INTESTINAL COCCIDIOSIS OF CALVES AND LAMBS (PSOROSPERMOSIS, HÆMORRHAGIC ENTERITIS, BLOODY FLUX, DYSENTERY, ETC.).
History. This disease is very common in the Avalon and surrounding districts, sometimes assumes the characteristics of a true epizootic, and affects young bovine animals between the ages of six months and two years, but is commonest and most contagious in animals of from ten to eighteen months old.
It attacks animals in good or bad condition, without distinction of breed or species. It begins towards the end of July, attains its maximum development towards the end of August and September, and disappears in October, though occasionally it continues until November. In exceptional cases Degoix has seen it during January and February in animals which had returned from the fields to the byres about the end of November. It develops earlier than verminous bronchitis, in conjunction with which, however, it often occurs. It is commonest in warm, moist, rainy years, and amongst animals pastured on swampy ground containing numerous springs and streams. Year after year it attacks animals occupying particular pastures in summer. The soil of these pastures is undoubtedly infested with the germs of the disease, just as in places the soil is infested with anthrax bacilli. The appearance of symptoms is preceded by an incubation period of one or two months. The length of this incubation period is fixed by the observations which Degoix has made during the past twenty years, and depends on the time which elapses between the animals being turned into infected pastures and the appearance of the preliminary symptoms.
Symptoms. The disease commences with liquid, serous, fœtid, greenish-black diarrhœa, the material being voided without special straining and the animals losing neither their spirits nor appetite. Fever can scarcely be detected, the temperature ranging between 38° and 39° C. On the second or third day the diarrhœa changes in character. Though it always remains fœtid, it now becomes mucous, reddish-black, or sanguinolent, and contains more or less frequent blood clots of varying size.
The passage of this material causes violent straining, which becomes more and more common, and is accompanied by very pronounced rectal tenesmus. The animals stand with their backs arched for one or two minutes, sometimes longer, and the liquid escapes in large quantities, soiling the quarters and hocks. The animals are dull, show a certain degree of colic, and frequently grind the teeth. Appetite is lost, thirst is severe, and rumination ceases. Wasting makes rapid strides, the coat stares, the animals have difficulty in standing on account of their weakness, fever sets in, and the temperature rises to 40° C. This condition may last from five to ten days and terminate either in recovery or death. Recovery is frequently rapid in animals which have continued to eat, and in which the acute period has been of short duration—five to seven days at most. On the other hand, it is slow if the appetite has disappeared and the acute period has been prolonged beyond ten days.
The diarrhœa, which has lost its sanguinolent character towards the sixth or eighth day, may continue for somewhat longer. The attacks of straining become rare, and cease between the tenth and fifteenth days. The appetite remains capricious for a long time.
Convalescence is marked by alternate improvement and retrogression. The animals are weak, and only recover quickly under energetic treatment and forced feeding with concentrated digestible foods like milk, soup, cooked grain, etc., administered for three weeks or more.
Death may occur towards the tenth or fifteenth day from exhaustion. The patients become very anæmic and thin, the eyes are withdrawn into the orbits, and the animals appear indifferent to what goes on about them. They still groan feebly, occasionally grind the teeth, and lie continually on the chest with the head extended. The body temperature falls and death follows.
In well-bred animals in good condition the disease sometimes assumes a much graver and more rapidly progressive form, with peracute symptoms, and makes as many, if not more, victims than that previously described.
The process is as follows: After suffering for a day from serous diarrhœa, to which the owners pay little attention, the animals show sanguinolent diarrhœa and pass blood clots. This is almost immediately followed by very violent convulsive attacks—true eclampsia. The animals are then unable to stand, lie on the side with the head outstretched and resting on the ground, the eyes withdrawn into the sockets and often showing pirouetting movements (nystagmus), the neck drawn upwards and backwards (opisthotonos), and the limbs rigidly extended. From time to time the whole body is shaken by extremely violent convulsive movements.
This condition, which is sometimes preceded by weakness of the hind quarters and symptoms of locomotor ataxia and inco-ordination, may continue from six to thirty-six hours; in nine cases out of ten it terminates in death.
Causation. On microscopic examination of the serous dejections one finds distributed throughout the liquid mass very small numbers of ovoid corpuscles having a double outline, and contents of varied appearance; these are the coccidia.
When the diarrhœa has become sanguinolent and muco-fibrinous, the fluid contains these coccidia in considerable quantities, and large numbers of them may be found in the mucus, where they are mixed with epithelial débris, blood corpuscles, and lymphatic cells, etc. They are rarer in the clots. Coccidia cannot be found in the fæces of healthy animals, even in those occupying the same pastures with the diseased. Should the clinical symptoms be thought insufficient of themselves clearly to identify the disease, a simple microscopic examination of the fæces will remove any doubt.
Lesions. Post-mortem examination immediately after death enables one exactly to identify the habitat of the parasite and the lesions it produces. These lesions are to be found throughout the large intestine, from the cæcum to the anus.
The large intestine is almost or entirely empty, the mucous membrane is reddish-brown in colour, lies in folds, is œdematous, and everywhere covered with a coating of mucus. This coating varies in character at different points; in places it forms more or less thickened patches of greyish or yellowish colour, and of a resistant character, as though mixed with coagulated fibrin. These patches are fairly well defined, they are irregular in form, and vary in width from some millimètres up to several centimètres. They are more or less adherent to the mucous membrane, from which they can easily be stripped away. The mucous membrane thus exposed is slightly depressed, and of a whitish colour, thus markedly contrasting with the surrounding red coloration. This depression represents a slight ulceration, which, though superficial, is clearly visible to the naked eye.
Microscopic examination of the mucus patches reveals the existence, both superficially and in the depths, of epithelial cells derived from the mucous membrane, of vesicular cells derived from the Lieberkuhnian follicles, of numerous blood and lymphatic corpuscles, and, distributed irregularly throughout this mass of cells, of coccidia, resembling those found in the dejections.
In thin sections of the intestine, made through the ulcerated mucus-covered patches, and in a direction perpendicular to the mucous membrane, one finds that the epithelial covering of the intestine has disappeared.
The Lieberkuhn’s follicles are shortened, their orifices are irregular and partly blocked with epithelial débris. In a large number of these follicles the blind extremity is dilated, and more or less filled with coccidia, varying in appearance according to their stage of development. The epithelial cells normally lining these blind ends seem to have disappeared, and to have been replaced by the parasites. This, however, is not really the case. It is easy to prove by suitable dissection (after maceration of the sections in 30 per cent. alcohol) that the coccidia are lodged in epithelial cells which have become modified in shape and undergone hypertrophy as the parasite has grown, whilst the nucleus has been pushed to one end and undergone atrophy.
Alongside the deceased glands may be found others which are quite healthy. In the parts which are most markedly affected the interglandular connective tissue is infiltrated and slightly thickened. Degoix has never discovered coccidia in the cells of the intestinal mucous membrane itself. The lesions may be met with throughout the large intestine, but are more numerous and grave as the rectum is approached.
This disease is characterised by extensive inflammation, affecting the entire mucous membrane of the large intestine, by more or less extensive ulceration of this bowel, the ulcers being covered with muco-fibrinous patches rich in coccidia, by localisation of the parasites in the epithelial cells of the glandular cul-de-sac, by the appearance of the disease at a special time of year and in special districts, where it assumes the form of an enzooty, and by the fact that it always appears in the same pastures. The mortality varies between 12 and 25 per cent. from year to year.
Microscopic appearances. The protozoa which produce this disease assume the form of ovoid cysts, varying in length from 18 to 25 µ, and measuring at the widest part about 13 µ. They possess a hyaline envelope whose existence is proved by its double contour line, and yellowish, granular, highly refractile contents. This granular material does not always occupy the whole of the cavity. At a certain stage of development it collects towards the centre, forming a nucleus and leaving clear spaces at the poles of the cell. At a later stage this nucleus divides into four portions which afterwards separate.
Treatment. The protozoa, in their cystic condition, are very resistant to destructive influences. The most common natural cause of their destruction is drying in the open air. Unfortunately, in the localities where the patients usually live, that is, filthy byres, wet pasturages, etc., this destruction only takes place to a very limited extent.
The disease can be attacked by prophylactic and therapeutic measures.
Prophylaxis consists—firstly, in destroying the parasites contained in the dejections by the free use of 3 per cent. sulphuric acid solution; and, secondly, in removing the young animals from infected fields during the months between June and September.
Therapeutic treatment comprises—firstly, stimulant applications to the abdomen; secondly, disinfection of the intestine by the administration of salol, benzo-naphthol, very diluted solutions of creolin, etc.; thirdly, intestinal irrigation by the administration of mucilaginous drinks containing bicarbonate of soda, supplemented by general tonic treatment and the supply of concentrated, very nourishing, and easily digested food (Degoix, Revue générale de Médecine Vétérinaire, No. 28, February 15th, 1904, p. 177).
McFadyean describes a similar disease to the above in two to three months old lambs (Jour. of Comp. Path. and Therap., March, 1896, p. 31). The mortality reached 10 per cent. The lambs at the time the disease broke out in the flock were closely folded together with the ewes on growing roots, which, needless to say, were much soiled with earth and fæces before they were completely consumed.
INTESTINAL HELMINTHIASIS IN RUMINANTS
(Ox, Sheep, Goat).
Fig. 117.—Head of Tænia alba of the ox and sheep. (After Neumann.)
Verminous disease of the intestine is often accompanied by similar disease of the stomach (gastro-intestinal strongylosis of the sheep, lumbricosis of the calf), but it also occurs apart from the presence of gastric parasites. Parasites are more frequent in the intestine than in the abomasum, because the alkaline intestinal juices prove a much more favourable medium for their development than do the acid juices of the stomach.
The actual parasites may include ascarides, strongyles, hooked worms, œsophagostomes, tricocephales, sclerostomes, and various tæniæ (Tænia expansa et alba). Many of these have already been, or will hereafter be, referred to.
Helminthiasis due to round worms like strongyles, and the various forms of hooked worm, is graver than that due to flat worms, but most extraordinarily varied collections are sometimes met with. Speaking generally, however, helminthiasis more particularly affects young animals like calves, lambs, and yearling sheep, is rarer in adults, and in all cases the complications it produces are of trifling importance in adults as compared with those caused in the young.
The persistence of verminous diseases in certain infested countries, districts, farms, or pastures is explained by the enormous number of eggs or embryos passed with the fæces and disseminated with manure, as well as by the high degree of resistance of the eggs and embryos to destructive influences.
Causation. The various forms of intestinal helminthiasis are all due to embryos or eggs of worms obtaining entrance to the stomach or bowels of susceptible animals. Nevertheless, external conditions largely favour infestation. The existence of marshes, ponds, and stagnant water on certain pastures, heavy annual rainfall, the occurrence of wet seasons, etc., favour the existence and growth of embryos, and, as a consequence, the infestation of animals.
Fig. 118.—Adult specimen of the fringed tapeworm (Thysanosoma actinioides). (After Stiles, 1893.)
The symptoms of intestinal helminthiasis are always very vague, whether the victims be oxen, sheep, or goats. They point to the slow and progressive development of a pernicious anæmia, characterised primarily by interference with appetite and digestion, then by anæmia, and finally by cachexia. The patients are dull, lose condition, suffer from depraved appetite, and, during the cachectic period, from diarrhœa, and die in a condition of exhaustion. These forms of helminthiasis are much more frequent in sheep than in oxen.
The diagnosis is only arrived at by discovering parasites in the fæces, or, in those doubtful cases where one has been led to make a microscopic examination of the excrement, by the detection of large numbers of eggs.
From an economic standpoint the prognosis is grave, because severely infected animals recover their condition very slowly, whatever treatment be adopted.
Treatment includes the measures previously indicated regarding the destruction of germs, eggs, or embryos distributed over the pastures, and the drainage of wet grounds and stagnant pools. Where such diseases are common, the pastures should be dressed with iron sulphate, and the stable manure disinfected or burned.
Curative treatment comprises the administration of such anthelmintics as can be given with the food. They should not require to be administered by force, as this proceeding would not only necessitate a great loss of time, but might result in accidents.
Arsenious acid, in doses of 15 grains per day, and tartar emetic, in doses of 75 to 150 grains, according to the animal’s size, are among the best drugs for oxen, and may be given for four or five days running. Benzine, oil of turpentine, and empyreumatic oil are more difficult to administer.
In the case of sheep, preference should be given to areca nut, in doses of 75 to 120 grains, according to the animal’s size, and to tansy, which are convenient to give, and can be added to bran, oats, or beetroot.
Adult tapeworms of oxen are of relatively minor importance, but one tapeworm of sheep, viz., the fringed tapeworm (Thysanosoma actinioides), also known as Tænia fimbriata; Moniezia fimbriata deserves notice, as at times it forms a veritable scourge to the sheep industry of North America and South America.
Fig. 119.—Ventral and apex views of the head of the fringed tapeworm (Thysanosoma actinioides). × 17. (After Stiles, 1893.)
Fig. 120.—Segments of the fringed tapeworm (Thysanosoma actinioides), showing canals and nerves, and (f) fringed border, (t) testicles, and (ut) uterus. Enlarged. (After Stiles, 1893.)
Disease. The disease in sheep caused by the fringed tapeworm has been studied in detail by Curtice, who considers that next to scab it is the most important sheep disease of the western plains of North America. The financial loss it causes is extensive, and results from the failure of the lambs to fatten, the small crop of wool, and the weakening of the animals, so that they cannot withstand cold winter weather. The parasites develop slowly, and are present in considerable numbers before their presence is suspected. Toward September the lambs fail to grow as they should; in November the symptoms are marked. First, the worms produce local irritation of the intestine, which finally develops into a chronic catarrhal inflammation; their presence in the gall-ducts produces similar results, and obstructs the flow of bile; infected lambs are large-headed, under-sized, and hidebound; their gait is rheumatic, and they appear more erratic than the other sheep, standing oftener to stamp at the sheep dogs or herds, and lagging behind the flock when driven; the general symptoms are those of malnutrition, and Curtice considers them nearly identical with the symptoms of the “loco” disease; in fact, he states that it is extremely difficult to distinguish between the two diseases, and believes that the fact that the worms “may tend to produce depraved appetites and a morbid craze for a particular food is also reason for suspecting that the loco disease may depend on the tapeworm disease.” General systemic disturbances result from malnutrition; the usual fat is absent; serous effusions are noticed in the body cavities, serous infiltration in the connective tissue.
Treatment is similar to that of parasitic gastro-enteritis of sheep and lambs (which see).
CHAPTER IX.
DISEASES OF THE LIVER.
From the physiological standpoint the liver is an organ of such importance that its pathology should be studied as completely as possible. Furthermore, it is often the seat of a number of varying lesions, either of parasitic, toxic, infectious, or cancerous origin.
In animals of the bovine species the liver is placed in the right retrodiaphragmatic region, so that it is somewhat difficult to examine by any of the ordinary methods, like palpation and percussion. Under normal conditions it is entirely concealed beneath the hypochondrium, except towards the upper margin of the thirteenth rib, where it can be examined by palpation. When, as in various morbid conditions, it is considerably increased in size, it extends as far as the margin of the hypochondriac circle, thus becoming directly accessible to palpation and percussion. Sometimes it even enters the hypochondriac region, passing outside the omasum and abomasum, which it then thrusts towards the middle of the abdominal cavity.
The margin of the liver exhibits a depression lodging the gall bladder nearly opposite the centre of its vertical depth.
As the liver is so deeply situated, percussion is found to be the method of examination which gives the best results. Beyond the limits of the zone of auscultation, percussion gives above a semi-dull sound, then, proceeding downwards, a dull sound due to the liver, the omasum, and the collection of liquid in the bowel. When this dulness is well defined, clear, broad from above downwards, and extends to or beyond the hypochondrium, it indicates hypertrophy of the liver. By deep palpation of the posterior margin of the hypochondrium the liver can then be sounded, and its excessive size detected.
The symptomatology of the liver is still very imperfectly understood, for in practice the urine is rarely tested for bile pigments, nor attempts made to ascertain whether the glycogenic function is normal by the test for alimentary glycosuria.
In this connection nothing has yet been done to assist in diagnosing certain hepatic conditions. Fortunately, those diseases of the liver which we have to study are more often of a parasitic nature than true diseases of the hepatic tissue.
The reported cases of venous or biliary cirrhosis, moreover, are too ill-defined and too incomplete to be taken as a type for description. We leave them on one side. In a similar way, apart from parasitic cholangeitis and cholecystitis, inflammations of the biliary ducts are little known, and are rare.
CONGESTION OF THE LIVER.
In bovine pathology only passive congestion of the liver, often a result of various primary affections with cardiac lesions, is well recognised.
Active congestions probably occur during infections or intoxications of various kinds, but have not been made the object of special research.
Among diseases likely to produce passive congestion must be included all those which interfere with the return circulation through the posterior vena cava. All cardiac affections with lesions of the valves or orifices of the right heart, all forms of pericarditis, tumours or lesions of the mediastinum compressing the posterior vena cava, produce stasis, passive congestion, and progressive development of what is called “cardiac liver.”
Symptoms. The liver is considerably hypertrophied, as a consequence of the stasis of blood and progressive dilatation of the portal system. Its zone of dulness increases in size, whilst on palpation its borders may sometimes be detected. This condition is always accompanied by digestive disturbance.
The function of the liver is more or less interfered with; the urine is scanty in amount and charged with deposit. Ascites of varying intensity frequently occurs; cardiac disturbance accompanies or usually precedes the above symptoms.
The lesions of passive congestion are represented by progressive dilatation of the entire portal venous system (nutmeg liver). In time this dilatation may produce biliary cirrhosis, as a result of chronic irritation of the blood-vessels and perivenous inflammation. This condition is known as “cardiac cirrhosis of the liver.”
The diagnosis of this pathological condition is generally easy, provided that the primary disease which causes it be recognised.
The prognosis is always grave, and the practitioner is limited to treating the primary affection, such as endocarditis, pericarditis, etc.
NODULAR NECROSING HEPATITIS.
This form of inflammation of the liver is somewhat rare in animals of the bovine species. The disease is difficult to diagnose, and is often only recognised on post-mortem examination.
Isolated tracts of the liver become inflamed, between which the rest of the tissue preserves its normal character; the parts affected appear to undergo complete degeneration, the cause of which is difficult to explain. On examining affected animals after death, the liver is found to be greatly enlarged, and apparently invaded by multiple tumours. On section, the parenchyma generally is of normal colour, but the diseased parts are represented by dirty greyish-yellow tissue of a lardaceous character, somewhat resistant to the knife.
The affected spots vary in size, between that of a lentil or hazel nut and an egg, and are formed of necrotic tissue.
The periphery is the seat of true chronic fibro-plastic inflammation.
Fig. 121.—Appearance of the liver in necrosing hepatitis
Causation. According to Stubbe, these lesions are produced by microbes, originating in the intestines, and carried to the liver by the mesenteric veins. The lesions and blood of the liver yield cultures of a microbe resembling that of necrosis; nevertheless, such lesions have not been experimentally reproduced.
According to Berndt, infection from the uterus is possible, and indeed probable. Moussu has only seen three cases of this particular condition of the liver in living animals. Two of these were in a working ox and a bull respectively, so that Berndt’s view would not seem to be exclusively applicable. Moussu is convinced that infection is of intestinal origin, and that it takes place through the mesenteric veins; he claims to have found the proof of this in the existence of multiple pylephlebitis and complete obliteration of the subhepatic veins in some cases.
Symptoms. The symptoms are so vague as to render diagnosis difficult. Berndt, on the other hand, regards it as fairly easy. He states that the disease occurs in old cows, which after parturition show loss of appetite, polydipsia, fever, dyspnœa, and short, feeble cough, suggesting pneumonia. After a few days the animals appear extremely weak, remain lying for long periods, and exhibit icterus. Percussion of the liver detects abnormal sensibility and hypertrophy.
The three cases seen by Moussu showed only slight yellowness of the membranes, general weakness and difficulty in walking, which at first glance appeared to suggest laminitis, marked hypertrophy of the liver, sensitiveness over the hepatic region, and, as complications, uncontrollable diarrhœa and peritonitis. But these symptoms are also noted in suppurating echinococcosis, and even in cancer of the biliary ducts, so that diagnosis does not appear easy. Nevertheless, there is always marked fever, and on post-mortem examination it is not unusual to find, in addition to the hepatic lesions, a certain amount of perihepatitis, partial peritonitis, and even pleurisy in the region of the diaphragm. The question is of little practical importance, for the gravity of the disease just described is such that economically no treatment is possible. The great point lies in correctly diagnosing disease of the liver, and that is relatively easy.
CANCER OF THE LIVER AND BILE DUCTS.
Cancer of the liver, that is, broadly speaking, the development in the liver of malignant tumours, capable of becoming generalised throughout the organism, is comparatively rare when compared with parasitic diseases of the same organ. It may be primary or secondary in character, but is much more frequently secondary. In bovines primary cancer assumes the forms of adenomata, trabecular epitheliomata, or adeno-carcinomata. Moussu describes a case in which the growths assumed the form of papillomata or adeno-papillomata extending throughout the biliary ducts, and partly obstructing the common bile duct, which was greatly dilated.
The real cause of these, as of all other primary tumours, remains shrouded in mystery.
Secondary cancer is more frequent; it occurs usually in the form of little isolated tumours (nodular cancer) of varying size and greyish colour.
Symptoms. Clinically the description, or rather the identification, of cancers of the liver is difficult, and the diagnosis particularly troublesome in cases of primary cancer.
In secondary cancer (following tumour of the testicle in oxen castrated by the method of bistournage, for example) the general condition, on the other hand, is usually so affected that attention is pointedly drawn to the seat of the secondary growths. The patients lose appetite, the fæces become fœtid, and diarrhœa sets in without clear signs of enteritis.
