Analysis of genetic characteristics of MTB and multi-drug resistance genes of 54 retreated rifampicin-resistant tuberculosis patients
Objective To analyze the genetic characteristics of Mycobacterium tuberculosis(MTB)strains and drug resistance gene mutations in 54 cases of retreated rifampicin-resistant tuberculosis(RR-TB)patients.Methods Fifty-four retreated RR-TB patients who retained both initial and recurrent MTB strains were included in the study.A total of 54 pairs(108 strains)of MTB were collected at the time of initial and recurrent treatment,and their genotypes were detected by RD105 gene deletion method.15-locus variable number tandem repeat genotyping experiment(MIRU-VNTR)was used to determine the cause of the recurrent disease.We constructed a minimum spanning tree(MST)based on the MIRU-VNTR results of 54 cases of recurrent MTB,and analyzed the genetic characteristics of the strains.Molecular linear probe assay was used to analyze the mutations of rifampicin-resistant rpoB gene and isoniazid-resistant katG and inhA genes in re-treated RR-TB strains.Results All 108 MTB strains from the patients with retreated RR-TB were Beijing genotype.The proportion of endogenous reactivation in retreated RR-TB patients was 77.8%(42/54),while the proportion of exogenous reinfection was 22.2%(12/54).MST showed that 54 retreated RR-TB strains were divided into 3 clone complexes(CC1,CC2,CC3)and 13 unique genotypes;they had 48 genotypes in total,with a clustering rate of 11.1%.Molecular linear probe assay showed that there were 40 cases of mutations in the isoniazid-resistance genes katG and inhA,with a multidrug resistance rate of 74.1%(40/54).The rifampicin-resistant rpoB gene was mainly mutated at the S531L site(63.0%,34/54),while the isoniazid-resistant katG gene was mainly mutated at the S315T1 site(75.0%,30/40).Conclusions En-dogenous reactivation was the main cause of retreated RR-TB patients in Beijing area.The predominant strain was the Bei-jing genotype,showing high genetic diversity and low clustering rate.Most of the multidrug-resistant gene mutation sites were rpoB gene S531L site and katG gene S315T1 site.
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