ArticleAntimicrobial agents and chemotherapy2011
DNA gyrase inhibition assays are necessary to demonstrate fluoroquinolone resistance secondary to gyrB mutations in Mycobacterium tuberculosis.
Article in Antimicrobial agents and chemotherapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.
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Who cites it
19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 35 citations in OpenAlex.
- Pooled it
- Systematic review of allelic exchange experiments aimed at identifying mutations that confer drug resistance in Mycobacterium tuberculosis.The Journal of antimicrobial chemotherapy · 2014Pooled it
- Trial
- The stress response factor SigH mediates intrinsic resistance to multiple antibiotics inMicrobiology spectrum · 2026Article
- Review
- From mutation detection to treatment decisions: CRISPR-enabled diagnostics for drug-resistant tuberculosis.Frontiers in bioengineering and biotechnology · 2026Review
- Molecular mechanism of a triazole-containing inhibitor ofiScience · 2024Article
- Exploring antibiotic resistance mechanisms inFrontiers in microbiology · 2024Review
- Functional Characterization of the DNA Gyrases in Fluoroquinolone-Resistant Mutants of Francisella novicida.Antimicrobial agents and chemotherapy · 2017Article
- Role of gyrB Mutations in Pre-extensively and Extensively Drug-Resistant Tuberculosis in Thai Clinical Isolates.Antimicrobial agents and chemotherapy · 2016Article
- Specific gyrA gene mutations predict poor treatment outcome in MDR-TB.The Journal of antimicrobial chemotherapy · 2016Article
- Molecular diagnosis of fluoroquinolone resistance in Mycobacterium tuberculosis.Antimicrobial agents and chemotherapy · 2015Article
- Prevalence and molecular characterization of fluoroquinolone-resistant Mycobacterium tuberculosis isolates in China.Antimicrobial agents and chemotherapy · 2014Article
- Detection of second-line drug resistance in Mycobacterium tuberculosis using oligonucleotide microarrays.BMC infectious diseases · 2013Article
- Importance of the genetic diversity within the Mycobacterium tuberculosis complex for the development of novel antibiotics and diagnostic tests of drug resistance.Antimicrobial agents and chemotherapy · 2012Review
- Molecular characterization of multidrug- and extensively drug-resistant Mycobacterium tuberculosis strains in Jiangxi, China.Journal of clinical microbiology · 2012Article
- Extending the definition of the GyrB quinolone resistance-determining region in Mycobacterium tuberculosis DNA gyrase for assessing fluoroquinolone resistance in M. tuberculosis.Antimicrobial agents and chemotherapy · 2012Article
- Impact of amino acid substitutions in B subunit of DNA gyrase in Mycobacterium leprae on fluoroquinolone resistance.PLoS neglected tropical diseases · 2012Article
- New insights into fluoroquinolone resistance in Mycobacterium tuberculosis: functional genetic analysis of gyrA and gyrB mutations.PloS one · 2012Article
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The main mechanism of fluoroquinolone (FQ) resistance in Mycobacterium tuberculosis is mutation in DNA gyrase (GyrA(2)GyrB(2)), especially in gyrA. However, the discovery of unknown mutations in gyrB whose implication in FQ resistance is unclear has become more frequent. We investigated the impact on FQ susceptibility of eight gyrB mutations in M. tuberculosis clinical strains, three of which were previously identified in an FQ-resistant strain. We measured FQ MICs and also DNA gyrase inhibition by FQs in order to clarify the role of these mutations in FQ resistance. Wild-type GyrA, wild-type GyrB, and mutant GyrB subunits produced from engineered gyrB alleles by mutagenesis were overexpressed in Escherichia coli, purified to homogeneity, and used to reconstitute highly active gyrase complexes. MICs and DNA gyrase inhibition were determined for moxifloxacin, gatifloxacin, ofloxacin, levofloxacin, and enoxacin. We demonstrated that the eight substitutions in GyrB (D473N, P478A, R485H, S486F, A506G, A547V, G551R, and G559A), recently identified in FQ-resistant clinical strains or encountered in M. tuberculosis strains isolated in France, are not implicated in FQ resistance. These results underline that, as opposed to phenotypic FQ susceptibility testing, the DNA gyrase inhibition assay is the only way to prove the role of a DNA gyrase mutation in FQ resistance. Therefore, the use of FQ in the treatment of tuberculosis (TB) patients should not be ruled out only on the basis of the presence of mutations in gyrB.
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