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Infection by Fasciola hepatica, the sheep liver fluke, results from ingestion of encysted metacercariae on watercress or other aquatic vegetables. Infection is prevalent in sheep-raising areas in many countries, especially parts of South America, the Middle East, and southern Europe, and it has increasingly been recognized in travelers to these areas. Fasciola gigantica has a more restricted distribution in Asia and Africa and causes similar findings. Eggs are passed from host feces into freshwater, leading to infection of snails, and then deposition of metacercariae on vegetation. In humans, metacercariae excyst, penetrate into the peritoneum, migrate through the liver, and mature in the bile ducts, where they cause local necrosis and abscess formation (eFigure 35–18).

eFigure 35–18.

Life cycles of Fasciola hepatica and Fasciola gigantica (liver flukes). Immature eggs are discharged in the biliary ducts and in the stool

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. Eggs become embryonated in water
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, eggs release miracidia
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, which invade a suitable snail intermediate host
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, including the genera Galba, Fossaria, and Pseudosuccinea. In the snail, the parasites undergo several developmental stages (sporocysts
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, rediae
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, and cercariae
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). The cercariae are released from the snail
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and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress
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. After ingestion, the metacercariae excyst in the duodenum
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and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults
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. In humans, maturation from metacercariae into adult flukes takes approximately 3–4 months. The adult flukes (F hepatica: up to 30 mm by 13 mm; F gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. F hepatica infects various animal species, mostly herbivores. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.)

Two clinical syndromes are seen, related to acute migration of worms and chronic infection of the biliary tract. Symptoms related to migration of larvae present 6–12 weeks after ingestion. Typical findings are abdominal pain, fever, malaise, weight loss, urticaria, eosinophilia, and leukocytosis. Tender hepatomegaly and elevated liver biochemical tests may be seen. Rarely, migration to other organs may lead to localized disease. The symptoms of worm migration subside after 2–4 months, followed by asymptomatic infection by adult worms or intermittent symptoms of biliary obstruction, with biliary colic and, at times, findings of cholangitis. Early diagnosis is difficult, as eggs are not found in the feces during the acute migratory phase of infection. Clinical suspicion should be based on clinical findings and marked eosinophilia in at risk individuals. CT and other imaging studies show hypodense migratory lesions of the liver. Definitive diagnosis is made by the identification of characteristic eggs in stool. Repeated examinations may be necessary. In chronic infection, imaging studies show masses obstructing the ...

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