[Development of experimental model animals for disseminated Mycobacterium avium complex infections using immunodeficient mice and rats].

In order to establish an animal model for disseminated M. avium complex (MAC) infections frequently encountered in AIDS patients, we studied growth of M. intracellulare in visceral organs (lungs, livers, spleens, kidneys), in blood, and in footpads of mice with defined immunodeficiencies, such as SCID mice with T and B cell-defect, BALB/c athymic nude mice with matured T cell-defect, and beige mice with NK cell-defect. In addition, Sprague-Dawley rats with acquired immunodeficiency induced by cyclosporine-treatment were also examined. The following results were obtained. 1) SCID mice: First, SCID mice were infected sc with 6.1 x 10(6) CFU of M. intracellulare N-260 (virulent SmT colonial variant) into the hind footpad. The organisms grew in the footpad remarkably during the 12 weeks after infection in SCID mice, where the growth rate was much greater than that in CB-17 strain mice with the same genotype as SCID mice and in BALB/c mice with Bcgs genotype (CB-17 and BALB/c mice are MAC-susceptible). Furthermore, in SCID mice, bacteremia and dissemination of organisms to the visceral organs were observed but not in the two control strains of mice. Second, SCID mice were infected i.v. with 4.8 x 10(6) CFU. The bacterial loads in the viscera of SCID mice after infection were larger than those of CB-17 mice except for livers. However, the incidence and the degree of gross lung lesions were much less in SCID mice compared to CB-17 mice, presumably due to the defect in T cell-mediated immune reactions in SCID mice.(ABSTRACT TRUNCATED AT 250 WORDS)