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

Int J Antimicrob Agents. 2005 May;25(5):358-73. doi: 10.1016/j.ijantimicag.2005.02.006.


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.

Publication types

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

MeSH terms

  • Animals
  • DNA Gyrase / genetics
  • DNA Topoisomerase IV / genetics
  • Drug Resistance, Bacterial / genetics
  • Escherichia coli / drug effects*
  • Escherichia coli / genetics
  • Escherichia coli Infections / drug therapy
  • Escherichia coli Infections / veterinary
  • Escherichia coli Proteins / genetics
  • Fluoroquinolones / pharmacology
  • Humans
  • Phenotype
  • Plasmids / genetics
  • Point Mutation
  • Quinolones / pharmacology*
  • Salmonella / drug effects*
  • Salmonella / genetics
  • Salmonella Infections / drug therapy
  • Salmonella Infections, Animal / drug therapy


  • Escherichia coli Proteins
  • Fluoroquinolones
  • Qnr protein, E coli
  • Quinolones
  • DNA Topoisomerase IV
  • DNA Gyrase