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Plasmid-mediated quinolone resistance in gram-negative bacterial species: an update

Vincent Cattoir1, Patrice Nordmann

  • 1INSERM U914, Emerging Resistance to Antibiotics, Service de Bactériologie-Virologie, hôpital de Bicêtre, Assistance Publique/Hôpitaux de Paris, Faculté de Médecine et Université Paris-Sud, K.-Bicêtre, France.

Current Medicinal Chemistry
|March 12, 2009
PubMed

Insights

Emergence of plasmid-mediated quinolone resistance (PMQR) is a growing concern. Mechanisms include Qnr proteins, AAC(6')-Ib-cr, and QepA efflux pumps, contributing to fluoroquinolone resistance in Enterobacteriaceae.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Antimicrobial Resistance

Background:

  • Quinolone and fluoroquinolone resistance has increased in human and veterinary medicine over 30 years.
  • Previously, resistance was attributed to chromosomal modifications, porin defects, and efflux pumps.
  • Plasmid-mediated quinolone resistance (PMQR) has emerged since 1998.

Purpose of the Study:

  • To review the mechanisms of plasmid-mediated quinolone resistance (PMQR).
  • To highlight the roles of Qnr proteins, AAC(6 extprime)-Ib-cr, and QepA in conferring resistance.
  • To discuss the global spread of these resistance determinants.

Main Methods:

  • Literature review of studies on quinolone resistance mechanisms.
  • Analysis of reported genetic determinants of PMQR.
  • Compilation of data on the prevalence and variants of Qnr proteins, AAC(6 extprime)-Ib-cr, and QepA.

Main Results:

  • Three main PMQR mechanisms identified: Qnr proteins, AAC(6 extprime)-Ib-cr, and QepA.
  • Qnr proteins (QnrA, QnrB, QnrC, QnrS) protect DNA gyrase and topoisomerase IV.
  • AAC(6 extprime)-Ib-cr acetylates fluoroquinolones; QepA extrudes hydrophilic fluoroquinolones.

Conclusions:

  • PMQR mechanisms significantly contribute to fluoroquinolone resistance in Enterobacteriaceae.
  • The global dissemination of Qnr, AAC(6 extprime)-Ib-cr, and QepA poses a significant public health challenge.
  • Understanding these mechanisms is crucial for developing strategies to combat antimicrobial resistance.

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