It seems appropriate in a symposium dedicated to the examination of septicemia, that one of the topics for discussion should be the examination of the factors which allow circulating bacteria to adhere to intracardiac or vascular endothelium. In the last 10-12 years our understanding of the pathogenesis of this disease has increased markedly. This can be attributed to a large extent to the development by Dr Freedman and hist colleagues at Yale of reproducible, simple, inexpensive animal model of infective endocarditis. The purpose of this discussion will by to summarize studies aimed at helping to explain why bacteria stick to cardiac valves, what forms the stimulus for vegetation propagation, and some new idea for possible prevention of this event.
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