Group B Streptococcal Colonization, Molecular Characteristics, and Epidemiology

Abstract

Streptococcus agalactiae or group B streptococcus (GBS) is a leading cause of serious neonatal infections. GBS is an opportunistic commensal constituting a part of the intestinal and vaginal physiologic flora and maternal colonization is the principal route of GBS transmission. GBS is a pathobiont that converts from the asymptomatic mucosal carriage state to a major bacterial pathogen causing severe invasive infections. At present, as many as 10 serotypes (Ia, Ib, and II–IX) are recognized. The aim of the current review is to shed new light on the latest epidemiological data and clonal distribution of GBS in addition to discussing the most important colonization determinants at a molecular level. The distribution and predominance of certain serotypes is susceptible to variations and can change over time. With the availability of multilocus sequence typing scheme (MLST) data, it became clear that GBS strains of certain clonal complexes possess a higher potential to cause invasive disease, while other harbor mainly colonizing strains. Colonization and persistence in different host niches is dependent on the adherence capacity of GBS to host cells and tissues. Bacterial biofilms represent well-known virulence factors with a vital role in persistence and chronic infections. In addition, GBS colonization, persistence, translocation, and invasion of host barriers are largely dependent on their adherence abilities to host cells and extracellular matrix proteins (ECM). Major adhesins mediating GBS interaction with host cells include the fibrinogen-binding proteins (Fbs), the laminin-binding protein (Lmb), the group B streptococcal C5a peptidase (ScpB), the streptococcal fibronectin binding protein A (SfbA), the GBS immunogenic bacterial adhesin (BibA), and the hypervirulent adhesin (HvgA). These adhesins facilitate persistent and intimate contacts between the bacterial cell and the host, while global virulence regulators play a major role in the transition to invasive infections. This review combines for first time epidemiological data with data on adherence and colonization for GBS. Investigating the epidemiology along with understanding the determinants of mucosal colonization and the development of invasive disease at a molecular level is therefore important for the development of strategies to prevent invasive GBS disease worldwide.

Within-Host Diversity and Vertical Transmission of Group B Streptococcus Among Mother-infant Dyads in The Gambia

“…This clone has also been linked to transmission between humans and cattle [21]. Several studies have associated ST196 with serotype IV [22]. We are aware of only one other study which reported one strain out of 102 prospectively collected strains to be ST196 with a serotype II capsular backbone [23].…”

Pan-GWAS of Streptococcus agalactiae highlights lineage-specific genes associated with virulence and niche adaptation

“…Streptococcus agalactiae (Group B Streptococcus, GBS) forms part of the normal gastrointestinal and urogenital microbiota, occasionally associated with causing lifethreatening invasive disease in infants, pregnant women and adults with co-morbidities [Shabayek and Spellerberg, 2018]. Since the 1970s, GBS has been reported as one of the leading causes of neonatal mortality and morbidity in the US [Dermer, et al, 2004] but it is increasingly recognised that the burden is greatest in low-to-middle income countries.…”

Capsular polysaccharide of Streptococcus agalactiae is an essential virulence factor for infection in Nile tilapia (Oreochromis niloticus Linn.)

“…Virulence‐associated factors including those driving bacterial adhesion and colonization (Lmb, DltA, BibA, FbsA, FbsB and pili), bacterial invasion (HylE, CspA, and Gap), immune evasion (CylE, CpsA, ScpB and sialic acid) and toxicity (CylE, HylB and Cfb) can promote GBS entry into host cells and facilitate the intracellular survival and spread of GBS (Kayansamruaj, Pirarat, Katagiri, Hirono, & Rodkhum, ; Shabayek & Spellerberg, ; Udo, Boswihi, & Al‐Sweih, ; Zhang et al, ). Additionally, the capsule covers the outer layer of GBS strains, which is mainly composed of the capsular polysaccharide (CPS).…”