, tends to undergo retrogressive changes notably fatty
degeneration, to which germs brought on the worms or in their alimentary
canals contribute. This together with the movements of the parasites
tends to break up the mass, and minute portions are washed on into the
different smaller vessels. Soon these reach divisions which are too
small to admit them, which are accordingly occluded and the circulation
through them abolished. The presence of microbes as well as fibrine
contributes to cause further coagulation, more absolute embolism and
arrest of the circulation.
It is further alleged that the sexual instinct in the summer months (May
to August) leads the worms to leave the aneurisms, to pass through the
smaller divisions to the cæcum or colon where alone full sexual
evolution is possible. In these migrations they cause the thrombosis of
the smaller trunks and determine the verminous congestions of the bowels
which are especially common in these months.
=Disturbances of the Intestinal Circulation.= As these usually occur in
the lines of distribution of the anterior mesenteric artery a knowledge
of its divisions and their destination and anastomosis, is essential to
an intelligent understanding of the pathogenesis and lesions. As first
pointed out by Lecoq the anterior mesenteric artery is divided into
three primary bundles: (a) a _left_ of 15 to 20 trunks which are
destined to the small intestine; (b) a _right_ which gives off cæcal
branches, one to the double colon, and one to the ilium to anastomose
with the last trunk of the left bundle; and (c) an _anterior_ which
gives one branch to the second division of the double colon and
anastomosis with the colic branch of the right bundle at the pelvic
flexure; and a second branch to the floating colon to anastomose with
the posterior mesenteric artery.
The divisions of the left bundle anastomose so freely with each other in
the mesentery and immediately above the intestine that the blocking of
any one branch cannot entirely arrest the circulation in the
corresponding part of the intestine. It may however produce a partial
local stagnation in the vessels of a short loop of intestine, resulting
in œdematous infiltration and thickening with resulting induration and
stricture of the gut. Chronic and permanent lesions are produced by such
blocking, but only rarely acutely fatal ones. Acute and fatal congestive
lesions of the small intestine from verminous embolism, occur only when
several adjacent divisions of the artery are blocked at once, and this
is a rare occurrence.
The right bundle of branches furnishes the only two arteries which are
supplied to the cæcum and the only artery furnished to the first half of
the double colon. The ileo-cæcal branch is less involved, first, because
being less dependent and smaller, it is less likely to receive an
embolus, and, second, because any lack of blood supply is
counterbalanced by the free anastomosis with the last iliac division of
the left bundle. When the embolus blocks the undivided trunk of the
right bundle this same principle comes into play, the free supply of
blood from the posterior branch of the left bundle supplying blood
through its anastomosis with the iliac and cæcal branches of the right.
But when the emboli are lower down, in the cæcal branches of the right
bundle, or in these and the colic branch, arrest of the circulation in
the intestinal walls ensues, followed by paresis, passive congestion and
hemorrhage. The cæcum and double colon thus become the seats of the
grave and fatal lesions of verminous embolism.
The resulting lesions are to be variously accounted for. The stagnation
of blood in the vessels below the embolus, determines a speedy
exhaustion of its oxygen and increase of its carbon dioxide, so that it
is rendered unfit to maintain the normal nutrition and functions of the
part, and the capillary and intestinal walls are alike struck with atony
or paresis. The blood filters into the stagnant vessels slowly from
adjacent anastomosing trunks, and the liquor sauguinis exudes into the
substance of the tissues and lumen of the intestine, leaving behind the
greater part of the blood globules so that the stagnant blood is
rendered more and more abnormal in composition. The walls of the
capillaries soon lose their cohesion as well as their contractility, and
giving way at different points, allow the escape of blood into the
tissues, bowels and peritoneal cavity. It has been further claimed that
the emboli already infected and in process of degeneration communicate
this to the walls of the vessels and to the stagnant blood, hastening
the process of degeneration and rupture.
Another series of circulatory disorders are liable to take place. The
blocking of the vessels of the right bundle, tends to increase the blood
pressure in the left bundle and the anterior one, and thus to determine
congestions, paresis and inflammations in the small intestines, the
second division of the double colon and the floating colon. The
resulting inflammation and increased vascular tension may lead
indirectly to implications of the brain and lung.
Extravasations so extensive as to appear like blood clots may be present
between the layers of the mesentery or in the mucosa and submucosa, and
blood, liquid or coagulated, may have accumulated in the abdominal
cavity. Blood effusion into the intestine gives a dark red coloration to
the contents which are further mixed with distinct clots.
The atonic bowels are always the seat of extensive fermentations and
tympany. The microbes engaged in these fermentations and their toxins,
are accountable for toxic changes occurring in the locally diseased
parts and in distant organs. To this may be attributed the congestion
and softening of the liver and the engorgements and hemorrhagic centres
in the spleen.