Examination of the liver always reveals hypertrophy, and sometimes sensitiveness. The patients rapidly lose flesh, become cachectic, and the proportionate number of red blood corpuscles diminishes. From the normal of six or seven millions the number may fall to one million or less, while that of the white corpuscles considerably increases. This leucocytosis, which accompanies all forms of visceral cancer, enables one to distinguish between cancer and chronic forms of diarrhœic enteritis; it must not be confused with leucæmia. Moderately developed ascites is common, in consequence of obstruction in the porto-hepatic circulation.
Fig. 122.—Portion of pig’s liver infested with echinoccocus hydatid, natural size. (Stiles, Annual Report, U.S.A. Department of Agriculture, 1900.)
The diagnosis of cancer of the liver or biliary ducts is surrounded with difficulty, and the prognosis is extremely grave, because no treatment is possible.
ECHINOCOCCOSIS OF THE LIVER.
This term is applied to the development in the depths of the hepatic parenchyma of hydatids of Tænia echinococcus.
The echinococcus hydatid is found in man, cattle, sheep, swine, etc. It represents an intermediate stage of development of the echinococcus tapeworm of dogs. Since this parasite develops its larval stage in man also, and further, since it is the most dangerous animal parasite found in man, it is important to thoroughly understand its life history in order to guard against infection.
Adult stage (Tænia echinococcus).
Hosts. Dog, dingo, jackal, wolf.
Fig. 123.—Portion of the intestine of a dog infested with the adult hydatid tapeworm (Tænia echinococcus) natural size. (After Ostertag, 1895.)
Fig. 124.—Adult hydatid tapeworm (Tænia echinococcus) enlarged. (After Leuckart, 1880.)
Fig. 125.—Hooks of adult hydatid tapeworm. a, From a hydatid; b, three weeks after feeding to a dog; c, from an adult; d, combined figures of a-c, showing the gradual changes in form. × 600. (After Leuckart, 1880.)
Life history. Starting with the adult tapeworm (Fig. 124) in the small intestine of the dog or wolf, the eggs are scattered over the ground and are swallowed by the intermediate host with the fodder or water. Upon arriving in the stomach the egg-shell is destroyed, and the six-hooked embryo, which is thus freed, bores its way through the intestinal wall, and wanders, actively or passively (that is, carried along by the blood), to various organs of the body—liver, lungs, ovaries, bones, skull, etc.—where it develops first into an acephalocyst, which may develop further, as shown by the accompanying illustrations. The heads which are formed, upon being devoured by a dog or wolf, then develop into adult tapeworms.
Young animals are most exposed to this disease; in adults or aged animals the migration and development of the embryo are more difficult.
Fig. 126.—Diagram of an echinococcus hydatid. cu, Thick external cuticle; pa, parenchym (germinal) layer; c, d, e, development of the heads, according to Leuckart; f, g, h, i, k, development of the heads according to Moniez; l, fully-developed brood capsule with heads; m, the brood capsule has ruptured, and the heads hang into the lumen of hydatid; n, liberated head floating in the hydatid; o, p, q, r, s, mode of formation of secondary exogenous daughter cyst; t, daughter cyst with one endogenous and one exogenous granddaughter cyst; u, v, x, formation of endogenous cyst, after Kuhn and Davaine; y, z, formation of endogenous daughter cysts, after Naunyn and Leuckart; y, at the expense of a head, z, from a brood capsule; evag, constricted portion of the mother cyst. (After R. Blanchard, 1886.)
These embryos perforate the tissue of the liver, become fixed in it, and derive from it the nourishment necessary for their conversion into cystic bladders of varying size, either sterile or fertile.
The number of vesicles is rarely large, and when only one or two are present they seldom produce sufficient disturbance to attract attention. On the other hand, when numerous they deform the liver, produce glandular atrophy, increase the total size of the organ, and lead to the appearance of clearly marked symptoms.
Fig. 127.—A racemose echinococcus, natural size. (After Leuckart, 1880.)
The cystic vesicles contain a clear, limpid, transparent fluid, in which float secondary, daughter, or granddaughter vesicles.
Fig. 128.—Section through a multilocular echinococcus, × 30. (After Leuckart, 1880.)
Symptoms. Echinococcosis of the liver has no well-marked symptoms, and is therefore difficult to diagnose in animals whose liver is deeply seated, and therefore beyond palpation. The signs which may characterise the period of penetration of the embryos through the intestine and into the depths of the liver, and which are probably represented by slight colic, vague pain and diarrhœa, usually pass unnoticed. But later, when the liver is extensively invaded appetite becomes irregular without apparent cause, animals show intractable diarrhœa, general feebleness, dulness, and wasting.
Fig. 129.—A multilocular echinococcus from the liver of a steer, natural size.—(After Ostertag, 1895.)
Fig. 130.—A multilocular echinococcus from the pleura of a hog, natural size. (After Ostertag, 1895.)
These symptoms do not point with sufficient clearness to a special visceral lesion, but as they call for a complete examination, the practitioner is almost forced to a certain conclusion by the fact that the examination remains negative except in regard to the liver. The liver seems large and sensitive, and may sometimes be considerably hypertrophied, for cases have been seen in the ox where the normal weight of 10 to 12 lbs. has been increased to 60 or even 100 lbs., while in the pig, whose liver normally weighs 4 lbs., the weight has been as high as 20 or 40 lbs. In such cases percussion and palpation show that the liver extends beyond the right hypochondriac region and invades a large portion of the corresponding flank. But such great enlargement is exceptional, and when only a dozen vesicles are present, although the functions of the liver may be seriously disturbed, the information obtained by physical examination is seldom sufficient to justify an exact diagnosis. The liver is found to be enlarged and thickened; otherwise the examination gives negative results.
Fig. 131.—Echinococcus bladder-worm or hydatid.
Fig. 132.—Tænia echinococcus.
The diarrhœa may result from failure of the liver to secrete sufficient bile to destroy intestinal toxins, or to carry on its glycogenic function; but it may possibly be the direct result of chronic intoxication by the contents of the vesicles.
Experience has shown, in fact, that in man, when a superficial vesicle becomes ruptured, the peritoneal cavity is flooded with the contents of the cyst; the daughter cysts adhere to the peritoneum, and that almost invariably vascular disturbance occurs, accompanied by itching of the skin and an eruption resembling that of urticaria.
The liquid of the vesicles contains an active toxalbumin.
Diagnosis. In certain cases, diagnosis is possible, and even easy, but in others it is extremely difficult and almost impossible.
Prognosis. The prognosis is always grave, for if the lesions in the liver do not produce death, as usually happens, they so profoundly affect the animals’ general state, that it is no longer worth while to keep them alive.
No practical treatment exists. In exceptional cases it certainly might be possible, although in the large herbivora always difficult, to expose the liver and to puncture and evacuate the contents of some of the cysts; but the result would be illusory, because some vesicles would always be inaccessible, and economically intervention would be incomplete and useless.
Fig. 133.—Pig’s liver with echinococcus cysts. (After Railliet.)
Although there is no useful method of treatment, prophylaxis is possible and valuable. It consists in preventing the development of tæniæ in farm and sporting dogs. For this purpose it is sufficient to prevent their obtaining raw offal containing vesicles of echinococci from sheep, oxen, or pigs, and also to free them from any helminths which they may harbour. In this way they no longer spread eggs of tæniæ with their fæces in the neighbourhood of ponds or drinking places, and the cattle do not ingest the embryos.
SUPPURATIVE ECHINOCOCCOSIS.
Causation. Simple echinococcosis may remain undetected for a long time, and young animals affected with it may grow up without exhibiting marked general disturbance. The old echinococci end by degenerating, the wall of the cyst becomes modified, the liquid it contains, turbid, lactescent, then caseous; the vesicle becomes wrinkled, and finally nothing resembling the primary vesicle remains. The liquid is soon absorbed, and the primary cyst is only represented by a caseous magma, which undergoes calcareous infiltration and progressive atrophy.
Under other circumstances the development of the echinococcus vesicles is less regular; they may become accidentally infected and transformed into encysted abscesses, constituting suppurative echinococcosis of the liver. The membrane of the vesicles usually resists the passage of microbes, but the fibrous tissue surrounding the cyst is very vascular; and if, in consequence of vascular disturbance in the liver (which may result simply from feeding, trifling infection or other visceral disease), the blood should for a short time be infected, microbes penetrate through solutions of continuity in the wall of the vesicle, which becomes a centre of suppuration. The liquid becomes turbid, the primary cyst is transformed into an abscess, and suppurative echinococcosis is set up.
Symptoms. The general condition resulting from the development of suppuration in echinococcus cysts is very different from that of true echinococcosis. If the abscess develops rapidly, acute generalised peritonitis or localised peritonitis of the right anterior abdominal region may almost immediately occur, producing all the characteristic symptoms of ordinary peritonitis. In all cases, even in the absence of well-marked peritonitis, perihepatitis occurs, and the liver becomes adherent to the posterior surface of the diaphragm, to the hypochondriac region, to the abdominal wall, or to one of the gastric compartments.
This perihepatitis is indicated by exceptional sensitiveness in the right hypochondriac region, and by respiratory disturbance due to fixation of the diaphragm.
In certain cases these abscesses seem to develop like “cold” abscesses—i.e., without fever, and this without producing very marked digestive disturbance; but the patients waste rapidly, become weak, show slight sub-icteric coloration of the membranes, and appear to lose their strength. Movement is slow and hesitating, as though the animals were suffering from laminitis, the anæmia becomes more marked from day to day, and examination of the blood reveals abundant leucocytosis, the existence of which often assists in the diagnosis of internal suppuration. In a few months, at least in the cases we have seen, the animals become cachectic.
In other and still more obscure cases suppuration of the liver is accompanied by total hypertrophy, excessive sensitiveness in the right hypochondriac region, progressive loss of appetite, excessive thirst, and uncontrollable diarrhœa and fever, although in the case mentioned above there was little fever and no diarrhœa. The course of these cases, which probably result from intestinal infection, is much more rapid. In a fortnight or three weeks, sometimes less, the patients are carried off by intoxication, generalised purulent infection, or septicæmia.
Diagnosis. The diagnosis of suppurative echinococcosis and of primary abscess of the liver is difficult to establish. It is attained chiefly by a process of exclusion, though the signs furnished by percussion of the right flank, and by examination of the blood, are of some assistance.
Fig. 134.—Thin-necked bladder-worm (Cysticercus tenuicollis), with head extruded from body, from cavity of a steer, natural size. (Stiles, Annual Report, U.S.A. Bureau of Agriculture, 1901.)
Fig. 135.—The marginate tapeworm (Tænia marginata), natural size. (Stiles, Annual Report, U.S.A. Bureau of Agriculture, 1901.)
Prognosis. The prognosis is extremely grave.
Treatment is of little value. Even supposing that the diagnosis has been exact, surgical intervention is out of the question, and only this would appear theoretically to offer a chance of success. The abscesses are multiple, deeply placed, separated from one another, and sometimes surrounded by enormous tracts of inflamed tissue. In fact, the condition is of such a character as entirely to prohibit active measures.
CYSTICERCOSIS.
Fig. 136.—Head of the marginate tapeworm (Tænia marginata). × 17. (Stiles, Annual Report, U.S.A. Bureau of Agriculture, 1901.)
This disease is produced by the thin- or long-necked bladder-worm (Cysticercus tenuicollis) found in cattle, sheep, and swine. The cysticercus represents an intermediate stage of development of the marginate tapeworm (Tænia marginata) of dogs and wolves.
It is by no means uncommon in Europe and America, and occurs in the body cavity of cattle, sheep, swine, and other animals, attached to the diaphragm, omentum, liver, or other organ.
When eaten by dogs or wolves, it develops into the marginate tapeworm, which was formerly confused with T. solium of man, and gave rise to the erroneous idea that the pork-measle tapeworm occurs in dogs as well as in man.
Fig. 137.—Small and large hooks of (A) Tænia marginata, (B) T. serrata, and (C) T. cœnurus. a, Small hooks; b, large hooks. × 480. (After Deffke.)
Fig. 138.—Sexually mature segment of the marginate tapeworm (Tænia marginata). cp, Cirrus pouch; gp, genital pore; n, nerve; ov, ovary; sg, shell gland; t, testicles; tc, transverse canal; ut, uterus; v, vagina; vc, ventral canal; vd, vas deferens; vg, vitellogene gland. Enlarged. (After Deffke.)
Fig. 139.—Egg of the marginate tapeworm (Tænia marginata), with six-hooked embryo, greatly magnified. (Stiles, Annual Report, U.S.A. Bureau of Agriculture, 1901.)
Fig. 140.—Portion of the liver of a lamb which died nine days after feeding with eggs of the marginate tapeworm (Tænia marginata), with numerous “scars,” due to young parasites. (After Curtice.)
Life history. In tracing the life history it is best to begin with the egg, produced by the adult tapeworm in the intestine of dogs. These eggs, containing a six-hooked embryo, escape from the dog with the excrements, and are scattered on the ground, either singly or confined in the escaping segments of the tapeworm. Once upon the ground, they are easily washed along by rain into the drinking water, ponds, or brooks, or scattered on the grass. Upon being swallowed with fodder or water, they arrive in the stomach of the intermediate host (cattle, sheep, etc.), where the eggshells are destroyed and the embryos set free. The embryos then traverse the intestinal wall, and, according to most authors, arrive either actively, by crawling, or passively, by being carried along by the blood, in the liver or lungs, where they undergo certain transformations in structure. While still in the finer branches of the blood-vessels of the liver, which they transform into small, irregularly shaped tubes about 12 to 15 mm. long and 1 to 1·5 mm. broad, the embryos lose their six hooks, and develop into small, round kernels, which are generally situated at one end of the tubes. The embryo can first be seen about four days after infection. The “scars” (Figs. 140 and 141) described in the liver of animals infested with Cysticercus tenuicollis are nothing more nor less than these tubes, or altered blood-vessels, caused by the growth and wandering of the parasites.
Curtice takes a somewhat different view—that is, he considers the liver as a place of destruction for the young parasites, rather than a normal place for their development; he also claims that the embryos, which may even travel the entire length of the intestine of the intermediate host, traverse the intestine and arrive directly in the position where they complete their larval development without first passing through the liver.
Fig. 141.—Cross-section of the liver of a lamb which died nine days after feeding with eggs of the marginate tapeworm (Tænia marginata). (After Curtis.)
After developing into the full-grown bladder-worm, the parasites remain unchanged until they are devoured by a dog or wolf, or until, after an undetermined length of time, they become disintegrated and more or less calcified.
If the hydatid is devoured by a dog or wolf, either when the latter prey upon the secondary host or when the dog obtains the cyst at a slaughter-house, the bladder portion is destroyed, the scolex alone remaining intact in the digestive fluids. The head holds fast to the intestinal wall with its suckers and hooks; by strobilation (transverse division) it gives rise to the segments, which as we have already seen, together with the head, go to make up the adult tapeworm. Reproductive organs of both sexes develop in the separate segments, and eggs are produced, within which are developed the six-hooked embryos, the point from which we started.
DISTOMATOSIS—LIVER FLUKE DISEASE—LIVER ROT.
In France the name of distomatosis has been given to a disease caused by the presence of distomata in the bile ducts. It is the “liver rot” of England, the Eberfäule of Germany, and is produced by the growth in the biliary ducts of oxen, sheep, and goats of two species of distomata, viz., the Distoma hepaticum or Fasciola hepatica, and the Distoma lanceolatum.
Fig. 142.—Fasciola hepatica. A, young; B, adult parasite. (After Railliet.)
In 1875 Zundel established the causative relation between the presence of distomata in the liver and the development of progressive fatal cachexia in most of the animals affected. This opinion was emphasised by the works of Leuckart and Thomas on the development of distomata, and at the present day the parasitic theory is accepted as beyond question.
Fasciola hepatica (Distoma hepaticum).—The common liver fluke of cattle, sheep, swine, etc.
Life history. The adult parasite, instead of producing young similar to itself and capable of developing directly into adults in cattle, produces eggs which develop into organisms totally different from the adult form, living a parasitic life in other animals. In scientific language, the parasite is subject to an alternation of generations, together with a change of hosts. The following summary of the life history will make this point clear:—
(a) The adult hermaphroditic worm (Figs. 144 and 145) fertilises itself (although a cross fertilisation of two individuals is not impossible) in the biliary passages of the liver, and produces a large number of eggs.
Fig. 143.—Eggs of Fasciola hepatica. A, from the bile duct; B, embryonic; C, after opening. (After Railliet.)
Fig. 144.—Common liver fluke (Fasciola hepatica), natural size. (Stiles, Annual Report, U.S.A. Bureau of Agriculture, 1901.)
Fig. 145.—The common liver fluke (Fasciola hepatica), enlarged to show the anatomical characters. a, Acetabulum; c, cirrus pouch; i, intestine; m, mouth with oral sucker; o, ovary; p, pharyngeal bulb; s, shell gland; t, profusely branched testicles; u, uterus; va, vagina; vg, profusely branched vitellogene gland. (After Stiles, 1894, p. 300.)
Fig. 146.—Egg of the common liver fluke (Fasciola hepatica), examined shortly after it was taken from the liver of a sheep. At one end is seen the lid or operculum, o; near it is the segmenting ovum, e; the rest of the space is occupied by yoke cells which serve as food; all are granular, but only three are thus drawn. × 680. (After Thomas, 1883, p. 281, Fig. 1.)
Fig. 147.—Egg of the common liver fluke containing a ciliated embryo (miracidium) ready to hatch out: d, remains of food; e, cushion of jelly-like substance; f, boring papilla; h, eye-spots; k, germinal cells. × 680. (After Thomas, 1883, p. 283, Fig. 2.)
(b) Eggs (Figs. 143, 146 and 147).—Each egg is composed of the following parts: (1) A true germ cell, which originates in the ovary and is destined to give rise to the future embryo; (2) a number of vitelline or yolk cells, which are formed in a specialised and independent portion (vitellogene gland) of the female glands—instead of developing into embryos the yolk cells form a follicle-like covering for the true germ cell, and play an important rôle in the nutrition of the latter as it undergoes further development; (3) a shell surrounding the germ cell and vitelline cells, and provided at one end with a cap or operculum. The eggs escape from the uterus of the adult through the vulva, are carried to the intestine of the host with the bile, then pass through the intestines with the contents of the latter, and are expelled from the host with the fæcal matter. Many of them become dried, and then undergo no further development; but others are naturally dropped in the water in marshes, or, being dropped on dry ground, they are washed into water by the rain, or are carried to a more favourable position by the feet of animals pasturing or passing through the fields. After a longer or shorter period of incubation, which varies with the temperature, a ciliated embryo (miracidium) is developed. At a temperature of 20° to 26° C. the miracidium may be formed in ten days to three weeks; at a temperature of 16° C. the development takes two to three months; at 38° C. it ceases entirely. Experiments have shown that as long as these eggs remain in the dark the miracidium will not escape from the egg-shell; accordingly it will not escape during the night. When exposed to the light, however, or when suddenly brought into contact with cold water, the organism bursts the cap from the egg-shell, crawls through the opening, and becomes a—
Fig. 148.—Embryo of the common liver fluke (Fasciola hepatica), boring into a snail. × 370. (After Thomas, 1883, p. 285, Fig. 4.)
Fig. 149.—Sporocyst of the common liver fluke which has developed from the embryo, and contains germinal cells. × 200. (After Leuckart, 1889, p. 109, Fig. 67 B.)
Fig. 150.—Sporocyst of the common liver fluke, somewhat older than that of Fig. 149, in which the germinal cells are giving rise to rediæ. × 200. (After Leuckart, 1889, p. 109, Fig. 67 C.)
(c) Free-swimming ciliated miracidium (Fig. 148).—As already stated, this organism is entirely different from its mother. It measures about 0·15 mm. long; is somewhat broader in its anterior portion than in its posterior portion; on its anterior extremity we find a small eminence, known as a boring papilla; the exterior surface of the young worm is covered with numerous cilia, which by their motion propel the animal through the water; inside the body we find in the anterior portion a simple vestigial intestine and a double ganglionic mass provided with a peculiar pigmented double cup-shaped eye-spot; in the posterior portion of the body cavity are found a number of germ cells, which develop into individuals of the next generation.
Fig. 151.—Redia of the common liver fluke (Fasciola hepatica), containing germinal cells which are developing into cercariæ. × 150. (After Leuckart, 1889, p. 269, Fig. 129 A.)
Fig. 152.—Redia of the common liver fluke, with developed cercariæ. × 150. (After Leuckart, 1889, p. 270, Fig. 130.)
Fig. 153.—Free cercaria of the common liver fluke, showing two suckers, intestine, large glands, and tail. (After Leuckart, 1889, p. 279, Fig. 137.)
Swimming about in the water, the miracidium seeks out certain snails (Limnæa truncatula, L. oahuensis, L. rubella), which it immediately attacks (Fig. 148). The miracidium elongates its papilla and fastens itself to the feelers, head, foot, or other exterior soft portion of the body of the snail; some of the parasites enter the pallial (lung) cavity and attach themselves there. After becoming securely fastened to the snail the miracidium discards its ciliated covering, and shortens to about half its former length (0·07 mm. to 0·08 mm.). The parasites now bore their way into the body of the snail, and come to rest in the liver or near the roof of the pallial cavity, etc.; the movements gradually cease, and we have before us the stage known as the—
(d) Sporocyst (Figs. 149 and 150).—The eye-spots, ganglionic swellings, and vestigial intestine become more and more indistinct, and are finally lost. The sporocyst grows slowly at first, then more rapidly, and at the end of fourteen days or so measures 0·5 mm. The germ cells mentioned as existing in the posterior portion of the miracidium now develop into individuals of a third generation, known as—
Fig. 154.—Portion of a grass stalk with three encapsuled cercariæ of the common liver fluke (Fasciola hepatica). × 10. (After Thomas, 1883, p. 291, Fig. 13.)
Fig. 155.—Isolated encysted cercaria of the common liver fluke. × 150. (After Leuckart, 1889, p. 286, Fig. 142.)
