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Cell wall thickness and the molecular mechanism of heterogeneous vancomycin-intermediate Staphylococcus aureus

J Cui1, H Zhang2, Z Mo1

  • 1Department of Pulmonary and Critical Care Medicine, Chinese PLA General Hospital, Beijing, China.

Letters in Applied Microbiology
|February 4, 2021
PubMed

Insights

Methicillin-resistant Staphylococcus aureus (MRSA) with reduced vancomycin (VAN) sensitivity shows thicker cell walls. Upregulated cell wall synthesis genes in hVISA strains may explain VAN resistance in MRSA infections.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Infectious Diseases

Background:

  • Methicillin-resistant Staphylococcus aureus (MRSA) exhibiting reduced vancomycin (VAN) sensitivity poses a significant clinical challenge.
  • Treatment failures linked to VAN-intermediate Staphylococcus aureus (hVISA) highlight the need to understand resistance mechanisms.

Purpose of the Study:

  • To elucidate the molecular mechanisms behind reduced VAN sensitivity in a hVISA strain.
  • To compare the hVISA strain with a VAN-sensitive MRSA (N315) strain.

Main Methods:

  • Transmission electron microscopy (TEM) to analyze cell wall thickness.
  • Real-time quantitative PCR (RT-qPCR) to assess gene expression levels related to cell wall synthesis.

Main Results:

  • The hVISA strain exhibited significantly thicker cell walls compared to the N315 strain (36.72 nm vs 28.15 nm).
  • Expression levels of cell wall synthesis genes (glmS, vraR/S, sgtB, murZ, PBP4) were significantly higher in the hVISA strain.

Conclusions:

  • Upregulation of cell wall synthesis genes is a potential molecular mechanism for cell wall thickening in hVISA.
  • This thickening may contribute to the observed reduced VAN sensitivity and resistance in MRSA.
Keywords:
MRSART-PCRTEMcell wall thicknesshVISAmolecular mechanism

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