Epidemiology and Pathology

Fasciola hepatica is a large fluke measuring approximately 3.0 x 1.3 cm. The adults live in the biliary passages of man or herbivores for 8-9 years, where the operculated eggs (140 x 80 µm) are laid and subsequently passed in the feces. After embryomating in water for 10-15 days, the miracidia escape from the eggs and penetrate a snail of the genus Lymnaea. In this intermediate snail host, the miracidium is transformed into a sporocyst and within 4-5 weeks rediae and, later, cercariae are produced. The mature cercariae leave the snail and swim about for several hours until they adhere to the surface of aquatic plants, such as watercress, where they encyst to become metacercariae. The metacercariae are ingested by animals eating the aquatic vegetation or drinking from the contaminated pools. These metacercariae excyst in the duodenum, migrate through the duodenal wall into the peritoneal cavity, and penetrate Glisson's capsule of the liver. They then migrate throughout the hepatic parenchyma, various alterations until they reach the biliary ducts, where they mature to adult flukes within 3-4 months. Man acquires fascioliasis by eating raw watercress or other aquatic plants in the form of salads or juices, or by drinking water contaminated with metacercariae in meadows frequented by sheep.

When sheep, goats or cattle are infected with F. hepatica, there is characteristically extensive liver damage (liver rot). On the other hand, fascioliasis in humans is usually a mild disease, related to the worm burden as in other helminthic infections; humans obviously ingest less contaminated watercress than grazing herbivores. However, in occasional patients with severe infection, the biliary ducts will show hyperplasia, necrosis, and cystic dilatation with leukocytic infiltration, with similar changes seen together with flukes in the gallbladder at times. Occasionally, adult worms may occlude the common bile duct or hepatic ducts (Fig. 21.27). Most patients recover spontaneously with evacuation of the flukes via the intestinal tract. Fibrosis of the portal tracts with compression of adjacent liver cells and calcification of the biliary ducts may occur.

In the stage of active invasion, the young larvae may destroy some liver parenchyma in their migrations and cause varying degrees of necrosis, fibrosis, and microabcesses. In extensive infections, the parasites may migrate back and forth into the liver parenchyma to deposit their eggs, producing additional liver damage and fibrosis. The association of fascioliasis with portal hypertension, splenomegaly, and ascites is as yet unproven. Migrating larvae may cause ectopic fascioliasis; flukes have been reported in the blood vessels, lungs, subcutaneous tissues, ventricles of the brain, and orbits.

Fig. 21.27 Fasciola hepatica flukes in the main bile ducts producing marked dilatation, thickening and tortuosity of the ducts in this necropsy specimen of the liver. The adjacent hepatic tissue is inflamed and compressed.