ArticleAntimicrobial agents and chemotherapy2016
Role of gyrB Mutations in Pre-extensively and Extensively Drug-Resistant Tuberculosis in Thai Clinical Isolates.
Article in Antimicrobial agents and chemotherapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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17 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Pre-extensively and extensively drug-resistant tuberculosis prevalence among multidrug-resistant tuberculosis cases in Ethiopia: A systematic review and meta-analysis.PLoS neglected tropical diseases · 2026Pooled it
- Emergence of extensively and pan-drug resistance in clinical bacterial isolates: A systematic scoping review from Ethiopian public health perspective.PLoS neglected tropical diseases · 2025Article
- Private and well drinking water are reservoirs for antimicrobial resistant bacteria.npj antimicrobials and resistance · 2024Article
- Multilevel Pre-extensively Drug-resistant Tubercular Spondylodiscitis: Underdiagnosed or Overlooked? A Case Report.Journal of orthopaedic case reports · 2024Article
- Quantitative measurement of antibiotic resistance in Mycobacterium tuberculosis reveals genetic determinants of resistance and susceptibility in a target gene approach.Nature communications · 2024Article
- Quantitative measurement of antibiotic resistance inResearch square · 2023Article
- OvercomingActa pharmaceutica Sinica. B · 2022Review
- Genome-wide association studies of global Mycobacterium tuberculosis resistance to 13 antimicrobials in 10,228 genomes identify new resistance mechanisms.PLoS biology · 2022Article
- Whole-genome sequencing ofEpidemiology and infection · 2022Article
- Elucidating the Antimycobacterial Mechanism of Action of Ciprofloxacin Using Metabolomics.Microorganisms · 2021Article
- Computational modeling and bioinformatic analyses of functional mutations in drug target genes inComputational and structural biotechnology journal · 2021Article
- Pre-extensively drug-resistant tuberculosis spondylodiscitis in an immunocompetent patient: a case report.The Pan African medical journal · 2020Article
- Detection of Second Line Drug Resistance among Drug Resistant Mycobacterium Tuberculosis Isolates in Botswana.Pathogens (Basel, Switzerland) · 2019Article
- Mutation and Transmission Profiles of Second-Line Drug Resistance in Clinical Isolates of Drug-ResistantFrontiers in microbiology · 2019Article
- Article
- A Review of Moxifloxacin for the Treatment of Drug-Susceptible Tuberculosis.Journal of clinical pharmacology · 2017Review
- Clinical outcomes and molecular characterization of drug-resistant tuberculosis in pre- and extensively drug-resistant disease based on line probe assays.The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious DiseasesArticle
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7 authors at 3 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
DNA gyrase mutations are a major cause of quinolone resistance in Mycobacterium tuberculosis We therefore conducted the first comprehensive study to determine the diversity of gyrase mutations in pre-extensively drug-resistant (pre-XDR) (n = 71) and extensively drug-resistant (XDR) (n = 30) Thai clinical tuberculosis (TB) isolates. All pre-XDR-TB and XDR-TB isolates carried at least one mutation within the quinolone resistance-determining region of GyrA (G88A [1.1%], A90V [17.4%], S91P [1.1%], or D94A/G/H/N/V/Y [72.7%]) or GyrB (D533A [1.1%], N538D [1.1%], or E540D [2.2%]). MIC and DNA gyrase supercoiling inhibition assays were performed to determine the role of gyrase mutations in quinolone resistance. Compared to the MICs against M. tuberculosis H37Rv, the levels of resistance to all quinolones tested in the isolates that carried GyrA-D94G or GyrB-N538D (8- to 32-fold increase) were significantly higher than those in isolates bearing GyrA-D94A or GyrA-A90V (2- to 8-fold increase) (P < 0.01). Intriguingly, GyrB-E540D led to a dramatic resistance to later-generation quinolones, including moxifloxacin, gatifloxacin, and sparfloxacin (8- to 16-fold increases in MICs and 8.3- to 11.2-fold increases in 50% inhibitory concentrations [IC50s]). However, GyrB-E540D caused low-level resistance to early-generation quinolones, including ofloxacin, levofloxacin, and ciprofloxacin (2- to 4-fold increases in MICs and 1.5- to 2.0-fold increases in IC50s). In the present study, DC-159a was the most active antituberculosis agent and was little affected by the gyrase mutations described above. Our findings suggest that although they are rare, gyrB mutations have a notable role in quinolone resistance, which may provide clues to the molecular basis of estimating quinolone resistance levels for drug and dose selection.
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