RESUMO
OBJECTIVE: To characterize the rpoB gene mutations of the rifampicin-resistant M. tuberculosis strains isolated in pulmonary tuberculosis patients from Mexico. MATERIAL AND METHODS: Thirty-seven clinical M. tuberculosis isolates cultured on Löwenstein-Jensen media and obtained from consecutive tuberculosis patients in 5 public hospitals were analyzed by PCR and the INNO-LiPA Rif TB for amplification and detection of mutations associated with rifampicin resistance, respectively. RESULTS: Twenty-three out of 37 isolates (62.2%) were found to be wild type (rifampicin susceptible), while 14 isolates (37.8%) contained mutations associated with rifampicin resistance. Seven out of the 37 isolates (18.9%) had a delta S1 mutation, in the nucleotide position number 511; one (2.7%) had a R4b mutation, in nucleotide H526D; five (13.5%) contained a R5 mutation, in nucleotide S531L; and one (2.7%) showed a double mutation delta S1/R4b. CONCLUSION: According to the marker used (rifampicin resistance), at least five different strains of M. tuberculosis circulate among pulmonary tuberculosis patients in Mexico. rpoB gene mutations associated with rifampicin resistance are common in Mexico. A single mutation in nucleotide 511 was the most frequently observed, followed by single mutations in nucleotides S531L and H526D.
Assuntos
Antibióticos Antituberculose/uso terapêutico , Farmacorresistência Bacteriana , Mutação , Mycobacterium tuberculosis/genética , Proteínas de Plantas/genética , Rifampina/uso terapêutico , Tuberculose Pulmonar/tratamento farmacológico , Tuberculose Pulmonar/microbiologia , RNA Polimerases Dirigidas por DNA , Hospitais Públicos , Humanos , México , Mycobacterium tuberculosis/efeitos dos fármacosRESUMO
A panel of samples, previously typed by serology, was retyped using a line probe assay. One sample from a Brazilian Caucasian individual was serologically typed as B52/B39, but showed an aberrant HLA-B pattern on the diagnostic strip and was typed as B*52012/B*39new. Further analysis by allele-specific amplification and subsequent sequencing of exons 2 and 3 revealed a G(B*3908)-to-T nucleotide substitution at position 467 (codon 156) resulting in an Arg (B*3908)-to-Leu substitution. Furthermore, the sequence revealed a silent mutation at position 174 (codon 58): a G(B*3908)-to-A nucleotide switch. The sequence has been sent to the EMBL databank and the HLA Nomenclature Committee, and the allele was named B*3913.