June 23, 2006
Endocarditis is a potentially deadly infection of the heart’s endocardium and often its valves and other nearby tissue. Its infectious hallmark is aggregations, or so-called vegetations, of various bacteria, immune cells called leukocytes, and a matrix of the blood-clotting protein fibrin and blood platelets. Of the bacteria inhabiting these vegetations, the most frequently identified belong to the genus Streptococcus. Previous animal studies in a well-established rat model of the condition indicate that the ability of streptococci to resist or avoid circulating immune cells may be an important step in the development of infective endocarditis. In the June issue of the journal Infection and Immunity, NIDCR scientists and colleagues take this discovery a step further with the oral bacterium Streptococcus gordonii, one of the well-established causes of endocarditis. Using a well-established rat model of endocarditis, they show “significant differences” in the virulence of seven representative species of S. gordonii. Importantly, these differences appear to be correlated solely with the interaction of the bacteria with leukocytes. The scientists found that after what should have been a deadly encounter with the leukocytes, nearly half of the strains responsible for severe endocarditis survived within the immune cells and ostensibly re-emerged to infect heart valves. Interestingly, among the non-infectious strains, nearly all were killed by the leukocytes. In future studies, by identifying the genes that help the resistant strains survive the leukocytes, scientists may be able to glean new insights into the development of infective endocarditis and discover new approaches for its prevention.