| Literature DB >> 27912841 |
José Manuel Rodríguez-Martínez1, Jesús Machuca2, María Eliecer Cano3, Jorge Calvo3, Luis Martínez-Martínez4, Alvaro Pascual2.
Abstract
After two decades of the discovery of plasmid-mediated quinolone resistance (PMQR), three different mechanisms have been associated to this phenomenon: target protection (Qnr proteins, including several families with multiple alleles), active efflux pumps (mainly QepA and OqxAB pumps) and drug modification [AAC(6')-Ib-cr acetyltransferase]. PMQR genes are usually associated with mobile or transposable elements on plasmids, and, in the case of qnr genes, are often incorporated into sul1-type integrons. PMQR has been found in clinical and environmental isolates around the world and appears to be spreading. Although the three PMQR mechanisms alone cause only low-level resistance to quinolones, they can complement other mechanisms of chromosomal resistance to reach clinical resistance level and facilitate the selection of higher-level resistance, raising a threat to the treatment of infections by microorganisms that host these mechanisms. Copyright ÂEntities:
Keywords: AAC(6′)-Ib-cr; OqxAB; Plasmid; QepA; Qnr; Quinolone; Resistance
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Year: 2016 PMID: 27912841 DOI: 10.1016/j.drup.2016.09.001
Source DB: PubMed Journal: Drug Resist Updat ISSN: 1368-7646 Impact factor: 18.500