Abstract

We previously reported that a mouse model reflected, at least in part, the pathogenic mechanism of bacteremia observed during streptococcal toxic shock syndrome caused by group A Streptococcus (GAS). We have extended this study by assaying the in vitro adhesion of these same isolates to mammalian cells. Unexpectedly, we found that high-virulence GAS isolates in the mouse model showed low adhesion to the host cells. Similarly, the rate of recovery from the peritoneal cavity and cardiac blood of mice after intraperitonial injection was higher for high- than for low-virulence strains. Levels of expression of molecules that affect the adhesion of GAS to host cells were not significantly correlated with GAS virulence. Taken together, these results indicate that the invasiveness of GAS, reflected as higher virulence, is correlated directly with lower adhesion to host cells.

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