Antigen-specific cellular and humoral responses are induced by intradermal Mycobacterium leprae infection of the mouse ear.

Leprosy is caused by infection with Mycobacterium leprae. The immune response of leprosy patients can be highly diverse, ranging from strong cellular responses accompanied by an apparent deficit of M. leprae-specific antibodies to strong humoral responses with a deficit of cell-mediated responses. Leprosy takes many years to manifest, and this has precluded analyses of disease and immune response development in infected humans. In an attempt to better define development of the immune response during leprosy we have developed an M. leprae ear infection model. Intradermal inoculation of M. leprae into the ear supported not only infection but also the development of a chronic inflammatory response. The inflammatory response was localized, comprising a T-cell infiltration into the ear and congestion of cells in the draining lymph nodes. The development of local chronic inflammation was prevented by rifampin treatment. Importantly, and in contrast to subcutaneous M. leprae footpad infection, systemic M. leprae-specific gamma interferon and antibody responses were detected following intradermal ear infection. These results indicate the utility of intradermal ear infection for both induction and understanding of the immune response during M. leprae infection and the identification or testing of new leprosy treatments.

Seasonal and spatial trends in the detectability of leprosy in wild armadillos.

A survey for leprosy among 565 armadillos from Louisiana and Texas found IgM antibodies to the phenolic glycolipid-1 antigen of Mycobacterium leprae in 16% of the animals. There were no geographic trends in the distribution of prevalence rates between the sites and the disease probably has a much greater range. Repeat observations in one location showed significant seasonal variations in the observable antibody prevalence rate, but the yearly average remained similar. Infected armadillos tended to be heavier, and the females usually had plasma progesterone concentrations indicative of sexual maturity. Using these characteristics to stratify the populations into adult and sub-adult cohorts, variations in the observable leprosy prevalence rate were seen to be proportional to changes in the age structure of the populations. Leprosy appears to be maintained in steady state within some regions, and nearly a third of the adult armadillos in Louisiana and Texas harbour M. leprae.

The effect of body temperature and cell-mediated immunity on the growth of Mycobacterium marinum and Mycobacterium leprae in mice.

Evidence is presented that the high susceptibility of armadillos to infection with Mycobacterium leprae cannot be explained solely in terms of body temperature because mutant mice maintained with a body temperature similar to that of armadillos do not become heavily infected with M. leprae. The depression of cell-mediated immunity accompanying the low body temperature is not sufficient to produce an overwhelming infection. The results obtained with M. marinum suggest that whereas lack of cell-mediated immunity or a low body temperature result in a moderately enhanced infection in the mouse a combination of both of these factors is required to produce an overwhelming infection involving the internal organs.

Airborne infection with Mycobacterium leprae in mice.

Although the portal of entry and mode of spread of M. leprae in human leprosy are still uncertain, it is widely held that direct person-to-person skin contact is important. This assumption has ignored the fact that patients with highly bacilliferous leprosy have nasal as well as dermal infection and that, since M. leprae is shed predominantly from the nose, leprosy might be an airborne infection. The present study was designed to investigate this possibility with mice exposed to airborne infection with M. leprae. The conditions are described in which thymectomised-irradiated CBA strain mice exposed to M. leprae aerosols sustained an immediate lung retention of 1 X 10(5) bacteria. Fourteen to 24 months later, 33% (10 of 30) of the mice had countable numbers of acid-fast bacilli (greater than 2 X 10(4)) with the characteristics of M. leprae in one or more homogenates prepared from ears, foot pads, nose or lungs. Evidence is presented from the distribution of M. leprae that the infection had arisen from systemic spresd of bacilli initially entering the lungs rather than from multiplication of organisms locally retained there, or in the nose, at the time of airborne infection. The relevance of these results to the possible route of infection of leprosy in man is discussed.