Passive immunization during experimental amebic liver-abscess development.
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Biomedical subjects
M Shibayama-Salas
Publications and source records attributed to M Shibayama-Salas.
Active immunization in hamsters with live Entamoeba histolytica trophozoites of low virulence.
Live trophozoites of Entamoeba histolytica of low virulence (LV) were inoculated intraportally in hamsters. One week later they were challenged intrahepatically with highly virulent (HV) trophozoites of the same strain and sacrificed 1 week later. Significant protection manifested by the production of smaller lesions was observed in immunized animals. Antiamebic IgG levels were significantly higher in the immunized group. Histologically, livers of immunized animals presented small lesions containing foamy macrophages, epithelioid cells, fibroblasts and devoid of amebas. Lymphocyte and plasma cell infiltrates were seen periportally.
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Early invasive intestinal amebiasis in Mongolian gerbils.
Mongolian gerbils were inoculated intracecally with E. histolytica trophozoites cultured monoxenically. During the first hours of interaction an increase in mucus production was observed. Microulcerative mucosal lesions appeared 24 to 72 h post-inoculation. Inflammatory infiltrate and edema of the lamina propria were associated with necrotic foci. At 96 h, the cecal mucosa was normal and live amebas were no longer detected. It is concluded that gerbils are useful as experimental models for studying the early stages of invasive intestinal amebiasis.
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Morphological characterization of experimental amebic liver lesions in gerbils.
Gerbils are susceptible to amebic liver abscess (ALA) production under experimental conditions. However, little is known about the histopathological changes that occur during the evolution of the lesion. We analyzed microscopically the sequence of cellular events of ALA in gerbils inoculated intraportally or intrahepatically with E. histolytica. At early stages trophozoites were associated with different degrees of inflammatory reaction. Amebas were also observed in areas devoid of inflammatory cells. Damaged hepatocytes were either related or not to inflammatory reaction. At late stages, lysis of macrophages and epithelioid cells were seen in relation to necrotic tissue and trophozoites. We conclude that amebic liver necrosis in gerbils at early stages may result from lysis of inflammatory cells as shown previously by us in hamsters, but also by direct contact and lytic activity of amebas to hepatocytes. The late destruction and expansion of hepatic tissue necrosis is apparently associated with damage of macrophages and epithelioid cells.
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Histological changes during healing of experimental amebic liver abscess treated with metronidazole.
Morphological changes during the healing of amebic liver abscess (ALA) in hamsters treated with metronidazole were studied. Animals with ALA of 4 days of evolution were treated orally with metronidazole (5 mg/100 g for 10 days). Liver samples were studied at different times from the beginning of treatment up to 22 days. The resolution of ALA was accompanied by chronic inflammatory reaction, increased number of foamy macrophages and gradual disappearance of the granulomas. Neoformed hepatocytes and blood vessels, and proliferation of biliary ducts were also observed. Foamy macrophages play an important role in the adequate healing of ALA.
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