Flukes (Liver, Lung, and Intestinal)

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Chapter 293 Flukes (Liver, Lung, and Intestinal)

Several different trematodes, or flukes, can parasitize humans and cause disease. Flukes are endemic worldwide but are more prevalent in the less developed parts of the world. They include Schistosoma, or the blood flukes (Chapter 292), as well as fluke species that cause infection in the human biliary tree, lung tissue, and intestinal tract. These latter trematodes are characterized by complex life cycles. Sexual reproduction of adult worms in the definitive host produces eggs that are passed in the stool. Larvae, called miracidia, develop in freshwater. These, in turn, infect certain species of mollusks (snails or clams), in which asexual multiplication by parasite larvae produces cercariae. Cercariae then seek a 2nd intermediate host such as an insect, crustacean, or fish or attach to vegetation to produce infectious metacercariae. Humans acquire liver, lung, and intestinal fluke infections by eating uncooked, lightly cooked, pickled, or smoked foods containing these infectious parasite cysts. The “alternation of generations” requires that flukes parasitize more than 1 host (often 3) to complete their life cycle. Because parasitic flukes are dependent on these nonhuman species for transmission, the distribution of human fluke infection closely matches the ecologic range of the flukes.

Liver Flukes

Fascioliasis (Fasciola hepatica)

Fasciola hepatica, the sheep liver fluke, infects cattle, other ungulates, and occasionally humans. This infection affects ~17 million people worldwide and has been reported in many different parts of the world, particularly South America, Europe, Africa, China, Australia, and Cuba. Although F. hepatica is enzootic in North America, reported cases are extremely rare. Humans are infected by ingestion of metacercariae attached to vegetation, especially wild watercress, lettuce, and alfalfa. In the duodenum, the parasites excyst and penetrate the intestinal wall, liver capsule, and parenchyma. They wander for a few weeks before entering the bile ducts, where they mature. Adult F. hepatica (1-2.5 cm) commence oviposition approximately 12 wk after infection; the eggs are large (75-140 µm) and operculated. They pass to the intestines with bile and exit the body in the feces (see Fig. 292-1). On reaching freshwater, the eggs mature and hatch into miracidia, which infect specific snail intermediate hosts to multiply into many cercariae. These then emerge from infected snails and encyst on aquatic grasses and plants.

Clinical manifestations usually occur either during the liver migratory phase of the parasites or after their arrival at their final habitat in upper bile ducts. Fever, right upper quadrant pain, and hepatosplenomegaly characterize the 1st phase of illness. Peripheral blood eosinophilia is usually marked. As the worms enter bile ducts, most of the acute symptoms subside. On rare occasions, patients may suffer from obstructive jaundice or biliary cirrhosis, with signs of cholestasis, ascending cholangitis, cholelithiasis and jaundice with elevation in liver enzymes, direct bilirubin, and γ-glutamyl transpeptidase (GGT). F. hepatica infection is diagnosed by identifying the characteristic eggs in fecal smears or duodenal aspirates. Diagnosis can be suggested by positive serology and imaging that reveals acute hypodense liver lesions that change over time. Presentation can be dramatic in children, with features including generalized edema, hepatic cirrhosis with esophageal varices, and, in severe cases, death from generalized organ failure.

The recommended treatment of fascioliasis is triclabendazole (10 mg/kg once or twice PO) or bithionol (30-50 mg/kg once daily PO on alternate days for a total of 10-15 doses). In the USA, bithionol is available from the Centers for Disease Control and Prevention (telephone: 404-639-3670).

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