An appraisal of the virulence factors associated with streptococcal endocarditis.
Platelet aggregation is believed to be a virulence factor in infective endocarditis. Other factors may be adhesion to components of thrombotic vegetations, particularly platelets, fibronectin and fibrinogen. Two strains from the Streptococcus sanguis group (SSG) were chosen for comparative study on the basis that one aggregated both human and rat platelets and the other lacked this capacity. Both strains caused endocarditis in the rat model but the aggregating strain was found in higher numbers in the excised vegetations. The nonaggregating strain was unable to bind to human or rat platelets but could bind insoluble fibronectin, insoluble fibrinogen and platelet-fibrin clots from both sources, albeit to a lesser extent than the aggregating strain. These results suggest that whereas adhesion to, and aggregation of, platelets are not essential events in the initiation of the pathogenesis of experimental endocarditis, they may be factors contributing to virulence.
Manning
J E
JE
Institute of Dental Research, United Dental Hospital, Sydney NSW, Australia.
Hume
E B
EB
Hunter
N
N
Knox
K W
KW
D000818:Animals; D001422:Bacterial Adhesion; D001792:Blood Platelets / Q000382:microbiology*; D004195:Disease Models, Animal; D004697:Endocarditis, Bacterial / Q000097:blood / Q000382:microbiology*; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005353:Fibronectins / Q000378:metabolism; D006801:Humans; D010974:Platelet Aggregation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013290:Streptococcal Infections / Q000097:blood / Q000382:microbiology*; D013298:Streptococcus sanguis / Q000378:metabolism / Q000472:pathogenicity*; D014774:Virulence
D005353:Fibronectins; D005340:Fibrinogen