PLASMID-MEDIATED QUINOLONE RESISTANCE – PMQR

Fluoroquinolones(FQ) are broad-spectrum antimicrobial agents widely used to treat a range of infections in clinical medicine. However, the surveillance studies demonstrate that fluoroquinolone resistance rates increased in Enterobacteriaceae in the past years. FQ inhibit bacterial DNA synthesis by interfering with the action of two bacterial enzymes - DNA gyrase and topoisomerase IV. There are two categories of quinolone resistance mechanisms: chromosomally encoded and acquired. Mutations in chromosomal genes encoding gyrase and topoisomerase IV are the most common mechanisms responsible for high-level fluoroquinolone resistance. Mutations can occur also in regulatory genes which control the expression of native efflux pumps located in bacterial membrane. Furthermore, three mechanisms of plasmid-mediated quinolone resistance (PMQR) have been discovered so far, including Qnr proteins, the aminoglycoside acetylotransferase variant - AAC(6’)-Ib-cr, and plasmid-mediated efflux pumps - QepA and OqxAB. Although the PMQR mechanisms alone cause only low-level resistance to fluoroquinolone, they can complement other mechanisms of chromosomal resistance and facilitate the selection of higher-level resistance. Moreover, plasmids with PMQR mechanisms often encode additional resistance traits (ESBLs, pAmpC, KPC) contributing to multidrug resistance (MDR). This review is focused on a range of molecular mechanisms which underlie quinolone resistance. 1. Introduction. 2. Mechanisms of fluoroquinolone action. 3. Chromosomally-encoded fluoroquinolone resistance. 3.1. Mutations changing the functions of target enzymes. 3.2. Reduction of drug concentration in the cytoplasm - efflux pump. 4. Plasmid-mediated quinolone resistance. 4.1. Qnr proteins. 4.2. AAC(6’)-Ib-cr enzyme. 4.3. Plasmid-mediated efflux pump: QepA i OqxAB. 4.4. The impact of PMQR on fluoroquinolone susceptibility level. 5. Summary

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