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Efflux pump-mediated quinolone resistance in Staphylococcus aureus strains wild type for gyrA, gyrB, grlA, and norA

J L Muñoz-Bellido1, M Alonzo Manzanares, J A Martínez Andrés

  • 1Departamento de Microbiologia, Hospital Universitario de Salamanca, Spain.

Antimicrobial Agents and Chemotherapy
|January 30, 1999
PubMed

Insights

Fluoroquinolone efflux was observed in some Staphylococcus aureus strains without typical resistance mutations. This suggests alternative mechanisms for fluoroquinolone resistance may exist in clinical settings.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Antimicrobial Resistance

Background:

  • Fluoroquinolones are critical antibiotics for treating Staphylococcus aureus infections.
  • Efflux pumps play a significant role in bacterial antibiotic resistance.
  • The norA gene and its promoter are known to be involved in fluoroquinolone resistance in S. aureus.

Purpose of the Study:

  • To investigate fluoroquinolone efflux in clinical strains of Staphylococcus aureus.
  • To determine if efflux occurs in strains lacking mutations in known resistance genes, including norA.

Main Methods:

  • Studied 47 clinical Staphylococcus aureus strains with varying ciprofloxacin Minimum Inhibitory Concentrations (MICs).
  • Assessed strains for mutations in gyrA, gyrB, grlA, and norA genes and its promoter region.
  • Quantified fluoroquinolone efflux in susceptible and resistant strains.

Main Results:

  • Forty-three of 47 strains were wild-type for gyrA, gyrB, grlA, and norA regions.
  • Forty strains (ciprofloxacin MICs 0.1-0.2 µg/ml) showed no detectable fluoroquinolone efflux.
  • Three strains (ciprofloxacin MICs 1-2 µg/ml) exhibited significant fluoroquinolone efflux.

Conclusions:

  • Fluoroquinolone efflux can be present in Staphylococcus aureus clinical isolates independent of mutations in norA and its promoter.
  • These findings indicate potential novel mechanisms of fluoroquinolone resistance in S. aureus.
  • Further research is needed to identify the specific mechanisms responsible for efflux in these strains.

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