Human IgG antibody to the type-specific polysaccharide antigen of group B Streptococcus type Ia in the sera of mice was measured by enzyme-linked immunosorbent assay, previously standardized by quantitative precipitation, 24 hr after passive immunization with human serum or affinity-chromatographed antibody. The concentrations of antibody needed to protect mice against 90% lethal dose challenge varied with the bacterial inoculum and ranged from 0.25 to 1 microgram/ml using five strains of group B Streptococcus type Ia. Affinity-chromatographed antibody gave results comparable to serum, indicating the specificity of the antibody and the absence of other humoral factors in protection with this serum. Sera from 11 infected infants and their mothers had concentrations of antibody of less than or equal to 0.17 micrograms/ml, below the protective level delineated in the experimental model. Twelve percent of 50 adult women and 36% of 25 women colonized with group B Streptococcus type Ia had antibody levels of greater than or equal to 1 microgram/ml.
Strain differences have been postulated to explain the observation that group B Streptococcus type III (GBS III) late-onset disease occurs in only a fraction of colonized infants. To determine the distribution of type-specific polysaccharide antigen (Ag) in GBS III, Ag was measured by rocket immunoelectrophoresis in both supernatant fluids and EDTA extracts and by radial immunodiffusion in multiple HCI extracts of the pellet from cultures of 10 strains of GBS III. Capsular Ag was defined as the sum of Ag in EDTA extracts + Ag in multiple HCI extracts. Both Ag in EDTA extracts and Ag in supernatant fluids correlated with capsular Ag (r = 0.94). GBS III strains were obtained from the blood of 19 infants with late-onset sepsis, from the cerebrospinal fluid or blood of 22 infants with late-onset meningitis, and from mucosal surfaces of both 18 infants and 12 mothers of infants with low levels of type-specific antibody and asymptomatic colonization. Mean values of Ag in supernatant fluids in strains from infants with late-onset sepsis (1.50 ± 0.08 ptg/ml) and late-onset meningitis (1.67 ± 0.09 pug/ml) were significantly greater than those in asymptomatic colonization strains (1.14 ± 0.05 ,ug/ml; P < 0.001). The number of organisms required for a 50% lethal dose in the chick embryo, determined in 29 strains, was inversely related to Ag in supernatant fluids (r =-0.60). The demonstration that the quantity of capsular Ag produced by GBS III strains is related to their virulence in chick embryos and to their invasiveness in susceptible infants supports the hypothesis that Ag is a virulence factor in humans.
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