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Laboratory Diagnosis The diagnosis of fascioliasis is established by serological tests and by identifying the large operculated eggs in feces or in material obtained by duodenal or biliary drainage. The eggs of F. hepatica cannot be reliably differentiated from those of Fasciolopsis buski, the giant intestinal fluke of man, which they resemble. Serodiagnosis is the diagnostic test of choice in fascioliasis, especially in the acute phase, since eggs are not present in stools for the first 2-3 months of infection. Serologic diagnosis using F. hepatica excretion-secretion antigens (e.g., ELISA) has been successful in endemic areas. Patients remain seropositive for many years after infection. There is some cross-reaction with other flukes, such as Schistosoma. F. hepatica antigen reportedly produces a specific intradermal reaction, and precipitin reactions also appear to be specific. The indirect hemagglutination test has a 100% diagnostic sensitivity and 97% specificity, if the metabolic antigen is used. The diagnosis of fascioliasis has also been made by liver biopsy, but this is usually accidental in biopsies done for other purposes. There is often a high blood eosinophilia in fascioliasis, up to 68% having been recorded in severe infections and in the pharyngeal tissue phase. Anemia and leukocytosis may be present. The erythrocyte sedimentation rate is increased and various liver function tests, such as cephalin flocculation and thymol turbidity tests, bilirubin, alkaline phosphatase, and transaminase may be elevated as a manifestation of liver dysfunction. Hypergammaglobulinemia is often present. Clinical Characteristics Clinical symptoms of fascioliasis will vary, depending on the severity of the infection and stage of the disease. In the acute invasive phase, where the young larvae are migrating through the liver parenchyma, there may be a transient period of dyspepsia with characteristically high fever lasting many weeks. There is pain over the liver, which is enlarged and tender. Other symptoms such as anorexia, prostration, muscle, joint and shoulder pains, headache, nausea and vomiting may also be present. Occasionally, marked wasting, jaundice, pruritus, urticaria, and pallor are seen. The acute phase of the disease is thus characterized by allergic, immunological and toxic reactions. The triad of painful, tender hepatomegaly, fever and marked eosinophilia is highly suggestive of fascioliasis in an endemic area. The chronic or latent phase of fascioliasis may last for months or even years, and develops after the larvae have reached the bile ducts and after the parenchymal destruction seen in the acute invasive phase subsides, with healing and regeneration. In the chronic phase, there are usually few symptoms unless the adult flukes have caused significant epithelial proliferation and obstruction of the biliary ducts with subsequent biliary cirrhosis and jaundice. Frequently, this chronic form of the disease is unrecognized in endemic areas, being misdiagnosed as biliary disease of other etiology. There may be diffuse abdominal pain, chiefly in the right upper quadrant and epigastrium, nausea, vomiting, dyspepsia, diarrhea, and occasionally hepatomegaly, splenomegaly and jaundice. Eosinophilia is seen in 50% of patients. Obstruction of the extrahepatic bile ducts by the adult flukes, biliary sludge and stones may produce a clinical picture similar to choledocholithiasis. At peritoneoscopy or surgical exploration the liver may be normal or diffusely enlarged. The gallbladder may be normal or involved with fibrosis, calculi, flukes, and empyema. The common bile duct may show marked dilatation and fibrosis and adult flukes and stones may be present. Some investigators conclude that the parasite is a factor in the formation of calculi, since stones in the gallbladder or common duct are not infrequent in patients with chronic fascioliasis. Mechanical obstruction and dilatation of the biliary ducts caused by the adult parasites, hyperplasia of the ductal epithelium, biliary sand or sludge, and fibrosis and calcification of the walls of the ducts have all been reported. Unlike clonorchiasis and opisthorchiasis, there is as yet no proven relationship between fascioliasis and cholangiocellular carcinoma. Pharyngeal Fascioliasis (Halzoun). In Lebanon, Armenia, and the Middle East, the local habit of eating raw sheep or goat livers causes halzoun, which results from the lodging of adult worms such as Fasciola hepatica or perhaps Linguatula serrata (tongue worms) on the pharyngeal mucosa, resulting in transient but distressing pharyngeal edema and occasionally obstruction. Dysphagia and dyspnea, with a feeling of suffocation, are commonly present. |
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Copyright: Palmer and Reeder