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Biosensor for Detection of Antibiotic Resistant Staphylococcus Bacteria
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Biosensor for Detection of Antibiotic Resistant Staphylococcus Bacteria

Published on: May 8, 2013

Distribution of fusidic acid resistance determinants in methicillin-resistant Staphylococcus aureus

F B McLaws1, A R Larsen, R L Skov

  • 1Antimicrobial Research Centre and Institute of Molecular and Cellular Biology, University of Leeds, Leeds, United Kingdom.

Antimicrobial Agents and Chemotherapy
|December 15, 2010
PubMed

Insights

Fusidic acid resistance in Staphylococcus aureus is rising, driven by both the spread of resistant strains and the transfer of resistance genes. Understanding these mechanisms is crucial for combating MRSA infections.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Antimicrobial Resistance

Background:

  • Increasing prevalence of fusidic acid resistance in Staphylococcus aureus, including methicillin-resistant S. aureus (MRSA), over the past two decades.
  • Limited understanding of the specific determinants mediating fusidic acid resistance and the relative contributions of clonal spread versus horizontal gene transfer.

Purpose of the Study:

  • To investigate the mechanisms and transmission routes of fusidic acid resistance in clinical MRSA isolates.
  • To determine the roles of specific resistance genes (fusB, fusC) and target mutations (fusA) in fusidic acid resistance.
  • To assess the impact of clonal dissemination versus horizontal gene transfer on the prevalence of fusidic acid resistance.

Main Methods:

  • Analysis of 1,639 MRSA isolates collected in Denmark between 2003 and 2005.
  • Determination of fusidic acid Minimum Inhibitory Concentrations (MICs).
  • Genotypic analysis to identify resistance determinants (fusB, fusC) and mutations in the fusA gene.

Main Results:

  • 17.6% of MRSA isolates exhibited resistance to fusidic acid (MIC >1 μg/ml).
  • Fusidic acid resistance was primarily mediated by the fusB or fusC genes (∼87% of resistant isolates), with the remainder due to fusA mutations.
  • The CC80-MRSA-IV clone carrying fusB accounted for 61% of resistant isolates, and a CC5 clone with fusC represented 12%.

Conclusions:

  • Clonal dissemination, particularly of CC80-MRSA-IV carrying fusB, is a major driver of fusidic acid resistance in European MRSA strains.
  • Horizontal transmission of fusidic acid resistance genes (fusB, fusC) has also contributed significantly, evidenced by their presence across diverse genetic lineages and mobile genetic elements.
  • Both clonal spread and horizontal gene transfer are critical factors in the rising prevalence of fusidic acid resistance in MRSA.

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