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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
Summary
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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