Mupirocin resistance in staphylococci: development and transfer of isoleucyl-tRNA synthetase-mediated resistance in

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Biosensor for Detection of Antibiotic Resistant Staphylococcus Bacteria

Published on: May 8, 2013

D G Thomas1, J M Wilson, M J Day

  • 1Welsh School of Pharmacy, Cardiff University, UK.

Journal of Applied Microbiology
|April 23, 1999
PubMed

Insights

High-level mupirocin resistance in Staphylococcus aureus can be plasmid-mediated, allowing transfer between bacteria. Other resistance forms likely stem from chromosomal mutations affecting isoleucyl-tRNA synthetase sensitivity.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Antimicrobial Resistance

Background:

  • Mupirocin is a crucial topical antibiotic for treating Staphylococcus aureus infections.
  • Emergence of mupirocin resistance poses a significant threat to clinical efficacy.
  • Understanding resistance mechanisms is vital for effective treatment strategies.

Purpose of the Study:

  • To investigate the transferability and genetic basis of mupirocin resistance in Staphylococcus aureus.
  • To determine the impact of different resistance levels on the sensitivity of isoleucyl-tRNA synthetase (IRS).

Main Methods:

  • Experimental transfer of mupirocin resistance between Staphylococcus species.
  • Enzymatic assays measuring mupirocin inhibition of crude isoleucyl-tRNA synthetases (IRS).
  • Determination of 50% inhibitory concentrations (IC50) for various resistant and sensitive strains.

Main Results:

  • High-level mupirocin resistance was transferable between Staphylococcus aureus, Staphylococcus epidermidis, and Staphylococcus haemolyticus via plasmids.
  • Moderately resistant strains and those with in vitro-induced resistance did not show plasmid-mediated transfer.
  • Enzyme assays revealed significantly higher IC50 values for IRS from highly resistant clinical isolates and transconjugants, indicating reduced drug sensitivity.

Conclusions:

  • High-level mupirocin resistance in clinical Staphylococcus aureus isolates is primarily plasmid-mediated, involving a distinct resistant IRS.
  • Moderate resistance and in vitro-acquired high-level resistance are likely due to chromosomal mutations affecting the native IRS sensitivity.

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