Growth, activities of enzymes in the small intestine, and ultrastructure of microvillous border in gerbils infected with Giardia duodenalis

Abstract

The aim of this study was to assess and correlate changes in weight gain, food intake, small intestinal disaccharidase activities and microvillous border surface area over the course of a primary Giardia duodenalis infection in weanling Mongolian gerbils (Meriones unguiculatus). Weight gain in infected animals was significantly impaired between days 8 and 20 postinoculation when compared to age-and weight-matched controls. No difference in food intake was observed between groups. Trophozoite population in the small intestine was maximal on day 4 and 6 of infection, and colonization persisted in the duodenum throughout the experiment (30 days). In infected gerbils, mucosal sucrase and maltase activities were significantly depressed in the duodenum and jejunum on day 4 and in all areas of the small intestine by day 6. Eight and 25 days postinoculation, disaccharidase activities had recovered in the jejunum and distal small intestine but remained depressed in the duodenum, the area where trophozoite colonization persisted. Diffuse loss of microvillous border surface area was observed in the duodenum and jejunum after 6 days of infection. Eight days postinoculation, microvillus surface area had returned to normal in the jejunum, but not in the duodenum. Our findings demonstrate that acute giardiasis in weanling gerbils impairs weight gain, depresses disaccharidase activities, and diffusely reduces mucosal microvillous border surface area. The brush border injury occurred at times and sites of maximal trophozoite colonization and correlated with disaccharidase impairment. This is the first report of a diffuse mucosal injury associated with giardiasis. We postulate that Giardia infection impairs small intestinal function by markedly decreasing microvillous border surface area and that this mechanism explains in part retarded growth and appearance of symptoms associated with the disease. © 1991 Springer-Verlag.