Protective Efficacy against Group B Streptococcal Infection in Neonatal Mice Delivered from Preimmunized Pregnants

Abstract

Neonatal mice delivered from mothers preimmunized with heated or formalinized whole cell vaccines of type Ia, Ia/c and III/c group B streptococci were infected with each type of bacteria, and then serum antibodies of mothers and neonates who survived the experiments were measured by enzyme-linked immunosorbent assay. The relationship between the protectivity in neonate mice and the antibody titers to the type specific polysaccharide antigens and the protein c antigen of their sera were examined.In the Ia-immunized group which showed high protection against the type Ia infection, anti-Ia IgG antibody titers were low, and anti-protein c IgG antibody was riot detected. Type Ia/c and Mk vaccines were highly effective against both type Ia/c and III/c infection, but less effective in type Ia infection. The protein c antigen was identified in both type strains by the double diffusion assay, and the IgG antibodies to the protein c were significantly high in sera of both maternal mice immunized with types Ia/c or III/c organisms and their newborn infants. High titers of the protein c IgG antibody retained 3 to 4 weeks after the last injection of vaccines which corresponded to the period of pregnancy and lactation. Small amounts of IgM antibody to all antigens were detected only in maternal sera.These results suggest that IgG antibodies to the protein c antigen and to the type-specific polysaccharide antigens are equally important protective factors which are transferable from preimmunized mothers to their newborn infants through placenta and/or lactation.Group B streptococcus is recognized as an important agent of sepsis and meningitis in neonates, and is transmitted to newborn infants in the maternal genital tracts (2, 12, 13). Group B streptococci (GBS) are known to be colonized in the vaginas of, at most, 70% of all pregnant women (1), but only about 1% of their newborns seem to develop serious GBS diseases (18). The low rate of apparent infection could be derived from defence mechanisms in the neonates. Baker and her colleagues (3)(4)(5) found that the susceptibility of neonates to infection with type III GBS is related to the absence of transmitted maternal immunoglobulin G (IgG) antibody to type III polysaccharide, which has been corroborated by others 297

A Novel Hexavalent Capsular Polysaccharide Conjugate Vaccine (GBS6) for the Prevention of Neonatal Group B Streptococcal Infections by Maternal Immunization

“…An active maternal immunization model [23] was used to evaluate protection of the pups resulting from vaccine-elicited immune responses in the dams. Female mice (2–10 per arm) were dosed at weeks 0, 3, and 6 with either 10 µg (CP/dose) of monovalent conjugate or 5 µg of GBS6 (CP/serotype/dose) formulated in 100 µL of 1 g/L AlPO 4 .…”

Characterization of the a antigen of the c proteins of group B streptococci (GBS) using a murine monoclonal antibody

“…Attempts to purify the c proteins using various extraction methods suggest that both the a and the fl antigen exhibit heterogeneity in molecular size ranging from 10-20 kD to 130 kD or more (3,8,13). Studies have indicated that the c-protein antigens may interfere with the resistance to opsonization and killing of GBS (8), and in vivo studies have shown a protective effect of anti-c-protein antibodies when the animals were preimmunized (9) or passively protected by injection of hyperimmune rabbit antisera (3,6,8,11).…”