| pubmed-article:10656117 | pubmed:abstractText | In this study we examined the mechanisms of resistance to rifampin (RMP) and isoniazid (INH) in 352 clinical isolates of Mycobacterium tuberculosis from Sevilla, Spain, using three different molecular methods: 1) PCR-single strand polymorphism analysis; 2) the commercial system Inno-LiPA RTB for RMP resistance; and 3) sequence analysis. Resistance to RMP was found in 21 strains, where the following mutations in the rpoB gene were detected: Ser531-->Leu (n = 14 strains); His526-->Asp (n = 3), Asn518-->Ser (n = 1), Gln513-->Leu (n = 1) and a nine nucleotide deletion (n = 1). Resistance to INH occurred in 29 strains, with mutations observed in: a) katG gene: Ser315-->Thr (n = 12), Ile304-->Val (n = 1), and a partial deletion (n = 4); b) regulatory region of the inhA gene: nucleotide substitution C209T (n = 3). No mutation was found in the ahpC promoter. | lld:pubmed |
