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Gentamicin-resistant menadione and hemin auxotrophic Staphylococcus aureus persist within cultured endothelial cells

J M Balwit1, P van Langevelde, J M Vann

  • 1Department of Medical Microbiology, University of Wisconsin Medical School, Madison.

Insights

Staphylococcus aureus auxotrophs showed reduced virulence but enhanced survival inside cells. Supplementation restored virulence, suggesting a mechanism for bacterial evasion of defenses and antimicrobial resistance.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Molecular Biology

Background:

  • Staphylococcus aureus is a significant human pathogen.
  • Understanding bacterial adaptation and survival mechanisms is crucial for developing new treatments.
  • Menadione and hemin are essential compounds for bacterial metabolism and virulence.

Purpose of the Study:

  • To investigate the role of menadione and hemin auxotrophy in Staphylococcus aureus virulence.
  • To determine the impact of menadione and hemin supplementation on bacterial growth, hemolytic activity, and intracellular survival.
  • To explore the potential of aminoglycoside selection for generating S. aureus variants with altered virulence properties.

Main Methods:

  • Generating menadione and hemin auxotrophs of Staphylococcus aureus using in vitro gentamicin selection.
  • Assessing hemolytic activity of parent and auxotrophic strains.
  • Evaluating intracellular survival of bacteria within cultured bovine aortic endothelial cells.
  • Supplementing auxotrophs with exogenous menadione or hemin to observe effects on growth and virulence.

Main Results:

  • Generated Staphylococcus aureus menadione and hemin auxotrophs exhibited reduced hemolytic activity.
  • These auxotrophs demonstrated enhanced intracellular survival within endothelial cells compared to the hemolytic parent strain.
  • Supplementation with menadione or hemin restored rapid growth, increased hemolytic activity, and reduced intracellular persistence.
  • The restored virulence matched that of the original hemolytic clinical parent strain.

Conclusions:

  • Aminoglycoside selection can generate Staphylococcus aureus auxotrophs with altered virulence.
  • Menadione and hemin auxotrophy influences S. aureus hemolytic activity and intracellular survival.
  • Persistence of these variants in the intracellular environment may contribute to immune evasion and antimicrobial resistance.
  • Targeting menadione and hemin metabolism could be a strategy to combat S. aureus infections.

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