Detection of Mutations in Mycobacterium tuberculosis by a Dot Blot Hybridization Strategy

Genomic variation in any organism is of interest, because it may influence the phenotype of the organism. Special interest currently focuses on prokaryotic pathogens regarding mutations associated with resistance to therapeutic drugs, as well as those mutations involved in the evolution of the bacillus. The molecular basis of drug resistance in Mycobacterium tuberculosis to the front-line drugs is not mediated via plasmids, but is largely, if not entirely, owing to mutations in specific genes of M. tuberculosis. To date, 13 genes are known to be linked to resistance and many functional mutations have been described in these genes (1,2). However, the katG463 (Arg→Leu) and gyrA95 (Thr→Ser) mutations have no apparent relationship to drug resistance, and the combination of these two polymorphisms has been used to place clinical isolates of the M. tuberculosis complex into three evolutionary distinct genotypic groups (3).