Contribution of sialic acid-binding adhesin to pathogenesis of experimental endocarditis caused by Streptococcus gordonii DL1

Abstract

An insertional mutation in hsa, the gene encoding the sialic acid-binding adhesin of Streptococcus gordonii DL1, resulted in a significant reduction of the infection rate of the organism and an inflammatory reaction in the rat aortic valve with experimental endocarditis, suggesting that the adhesin contributes to the infectivity of the organism for heart valves.

FIG. 1.

Bacterial density in vegetations infected with S. gordonii DL1 (filled dots) or EM230 (open dots). Each dot in a column represents the bacterial density in a vegetation (log₁₀ CFU/mg of vegetation) in a single rat. Dots below the zero level represent culture-negative vegetations. Differences in median vegetation bacterial densities and differences in rates of valve infections were evaluated by the Mann-Whitney U test and Fisher's exact probability test, respectively. N.S., not significant.

FIG. 2.

Histopathological aspects of vegetation that developed on aortic valves of rats after catheterization and challenge with S. gordonii DL1R2 or EM230. Paraffin sections of cardiac tissues including aortic valves were stained with hematoxylin and eosin. Bars in the upper panels (low magnification) and lower panels (high magnification) represent 1 mm and 0.1 mm, respectively. There is no catheter space in the upper right panel because the vegetation was too small to be associated with the catheter. A, aortic wall; AV, aortic valve; C, space formed by catheter; ML, myocardium of left ventricle.

FIG. 3.

Bacterial densities in vegetations infected with S. gordonii DL1 (filled dots) and EM230 (open dots). Six catheterized rats were challenged with a 1:1 mixture of both strains. Each pair represents the bacterial density of the vegetation (log₁₀ CFU/mg of vegetation) in a single rat. Differences between the means of bacterial densities in vegetations were evaluated by the paired t test.