Chapter IX: Part 9

This is not a common affection in cattle, yet it does occur in weak and debilitated conditions, and in animals fed on fibrous and innutritious aliments. The ingesta are delayed in the gut, their liquid portion absorbed and the remainder accumulates in a hard mass, which distends and weakens the bowel. Dry winter feeding, with a scarcity of water strongly contributes to its production. Astringent plants in the hay, or smut or ergot may add to the tendency.

_Symptoms._ The fæces are hard and firm, glazed on the surface, coated with mucus and sometimes stained with blood. They are passed in small quantity and with much effort and straining, and finally the bowels become completely blocked, nothing whatever being passed. Tympany of the rumen now appears, especially after feeding, appetite and rumination fail, there is much dullness, debility, and loss of flesh and unless relieved, the animal dies in marasmus. Pressure on the right side of the abdomen made suddenly and forcibly produces a sound of liquid splashing in an air space, derived apparently from the accumulation above the obstruction. The oiled hand introduced into the rectum may feel the solid impaction, but in any case causes pain and moaning when the seat of the impaction is pressed upon.

_Treatment._ In the milder cases and earlier stages a change to sloppy food, green food, or boiled flaxseed, with plenty of salt, free access to water, and scruple doses of nux vomica may prove successful.

In the more advanced conditions with complete obstruction, give ½ lb. to 1 lb. each of sodium chloride, and sodic sulphate, and ½ dr. nux vomica, inject hypodermically 3 grs. eserine or 7 grains barium chloride, give water _ad libitum_, and frequent and large injections of soapsuds. If these latter are given cold they will still further stimulate the missing peristalsis. In obstinate cases a second dose of the salts, or 1 quart of castor oil may be given with the addition of 20 drops of croton oil.

When relief has been obtained, a laxative and nutritive diet and a course of bitters should follow.

INDIGESTION WITH OBSTRUCTION OF THE COLON IN SWINE.

Causes: green leguminosæ, dew, rain, dry indigestible food, lack of
water or exercise, debility, torpid liver. Symptoms: firm, small,
coated stools, obstruction, straining, tympany, rumbling, vomiting,
anorexia, lies on belly, secludes himself, restless, grinding teeth,
diarrhœa. Diagnosis from hog cholera. Treatment: laxatives, enemata,
antiferments, rubbing, massage, mechanical unloading of rectum,
puncture, dieting, bitters.

_Causes._ The leguminosæ in their green state are liable to produce indigestion and flatulence in the pig. If covered by dew or rain this tendency is increased. Dry, fibrous or indigestible food with privation of water and of exercise tends to intestinal impaction. Debility from any cause, by weakening the contractility and secretory power of the bowel strongly predisposes to this condition. Torpid liver with diminished secretion of bile is another common factor.

_Symptoms._ The defecations are infrequent, and small, and covered by a mucus film on a glazed surface. This increases steadily until they cease altogether, when straining, tympany, rumbling and vomiting follow. The animal refuses food, and lies on its belly, hiding under the straw when that is available. Restlessness with frequent change of place and grinding of the teeth are noticed. A spontaneous cure may take place by a free secretion of liquid in which the impacted mass is loosened, disintegrated and floated off, the costiveness being succeeded by diarrhœa. Once established this diarrhœa may become persistent, causing serious loss of condition, and simulating hog cholera. It may be distinguished by the fact that it occurred without the introduction of a _contagium_, is easily accounted for by the nature of the food and is not communicated to adjacent herds treated in a different way. There is also the absence of the petechiæ on the skin, and, on post mortem, of the specific round necrotic intestinal ulcers of hog cholera.

