Correlation of epithelial cell invasiveness of group B streptococci with clinical source of isolation.

Neonatal infections caused by Group B streptococci (GBS) may lead to pneumonia, sepsis, or meningitis indicating that GBS are able to invade tissues and enter the bloodstream from infected sites. In this study, we showed that the tissue invasiveness of GBS may be related to their ability to invade epithelial cells in vitro by correlating the degree of GBS invasion of cultured human respiratory epithelial cells with the clinical source of isolation. Among 77 isolates tested, those from invasive infections of neonates and adults were significantly (P < 0.001) more invasive than those from vaginal carriers and colonised neonates without clinical symptoms. Furthermore, isolates from the blood were more invasive (P < 0.05) than those from other sites. GBS invasion seemed to be mediated by bacterial surface proteins since trypsin treatments of streptococci significantly reduced their invasion into epithelial cells and invasiveness was not limited to a certain capsular serotype. The two major GBS surface protein antigens c and R, however, were not involved in the invasion process. These results indicate that in vitro invasion of cultured human cells reflects the in vivo invasive property of GBS and involves bacterial surface components different from known virulence factors such as capsule or protein antigens c and R.