(e) Rediæ (Figs. 151 and 152).—The rediæ escape from the sporocyst when the latter are from two weeks (in summer) to four weeks (in late fall) old. Upon leaving the body of the sporocyst they wander to the liver of the snail, where they grow to about 2 mm. long by 0·25 mm. broad. Each redia consists of a cephalic portion, which is extremely motile, and which is separated from the rest of the young worm by a ridge; under the latter is situated an opening, through which the next generation (cercariæ) escape. The posterior portion of the worm is provided, at about the border of the third and the last fourths of the body, with two projections. There is a mouth with pharynx situated at the anterior extremity, the pharynx leading to a simple blind intestinal sac. The redia, as well as the sporocyst, may be looked upon as a female organism, and in its body cavity are found a number of germ cells, which develop into individuals of the next generation, known as—
(f) Cercariæ (Figs. 153—155).—These organisms are similar to the adult parasites into which they later develop. The body is flat, more or less oval, and provided with a tail inserted at the posterior extremity. The oral sucker and acetabulum are present as in the adult, but the intestinal tract is very simple; on the sides of the body are seen two large glands, but the complicated genital organs of the adult are not visible. The cercaria leaves the redia through the birth opening, remains in the snail for a longer or shorter time, or passes out of the body of the snail and swims about in the water. After a time it attaches itself to a blade of grass (Fig. 154) or some other object, and forms a cyst around itself with material from the large glands, at the same time losing its tail. It now remains quiet until swallowed by some animal. Then, upon arriving in the stomach—of a steer, for instance—the cyst is destroyed, and the young parasite wanders through the gall-ducts or, as some believe, through the portal veins to the liver, where it develops into the adult hermaphrodite.
Fig. 156.—Drawing from a microscopic preparation, showing a hæmorrhage in the parenchyma of the liver caused by the common liver fluke (Fasciola hepatica). a, Atrophic liver tissue; b, round-cell infiltration; c, a portion of the parasite; d, hæmorrhage. (After Schaper, 1890, Pl. I., Fig. 1.)
From the above we see that this parasite runs through three generations, namely:
(1.) Ovum, miracidium, and sporocyst ... first generation.
(2.) Redia ... second generation.
(3.) Cercaria and adult ... third generation.
During this curious development, which lasts about ten to twelve weeks, there is a constant potential increase in the number of individuals, for each sporocyst may give rise to several (five to eight) rediæ, each redia to a larger number (twelve to twenty) cercariæ, and each adult to an enormous number (37,000 to 45,000) of eggs. This unusual fertility of the parasite is necessary because of the complicated life history and the comparatively small chance any one egg has of completing the entire cycle.
Hosts. An interesting and, from an agricultural standpoint, an important matter connected with this fluke is that it is found in a large number (about twenty-five) of domesticated and wild animals, and this fact probably explains to some degree the wide geographical distribution of the parasite.
Fig. 157.—Drawing from a microscopic preparation, showing the glandular hyperplasia of the mucosa of a gall-duct caused by the common liver fluke (Fasciola hepatica). a, Hypertrophied submucosa; b, interstitial connective tissue; c, compressed lobule; d, lumen of the gall-duct—thickened fibrous wall of the gall-duct. (After Schaper, 1890, Pl. I., Fig. 2.)
Symptoms. The symptomatology of this disease may clinically be divided into three well-marked periods:
I. Primary period. The primary phase commences with the penetration of the embryos of the parasite into the body, firstly into the intestine, and then into the liver by ascending the bile ducts. This phase occurs during the last months of the year, October, November, and December, and is rarely accompanied by alarming symptoms. At this time the sheep appear in good health, the summer being over, and the animals, being well nourished and fat, are able to resist the first attacks of the parasite, so that even an observant shepherd only notices a little dulness, want of condition, and muscular weakness. It requires a carefully trained eye to note these very general symptoms, for the bodily condition only changes very slowly and progressively, the appetite remaining good. Experienced butchers, however, in the districts where distomatosis is common, readily detect this condition. The animals make little resistance when handled.
Fig. 158.—Drawing from a microscopic preparation showing a fluke in the tissue of the liver. a, Necrotic liver tissue; b, atrophic liver cells; c, spines on the fluke, showing the outline of the body. (After Schaper, 1890, Pl. III., Fig. 5.)
Nevertheless, even in this primary phase, the conditions are not always as above sketched, and a certain number of deaths may occur. Gerlach has mentioned the possibility of death by cerebral apoplexy, in consequence of the young distomata penetrating to the brain. Moussu has certainly never seen such a complication, but has seen death from hepatitis, perihepatitis, and secondary pericarditis in animals gravely infested. The young embryos, whether they penetrate only by the bile ducts, as has been stated, or are carried to the liver by the blood stream, often excavate canals in the substance of the gland before establishing themselves in the bile ducts. They make their way as far as Glisson’s capsule, and may even penetrate it; and as they carry with them innumerable intestinal germs, when they arrive viâ the bile ducts, they set up hepatitis, perihepatitis, with the formation of numerous false membranes, or even infectious fibrinous peritonitis. Should the patients die during this phase one finds young distomata at the surface of the liver, or even in the thickness of the false membranes.
Fig. 159.—Tabular diagram of the occurrence of the common liver fluke (Fasciola hepatica) during different months of the year. a, Cattle; b, sheep; c, swine. (After Leuckart, 1889, p. 301, Fig. 147.)
When infestation is discrete the appearances are quite different. Careful breeders have even stated that at this period the young sheep appear to show a greater tendency to fatten.
II. Second period. In the primary phase deaths are exceptional; they only become common towards the end of the winter. During the second or middle period (December and January) the patients lose flesh, appear less active, show less regular appetite and greater thirst. The conjunctiva becomes pale and swollen, the sclerotic has a bluish tint, and the eyelids are somewhat infiltrated. The wool appears drier and less curly; locks of wool part readily from the skin, and the individual fibres become dry and fragile.
Fig. 160.—The large American fluke (Fasciola magna), natural size. (Stiles, Annual Report, U.S.A. Bureau of Agriculture, 1901.)
This phase is accompanied by very marked anæmia, rapid exhaustion during movement, and inability to run for any length of time.
The different methods of examination reveal nothing specially striking, except that the valvular sounds of the heart are sharper, and that trifling œdema occurs under the thorax and abdomen.
Microscopic examination of the fæces reveals the presence of eggs of distomata. The sheep rapidly become thin from about the end of January, even although the appetite persists and nourishing food is given.
III. Third, or wasting, period. The decline, which sets in about February, appears extremely obstinate, and resists all treatment.
The patients become feeble, eat less, and digest badly. Submaxillary œdema, common to advanced wasting diseases, then appears. If the sheep are removed from the fold to pasture, the swelling of the submaxillary space is very noticeable. It consists in an indolent œdematous tumefaction, which disappears when the animals are travelled, but reappears when grazing on account of the low position in which the head is then held.
The condition then becomes complicated with diarrhœa, and soon grows alarming. On examination, extensive dropsy may often be found in the thorax, pericardium, and abdomen.
Death results from exhaustion; the animals do not appear to suffer, but become extraordinarily anæmic, and perish without a struggle. The blood is simply rosy in colour, like gooseberry syrup; the clot is soft and gelatinous; the number of red blood corpuscles has fallen from about seven millions to a few hundred thousand.
Icterus is rare, though certain cases have been described where it has appeared during the last and even during the middle stage.
When animals begin to die in a district which has long been infested, the losses are enormous, the condition sometimes constitutes a perfect scourge. It should be remarked, however, that all those affected do not die; animals kept under good conditions may even survive for several months, although greatly wasted.
Towards March and April the parasites leave their position, and are conveyed by the current of bile towards the intestine, to be rejected with the fæces. This is the period of convalescence and recovery; but recovery is only relative, for the parasites are never entirely evacuated. The distomata then recommence their life cycle outside the animal body.
Fig. 161.—Macerated specimen of large American fluke, showing the digestive system and acetabulum. X 2. (After Stiles, 1894, p. 226, Fig. 2.)
Unfortunately the mortality caused by distomata is accidentally aggravated by other diseases, and the scourge then becomes an absolute disaster for the districts where such complications occur. Thus Besnoit and Cuillé, of Toulouse have shown that distomatosis may become complicated with a form of very rapidly fatal hæmorrhagic septicæmia, produced by an ovoid bacterium.
Distomatosis, already sufficiently grave, then becomes infinitely more serious, if only from the fact that it may prove the point of origin of an absolutely fatal complication.
In bovine animals the symptoms develop exactly as in sheep, though the cachectic period is uncommon and the injury done is often less important than in sheep. The patients exhibit irregular appetite, wasting without appreciable cause, anæmia, and even diarrhœa. In spite of excellent winter feeding they do not regain condition, and relative recovery only sets in with the approach of spring. Death from simple distomatosis is exceptional, but in animals so predisposed enteritis develops more easily, as do all forms of infection of intestinal origin.
The disease is, however, also grave for bovines because successive reinfection occurs, and the disease may be prolonged for years.
Causation. Distomatosis is due to one cause, viz., the entrance of embryo flukes into the digestive apparatus of herbivora.
The adult distomata in the biliary ducts continually discharge large quantities of eggs, though the process is most active between February and June or July. The eggs are carried away with the bile and fæces and pass on to the pastures, where they continue their life cycle, thanks to moisture and the presence of stagnant water. The embryos, having escaped from the egg, enter the bodies of the snails found in or near stagnant water (Limnæa truncatula), become converted into sporocysts, and afterwards into rediæ and cercariæ. The cercariæ become encysted on the lower surface of blades of grass in damp pastures, whence they are transferred to the animals’ stomachs along with the grass itself.
Fig. 162.—Limnæa truncatula. Natural size and magnified. (After Railliet.)
As the Limnæa truncatula lives not only in marshy regions, but also in all damp situations, the embryos of distomata are distributed over enormous areas, and the disease itself is equally widespread. The embryo, after ingestion, is set at liberty, and passes from the intestine into the innermost recesses of the liver, being guided up the bile ducts by the current of bile. At this point it attaches itself to the wall of the bile duct, passes through its various stages of evolution, and attains the adult form. It then begins laying eggs, and thus starts a new evolutionary cycle.
The life cycle of Distoma lanceolatum is not yet known, and this variety, moreover, is less widely distributed than the Distoma hepaticum.
The bile ducts are more easily penetrated by the distoma in young animals, a fact which explains why calves and lambs are particularly affected. Adults present a less favourable nidus, a fact which renders them less easily infected, but does not entirely prevent the parasites from attacking them. Old animals, although unable to resist entirely, seldom harbour many of the parasites.
Wet years appear to favour the extension and propagation of distomatosis in an extraordinary fashion, a fact which is easily understood, if we regard the phases of evolution of the parasite. The autumn appears particularly favourable to the infection of herds. This is explained by the fact that, during the summer, the dryness of the fields entirely prevents the development of such eggs as may be distributed over them; whilst wet periods during the autumn favour this development.
On the other hand, the grass becomes eaten down in autumn, so that the animals gather it almost level with the ground. As the cercariæ attach themselves to the lowest leaves they are then ingested in much larger quantities. The bad effects of wet seasons are not immediately apparent, but appear during the following spring.
Distomatosis is common throughout almost the whole of Europe, Africa, and America. In France it is most serious in the moister regions of Sologne, in Berry, the mountainous and wet districts of the great central plateau, and particularly in the Pyrenees. It particularly attacks oxen in the valley of the Meuse, the marshes of Picardy, the lower regions of Normandy, and in all the mountainous pastures of the central plateau.
Lesions. The lesions of distomatosis vary with the stage of development of the parasites. During the primary phase of invasion of the bile ducts by young distomata one finds interstitial diffuse hepatitis, due to perforation of the gland by young parasites, adhesive perihepatitis, with the formation of false membranes, and not uncommonly slight peritonitis.
Zoologists state that the young distomata penetrate the liver by passing upwards against the current of bile. It does not appear impossible, however, that they may penetrate by another path, particularly as so-called “erratic” forms of distomatosis like distomatosis of the lung, heart, lymphatic glands, and various other tissues are not uncommon. It has been suggested that the young distomata, arriving in the bile ducts, perforate the gland, giving rise to these lesions of perihepatitis, peritonitis or erratic distomatosis; but this view is scarcely in harmony with the fact that the parasites are usually found in the bile ducts.
During the second phase, corresponding to the development of almost adult distomata, the perihepatitis and peritonitis set up either produce fatal results by secondary infection or diminish and disappear. The parasites develop in the bile ducts, in which they attain the adult condition. They steadily ascend towards the origins of the ducts, dilating them in their passage in an extraordinary way. The number of parasites varies greatly: sometimes there are but few, and they are only discovered on post-mortem examination; in other cases the bile ducts are crammed with them, as many as six or seven hundred or even a thousand being present. The distended bile ducts always show chronic peripheral inflammation, which steadily becomes aggravated, producing pericanalicular atrophying sclerosis. This condition is followed by change in and disappearance of a certain quantity of hepatic tissue, and by various forms of vascular and secretory disease.
This is the period of greatest disturbance, not only in consequence of the actual presence, but also of the mode of living, of the parasites.
Moussu declares that the parasites live principally on blood, at least during the first and second stage of their sojourn in the liver, adducing as proof that if one completely injects the vascular system of the liver (arteries and veins), some of the injected matter will be found a day afterwards in the digestive apparatus of the parasites.
The disturbances which they produce are therefore due to their actual presence and its consequences, to their mode of life, and to the intercurrent infections of which they are sometimes the initial cause.
It is idle to object that the part played by these parasites is less important than has been suggested, and that the mortality results from intercurrent infection, and not from the parasites themselves. It is equally idle to point out that carcases of animals suffering from severe infection with distomata, particularly the carcases of sheep, are frequently found in slaughter-houses, in perfectly fat condition, and with the appearance of not having suffered in any way. These observations are perfectly correct and well founded. But it matters little that death results from an infection superadded to the distomatosis, if the presence of distomata is the determining factor in causing the superadded infections, and if such infection is, as Moussu believes, almost inevitable in animals already exhausted by the action of the parasites.
The fact that animals suffering from distomatosis and slaughtered for food are well nourished is not a valid objection; for it has long been known that wasting and anæmia are not immediate consequences, and that before they are clearly apparent the distomata must have been present in the liver for several months. Bakewell and the Marquis of Behague have shown that in moderately infected animals there is a tendency to lay on flesh during the first and a portion of the second stage of development of the disease.
If the animals are slaughtered before the period of progressive decline sets in, it is quite possible to form entirely wrong views regarding the importance of these parasites.
The wasting process commences towards the end of the second phase of the disease, and then makes rapid progress. The parasites, which have then been continuously drawing on the blood for their nourishment for a long time, produce anæmia, and some infection of the bile ducts, and usually a certain degree of icterus.
The third phase is accompanied by general signs of cachexia, which need not again be described. They are similar to those of all progressive cachexias. In animals which survive this phase and are ultimately slaughtered the liver always shows very marked sclerosis, commencing around the biliary ducts. Even after the parasites have been evacuated, these ducts appear indurated, thickened, fibrous, and sometimes encrusted with biliary deposits or obstructed with true calculi. These calculi may or may not contain parasites; sometimes they simply contain eggs: they are open, tubular, and perforated, but always irregular on the surface.
When in addition complications have appeared, one usually finds general lesions of septicæmia and blood infection.
In erratic distomatosis, which is of no importance clinically, distomata may become encysted in the lung or other viscus, and in time die. The cysts, which only contain one and rarely two parasites, present a fibrous shell, enclosing a blackish, pultaceous, grumous magma, which sometimes has undergone a certain amount of calcareous infiltration. The parasite may be entirely destroyed.
Diagnosis. Early diagnosis is difficult, and can only be established by microscopic examination of the excreta and the discovery of eggs. On an average one may find one egg in each preparation when the liver contains 80 to 100 flukes. When wasting is very marked, and particularly when there has already been a number of deaths, diagnosis becomes extremely easy. It is sufficient to find flukes in any form (Distoma hepaticum rel lanceolatum) to be assured as to the cause of disease.
Prognosis. In severely infested cases the prognosis is extremely grave, because no efficient method of treatment exists. Embedded in the liver, the parasites resist the action of all drugs, and we know of no anthelmintic eliminated by the bile which in any way affects their vitality. When the disease is recognised early, the most economical method is to fatten the animals as rapidly as possible and prepare them for slaughter.
Treatment. There is no reliable curative treatment. The drugs which one might employ would kill the animal before poisoning the parasites embedded in the liver. Various mixtures containing sulphate of iron, juniper leaves, etc., have been recommended; but rich food constitutes the best of all treatment, both from a curative and a prophylactic standpoint.
With the view of preventing the disease, however, and protecting flocks from attack in places where the disease is common, certain precautions should be adopted. They comprise—(a) providing a free supply of rock-salt, either in masses placed in the mangers or distributed with the food; the salt increases gastric secretion, and has a slight action on the parasites: (b) adding to the food during the first months of winter branches of birch, juniper, willow, and broom; the leaves of these plants contain aromatic or resinous principles which act on the liver, are eliminated by the bile, and may have valuable results.
But of all preventive measures the most effective consist in draining, cleansing, and drying low, moist, or marshy lands, because the molluscs which are essential to the life cycle of the parasites are unable to develop where the soil is dry. The manure containing the eggs of the parasites may be disinfected by adding to it lime, sulphate of iron, or common salt. Common salt and lime spread over the pastures has a double beneficial influence, acting both as a manure and as a parasiticide. From May to August is the best time for spreading this dressing.
The fluke embryos are destroyed by 1 to 2 per cent. solutions of common salt, and by ¾ per cent. solutions of lime.
In over-stocked fields the animals are obliged to graze very close to the ground, and are thus more exposed to infection. Over-stocking should therefore be avoided. Animals should not be left too long on the same ground. If infected they should at once be driven to higher pastures. Raised water tanks can be placed in the pastures—they are less likely to become infected. Animals from known infected flocks or herds should not be purchased. Livers from infected animals should be cooked or destroyed. If eaten raw by dogs the eggs pass uninjured through the dog’s intestine and infect fresh pastures.
Sulphate of iron distributed in quantities of 250 to 400 lbs. per acre is valuable as a manure, and would probably have a greater effect in destroying the embryos.
SECTION III.
RESPIRATORY APPARATUS.
CHAPTER I.
EXAMINATION OF THE RESPIRATORY APPARATUS.
From the clinical standpoint a study of the respiratory apparatus implies the examination of the nostrils, nasal cavities, frontal and maxillary sinuses, larynx, trachea, and, for the purpose of ascertaining the condition of the lungs and pleura, of the chest.
Nasal cavities. Examination of the external portion of the nasal cavities is extremely simple. The observer notes the degree to which the orifices are dilated, the frequency of the respiratory movements and the condition of the muzzle. He may find various eruptions, crusts due to discharge, etc., and will remark any peculiarities presented by these. The depths of the nasal cavities can only be examined through the nostrils to a very limited extent; but the condition of the pituitary mucous membrane, its degree of vascularity, and the existence of ulcerations or of vegetations can be observed.
Digital examination is sometimes useful in discovering the condition of the lower portions of the turbinated bones. The electric light does not greatly assist the observer, on account of the narrowness of the air passages. On the other hand, examination of the face, and palpation and percussion over the region of the frontal sinuses is of considerable value. By inspection, one discovers deformity caused by tumours, by ossific inflammation, or other lesions; and detection is rendered easier by the fact that deformities are usually asymmetrical, only occurring on one side.
Palpation reveals the degree of resistance and flexibility of the external bony wall as well as the condition of the subcutaneous tissues.
Percussion sometimes discloses absolute dulness, due to tumours of the mucous membrane, of the turbinated bones, or of the bones of the face.
The pharyngeal portion of the nasal cavities is difficult to reach, but can be examined by passing the hand, palm upwards, into the pharyngeal cavity, when the fingers may be slipped behind the soft palate and thus introduced into the posterior nasal chamber. The animals should first be very carefully secured and a strong gag introduced into the mouth.
Sinuses. Frontal sinus.—The frontal sinus occupies the greater part of the anterior cranial region and the summit of the head, extending from the highest point of the poll as far forward as a line drawn between the two orbits. Above, it directly communicates with the sinus of the horn core. In this upper region, where it abuts on the sinus of the opposite side along the median line, it is of greatest size. Below, on the other hand, it is very narrow, much broken up and incompletely divided into a series of cells, by thin, bony plates running in all directions.
Fig. 163.—Median section through an ox’s head. Sf, Frontal sinus; N.Ph. nasopharnyx; Vp., hard palate; C., turbinated bones; V., vomer; L., tongue; V. pa., soft palate; E., epiglottis; La., larynx; Œ., œsophagus.
It is in direct communication with the nasal cavity.
The frontal sinus, then, occupies all the supero-lateral portion of the cranial box, which is thus provided with a double wall. At one point, however, over a lozenge-shaped area, the cranial cavity is only protected by a single wall. It is in this region that the slaughterman strikes the animal when killing it.
The frontal sinus may be examined by inspection and palpation. Inspection sometimes reveals deformity of the external wall of the sinus. Such deformity, however, is rare, and Moussu has only observed it in two cases of tuberculosis of the bones forming the cranial wall.
By percussion one detects abnormal sensibility, and partial or complete dulness over certain areas.
Fig. 164.—General arrangement of the sinuses. The circular openings indicate points at which trepanation is performed.
Maxillary sinus.—The maxillary sinus occupies the whole lateral region of the face, from the inferior extremity of the maxillary spine as far as the sub-orbito-palatine region. In front its external wall is very solid, but behind, below the orbit, is extremely thin. Externally the sinus is largely protected by the anterior insertion of the external masseter muscle, a fact which explains how rarely it is injured.
Larynx. In consequence of its deep situation, the larynx can scarcely be examined except by inspection, external palpation, internal digital palpation, and auscultation.
External examination presents no difficulty, and enables one to detect lesions around or near the larynx.
Palpation reveals the existence of œdematous swellings, enlargements of the retro-pharyngeal lymphatic glands, inflammatory engorgements, etc.
Internal digital examination, like examination of the pharynx, can only be performed after very firmly fixing the animal in position, and inserting a gag in the mouth.
