Cell Surface and Cytosolic Proteins of Group B Streptococcus Adding New Dimensions in Its Colonization and Pathogenesis

Streptococcus agalactiae or Group B streptococcus (GBS) is an opportunistic human pathogen known for their invasive diseases caused in newborns, pregnant women, and nonpregnant adults. This pathogen even being an asymptomatic colonizer of adult humans, still they result in a broad range of disease manifesta-tions starting from mild skin diseases to pneumonia, meningitis, and septicemia. Of the 10 GBS capsular types, the majority of invasive neonatal diseases are associated with the serotype III. GBS is a pathogen that has developed some strategies to resist host immune defenses. The formidable array of GBS virulence factors makes this bacterium at the forefront of neonatal pathogens. The involvement of bacterial components in the host-pathogen interaction of GBS pathogenesis and its related diseases is thought to be due to a variety of virulence factors expressed by Streptococcus agalactiae . Pathogenic factors of streptococcus promote infections by their coordinated activity. These factors/determinants initially get a stimulus by the communication between specific ligands and their respective receptors in a host-pathogen interaction. These in turn activate adhesion and invasion mechanisms by mediating the attachment of pathogen via cell wall associated/secretory proteins, e.g., adhesins followed by their entry into the host cell eventually deciding their fate to live by activation of mechanisms like phagocytosis. These mediators/deter-minants also modulate the immune responses by the host toward the pathogen. A number of new GBS surface-exposed or secreted proteins have been identified (GBS immunogenic bacterial adhesion protein, leucine-rich repeat of GBS, serine-rich repeat proteins), the three-dimensional structures of known streptococcal proteins ( α C protein, C5a peptidase) have been solved, and an understanding of the pathogenetic role of “old” and new determinants