Plasmid-mediated quinolone resistance: Two decades on

被引:150
|
作者
Manuel Rodriguez-Martinez, Jose [1 ,2 ]
Machuca, Jesus [1 ,2 ,3 ]
Cano, Maria Eliecer [2 ,4 ]
Calvo, Jorge [2 ,4 ]
Martinez-Martinez, Luis [2 ,4 ,5 ]
Pascual, Alvaro [1 ,2 ,3 ]
机构
[1] Univ Seville, Dept Microbiol, Seville, Spain
[2] Inst Salud Carlos III, Spanish Network Res Infect Dis REIPI RD12 0015, Madrid, Spain
[3] Hosp Univ Virgen Macarena, Unidad Enfermedades Infecciosas & Microbiol Clin, Seville, Spain
[4] Hosp Univ Marques de Valdecilla, IDIVAL, Santander, Spain
[5] Univ Cantabria, Dept Biol Mol, Santander, Spain
关键词
Resistance; Plasmid; Quinolone; Qnr; AAC(6 ')-lb-cr; QepA; OqxAB; PENTAPEPTIDE REPEAT PROTEINS; CTX-M-15-PRODUCING KLEBSIELLA-PNEUMONIAE; FLUOROQUINOLONE-MODIFYING ENZYME; MUTANT PREVENTION CONCENTRATIONS; ESCHERICHIA-COLI STRAINS; IN-VIVO SELECTION; 16S RIBOSOMAL-RNA; ANTIBIOTIC-RESISTANCE; EFFLUX PUMP; MULTIDRUG-RESISTANCE;
D O I
10.1016/j.drup.2016.09.001
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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')-lb-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. (C) 2016 Elsevier Ltd. All rights reserved.
引用
收藏
页码:13 / 29
页数:17
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