Mechanisms of quinolone resistance in Escherichia coli and Salmonella: Recent developments

Katie L. Hopkins*, Robert H. Davies, E. John Threlfall

*Corresponding author for this work

Research output: Contribution to journalShort surveypeer-review

381 Citations (Scopus)

Abstract

Fluoroquinolones are broad-spectrum antimicrobials highly effective for treatment of a variety of clinical and veterinary infections. Their antibacterial activity is due to inhibition of DNA replication. Usually resistance arises spontaneously due to point mutations that result in amino acid substitutions within the topoisomerase subunits GyrA, GyrB, ParC or ParE, decreased expression of outer membrane porins, or overexpression of multidrug efflux pumps. In addition, the recent discovery of plasmid-mediated quinolone resistance could result in horizontal transfer of fluoroquinolone resistance between strains. Acquisition of high-level resistance appears to be a multifactorial process. Care needs to taken to avoid overuse of this important class of antimicrobial in both human and veterinary medicine to prevent an increase in the occurrence of resistant zoonotic and non-zoonotic bacterial pathogens that could subsequently cause human or animal infections.

Original languageEnglish
Pages (from-to)358-373
Number of pages16
JournalInternational Journal of Antimicrobial Agents
Volume25
Issue number5
DOIs
Publication statusPublished - May 2005

Bibliographical note

Funding Information:
This work was funded by the UK Department for Environment, Food and Rural Affairs, project number VM02136. The authors thank their scientific colleagues for helpful comments on the manuscript.

Keywords

  • DNA gyrase
  • Escherichia coli
  • Fluoroquinolones
  • Salmonella
  • mar
  • qnr

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