Fig. 33.—A, Succinea putris, infested by B, Leucochloridium paradoxum, or the fully-formed sporocyst of Distomum macrostomum. (After Heckert.) A, Natural size; B, × 7.
The egg of this Distome thus gives rise to a larva which enters the tissues of one particular Mollusc. Here it becomes a branched sporocyst within which the sexual worms are formed, apparently each from a single embryonic blastomere ("Keimzelle"), by a process comparable with the development of a parthenogenetic ovum, and the whole cycle has been termed Alloiogenesis, i.e. alternation of sexual and parthenogenetic generations (Grobben).[[80]] Leuckart[[81]] and Looss,[[82]] however, consider that what was once a metamorphosis of an individual (as in the Holostomatidae) has now become, by maturation of the Cercaria in the comparatively modern warm-blooded bird, a metamorphosis extending over two or more generations.
Distomum (Fasciola) hepaticum.—The liver-fluke of the Sheep, which produces the disastrous disease, liver-rot, has a distribution as wide as that of a small water-snail, Limnaea truncatula, the connexion between the two being, as Thomas[[83]] and Leuckart discovered, that this snail is the intermediate host in which the earlier larval, sporocyst, and redia stages are passed through, and a vast number of immature flukes (Cercariae) are developed. These leave the snail and encyst upon grass, where they are eaten by the sheep. Over the whole of Europe, Northern Asia, Abyssinia, and North Africa, the Canaries, and the Faroes, the fluke and the snail are known to occur, and recently the former has been found in Australia and the Sandwich Islands, where a snail, apparently a variety of Limnaea truncatula, is also found.[[84]] Over these vast areas, however, the disease usually only occurs in certain marshy districts and at certain times of the year. Meadows of a clayey soil, liable to be flooded (as in certain parts of Oxfordshire), are the places where this Limnaea occurs most abundantly, and these are consequently the most dangerous feeding-grounds for sheep. The wet years 1816, 1817, 1830, 1853, and 1854—memorable for the occurrence of acute liver-rot in England, Germany, and France—showed that the weather also plays a considerable part in extending the suitable ground for Limnaea over wide areas, which in dry years may be safe pastures. In 1830 England lost from this cause,[[85]] one and a half million sheep, representing some four millions of money, while in 1879-80 three millions died. In 1862 Ireland lost 60 per cent of the flocks, and in 1882 vast numbers of sheep perished in Buenos Ayres from this cause. In the United Kingdom the annual loss was formerly estimated at a million animals, but is now probably considerably less. After infection during a wet autumn, it is usually in the succeeding winter that the disease reaches its height.
The symptoms of "rot" appear about a month after infection, more acutely in lambs than in sheep, and again, less in oxen than in sheep. At first, death may result from cerebral apoplexy, but if the first few weeks are passed through, a pernicious anaemia sets in, the sheep are less lively and fall at a slight touch, the appetite diminishes, and rumination becomes irregular. The conjunctiva is of a whitish-yellow colour, the dry, brittle wool falls off, and there is sometimes fever and quickened respiration. In January, about three months after infection, the wasting, or fatal, period sets in. Oedemas or swellings, usually visible before, become larger at the dependent parts of the body, a large one in the submaxillary region being especially well marked, and this is considered one of the most characteristic symptoms ("watery poke"). Through this period few of the infected sheep survive, but should they do so, the flukes begin to migrate, though some remain much longer within the liver. Migration is effected through the bile-duct into the duodenum and outwith the faeces, in which the altered remains of the Distomum are sometimes scarcely recognisable. Under these circumstances (or owing to death of the fluke in situ) the sheep recover more or less fully.
The preventive measures seem to be: (1) Destruction of the eggs and of the manure of rotten sheep; (2) slaughter of badly fluked sheep; (3) adequate drainage of pastures; (4) an allowance of salt and a little dry food to the sheep; and (5) dressings of lime or salt on the ground to destroy the embryos.[[86]]
Distomum hepaticum, contrary to most Trematodes, enjoys a wide range of hosts. Man himself occasionally falls a victim; thus in Dalmatia, in the Narenta Valley, the disease is endemic but slight in its effects. The horse, deer, camel, antelopes, goat, pig, rabbit, kangaroo, beaver, and squirrel have all been known to harbour this fluke occasionally. In the Italian deer-parks at Mandria a large species, D. magnum, decimated the herds some years ago; and this species, probably imported from Italy, is now almost as dangerous a parasite on the western plains of the United States as D. hepaticum.
Bilharzia haematobia.[[87]]—This formidable parasite was discovered by Bilharz in 1853 in the veins of the bladder of patients at the Cairo Hospital, and is remarkable from its abundance on the east coast and inland countries of Africa from Egypt to the Cape, as well as in the districts bordering Lake Nyassa and the Zambesi river, while westwards it occurs on the Gold Coast. Mecca is a source of infection whence Mohammedans carry the disease to distant places. In Egypt about 30 per cent of the native population is affected by the serious disease known as Haematuria, resulting from the attacks of Bilharzia, so that, of the many scourges from which in Africa man suffers, this one is perhaps the most severe.
Fig. 34.—Bilharzia haematobia Cobb. × 10. The female (♀) lying in the gynaecophoric canal of the male (♂). d, Alimentary canal; ms, oral sucker of male; vs, ventral suckers. (After Leuckart.)
The worm is found usually in couples, which have been proved to be male and female individuals (Fig. 34), often in considerable numbers in the veins of the pelvic region, chiefly the veins of the bladder and of the large intestine, and it is tolerably certain that Bilharzia enter these vessels from the portal vein. Their long slender bodies enable them to penetrate into the finer vessels, which get partially or entirely choked up, and the circulation accordingly impeded. But the most serious consequences are observed in the urinary bladder. The mucous membrane is swollen and inflamed here and there, chiefly on the dorsal surface, the capillaries appear varicose and covered with mucus, mixed with blood-extravasations in which Bilharzia-eggs are noticeable. The eggs also cause numerous swollen knots in the submucous tissue. Should the disease not pass beyond this stage (and such is usually the case, especially in South Africa), a temporary haematuria ensues. The urine, which is only expelled with great effort, accompanied by intense pain, is mixed with blood, mucous clots, and masses of Bilharzia-eggs, from which some of the embryos have already hatched out. The symptoms, however, may gradually pass away, and a more or less complete recovery accomplished. The disease may indeed be of a far less severe character, and may not interfere with the usual occupations of the patient; but, on the other hand, a far more extensive thickening of the wall of the bladder sometimes occurs; hard masses of eggs, uric acid crystals, and other deposits, may lead to the formation of stones, degeneration of the substance of the ureter, and eventually to that of the kidney itself. The stone, indeed, has long been known to be a prevalent disease in Egypt, and it is now known to arise from concretions formed round masses of Bilharzia eggs. From the portal vein, again, other Bilharzia may gain access to the rectum, or the liver, and it has also been found in the lungs, and may give rise to most serious complications, if indeed the patient lives.