Platelet-bacterial interactions in the pathogenesis of infective endocarditis. Part I: The Streptococcus

Infective endocarditis (IE) is a life threatening disease caused by a bacterial infection of the endocardial surfaces of the heart. It is typified by the formation of septic thrombi or vegetative growth on the heart valve. Typically, both platelets and fibrin are deposited on exposed extracellular matrix proteins as part of the normal response to damage of the endocardium [1]. However, this sterile platelet-fibrin nidus facilitates colonisation of the endocardium by bacteria in the bloodstream [2]. Following attachment, bacteria can recruit platelets from the circulation inducing platelet activation and platelet aggregation. This results in the development of large macroscopic vegetations which resist infiltration by both immune cells and antibiotics making IE a difficult disease to treat. These vegetations commonly occur on the heart valves and can disrupt hemodynamic patterns within the heart. This puts undue force on often already compromised valves, leading to congestive heart failure [3]. IE is notoriously difficult to treat, requiring aggressive multi-antibiotic therapy often coupled with surgery to remove vegetations and/or replace the infected valve [4]. Therapy is successful when all traces of bacteria are absent from the blood stream. Multiple species of bacteria have been isolated from the infected vegetations of patients [5, 6] with IE but the streptococci are amongst the most common cause, second only to the staphylococci whose interactions with human platelets are discussed elsewhere in this book (Chapter X). Indeed, in a recent prospective study, the role of streptococci in IE is masked by the growing incidence of staphylococcal IE resulting from the increased use of medical procedures leaving streptococci as a main cause of IE in the normal population [7, 8].