Abstract

The incidence of GBS colonization at birth was determined prospectively among 96% of 2,407 infants born over a 12-month period in an urban community hospital. GBS were recovered from one or more of the four sites cultured in 290 (12.5%) of these newborn infants, 91 of whom were heavily colonized (3 to 4 sites positive). Sepsis or meningitis occurred in 13 infants, an attack rate of 5.4/1,000 live births. Attack rates for early and late onset disease, respectively, were 3.7 and 1.7 per 1,000 live births. All serotypes were found to cause disease. The incidence of early sepsis was strikingly high (8%) in heavily colonized infants. Those colonized at 1 to 2 sites were at no greater risk than noncolonized infants. The maternal vaginal colonization rate at delivery was 19%, with acquisition from the mother documented as the primary source of the organism in early onset infections. Perinatal events, including maternal complications and signs of illness at or immediately after birth, suggested ascending infection with exposure in utero to be likely in six infants. Passive acquisition of GBS (intrapartum exposure) probably occurred in the three remaining early onset cases. This mechanism was also likely responsible for five nonbacteremic infections. The four infants with late onset sepsis or meningitis were not colonized at birth or when discharged from the nursery (day 3); a possible maternal source for infection was found in only one of these infants.

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