_Treatment._ The first object is to rid the intestines of the irritating impacted masses, and this may be secured by giving 1 oz. castor oil, 2 drs. jalap, or 3 grs. croton farina to a 150 lb. pig. This may be seconded by frequent and copious injections of soapsuds. If fermentation and tympany are troublesome 30 grs. chloral hydrate may be given and repeated as circumstances demand it. Active rubbing of the abdomen or kneading of the same will prove useful. If tympany becomes dangerous the gas may be safely evacuated by trochar and cannula, the point of puncture being selected by the clearness of the resonance. When the impaction has reached the rectum and prevents the use of enemata, it may be extracted with the oiled fore finger. An injection of sweet oil may then be given and the finger may be used again and again as the impacted fæces come within reach. When diarrhœa has set in it may be checked by doses of 30 to 60 drops of laudanum, and a diet of boiled milk, well boiled flaxseed or other starchy gruel or mush. A course of bitters with chalk, bismuth or antiseptics will prove serviceable during convalescence.

INTESTINAL INDIGESTION IN THE DOG WITH CONSTIPATION.

Usual seat. Causes: house life, neglect of call to defecate, lack of
exercise, overdistension, atony, watch dogs, over feeding, obesity,
ill health, debility, loss of teeth, paraplegia, spiced and sweet
food, matting of hair over anus, tumors round anus. Symptoms: small,
hard, white, glazed stools, straining, no stools, hot, tender,
swollen, bulging anus, abdominal manipulation, dullness, laziness,
seeking seclusion, colics, tender abdomen, stiffness, arched back,
drooping head and tail, vomiting—sometimes feculent, fever. Lesions:
impacted mass of hard, gritty particles, catarrhal congested or
necrotic mucosa, and outer coats, perforating ulcers. Treatment: air,
exercise, laxative diet, mechanical extraction, purgatives, enemata,
demulcents, laparotomy, enterrectomy.

In the dog, atony and impaction are common especially in the rectum, where the fæces are unduly retained in connection with house life until accumulated and dried. The impaction tends to extension forward, the new material adding continually to the old, and the overdistended rectum becoming more and more atonic in proportion to the increase of the distension.

_Causes._ The most prominent factor is denial of nature’s call to defecate, on the part of house dogs trained to habits of cleanliness. The accumulated mass distends and weakens the rectum, enabling it to hold more without suffering, making the call of nature less imperious, and diminishing the power of expulsion. Lack of exercise usually operates in the same animals, as it also does in watch dogs, the movements of which are limited by the length of their chains.

Overfeeding contributes, in various ways, by increasing the amount of feculent matter passed on into the rectum, by hastening the food through stomach and small intestine imperfectly digested and therefore in a more irritating condition, and by contributing to obesity and lack of tone.

In mastiffs, hounds, bull-dogs, etc., which are naturally gluttonous and swallow animal food in large masses without tearing apart, or mastication, portions pass into the intestine undigested and tend to disturb and block the terminal bowel.

Dogs that are out of health, and which lack tone in general have usually torpid bowels and suffer from delay and impaction of contents. Hence all chronic and debilitating diseases are liable to become aggravated by this troublesome complication.

Old dogs with the teeth worn out and the general tone of the stomach and intestines low are habitual sufferers.

Paralysis of the posterior limbs is usually associated with paresis of the rectum and accumulation, and various other atonic nervous disorders act in the same way.

The sympathy between the skin and alimentary tract shows itself in common disorders, indigestions and catarrh becoming complicated by skin eruptions acute and chronic, by indigestions and impactions. To both conditions the nature of the food of house dogs largely contributes, the habit of eating abundantly at each meal time of the master, the consumption of highly spiced meats, of sweet cakes, pastry and puddings, and even the exclusive diet of white bread or farinaceous and starchy aliment.

In long haired dogs, the matting of these hairs together across the anus proves a factor by rendering defecation difficult and painful.

The formation of tumors around the anus, or inflammation and swelling of the anal glands are additional causes.

_Symptoms._ As in other animals this condition may be chronic, lasting for a long time without leading to complete obstruction. The fæces are passed in hard fœtid, whitish masses, often partly divided, in pellets, dry, and polished on the surface and covered with a film of mucus, sometimes blood. They are passed at considerable intervals, slowly and with painful effort and straining.

