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Group B streptococci has been a common cause of invasive infection in neonates and young infants for several decades.1 In recent years, it has been understood that group B streptococci also is an important cause of maternal obstetrical morbidity and of fetal loss. Within the past decade, a significant decline in the incidence of early-onset group B streptococcal neonatal infections has been observed in association with universal culture-based screening of pregnant women and administration of intrapartum antibiotic prophylaxis to women colonized with group B streptococci.


Rates of maternal rectal and vaginal colonization with group B streptococci during pregnancy range from 20% to 30%. Without interruption of transmission, approximately 50% of infants delivered of a colonized mother acquire mucous membrane colonization. The risk for invasive infection among colonized infants is approximately 1%. This risk is increased when there is premature onset of labor, maternal chorioamnionitis, a prolonged interval between rupture of membranes and delivery, twin pregnancy, or maternal postpartum bacteremia, among other factors. Heavy maternal colonization also increases the risk for neonatal infection. Fetal aspiration of infected amniotic fluid can result in the development of congenital pneumonia with symptoms at or shortly after birth.

Group B streptococci are gram-positive cocci that grow readily as white to gray white colony-forming units with a narrow zone of β-hemolysis when inoculated on blood agar. Group B streptococci have been classified, based on capsular polysaccharide antigens, into 8 types. Contemporary data indicate that types Ia, III, and V predominate in early-onset disease, accounting for more than three quarters of isolates from infants with invasive infection.2,3 Together with types Ib and II, these 5 types account for 99% of isolates from infant invasive early-onset disease. Among late-onset cases of group B streptococcal infection, type III strains predominate, accounting for approximately two thirds of infections. Serotype III strains also account for approximately 90% of isolates from infants with meningitis.

Clinical Manifestations

The clinical features of early-onset and later-onset group B streptococcal infections are shown in Table 286-1. Risk for early-onset infection is increased in the setting of maternal obstetric complications but term infants usually present with no risk factors other than maternal colonization. The three common clinical presentations for early-onset disease are septicemia without a focus, pneumonia, and meningitis. In excess of 75% of infants present with respiratory signs, including tachypnea, grunting, or cyanosis. Radiographic findings can be suggestive of surfactant deficiency, transient tachypnea, or congenital pneumonia. Other signs of early-onset infection are those common to neonatal sepsis, including temperature or vascular instability, poor feeding, and lethargy. Clinical signs suggesting meningeal involvement can be unapparent at the initial presentation, but seizures develop within 24 hours of presentation in 50% of infants with meningitis.

Table 286-1. Differential Characteristics of Early versus Later-Onset Group B Streptococcal Infections in Early Infancy

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