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Published on: March 2, 2020

Fluoroquinolone resistance in Neisseria meningitidis in Spain

Rocío Enríquez1, Raquel Abad, Celia Salcedo

  • 1Reference Laboratory for Meningococci, Servicio de Bacteriología, National Centre for Microbiology, National Institute of Health Carlos III, Majadahonda, Madrid, Spain.

The Journal of Antimicrobial Chemotherapy
|November 23, 2007
PubMed
Abstract

Insights

Ciprofloxacin resistance in Neisseria meningitidis is mainly due to gyrA mutations. Other genetic changes in gyrA, parE, and mtrR also contribute to reduced susceptibility in these meningococcal isolates.

Area of Science:

  • Microbiology
  • Genetics
  • Pharmacology

Background:

  • Neisseria meningitidis is a significant human pathogen.
  • Quinolones, including ciprofloxacin, are used to treat bacterial infections.
  • Understanding antimicrobial resistance mechanisms is crucial for effective treatment.

Purpose of the Study:

  • To investigate ciprofloxacin resistance in Neisseria meningitidis.
  • To identify genetic mutations associated with quinolone resistance.

Main Methods:

  • Susceptibility testing of 5300 Neisseria meningitidis isolates.
  • Analysis of mutations in quinolone resistance-determining regions (QRDRs) of gyrA, gyrB, parC, and parE genes.
  • Investigation of mutations in the mtrR gene and their effect on the MtrCDE efflux system.

Main Results:

  • Ten isolates exhibited reduced susceptibility to ciprofloxacin (MICs 0.06–0.25 mg/L).
  • Single mutations in the gyrA gene, particularly Thr-91-->Ile, were the primary mechanism of resistance.
  • No mutations were found in the QRDRs of parC and gyrB.
  • Three strains had a His-495-->Asn substitution in the parE gene.
  • Two alterations in the mtrR gene were identified, potentially affecting the MtrCDE efflux system.

Conclusions:

  • Single gyrA mutations are the predominant mechanism for ciprofloxacin resistance in Neisseria meningitidis.
  • Mutations in parE and alterations in the mtrR gene may also contribute to reduced quinolone susceptibility.
  • These findings highlight the genetic basis of meningococcal resistance to fluoroquinolones.

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