The life cycle is direct. Environmentally resistant and infectious cysts are passed in the feces. Excystation occurs following ingestion. The minimum infectious dose for a mouse is approximately 10 cysts. Shortly after excystment, trophozoites divide longitudinally and colonize the mucosal surface of the proximal small intestine, adhering to columnar cells near the bases of intestinal villi and moving within the mucus layer on the mucosa.
Most infections are asymptomatic.
When apparent, clinical signs are nonspecific and include weight loss, stunted growth, rough coat, and enlarged abdomen. Strain differences in susceptibility have been observed. The bases for these differences are unknown, although both MHC and non-MHC genes appear to influence the outcome of primary G. muris infections. In addition, male mice shed cysts in their feces longer than females do and trophozoites are present in their intestines for a longer period than in females. Protective immunity is dependent upon both cellular and humoral mechanisms, with IFN-gamma somehow playing a role in clearance of trophozoites.