FIMA, A MAJOR VIRULENCE FACTOR ASSOCIATED WITH STREPTOCOCCUS-PARASANGUIS ENDOCARDITIS

Adherence of microorganisms to damaged heart tissue is a crucial event in the pathogenesis of infective endocarditis. In the present study, we investigated the role of the FimA protein as a potential virulence factor associated with Streptococcus parasanguis endocarditis. FimA is a 36-kDa surface protein that is a recognized adhesin in the oral cav ity where it mediates adherence to the salivary pellicle. An insertion mutant and a deletion mutant of S. parasanguis were employed in the r at model of endocarditis to determine the relevance of FimA in endocar ditis pathogenesis. Catheterized rats were infected with either the fi mA deletion mutant VT929, the fimA insertion mutant VT930, or the isog enic, wild-type S. parasanguis FW213. Rats inoculated,vith FW213 devel oped endocarditis more frequently (50.9%) than animals inoculated with either the deletion mutant (2.7%) or the insertion mutant (7.6%) (P < 0.001). A series of in vitro assays were performed to explore the mec hanism(s) by which FimA enhanced the infectivity of S. parasanguis. Fi mA did not inhibit the uptake or the subsequent killing of S. parasang uis by phagocytic granulocytes. Similarly, FimA did not play a role in the adherence to or the aggregation of platelets. Significant differe nces were noted between FW213 and VT929 (P < 0.05) and FW213 and VT930 (P < 0.001) in their abilities to bind to fibrin monolayers. The mean percent adherence of FW213 to fibrin monolayers (2.1%) was greater th an those of VT929 (0.5%) and VT930 (0.12%). Taken together, these resu lts indicate that FimA is a major virulence determinant associated wit h S. parasanguis endocarditis and further suggest that its role is ass ociated with initial colonization of damaged heart tissue.