Pathogenesis

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After excystment, the metacercariae penetrate the intestine and enter the peritoneal cavity as immature flukes. They migrate to the liver after several days and penetrate Glisson's capsule during the acute hepatic phase of infection. After migration through the liver for 5-6 weeks, the worms enter the bile ducts to begin

Fig. 17.3 Fasciola hepatica adult (A) (~ 30 x 13 mm) and egg (B) (~ 140x75 |im). Reproduced by courtesy of Professor Prayong Radomyos, Faculty of Allied Health Services, Thammasat University, Thailand

the chronic biliary phase. The flukes mature after 3-4 months and begin to secrete eggs. Other routes of migration have been proposed including a hematogenous and biliary route (directly from the intestine). These theories seem less probable since worms have not been found in the circulation and do not reach the biliary tree until late in the disease course (Naquira-Vildoso and Marcial-Rojas, 1971).

The pathologic findings of the acute stage include focal hemorrhage and inflammation in the duodenum. When the flukes enter the liver, they digest hepatic tissue and cause inflammation, hemorrhage, dilated intrahepatic bile ducts, subcapsular cavities and surface liver nodules of 5-15 mm in diameter. Migration tracks from some of these nodules extend 1-2 cm into the parenchyma. These tracks contain cellular debris, Charcot-Leyden crystals, eosinophilic inflammation and sometimes flukes. The gall bladder also contains nodules as well as adhesions (Acosta-Ferreira et al., 1979). Inflammation is often present, which can result in fibrosis, thickening and dilatation of the extrahepatic bile ducts and gall bladder.

vaccines in animals include hemoglobin and a fatty-acid binding protein. Vaccination studies in mice with a schistosome antigen related to this fatty acid-binding protein protected against F. hepatica and schistosome challenge infection and raised the possibility of a dual helminth vaccine (Tendler et al., 1996).

F. hepatica has a number of immune evasion mechanisms that allow for chronic infections. Among the proposed mechanisms are rapid turnover of the glycocalyx and cleavage of surface-bound immunoglobulins by secreted proteases in order to prevent antibody-dependent cellular cytotoxicity (Carmona et al., 1993; Hanna, 1980; Hughes, 1985). These proteases have also been shown to be directly toxic to host cells and to be capable of degrading extracellular matrix components, which may assist in tissue migration (Berasain et al., 1997; Goose, 1978). Finally, these proteases may have host cytokine mimicry, which enables the fluke to control the immune response. A 28kDa protein has been isolated with interleukin-5-like activity, which stimulates production of a T helper cell type 2 response that may favor tolerance of the infection (Rifkin et al., 1996).

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