Fig. 165.—Manual examination of the larynx in the ox.
The hand is introduced, palm downwards, and passed as far as the pharyngeal cavity. The index finger can then easily be slipped into the glottis. Exploration must be effected rapidly and without violence. It reveals the condition of the glottis, the presence, position and form of growths like myxomata and of new tissues, due to the presence of actinomyces, as well as tuberculous vegetations or ulcerations.
By auscultation we discover the presence of normal or abnormal laryngeal sounds—roaring, whistling, or bubbling sounds, etc.
Trachea. The trachea may be examined by palpation and auscultation.
Palpation reveals the degree of sensitiveness, abnormalities in position or form, the presence of peripheral inflammations, fractures of rings, etc.
Auscultation indicates whether the tracheal sound be normal or otherwise, or accompanied by abnormal sounds, like mucous râles, or by pathological sounds conveyed from the chest.
Thorax. The thorax can be examined by inspection, palpation, percussion, and auscultation.
By inspection we discover whether the formation of the thorax as a whole is normal, or whether there exist congenital or acquired deformities, asymmetry like that produced by pneumo-thorax or deviations of ribs from the normal line, etc. One also notes the breathing movements, the manner in which the sides expand and contract, the respiratory rhythm, and any special peculiarities of inspiration or expiration.
Palpation reveals the degree of sensitiveness of the thoracic wall and of the intercostal spaces, the existence of more or less extensive local œdematous infiltration, and the presence or disappearance of thoracic conditions like hydro-thorax.
Percussion indicates the degree of sonority of the chest in different parts. It can either be practised directly with the hand or through the medium of a pleximeter. The latter method is preferable when dealing with fat animals. Percussion, however, gives slightly different results, according to the degree of fatness of the subjects. It should be practised both in a vertical as well as in a horizontal direction.
At all points where the muscles are thick or well developed the results produced are negative, in the sense that only a dull sound is obtained. This is the result obtained in auscultating the areas marked 1, where one meets with the ileo-spinal and common intercostal muscle, and in that marked 4, where the olecranian muscles are encountered (Fig. 166). Over the middle and inferior zones, however, the results are much more instructive.
On the right side percussion of the middle zone gives, under normal conditions, a clear sound and perfect resonance from above downwards, and from in front backwards, between the fourth intercostal space and the ninth rib. Beyond this point lies the liver, which gives a partial dull sound, and absolute dulness from the ninth to the twelfth rib, in consequence of its position, and of the projection of the diaphragm towards the thoracic cavity.
Percussion of the inferior zone produces less marked resonance, which diminishes more and more towards the base, in consequence of the thinness of the pulmonary lobes at this point. This resonance does not extend as far as the hypochondriac region, because the lower part of the abomasum insinuates itself beneath the costal cartilages and causes a region of dulness.
On the left side percussion gives precisely similar results, except in the upper portion of the middle zone. Beyond the ninth intercostal space the sound changes, and has a tympanic character; because here the anterior and upper portions of the rumen are encountered, as they are lodged beneath the hypochondrium. Below, the sound is dull, on account of the gastric compartments generally being full of food.
Certain trifling modifications of this normal condition may be noted, depending on the degree of fatness or thinness of the subjects. The pathological changes which may occur are as follows:—
A tympanic sound, with or without metallic character, may be found at a point where normally one would expect a clear sound (pneumo-thorax, diaphragmatic hernia). A dull sound may be met with in the same regions, all resonance being lost (pneumonia, broncho-pneumonia, pleural exudate, etc.). Partial dulness and partial loss of resonance may occur in regions which ought to give a resonant sound (deep pneumonia, tuberculous lesions, the presence of echinococcus cysts, etc.).
Auscultation—i.e., examination by means of the ear—is the most valuable method of discovering and localising pulmonary, pleural, or cardiac lesions.
Various sensations are conveyed to the ear, depending on the method in which the normal or pathological sounds are produced.
The deductions to be drawn as regards the nature of existing disease are based on the intensity, character, duration, and special attributes of the sounds noted.
Direct auscultation is the most certain method, but the ear cannot be applied with equal facility at all points. Under such circumstances a simple or binaural stethoscope, or the phonendoscope, may be used with advantage.
To properly appreciate the sounds heard it is essential to be exactly acquainted with the relation between the lung and thorax. On the left side (Fig. 60) the anterior pulmonary lobe occupies the space between the first and fourth ribs, in front and above the base of the heart. The middle, or cardiac, lobe covers the left upper and postero-lateral part of the heart from the fourth to the sixth rib. The posterior lobe occupies all the region beyond the sixth rib as far as the twelfth.
On the right side the arrangement is similar, but the anterior lobe and the cardiac lobe are more developed (Fig. 62).
Under ordinary circumstances the extensive movement of the lung which occurs during inspiration produces a special sound known as the respiratory or vesicular murmur. Contrary to what has been written, and said, this sound in animals possessing absolutely sound lungs ends with inspiration. Expiration is silent, though it is easy to estimate its duration.
In auscultating the lung, we may distinguish four zones, a superior zone, a middle zone, an inferior zone, and a scapular zone.
The superior zone is bounded by the vertebro-costal gutter, descends approximately as far as the inferior line of insertion of the common intercostal muscle, and extends from the summit of the scapula in front to the hypochondrium behind.
Auscultation of this region through the ileo-spinal and common intercostal muscle will always reveal, except in very fat animals, the vesicular murmur to a point as far back as the eleventh intercostal space. Nevertheless, this vesicular murmur is relatively feeble, and becomes imperceptible beyond the eleventh rib.
The middle zone comprises the most convex portion of the ribs, and at this point the wall of the thorax is thinnest, while the lung below is thickest.
Fig. 166.—The areas over which auscultation of the chest may be performed, showing their extent, position and relations to the thoracic wall. 1, Upper zone; 2, middle zone; 3, inferior zone; 4, subscapular zone.
For these reasons the vesicular murmur is heard at its maximum intensity at this point. Towards the upper and lower limits of this zone are found the great bronchial divisions, so that auscultation should always be practised with the greatest care at this point. The middle zone occupies approximately one-third of the total depth of the thorax. The vesicular murmur becomes weaker as one passes backwards, and finally disappears at a considerable distance from the angle of the hypochondrium, following a curved line the convexity of which is directed forwards, and which is continuous with that limiting the upper zone.
These peculiarities are due to the anatomical arrangement and mode of insertion of the diaphragm on the internal surface of the hypochondrium.
The inferior zone is very limited, and corresponds externally to the inferior third of the thorax, and topographically to the cardiac lobe or middle lobe of the lung and to the inferior portion of the posterior lobe.
As these pulmonary lobes are of comparatively slight thickness, the vesicular murmur is feeble. It can be heard over a trapezoidal space, forming a prolongation of the middle zone, but not below in the region of the sternum or pectoral muscles.
The fourth zone extends over the mass of the olecranian muscles. It is of triangular form, in consequence of the inclination of the scapula and humerus. Except in very fat animals the vesicular murmur is readily audible through the muscular mass on the right side better than on the left, on account of the development of the right anterior pulmonary lobe.
On the left side the beating of the heart is heard above the pulmonary sounds.
Clinically one may hear an exaggeration of the ordinary respiratory murmur whenever the lung is actively exercised, as, e.g., immediately after trotting. This exaggeration, however, is often pathological. It is known as “juvenile or supplementary respiration,” when due to the fact that some other portion of the lung is not acting.
The respiratory murmur may be lessened in certain morbid conditions, such as emphysema and congestion of the lung, and may completely disappear in pneumonia or broncho-pneumonia, a fact which is even of greater significance.
In various pathological conditions the respiratory murmur may also be modified. On the other hand, the movement of air in the bronchi also produces various sounds of importance.
A number of different bronchial sounds may be distinguished; these include both inspiratory and expiratory sounds, for sometimes an expiratory sound may become audible and clearly appreciable, or may acquire characters of the greatest importance.
The inspiratory sound may be strong, rough, rasping, painful, moist or rattling. The pathological expiratory sounds may vary between audible, strong, rough, prolonged, or rattling. The varieties of souffle, or rattle, are the tubal souffle of inspiration or expiration (met with in pneumonia or broncho-pneumonia); the soft, deep-seated pleuritic souffle (peripneumonia); the continuous cavernous souffle (met with in tuberculosis); the broad amphoric souffle, in which the vibrations are extensive and of metallic character (met with in pneumo-thorax).
As to the varieties of râles which usually accompany these souffles, they may all be met with in tuberculous animals, and comprise crepitant and sub-crepitant, mucous, cavernous, snoring and sibilant râles.
CHAPTER II.
NASAL CAVITIES.
SIMPLE CORYZA.
Simple acute coryza, or inflammation of the mucous membrane of the nasal cavities, is of comparatively trifling importance in bovine animals, and, were it not for the possibility of gangrenous coryza being confused with it, there would scarcely be any necessity for a special description.
The onset of coryza is indicated by repeated sneezing and coughing, by congestion of the pituitary mucous membrane, which soon begins to secrete abnormally, and by difficulty in respiration, which becomes snoring or whistling.
The discharge, transparent at first, then mucous and muco-purulent, is abundant in quantity; the inflammation is arrested at this point or extends towards the facial sinuses, the pharynx and larynx; the eyes are swollen and watering, and almost all the characteristic symptoms appear which mark the onset of gangrenous coryza. Two signs, however, are wanting. The appetite is fairly well maintained, and the temperature little above normal. Simple coryza occurs at all times of the year in consequence of sudden chills, but is commonest in spring and autumn.
At first the distinction between this condition and gangrenous coryza can only be ascertained after taking the temperature.
The prognosis is absolutely favourable, and often in forty-eight hours every symptom disappears.
Treatment is confined to keeping the animals in stables at a suitable temperature, sheltered from draughts. Emollient fumigations and inhalations of turpentine, creosote, or eucalyptus oil rapidly check the more alarming symptoms. Warm drinks and foods and cooked roots are recommended.
In sheep, acute coryza as a consequence of chills, etc., occurs in autumn, but is more commonly due to a parasitic cause, viz., invasion of the nasal cavities by larvæ of certain œstridæ. During the succeeding winter it continues under the form of chronic coryza, as a result of the larvæ retaining their position in the sinuses.
Treatment of this parasitic coryza consists in trephining the sinuses and destroying the larvæ.
GANGRENOUS CORYZA.
Gangrenous coryza is a grave disease of diphtheritic character, which at first seems to be localised in the mucous membrane of the upper respiratory passages, but which exhibits a tendency to affect all the mucous membranes of the system.
The term “gangrenous coryza,” adopted in France, has been replaced in other countries, especially in Germany, by such descriptions as “contagious disease of the head,” and “malignant catarrhal fever of the ox.” Old writers describe gangrenous coryza as a disease common in the Jura, the eastern parts of France generally, and in the valley of the Saône. In reality this disease occurs everywhere, both in the centre, west and north of France, as well as in the eastern regions. Serious outbreaks frequently occur in Germany and Italy.
Symptoms. Gangrenous coryza assumes three different forms, which, however, only represent successive degrees of intensity of the attack. In the peracute form death occurs in three to five days, even when the characteristic signs are not all as yet apparent. In the acute, and by far the most frequent form, the disease lasts from fifteen to twenty days, and also ends in death in by far the greater number of cases. Finally, in the form usually termed chronic, the disease lasts from four to eight weeks, and most frequently ends in recovery.
Acute and peracute forms.—The onset is marked by very striking symptoms, which precede the local symptoms by some hours, or by a day or more.
The temperature rises rapidly from the normal to 103° or 105° Fahr. (39·5° to 41° C.), or even higher. Appetite and rumination are entirely suspended; the respiration becomes rapid and difficult, while the heart beats strongly and tumultuously; the muzzle is dry, the mouth hot, and salivation so abundant as to suggest an attack of foot-and-mouth disease. Fæces and urine are only passed at long intervals, and dysuria is present.
At first everything seems to indicate the development of an acute infectious disease; but soon afterwards appear local indications affecting the respiratory, ocular, digestive, urinary, nervous and cutaneous systems.
The respiratory symptoms are most important, and almost characteristic. Respiration becomes difficult, rough as in acute coryza, but soon assumes a snoring character, and is accompanied by a discharge, containing false membranes, from both nostrils.
The serous and muco-purulent discharge becomes rusty or reddish-brown, soon acquires a very fœtid smell, and is found to contain epithelial débris and yellowish-green false membranes. After the least effort to cough or the slightest touch on the membranes themselves—sometimes without any visible cause at all—epistaxis sets in, the blood being mixed with the discharge or simply escaping in the form of reddish strings, like that occasionally seen in glanders.
The mucous membrane of the nasal cavities is red, turgid, apt to bleed, and painful to the touch.
Percussion of the nasal cavities, sinuses, and even of the horns reveals everywhere exceptional sensibility.
Sometimes, but only in certain subjects, the lower portions of the head, including the muzzle, nostrils, lips and forehead, become infiltrated, as though the case were one of purpura. Thoracic complications are rarely absent, unless the disease is treated. Towards the end of the first week the respiration, still painful and snoring, becomes more rapid; and auscultation reveals at various points in the lungs areas of bronchitis and of broncho-pneumonia, indicated by bronchial râles, rattling breathing, and tubal souffles, etc. These complications are accompanied by attacks of coughing, which increase the discharge, and may threaten to end in suffocation. This happens when large masses of false membranes from the bronchi are thrown into the larynx and cannot readily be ejected through the glottis, which has been reduced in size by œdematous infiltration and inflammation.
Percussion is generally useless. The appearance of the eyes is also very significant. These symptoms develop simultaneously with the respiratory disturbance, and are marked by infiltration of the eyelids, œdematous conjunctivitis, and ophthalmia. The cornea becomes whitish, infiltrated, opaque, and sometimes shows ulcerative keratitis; or, on the other hand, it remains simply semi-transparent, and through it the media of the eye may be seen to have become opalescent. Ulcerative keratitis may develop rapidly and end in perforation of the cornea.
In certain rare instances examination with the ophthalmoscope has revealed the existence of exudative iritis; this condition may be complicated with syncchia, intra-ocular hæmorrhage, and result in permanent loss of vision.
These ocular symptoms are accompanied by continuous, abundant and prolonged discharge of tears, intense photophobia, and exceptional sensitiveness to manual examination, etc.
Digestive disturbance appears less important, and may be regarded as consequent on the febrile reaction, the general disturbance, or the condition of the respiratory apparatus. But complete examination will show that from the onset of the disease a special form of stomatitis occurs. From the first the mouth is hot and dry: soon afterwards abundant reflex salivation occurs, and the discharge, like that from the nose, becomes excessively fœtid. This stomatitis differs entirely from ordinary forms of stomatitis and from the stomatitis peculiar to foot-and-mouth disease, and is characterised by the necrosis of fragments of epithelium forming false membranes. These on being shed leave exposed numerous ulcers distributed over the tongue, cheeks, and lips. Neither vesicles nor pustules are produced, but merely false membranes of small dimensions.
The false membranes and ulcerations occur on the soft palate and in the pharynx.
When the patients survive for a certain time, croupal enteritis and ulcerative enteritis, sometimes accompanied by hæmorrhage, develop. The administration of enemata is followed by the passage of fæces containing considerable fragments of epithelium or of streaks of blood. From the outset these digestive complications are indicated by failure to ruminate, by cessation of peristalsis and by constipation, which is usually succeeded by abundant fœtid diarrhœa.
Functional disturbance of the genito-urinary apparatus is rarer, or at least more difficult to detect. The animals refuse drink; micturition seems to be suspended or very difficult. The urine may be albuminous or rose-coloured, in consequence of the presence of hæmatin; more rarely it is purulent or sanguinolent. There may also be urethritis, cystitis, pyelitis, and nephritis, with the passage of hyalin cylinders in the urine, although this is not always the case.
In females the mucous membrane of the vagina and lips of the vulva usually seem congested and œdematous; but it is rare to find diphtheritic false membranes, as on the buccal and nasal mucous membranes, etc. On the other hand, vaginitis and exudative metritis are common.
Cutaneous outbreaks also constitute important symptoms by which this disease is recognised. At points where the skin is fine, on the inner surface of the thighs, around the girth, on the inner surface of the forearm, and on the mammæ, etc., an exanthematous eruption occurs, followed later by the development of pustules, which at first sight might suggest cow-pox.
These pustules are prominently apparent, and can readily be detected on palpation. They are more or less confluent, hard, and without a peripheral œdematous zone.
In the case of the mammæ these pustules occur most commonly on the teats, are round or slightly oval in form, bright red in colour, and sometimes violet-red. They never become converted into vesico-pustules, as in cow-pox, or into vesicles; and in no way resemble the skin eruption peculiar to foot-and-mouth disease.
Certain nervous symptoms have also been described, comprising trembling, epileptiform convulsions, and paraplegia of the hind quarters.
Moussu has never seen nervous disturbance assume the form of epileptiform convulsions, and it is possible that the paraplegia referred to simply marks the last stage of the disease.
Causation. The essential cause of gangrenous coryza has not yet been definitely ascertained. Within recent years teachers of the highest authority have represented the disease as a general affection belonging to the hæmorrhagic forms of septicæmia (Nocard and Leclainche). Nocard has found ovoid bacteria in the false membranes of the larynx, and Leclainche a paracoli-bacillus in the mesenteric ganglia and the intestines, but the disease has never been reproduced in a characteristic and complete form similar to the clinical type.
Other microbes have also been described as occurring in the blood or discharges; but attempts to transmit the disease by using cultures or the different morbid products which observers have collected have invariably failed, and it has therefore been concluded that the disease is not contagious, but merely infectious.
Moussu does not regard this disease as a hæmorrhagic septicæmia, because the blood proves sterile unless grave pulmonary, intestinal or renal complications occur, and because the disease appears capable of being cured in a short time by simple methods. In the present state of knowledge he prefers to regard it as an infectious disease of diphtheritic form, at first localised in the upper respiratory and digestive tracts, always tending towards a grave toxæmia, and towards complications due to various other infections.
Even though direct contagion has not been proved, it is impossible to doubt that stables may become infected. This is sufficiently proved by the continued appearance of the disease when disinfection is neglected after the occurrence of the first case.
It is possible that the causes formerly assigned—viz., chills, the influence of draughts, and a morbid predisposition—may increase susceptibility in animals otherwise well cared for, but it is quite certain that infection of the stable is an important factor.
Lesions. The lesions vary with the complications, but those shown in the beginning are always identical. The mucous membrane of the nasal cavities is congested, inflamed, sphacelated, and ulcerated at different points. The turbinated bones and the ethmoid cells may become necrotic; in the larynx the region of the glottis is always most markedly affected; the mucous membrane becomes ulcerated in the neighbourhood of the vocal cords, and the tissues may become more deeply attacked.
In the trachea and bronchi the mucous membrane undergoes desquamation, and may become ulcerated at the points where false membranes have formed. The mucous membrane of the sinuses is always affected, but is rarely ulcerated.
Such complications as capillary bronchitis, broncho-pneumonia, and gangrene of the lung may be noted.
The mucous membrane of the mouth presents a violet-red or blackish-red colour; the tongue and gums are swollen, and ulcers as large as a lentil or a halfpenny may occur either singly or in a confluent form.
The genito-urinary apparatus reveals signs of croupal cystitis, submucous effusions of blood, vaginitis with the formation of false membranes, acute pyelitis, etc.
Diagnosis. When the symptoms are fully developed the diagnosis of gangrenous coryza is extremely simple, but the absence of some of these may justify hesitation in forming an opinion. If the examination is carefully carried out, it is always possible to distinguish this disease from simple coryza, which is only accompanied by trifling fever, and in which appetite is preserved; from foot-and-mouth disease, with its very characteristic buccal eruption and absence of lesions from the upper portions of the respiratory tract; and from contagious ophthalmia.
Prognosis. Up to the present time the prognosis has always been regarded as extremely grave, the mortality being sometimes as high as from 90 to 100 per cent., and moreover the cases which recover are invariably those of what is considered the chronic form. Sudden sinking of temperature during the disease is an unfavourable sign. From 1894 to 1900 Moussu never cured a single case, whatever his method of treatment; nevertheless, it now seems possible to regard the condition a little more hopefully, provided that no incurable complication occurs before the beginning of treatment.
Treatment. Of all the modes of treatment suggested—viz., anti-febrile agents, general stimulants, purgatives, diuretics, external stimulant applications, etc.—none have succeeded. Antiseptics injected into the nasal cavities, antiseptics given internally, milk diet, and all the methods hitherto suggested are equally useless.
The only treatment which appears to have achieved any degree of success is that of injecting physiological salt solution in large doses (up to six quarts per day, divided into three parts). All the animals treated by this method recovered, provided they presented no broncho-pulmonary complications.
The sole inconvenience of this treatment is the difficulty in carrying it out when the animals are at a distance from the practitioner. It is indispensable that they should be close at hand, in order that he himself may make the injections at the proper time. There is some reason for hoping, however, that serum from animals which have recovered will prove to be more active than saline injections.
This method of treatment should be followed up by the most rigid hygienic precautions. The mouth, nasal cavities and eyes should frequently be washed with antiseptic solutions. The stables should be freely ventilated, and the floors and bed kept in the cleanest possible condition, etc.
Whenever a case of gangrenous coryza is observed it should be isolated, and the stables should most carefully be disinfected.
TUMOURS OF THE NASAL CAVITIES.
Apart from actinomycosis of the upper jaw, tumours of the nasal cavities or of the sinuses are not frequent in bovine animals. They are, however, occasionally met with, and present symptoms which must be carefully studied in order to avoid errors of diagnosis. Usually they are of the nature of myxomata, more rarely of fibro-myxomata.
Fig. 167.—Transverse section through the nasal cavities near their centre (normal).
Symptoms. The dominant symptom is difficulty in breathing, both when moving and eating, a difficulty which is sometimes so considerable as to cause snoring respiration or roaring. Nevertheless, examination of the trachea and of the lung, visual examination of the lower portions of the nasal cavities, and manual examination of the pharynx, larynx and glottis give only negative results. It may even happen, as occurred in the case from which the illustration herewith was taken, that percussion of the maxillary sinus reveals normal resonance.
