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JAC Advance Access published online on May 13, 2008
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkn206
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Research letter

First detection of plasmid-mediated, quinolone resistance determinants qnrA, qnrB, qnrS and aac(6')-Ib-cr in extended-spectrum β-lactamase (ESBL)-producing Enterobacteriaceae in Budapest, Hungary

Dóra Szabó1,*,{dagger}, Béla Kocsis1,{dagger}, László Rókusz2, Júlia Szentandrássy3, Katalin Katona3, Katalin Kristóf1 and Károly Nagy1

1 Institute of Medical Microbiology, Semmelweis University, Nagyvárad tér 4, H-1089 Budapest, Hungary 2 First Department of Medicine, State Health Center, Ministry of Defense, Róbert K. krt. 44, H-1134 Budapest, Hungary 3 Department of Microbiology, State Health Center, Ministry of Defense, Róbert K. krt. 44, H-1134 Budapest, Hungary

* Corresponding author. Tel/Fax: +36-1-210-2959; E-mail: szabdor@net.sote.hu

Key Words: fluoroquinolones , antimicrobial resistance epidemiology , mechanisms of resistance

The first 10% of the full text of this article appears below.

Sir,

Quinolone resistance in Enterobacteriaceae usually results from mutations in genes coding for chromosomally encoded type II topoisomerases, efflux pumps or porin-related proteins. Recently, transferable, plasmid-borne, quinolone resistance genes—qnrA, qnrB, qnrS, cr variant of aac(6')-Ib, qepA and oxqB—have been observed in clinical isolates, more frequently among strains producing plasmid-mediated, extended-spectrum β-lactamases (ESBLs).1

The objective of this study was to determine the prevalence of qnrA, qnrB, qnrS and aac(6')-Ib-cr genes in ESBL-producing clinical isolates of 70 . . . [Full Text of this Article]


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