Aggregation of platelets by bacteria is a potential factor in the pathogenesis of infective endocarditis. Twenty-five strains from the group, including 15 recent isolates from cases of endocarditis, were compared for their ability to aggregate human and rat platelets over periods of 15 and 25 min, respectively. In each case, 76% of strains caused aggregation; the median time to onset of aggregation was longer for human platelets (12 min) than for rat platelets (1 min). Strains unable to aggregate human platelets included three from cases of endocarditis. There was no correlation between the ability to aggregate human and rat platelets, although the majority of strains (60%) aggregated both. Tests on representative strains for their ability to aggregate rabbit platelets gave results similar to those for rat platelets, including a median time of 1 min to onset of aggregation. The differences in the ability of individual bacterial strains to aggregate human and animal platelets indicate that caution is needed in extrapolating in-vitro observations to the in-vivo situation.


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