In the more advanced and violent cases defecation becomes absolutely impossible, though the animal strains violently and frequently. The anus and rectum bulge as a rounded swelling and the congested and bleeding mucous membrane may be exposed, but nothing is passed. The anus is hot and tender to the touch and the anal glands swollen. Manipulation of the abdomen between the two hands can detect the impacted gut extended forward for a considerable distance, and even implicating the colon. The oiled finger in the rectum may detect the impacted matter as a conglomerate mass of gritty materials. If the appetite continues this becomes all the more extensive. The affected animal is dull, prostrate and indisposed to exertion, seeking a dark retired place where he can rest undisturbed curled up into a ball. Sometimes he starts with a sharp yelp. Especially does he shrink and complain when the belly is handled. If made to walk, he does so stiffly, hangs head and tail, arches the back and tucks up the belly. The face and eyes express severe suffering. Vomiting is a frequent complication, the rejected matters being often feculent. Colicy pains are indicated by yelping or moaning, enteritis and peritonitis by hyperthermia and extreme abdominal tenderness. The acute disease may last from one to two weeks, and death may be preceded by auto-infection, by nervous symptoms of various kinds or by enteritis or peritonitis.

_Lesions._ These may be stated shortly as impaction, catarrh or necrotic changes of the mucosa, more or less extensive inflammations of the bowels and peritoneum, perforations, and congestions of the liver and kidneys.

_Treatment._ In the milder cases plenty of open air exercise and a laxative diet may succeed. In the more severe cases it is usually requisite to unload the rectum mechanically. The dog is laid on a table, and the oiled finger introduced through the anus, lubricates the mucosa as far as it can be reached. Then little by little the firm mass may be disintegrated and removed being steadied by the other hand applied on the abdomen. The handle of a teaspoon or a special spoonshaped curette may at times replace the finger to advantage, but must be used with due judgment, in view of the thinness and friability of the walls of the gut.

When the gut has been emptied in this way, or in the less severe cases without this preliminary, purgatives and frequent injections can be used to advantage. Jalap ½ dr. and calomel 5 grains, or castor oil ½ oz., or syrup of buckthorn have been usually employed. The impaction is usually too firm for the transient action of eserine or pilocarpin. As injections, castor oil, soapsuds, decoctions of flaxseed, mallow or elm bark may be employed being repeated as often as they are expelled and supplemented by the mechanical removal of all solid matters that come within reach.

In cases so extensive as to resist the above measures we can resort to laparotomy. The incision can be made close and parallel to the linea alba, the rectum, or floating colon drawn out through the wound, the other intestines being carefully held back by an assistant, the gut is then incised longitudinally and its solid contents removed. The wound is thoroughly cleansed, washed with an antiseptic (mercuric chloride 1:2000), and sutured with catgut, the mucosa being carefully turned in and the muscular and peritoneal coats kept in accurate contact. Finally the abdominal wound is closed by silk sutures. The patient must be placed for a week or ten days on well boiled gruels and the rectum frequently emptied by injections of tepid water.

In case the bowel is found to be necrotic, the gangrenous section may be excised and the ends brought together by Murphy’s button, or simply sutured with catgut over a hollow tube of raw potato.

INTESTINAL INDIGESTION AND OBSTRUCTION IN BIRDS.

Causes: Age, debility, atony, matting of feathers, dry or indigestible
food, lack of water, diseased oviducts, sand or gravel, lack of
pebbles or power in gizzard. Lesions: masses of egg, uric acid, or
fæces in cloaca, implicating colon and cæca. Symptoms: dullness,
stupor, vertigo, staggering, erect plumage, trailing wings and tail,
bulging anus, covered with matted feathers, impaction felt by finger.
Treatment: extract mass, castor oil, laudanum, chalk, bismuth, pepper,
demulcents, phenol, exercise, silage, green food, pebbles.

_Causes._ These resemble those already noted for the dog. Old age, debility, and atony of the bowel, the matting together of feathers across the anus, dry feeding, indigestible food, scarcity of water, and lack of exercise are especially to be noted. Malformations or other changes lead to obstruction of the cloaca, and of defecation. Sand and gravel passing from an atonic gizzard accumulate in the small intestine or in the cæca distending them to great excess. Imperfect trituration in the gizzard, from lack of pebbles, may prove a factor in stoneless prairies.

