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Characterization of the molecular mechanisms of quinolone resistance in Yersinia enterocolitica O:3 clinical isolates

  • S. Capilla
    ,
  • ,
  • P. Goñi
    ,
  • M. C. Rubio
    ,
  • M. T. Jiménez de Anta
    ,
  • R. Gómez-Lus
  • University of Zaragoza
    ,
  • ,
  • U.A.S.P.
    ,
  • Hospital Clínic – Universitat de Barcelona
Research Output: Contribution to journal Article Peer-review

Open access

Publication Information

Output type

Research Output: Contribution to journal Article Peer-review

Original language

English

Pages from-to (Number of pages)

Pages 1068-1071 (4 pages)

Journal (Volume, Issue Number)

Journal of Antimicrobial Chemotherapy (Volume 53, Issue 6)

Publication milestones

  • Published - 06/2004

Publication status

Published - 06/2004

ISSN

0305-7453

Publication IDs

  • Scopus: 3042685848
  • PubMed: 15117921

Abstract

Objectives: The aim of this study was to determine the roles of mutations in the gyrA and parC genes and the overexpression of efflux pump(s) as mechanisms of resistance to quinolones. Forty-five Yersinia enterocolitica O:3 clinical isolates (41 nalidixic acid-resistant, three nalidixic acid-susceptible and one nalidixic acid-resistant strain obtained in vitro) were analysed. Results: All the nalidixic acid-resistant strains showed mutations in the gyrA gene and none in the parC gene. The presence of the inhibitor produced decreases in the MIC values of nalidixic acid by two to six serial dilution steps in 37 of the 41 nalidixic acid-resistant strains. Meanwhile, the MIC value of ciprofloxacin was affected in two strains whose values diminished three serial dilution steps. The nalidixic acid-resistant mutant obtained in vitro was also affected by the inhibitor decreasing the MIC value of nalidixic acid three serial dilutions steps whereas the MICs for the nalidixic acid-susceptible strains were not affected. Conclusions: Our results show that the high level of resistance to nalidixic acid is likely due to an overexpression of an efflux pump plus a mutation in the gyrA gene, whereas decreased susceptibility to ciprofloxacin is only associated with the presence of a mutation in the gyrA gene.

Funding Details

This work has been partially supported by grants FIS02/0353 from the Ministry of Health, Spain, and 2002 SGR00121 from the Depart- ament d’Universitats, Recerca I Societat de la Informació de Generalitat de Catalunya, Spain.
FundersFunding numbers
Ministry of Health, Spain
2002 SGR00121
DURSI
-

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