Expanded-spectrum β-Lactamase and Plasmid-mediated Quinolone Resistance

To the Editor: The emergence of plasmid-mediated, and thus transfer-able, quinolone resistance determinants has been recently discovered (1) and shown to involve the pentapeptide repeat protein Qnr, which interacts with DNA gyrase and topoisomerase IV to prevent quinolone inhibition (2,3). Qnr determinants confer resistance to nalidixic acid and reduced susceptibility to fl uoroquinolones (3). They have been identifi ed worldwide in a variety of enterobacterial species and were often associated to expanded-spectrum β-lactamases (ESBLs) (2). The association between the ESBL VEB-1 and the QnrA1 determinants was reported (4). Because plasmid co-localization of QnrA and VEB-1 encoding genes has been reported repeatedly from scattered clonally-unrelated entero-bacterial isolates, our objective was to use replicon typing to trace a possible dissemination of a common plasmid worldwide. The bla VEB-1-and/or qnrA-positive plasmids that have been included in the study were from 17 isolates previously described in detail (3–8) (Table). Escherichia coli transconjugants (Tc) were obtained for 14 of 17 clinical isolates, allowing an accurate replicon typing since original clinical isolates might harbor several plasmids. They were collected from 1999 to 2005, from patients hospitalized in different parts of the world (Table). The 13 bla VEB-1-positive isolates were from 5 countries (France, Turkey, Algeria, Thailand, and Canada), scattered on 4 continents. Among them, the Provi-dencia stuartii and Proteus mirabilis isolates from Algeria were negative for qnrA1. In addition, 4 bla VEB-1-negative but qnrA1-positive isolates recovered from France and Australia were also included in the study. to type the resistance plasmids from all the strains.