_Lesions._ The most common seat of obstruction is at the cloaca, and the impacted matter may be yellow partaking of the nature of yolk of egg, or it may consist of feculent matters and uric acid in various proportions, white, hard and fœtid. As in the dog this distension may be continued forward blocking the colon and cæca as well. Lucet mentions a case in which the impacted mass measured seven inches long, and eight in circumference at its posterior and larger end.

_Symptoms._ The bird is dull, sluggish, stupid, giddy or unsteady on its limbs, with feathers erect, wings, tail and head pendent and loses flesh rapidly. Often a felted mass of feathers and fæces cover the anus. In its absence there appears the rounded swelling or on manipulation the impacted cloaca or rectum can be felt firm and resistant.

_Treatment._ Soften and remove the external mass of fæces by the aid of tepid water, clip off the feathers, which would tend to restore it, then by the oiled finger and warm water injections break up and extract the contents of cloaca and rectum. If impaction remains farther forward give a teaspoonful of castor oil. If diarrhœa has already set in, give 5 drops laudanum, and mix chalk or bismuth and pepper in a mush to be fed to the patient. Injections of slippery elm containing a teaspoonful of carbolic acid in the pint will prove useful.

The bird should be allowed plenty of exercise, its grain being fed on a floor covered lightly with straw to encourage scratching, and silage or green food should be allowed. On the prairies where pebbles cannot be secured, imported gravel or vitrified brick broken into small pieces should be allowed.

COLIC IN SOLIPEDS FROM VERMINOUS EMBOLISM. INTESTINAL CONGESTION.

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.

NON-VERMINOUS INTESTINAL CONGESTION IN SOLIPEDS.

Causes: sudden changes to green food, or leguminous fodder, newly
harvested fodder, frosted food, iced water, microbian infection, toxin
poisoning, intestinal fermentations, experiments, volvulus,
invagination, strangulation, compression, atony. Symptoms: as in
verminous aneurisms. Diagnosis: absence of worms, presence of other
causes. Treatment.

_Causes._ Acute intestinal congestion apart from verminous aneurisms is ascribed to a variety of causes. Sudden changes of food especially to green food, in spring, or to some of the leguminous fodder plants (alfalfa, cowpea, clover, tares, vetches), newly harvested grain or hay, fodders covered with hoarfrost, iced water, and microbian infection or poisoning with toxins or other irritant products of intestinal fermentations. Experimentally the injection into the circulation of pyogenic toxins and putrid matters has determined intestinal congestion and hemorrhage. In the same way musty hay or grain have proved the occasion of these attacks. Finally mechanical blocking of the circulation of the intestine as by volvulus, invagination, strangulated hernia, or even compression by bulky food has seemed to operate in this way.

It ought to be borne in mind that the habitual microbes of the healthy bowel may become pathogenic when brought in contact with a mucosa which is the seat of irritation, atony or any condition of debility.

_Symptoms and Lesions._ The verminous aneurisms and thrombosis aside, the symptoms and lesions of this form of congestion so closely resemble those of the verminous affection that it seems needless to repeat them.

_Diagnosis_ is difficult but the absence of worms in the affected animals and their fellows, and the presence of some one of the other recognized causes may lead to a fair conclusion.

_Treatment_ of the affection is more hopeful than in the verminous affection, and may be conducted on the same general lines.

PSEUDOMEMBRANOUS (CROUPOUS) ENTERITIS IN SOLIPEDS.

Definition. Causes: As in ordinary enteritis, with added infections or
toxins. Symptoms: As in enteritis, nervous symptoms, diarrhœa.
Lesions: Congested mucosa, whitish or grayish false membranes, in
patches or tubular casts, granular, mucous, albuminoid, fibrinous.
Diagnosis: False membranes in stools. Treatment: Glauber salts,
calomel, alkaline carbonates or tartrates, oils, antiferments,
demulcents, careful diet, bitters.

_Definition._ An inflammatory affection of the bowels characterized by the ejection with the fæces of false membranes.