In the case of tumours of small size the forehead is not deformed. When, on the other hand, the tumour partly obstructs the nasal cavities it may thrust on one side the septum nasi and externally cause well-marked asymmetry of the face. Sero-mucous or muco-purulent discharge then occurs.
The diagnosis is somewhat difficult, for continuous or temporary roaring (or at any rate difficulty of respiration), being the dominant symptom, must be distinguished from roaring due to a laryngeal lesion like paralysis or tumour formation, from perilaryngeal compression due to enlarged retro-pharyngeal glands, and from tracheal or pulmonary lesions; and its origin must be located in the nasal cavities.
Fig. 168.—Transverse section through the nasal cavities: myxoma of the right side and of the maxillary sinus. Deformity of the forehead and face.
The prognosis is grave, in consequence of the difficulty of exploring the depth of these cavities and of the possible nature of the tumour. Nevertheless, in the case of simple myxomata permanent recovery usually follows extirpation.
Treatment is confined to extirpation, which is quite possible in the case of pedunculated tumours; in the case of sessile tumours free trepanation of the roof of the nasal cavities becomes necessary. The operation is quite safe.
PURULENT COLLECTIONS IN THE NASAL SINUSES. NASAL GLEET.
From the clinical point of view two varieties of this condition may be distinguished—inflammation of the mucous membrane of the maxillary sinus and inflammation of the mucous membrane of the frontal sinus and of the horn core. These forms of inflammation frequently lead to suppuration. The pus collects in the depressions and divisions of the frontal or maxillary sinus.
PURULENT COLLECTIONS IN THE FRONTAL SINUS.
Causation. In the majority of cases inflammation of the mucous membrane of the frontal sinus is produced by external causes: fractures of the horns and horn core accompanied by hæmorrhage into the horn core; fractures of the horn with exposure of the sinus of the horn core; wounds and violent blows on the occipital region or the frontal bone; cracks or depressions of the external wall of the sinus, etc.
In all these cases, whether blood is effused or the mucous membrane of the sinus is merely infiltrated with serum, infection may be produced by germs being deposited from the air passing through the nasal cavities and causing suppuration.
Purulent collections in the frontal sinus may result from continued irritation, like that due to a badly fitting yoke. They also occur as an accidental complication of general diseases like gangrenous coryza.
Symptoms. The catarrh or purulent collection in the sinus may be unilateral or bilateral, and the symptoms vary, according to the form which it assumes.
Unilateral collections.—Nasal hæmorrhage is often the first symptom, but this is often regarded as of little importance, because the formation of pus does not occur until very much later. The animal shows ill-defined pain, loses appetite, remains dull and somnolent, and carries its head on one side. The horn on the injured side is hot and sensitive, and at a later stage the eye becomes affected by contiguity of tissue. It is then swollen, closed, and watery; the conjunctiva is infiltrated, and somewhat inflamed. Sensibility and partial or complete dulness of the affected side may be detected by palpation and percussion. On the animal being made to cough, a yellowish or greyish-white discharge of very fœtid and sometimes putrid character escapes.
Bilateral collections.—Catarrh is rarely bilateral at first; but if the unilateral lesion is not treated, it affects the median septum dividing the two cavities, and the inflammation extends to the second sinus. The animal then shows dull pain, and exhibits marked depression; sometimes it appears quite prostrate. The head is carried low and inclined towards the ground, while the above-mentioned ocular symptoms and the indications furnished by palpation and percussion extend to both sides. Coughing produces momentarily a double discharge, which the animal disposes of after the fashion of horned cattle.
Diagnosis. The diagnosis only presents difficulty in the early stages. Later the warmth and sensitiveness of the horns, the partial dulness, offensive character of the discharge, etc., render diagnosis easy.
The disease is not likely to be mistaken for gangrenous coryza, despite the condition of the eyes, because it develops slowly, progressively, and without marked fever.
Prognosis. If treated early, unilateral or bilateral collections of pus in the sinuses are capable of cure, but later when bodily health is impaired and the local lesions of the mucous membrane very pronounced, there is less chance of success.
Lesions. The initial lesions consist in cracks, fissures, or fractures of the bones of the face or exostoses of traumatic origin. In other cases the mucous membrane alone is affected. As a result of chronic irritation it becomes thickened, inflamed, and ulcerated, and granulates freely. The depressions in the sinuses contain grumous, fœtid pus, which irritates the surrounding tissues and produces pain and general symptoms of cerebral irritation, which are sometimes very disquieting.
Treatment. Numerous methods of treatment were formerly recommended, such as absolute rest, bleeding, cold affusions, perforation of a horn, section of a horn, etc. None of these is of any value.
At first, provided only a certain degree of sensitiveness and simple catarrh without suppuration exist, antiseptic fumigations with tar, carbolic acid, thymol, etc., are useful; but later, when pus has formed, they are useless. At this period the only rational and efficacious treatment consists in trepanation. In unilateral collections three openings are necessary.
The first is an opening into the sinus of the horn core. It is made ⅜ to ¾ of an inch above the horn-secreting band of the horn. It must not be forgotten, however, in planning such an opening that the sinus of the horn core only exists in a rudimentary condition in young animals, and that it is scarcely possible to trephine the horns before the patient is three years of age.
The second opening is made towards the upper part of the frontal sinus about ¾ inch below the horn-secreting ring at the base of the horn and in a line with the axis of the horn core itself. Whatever the animal’s age and however little the sinuses may be developed, this opening is certain to expose the cavity of the frontal sinus.
In old animals where the frontal sinus is enormously developed, and where very large depressions exist in the orbital region, a third opening should be made just above a transverse line uniting the upper margins of the two orbits and inside the suborbital suture.
These openings having been made, treatment consists—firstly, in completely washing out the cavity with boiled water, cooled to 95° or 100° Fahr.; and, secondly, in injecting antiseptic and astringent solutions so as to check the formation of pus. Among such may be mentioned 3 per cent. carbolic solution, 5 per cent. carbolic glycerine, 2 per cent. solution of iodine in iodide of potassium, etc.
Whatever the drugs employed, the cavities should be washed out every day, first with plain sterilised water, and then with antiseptic solutions at the body temperature, since cold solutions often cause inflammation of the mucous membrane of the opposite sinus.
PURULENT COLLECTIONS IN THE MAXILLARY SINUS.
This disease is much rarer than that of the frontal sinus, and only within the last few years (Ries, 1899) has a really good description been given of it.
The causation is imperfectly understood. Injuries to the suborbital region and maxillary ridge, caries of the molar teeth, and inflammation occurring during the development of general diseases represent the principal causes.
The dominating and characteristic symptom of the presence of pus in the maxillary sinus consists in incessant snorting, accompanied by violent movements of the head and the discharge of purulent or muco-purulent material.
At the beginning of these attacks of snorting, which are produced by the reflux of pus from the sinus towards the nasal cavities, the respiration becomes snoring and rapid, and the animal makes sniffing movements as though the nasal cavities were partially obstructed. After these crises, the respiration again becomes silent.
Contrary to what has been observed in purulent collections in the frontal sinus, the discharge is unilateral, reddish yellow in colour, viscous in consistence, and is accompanied by clots of a gelatinous material or even of blood.
During the attacks of snorting, the discharge resembles that of croupal or pseudo-membranous bronchitis, but the material discharged is not moulded on the internal shape of the bronchi. The masses of discharge are irregular in form, and appear as though made up of fibrous tissue matted together. Attention having been attracted by the discharge, exploration of the trachea and chest reveals nothing; on an examination of the sinuses, however, palpation and percussion betray a certain amount of sensitiveness, together with partial or complete dulness, and the lesion is discovered.
Diagnosis. Confusion between pus formation in the maxillary and frontal sinuses can be avoided by careful examination.
Prognosis. The prognosis is not very grave; the animals maintain their appetite, but become thinner, and the condition shows no tendency to spontaneous cure.
Treatment. The only rational treatment consists in trephining, an operation practised immediately above the maxillary tuberosity and over the lowest part of the sinus (Fig. 164). This opening allows the cavity to be washed out and the sinus drained.
Antiseptic treatment exactly resembles that of purulent collections in the frontal sinus. Injections of astringents, dilute carbolic acid and iodine solutions, etc., are recommended.
ŒSTRUS LARVÆ IN THE FACIAL SINUSES OF SHEEP.
(FALSE STURDY.)
Causation. This disease of sheep, which sometimes produces vertigo resembling that shown in gid or sturdy, is produced by the growth of larvæ of Œstrus ovis in the frontal sinuses. The œstrus of the sheep assumes perfect insect form during the fine days of summer from July to September. The females swarm around the flocks and attempt to alight on the animal’s head close to the nostrils, where they deposit their eggs or larvæ. The larvæ crawl into the nostrils, thence into the nasal cavities, the meatus, and finally the sinuses, where they become fixed. In these sinuses they undergo complete development, increasing from a length of about ⅒ inch to from ¾ to 1 inch before their transformation into the nymph and perfect insect. They remain in the sinus for eight to ten months. When numerous and well developed they may fill the whole of the cavity.
Symptoms. It is easy for a careful observer to note the time at which the larvæ penetrate the sinus. During the hottest hours of the day the adult insects are continually hovering over the flocks, and on watching carefully one sees sheep suddenly become excited, tap with their feet, rub their faces against any hard, resisting object in the neighbourhood, plunge their nostrils into the dust, and snort violently.
When the larvæ have penetrated the nasal cavities they produce frequent attacks of sneezing by irritating the mucous membrane, and cause an intense sero-mucous and afterwards a moderate muco-purulent coryza. As long as the larvæ remain of small size, the apparent results they produce are insignificant, as during the first months of winter; but when they are numerous, and have become of considerable size, they cause symptoms which might suggest an attack of gid or sturdy.
Thus the bodily movements become spasmodic, the gait irregular, and the animals show attacks of vertigo. They stagger and fall, making convulsing movements, grinding their teeth and rolling their eyes, while frothy saliva escapes from the mouth, etc.
Death may occur during such attacks, which, however, are happily very rare. Most commonly the animals are simply dull and somnolent. They feed badly, carry their heads low, and sometimes hide themselves under the mangers or in corners.
In exceptional circumstances they bury their heads in the wool or carry them high in the air in walking, while they lift their front legs high, with a stepping movement.
Fig. 169.—Parasitic invasion of the sinuses and cœnurosis (showing the seat of operation in either condition).
Diagnosis. The diagnosis of parasitic invasion of the sinus in the sheep is rather difficult, because certain of the symptoms suggest gid. One never finds the signs of true gid, however, and, on the other hand, a certain amount of discharge and attacks of snorting always exist. Finally, gid (cœnurosis) only attacks young animals, whilst the larvæ of œstridæ are commonest in adults.
To confound the disease with verminous bronchitis is still less likely, for although a discharge exists in both cases, this is accompanied by cough in bronchitis, and only by sneezing attacks in infection of the sinuses.
Finally, in bronchitis, histological examination leads to the discovery of eggs or embryos of the strongyles. The diagnosis becomes very easy on post-mortem examination, the identification of the larvæ of œstridæ being extremely simple.
Prognosis. The prognosis is only grave when infestation is very pronounced. Most commonly the parasites complete their development without producing disquieting symptoms; as summer approaches they are expelled and recovery occurs.
Lesions. The only lesions consist in very active inflammation of the mucous membrane of the sinus, which appears excessively hypertrophied, and in the existence of larvæ. These develop in the midst of a magma of purulent, fœtid discharge. The number of parasites usually ranges from two to twenty, although Zürn declares that he has found as many as eighty in one subject.
Treatment. Many precautions have been suggested for preventing infestation. Many are impossible or difficult to carry out in current practice, even the soaking of the nostrils in empyreumatic oil, and the majority are useless. The only suggestion to which we attribute any importance consists in trying to prevent the perfect insects from obtaining a lodgment in cavities in the walls or roofs of sheep-sheds.
The really efficacious modes of treatment are also few in number, for the larvæ are so firmly lodged in the mucous membrane of the sinuses that they can only be detached after these have been trephined. The use of nasal injections, embrocations and powders, with the object of making the animal sneeze, are ineffectual.
Trepanation should not be performed until it is quite clear that the flock is badly infested, and when serious symptoms appear to threaten the lives of some of the animals.
The operation, although very simple, requires care on account of the thinness of the bones.
The anatomical directions are the middle line of the head, and a transverse line uniting the upper margin of the two orbits. The orifices are made in the two lower angles produced by the intersection of these lines (Fig. 169).
It is then easy to remove with the fingers or forceps the larvæ situated immediately below the point of trepanation, and afterwards to wash out thoroughly the cavities of the sinuses. If some lie at points which cannot be directly reached, they can be killed by injecting a little benzine and water. This proceeding is quite safe.
CHAPTER III.
LARYNX, TRACHEA AND BRONCHI.
LARYNGITIS.
Laryngeal diseases are common, but are usually only the local expression of some grave general infection, such as foot-and-mouth disease, gangrenous coryza, or tuberculosis. Pathological conditions such as these can be disregarded for the moment, as they will receive attention under special heads.
The two current forms of laryngeal disease are acute laryngitis and stridulous laryngitis.
ACUTE LARYNGITIS.
Acute laryngitis, like simple coryza, of which it is often only an accompaniment, is caused by chill, by irritant vapours, by smoke, etc., or by external traumatic causes.
The cough is dry and painful at first; afterwards it is accompanied by a discharge or by the swallowing of mucus or muco-purulent products. The respiration sometimes appears accelerated and difficult, but roaring or whistling and marked fever are rare. The slightest pressure over the laryngeal region causes pain and attacks of coughing. The respiration is normal while the animal is at rest, provided that the laryngitis remains localised; frequently, however, it is complicated with bronchitis.
The appetite is somewhat diminished, but all these symptoms very rapidly improve.
The diagnosis is based on the frequency of the cough and the sensitiveness of the throat region.
The prognosis is favourable in cases of simple laryngitis.
Treatment consists in the administration of steam inhalations, warm drinks, the application of mustard plasters or blisters around the laryngeal region, and the administration of expectorants to facilitate mucous discharge.
PSEUDO-MEMBRANOUS LARYNGITIS.
Pseudo-membranous laryngitis, also termed by German authors croupal or diphtheritic laryngitis, because it bears a certain resemblance to human croup, is characterised by the formation of false membranes on the vocal cords, arytenoid cartilages, and subglottal region, etc.
In France it has been described under the name of stridulous laryngitis, because its dominant symptom consists in attacks of intense dyspnœa, during which the respiration is accompanied by whistling. Without making any attempt to prejudge the nature of the disease, which resembles the pseudo-diphtheritic forms of laryngitis in man, we prefer the term pseudo-membranous laryngitis. Moreover, this pseudo-membranous laryngitis very frequently accompanies pseudo-membranous sore throat, tracheitis and bronchitis, with formation of false membranes.
Causation. The causes suggested are similar to those of simple sore throat: they include chills, the ingestion of ice-cold water, or the inhalation of irritant gases, during outbreaks of fire, etc., etc.; but it is quite certain that here, as in many similar cases, a primarily simple laryngitis is complicated by a well-marked infection.
Symptoms. The general symptoms seen during the early stages consist in loss of appetite, general depression, rigors, and a rise in temperature of 1° to 2° Fahr.
Then, after twenty-four or forty-eight hours, the respiration becomes more rapid, difficult, whistling and dyspnœic, with intermittent attacks of suffocation.
Examination of the chest gives negative results, but, on the throat being manipulated, the slightest pressure exercised over the larynx produces attacks of coughing. During the first few days these attacks are loud, spasmodic, and difficult, but on succeeding days they lead to the discharge, from the nostrils or mouth, of masses of false membrane accompanied by whitish and sometimes blood-stained fluid. Secondarily the mucous membrane of the nasal fossæ appears inflamed to a varying degree. The conjunctiva is also affected, the eyes are watering. An important symptom consists in the fact that this watering is accompanied by internal ophthalmia, as in gangrenous coryza.
In consequence of the respiratory difficulty, the animal takes up a characteristic attitude, holding its neck stiffly in a horizontal position and its head completely extended; the nostrils are widely dilated. When the disease is fully-developed rumination is suppressed, the bowels are constipated and the fæces are coated as in grave cases of enteritis, the yield of milk diminishes, the heart beats feebly, the pulse remains small; death may occur from asphyxia, and probably also from intoxication.
The disease usually lasts from eight to ten days, but death may occur earlier. In the majority of cases, however, the animal can be saved. All the symptoms diminish, the temperature falls, rumination again appears and with it appetite, and the whole condition becomes normal. Many animals, however, remain thin and recover slowly; these are principally cases which have suffered from pseudo-membranous bronchitis.
Lesions. The lesions may be confined to the larynx, but may also invade neighbouring cavities. They consist in the formation of mucoalbuminous and fibrinous exudates, covering the mucous membrane in superposed layers, penetrating the epithelial stratum, and adhering so strongly to the corium that attempts to loosen them cause the deeper seated structures to bleed.
Diagnosis. The symptoms are sufficiently well marked to prevent any confusion arising except with gangrenous coryza, but in this case there is no ophthalmia lesion of the nasal cavities, cutaneous eruption, or eruption over the claws.
The prognosis is grave when the disease attacks debilitated or exhausted animals.
The treatment is confined entirely to treating symptoms. As in all acute inflammatory affections, moderate bleeding, sinapisms over the region of the larynx, repeated as often as necessary, or applications of antimonial ointment have been recommended. Applications of moxas or setons in the neighbourhood of the dewlap might possibly prove of value.
Internally tartar emetic, in doses proportioned to the size of the animal (2½ to 3 drachms in adults), has been recommended; also iodide of potassium.
General stimulants, like alcohol, coffee, tea, acetate of ammonia, and suitable hygienic conditions suggest themselves. Tepid drinks can be given freely. Nourishing and easily digested food, and a ration of milk complete the treatment.
Emollient and antiseptic fumigations are also of value, as in ordinary sore throat or laryngitis, for they favour the separation and discharge of the false membranes.
TUMOURS OF THE LARYNX.
Acute forms of pseudo-membranous laryngitis, or even tuberculous laryngitis, are not the only diseases which affect the larynx. It is by no means exceptional to discover intra-laryngeal tumours, mucous polypi, tuberculomes, and growths due to actinomyces, etc.
The presence of these tumours is indicated by difficulty in respiration, fits of coughing, and threatened suffocation, accompanied by discharges of varying character.
When the tumour is largely sessile, the respiration may simply be snoring or whistling, without any suggestion of suffocation; but if, on the other hand, it is pedunculated, displacement of the polypus produced by the currents of air during inspiration and expiration causes spasm of the glottis, fits of coughing and threatened suffocation.
The diagnosis is not always easy, though examination of the nasal cavities, the sinuses, trachea and chest gives negative results. Auscultation of the larynx may suggest the existence of the lesion, but an exact diagnosis can only be attained by digital examination of the larynx through the pharynx.
Fig. 170.—Sessile form of intra-laryngeal polypus.
The prognosis of these tumours is grave, because death from asphyxia may occur during an attack of coughing or as a consequence of the fits of suffocation.
Treatment. As it is usually extremely difficult, if not impossible, to discover the exact nature of the tumour, medical treatment, except for instance in the case of actinomycosis, is of very uncertain value.
Surgical treatment alone suggests itself. Before attempting an operation tracheotomy should be performed and a metal canula inserted. The animal having been cast, and the upper laryngeal region anæsthetised by means of cocaine, a vertical incision is made in the median line below the larynx, passing through the skin, the vertical junction between the neck muscles and the three first circles of the trachea, and access is thus obtained to the larynx and subglottal region. The operation should only be performed in exceptional cases, such as that of a valuable stud animal.
Provided that the new growth has a well-developed pedicle it can be removed through the mouth by the use of an écraseur or simply by tearing out.
BRONCHITIS.
Diseases of the bronchi in bovine animals reveal very different characters, according to the nature of the primary cause, for which reason cases occur of simple acute bronchitis, verminous bronchitis, simple chronic bronchitis, pseudo-membranous bronchitis, tuberculous bronchitis, etc.
SIMPLE ACUTE BRONCHITIS.
Simple acute bronchitis co-exists with, or is often only the logical and inevitable complication of, coryza and acute laryngitis. It is commonly associated with inflammation of the mucous membrane of the trachea.
It accompanies cold and wet seasons, and usually appears with the autumn frosts, in animals still at grass. In animals under shelter it occurs after undue exertion followed by chills, and after sudden rain storms. It also attacks working oxen, which are much exposed to the weather.
The symptoms follow very rapidly on the determining cause. They are ushered in by rigors, trembling attacks, diminution or loss of appetite, arrest of rumination, acceleration of breathing, and the appearance of a rough and spasmodic cough.
In ordinary cases these symptoms rapidly diminish, even without treatment. The appetite again becomes moderate, rumination returns, but the cough remains more or less rough and spasmodic, ending in the discharge, or more often in the swallowing, of abundant bronchial mucus.
This is the condition at the period of crisis. Percussion of the thorax reveals normal resonance. On auscultation of the sides during the period of onset, rough râles are heard, which at the period of crisis are replaced by mucous râles. The cough diminishes in frequency, and after a fortnight everything again becomes normal.
The diagnosis is very easy, the important point being not to confuse common bronchitis with tuberculous bronchitis, which very often assumes a chronic form.
Prognosis. The prognosis is not grave, even though the disease may assume a chronic condition.
Treatment does not differ from that of acute bronchitis in the horse. It consists in antiseptic and steam fumigations, tepid drinks, the administration of doses of 2 to 3 drachms Kerme’s mineral in adult animals, and of 1 to 1½ drachms of iodide of potassium, given in a mash or in honey electuary. During convalescence tar water should be administered.
CHRONIC BRONCHITIS.
