A serologic study of naturally acquired leprosy in chimpanzees.

Data from longitudinally obtained serum samples spanning several years has permitted us to identify two chimpanzees with leprosy and to estimate the time of Mycobacterium leprae exposure/infection. The results confirm high levels of specific anti-M. leprae phenolic glycolipid-I (PGL-I) as well as anti-lipo-arabinomannan (anti-LAM) antibodies in both chimpanzees, and identify additional chimpanzees with possible M. leprae exposure. The observations are consistent with the hypothesis that leprosy exists in chimpanzees in the U.S.A. and suggest the possibility that M. leprae may be transmitted among chimpanzees. The data suggest that monitoring anti-PGL-I and anti-LAM IgG and IgM levels longitudinally in leprosy contacts may be useful in the recognition of preclinical leprosy.

HLA-linked control of predisposition to lepromatous leprosy.

In order to investigate if genes conferring susceptibility to leprosy and/or predisposition to a particular leprosy type are linked to HLA, we performed HLA-A and HLA-B typing on members of 29 families containing at least two siblings affected with leprosy from a leprosy endemic area in Jiangsu Province, People's Republic of China. Moreover, we performed a lepromin test in nearly all of the members of eight families containing at least two siblings affected with lepromatous leprosy. For 26 families the data permitted analyses of the segregation of parental HLA-haplotypes observed among children in relation to leprosy status. Siblings affected with lepromatous (LL or BL) leprosy shared parental HLA-haplotypes significantly more often than expected (p less than 0.05), and a highly significant deficit (p less than 0.0005) of shared HLA-haplotypes was observed among affected siblings discordant for leprosy type. These data confirm the HLA-linked control of leprosy type and, in particular, recently obtained evidence for linkage of predisposition to lepromatous leprosy with HLA. Healthy siblings did not share a haplotype more often than expected, and those haplotypes which were shared among all leprosy patients of a sibship did not occur less frequently than expected among the healthy siblings of the same sibship. The latter data confirm the absence of linkage of genes conferring susceptibility or resistance to leprosy with HLA. An analysis of the lepromin test results observed among healthy siblings showed no evidence for cosegregation of the results with HLA.