ArticleBrazilian journal of microbiology : [publication of the Brazilian Society for Microbiology]2014
Molecular mechanism of fluoroquinolones resistance in Mycoplasma hominis clinical isolates.
Article in Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology], 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Sternal wound infection caused by Mycoplasma hominis in an adult patient: a case report and literature review.BMC infectious diseases · 2025Review
- Chinese advances in understanding and managing genitourinary tract infections caused by Mycoplasma genitalium, Mycoplasma hominis, and Ureaplasma urealyticum.Archives of microbiology · 2024Review
- Clinical and Microbiological Characterization of Bloodstream Infections Caused by Mycoplasma hominis: An Overlooked Pathogen.Infectious diseases and therapy · 2022Article
- Mycoplasma hominis meningitis in an extremely preterm newborn: a case report.BMC pediatrics · 2021Article
- Antimicrobial Resistance in ClinicalAntimicrobial agents and chemotherapy · 2020Article
- Article
- Article
- Mycoplasmas and Their Antibiotic Resistance: The Problems and Prospects in Controlling Infections.Acta naturaeArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To evaluate the molecular mechanism of fluoroquinolones resistance in Mycoplasma hominis (MH) clinical strains isolated from urogenital specimens. 15 MH clinical isolates with different phenotypes of resistance to fluoroquinolones antibiotics were screened for mutations in the quinolone resistance-determining regions (QRDRs) of DNA gyrase (gyrA and gyrB) and topoisomerase IV (parC and parE) in comparison with the reference strain PG21, which is susceptible to fluoroquinolones antibiotics. 15 MH isolates with three kinds of quinolone resistance phenotypes were obtained. Thirteen out of these quinolone-resistant isolates were found to carry nucleotide substitutions in either gyrA or parC. There were no alterations in gyrB and no mutations were found in the isolates with a phenotype of resistance to Ofloxacin (OFX), intermediate resistant to Levofloxacin (LVX) and Sparfloxacin (SFX), and those susceptible to all three tested antibiotics. The molecular mechanism of fluoroquinolone resistance in clinical isolates of MH was reported in this study. The single amino acid mutation in ParC of MH may relate to the resistance to OFX and LVX and the high-level resistance to fluoroquinolones for MH is likely associated with mutations in both DNA gyrase and the ParC subunit of topoisomerase IV.
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