Chronic inflammation of the mucous membrane of the large bronchi and trachea may follow acute bronchitis, but it is also a frequent termination of verminous bronchitis. It is found in fully developed animals, adult or old, and particularly in those inhabiting wet, cold valleys.
It is characterised by frequent paroxysms of coughing, which appear on the slightest provocation, such as the action of cold air on leaving the stable or of the air of a confined space on animals returning from the open; concussion of the chest by the pleximeter, squeezing of the loins, rapid movement, etc.
This coughing is accompanied by the discharge of mucus, which rarely arrives at the nostrils, but is swallowed in passing through the pharynx. Such mucus is always thick, greenish yellow in colour, and without smell.
The respiration, although regular whilst the animal is at rest, becomes accelerated on moving, and after attacks of coughing. It is sometimes rapid and whistling.
Percussion discloses neither partial nor complete dulness, but everywhere irregularly distributed mucous rattling and sibilant râles are revealed by auscultation.
There is no fever, the appetite is maintained, and, what is an even more important point, animals in good condition preserve their flesh. Interlobular pulmonary emphysema and emphysema resulting from dilatation are inseparable accompaniments of chronic bronchitis, for which reason the flank respiratory movement is frequently very marked.
The diagnosis is of only moderate difficulty, because although in certain conditions the disease may be mistaken for tuberculosis or emphysema, it can be distinguished by bacteriological examination of the discharge, by an injection of tuberculin, by careful auscultation, and by consideration of the general condition.
Lesions. The walls of the bronchi are thickened, the submucous connective tissue is sclerosed, the muscular fibres are modified in structure, and have become fibrous, while the epithelial layer is desquamated and suppurating. The peribronchial tissue also undergoes sclerosis, and in certain cases the smaller bronchi present marked dilatations resembling small caverns (bronchi-ecstasis).
Treatment can never be more than palliative; the aim should be to prevent the lesions becoming aggravated, and to check the pathological secretion from the bronchi, but the lesions already existent can never be removed. Tar water should be perseveringly administered. Essence of turpentine in doses of 2 to 2½ drachms per day in electuary (adults), creosote in doses of 1¼ to 1½ drachms, and terpine in doses of ¾ to 1 drachm give the best results, and produce a marked improvement.
PSEUDO-MEMBRANOUS BRONCHITIS.
The pseudo-membranous forms of bronchitis, formerly termed “croupal or diphtheritic bronchitis,” are rare. They develop suddenly or follow pseudo-membranous laryngitis. Like the latter, they are due to a specific infection, possibly aided by accidental causes.
Their causation is imperfectly understood, and they cannot be compared, still less homologated, with diphtheritic disorders in man. They are characterised by the formation of false membranes, which develop on the mucous surface, mould themselves over the internal surface of the large bronchi, and ramify throughout the bronchial channels like branches of trees. They are of greyish-yellow colour, and appear to be formed of fibrin, coagulated albumen, and epithelial débris cemented together with mucus.
Symptoms. At the outset these pseudo-membranous forms of bronchitis have the same characters as acute bronchitis, which at the crisis would be marked by the expulsion of fragments of false membrane by coughing. Most frequently it seems that the bronchitis follows its regular course, and in such case it is only during convalescence or a considerable time afterwards that the membranes begin to be discharged during paroxysms of coughing.
The patients are subject to intense dyspnœa, appear about to suffocate, and during the efforts then made the false membranes are discharged in the form of half-organised layers, or, on the other hand, in branched masses, resembling twigs.
The dyspnœa at once ceases. Despite the development of these false membranes in the bronchi, no alarming symptoms are produced, which is explained by the fact of the false membranes being adherent only to the inner surface of the principal conduits, without closing or even markedly obstructing them or the smaller passages leading to the pulmonary alveoli. When, however, they are displaced, violent reflex spasms are produced as soon as the fragments approach the larynx.
Diagnosis. The diagnosis rests entirely on examination of the expectorated material.
So far as the prognosis is concerned, it is less grave than might be supposed from the symptoms. The gravity arises from the fact that this disease has a certain tendency to become chronic.
Treatment scarcely differs from that of ordinary bronchitis. Tar, creosote in doses of 2½ to 5 drachms given in oil; terpine in doses of ½ to ¾ drachms per day can be recommended. Iodide of potassium also has certain advantages.
VERMINOUS BRONCHITIS IN SHEEP AND CATTLE (HUSK, HOOSE, ETC.).
Lambs, young sheep, and calves sometimes suffer severely from infestation with lung worms, which set up great irritation in the bronchial passages, leading to chronic bronchitis. The animals show frequent attacks of paroxysmal coughing, during which some of the parasites may be expelled. The irritation produced causes serious loss of condition, and if not alleviated may lead to death. The parasite of the sheep is known as Strongylus filaria (sheep lungworm), that of the calf Strongylus micrurus. The worms are from 2 to 4 inches long, whitish in colour, and of the diameter of a hat-pin.
Treatment. According to generally accepted views among veterinarians and zoologists, it is a comparatively simple matter to kill worms in the bronchial tubes, and a number of cases of the disease are reported in literature which are alleged to have been cured. These views, however, are open to very serious doubt.
Neumann (1892b, pp. 590, 591, 593, 594) summarises the subject of treatment as follows:—
Two different procedures in treatment are pursued. In one, substances are passed into the digestive canal, which, being diffused in the blood, are believed to be capable of attacking the worms in the bronchial tubes. With this view, the picrate of potash (0·20 to 0·40 gram per head) is given, dissolved in thin gruel or mucilage; creosote; oil of turpentine; a mixture of equal parts of oil of turpentine and tincture of camphor—a teaspoonful every day to each lamb in a mucilaginous fluid; a mixture of creosote 120 grams, spirits of wine 500 grams, and water 700 grams—an ordinary spoonful every day to each animal; or creosote 60 grams, benzine 300 grams, water 2 litres—an ordinary spoonful given every day for eight days to each sheep. Hall states he has successfully employed prussic acid in ten-drop doses, morning and evening.
But experience has shown that, while such treatment is troublesome to carry out, its efficacy cannot be relied upon.
Success is more certain with fumigations, as they penetrate directly to the worms, stupefy them, and induce fits of coughing that cause expulsion. They are practised in buildings from which all forage is previously removed, and which are well closed. Into these the diseased [animals] are introduced, and on a red-hot shovel are placed rags, horns, feathers, hair, old pieces of leather, empyreumatic oil, tar, juniper berries, asafetida, etc. The intensity, duration, and number of these fumigations are graduated as the sheep become accustomed to them. At first once a day may suffice, and then the intensity should be moderate and the duration about ten minutes; afterwards two, and finally three, may be given during the day, each lasting for twenty minutes. Kowalewsky says he has obtained very good results from similar fumigations. Fumigations with chlorine, sulphur, and sulphuret of mercury or cinnabar have been recommended, but they are dangerous.
(Stephen recommends as follows: Put about forty lambs at a time into an air-tight house, and place tar, sulphur, and turpentine in a pot of burning coals, suspended by a chain from the ceiling and brought as near to the heads of the animals as possible; the fumes are to be allowed to fill the house, and more ingredients are added as required, the lambs being kept in the place for twenty-five minutes each time, and the process to be repeated on three occasions.)
Tracheal injections in the verminous bronchitis of calves are of great utility; but for a flock of sheep they would be troublesome and difficult to administer. However, Nieman, has successfully employed them on 384 sheep belonging to several small owners. He used a solution of 2 parts iodine and 10 parts iodide of potassium in 100 parts of distilled water. This fluid was mixed, in equal parts, with oil of turpentine, and made into an emulsion with olive oil; each sheep received 5 to 8 grams of the mixture, and the number of the injections varied according to the gravity of the disease—from two to three at two days’ interval. The worms were killed and expelled during the paroxysms of coughing, and the bronchitis was modified.
The medical treatment should be assisted by very nourishing food, and by bitter, stimulating, and ferruginous tonics, which arouse the digestive functions and allow those animals which are least exhausted to reach the period of elimination of the parasites.
At the commencement of any kind of treatment it is well to have an examination of the flock, with the object of sending the worst cases to the butcher.
The same medicaments have been employed in treating this malady in calves as in that of sheep, and no better results have been obtained. Neumann and Janné have, however, been successful with asafetida (30 grams), Chabert’s empyreumatic oil (60 grams), and a mucilaginous decoction (500 grams)—a spoonful of this mixture being given in a half litre of milk, and the treatment continued for about a month.
The results are less uncertain if the worms lodged in the bronchial tubes are directly acted upon, either by means of injections of the same kind as those employed for sheep, or fluid medicaments introduced directly into the bronchi.
Read says he has cured calves worn down almost to skeletons by verminous bronchitis by the following procedure: The head of the calf is slightly elevated, and about 2 drachms of ether, chloroform, oil of turpentine, or rectified oil of amber—single or combined—are poured into each nostril and allowed to vaporize there; it will then, by the respiration, be carried into the air passages, and thus destroy the filariæ. In some cases it must be repeated two or three times, but once has frequently the desired effect.
The method of treatment by intra-tracheal injection, introduced by Levi, of Pisa, has yielded very satisfactory results. Levi has been completely successful with a sheep. Éloire has employed it in sixteen calves affected with the disease, and all were cured. He used the following mixture: Black poppy oil, 100 parts; oil of turpentine, 100 parts; carbolic acid, 2 parts; purified cade oil, 2 parts. Each calf received 10 grams of this mixture daily for three days.
The injection, which should be given slowly, is followed by a fit of coughing, and the expired air has the odour of turpentine. This treatment has also been successful at Milan. Similar favourable results have followed Hutton’s treatment of eight calves, some of which were in the last stage of verminous bronchitis. He employed a mixture of oil of turpentine, tincture of opium, pure carbolic acid, and water—the oil of turpentine forming one-half of the mixture. The dose was ½ an ounce, and in the serious cases this was given every day for three days, and in other cases every second or third day. Kriwonogow has likewise cured twenty-two calves by giving each of them two tracheal injections of 8 grams of the following mixture: Essence of cloves and oil of turpentine, 360 parts of each; carbolic acid and olive oil, 30 parts of each.
(Williams speaks highly of the administration of prussic acid. Penhale gives—by intra-tracheal injection, and slowly—oil of turpentine 2 drams, carbolic acid 20 minims, and chloroform ½ a dram.)
CHAPTER IV.
LUNGS AND PLEURÆ.
PULMONARY CONGESTION.
Besides passive congestions of the lung, which it is unnecessary to describe here, and which result from cardiac or pericardiac affections or the compression of important vessels, there sometimes occur, particularly among young animals, cases of active congestion of the lung. Such cases are produced by over-exertion on the part of animals which have escaped from control or have been chased by dogs.
They are most common in animals usually kept in stables, but which have accidentally escaped, or in very fat animals.
Dyspnœa and cough are the chief symptoms. The animals stop as though exhausted, extend their neck and head, dilate their nostrils and thrust their limbs out on either side of the body, while at the same time they appear in a condition of terrible distress.
The respiration is rapid and short, the patient can scarcely breathe, and asphyxia seems imminent. On auscultation it seems that the respiratory murmur has disappeared over almost the entire extent of the lung.
Death may occur very quickly.
The diagnosis is extremely easy, provided that the history is known.
The prognosis is grave.
One of the most successful methods of treatment consists in free bleeding. In a great majority of cases this causes the symptoms to abate as though by enchantment. Cutaneous stimulation by mustard and similar irritants, as well as ablutions of cold water, are useful. The animal should be placed in a very airy spot.
SIMPLE PNEUMONIA.
History. Veterinary surgeons have long been divided in opinion on the question whether simple pneumonia occurs in animals of the bovine species. Whilst some affirm it, others think that all lesions of the lung in the ox, apart from pneumonia due to foreign bodies, should be regarded as of the nature of peripneumonia.
Some ten years ago two veterinary surgeons of the department of the Aisne, Coulon and Ollivier, practising in a district where peripneumonia rages, made some extremely interesting observations on pneumonia in the ox. Their object was to distinguish between contagious peripneumonia and simple pneumonia during life, simple pneumonia having formerly been regarded as a non-contagious peripneumonia. Despite the rather unfavourable conditions in which ordinary practitioners are frequently placed, these gentlemen performed a work of great value. The facts which point to the occurrence of simple pneumonia are as follows:—
The disease is not contagious. One may allow affected animals to mix with normal subjects without the disease being communicated. Pulmonary exudate from cases of simple pneumonia can be injected into the dewlap and hind quarters of young and adult animals, without pathological results.
The lesions and course of simple pneumonia entirely differ from those of peripneumonia.
Causation. Simple pneumonia is not common, and only occurs quite exceptionally in fat stock, or in milch cows kept in stables at a regular temperature, as in the north of France and near Paris.
It occurs most commonly in working animals, which are exposed to variations in temperature and to chills. By causing vascular disturbance, chill favours microbic infection and visceral inflammation. Trasbot has described the case of an ox which, after having worked hard, and whilst freely sweating, was left exposed to the wind under a shed for about three hours. This animal contracted unilateral pneumonia the following day.
Coulon and Ollivier have seen the disease in animals living in damp, low-lying valleys, or valleys exposed to the north wind, which are exposed in consequence to great variations in temperature.
The symptoms follow almost the same course as in the horse, and one may distinguish three periods:—
I. Period of onset. The symptoms which mark the onset of the disease are moderate fever, which progressively increases, and acceleration of respiration and of circulation. The number of the respiratory movements rises to twenty or twenty-five per minute, those of the pulse to fifty, sixty, or eighty. The conjunctiva becomes injected, and then of a yellow tint. At this period the appetite never disappears completely, rumination is regular, and there is neither tympanites nor colic.
These general symptoms, which are not of special significance, are supplemented by more precise local symptoms—an abortive, difficult and painful, cough which is easily induced, and a whitish discharge. The rusty expectoration which is characteristic of simple pneumonia in the horse and in man has never been observed.
Percussion discloses partial dulness, usually on one side, in the lower region of the chest: the respiratory murmur in this region is ascertained by auscultation to have diminished, whilst in the upper part and also on the opposite side the respiratory murmur is increased.
II. Period of exacerbation. This period is characterised by accentuation of all the symptoms: the temperature rises, and may attain 104° Fahr.; the submaxillary artery is tense; the dulness becomes more marked, whilst crepitant and mucous râles are heard. In the portions still unattacked the function of the lung is exaggerated in order to make up for the defect of the diseased parts, and the respiration becomes juvenile.
The appetite, which previously had been maintained, diminishes considerably, without, however, entirely disappearing, and intense thirst sets in, as a consequence of the fever.
III. Period of crisis. The general symptoms remain stationary for four or five days; the respiration, which is always affected, sometimes becomes as rapid as thirty to forty per minute; the tubal souffle which invariably occurs in pneumonia of the horse is not always clearly audible.
Terminations. (1.) Resolution.—This is indicated by the attenuation of all the symptoms and the disappearance of fever, which gradually sinks from 105° to 101° Fahr. The respiratory movements become fuller and fewer in number, the pulse slower, and the artery softer and more compressible. The cough changes its character, is stronger, more sonorous and prolonged, and is accompanied by the free discharge of muco-pus. The dulness descends, and the tubal souffle, if previously existing, is replaced by the returning crepitant râle. In general the disease runs its course in eight to ten days in young and in fourteen to fifteen days in aged subjects.
(2.) Death by asphyxia is almost the only fatal termination of pneumonia in the ox. It occurs in one-third to one-fourth of the subjects attacked. Its approach is announced by a deep mahogany-red coloration of the conjunctiva. The pulse becomes very rapid, 100 to 110 per minute, thready, small, and almost imperceptible, whilst the beating of the heart is strong and tumultuous. Respiration is rapid and very laboured (50 to 70 per minute). The animal’s attitude is typical; it stands with its limbs thrust out, its head extended, its nostrils dilated, and its mouth half open, discharging foamy and viscous saliva. Throughout the greater portion of the lung gurgling sounds and crepitant mucous râles can then be detected.
(3.) Cases ending in gangrene and suppuration are excessively rare, and others resulting in chronic pneumonia have not been authoritatively described.
Pneumonia is distinguished from broncho-pneumonia by the existence of dulness at the period of crisis, whilst in the case of broncho-pneumonia this period is only marked by partial dulness, which is even then sometimes slight. Moreover, broncho-pneumonia usually develops much more slowly.
The disease, then, is distinguished from peripneumonia by the following points:—
(a) By the character of the temperature curve, which is regular in pneumonia, only attaining its highest point at the period of crisis, whilst in peripneumonia it ascends suddenly, and presents sudden oscillations.
(b) The appetite remains, although diminished.
(c) Sensitiveness in the region of the ribs is but feebly marked, or is entirely absent, simple pneumonia not being accompanied by pleurisy.
(d) The dewlap never shows œdema, a symptom which usually accompanies the period of crisis in peripneumonia, when the jugular veins and the anterior vena cava are compressed.
(e) These signs alone are almost sufficient on which to base the diagnosis, but they are often supplemented by two others, of some what less importance (for in exceptional cases they may also be observed in simple pneumonia), viz.—the absence in most instances of a membranous sound, and of a well-marked souffle.
Prognosis. Two-thirds of the cases recover. This proportion might be increased if the veterinary surgeon were called in at the beginning.
Lesions. Post-mortem examination reveals neither pleural exudate nor pleural lesions. The lung is large and of increased weight, hepatised along its lower borders, and congested in its upper part.
The sero-hæmorrhagic infiltration of the interlobular spaces varies, according to the region examined: the upper regions are engorged and black, owing to capillary hæmorrhages and blood clots, which completely surround the pulmonary lobule, the latter being violet or brownish-red in colour. In the hepatised portions the lobules are of a washed-out reddish tint, and the interspaces of a whitish colour.
The bronchi are filled with frothy, whitish mucus; the small bronchi sometimes contain fibrous concretions and the mucous membrane is injected, and may be destroyed in places. The bronchial lymphatic glands are enlarged, congested, and contain small hæmorrhages.
It is important in making a post-mortem examination to be able to distinguish pneumonia from peripneumonia. This is comparatively easy if one bears in mind that in the latter pleurisy always exists, that the interlobular connective tissue spaces are always greatly distended with a citrine-coloured serosity, that on section the peripneumonic lung resembles a mosaic; and that, finally, the course of hepatisation is centripetal, the inflammation commencing at the periphery of the lobule, and progressively extending towards the centre. In pneumonia, on the contrary, pleurisy is always absent; the interlobular connective spaces are only distended slightly, if at all, and always contain a brownish-red serosity: the course of hepatisation is centrifugal; it commences in the pulmonary alveoli, and extends towards the periphery and the interlobular divisions. The following table gives a résumé of the other differences between the two diseases:—
| Peripneumonia. | Pneumonia. |
|---|---|
| Œdema of the dewlap. | No œdema of the dewlap. |
| Pleural exudate. | No pleural exudate. |
| Centripetal lobular hepatisation. | Ascending centrifugal lobar hepatisation. |
| Extreme infiltration of the interlobular connective tissue spaces (primary yellow infiltration). | Moderate infiltration of the interlobular connective tissue spaces (secondary reddish-brown infiltration). |
Treatment. Good hygiene, regular ventilation, moderate warmth, and the administration of tepid drinks facilitate recovery.
Certain German authors recommend cold compresses to the thorax, douches, and cold enemata in pneumonia. We do not think that such treatment has proved very successful, although it has been well tried.
The classic treatment commences with moderate bleeding, the free application of mustard to the sides, the application of moxas, frictions with antimonial or blister ointment, and the administration of draughts containing 2 to 2½ drachms of tartar emetic per day, or considerable doses of alcohol; and this treatment seems to have given the best results. Antithermic agents, like acetanilide, phenacetin and quinine sulphate, are too costly to be greatly used in bovine medicine. Salicylate of soda is preferable.
In order to assist circulation, support the tone of the heart and avoid engorgement of the lung and asphyxia; digitalis should be given in doses of ¾ to 1 drachm per day, or digitalin in subcutaneous injections of 5 to 6 milligrammes, continued for five or six days. Finally, iodide of potassium may be given in doses of 1 to 1½ drachms, to reduce inflammation and as an expectorant.
PNEUMONIA DUE TO FOREIGN BODIES—MECHANICAL PNEUMONIA.
It may happen that in examining a patient pneumonia is diagnosed under circumstances which seem to forbid its being regarded as simple or primary. This may be explained by the fact that ruminants are very apt to suffer from pneumonia produced by foreign bodies. The lung may be penetrated either by some sharp object making its way forwards from the rumen or reticulum or by liquid or solid material passing into the trachea. These are two common methods by which this form of pneumonia is produced.
PNEUMONIA DUE TO THE MIGRATION OF FOREIGN BODIES FROM THE RETICULUM.
Causation. The conditions under which food is swallowed by ruminants after preliminary mastication permit indigestible objects, such as stones, fragments of wood, nails, needles, bits of iron wire, etc., to enter the rumen, whence they reach the reticulum in consequence of peristaltic movements. Sharp, perforating objects, like needles or fragments of iron wire, penetrate the walls of the gastric compartments, and, impelled by the movements of these organs, pass through the intervening tissues, usually in the direction of the heart. Under conditions which cannot precisely be defined, these foreign bodies make their way towards the pleural cavity (usually the right, in consequence of the situation of the reticulum), traverse the diaphragm, and directly penetrate the base of the lung.
As the migrating object is usually infected, its passage through the diaphragm always produces a localised patch of diaphragmatic pleurisy. Although possible, it is only rarely that the pleural sac becomes generally infected, or that rapidly fatal septic pleurisy is set up. Usually the localised pleurisy causes the base of the lung to become adherent to the anterior surface of the diaphragm. The foreign body continuing its movements, passes into the lung, and there sets up pneumonia.
Symptoms. When the practitioner is first consulted he often finds only indications of the crisis period of a localised pneumonia at the base of the affected lung. The symptoms include fever, accelerated breathing, moaning, loss of appetite, cough without discharge, dulness over the base of the lung on percussion, disappearance of the respiratory murmur in the dull area, souffle opposite the inferior bronchi, and normal or juvenile respiration towards the front, i.e., in the anterior lobe, and sometimes in the cardiac lobe.
