ArticleThe Journal of infectious diseases2012
Impact of fluoroquinolone resistance mutations on gonococcal fitness and in vivo selection for compensatory mutations.
Article in The Journal of infectious diseases, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 83 citations in OpenAlex.
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- Quantifying the real-world impact of antibiotic use and genetic determinants of resistance on gonococcal dynamics.Nature microbiology · 2026Article
- Commensal Fitness Advantage May Contribute to the Global Dissemination of Multidrug-Resistant Lineages of Bacteria-The Case of UropathogenicPathogens (Basel, Switzerland) · 2023Article
- Vertebrate and Invertebrate Animal and New In Vitro Models for StudyingPathogens (Basel, Switzerland) · 2023Review
- Extra-genitalInternational journal of STD & AIDS · 2023Article
- Emergence and Genomic Characterization of Neisseria gonorrhoeae Isolates with High Levels of Ceftriaxone and Azithromycin Resistance in Guangdong, China, from 2016 to 2019.Microbiology spectrum · 2022Article
- c-di-AMP signaling plays important role in determining antibiotic tolerance phenotypes of Mycobacterium smegmatis.Scientific reports · 2022Article
- Global Emergence and Dissemination of Neisseria gonorrhoeae ST-9363 Isolates with Reduced Susceptibility to Azithromycin.Genome biology and evolution · 2022Article
- Auranofin exerts antibacterial activity against Neisseria gonorrhoeae in a female mouse model of genital tract infection.PloS one · 2022Article
- Selection of Resistant Bacteria in Mallards Exposed to Subinhibitory Concentrations of Ciprofloxacin in Their Water Environment.Antimicrobial agents and chemotherapy · 2021Article
- Persistence Dynamics of Antimicrobial-ResistantAntimicrobial agents and chemotherapy · 2020Article
- Biological feasibility and importance of a gonorrhea vaccine for global public health.Vaccine · 2019Review
- Evidence of Recent Genomic Evolution in Gonococcal Strains With Decreased Susceptibility to Cephalosporins or Azithromycin in the United States, 2014-2016.The Journal of infectious diseases · 2019Article
- Impact of an Antimicrobial Stewardship Intervention on Within- and Between-Patient Daptomycin Resistance Evolution in Vancomycin-Resistant Enterococcus faecium.Antimicrobial agents and chemotherapy · 2019Article
- Applications of genomics to slow the spread of multidrug-resistant Neisseria gonorrhoeae.Annals of the New York Academy of Sciences · 2019Review
- Genomic surveillance of Neisseria gonorrhoeae to investigate the distribution and evolution of antimicrobial-resistance determinants and lineages.Microbial genomics · 2018Article
- Article
- Impact of Rapid Susceptibility Testing and Antibiotic Selection Strategy on the Emergence and Spread of Antibiotic Resistance in Gonorrhea.The Journal of infectious diseases · 2017Article
- Cryptic Microheteroresistance Explains Mycobacterium tuberculosis Phenotypic Resistance.American journal of respiratory and critical care medicine · 2017Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundQuinolone-resistant Neisseria gonorrhoeae (QRNG) arise from mutations in gyrA (intermediate resistance) or gyrA and parC (resistance). Here we tested the consequence of commonly isolated gyrA(91/95) and parC86 mutations on gonococcal fitness.
methodsMutant gyrA(91/95) and parC86 alleles were introduced into wild-type gonococci or an isogenic mutant that is resistant to macrolides due to an mtrR(-79) mutation. Wild-type and mutant bacteria were compared for growth in vitro and in competitive murine infection.
resultsIn vitro growth was reduced with increasing numbers of mutations. Interestingly, the gyrA(91/95) mutation conferred an in vivo fitness benefit to wild-type and mtrR(-79) mutant gonococci. The gyrA(91/95), parC86 mutant, in contrast, showed a slight fitness defect in vivo, and the gyrA(91/95), parC86, mtrR(-79) mutant was markedly less fit relative to the parent strains. A ciprofloxacin-resistant (Cip(R)) mutant was selected during infection with the gyrA(91/95), parC86, mtrR(-79) mutant in which the mtrR(-79) mutation was repaired and the gyrA(91) mutation was altered. This in vivo-selected mutant grew as well as the wild-type strain in vitro.
conclusionsgyrA(91/95) mutations may contribute to the spread of QRNG. Further acquisition of a parC86 mutation abrogates this fitness advantage; however, compensatory mutations can occur that restore in vivo fitness and maintain Cip(R).
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.