Plasmid-mediated quinolone resistance in gram-negative bacterial species: an update.

Abstract:

:Resistance to quinolones and fluoroquinolones has been increasingly reported among human and veterinary isolates during the last three decades related to their wide clinical use. Until recently, the mechanisms of resistance to quinolones in Enterobacteriaceae were believed to be only chromosome-encoded, i.e. related to modifications of the molecular targets (DNA gyrase and topoisomerase IV), decreased outer-membrane permeability (porin defect) and overexpression of naturally-occurring efflux. However, emergence of plasmid-mediated quinolone resistance (PMQR) has been reported since 1998. Three mechanisms are known to date: Qnr proteins, aminoglycoside acetyltransferase AAC(6')-Ib-cr, and efflux pump QepA. The Qnr proteins protect DNA gyrase and type IV topoisomerase from quinolone inhibition. Four types of Qnr protiens have been reported: QnrA (six variants), QnrB (19 variants), QnrC (one variant), and QnrS (three variants). The AAC(6')-Ib-cr determinant acetylates several fluoroquinolones, such as norfloxacin and ciprofloxacin. The protein AAC(6')-Ib-cr contains two amino acid substitutions as compared to the wild-type enzyme AAC(6')-Ib. Both Qnr and AAC(6')-Ib proteins have been reported worldwide. Lately reported, the plasmid-encoded QepA efflux pump may extrude hydrophilic fluoroquinolones (eg. norfloxacin, ciprofloxacin, and enrofloxacin).

journal_name

Curr Med Chem

authors

Cattoir V,Nordmann P

doi

10.2174/092986709787581879

subject

Has Abstract

pub_date

2009-01-01 00:00:00

pages

1028-46

issue

8

eissn

0929-8673

issn

1875-533X

journal_volume

16

pub_type

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