Clinical Pearls & Morning Reports
Fasciola hepatica is found throughout the world, with an estimated 2.4 million to 17 million persons infected. Since fascioliasis is not a reportable disease in the United States, accurate prevalence estimates are not available. Although the intermediate host — snails of the Lymnaeidae family — exists in the United States, most clinical cases in the United States are diagnosed in immigrants and returning travelers. Read the NEJM Clinical Problem-Solving Article here.
Q: How do humans become infected with F. hepatica?
A: Fascioliasis is a helminthic infection resulting from exposure to F. hepatica or F. gigantica. F. hepatica infection is common in sheep and cattle, but the pathogen can also cause disease that is sporadic or endemic in humans. Human fascioliasis most often results from the consumption of freshwater plants such as watercress and water chestnuts, to which the infective metacercariae attach themselves.
Q: What test is the mainstay of diagnosis in patients with acute F. hepatica infection?
A: Once they are ingested by humans, the metacercariae excyst (i.e., emerge from a cyst) in the intestine, and within a period of 2 to 24 hours, they migrate into the peritoneal cavity as immature flukes. After 48 hours, the larvae penetrate Glisson’s capsule, and over a period of 7 weeks, the immature flukes migrate through the liver parenchyma, resulting in necrosis and an eosinophilic infiltration. During this larval stage, the clinical symptoms and signs include right-upper-quadrant abdominal pain, weight loss, and fever, as well as eosinophilia resulting from the inflammatory response to the migrating larvae. Since antibodies to Fasciolidae can develop within 2 to 4 weeks after cyst ingestion, serologic testing is the mainstay of diagnosis in patients with an acute infection.
A: The acute symptoms of infection generally last 2 to 3 months and can include abdominal pain and nausea, which are related to larval migration through the intestine and liver parenchyma. During acute infection, immature larvae do not release eggs and are therefore not detected on stool examination. Dermatologic manifestations of acute infection include urticaria and migrating cutaneous nodules as a result of larval migration to the skin. Imaging of the liver shows characteristic hypoattenuating tracks extending from the liver capsule into the parenchyma due to larval penetration and migration. In the chronic, or biliary, stage of fascioliasis, adult hermaphrodite flukes release eggs in the hepatic and common bile duct of the host. This latent stage, which can last for decades, may be characterized by biliary obstruction, ascending cholangitis, acute pancreatitis, or mucosal erosion and hemobilia.
A: Although the treatment of choice for other trematodes is praziquantel, this agent is ineffective against F. hepatica. Triclabendazole has been used in veterinary practice for fascioliasis since 1983, with demonstrated efficacy against immature and mature forms of the liver fluke. After an outbreak of fascioliasis in Iran in 1989, a formulation of triclabendazole for use in humans was developed in Egypt and registered in December 1997. Triclabendazole is administered as a single dose of 10 mg per kilogram; two doses of 10 mg per kilogram, administered 12 to 24 hours apart, are given in severe cases.