_Causes._ It has been long attributed to the causes which produce other forms of enteritis and indigestions, as youth, rich stimulating feeding, sudden change to green food in spring, sudden chills, over-fatigue, confinement indoors, and prolonged costiveness. In man it is found as a sequel of infectious diseases (pneumonia, pyæmia), in Bright’s disease, cirrhosis of the liver and cancer, and in poisoning by lead, mercury or arsenic (Osler). Cadeac, who found great numbers of streptococci in the false membranes in animals, is certain it is a microbian disease, and this is doubtless true, if qualified by the statement that the microbe as is so often the case with other intestinal affections, requires an occasion in the form of a diseased or debilitated condition of the mucosa to enable it to become pathogenic. The disease is not known to propagate itself indefinitely or without such a predisposing occasion.

_Symptoms._ There are dullness, prostration, langor, hyperthermia, accelerated pulse, and colics which may be slight or very severe. In some cases nervous symptoms have been observed, such as irritability or stupor and somnolence with icterus and fœtid stools. The fæces are usually semi-liquid, implying an excessive liquid secretion as well as the exudation of the membranous matter.

_Lesions._ There is a pink congestion of the intestinal mucosa more or less generally distributed. Whitish false membranes cover patches chiefly on the terminal portion of the small intestine, but frequently also on the cæcum and colon, covering an especially red and angry mucosa. They may occur as simple patches, as ribbon shaped pieces, or as hollow cylinders lining the entire circumference of the intestine. They appear as if fibrillated, but contain abundance of granular matter and seem to be composed mainly of mucus with albuminoid matter and probably a little fibrine. The deeper layers, in contact with the inflamed surface are soft and gelatinoid. It is alleged that coexisting wounds on other parts of the body become covered by a soft pultaceous false membrane.

_Diagnosis_ is based on the presence of the false membranes of a considerable thickness, so that they can be distinguished from the film of mucus which covers the fæcal balls in constipation or enteric catarrh.

_Treatment._ Facilitate the secretion from the mucosa, and the separation of the false membrane by giving 1 lb. Glauber salts, or give this agent in doses of 5 or 6 ozs. per day. Calomel 1 dr. may be used instead and has the additional advantage of acting as a disinfectant. The alkaline carbonates or tartrates or even olive or castor oil may be used as substitutes. Antiferments like salol, naphthol, salicylic acid, and salicylate of soda have been prescribed to check the multiplication of the germ. Flaxseed tea, elm bark, and other mucilaginous agents may also be given. An easily digestible and laxative diet and a course of bitters may follow.

PSEUDOMEMBRANOUS (CROUPOUS) ENTERITIS IN CATTLE.

Causes: as in solipeds, youth, overfeeding, plethora, dietetic
blunders, temperament, over-exertion, chill when heated, gestation,
foul water, irritants, drastics, infections. Symptoms: as in enteritis
with false membranes, complications. Duration. Lesions: false
membranes, extent, color, structure, composition, congested mucosa.
Treatment: Glauber and other salts, pilocarpin, potassium iodide,
antiseptics, sulphites, sulphides, borax, bismuth, naphthol, creolin,
muriatic acid, bitters.

_Causes._ The same causes are quoted as in solipeds, youth, extra high condition, rich feeding, sudden change to the green food of spring, climatic vicissitudes of the same season, a sanguineous (Reynal) or lymphatic (Friedberger and Fröhner) temperament, overwork, exhausting travel, suppressed perspiration, gestation, plethora, foul drinking water, special irritant plants (chicory, Huzard), and drastic purgatives. Cadeac suggests bacteria, quoting instances of a fifth or a fourth of a herd suffering at once. The same would come from any other cause acting on the whole herd and it seems probable that a microbian factor is present but can find occasion for its pathogenesis only in given morbid conditions of the mucous membrane. This would explain the failure of the affection to propagate itself like a plague, and at the same time its tendency to manifest itself extensively in given herds with a common predisposing condition.

