Review examines pathophysiology of Group B Streptococcus infections in neonates, suggesting vaccine need.
Group B Streptococcus (GBS) remains a leading cause of neonatal morbidity and mortality worldwide. About 18% of pregnant women are colonized in the gastrointestinal or genitourinary tracts. Vaginal colonization can result in ascending intrauterine infection, enabling GBS to reach the amniotic fluid and infect the fetus during pregnancy or the newborn at delivery, leading to invasive GBS (iGBS) disease. Early-onset disease (EOD) typically manifests as sepsis, whereas late-onset disease (LOD) is more often associated with meningitis. Intrapartum antibiotic prophylaxis (IAP), based on screening at 36-37 weeks' gestation, has substantially reduced EOD but not LOD, and implementation remains difficult in low- and middle-income countries (LMICs) with limited resources. This underscores the urgent need for a safe, effective, and affordable maternal GBS vaccine. This review examines how GBS virulence factors interact with host factors, causing iGBS. Understanding these mechanisms is essential for vaccine design and therapeutic development.
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Hamimi et al. (2026) studied this question.
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