AI Article Synopsis
- The study investigates the molecular mechanisms behind fluoroquinolone resistance in Mycoplasma hominis isolated from urogenital samples.
- 15 clinical isolates were analyzed for mutations in key genes related to antibiotic resistance, particularly focusing on DNA gyrase and topoisomerase IV.
- Results showed that many resistant isolates had mutations in gyrA or parC, indicating that these mutations contribute to fluoroquinolone resistance, particularly linked to specific antibiotics like Ofloxacin and Levofloxacin.
Article 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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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4059304 | PMC |
| http://dx.doi.org/10.1590/s1517-83822014000100034 | DOI Listing |
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