_Symptoms._ There are indications of enteric inflammation and fever, rigors, slight hyperthermia, drying up of the milk secretion, impaired or suspended appetite and rumination, constipation, colicy pains, increasing dullness and prostration. As the disease advances the excrements become soft, pultaceous or watery, with floating hard baked pieces, dark and even glistening on the surface and more or less false membranes. These are sometimes stained with blood, which may also be mingled with the liquid debris. As in solipeds these membranes constitute the only true diagnostic symptom. They may appear as shreds, bands or complete cylindroid casts of the intestine.

Other complications, like pseudomembranous exudate on wounds, abortions and profound weakness are sometimes noted. The disease may last eight days before ending in recovery. When death takes place it is about the fourth or sixth day.

_Lesions._ The false membranes are found on the ilium and colon, in thin films or in thick masses, or tubular casts. In extreme cases the membrane has covered an extent of 24 feet in length, and if recent it is soft and friable. If older it may be firm, consistent and yellow or stained by the blood or ingesta. As in solipeds it shows a reticulated network and a fine granular structure, and is composed mainly of inspissated mucus with albuminoids and fibrine. The exudate covers a surface of extreme redness, with points of darker blood-staining and even abrasion or ulceration. The surrounding mucosa is also congested, the villi hypertrophied, the mucous follicles swollen.

_Treatment._ In the early stages a laxative of soda sulphate is of especial value in depleting from the inflamed mucosa, liquefying the secretions and dissolving and loosening the false membranes. Epsom salts, cream of tartar, Rochelle salts, calomel, and pilocarpin are more or less valuable substitutes. Iodide of potassium is most valuable in dissolving the exudate and acting as a microbicide (dose 3–4 drs.).

Other alkaline salts may be substituted or as antiseptics the sulphites, hyposulphites, or sulphides of potash or soda. Borax, bismuth, naphthol and creolin have also been recommended. Enemata of warm water are desirable.

In very adynamic conditions, muriatic acid (½ dr. doses) may be given with vegetable bitters and the same may be allowed during convalescence.

PSEUDOMEMBRANOUS (CROUPOUS) ENTERITIS IN SHEEP.

Causes: As in cattle, draughts in folds, overfeeding. Symptoms: fever,
inappetence, weakness of hind parts, diarrhœa, tenesmus, false
membranes, blood in stools, tympany. Treatment: change diet of dam,
exercise, Glauber salts, potassium iodide, bismuth, flaxseed, elm
bark, mallow, gum, carminatives, bitters, antiseptics.

_Causes._ The same causes are claimed as for cattle. Clavel attributed it to too rich milk, and exposure to cold draughts, in folded lambs.

_Symptoms._ To the general symptoms of fever are added refusal of the teat, weakness or paresis of the hind limbs, looseness of the bowels and the ejection of false membranes with an unusual amount of straining. The dejections may be watery and mixed with blood. In some cases defecation is suppressed, the intestines being blocked by the membranes, and then acute indigestion and fatal tympany may follow.

The pathological anatomy and lesions resemble those seen in the ox.

_Treatment._ Change the diet of the ewe, and allow more outdoor exercise. Give the lamb Glauber salts (½ to 1 oz.) with potassium iodide (10 grs.), and bismuth (1 dr.). Decoctions of flaxseed, or solutions of elm bark, mallow or gum arabic are desirable, and infusions of aromatic plants or oils of peppermint, anise, or fennel may be added with quinia. As in the other animals such antiseptics as salol, naphthol, naphthalin, boric acid, or salicylate of soda may be administered.

PSEUDOMEMBRANOUS (CROUPOUS) ENTERITIS IN DOGS.

Complication of other diseases like distemper. Symptoms: fever,
retching, vomiting, tense, tender, tympanitic abdomen, irregular
bowels, false membranes. Lesions: stomach empty, congested, croupous
exudate, extravasations. Treatment: sodium sulphate, boric acid,
sodium salicylate, salol, bismuth, by mouth or enema, strychnia,
vermifuges.

In dogs the formation of false membranes on the intestinal mucosa seems to have less of an individual character, and is found associated with other affections, like canine distemper and parasitism. In the absence, however, of accurate knowledge of the specific cause of croupous enteritis in other animals it seems permissible for the present, to arrange the whole in one class characterized by the presence of false membranes.

