Group B Streptococcus GAPDH and Immune Evasion
Paula Ferreira1,2 and Patrick Trieu-Cuot3
- 1ICBAS, Instituto de CUncias Biomedicas de Abel Salazar, Universidade do Porto, Porto, Portugal
- 2 Instituto de Investigagao e Inovagao em Saude, Universidade do Porto, Porto, Portugal
- 3 Unite de Biologie des Bacteries Pathogenes a Gram-positif, Institut Pasteur, CNRS ERL 3526,28 rue du Dr ROUX, Paris, France
The Bacterium GBS
Streptococcus agalactiae, also known as Group B Streptococcus (GBS), is a major neonatal pathogen causing pneumonia, sepsis, and meningitis (Edwards and Baker 2005; Johri et al. 2006; Phares et al. 2008; Verani et al. 2010). GBS is also responsible for significant morbidity in pregnant women and the elderly, and a cause of mortality in immunocompromised adults (Dermer et al. 2004; Edwards and Baker 2005). This Gram-positive encapsulated bacterium is a commensal of the gastrointestinal and genitourinary tracts and colonizes the birth canal of up to 30% of healthy pregnant women (Johri et al. 2006; Verani et al. 2010). Vaginal colonization during pregnancy increases the incidence of premature delivery and perinatal transmission of the bacterium (Ferrieri et al. 1977; Schuchat 2000). Neonates likely acquire part of the mother vaginal microflora, including GBS, by vertical transmission during labor through aspiration of the infected amniotic fluid. Despite early antimicrobial treatment and improvement in neonatal intensive care, up to 10% of neonatal invasive GBS infections are lethal and 25-35% of surviving infants with meningitis experience permanent neurological sequelae (Edwards and Baker 2005). As with most extracellular pathogens, GBS survival depends on its ability to evade the host immune system; neonates, particularly those born prematurely, are of course highly vulnerable to life-threatening infections.