Abstract:In Streptococcus sanguinis (sanguis) induced experimental endocarditis, we sought evidence that the development of aortic valvular vegetation depends on the availability of fibrin. Endocarditis was induced in New Zealand white rabbits by catheter placement into the left ventricle and inoculation of the bacteria. Fibrin was localized in the developing vegetation with 99mTechnetium (Tc)-Iabeled anti-fibrin antibody one or three days later. When rabbit anti-fibrin antibody was given intravenously on day 1, the mass of aortic valvular vegetation was significantly reduced at day 3; infusion of non-specific rabbit IgG showed no effect. The 99mTc-labeled anti-fibrin antibody also labeled kidneys that showed macroscopic subcapsular hemorrhage. To learn if the deposition of fibrin in the kidneys was a consequence of endocarditis required a comparison of farm-bred and specific pathogen-free rabbits before and after the induction of endocarditis. Before induction, the kidneys of farm-bred rabbits were labeled, but specific pathogen-free rabbits were free of labeling and signs of macroscopic hemorrhage. After 3 days of endocarditis, kidneys of 10 of 14 specific pathogen-free rabbits labeled with 99mTc-labeled anti-fibrin antibody and showed hemorrhage. Kidney lesions were suggested to be a frequent sequellae of S. sanguinis infective endocarditis. For the first time, fibrin was shown to be required for the continued development of aortic valvular vegetations.
Key words: Fibrin, Anti-fibrin antibody, Endocarditis, Streptococcus sanguinis (sanguis)The pathogenesis of infective endocarditis is complex and involves the formation of platelet and fibrin-rich, septic vegetation on previously damaged heart valves (18,19). Although previous valvular disease is a major risk factor, the viridans group of streptococci have been frequently implicated as pathogens consequent to the occurrence of bacteremia (29,31). When bacteria adhere to injured valves, a platelet-fibrin matrix forms, developing into vegetation that enlarges over time as indicated by histological evidence from rabbits (10). The vegetation appears to increase in mass by the growth of infecting microbial colonies and accumulation of platelets; fibrin deposition is prominent. Yet there is no clear evidence that the developing mass of vegetation requires the unimpeded polymerization of fibrin.As the vegetation develops, the tissue factor is expressed locally through an activation of the extrinsic pathway of coagulation (3,4 sion is generally accompanied by clotting and coagulation, the vegetation is therefore suggested to form as a septic thrombus. As expected for a septic thrombus, the fibrinolytic treatment of experimental endocarditis with tissue plasminogen activator reduces the accumulation of platelets and inhibits the continued development of the vegetative mass (25). During endocarditis, therefore, the increasing mass of valvular vegetation is expected to be dependent on the accumulation of fibrin if the lesions are thrombus-like.To study the hypothesis tha...