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Experimental Endocarditis Model of Methicillin Resistant Staphylococcus aureus (MRSA) in Rat
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DltABCD- and MprF-mediated cell envelope modifications of Staphylococcus aureus confer resistance to platelet

Christopher Weidenmaier1, Andreas Peschel, Volkhard A J Kempf

  • 1Cellular and Molecular Microbiology Division, Medical Microbiology and Hygiene Department, University of Tübingen, 72076 Tübingen, Germany.

Infection and Immunity
|November 22, 2005
PubMed

Insights

Mutations in Staphylococcus aureus dltA and mprF genes increase susceptibility to antimicrobial peptides and reduce virulence in endovascular infections, highlighting the role of surface charge in pathogenesis.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Bacterial Pathogenesis

Background:

  • Staphylococcus aureus surface charge modifications by DltABCD and MprF proteins enhance resistance to cationic antimicrobial peptides (CAPs).
  • These modifications are crucial for S. aureus pathogenesis, particularly in endovascular infections where CAPs like thrombin-induced platelet microbicidal protein 1 (tPMP-1) play a role.

Purpose of the Study:

  • To investigate the impact of dltA and mprF mutations on S. aureus susceptibility to tPMP-1.
  • To assess the effect of these mutations on bacterial adherence to endothelial cells (EC) and matrix proteins.
  • To evaluate the in vivo virulence of mutant strains in a rabbit endocarditis model.

Main Methods:

  • Generated dltA and mprF mutant strains of S. aureus.
  • Assessed in vitro susceptibility to tPMP-1.
  • Measured bacterial adherence to EC, fibronectin, fibrinogen, and platelets.
  • Utilized a rabbit endocarditis model to evaluate in vivo virulence, including colonization, proliferation, and metastatic infection.

Main Results:

  • Both dltA and mprF mutations significantly increased S. aureus susceptibility to tPMP-1 in vitro.
  • The dltA mutation, but not mprF, reduced bacterial adherence to EC in vitro.
  • Both mutations attenuated virulence in vivo, reducing colonization and proliferation in vegetations; only dltA significantly reduced metastatic infections.

Conclusions:

  • Surface charge modifications mediated by DltABCD and MprF are critical for S. aureus resistance to CAPs and virulence in endovascular infections.
  • Teichoic acid-dependent endothelial cell interactions are important for pathogenesis.
  • Targeting these surface modifications offers potential therapeutic strategies against S. aureus endovascular infections.

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