Prevalence of plasmid-mediated quinolone resistance determinants QnrA, QnrB, and QnrS among clinical isolates of Klebsiella pneumoniae in Scotland
Abstract number: P1531
Younes A., Hamouda A., Dave J., Gibb A., Amyes S.G.B., Schneiders T.
Introduction: Quinolone resistance results from mutations in the chromosomally-encoded type II topoisomerases, and via the upregulation of efflux pumps, or porin-related genes. Recent studies demonstrate that the plasmid-mediated qnr genes (QnrA, B and S) play an emerging role in the dissemination of fluoroquinolone resistance. The first plasmid-mediated quinolone resistance protein Qnr was identified in a Klebsiella pneumoniae isolate in 1994 where the presence of the qnr gene increased the MICs to nalidixic acid and fluoroquinolones by four- to eight-fold. The qnr gene has been identified in complex In4 family class 1 integrons, known as complex sul1-type integrons that may act as a recombinase for mobilisation of the antibiotic resistance genes located nearby (e.g., qnr, blaCTX-M and ampC). In addition, an association of quinolone resistance with the production of ESBLs has been reported. This study aimed to determine the prevalence of qnr genes and its association with the presence of ESBLs in clinical K. pneumoniae isolates from Scotland.
Methods: Isolates of K. pneumoniae were collected from the Royal Infirmary Edinburgh in 2007. The qnrA, qnrB, and qnrS genes were detected by PCR. MICs of ciprofloxacin, nalidixic acid, cefotaxime, ceftazidime, ceftriaxone, cefoxitin and meropenem were performed according to the BSAC guidelines. ESBL production was confirmed by double and combination disk methods.
Results: Of the 95 isolates tested, 27 were found to be positive by PCR for the qnr genes. These positive isolates were further assessed by PCR where 11 possessed the qnrB gene, 10 contained the qnrA gene and 2 harboured the qnrS gene. Interestingly four isolates were found to harbour both the qnrB and qnrS genes. Out of the 27 qnr positive isolates, 12 (44.4%) isolates were found to be resistant to nalidixic acid, while the remaining 15 (55.6%) were sensitive to nalidixic acid. Six of the qnrB positive isolates were associated with CTX-M, SHV and TEM, one isolate with TEM and SHV b-lactamases. Two qnrA positive isolates were associated with TEM and SHV only. However of the isolates that were tested none were found to harbour an ESBL and the qnrS gene.
Conclusion: These findings indicate the high prevalence of qnr genes and the co-expression of fluoroquinolone and extended-spectrum b-lactam resistance among Klebsiella pneumoniae isolates in Scotland.
|Session name:||18th European Congress of Clinical Microbiology and Infectious Diseases|
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