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Clinical Microbiology Reviews, October 2009, p. 664-689, Vol. 22, No. 4
0893-8512/09/$08.00+0     doi:10.1128/CMR.00016-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Plasmid-Mediated Quinolone Resistance: a Multifaceted Threat

Jacob Strahilevitz,1* George A. Jacoby,2 David C. Hooper,3 and Ari Robicsek4 Author Bios

Department of Clinical Microbiology and Infectious Diseases, Hadassah-Hebrew University, Jerusalem 91120, Israel,1 Lahey Clinic, Burlington, Massachusetts 01805,2 Division of Infectious Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114,3 Department of Medicine, NorthShore University HealthSystem, University of Chicago Pritzker School of Medicine, Evanston, Illinois 602014

Summary: Although plasmid-mediated quinolone resistance (PMQR) was thought not to exist before its discovery in 1998, the past decade has seen an explosion of research characterizing this phenomenon. The best-described form of PMQR is determined by the qnr group of genes. These genes, likely originating in aquatic organisms, code for pentapeptide repeat proteins. These proteins reduce susceptibility to quinolones by protecting the complex of DNA and DNA gyrase or topoisomerase IV enzymes from the inhibitory effect of quinolones. Two additional PMQR mechanisms were recently described. aac(6')-Ib-cr encodes a variant aminoglycoside acetyltransferase with two amino acid alterations allowing it to inactivate ciprofloxacin through the acetylation of its piperazinyl substituent. oqxAB and qepA encode efflux pumps that extrude quinolones. All of these genes determine relatively small increases in the MICs of quinolones, but these changes are sufficient to facilitate the selection of mutants with higher levels of resistance. The contribution of these genes to the emergence of quinolone resistance is being actively investigated. Several factors suggest their importance in this process, including their increasing ubiquity, their association with other resistance elements, and their emergence simultaneous with the expansion of clinical quinolone resistance. Of concern, these genes are not yet being taken into account in resistance screening by clinical microbiology laboratories.

* Corresponding author. Mailing address: Department of Clinical Microbiology and Infectious Diseases, Hadassah Ein-Kerem, Jerusalem 91120, Israel. Phone: 972-50-894 6353. Fax: 972-2-641 9545. E-mail: jstrahilevitz{at}hadassah.org.il

Clinical Microbiology Reviews, October 2009, p. 664-689, Vol. 22, No. 4
0893-8512/09/$08.00+0     doi:10.1128/CMR.00016-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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