_Symptoms._ Along with the general symptoms of fever and the special ones of the existing specific disease there is more or less disturbance of the digestive organs, anorexia, vomiting, tense, tender, perhaps tympanitic abdomen, irregularity of the bowels and the passage of the false membranes. A morose disposition and tendency to snap has been noticed by Röll.

_Lesions._ The stomach is empty with red or dark mottled mucosa, the intestinal mucosa is congested covered with a layer of mucopurulent exudate, and at intervals patches of false membranes which are also found in shreds floating in the glairy contents. The exudates are of a yellowish gray color, more or less streaked with blood, and the mucosa infiltrated, swollen, highly congested and with spots of extravasation of blood.

_Treatment._ Small doses (1 to 2 drachms) of sulphate of soda may be given by the mouth, or boric acid (1 scruple), salicylate of soda (10 grains), salol (5 grains), or bismuth nitrate (½ drachm). Injections of boric acid, borax, sodium hyposulphite, or even Glauber salts prove useful, and powdered nux vomica (1 grain twice daily) may be added.

In case of intestinal parasites vermifuges must be resorted to.

PSEUDOMEMBRANOUS (CROUPOUS) ENTERITIS IN BIRDS.

In pigeons: Ærobic, non-motile bacillus, in lesions, membrane and
internal organs, pathogenesis, in chickens pathogenesis differs, also
in man, parts attacked, exudate, other symptoms, mortality early and
late in outbreak, American form, pathogenesis to rabbits and
Guinea-pigs. Prevention: Avoidance of infection, quarantine of birds,
separation of sick, disinfection, accidental bearers of infection,
pigeons, buzzards, carrion crows, dogs, men, cleanliness. Treatment:
Locally antiseptics, phenol, boric acid, generally, phenol.

This has been especially seen in pigeons in which it has been studied by Löffler, Cornil and Megnin, and Babes and Puscarin. Löffler found an ærobic, non-motile, non-liquefying bacillus in the false membranes, inflamed tissues, liver, lungs and blood, even in the leucocytes. It formed irregular masses, and grew in nutrient gelatine, blood serum and potato. It proved pathogenic to pigeons, linnets, rabbits and mice, but not to hens, Guinea-pigs, rats or dogs. Chickens, however, suffer from an acute diphtheritic affection caused by a nearly allied bacillus, and it remains to be seen whether the varying pathogenesis may not be due to the habit of long continued growth in a particular genus and an acquired unfitness for growing in the other. The pathogenesis is also different from the bacillus of diphtheria of man, and the two diseases are not usually inter-communicable, in spite of the fact that in rare instances infection has appeared to have taken place from man to birds.

In pigeons and fowls the upper parts of the air passages and digestive tract are mainly involved, the tongue, fauces, corners of the mouth, nares, larynx, and conjunctiva. The bowels suffer less frequently and mostly concurrently with the mouth, nose and throat. The mucosa is deeply congested and in part covered by a yellowish exudate which may accumulate in masses, and dry into a firm substance. The disease affects particularly high bred birds, kept in close warm houses, and is often imported by prize animals returned from a show. There may be dullness, listlessness, sunken head, trailing wings and tail, erect plumage, diarrhœa, and, if the nose and throat are affected, a modification of the voice as in roup. Death may occur from asphyxia from the second to the fourth day near the beginning of an outbreak or the illness may last twenty days, after the more susceptible birds have been killed off.

In investigating a series of outbreaks of roup in chickens in America, Dr. V. A. Moore found a non-motile bacillus allied to the colon bacillus which proved much more deadly to rabbits and guinea pigs than to chickens, and which was not found in the blood nor internal organs but only in the local lesions where inoculated. The disease tended to assume a chronic type in place of the acute form as seen in Europe. Three inoculated chickens escaped the disease altogether. It would appear therefore that we have here a disease distinct from that described by Lœffler, or that there was an absence of some unknown predisposing or contributing conditions that were present in the European outbreaks. In both diseases however infection is an undoubted factor and similar measures of prevention and even of treatment may be followed.