Prevalence of mechanisms decreasing quinolone-susceptibility among Salmonella spp. clinical isolates

Autors/ores

  • Amy D. Lunn Department of Microbiology, Hospital Clinic, School of Medicine, University of Barcelona, Spain School of Medicine, University of Sheffield, Sheffield, United Kingdom
  • Anna Fàbrega Department of Microbiology, Hospital Clinic, School of Medicine, University of Barcelona, Spain
  • Javier Sánchez-Céspedes Department of Microbiology, Hospital Clinic, School of Medicine, University of Barcelona, Spain
  • Jordi Vila Department of Microbiology, Hospital Clinic, School of Medicine, University of Barcelona, Spain

Paraules clau:

Salmonella · quinolones · efflux pumps · gene gyrA · plasmid-encoded genes · antibiotic resistance

Resum

Fluoroquinolone treatment failure has been reported in patients with nalidixic acid-resistant Salmonella infections. Both chromosomal- and plasmid-mediated quinolone-resistance mechanisms have been described. The objective of this study was to identify the prevalence of these mechanisms in a collection of 41 Salmonella spp. clinical isolates causing acute gastroenteritis, obtained in the Hospital Clinic, Barcelona. The minimum inhibitory concentrations (MICs) of nalidixic acid and ciprofloxacin were determined by Etest. Mutations in the quinolone-resistance determining regions (QRDRs) of the gyrA, gyrB, and parC genes and the presence of the qnr, aac(6′)-Ib-cr, and qepA genes were detected by PCR and DNA sequencing. All isolates showed constitutive expression of an efflux pump. None of the isolates were ciprofloxacin-resistant, whereas 41.5% showed nalidixic acid resistance associated with a mutation in gyrA and overexpression of an efflux pump. Although qnrS1, qnrB6, and qepA were found in four isolates, the expression of these genes was not associated with decreased quinolone susceptibility. Mutations in the gyrA gene and overexpression of an efflux pump were critical for nalidixic acid resistance and decreased susceptibility to ciprofloxacin in these isolates. However, plasmid-mediated quinolone resistance did not seem to play a major role. To our knowledge, this is the first description of qepA in Salmonella. [Int Microbiol 2010; 13(1):15-20]

Biografies de l'autor/a

Amy D. Lunn, Department of Microbiology, Hospital Clinic, School of Medicine, University of Barcelona, Spain School of Medicine, University of Sheffield, Sheffield, United Kingdom

Department of Microbiology, Hospital Clinic, School of Medicine, University of Barcelona, Spain
School of Medicine, University of Sheffield, Sheffield, United Kingdom

Anna Fàbrega, Department of Microbiology, Hospital Clinic, School of Medicine, University of Barcelona, Spain

Department of Microbiology, Hospital Clinic, School of Medicine, University of Barcelona, Spain

Javier Sánchez-Céspedes, Department of Microbiology, Hospital Clinic, School of Medicine, University of Barcelona, Spain

Department of Microbiology, Hospital Clinic, School of Medicine, University of Barcelona, Spain

Jordi Vila, Department of Microbiology, Hospital Clinic, School of Medicine, University of Barcelona, Spain

Department of Microbiology, Hospital Clinic, School of Medicine, University of Barcelona, Spain

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Publicat

2010-07-28

Número

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Articles