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.

在发现质粒介导的喹诺酮抗药性（PMQR）的二十年后，与该现象相关的三种不同机制：靶标保护（Qnr蛋白，包括具有多个等位基因的多个家族），主动外排泵（主要是QepA和OqxAB泵）和药物修饰[AAC（6'）-Ib-cr乙酰转移酶]。PMQR基因通常与质粒上的移动或转座元件相关，对于qnr基因，通常将它们整合到sul1中型整数。在世界各地的临床和环境分离物中都发现了PMQR，并且似乎正在传播。尽管仅三个PMQR机制仅引起对喹诺酮类药物的低水平耐药性，但它们可以补充其他的染色体耐药性机制以达到临床耐药性水平，并有助于选择较高水平的耐药性，从而对宿主微生物感染的治疗提出了威胁。这些机制。