Emergence of plasmid-mediated resistance to quinolones in Enterobacteriaceae

J Antimicrob Chemother. 2005 Sep;56(3):463-9. doi: 10.1093/jac/dki245. Epub 2005 Jul 14.

Abstract

Although quinolone resistance results mostly from chromosomal mutations in Enterobacteriaceae, it may also be mediated by plasmid-encoded Qnr determinants. Qnr proteins protect DNA from quinolone binding and compromise the efficacy of quinolones such as nalidixic acid. Qnr proteins (QnrA-like, QnrB and QnrS) have been identified worldwide with a quite high prevalence among Asian isolates with a frequent association with clavulanic acid inhibited expanded-spectrum beta-lactamases and plasmid-mediated cephalosporinases. The qnrA genes are embedded in complex sul1-type integrons. A very recent identification of the origin of QnrA determinants in the water-borne species Shewanella algae underlines the role of the environment as a reservoir for this emerging threat. It may help to determine the location of in vivo transfer of qnrA genes. Further analysis of the role (if any) of quinolones for enhancing this gene transfer may be conducted. This could prevent the spread, if still possible, of this novel antibiotic resistance mechanism.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Amino Acid Sequence
  • Bacterial Proteins / genetics
  • Bacterial Proteins / metabolism
  • Cephalosporinase / genetics
  • Cephalosporinase / metabolism
  • Drug Resistance, Bacterial / physiology*
  • Enterobacteriaceae / drug effects*
  • Enterobacteriaceae / genetics*
  • Escherichia coli Proteins / genetics
  • Gene Transfer, Horizontal
  • Integrons
  • Molecular Sequence Data
  • Plasmids / drug effects
  • Plasmids / genetics*
  • Quinolones / pharmacology*
  • beta-Lactamases / genetics

Substances

  • Bacterial Proteins
  • Escherichia coli Proteins
  • Qnr protein, Klebsiella pneumoniae
  • Quinolones
  • Sul1 protein, E coli
  • Cephalosporinase
  • beta-Lactamases