Fasciolosis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
The development of infection in definitive host is divided into two phases: the parenchymal (migratory) phase and the biliary phase.[1] The parenchymal phase begins when excysted juvenile flukes penetrate the intestinal wall. After the penetration of the intestine, flukes migrate within the abdominal cavity and penetrate the liver or other organs. F. hepatica has a strong predilection for the tissues of the liver.[2] Occasionally, ectopic locations of flukes such as the lungs, diaphragm, intestinal wall, kidneys, and subcutaneous tissue can occur.[3][4] During the migration of flukes, tissues are mechanically destroyed and inflammation appears around migratory tracks of flukes. The second phase (the biliary phase) begins when parasites enter the biliary ducts of the liver. In biliary ducts, flukes mature, feed on blood, and produce eggs. Hypertrophy of biliar ducts associated with obstruction of the lumen occurs as a result of tissue damage.
References
- ↑ Dubinský, P., 1993. Trematódy a trematodózy. In: Jurášek, V., Dubinský, P. a kolektív, Veterinárna parazitológia. Príroda a.s., Bratislava, 158–187. (in Slovakian)
- ↑ Behm, C.A., Sangster, N.C., 1999. Pathology, pathophysiology and clinical aspects. In: Dalton, J.P. (Ed.), Fasciolosis. CAB International Publishing, Wallingford, pp. 185–224.
- ↑ Boray, J.C., 1969. Experimental fascioliasis in Australia. Adv. Parasitol. 7, 95–209.
- ↑