CHAPTER IX.. Diseases of the Liver.

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.

=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.

=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.

=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.

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.

The cystic vesicles contain a clear, limpid, transparent fluid, in which float secondary, daughter, or granddaughter vesicles.

=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.

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.

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.

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.

=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.

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.

=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.

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.

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.

(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—

(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.

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—

(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.

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.

=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.

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.

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.

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.

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.

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.