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American Journal of Pathology, Vol 117, 81-91, Copyright © 1984 by American Society for Investigative Pathology
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V Tsutsumi, R Mena-Lopez, F Anaya-Velazquez and A Martinez-Palomo
The complete sequence of morphologic events during amebic liver abscess formation in the hamster has been studied, from the lodgement of amebas in the hepatic sinusoids to the development of extensive liver necrosis. Following intraportal inoculation of live amebas, the early stages of the lesion (from 1 to 12 hours) were characterized by acute cellular infiltration composed of an increasingly large number of polymorphonuclear leukocytes, which surrounded centrally located trophozoites. Histiocytes and lysed leukocytes were situated on the periphery of the lesions. Hepatocytes close to the early lesions showed degenerative changes which led to necrosis; however, direct contact of liver cells with amebas was very rarely observed. At later stages, the extent of necrosis increased, macrophages and epithelioid cells replaced most leukocytes, and well-organized granulomas developed. Extensive necrosis associated with fused granulomas was present by Day 7. The results suggest that Entamoeba histolytica trophozoites do not produce amebic liver abscesses in hamsters through direct lysis of hepatocytes. Rather, tissue destruction is the result of the accumulation and subsequent lysis of leukocytes and macrophages surrounding the amebas.
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