Since Mycobacterium leprae, the causative organism of Leprosy, proliferate inside macrophages, it has been speculated that catalase encoded by the katG gene may protect acid-fast bacilli from the deleterious effects of peroxide generated from
macrophage
and may play a crucial role in the survival of M. leprae in vivo. The homology of E. coli katG gene is also identified from M. tuberculosis and M. leprae recently. However, the katG gene of M. leprae is thought to be a pseudogene, unlike that of
M.
tuberculosis, because it contains multiple deletions, implicating that isoniazid(INH), which is activated to a potent tuberculocidal agent by catalase encoded by the katG gene, is unlikely to be of therapeutic benefit to leprosy patients.
We have tested 1) the role of KatG protein in activation of INH by using INH susceptible test of M. smegmatis mc2155 and BH1, and 2) the effect of INH on M. leprae growth by radiorespirometric assay to examine the catalase-like activity in M.
leprae. It
was found that the viability of M. leprae was decreased at 20㎍/㎖ of INH and higher concentrations.
We confirmed the role of KatG protein in activation of INH and our results suggest that a catalase-like activity other than katG is present in M. leprae.
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