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Review
. 2014 Oct;2(5):10.1128/microbiolspec.PLAS-0006-2013.
doi: 10.1128/microbiolspec.PLAS-0006-2013.

Plasmid-mediated Quinolone Resistance

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Free PMC article
Review

Plasmid-mediated Quinolone Resistance

George A Jacoby et al. Microbiol Spectr. .
Free PMC article

Abstract

Three mechanisms for plasmid-mediated quinolone resistance (PMQR) have been discovered since 1998. Plasmid genes qnrA, qnrB, qnrC, qnrD, qnrS, and qnrVC code for proteins of the pentapeptide repeat family that protects DNA gyrase and topoisomerase IV from quinolone inhibition. The qnr genes appear to have been acquired from chromosomal genes in aquatic bacteria, are usually associated with mobilizing or transposable elements on plasmids, and are often incorporated into sul1-type integrons. The second plasmid-mediated mechanism involves acetylation of quinolones with an appropriate amino nitrogen target by a variant of the common aminoglycoside acetyltransferase AAC(6')-Ib. The third mechanism is enhanced efflux produced by plasmid genes for pumps QepAB and OqxAB. PMQR has been found in clinical and environmental isolates around the world and appears to be spreading. The plasmid-mediated mechanisms provide only low-level resistance that by itself does not exceed the clinical breakpoint for susceptibility but nonetheless facilitates selection of higher-level resistance and makes infection by pathogens containing PMQR harder to treat.

Figures

Fig. 1
Fig. 1
The rod-like structure of the QnrB1 dimer is shown above with the sequence of the monomer below. The sequence is divided into four columns representing the four faces of the right-handed quadrilateral β-helix. Face names and color are shown at the top along with the naming convention for the five residues of the pentapeptide repeats. Loops A and B are indicated by one and two asterisks, respectively, with their sequences indicated below and the loops shown as black traces on the diagram. The N-terminal α-helix is colored salmon. The molecular 2-fold symmetry is indicated with a black diamond. Type II turn (235) containing faces are shown as spheres and type IV-containing faces as strands. Adapted from reference (44). © the American Society for Biochemistry and Molecular Biology.
Fig. 2
Fig. 2
QnrB1 protection of DNA gyrase from ciprofloxacin inhibition of supercoiling. Reaction mixtures of 30 μl were analyzed by agarose gel electrophoresis. Reaction mixtures contained 0.2 μg relaxed pBR322 DNA (lanes 1 to 14), 6.7 nM gyrase (lanes 2 to 14), 2 μg/ml ciprofloxacin (lanes 3 to 14), and QnrB-His6 fusion protein at 25 μM (lane 4), 5 μM (lane 5), 2.5 μM (lane 6), 0.5 μM (lane 7), 50 nM (lane 8), 5 nM (lane 9), 0.5 nM (lane 10), 50 pM (lane 11), 5 pM (lane 12), or 0.5 pM (lane 13). Reprinted from (27)
Fig. 3
Fig. 3
Genetic environment of qnr alleles.
Fig. 4
Fig. 4
Survival at increasing fluoroquinolone concentrations for Escherichia coli J53 and J53 pMG252. A large inoculum (1010 colony forming units) and appropriate dilutions were applied to Mueller-Hinton agar plates containing the indicated concentration of ciprofloxacin, and surviving colonies were counted after incubation for 72 h at 37°C [from (215)] with permission.

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