Streptococcus group B (GBS) is almost exclusively a perinatal pathogen (Baker, 1977). While infections have been reported outside the perinatal period, primarily in individuals with impaired immune function, the major concern is with pregnant women and newborn infants. GBS is a common cause of urinary tract infection, amnionitis, and endometritis during pregnancy and is the principal cause of serious bacterial infection in the newborn. Early-onset disease occurs within the first few days of life, often resulting from intrauterine infection. Clinical manifestations range from respiratory distress and apnea to septic shock. Late-onset disease may occur from the end of the first week of life to three or four months of age. The usual clinical presentation is meningitis, with or without bacteremia.

GBS meningitis is followed by the usual sequelae: mental retardation, neurologic disease, seizure disorders, or deafness occur in about one-fourth of survivors. Epidemiologic studies have demonstrated that early-onset GBS disease is associated with several risk factors, including maternal amnionitis, prolonged rupture of placental membranes, deficiency of antibody to the type-specific polysaccharide antigen (Ia, Ib, II, and III), and prematurity (Boyer et al., 1983). Although the incidence of GBS is higher in premature infants than in term births, the number of term births is much higher, so term infants may account for more than 50 percent of clinically significant GBS infections, in some of these cases there are no identifiable maternal risk factors (Cochi and Feldman, 1983).

For early onset disease, a potential maternal source for the organism is an identified risk factor for GBS infection (Pass et al., 1979), but it is difficult to predict which infants born to carrier mothers are at greatest risk of disease. Degree of exposure (presumably inoculum size) appears to affect development of disease (Boyer, 1983; Pass et al., 1979; Pyati et al., 1983).