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Staphylococcus aureus response and adaptation to vancomycin.

Anaëlle Fait1, Stephanie Fulaz Silva2, Jack Åke Harry Abrahamsson2

  • 1Department of Veterinary and Animal Sciences, University of Copenhagen, Frederiksberg, Denmark; Department of Environmental Systems Science, ETH Zürich, Zürich, Switzerland.

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Summary

Antibiotic resistance in Staphylococcus aureus is a growing threat. This review details vancomycin-intermediate (VISA) and heterogeneous vancomycin-intermediate (hVISA) strains, focusing on detection and treatment strategies for these challenging infections.

Keywords:
CollateralEpistasisGraXSRLipid IIRpoBVISAVraTSRWalRKhVISA

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Area of Science:

  • Microbiology
  • Infectious Diseases
  • Antimicrobial Resistance

Background:

  • Antibiotic resistance in Staphylococcus aureus, particularly Methicillin-resistant S. aureus (MRSA), poses a significant global health challenge.
  • A subset of MRSA strains exhibit reduced susceptibility to vancomycin, the primary treatment, manifesting as vancomycin-intermediate S. aureus (VISA) or heterogeneous vancomycin-intermediate S. aureus (hVISA).
  • VISA/hVISA strains are characterized by cell wall thickening and diminished vancomycin binding, leading to subtle and variable susceptibility changes, complicating detection.

Purpose of the Study:

  • To review current knowledge on VISA and hVISA strains of Staphylococcus aureus.
  • To explore factors influencing VISA development, including genetic background and transient resistance mechanisms.
  • To investigate collateral susceptibility and the impact of specific mutations on antibiotic resistance.

Main Methods:

  • Literature review summarizing current understanding of VISA and hVISA.
  • Discussion of genetic epistasis and transient VISA mechanisms mediated by signal transduction systems (e.g., VraTSR, GraXSR, WalRK).
  • Analysis of mutations in rpoB and their structural impact on RNA polymerase, relating to rifampicin resistance.

Main Results:

  • VISA/hVISA strains result from accumulated mutations affecting cell wall synthesis and vancomycin binding.
  • Transient VISA phenotypes can emerge due to altered gene expression via specific regulatory pathways.
  • Mutations in rpoB can influence protein structure and potentially confer cross-resistance or collateral susceptibility.

Conclusions:

  • Understanding the genetic and transcriptional underpinnings of VISA/hVISA is crucial for improved detection.
  • Identifying strains at risk for VISA development can guide targeted antibiotic therapy.
  • Further analysis of these strains may help preserve vancomycin's efficacy for future treatments.