Platelet-bacterial interactions in the pathogenesis of infective endocarditis. Part II: The Staphylococcus
Infective Endocarditis is a microbial infection characterised by the presence of septic vegetations on the surface of the endocardium (Moreillon and Que, 2004). Infection most commonly occurs on the heart valves that has been damaged by congenital defects such as previous disease or trauma (Durack, 1995). As a result these sites have the ability to generate turbulent blood flow which in turn can cause damage to inner most lining of the blood vessels, the endothelium, which causes surface damage leading to exposure of underlying matrix protein (Ruggeri, 2009). Once exposed this highly thrombogenic surface leads to rapid platelet deposition and the formation of a fibrin network. Circulating bacteria from a transient bacteremia in turn binds to this sterile platelet fibrin nidus which allows a secondary accumulation of platelets that encase the bacteria leading to stable thrombus formation (Moreillon and Que, 2004).
Despite improvements in medical and surgical therapy, invasive staphylococcal disease causing infective endocarditis is still associated with a severe prognosis and remains a significant therapeutic challenge. Once a disease primarily affecting younger patients presenting with rheumatic heart disease, modern times see a significant increase in newer ‘at risk’ categories including patients with long term indwelling central venous catheters, patients undergoing haemodialysis and invasive intravascular procedures such as arthroplasty, immunocompromized patients and intraveneous drug abusers (Thuny et al., 2012). Treatment of infective endocarditis usually requires a multidisciplinary approach involving specialists in infectious disease, cardiologists and cardiac surgeons. Current treatment regimes consist of aggressive prolonged antibiotic therapy, frequently combined with surgery (Prendergast and Tornos, 2010, Wilson et al., 2007). Prolonged antibiotic use is often less than successful as 40% of patients relapse within 2 months of finishing clinically effective therapy.