The pathogenesis of leprosy in the nine-banded armadillo and the significance of IgM antibodies to PGL-1.

Twenty-seven nine-banded armadillos captured from the wild and tested free of wild M. leprae infection were distributed into four groups. They were injected at the right hind footpad with saline suspensions of M. Leprae at doses of 10(3), 10(4), 10(5) and 10(6). PGL-1 antibody levels were estimated using an ELISA test, twice during six months before the infection and every two months after the infection. One animal from each group was sacrificed at 6, 12, 18, 24, and 30-month intervals and another eight at unspecified intervals. A thorough autopsy and histopathological examination were conducted on all of them. Of the 27 animals, 18 developed the infection. In 10, there were granulomas at the site of inoculation and in 17 the regional lymph nodes were infected. The disease spread extensively to other lymph nodes and to the liver and spleen and then to the other organs. Peripheral nerves were invaded by M. leprae in only five animals. PGL-1 antibody levels registered a positive reading in only six of the 18 animals with the infection. In armadillo leprosy, the lesions did not persist at the site of entry in all animals M. leprae multiplied in the macrophages at the site of inoculation and the reticuloendothelial cells of the lymph nodes before they spread to other organs. There was evidence of invasion of endothelial cells of capillaries and possible bacteraemia even at an early phase of the infection. Peripheral nerves were not the preferred sites of entry or multiplication of M. leprae. Progressive increase in PGL-1 antibodies was recorded in five lepromatous armadillos with disseminated infection and high bacterial load. However, PGL-1 antibodies response was not sensitive enough to detect early disease.

Early infection with M. leprae and antibodies to phenolic glycolipid-I in the nine-banded armadillo.

Nine-banded armadillos were intravenously infected with 10(9) M. leprae. IgM antibodies to PGL-I were evaluated three times during the six months before and every two months after the infection. A thorough autopsy examination was done on animals that died or were sacrificed at intervals of 3, 4, 6, 12, 15 and 18 months after the infection. Three animals which had acquired the infection in the wild and one experimentally infected animal showed significant increases in antibody levels corresponding to their high bacterial load. In the other five experimentally infected animals, M. leprae infection was established in the cells of the reticulo endothelial system (RES) long before the IgM antibody levels to PGL-I became positive. It is possible that in human leprosy also M. leprae may enter and multiply in the RES initiating antibody production during the incubation period before clinical disease with neuritis becomes manifest.