The temptation under such circumstances is to deliver a diagnosis of simple pneumonia with prognosis of probable recovery. It should be remembered, however, that in all cases of basilar pneumonia without affection of the anterior lobes there is a considerable chance of the condition being due to the presence of a foreign body. On more careful examination it is found that the intercostal spaces opposite the affected region are very sensitive, and that the circle of the hypochondrium is correspondingly sensitive. The owner, moreover, almost always informs the practitioner that for several weeks his animal has coughed, shown tympanites, diminished appetite, etc.
Compression of the roots of the corresponding diaphragmatic nerve at the base of the neck always produces coughing.
These symptoms rarely accompany the development of simple pneumonia. Furthermore, the course of this accidental pneumonia is entirely different. Instead of developing regularly according to the above-described cycle, pneumonia due to foreign bodies develops slowly, and only becomes well defined after several weeks, whilst its tendency is to grow more and more aggravated. The zone of dulness extends both in a forward and upward direction. The souffle extends forwards. Auscultation and palpation sometimes reveal the formation of an abscess or local gangrene; while there is slight œdema of the wall of the chest, as well as a gurgling sound at the moment when the lung is displaced, high fever, intensely coloured urine, and very marked leucocytosis, etc. Death is inevitable, and when gangrene exists it sometimes occurs suddenly.
Diagnosis. The diagnosis is based on the information furnished with regard to the course of the disease, the localisation of the hepatised zone, and the progressive character of the affection.
The diagnosis, nevertheless, is always a little doubtful, but may be so far assured as to attain the position of a quasi-certainty.
Prognosis. The prognosis is unequivocal.
Treatment. No practical treatment, either to extract the foreign body or to combat the special pneumonia which it has produced, can be attempted. All the interlobular connective layers and the lobules themselves are invaded by various microorganisms carried by the foreign body. Numerous fragments of tissue serve as centres of suppuration and gangrene, and the only chance would lie in attempting resection of the lung. Such intervention has no practical interest in veterinary surgery. It is true that when the existence of an abscess is suspected, an aseptic exploratory puncture may be made, and, in the event of the diagnosis being so far confirmed, the abscess might be opened through an intercostal space. Under such circumstances, however deep the point of penetration of the foreign body, the development of the resulting abscess causes local pleurisy and adherence between the pleura and lung, so that there is no immediate danger of producing purulent pleurisy and pneumo-thorax. If small the foreign body might possibly be discharged through the passage thus afforded.
In practice the best plan is to recommend slaughter as soon as the diagnosis becomes certain, provided that the meat can still be utilised.
PNEUMO-MYCOSIS DUE TO ASPERGILLI.
The term pneumo-mycosis, or pulmonary aspergillosis, is used to denote a condition due to the growth in the respiratory apparatus of a fungus of the order aspergillus (family, Perisporiæ; sub-order, Perisporiaceæ; order, Ascomycetes).
In ruminants, as in all other animals, pulmonary aspergillosis occurs accidentally, and may often pass unperceived, in spite of the indications given by Lucet and Bournay regarding its development and symptoms.
It seems most frequently to be caused by Aspergillus niger and Aspergillus fumigatus, particularly by the latter, which, according to Rénon’s work, also appears to be the most pathogenic. It only develops in animals whose respiratory apparatus is injured and is the seat of such lesions as those of chronic bronchitis, bronchi-ectasis, and of parasitic lesions or those containing cavernous spaces resulting from abscess formation, etc., etc.
The fungi, or more properly the spores, which have accidentally penetrated into the respiratory channels germinate and develop in the pathological dilatations, causing disseminated areas of pneumonia and some mechanical disturbance, but not producing intoxication by liberating toxins.
Causation. Infection occurs through the air passages, in consequence of the inspiratory current carrying spores of the fungi into the ramifications of the bronchi, where they develop if the soil is favourable. Development is favoured if the animals exposed to contamination are in bad condition, or if, as sometimes happens, the walls of the stables are not kept clean, and are covered with various forms of fungi.
Prolonged feeding on musty fodder may also favour respiratory infection; but it seems highly improbable that under ordinary conditions infection can occur through the digestive tract. Infection of the lung must also be regarded as exceptional, if one bears in mind the frequency with which oxen are fed on musty or mildewed fodder and the small number of accidents recorded.
Symptoms. The symptoms are obscure, and pulmonary aspergillosis is often only discovered on post-mortem examination. A cough is the chief symptom. It is dry at first. Afterwards it becomes spasmodic and frequent.
Respiration is difficult, dyspnœic, effected only with effort, and sometimes even discordant. Expiration is sighing.
Percussion reveals zones of partial or complete dulness when the lesions are near the surface of the lung, which, however, is rare. Bournay has noted the occurrence of a musical sound resembling that obtained by tapping a small crystal or glass bell.
Auscultation is said to reveal rough or sibilant râles, but as the lesions occur only in animals whose respiratory apparatus has already been impaired, it is difficult to offer an opinion on the subject.
These signs are invariably accompanied by a certain amount of general ill-health, wasting, and irregularity of appetite and of rumination.
On post-mortem examination the lung of the affected animal appears strewn with nodules, varying in size between a hazel-nut and a walnut. On section, Bournay claims to have found a wall or fibrous shell covering a greenish cryptogamic growth, in the centre of which was a yellowish, sharply defined kernel formed of masses of fungi (Mycelium, sterigmata and spores). In cases of rapid development, the pulmonary tissue around the parasitic lesion is completely hepatised.
Diagnosis. Diagnosis is impossible without recourse to microscopic examination of the discharge. This examination, which, however, is somewhat difficult, may, after staining, result in the detection of débris of the mycelial filaments and of spores, with or without bacilli of tuberculosis. The diagnosis as regards fungi can only be assured by preparing cultures.
Prognosis. The prognosis is grave, because the disease is always superadded to lesions, which of themselves would justify a sombre view.
Treatment. In consequence of the small number of observations published and the difficulty in diagnosis, no rational treatment has hitherto been laid down. From a purely theoretical standpoint, fumigations with tar and essence of turpentine and the inhalation of carbolic spray have been recommended. Life in the open air would, without doubt, be equally or more efficacious. Preventive treatment consists in withholding musty fodder and keeping the stables clean.
GANGRENOUS BRONCHO-PNEUMONIA DUE TO FOREIGN BODIES.
Foreign bodies which find their way into the trachea instead of the œsophagus provoke in most cases broncho-pneumonia, which very rapidly terminates in gangrene and death.
Causation. Forced feeding of sick animals which have lost their appetite is one of the principal causes of this grave condition. In order to administer food such as mashes, gruel, hay tea, etc., the oxherds have a bad habit of lifting the entire head and drawing forward the tongue whilst they pour the concoctions into the animal’s mouth. The liquid cannot then be divided into portions, deglutition in the pharynx is badly effected, and the substances administered find their way partly into the larynx and partly into the œsophagus. In the case of astringent, bitter, or highly stimulating drugs, a similar accident may be caused by spasm of the pharynx or œsophagus, where the tongue has not been left free and excessive quantities have been given.
Again, during the course of diseases complicated with paralysis of the pharynx (cow-pox, parturient apoplexy), obstruction of the pharynx and œsophagus (tympanitic indigestion), intense pharyngeal dysphagia (foot-and-mouth disease), etc., the risk of broncho-pneumonia due to foreign bodies is much greater still. It may even occur spontaneously in animals in the enjoyment of complete freedom (foot-and-mouth disease).
Lastly, cases of broncho-pneumonia have been described as a consequence of inhaling foreign bodies, when the animals are fed, for example, with meal made from undecorticated cotton-seed. Under such circumstances the lesions produced are similar to those of pneumoconiosis in man (the chronic forms of pneumonia of miners, charcoal-burners, quarrymen, stonemasons, etc.).
Symptoms. The symptoms of gangrenous broncho-pneumonia become apparent immediately after the foreign body has entered the trachea. They commence with a violent, spasmodic cough, produced by reflex action, which in its turn is due to the laryngeal mucous membrane having been touched. But this cough is now too late to be of use, for the food, drug or liquid has passed into the depths of the trachea, and cannot be ejected. The cough soon ceases, and the animals may even return to their food. These appearances, however, are deceptive, for twelve, twenty-four or forty-eight hours later the cough reappears, whilst appetite diminishes. The attacks of coughing are succeeded by the discharge of a greyish or reddish-grey offensively smelling material; respiration becomes more rapid, the heart’s action violent, and the temperature rises to 103° or even 105° Fahr. (39·5 to 40·5° C.).
The patients soon refuse all solid food, and if the chest is then examined by percussion one finds partial dulness, rarely simple dulness, over the cardiac lobes opposite the point where the girth passes. The partial dulness may rise to a varying height on both sides; sometimes it is confined to one side.
On auscultation the respiratory murmur in the upper two-thirds of the lung appears exaggerated on both sides, and is found to have greatly diminished, or disappeared altogether in the inferior zone.
Auscultation through the scapula almost always shows that the anterior lobes are affected; but, at all events, in the examinations we have made, checked by post-mortem examination, the cardiac lobes have always proved to be most affected, a fact attributable to the direction of the principal bronchi. The lower portion of the posterior lobes may also be affected, but this is rarer. All the lower zone is irregularly hepatised, and on auscultation one hears large moist râles, whilst respiration sometimes appears of a blowing character, and divided by a pause, but there is no tubal souffle. If the patient survive for a certain time, the sounds heard on auscultation undergo change; gurgling noises and sometimes true cavernous souffles are heard, as a result of suppuration in the bronchi and gangrene of one or more areas in the lung. Diffuse gangrene is rare, and the inferior zone is usually the only portion affected.
During this phase the expired air has an absolutely characteristic gangrenous odour.
Death occurs by asphyxia and intoxication, but some animals hold out for a fortnight and more.
Lesions. Post-mortem examination reveals a suppurative but secondary inflammation of the mucous membrane of the nasal cavities, pharynx, larynx, and trachea.
In the bronchi, sometimes very deeply placed, remains of foreign bodies are found in cases where some solid material has been inhaled. The mucous membrane of the bronchi is violet in colour, in places appears to be sloughing, and is covered by gangrenous patches immersed in a reddish-grey putrid fluid of offensive odour. In places the pulmonary tissue has undergone gangrene; and incision of the diseased centres discovers irregular cavities, filled with a pultaceous, greyish material, which often makes its way into the bronchi. These are the irregular cavities which give rise to the gurgling sounds. The walls of these cavities are formed of disintegrating pulmonary tissue, which again is surrounded by a zone of grey hepatisation. The gangrenous areas may unite, forming vast caverns. If near the surface they cause adhesive or septic pleurisy.
Diagnosis. The diagnosis is not very difficult, provided that an exact account can be obtained of the circumstances which preceded the appearance of the disease. The signs furnished by the discharge, the expired air, percussion and auscultation are sufficiently significant to remove any doubt.
Prognosis. The prognosis is extremely grave, and in the great majority of cases fatal.
Treatment. There is very little chance of recovery, no matter what treatment may be employed. The most favourable termination consists in the gangrene remaining limited to the bronchi and to a small fragment of the lung, so that the damaged tissues, being gradually delimited and sloughed off, may finally be discharged by coughing.
This is an exceptional termination, but attempts may be made to assist its evolution by giving alcohol in doses of 8 to 10 ounces per day, and salicylate of soda in doses of 4 to 5 drachms. When the condition can be early diagnosed before intense and continued fever has set in, and when the animal’s condition is good, it is often preferable to slaughter the patient.
INFECTIOUS BRONCHO-PNEUMONIA.
The ox’s lung is liable to so many and such extremely varied diseases that it seems desirable to add to the above descriptions some remarks on infectious broncho-pneumonia of external or internal origin.
Anatomically these forms of broncho-pneumonia are characterised by the occurrence of “islands” of pulmonary hepatisation, more rarely by extensive (massive) hepatisation; in all cases the hepatisation is irregular, and in no way resembles that of simple pneumonia.
Causation. The internal causes are numerous and varied. They are due to primary infection of an organ whence arises a general infection, sometimes even true septicæmia. Some form of broncho-pneumonia, such as simple broncho-pneumonia, purulent broncho-pneumonia, gangrenous broncho-pneumonia, etc., then follows as a complication. These broncho-pneumonias are therefore only manifestations of purulent infection or septicæmia. They frequently follow post-partum infections, vaginitis, metritis, and suppurative mammitis.
Symptoms. The general symptoms first attract attention, and are extremely acute. They comprise high fever, loss of appetite, cessation of rumination and of milk secretion, breathlessness, blowing, etc.—all signs of grave and rapidly progressive infection.
Sometimes at this period nothing more than the primary lesion, such as metritis or mammitis, can be detected. It may even happen that the uterus seems little affected, and, despite the accelerated respiration, neither partial nor complete dulness of the lung is discovered.
Hepatisation only occurs some days afterwards, and with it irregular partial dulness localised in the lower zones, disappearance of the respiratory murmur in the corresponding regions, exaggeration in the infected regions, an expiratory sound which is barely perceptible or may be of a blowing character, or, again, after several days may be transformed into a tubal souffle.
The cough then becomes frequent, generally difficult, paroxysmal, feeble, and easily provoked. The appetite suffers, the patients seem to prefer fluid nourishment and lose flesh very rapidly.
If the broncho-pneumonia is about to terminate in suppuration or gangrene, the respiration becomes sighing, the breath fœtid, and the cough is accompanied by a greyish muco-purulent or gangrenous discharge.
When the abscesses are deep-seated, the alarming symptoms retain their primary degree of intensity for weeks, until the animals are completely exhausted. Abscesses, originating in deep-seated parts, may even extend towards the surface of the lung, and produce either adhesive pleurisy that can be detected by palpation, or exudative pleurisy, easily recognised on percussion.
When the infective microbes are not pyogenic the general condition appears less grave, the animals exhibit only moderate fever, appetite is diminished but not lost, wasting is slower, and may continue for months, but the affected portions of lung become converted into fibrous masses or a material resembling spleen pulp.
The duration of infectious broncho-pneumonia, therefore, varies with the nature of the infecting organism. In cases which terminate in gangrene, the animals may survive for three or four weeks; in those where suppuration occurs, for several months. In short, recovery is the rule in simple broncho-pneumonia; but from an economic standpoint there is little reason for keeping the animals alive.
Diagnosis. The diagnosis is not generally very difficult; for if at first the case may be mistaken for one of simple pneumonia, the persistence or prolonged aggravation of the symptoms and the irregularity in position of the lesions revealed by percussion and auscultation enable the condition to be distinguished at an early period from simple pneumonia.
Confusion with acute or chronic pleuro-pneumonia may easily be avoided by noting the absence of pleural effusion, and of the soft pleuritic souffle of peripneumonia, etc.
Where auscultation is chiefly relied upon it is more difficult to differentiate between this disease and acute tuberculosis, and between it and broncho-pneumonia produced by foreign bodies, although the latter disease develops differently.
Prognosis. The prognosis is always extremely grave and, in cases where there is gangrene or abscess formation, fatal. From the economic standpoint the chronic form is also very grave.
Treatment. As broncho-pneumonia is frequently of a secondary character, treatment should at first be particularly directed against the primary condition, whether in the mammary gland, uterus or elsewhere. Early treatment of suppurative mammitis, metritis, etc., is therefore necessary.
Broncho-pneumonia is treated by free vesication of the walls of the chest, the administration of tonics and antiseptics, alcohol in small doses, acetate of ammonia in doses of 1 to 2 drachms, salicylate of soda in doses of 5 to 8 drachms per day, salicylic acid in doses of 1 drachm, and creosote in doses of 1½ to 5 drachms, given in electuary, etc.
Diuretics, farinaceous gruels, etc., may be used freely, and are of value.
If the symptoms persist or become aggravated, and suggest the development of an abscess or gangrene, it is better to slaughter the animal.
BRONCHO-PNEUMONIA OF SUCKING CALVES.
Young animals still with the mother, particularly calves during the first few weeks of life, are liable to broncho-pneumonia of a specialised character, as regards not only its causes, but its development and duration.
Causation. The causes may be grouped under two principal heads:—
(a) In slow or difficult cases of parturition, the fœtus may be injured whilst being delivered, as a consequence of direct compression of the great blood-vessels, etc. (particularly of compression of the umbilical cord, compression of the thorax in the cardiac region, or partial premature separation of the envelopes), and may thus by reflex action make automatic inspiratory movements.
Respiration being impossible, inasmuch as the thorax has not yet passed the posterior passages, such inspiratory efforts made during the passage through the pelvis may cause amniotic liquid to pass into the bronchi. This accident is particularly liable to occur during deliveries with breech presentation. If, as happens frequently, the amniotic liquid has become infected either prior to or as a consequence of obstetrical manipulation, the result is fatal; for the passage of infected amniotic fluid into the bronchi develops a broncho-pneumonia of a degree of gravity depending on the character of infection.
(b) By an entirely different mechanism broncho-pneumonia may occur in sucking calves during the first few weeks of life, even in the case of animals born in a vigorous condition, and kept in warm and well-arranged stables. This form follows diarrhœa, and constitutes a final complication which is always of very marked gravity, and in most cases fatal.
Such secondary broncho-pneumonia only occurs when the diarrhœa has resisted treatment, and it is important to note that the pectoral lesions appear at a time when the intestinal mischief seems to have diminished, the diarrhœa having lessened or disappeared. This variety of broncho-pneumonia of young animals is by far the most frequent. It has been termed broncho-pneumonia of intestinal origin, and exactly resembles, so far as its development and gravity are concerned, the broncho-pneumonia in young infants described by Sevestre and Lesage.
The term broncho-pneumonia, moreover, is not strictly correct, or at least is not exclusive; for the rapid forms often exhibit lesions other than those of broncho-pneumonia. Post-mortem examination reveals pleurisy and pericarditis.
Pathogeny. At the outset of these attacks of broncho-pulmonary disease, a careful bacteriological examination of the organisms to be found in the discharge of bronchial mucus leads to the discovery of bacilli which do not stain with Gram, and which resemble varieties of the colon bacillus; in other cases of streptococci. At a later stage, when the animal has become weak, microorganisms are present in much greater variety. Nocard found in lung abscesses the bacillus of epizootic lymphangitis. It seems that the development of various lesions in the thoracic cavity may be due to auto-infection, i.e., to the penetration from the intestine of germs which, after passing through the circulation, establish themselves at some point in the lung. The pleura is attacked at a later period as a consequence of continuity and contiguity of tissue.
In a similar way pericarditis and even valvular endocarditis may be produced.
Symptoms. The symptoms are similar to those of all forms of broncho-pneumonia. Where diarrhœa has been neglected, the conditions may apparently improve without evident cause, whilst the respiration becomes more frequent. The patient soon suffers from cough, and in a few hours the existence of broncho-pneumonia is clearly apparent. Acceleration of breathing is the dominant symptom. The respirations may rise to fifty to sixty per minute, at which they continue, while fever sets in. On percussion the thorax may appear of normal resonance throughout; but when pleural lesions and exudates exist, resonance gives place to partial or complete dulness. Should pericarditis or small cardio-pericardial adhesions exist, they may escape observation, but if the exudate is abundant or the adhesions multiple or of large size the usual symptoms of pericarditis develop progressively.
On auscultation the respiratory murmur is always found to be greatly exaggerated in the healthy parts, usually the upper portions of the lung. On the contrary, it is attenuated or suppressed in the affected regions. The other signs vary greatly, according to the extent, intensity, and more or less advanced condition of the lesions. Crepitant and bronchial râles, blowing respiration and tubal souffles, etc., are among the symptoms.
The duration of the disease varies; some patients may be carried off in five or six days, while others survive for one or two months, or even longer. A few recover, but they remain thin, puny, and atrophied, and are not worth keeping alive.
Lesions. The lesions extend to the bronchi, the pulmonary tissue, and sometimes the pleura and pericardium. They consist in lesions of diffuse broncho-pneumonia, pleurisy with false membranes and parietopulmonary adherences, and pericarditis with partial cardio-pericardial adhesions.
In rare cases abscesses caused by pyogenic streptococci may be found.
The anterior lobes, cardiac lobes, and lower part of the posterior lobes are those singled out for attack.
Diagnosis. The diagnosis is not difficult, provided that the circumstances preceding the appearance of the pulmonary lesions are known.
Prognosis. The prognosis is very grave.
Treatment. Treatment very often proves useless, because the patients have little resisting power and are exhausted, and also because they are suffering from a slowly progressive septicæmia. It may, however, be worth while in the early stages to apply blisters to the chest and administer general stimulants: alcohol in doses of 8 to 12 drachms per day, divided into two parts and mixed with milk; acetate of ammonia in doses of ½ to 1 ounce; and tinctura digitalis 5 to 6 drops.
The primary disease of the intestine is masked by the pulmonary symptoms, but should not be overlooked. Rice water, subnitrate or salicylate of bismuth may be added to the milk or albuminous solutions constituting the diet. When an epizootic of broncho-pneumonia complicates the diarrhœa it is necessary to take all the preventive measures which have been suggested in connection with white scour and umbilical diseases in calves. These comprise disinfection of the premises and local disinfection of the animals affected.
SCLERO-CASEOUS BRONCHO-PNEUMONIA OF SHEEP.
The sheep suffers from a special form of broncho-pneumonia, which is seldom seen except in isolated cases, but which, under exceptional circumstances, may nevertheless attack a certain number of animals in a particular flock. It was first noticed and described by Liénaux in 1896, and has more recently been studied by Sivori (1899). Moussu has only seen it in flocks in the north of France.
Causation. The causes of this disease are still imperfectly understood.
Sivori’s researches show that the disease may be referred to a microorganism, but we do not yet know exactly by what path infection occurs.
The agent of sclero-caseous broncho-pneumonia in the sheep appears similar to that described by Preisz and Guinard in 1891, and identical with the microbe of ulcerative lymphangitis of the horse (Nocard, 1897). It is probable that infection occurs through the respiratory apparatus.
