Time to rethink prevention of neonatal group B streptococcal disease

Group B Streptococci (GBS) are both natural colonizers and important invasive pathogens in newborns. The introduction of intrapartum antibiotic prophylaxis has led to a significant decrease in the incidence of early onset sepsis. In contrast, late onset sepsis, which accounts for up to 50% of cases, has not declined. IAP impacts microbiome development during infancy, specifically it reduces the abundance of Bifidobacterium and Bacteroides spp., which might be associated with long-term health outcomes such as asthma development and obesity. This review highlights the challenges and risks associated with GBS colonization in neonates, including the role of virulence factors and specific contribution of host immunity. Bacterial pathogenicity factors involved in adhesion and colonization, e.g. GBS pilus islands, barrier disruption, e.g. pore-forming toxin ß-hemolysin, or evasion of neonatal immune defense mediated by GBS capsular polysaccharide and membrane glycolipids are important targets to suppress the translocation of GBS and progression to invasive disease. In line with this, metabolic programming of neonatal immune cells, e.g. glycolytic capacity, is GBS strain-specific which also argues for a more tailored strategy of prevention. Given the benefits and risks of IAP, it is important to rethink strategies of preventing GBS disease including alternative strategies such as vaccination and probiotic supplementation. Further studies need to focus on modulating the developing immune-microbiome interplay including the metabolic milieu to the advantage of the vulnerable newborn.