Staphylococcus aureus is a versatile microbial pathogen and among the most frequently isolated from nosocomical infections. The clinical manifestations are widespread and include bacteremia, endocarditis, pneumonia, osteomyelitis, septic arthritis, suppurative thrombophlebitis and abscess formation. Bacterial adherence is likely to play a central role in the disease pathogenesis of this predominantly extracellular pathogen. S. aureus expresses various adhesins as a function of growth phase that promote adherence to host cells such as platelets and/or soluble plasma proteins such as fibrinogen or fibronectin. Our current study focuses on early exponential phase S. aureus and its adhesion to immobilized platelets in the presence of physiologically relevant wall shear stresses. The mechanisms governing S. aureus adhesion to immobilized platelets via plasma, fibrinogen and fibronectin have also been investigated. Clumping factor A (ClfA) is the primary adhesin involved in S. aureus-platelet interactions at all investigated vascular shear stresses. Our results suggest that fibrinogen is the key protein at this growth phase supporting S. aureus-platelet binding. In this study, we also demonstrate shear dependant adhesion of S. aureus to platelets via fibronectin binding proteins (Fnbps) in the presence of exogenously added fibronectin. However, the contribution of this binding mechanism is minimal in comparison to fibrinogen-mediated interactions. The above findings further our understanding of the complex events underlying S. aureus pathogenesis and may ultimately lead to the development of novel therapeutics to combat staphylococcal infections.