The sequence of changes in the activity of six disaccharidases in the small intestine of gerbils during primary and secondary G lamblia infections was examined. The primary G lamblia infection induced a transient reduction in disaccharidase activity which was related to the highest trophozoite burden in the small intestine. During the primary exposure, a 30% to 85% decrease in the activity of enzymes was observed on days 10 and 20 after infection. Secondary exposure of gerbils to G lamblia caused a sharp decrease in disaccharidase activity as early as 24 h after challenge. The reduction in the enzyme activity was not influenced by the size of the challenge inoculum and occurred even when there were no live trophozoites in the small intestine. Disaccharidase deficiency could also be induced by challenge with the soluble extract of the trophozoites. Multiple challenge administrations of G lamblia trophozoites to gerbils induced a persistent disaccharidase deficiency. The results indicate that disaccharidase deficiency associated with the primary G lamblia infection probably represents a direct effect of the parasite on the brush border of the small intestine. On the other hand, the observed disaccharidase deficiency in the secondary G lamblia infection appears to be induced by the local immune responses of the host.
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