Various micro-organisms have been implicated as causative agents for bacterial endocarditis, including lactobacilli and in particular the viridans streptococci which are more commonly associated with dental caries. Of these, the most frequently isolated one has the descriptive name Streptococcus sanguis. The disease is characterized by growth of micro-organisms within a platelet-fibrin thrombus protruding from a valve leaflet. An understanding of the pathogenesis involves knowledge of the mechanisms of conversion of the normal vascular surface to a thrombogenic one and the adhesion of micro-organisms to such surfaces. Model systems to study this interaction include experimental animals, mammalian epithelial cells and platelets, and proteins such as fibronectin and fibrinogen. Microbial protein surface components (adhesins) and lipoteichoic acid have also been implicated. Capsular polysaccharides may be involved, but the role of dextrans formed from sucrose has been over-emphasized as the polymers are not formed in situ. Antibiotic prophylaxis for patients at risk is based on bacteriostatic or bactericidal action. However, bacterial cell surface components involved in adhesion may also be affected, and knowledge of such reactions could provide a more rational basis for antibiotic prophylaxis.