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The msaABCR operon regulates resistance in vancomycin-intermediate Staphylococcus aureus strains

Dhritiman Samanta1, Mohamed O Elasri2

  • 1The University of Southern Mississippi, Hattiesburg, Mississippi, USA.

Antimicrobial Agents and Chemotherapy
|August 27, 2014
PubMed

Insights

The msaABCR operon plays a key role in vancomycin resistance in Staphylococcus aureus (S. aureus). Deleting this operon significantly reduced vancomycin resistance and cell wall thickness in clinical strains.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Public Health

Background:

  • Vancomycin-intermediate Staphylococcus aureus (VISA) poses a significant public health threat.
  • The molecular mechanisms underlying VISA are not fully understood.
  • Identifying novel resistance mechanisms is crucial for developing effective treatments.

Purpose of the Study:

  • To elucidate the role of the msaABCR operon in vancomycin resistance in clinical VISA strains.
  • To investigate the impact of msaABCR operon on cell wall synthesis and vancomycin binding.

Main Methods:

  • Genetic manipulation: Deletion of the msaABCR operon in three clinical VISA strains (Mu50, HIP6297, LIM2).
  • Phenotypic analysis: Determination of vancomycin Minimum Inhibitory Concentration (MIC), cell wall thickness measurement, and growth rate assessment in the presence of vancomycin.
  • Biochemical assays: Evaluation of vancomycin binding capacity to bacterial cells.

Main Results:

  • Deletion of the msaABCR operon led to a significant decrease in vancomycin MIC (from 6.25 to 1.56 μg/ml) in Mu50 and HIP6297 strains.
  • Reduced cell wall thickness was observed in the msaABCR deletion mutants.
  • Mutants exhibited decreased growth rates in vancomycin-containing media and reduced vancomycin binding capacity.

Conclusions:

  • The msaABCR operon is a significant contributor to vancomycin resistance in S. aureus.
  • This operon influences cell wall synthesis and vancomycin susceptibility.
  • Targeting the msaABCR operon may offer a novel strategy to combat VISA infections.

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