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Eur J Clin Microbiol Infect Dis. 2017 Mar;36(3):421-435. doi: 10.1007/s10096-016-2847-x. Epub 2016 Nov 26.

Plasmid-mediated quinolone resistance in Enterobacteriaceae: a systematic review with a focus on Mediterranean countries.

Author information

1
Laboratoire d'Ecologie Microbienne, FSNV, Université de Bejaia, 06000, Bejaia, Algeria.
2
Department of Microbiology, University of Seville, Seville, Spain.
3
Spanish Network for the Research in Infectious Diseases (REIPI RD12/0015), Instituto de Salud Carlos III, Madrid, Spain.
4
Laboratoire d'Ecologie Microbienne, FSNV, Université de Bejaia, 06000, Bejaia, Algeria. ziz1999@yahoo.fr.

Abstract

Quinolones are a family of synthetic broad-spectrum antimicrobial drugs. These molecules have been widely prescribed to treat various infectious diseases and have been classified into several generations based on their spectrum of activity. Quinolones inhibit bacterial DNA synthesis by interfering with the action of DNA gyrase and topoisomerase IV. Mutations in the genes encoding these targets are the most common mechanisms of high-level fluoroquinolone resistance. Moreover, three mechanisms for plasmid-mediated quinolone resistance (PMQR) have been discovered since 1998 and include Qnr proteins, the aminoglycoside acetyltransferase AAC(6')-Ib-cr, and plasmid-mediated efflux pumps QepA and OqxAB. Plasmids with these mechanisms often encode additional antimicrobial resistance (extended spectrum beta-lactamases [ESBLs] and plasmidic AmpC [pAmpC] ß-lactamases) and can transfer multidrug resistance. The PMQR determinants are disseminated in Mediterranean countries with prevalence relatively high depending on the sources and the regions, highlighting the necessity of long-term surveillance for the future monitoring of trends in the occurrence of PMQR genes.

PMID:
27889879
DOI:
10.1007/s10096-016-2847-x
[Indexed for MEDLINE]

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