Streptococcus agalactiae, also known as Group B Streptococcus (GBS), is a commensal bacteria that is commonly found in the vagina of approximately 30% of healthy women. While GBS does not normally pose a health risk to humans, GBS infection is a serious risk for neonatal infants. This otherwise innocuous bacterium is the leading cause of neonatal septicemia, pneumonia, and meningitis. Neonatal GBS infection carries with it a 10% mortality rate, and meningitis caused by GBS leaves 25 to 35% of survivors with permanent neurological damage. Current treatment of GBS is focused on the identification of “at-risk” mothers and the prevention of mother-infant transmission through intrapartum antibiotic prophylaxis (IAP). In IAP, a mother who has been identified as a GBS carrier is treated with antibiotics during her pregnancy, particularly during the third trimester. While this preventative treatment has been effective in reducing the incidence of early-onset disease (EOD), it is not without its problems. IAP has been unable to prevent a rise in infant mortality in the last decade due to late-onset disease (LOD), which occurs after the first week of life. Unfortunately, LOD is the most damaging form of GBS infection, as it tends to cause meningitis. At the same time, the rise of antibiotic-resistant strains of GBS has been linked to the widespread use of IAP as a preventative measure (11, 12).
Due to the problems with current GBS treatments, current research is focused on the development of an effective vaccine. While the fragility of the fetal and neonatal immune system makes immunizing the fetus itself impractical, neonates may develop immunity to diseases against which their mother has been vaccinated. This occurs through a phenomenon known as passive immunity, in which antibodies produced by the mother cross the placenta and enter the fetal bloodstream. Previous attempts to design vaccines for GBS have been met with difficulty due to the wide variety of infectious GBS strains. Ideally, a vaccine would target a protein that is both required for infection – also known as a virulence factor – and that is shared by all infectious strains of GBS. A second difficulty with promoting GBS immunity in infants is that the reasons for neonatal susceptibility to GBS have not previously been well-understood. While it is clear that GBS is able to prevent an effective immune response, the methods by which it does so had not been characterized.
