The role of platelets in infective endocarditis.
There is growing evidence that platelets play an important role in the development of infective endocarditis (IE). This review focuses on interactions between bacteria and platelets. Many types of microorganism are capable of causing endocarditis. The oral streptococci, particularly Streptococcus sanguis and S. oralis, remain the most common causative bacteria in IE but Staphylococcus aureus is becoming an increasingly important agent. Several species of bacteria and fungi are able to cause platelet aggregation in vitro, and there are indications that this ability is associated with the production of severe disease. Different bacteria appear to utilise different mechanisms of aggregation, and mechanisms for adhesion may be distinct from those responsible for aggregation. At least one commonly studied strain of S. sanguis apparently utilises the host's IgG and complement responses to induce platelet activation. IE may therefore be among the number of diseases in which immunological activation of platelets is thought to be of importance. Other bacterial strains have their own adhesins and agonists. The more virulent bacteria, notably the staphylococci, also possess proteolytic enzymes and may directly activate coagulation pathways, whereas less virulent, opportunistic pathogens, such as some streptococci and Candida albicans, may rely on interactions with host factors for colonisation and proliferation. It is proposed that platelets are involved in formation of the non-bacterial thrombotic vegetation (NBTV) and are necessary for the effective adhesion of bacteria to the NBTV, and that platelets also influence the persistence and clinical outcome of the disease through proliferation of the thrombotic vegetation. It is hypothesised that successful colonisation of the heart valves by a micro-organism depends on effective adhesion of the bacteria or fungi to platelets, in combination with the ability to induce platelet activation and aggregation.
Ford
I
I
Department of Medicine and Therapeutics, University of Aberdeen, Foresterhill, Aberdeen, Scotland. i.ford@abdn.ac.uk
Douglas
C W
CW