_Symptoms._ An animal, perhaps known to harbor the sclerostoma equinum,
is suddenly attacked with violent and persistent colic. He trembles,
paws, moves his hind feet uneasily, kicks the abdomen, throws anxious
looks at the flanks, crouches, lies down, rolls, gets up, and at once
gets down again. The intensity of the suffering rapidly increases, the
face is drawn and pinched, the eye is extremely anxious, the patient no
longer lies down, but throws himself down reckless of consequences, when
down he is not quiet for an instant, but now on his breast, then on his
side, then on his back, the limbs struggling and jerked violently, the
head turned first to one side and then to the other, he is a picture of
extreme agony. If made to walk the same indications continue; he walks
with head down and limbs semiflexed ready to drop at any moment, and
often he will drop suddenly in spite of every effort to keep him on his
feet. The pulse is at first strong and full, but as extensive effusion
takes place into the bowels or abdomen, or as the animal is poisoned by
toxins, it becomes small, weak, and it may be imperceptible. Breathing
is quick and catching, and the mucous membranes are dark red. Sweating
which shows first about the elbows or flanks or back of the ears finally
becomes general, the surface cold and the limbs especially so. Fæces may
be passed at first, a few dry balls at a time from the floating colon or
rectum, but soon they are suppressed entirely. Some patients strain
frequently to micturate but pass little at a time.
In some instances the acute pain seems to suddenly cease, but there is
no general improvement, the patient stands with head depressed, eyes
sunken and expressionless, ears lopped, cold perspiration, chilly limbs,
unsteady gait and imperceptible pulse. It implies merely a paralysis of
the affected bowels in connection with the extensive congestion and
extravasation.
_Course._ _Duration._ The more acute cases reach their acme with great
rapidity, death may occur after two hours illness, and in other cases it
may be delayed ten or even twenty-four hours. It may be caused by
indigestion and tympany, by volvulus or invagination, by excessive
hemorrhage, or by poisoning with toxic matters.
Recovery occurs when the vessel blocked is an unimportant one as a
branch of the left bundle so that circulation may be reëstablished from
collateral trunks; or when a more important trunk has been but partially
blocked, and after a time it either clears itself, or collateral
circulation comes in with sufficient compensation. There is a more or
less rapid disappearance of the colics and other symptoms, a free
passage of urine, the rejection of fæces, it may be in a liquid,
semi-liquid or sanguineous condition, yet enough to indicate the
restoration of intestinal tone. The patient begins to pick morsels of
food and soon acquires his former appetite.
In some instances, however, the recovery is not complete. Trasbot has
noted a case of laminitis occurring within fifteen hours after the
improvement, and in other cases there remain chronic debility and
catarrh of the intestines. The appetite remains poor, there are
occasional colics, the bowels are irregular, loose or costive, and the
fæces are dry, glossy and covered with mucus. The back is arched, the
belly tucked up, strength and vigor are both lacking, and the patient
spends much time in the recumbent position.
Complications of various kinds may follow as in other diseases of the
intestines. After even the best recoveries, a relapse is always to be
apprehended as the original cause remains and the animal is liable to be
cut off at any time.
_Treatment._ This is very unsatisfactory as the original source of
trouble, the worms, being in the blood-vessels, cannot be reached by
vermifuges that would be harmless to the host, and clots blocking the
smaller intestinal vessels, cannot be dissolved and removed. Moreover,
although we could compass the death of the worms in the aneurisms, we
would leave their dead bodies as sources of septic change, blood
coagulation and embolism.
A certain number of cases, however, are not necessarily fatal, and the
worms of the blood-vessels have not an indefinite period of life, so
that there is some encouragement for both therapeutic and preventive
treatment. During the attack we must be content to treat symptoms.
French veterinarians still trust largely to general bleeding, adopted at
the very outset and to the extent of 6 to 10 quarts. It will temporarily
lessen the vascular tension, more permanently dilute the blood, and calm
nervous excitement, and in the most violent cases, as a kind of forlorn
hope, it might be tried with the view of tiding over the acute stage
until a freer collateral circulation could be established.
The use of anodynes will be more generally acceptable to American
practitioners. Two to four grains of sulphate of morphia or codeine may
be given hypodermically in combination with 1½ gr. eserin, 7 grs. barium
chloride, or 2 grs. pilocarpin, to secure a speedy movement of the
bowels.
To counteract intestinal fermentation perhaps no better agent can be got
than chloral hydrate, ½ oz. of which may be given by the mouth in water,
and ½ oz. more by the rectum.
Wet compresses to the abdomen, or fomentations with water rather hotter
than the hand can bear or even the application of mustard is sometimes
useful as a soothing or derivative agent.
In the absence of morphia or chloral, laudanum, ether, chloroform,
camphor or assafœtida have been recommended.
It is important to keep the patient on a soft, littered floor to prevent
injury from his throwing himself down, and walking him around may be
resorted to for the same purpose.
_Prevention._ After a non-fatal attack and in every case in which a
horse is found to harbor the sclerostoma equinum in quantity, measures
should be taken to expel those present in the bowels and to prevent the
entry of embryos. The infested horse may be purged and put on two
drachms each of tartar emetic and sulphate of iron every morning in a
handful of feed half an hour before the first meal. After six doses he
may take a second active purgative. In case of need the addition of 6
grains arsenious acid and a drachm of carbolic acid to each dose will
render them much more effective. All water must be withheld that comes
from streams running by farm-yards, from ponds or open wells in
barn-yards, from uncovered cisterns and from any source which receives
drainage or leaching from land occupied by solipeds or spread with their
manure.
A course of vermifuge medicine should be given at intervals of two or
three months to get rid of the worms which have passed in the interval
from the cysts of the colon, into the intestine.