Staphylococcus aureus is one of the most common causes of community- and hospital-acquired infections. Many common diseases caused by S. aureus include infectious endocarditis, osteomyelitis, septic arthritis, pneumonia and septicemia. The recent surge in methicillin resistant S. aureus (64.4% of cases) and continued appearance of vancomycin resistant S. aureus highlights the need to develop a clearer understanding of the pathogenesis and infective mechanisms of the bacterium. In the initial stages of infection, S. aureus adheres to surface tissues. Once inside the bloodstream, the bacterium can be carried to any location in the body and promote new infections. The overall goal of this project is to understand how bacteria incorporate into growing thrombi and the effects of the bacterial presence on thrombus formation. The first part of my research quantifies bacterial incorporation into growing thrombi both at the surface and in the aggregate. Our results demonstrate that the fibrinogen receptor ClfA plays the dominant role in promoting S. aureus incorporation. The second and third part of our research demonstrated that bacterial presence in whole blood modulates thrombus formation through both receptor-mediated interaction and physical interaction. The fourth part of our research seeks to evaluate the feasibility of using the parallel plate flow chamber to conduct more complex experimental designs such as evaluating thrombus formation on a biofilm. We conclude that the current parallel plate flow chamber system and design can accommodate more complex systems, but the practicality of the experiments depends on the experimental design and budget. In summary, this project demonstrates the importance of the ClfA receptor in bacterial integration into growing thrombi and S. aureus receptors and physical presence to modulate thrombus formation.