Investigation of fluoroquinolone resistance mechanism in Mycoplasma hominis isolated from urogenital samples in a Chinese hospital
Zhang, Hongyan and Zheng, Liangjian and Zhao, Juan and Ding, Shaochuan and Xia, Yun,, 68, 206-210 (2019),
doi = https://doi.org/10.1099/jmm.0.000913,
publicationName = Microbiology Society,
issn = 0022-2615,
abstract= Purpose. Mycoplasma hominis is considered among the causes of urogenital infections and shows increasing resistance to fluoroquinolones. However, data regarding the fluoroquinolone resistance mechanism of M. hominis in Southwest China are limited. This study aimed to investigate gene mutations of quinolone resistance-determining regions (QRDRs) of M. hominis isolated from clinical urogenital samples in a Chinese hospital. Methodology. Strains of M. hominis were identified by 16S rRNA gene sequencing. The minimal inhibitory concentrations (MICs) of fluoroquinolones were determined by the broth microdilution method, following CLSI guidelines. PCR was used to amplify the QRDRs of the genes gyrA, gyrB, parC and parE. Positive products were sequenced, and gene mutations and amino acid substitutions were analysed by DNAMAN software and BLAST. Results. The resistance rates of M. hominis to ciprofloxacin (CIP), levofloxacin (LVX), moxifloxacin (MXF) and gatifloxacin (GAT) were 90.5, 85.7, 73.8 and 71.4 %, respectively. A total of 57 isolates of M. hominis were screened, among which 52 strains demonstrated different resistant phenotypes to fluoroquinolones, 41 harboured amino acid substitutions of GyrA S153L, 51 harboured ParC S91I and 22 harboured ParC K144R. ParE A463S and ParC A154T were recorded for the first time and no amino acid change was detected in GyrB. Conclusion. The resistance of M. hominis to fluoroquinolones in Southwest China is mainly related to mutations in QRDRs of either gyrA or parC. High-level resistance is associated with mutations in both DNA gyrase and topoisomerase IV.,
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