JAC Advance Access originally published online on September 7, 2007
Journal of Antimicrobial Chemotherapy 2007 60(5):1176-1178; doi:10.1093/jac/dkm308
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Correspondence |
Detection of qnrA among Enterobacteriaceae from South-East England with extended-spectrum and high-level AmpC ß-lactamases

1 Antibiotic Resistance Monitoring and Reference Laboratory, Centre for Infections, Health Protection Agency, London, UK 2 Laboratory of Healthcare Associated Infection, Centre for Infections, Health Protection Agency, London, UK
* Corresponding author. Tel: +44-208-327-7259; Fax: +44-208-200-7449; E-mail: matthew.ellington{at}hpa.org.uk
Keywords: quinolone resistance , Qnr , Enterobacter spp.
The plasmid-borne qnrA gene confers decreased susceptibility to quinolones in Enterobacteriaceae.1 Moreover, the presence of the gene increases the likelihood that higher-level, clinically relevant, resistance may arise2 via secondary changes in cell permeability, efflux or the DNA gyrase/topoisomerase proteins.3 The qnrA gene has been reported worldwide, with varying prevalence rates from 0.3% to 7.7%, based on studies with variable sample sizes, sources and selection criteria.1,4 A study of ciprofloxacin-resistant Enterobacteriaceae isolates in the UK reported qnrA in 32% of a relatively small, local sample (n = 47).5
Among 1122 confirmed oxyimino-cephalosporin-resistant Enterobacteriaceae isolates, collected in 16 hospitals in London and South-East (SE) England during a 2004 survey, 658 were resistant to ciprofloxacin (59%) according to the 2005 BSAC criteria (MIC > 1 mg/L).6 In order to seek qnrA-positive isolates, isolates with ciprofloxacin MICs
0.125 mg/L (n = 821/1122) were PCR-tested using standard reactions with cell suspensions of isolates and the primer pair QnrA (5'-GGGTATGGATATTATTGATAAAG-3')/QnrB (5'-CTAATCCGGCAGCACTATTA-3').7 Among these 821 isolates, 25 (3%) possessed qnrA. DNA sequencing confirmed that the 661 bp amplicons from six randomly chosen qnrA-positive isolates were identical to the qnrA1 allele (GenBank accession no. AY070235
[GenBank]
). The 25 qnrA-positive isolates were from 10 of 16 survey hospitals (Figure 1) and comprised 23 Enterobacter cloacae from 10 different hospitals, along with single representatives of Citrobacter freundii and Klebsiella pneumoniae, as identified by API20Etests (bioMerieux, Marcy-l'Étoile, France). Despite being isolated from the urinary tract of the same patient, the K. pneumoniae and E. cloacae isolates did not carry the same qnrA resistance plasmid, as determined by plasmid transfer and analyses (data not shown).
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Of the 23 qnrA-positive E. cloacae isolates, 9 were extended-spectrum ß-lactamase (ESBL) producers; 1 with a CTX-M enzyme and 8 with non-CTX-M ESBLs. The remaining 14 had copious AmpC ß-lactamase activity, which was presumed to be chromosomally encoded (Figure 1). Only 2 of 25 isolates (1 E. cloacae and 1 C. freundii) were susceptible to gentamicin (MICs
1mg/L), whereas all 25 isolates were susceptible to imipenem (Figure 1) and meropenem (data not shown); only 9 were susceptible to ciprofloxacin (MIC
1 mg/L), suggesting that most had additional mechanisms of quinolone resistance. Using an 85% similarity cut-off value to define strains by PFGE of XbaI-digested genomic DNA, 14 distinct types were detected among the 23 E. cloacae isolates. One strain was represented by six isolates from three geographically remote centres; all these isolates had similar antibiograms (Figure 1). A further two pairs of related isolates, one from a single centre (centre F) and the other from separate centres (D and A), were also detected, along with a group of three isolates from two centres (centres A and F) (Figure 1). The remaining 10 isolates were unique types by PFGE.
These data indicate that qnrA-positive E. cloacae isolates are widely scattered in SE England, at least, and that one strain with the mechanism has spread among three hospitals. Equally significant, however, was the absence of qnrA from the large number of CTX-M ß-lactamase-positive Escherichia coli and Klebsiella investigated, although virtually all of these were also quinolone-resistant. Many of these latter isolates have fluoroquinolone resistance co-mediated by plasmids that encode the aminoglycoside/ciprofloxacin modifying enzyme AAC(6 )-Ib-cr along with the CTX-M-15 ß-lactamase.8
This work was supported by the Health Protection Agency.
None to declare.
Footnotes
Present address. Laboratory of Healthcare Associated Infection, Centre for Infections, Health Protection Agency, 61 Colindale Avenue, London NW9 5EQ, UK ![]()
Acknowledgements
We would like to acknowledge Nicola Potz and the 2004 South East England ESBL survey for providing strains for this study. Parts of this work were presented at the Forty-fifth Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC), Washington, DC, 2005 (Ellington MJ, Hope R, Turton J, Livermore DM, Woodford N. In: Abstracts of the Forty-fifth Interscience Conference on Antimicrobial Agents and Chemotherapy, Washington, DC, 2005. Abstract C2-786, p. 119. American Society for Microbiology, Washington, DC, USA).
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