The results presented here demonstrate a differential mechanism and binding efficiency for the adhesion of early versus late growth phase S. aureus to immobilized platelets.

Objective-The objective of this study is to delineate the molecular mechanisms responsible for Staphylococcus aureus-platelet adhesion as a function of physiologically relevant wall shear stresses. Methods and Results-A parallel plate flow chamber was used to quantify adhesion of wild-type, Spa Ϫ , ClfA Ϫ and SdrCDE Ϫ strains to immobilized platelet layers. In the absence of plasma, adhesion increases with increasing wall shear rate from 100 to 5000 seconds Ϫ1 . The presence of plasma significantly enhances adhesion at all shear levels. Addition of exogenous fibrinogen yields adhesion levels similar to plasma in the lower shear regimes, but has a diminishing effect on potentiating adhesion at higher shear rates. Alternatively, as shear rate increases von Willebrand factor (VWF) plays an increasingly significant role in mediating binding. Conclusions-Addition of plasma proteins potentiates S aureus-platelet

The results presented herein demonstrate that the mode of growth, temporal adhesin expression pattern, and hydrodynamic shear govern S. aureus adhesion to immobilized platelets. ClfA was identified as the critical binding adhesin, regardless of the mode or phase of growth.