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Plasmid-mediated quinolone resistance: a multifaceted threat
Jacob Strahilevitz1, George A Jacoby, David C Hooper
1Department of Clinical Microbiology and Infectious Diseases, Hadassah Ein-Kerem, Jerusalem 91120, Israel. jstrahilevitz@hadassah.org.il
Plasmid-mediated quinolone resistance (PMQR) genes like qnr, aac(6')-Ib-cr, oqxAB, and qepA are emerging globally. These genes, though conferring low-level resistance, facilitate the selection of higher quinolone resistance levels.
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- Plasmid-mediated quinolone resistance (PMQR) has become a significant concern in recent decades.
- The qnr genes, likely originating from aquatic environments, represent the most studied PMQR mechanism.
- Emerging resistance mechanisms include aac(6 ext extprime)-Ib-cr and efflux pumps (oqxAB, qepA).
Purpose of the Study:
- To review and characterize the known mechanisms of plasmid-mediated quinolone resistance.
- To highlight the significance of PMQR in the broader context of quinolone resistance.
- To underscore the need for incorporating PMQR detection in clinical diagnostics.
Main Methods:
- Literature review of studies on PMQR genes.
- Analysis of the molecular mechanisms of qnr, aac(6 ext extprime)-Ib-cr, oqxAB, and qepA.
- Examination of the clinical implications and spread of PMQR.
Main Results:
- Qnr proteins protect DNA gyrase and topoisomerase IV from quinolone inhibition.
- aac(6 ext extprime)-Ib-cr inactivates ciprofloxacin via acetylation.
- oqxAB and qepA function as quinolone efflux pumps.
- These genes contribute to increased minimum inhibitory concentrations (MICs) and facilitate selection for higher resistance.
Conclusions:
- PMQR genes are increasingly prevalent and associated with other resistance determinants.
- The spread of PMQR is concurrent with rising clinical quinolone resistance.
- Current clinical microbiology laboratory screening methods do not account for these PMQR genes.
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