Infection of normal mice by the intestinal protozoan Giardia muris is self-limited and is followed by resistance to subsequent reinfection (1, 2). Similar observations have been made in G. lamblia infection in limited studies in human volunteers (3). The nature and mechanism of this parasite elimination are, however, unclear. Immune mechanisms may be suspected in human infection with G. lamblia because of the high prevalence of chronic giardiasis in persons with variable immune deficiency syndrome (4). Congenitally hypothymic (nude, nu/nu) mice provide a useful model to test the contribution of thymus-dependent immune mechanisms in resolution of this protozoan infection. We have previously described the natural history of G. muris infection in mice (1). The infection can be measured by counting trophozoites in small intestine and cysts in feces; peak fecal cyst excretion occurs 1 to 2 weeks after oral inoculation of cysts in CF-1 outbred mice and in A/J and BALB/c inbred strains followed consistently by resolution of infection in 4 to 7 weeks (1, 2).


This work was supported by a grant-in-aid from the Rockefeller Foundation.

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