Filament genes and biofilm formation in Streptococcus agalactiae

Abstract

Streptococcus agalactiae is the prominent cause of bacterial sepsis and meningitis in neonates and is also the contributing agent of a number of serious infections in immunocompromised adults. S. agalactiae run into multiple niches through an infection, suggesting that regulatory mechanisms control the expression of specific virulence factors in this bacterium. Like other Gram-positive bacteria, Group B streptococcus (GBS) can create three-dimensional structures, such as biofilms that can increase their ability to colonize and maintain in the host. Biofilm formation has been investigated by GBS under laboratory conditions and is clearly controlled under environmental conditions. Significantly, antibodies that act against the proteins of the pili can prevent the creation of biofilms. The consequences of biofilm formation in the field of asymptomatic colonization and its dissemination remain invasive and its details are examined. The complex pathway leading to biofilm development in different species of microorganisms involves the contribution of both environmental conditions and genetic factors. Numerous genes or factors have been identified as being essential or required for biofilm formation. Such genes include those that regulate surface-exposed proteins, appendages, such as pili or fimbriae, and extracellular polymeric substance (EPS) matrix materials. Pilus seems to play a key role in adhesion and attachment to host cells both in Gram-negative and Gram-positive pathogens. Their involvement in the transition from planktonic growth to a surface-attached multicellular community has also been demonstrated in many studies. Three different types of pili have been characterized in GBS as potential virulence factors. For example, type 2a pili are involved in biofilm formation.