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.