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- Title
Impact of co-existence of PMQR genes and QRDR mutations on fluoroquinolones resistance in Enterobacteriaceae strains isolated from community and hospital acquired UTIs.
- Authors
Kotb, Dalia Nabil; Mahdy, Wafaa Khairy; Mahmoud, Mahmoud Shokry; Khairy, Rasha M. M.
- Abstract
<bold>Background: </bold>Fluoroquinolones are commonly recommended as treatment for urinary tract infections (UTIs). The development of resistance to these agents, particularly in gram-negative microorganisms complicates treatment of infections caused by these organisms. This study aimed to investigate antimicrobial resistance of different Enterobacteriaceae species isolated from hospital- acquired and community-acquired UTIs against fluoroquinolones and correlate its levels with the existing genetic mechanisms of resistance.<bold>Methods: </bold>A total of 440 Enterobacteriaceae isolates recovered from UTIs were tested for antimicrobial susceptibility. Plasmid-mediated quinolone resistance (PMQR) genes and mutations in the quinolone resistance-determining regions (QRDRs) of gyrA and parC genes were examined in quinolone-resistant strains.<bold>Results: </bold>About (32.5%) of isolates were resistant to quinolones and (20.5%) were resistant to fluoroquinolones. All isolates with high and intermediate resistance phenotypes harbored one or more PMQR genes. QnrB was the most frequent gene (62.9%) of resistant isolates. Co-carriage of 2 PMQR genes was detected in isolates (46.9%) with high resistance to ciprofloxacin (CIP) (MICs > 128 μg/mL), while co-carriage of 3 PMQR genes was detected in (6.3%) of resistant isolates (MICs > 512 μg/mL). Carriage of one gene only was detected in intermediate resistance isolates (MICs of CIP = 1.5-2 μg/mL). Neither qnrA nor qnrC genes were detected. The mutation at code 83 of gyrA was the most frequent followed by Ser80-Ile in parC gene, while Asp-87 Asn mutation of gyrA gene was the least, where it was detected only in high resistant E. coli isolates (MIC ≥128 μg/mL). A double mutation in gyrA (Lys154Arg and Ser171Ala) was observed in high FQs resistant isolates (MIC of CIP < 128 μg/mL).<bold>Conclusion: </bold>FQs resistance is caused by interact between PMQR genes and mutations in both gyrA and parC genes while a mutation in one gene only can explain quinolone resistance. Accumulation of PMQR genes and QRDR mutations confers high resistance to FQs.
- Subjects
URINARY tract infections; DRUG resistance in microorganisms; PLANT resistance to viruses; ENTEROBACTERIACEAE; MICROBIAL sensitivity tests; GENES; BACTERIAL protein metabolism; ANTIBIOTICS; BACTERIAL proteins; CIPROFLOXACIN; CROSS infection; GENETIC mutation; QUINOLONE antibacterial agents; ENTEROBACTERIACEAE diseases; PHARMACODYNAMICS
- Publication
BMC Infectious Diseases, 2019, Vol 19, Issue 1, pN.PAG
- ISSN
1471-2334
- Publication type
journal article
- DOI
10.1186/s12879-019-4606-y