A model for experimental cecal and hepatic amebiasis was developed and characterized in the gerbil (Meriones unguiculatus). Pathogenic and non-pathogenic Entamoeba histolytica strains were shown to cause damage in the cecum, proportional to their previous behavior in humans. Secretion of intestinal mucus, crypt hyperplasia and cytolysis of interglandular epithelium were prerequisites for amebic invasion. Ulcerative lesions with destruction of mucosal and submucosal tissues led to amebic dissemination to the liver. Formation of amebic liver abscesses followed subacute changes in the liver. Liver lesions resulted from the cytolytic effects of the enzymes of destroyed neutrophils. Growth of liver abscesses followed cytolysis of the fibrogranuloma walls. Immunodepression in amebiasis was confirmed by serologic findings and histologic alterations in the lymph nodes and spleen, and by a lowered antiamebic effect of lymphoid cells in vitro. A neutrophil stimulating and chemotactic factor from pathogenic amebic membranes was isolated and characterized. It was shown that both host and parasite factors are involved in the pathogenesis and pathology of amebiasis.

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Studies using Mongolian gerbils found that during a primary infection with Giardia lamblia trophozoites, disaccharidase activities were decreased from day 10 post-infection (p.i.) until well past elimination of the parasite. However, during a challenge infection, enzyme deficiencies were short-lived. A challenge with a soluble extract of G. lamblia trophozoites also resulted in reductions in disaccharidase activity. The degree of these reductions in enzyme activity was dependent on the extract dose. Gel filtration of the trophozoite crude extract resulted in fractions F1, F2, and F3. However, only a challenge with F1 led to disaccharidase deficiencies. Further separation of F1 resulted in fractions F1a and F1b. Impairments of enzyme activity were obtained only in gerbils challenged with F1b. Protein analysis of F1b revealed several high and low molecular weight bands. When gerbils previously exposed to G. lamblia were challenged with an extract of Entamoeba histolytica trophozoites, disaccharidase activities remained comparable to controls. Moreover, enzyme levels in gerbils challenged with excretory/secretory G. lumblia products were affected in a manner which was inconsistent with the live parasitic challenge. Results suggest that the disaccharidase deficiencies in giardiasis are parasite-specific and are induced by a heat-stable constituent(s) of fraction F1b, possibly through an immune response to an antigenic component of this parasite fraction.

No description available.