Symptoms. The clinical development of the disease is difficult to describe, because its course is slow and unaccompanied by well-marked external signs.
The animals lose flesh, pant for breath when moved, drop to the rear of the flock, cough frequently, feed badly and end by becoming cachectic. Many suffer from the disease and yet remain in fair bodily condition.
On post-mortem examination the lungs are found not to collapse, having lost their elasticity, and are of a yellowish-white colour, which is only seen in this disease. On section the pulmonary tissue appears dense, hard, and of a fibrous and lardaceous character. At various points nodules with fibrous envelopes and caseous, yellowish or greenish contents are found.
When the caseous nodules are near the surface the pleura may be chronically inflamed and thickened. The liver and kidney frequently contain caseous lesions.
Diagnosis. The diagnosis becomes easy after the first post-mortem examination, for the lesions discovered cannot be mistaken for those of parasitic broncho-pneumonia, degenerated pulmonary echinococcosis or tuberculosis. In the living animal, on the contrary, the diagnosis is extremely difficult.
Prognosis. The prognosis is grave. No special method of treatment is known.
PULMONARY EMPHYSEMA.
Pulmonary emphysema, i.e., exaggerated dilatation of the pulmonary tissue by air, is not uncommon in the bovine species, and occurs under the two classical forms—(1) alveolar or intra-lobular emphysema limited to dilatation of the alveoli; and (2) interlobular emphysema, produced by the entrance and diffusion of air in the interlobular spaces in consequence of rupture of the lobules.
These two forms are very frequently associated:—
(1.) Emphysema by dilatation usually begins in the right pretracheal lobe; also in the cardiac and even in the posterior lobes.
(2.) Interlobular emphysema begins in the same regions, but it spreads readily in a backward direction, remaining interstitial; or, on the other hand, becoming subpleural at the periphery of the lung.
In both cases the pulmonary tissue is pale, the blood-vessels are partially obliterated by compression; circulation and aeration of the blood are impeded—hence the appearance of the disturbance noted.
Causation. Emphysema is seen in adult working oxen; also, and to an even greater degree, in aged cows. It is produced by excessive strains in draught, or more often by the paroxysms of coughing so common during simple or parasitic bronchitis, broncho-pneumonia, pneumonia, chronic broncho-pneumonia, etc. Successive gestations also produce it.
All these pathological conditions also interfere with the nutrition of the bronchial mucous membrane, particularly of its deep-seated muscular layer, which is then incapable of regulating the distribution of air in the bronchial channels. The distribution being no longer regulated by reflex action, air accumulates at certain points as a result of the expiratory efforts made during coughing, and dilatation of the vesicles or lobules occurs.
Diseases of the digestive apparatus, acute or chronic tympanites in particular, may play a certain part by compressing the diaphragm, causing expiratory efforts and fits of coughing.
Furthermore, swelling of the lymphatic glands at the entrance to the chest, by compressing the pneumo-gastrics, provokes reflex cough and finally emphysema.
Symptoms. Pulmonary emphysema is marked by accelerated respiration due to diminution in the respiratory capacity, which is often very seriously affected; to insufficient absorption of oxygen in consequence of diminution in the space available for exchange of gases in the lung, and to insufficiency of expiration. This acceleration in breathing, though little marked during repose, becomes very pronounced after exercise, or during hot weather; and under these circumstances is accompanied by a paroxysmal, feeble but shrill cough, without discharge. This cough without discharge is frequently followed by swallowing.
Percussion reveals an important point, viz., increase in the normal resonance of the thorax.
On auscultation the vesicular murmur is found to be diminished, the respiration assumes a rough and rasping character, inspiration is difficult, expiration painful, and often divided into two periods, as indicated by a slight double movement of the flank. Expiration is clearly audible. Its duration is generally less than that of inspiration, although in some cases it is equal or even longer. It is accompanied by sibilant and snoring râles, sometimes even mucous râles, of an intermittent character. In rare cases there may be difficulty of respiration, as in broken-winded horses.
Diagnosis. The diagnosis may suggest a doubt as to whether emphysema or tuberculosis is present, but in the latter there is fever, the general condition is poor; on percussion the thorax reveals areas of partial dulness; and expiration is rough and prolonged, sometimes of a blowing character, a peculiarity which is exceptional in emphysema.
Prognosis. The prognosis is not very grave, except where emphysema is only an accompanying symptom of another disease, such as chronic bronchitis, tuberculosis, etc.
Treatment. Little can be done to check the development of the above described pulmonary lesions; but the cough may be relieved, and the pulmonary circulation improved by assisting the heart.
The most prompt and efficacious assistance is given by digitalis in doses of ½ to 1 drachm per day for adults, iodide of potassium in doses of 1 to 1½ drachms, and bromide of potassium in doses of 1 drachm to guard against reflex excitability of the pneumo-gastric. This treatment, however, should not be followed for more than five or six days, and should then be replaced by the administration of arsenious acid in doses of 15 grains per day, ground horse-chestnuts in doses of 3 ounces per day, etc., etc.
DISEASES OF THE PLEURA.
Primary inflammation of the pleura is very rare in animals of the bovine species, but secondary diseases of this membrane, on the other hand, are frequent.
ACUTE PLEURISY.
Cruzel, Fabry, and a number of practitioners have described the occurrence in working animals of acute pleurisy à frigore or serofibrinous pleurisy in consequence of severe, sudden variations in temperature, or prolonged chills. At the present day it seems fairly well established that pneumonia, and not pleurisy, is commonest under such conditions, and Moussu disclaims ever having seen primary pleurisy. On the other hand, pleuritic effusions are very common in contagious pleuro-pneumonia, secondary pleurisy due to pericarditis produced by foreign bodies, septic broncho-pneumonia or broncho-pneumonia due to foreign bodies, and the pleurisy which accompanies septicæmia consequent on parturition, etc. These forms of disease, however, are not simple serofibrinous pleurisy, but septic or suppurative pleurisy, still little understood in veterinary surgery.
Tuberculosis of the pleura, although very frequent, is rarely accompanied by marked exudation. Like secondary disseminated pleural carcinoma, it usually assumes the vegetative and adhesive form, with adhesions of greater or less extent between the lung and wall of the chest.
Symptoms. In all these morbid conditions the symptoms vary greatly, and it would be difficult to give an accurate general description of them.
In acute pleurisy à frigore shivering attacks, moderate fever, dulness, loss of appetite, interference with rumination, dryness of the skin, rapid wasting and intercostal pain, first indicated by dull colic, constitute the usual symptoms.
The respiration is short and irregular, interrupted when the exudation is abundant. Pressure over the intercostal spaces produces pain, as does strong percussion. Percussion reveals an area of dulness bounded above by a horizontal line.
Auscultation shows the respiratory murmur to have disappeared throughout the zone of dulness, and reveals the presence of a soft pleuritic souffle (a soft tubal souffle quite different from that of contagious pleuro-pneumonia) when pleural exudation is abundant. In septic or suppurative pleurisy fever is higher, loss of appetite more marked, wasting more rapid, and depression extreme, with, however, identical local symptoms.
Diagnosis. The diagnosis of pleural exudation presents little difficulty, because of the peculiar characters of the dulness and the pathognomonic indications obtained by auscultation. The exudation is usually unilateral, the mediastinum being very resistant and not perforated in the ox.
By passing the needle of a Pravaz’s syringe with antiseptic precautions through the intercostal space a little fluid may be drawn off and the diagnosis formed, the form and nature of the pleurisy being simultaneously established. The liquid extracted can be examined bacteriologically, and can be grown on nutritive media, or inoculated into experimental animals.
The prognosis is grave, because in the ox pleurisy is very often of a secondary character. The outlook varies, however, with the form of the pleurisy and the nature and virulence of the infecting organism.
Treatment. Treatment consists firstly in applying an energetic vesicant like antimonial ointment or liquid cantharides blister; internally diuretics such as soda bicarbonate, nitrate of potash, resin, and decoctions of pellitory, dogs’ grass, etc., may be given. If thought desirable the chest may be tapped and the pleural cavity washed out with an antiseptic solution.
CHRONIC PLEURISY.
Chronic pleurisy is frequent in aged animals, but usually assumes the form of local adhesive pleurisy. The adhesions between the lung and pleura are more or less extensive; they result from verminous broncho-pneumonia, echinococcosis, external injuries, etc. Clinically this form is of no importance, and is almost impossible to diagnose. During the development of pleural tuberculosis, on the contrary, adhesive dry pleurisy is frequent, and sometimes becomes so well marked that almost the whole of the opposing pleural surfaces may become united.
PNEUMO-THORAX.
The name pneumo-thorax is given to the condition produced by the entrance of air or gas into one of the pleural cavities.
The accident is usually produced by rupture of the parenchyma of the lung and of the pleura, a rupture which produces a communication between the alveoli or a bronchus and the corresponding pleural cavity. As soon as the rupture occurs air passes from the lung into the pleural cavity, and the lung collapses in consequence of the resilience of its elastic constituents.
Under other, much rarer, circumstances pneumo-thorax occurs in consequence of gas generated in the digestive tract passing into the pleural spaces. The condition then makes rapid progress, and death occurs in a few days.
Fig. 171.—Schema illustrating open pneumo-thorax. Right lung collapsed; pericardium and heart displaced towards the right.
Symptoms. The symptoms are well defined. As soon as the accident occurs the animal exhibits extremely marked and sudden dyspnœa, accompanied by heaving at the flank or general agitation of all the muscles of the body. One of the lungs, in fact, has suddenly been called on to perform the functions of both, and at first it naturally has great difficulty in meeting this demand.
The heaving at the flank and the general agitation of the body muscles is due to the fact that the regularity and rhythm of contraction of the diaphragm are disturbed, and the mechanical conditions have become different on the two sides. From the first, respiration is moaning and expiration becomes rapid, stertorous and deep, while the face is anxious-looking, and the nostrils are dilated as though the animal was on the point of suffocation. On examining the animal from in front or behind, the thorax is easily seen to be wanting in symmetry, the side on which the pneumo-thorax has occurred being immobile as compared with the sound side. The latter, moreover, is dilated in order to compensate for the loss of function of the collapsed lung.
Percussion reveals greatly increased resonance on the side of the pneumo-thorax. On the other hand, the opposite side yields a normal sound.
Auscultation reveals an increase of the respiratory murmur on the side which is still acting and, on the contrary, complete and total suppression of the respiratory murmur on the affected side. On applying the ear to the chest wall, a large soft, amphoric souffle of well-marked metallic character is heard. This is particularly clear on respiration, giving the impression of the existence of a large cavity beneath the ear. The sighing sound heard on auscultation of the chest wall is louder than that heard externally or over the region of the nostrils or larynx; and it seems to be reinforced, as though by the resonance of a large cavity with thin metallic walls. Once or twice per minute, moreover, a sound may be heard like that of dropping water. It is of a very special character, resembling that produced by drops falling to the bottom of a hollow metallic vase, and setting up prolonged vibration.
As secondary symptoms the heart’s action is accelerated, the number of beats rising to 80 or even 120 or 130 beats per minute; appetite is lost; slight tympanites develops as a result of rumination and eructation being suspended; the peristaltic movements of the rumen are interrupted, and constipation develops.
Diagnosis. The diagnosis of pneumo-thorax is easy, and the condition can scarcely be mistaken for any other except diaphragmatic hernia; but the indications derived from percussion and auscultation are so different in the two cases that they need not be further emphasised.
The task becomes more difficult, however, when an attempt is made to identify the exact form of pneumo-thorax, for three principal varieties are recognised.
In open pneumo-thorax, the first and most frequent form, air passes from the lung into the pleura at each inspiration, and flows back from the pleural cavity towards the bronchus at each expiration. The intra-pleural pressure is then approximately equal to the intra-bronchial pressure, and undergoes similar oscillations. (It should be noted that the aperture in the lung is seldom sufficiently large to establish an absolute equality of pressure between the bronchus and the pleural cavity. Respiration, therefore, though very seriously impeded, generally continues in a modified form.)
In a second variety, termed “valvular pneumo-thorax,” air passes freely from the lung into the pleural cavity, but is unable to return from that cavity towards the lung, because a flap of tissue acts as a valve and closes the orifice at the commencement of expiration. As soon as intra-pleural pressure rises above that of the inspiratory effort, the valve remains permanently closed.
In the third variety, called “closed pneumo-thorax,” the orifice of communication is obstructed by some mechanism, and the pleural sac only contains a film of air.
In practice, valvular pneumo-thorax is recognised by the movement of the thoracic wall (which in open and closed pneumo-thorax remains depressed), as well as by extreme intensity of the dyspnœa and attacks of threatened suffocation. Closed pneumo-thorax, which is only a termination and a stage in the cure of open pneumo-thorax and of valvular pneumo-thorax, is suggested by progressive improvement in the symptoms. Scientifically it is very easy to make this diagnosis by putting a manometric apparatus in communication with the pleural cavity by means of a simple hollow needle provided with a thick-walled rubber tube.
In open pneumo-thorax the liquid column in the manometer undergoes rhythmic oscillations corresponding to the respiratory movements; in valvular pneumo-thorax the intra-pleural pressure increases progressively until it becomes higher than the external pressure; and finally, in closed pneumo-thorax, the column of the manometer assumes a certain level at which it rests.
Prognosis. The prognosis is very variable, according to the primary cause of the accident. Animals might recover, but economically there is little advantage in preserving them when the diagnosis is assured, except in cases of animals of great value, and when the primary disease admits of it.
Causation. Pneumo-thorax may be produced by various causes. The most frequent cause in large animals is pulmonary echinococcosis, during the course of which a peripulmonary vesicle, after having injured several lobules, one of the air passages or even a bronchiole, may break through the pleura, thereby setting up direct communication between the bronchi and the pleural cavity.
To pulmonary tuberculosis, with peripheral softened tubercles, perforating simultaneously into an alveolus or a small bronchus and into the pleura, must be assigned the second place.
Vesicular and interstitial subpleural pulmonary emphysema is also a frequent cause of pneumo-thorax, the pleura being ruptured over the emphysematous points.
Finally, and exceptionally, an abscess of the lung may open into the pleura and form sinuses, which may establish a communication between the digestive reservoirs and pleural sacs; but such accidents produce pyo-pneumo-thorax and septic pleurisy of a rapidly fatal character.
The diagnosis of pneumo-thorax, and even of its varieties, does not, however, enable one to form a prognosis; the important point is to ascertain the original cause.
Treatment. It may be said of pneumo-thorax that no treatment exists, and that the position is one of expectancy. In fact, we possess no means of directly dealing with such diseases as echinococcosis, tuberculosis, or emphysema. For this reason it is best as a rule to advise slaughter. Nevertheless, when the condition is due simply to pulmonary echinococcosis of a discrete character, there is some chance that after several months the animal may recover spontaneously. The communicating orifice becomes closed by reparative processes (cicatricial contraction, the formation of a false membrane, limited adhesion between the two walls of pleura, etc.); the layer of air imprisoned within the pleural cavity is progressively absorbed, provided that it has not been accidentally infected; the collapsed and partially splenised lung progressively regains its function under the inspiratory efforts, and after some months complete recovery may occur. This termination cannot always be confidently predicted, because complications may arise at any moment; under no circumstances can complete recovery be anticipated when the primary disease is tuberculous.
Fig. 172.—Hydro-pneumo-thorax. I, Point of adhesion of the pleura; P, healthy lung; Ps, splenised lung; E, liquid or purulent exudate; Ca, air cavity constituting pneumo-thorax; C, heart.
In cases of valvular pneumo-thorax with extreme oppression, attacks of suffocation threatening death as a consequence of excessive intra-pleural pressure, displacement of the mediastinum towards the opposite side, compression of the heart, and functional disturbance of the sound lung, it may be worth considering whether the attacks of suffocation and threatened asphyxia can be modified or removed by preventing the excess of intra-pleural pressure. By simply passing a stout hollow needle through one of the intercostal spaces, the intra-pleural pressure may be reduced to that of the external atmosphere, and the effects of compression removed. This, however, is a last resort, and has no permanent effect.
HYDRO-PNEUMO-THORAX AND PYO-PNEUMO-THORAX.
When pneumo-thorax is set up, it rarely remains simple. In the great majority of cases the pleura becomes infected, either directly, by the lesion which has determined the pneumo-thorax (tubercle, superficial abscess, actinomycotic lesion, etc.), or secondarily, by the penetration of germs from the air or from the bronchus (echinococcosis, emphysema). Simple pneumo-thorax then becomes converted into hydro-pneumo-thorax or pyo-pneumo-thorax, according to circumstances—that is to say, whether the exudation into the pleural cavity is of a simple character or is of the nature of pus.
Symptoms. Hydro-pneumo-thorax is characterised by the signs common to true pneumo-thorax, which constitutes the primary lesion, viz., sudden difficulty in breathing, exaggerated unilateral resonance, amphoric souffle accompanied by a sound like that of drops of water falling into a metallic vessel, and by the signs of secondary exudative pleurisy, viz., moderate fever, dulness over the lower zones of the chest, limited above by a horizontal line, slight splashing sound, and a soft distant pleuritic souffle.
All the secondary symptoms—loss of appetite, suppressed rumination, sighing, accelerated pulse, etc.—are found in a more or less accentuated form.
In pyo-pneumo-thorax fever is more marked, while the signs noted on auscultation and percussion are identical, and are accompanied by digestive disturbance and marked œdema of the wall of the chest, which can be seen or detected by palpation.
Diagnosis. The diagnosis is relatively easy when the lesion is secondary; but the difficulty (as in simple pneumo-thorax) is to identify the exact character of the primary affection.
On the other hand, pyo-pneumo-thorax and hydro-pneumo-thorax are not always complete; adhesions of very varying character may exist between the lung and the chest wall; hence it is impossible to group together all the possible symptoms.
Diagnosis is facilitated by aseptically puncturing the chest with a Pravaz’s syringe.
Prognosis. The prognosis is extremely grave even in cases of hydro-pneumo-thorax. Treatment is useless, for even allowing that the primary disease might be cured, this process of cure, after reabsorption of the transudate, would be extremely tedious, and the animals would long remain in poor condition.
Treatment. In hydro-pneumo-thorax no treatment is advisable. Nothing is gained by thoracentesis, at least at an early stage, or before the lesion causing the pneumo-thorax has closed.
In pyo-pneumo-thorax, on the contrary, the theoretical course is to evacuate the pus and completely wash out the pleural sac with lukewarm non-irritant solutions of antiseptics.
CHAPTER V.
DISEASES OF STRUCTURES ENCLOSED WITHIN THE MEDIASTINUM.
The mediastinum is a space enclosed in the median plane of the thorax by the approach of the two opposite layers of pleura. Needless to say, at those points where the layers are in apposition, the space is theoretical only. It extends from the suprasternal region to the dorsal subvertebral region, and encloses all the vessels which pass from or to the base of the heart, the trachea, the œsophagus, the pneumo-gastric, diaphragmatic and cardiac nerves, etc., as well as the pericardial sac and the heart. The organs most frequently affected are the lymphatic glands lodged in the thickness of the mediastinum, the glands placed at the entrance to the chest, the bronchial glands, and the glands situated in the posterior mediastinum.
Inflammation of the mediastinum may coincide with inflammation of the mediastinal layers of the pleura; but this can only be detected on post-mortem examination. The lesions which can be recognised during life are simple inflammation of glands, resulting from pulmonary or pleural diseases, tuberculous inflammation of glands, and the presence of cancerous tumours of the mediastinum and hypertrophy of glands due to lymphadenitis.
Simple inflammation of the lymphatic glands is secondary and consecutive to broncho-pneumonia, verminous bronchitis, infectious bronchitis, etc.
It produces reflex irritation by compressing the pneumo-gastric and laryngeal nerves, and is indicated by loud, spasmodic coughing.
Treatment consists in administering iodide and bromide of potassium, terpine, in doses of 1 drachm per day for adults, essence of turpentine and tar water.
Tuberculous inflammation of glands, inseparable from pulmonary tuberculosis, has very special characteristics peculiar to tuberculosis.
Inflammation due to lymphadenitis is also very easy to diagnose as a rule, in consequence of the symmetrical enlargement of lymphatic glands elsewhere.
TUMOURS OF THE MEDIASTINUM.
Sarcomata, carcinomata, lymphomata, and lympho-sarcomata all occur in the mediastinum. They attack young healthy animals, and sometimes develop with such rapidity that in a few weeks they become generalised and invade the heart, lungs, and principal viscera. Their cause is as yet unknown.
Symptoms. At first sight the symptoms are much like those of pericarditis caused by foreign bodies. They consist in deformity of the presternal region, swelling of the jugulars, submaxillary œdema, irregular pretracheal tumefaction, etc.
The tumour, whatever its nature, commences in the mediastinum, develops towards the entrance to the chest, where it projects, and before long produces in the pretracheal region clearly marked œdematous swelling.
Between the two first ribs the tumour compresses the carotids, the jugulars, the nerve trunks, and also the trachea and œsophagus, producing difficulty in the return circulation, especially in the jugulars, swelling in the submaxillary space, loss of appetite and dyspnœa.
Palpation affords indication of a tumour of soft consistence, bosselated, more or less adherent to the skin, usually painless on pressure, and of irregular development. Compression of the œsophagus interferes with the deglutition of rough forage, impedes rumination, prevents eructation, and thus produces trifling but permanent tympanites.
The heart is affected reflexly or directly as a result of generalisation of the tumour, and the pulse may rise to 70 or even 120 per minute.
During the first stages neither auscultation nor percussion points to any pulmonary lesion. At a later stage the lung itself may be affected. The other important functions are normal.
Animals suffering from sarcoma, carcinoma, or lympho-sarcoma of the mediastinum waste very rapidly, lose appetite, become feverish, and soon develop cachexia.
Diagnosis. The diagnosis of tumour of the mediastinum is easy, because of the well-marked character of the apparent symptoms.
Prognosis. The prognosis must be regarded as extremely grave, and in most cases fatal, for there is no active method of intervention, extirpation being impossible.
There is no treatment. The animal should at once be slaughtered.