Abstract
The plasmid-encoded quinolone resistance gene qnrS1 was recently found to be commonly associated with ciprofloxacin resistance in Nigeria. We mapped the qnrS1 gene from an Escherichia coli isolate obtained in Nigeria to a 43.5 Kb IncX2 plasmid. The plasmid, pEBG1, was sufficient to confer ciprofloxacin non-susceptibility, as well as tetracycline and trimethoprim resistance, on E. coli K-12. Deletion analysis confirmed that qnrS1 accounted for all the ciprofloxacin non-suceptibility conferred by pEBG1 and tetracycline and trimethoprim resistance could be attributed to tetAR and dfrA14 genes respectively. While it contained a complete IncX conjugation system, pEBG1 was not self-transmissible likely due to an IS3 element inserted between the pilX5 and pilX6 genes. The plasmid was however efficiently mobilizable. pEBG1 was most similar to another qnrS1-bearing IncX2 plasmid from Nigeria, but both plasmids acquired qnrS1 independently and differ in their content of other resistance genes. Screening qnrS1–positive isolates from other individuals in Nigeria revealed that they carried neither pEBG1 nor pNGX2-QnrS1 but that IncX plasmids were prevalent. This study demonstrates that the IncX backbone is a flexible platform that has contributed to qnrS1 dissemination in Nigeria.
Highlights
When antibacterial quinolones were first introduced into clinical practice, it was thought that resistance would be slow to appear and that transmissible resistance was improbable [1]
Quinolone-non-susceptible strain 09/22a from Nigeria carries its qnrS1 gene on an IncX plasmid
Strain 09/22a is a quinolone-non-susceptible E. coli isolate from Nigeria that tested positive for qnrS1 by PCR in a recent study [5]
Summary
When antibacterial quinolones were first introduced into clinical practice, it was thought that resistance would be slow to appear and that transmissible resistance was improbable [1]. Initial reports of quinolone resistance were due to point mutations in the genes encoding their gyrase and topoisomerase targets that made them less sensitive to the drug. In 1998, Martinez-Martinez et al [2] described a plasmid-borne gene, termed qnrA, which conferred four-to-sixteen-fold resistance to quinolones on Enterobacteriaceae. QnrA is a pentapeptide repeat protein that protects DNA gyrase from quinolone binding and inhibition [3]. Transmissible quinolone resistance is attributable to genes encoding plasmid-encoded efflux pumps, such as qepA and oqx and, in the case of ciprofloxacin, the acetylating enzyme aac(69)-Ib-cr. While plasmid-encoded quinolone-resistance genes generally confer low-level resistance, their overall impact is great because they shield otherwise susceptible bacteria from the lethal effects of the quinolones, allowing them greater time and opportunity to evolve higher-level resistance
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