Bacterial Adherence The ability of various microbial species to adhere to specific sites determines the anatomic localization of infection caused by these microorganisms. Mediators of bacterial adherence serve as virulence factors in the pathogenesis of IE. Numer- ous bacterial surface components present in streptococci, staphylococci, and enterococci have been shown in animal models of experimental endocarditis to function as critical adhesins. Some viridans group streptococci contain a FimA protein that is a lipoprotein receptor antigen I (LraI) that serves as a major adhesin to the fibrin platelet matrix of NBTE.17 Staphylococcal adhesins function in at least 2 ways. In one, microbial surface components recognizing adhesive matrix molecules facilitate the attachment of staphylococci to human extracellular matrix proteins and to medical devices that become coated with matrix proteins after implantation. In the other, bacterial extracellular structures contribute to the formation of biofilm that forms on the surface of implanted medical devices. In both cases, staphylococcal adhesins are important virulence factors. Both FimA and staphylococcal adhesins are immunogenic in experimental infections. Vaccines prepared against FimA and staphylococcal adhesins provide some protective effect in experimental endocarditis caused by viridans group strepto- cocci and staphylococci.18,19 The results of these experimen- tal studies are highly intriguing, because the development of an effective vaccine for use in humans to prevent viridans group streptococcal or staphylococcal IE would be of major importance. Proliferation of Bacteria Within a Vegetation Microorganisms adherent to the vegetation stimulate further deposition of fibrin and platelets on their surface. Within this secluded focus, the buried microorganisms multiply as rap- idly as bacteria in broth cultures to reach maximal microbial densities of 108 colony-forming units per gram of vegetation within a short time on the left side of the heart, apparently uninhibited by host defenses in left-sided lesions. 