The wide spread emergence of isolates of Mycobacterium tuberculosis(M. tuberculosis) resistant to one or more antituberculous drugs represents one of the most alarming corollaries of AIDS related tuberculosis during recent years. Delayed detection, identification, and susceptibility testing of drug resistant isolates and failure to appropriately isolate contagious patients and to begin adequate chemotherapy have all been identified as predisposing factors of transmission of drug resistant M. tuberculosis (1). Molecular bases of drug resistance have been identified for all of the main antituberculous drugs, and drug resistance results from changes in several target genes, some of which are still undefined (2,3). These factors highlights the need to implement the rapid detection of drug resistance, for better management of patients as well as for control of the outbreaks and prevention of future nosocomial drug- resistant tuberculosis transmission (4).
Drug resistance in M. tuberculosis is due to the acquisition of mutations in chromosomally encoded genes and the generation of multidrug resistance is a consequence of serial accumulation of mutations primarily due to inadequate therapy (5, 6).
Several studies have shown that resistance to isoniazid (INTI) is due to mutaions in kat G gene. The rpo B gene, which encodes te subunit of RNA polymerase, harbors a mutation in an 81 bp region in about 95% of rifampicin (RIF) reistant M. tuberculosis strains recovered globally (6,7). Streptomycin (STR) resistance is due to mutations in rrs and rpsl genes which encodes 16S SrRNA and ribosomal protein S12 respectively (6, 8). Approximately 65% of clinical isolates resistant to ethambutol have a mutation in the embB gene (9, 10)
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