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Streptococcus agalactiae, or Group B Streptococcus (GBS), was first identified as a pathogen in cattle, associated with bovine mastitis.1,2 Widespread recognition of GBS as a significant human pathogen occurred in the 1960s–1970s, when it emerged as the most common cause of neonatal sepsis and an important cause of bacterial meningitis in infants less than 3 months of age in the United States.3–5 It was later shown that maternal colonization with GBS in the genital or gastrointestinal track represented the most important risk factor for early-onset (between 0 and 6 days of life) GBS disease in the newborn6,7 and that administration of intrapartum antibiotics to colonized women could prevent most cases of early-onset neonatal GBS infections.8,9 Consensus guidelines for the prevention of neonatal GBS disease, developed through collaboration between public health, academic investigators, and professional organizations including obstetricians and pediatricians, with the strong support of parent advocacy groups, were first published in 1996.10–12 These guidelines, revised in 2002 to include universal screening of pregnant women for GBS colonization, resulted in dramatic declines in early-onset GBS disease in the United States.13 However, early-onset cases still occur and rates of late-onset GBS disease (between 7 and 89 days of life) have not declined despite relatively high uptake and implementation of the guidelines.14 At least ten capsular serotypes have been described; serotypes Ia, Ib, II, III, IV, and V are the most common in the United States.


GBS infections remain a leading cause of morbidity and mortality in infants in the United States and worldwide.14,16 Early-onset disease occurs in the first week of life (most in the first 48 hours of life) and often manifests as sepsis, pneumonia, and less frequently as meningitis.14,15,17 More than a quarter of cases are in preterm infants.15 Late-onset disease occurs between 7 and 89 days of life and almost a third will present with meningitis. Other presentations include bacteremia without focus (61–65%), and rarely cellulitis and pneumonia.15,17 In the era since introduction of intrapartum antibiotic prophylaxis (IAP) in the United States, the rate of early-onset GBS infection in newborns declined to 0.23/1000 live births and late-onset disease remained stable at 0.31/1000 live births in 2015.15 More than 99% of the isolates from neonatal disease fell into six common serotypes (Ia, Ib, II, III, IV, and V). Serotype III accounted for more than half (56.2%) of late-onset neonatal infections in the United States.15 In a worldwide, systematic review and meta-analysis performed by an international Infant GBS Investigator Group, the pooled incidence of invasive GBS disease in neonates was 0.41/1000 live births for early-onset disease and 0.26/1000 live births for late-onset disease. Rates were highest in Africa (1.12) and lowest in Asia (0.30). These pooled rates were considered to be underestimated given significant constraints in case identification and availability of optimal diagnostic capacity in low- ...

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