Leishmaniasis in beige mice

Abstract

The courses of two protozoal diseases, cutaneous and visceral leishmaniasis, were examined in three groups of C57BL/6J mice. One group of mice was homozygous recessive for the beige gene (bg/bg). Beige mice are the genetic homologue of the human Chediak-Higashi syndrome and, among other defects, are profoundly deficient in natural killer cell activity. Wild-type (+/+) mice, which respond to experimental cutaneous or visceral leishmaniasis by eventually eliminating their parasites, and heterozygous beige (bg/+) mice served as controls; both are phenotypically normal in natural killer cell activity, which is particularly high in the spleen. In bg/bg mice, the course of Leishmania tropica, a causative agent of cutaneous leishmaniasis, was similar to that in control mice after both primary and cellular immune response to L. tropica antigen. However, bg/bg mice failed to eliminate mastigotes of Leishmania donovani, a causative agent of visceral leishmaniasis, from their spleens over an observation period of 56 days, in contrast to bg/+ and +/+ controls. Similar levels of anti-leishmanial antibody were produced by all groups of mice, and all mice responded comparably to footpad injections of L. donovani antigen. The results of this study suggest a possible role for natural killer cells in recovery from L. donovani but not from L. tropica infection.