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Updated: Apr 17, 2026

A Murine Model of Group B Streptococcus Vaginal Colonization
Published on: November 16, 2016
Natural acquired humoral immunity against serotype-specific group B Streptococcus rectovaginal colonization
G Kwatra1, P V Adrian1, T Shiri1
1Medical Research Council, Respiratory and Meningeal Pathogens Research Unit, University of the Witwatersrand, Johannesburg, South Africa; Department of Science and Technology/National Research Foundation, Vaccine Preventable Diseases, University of the Witwatersrand, Johannesburg, South Africa.
Group B Streptococcus (GBS) rectovaginal colonization in pregnant women is associated with invasive GBS disease in newborns, preterm delivery and stillbirths. We studied the association of GBS serotype-specific capsular polysaccharide (CPS) antibody on new acquisition and clearance of rectovaginal GBS colonization in pregnant women from 20 weeks until 37 to 40 weeks' gestation. Serum serotype-specific CPS IgG antibody concentration was measured by multiplex enzyme-linked immunosorbent assay and opsonophagocytic activity (OPA) titres. Rectovaginal swabs were evaluated for GBS colonization, using standard culture methods and serotyping by latex agglutination, at five to six weekly intervals. Higher serotype III CPS antibody concentration was associated with lower risk of rectovaginal acquisition of serotype III during pregnancy (p 0.009). Furthermore, serotype-specific OPA titres to Ia and III were higher in women who remained free of GBS colonization throughout the study compared to those who acquired the homotypic serotype (p <0.001 for both serotypes). Serum CPS IgG values of ≥1μg/mL for serotype V and ≥3μg/mL for serotypes Ia and III were significantly associated with protection against rectovaginal acquisition of the homotypic serotype. A GBS vaccine that induces sufficient capsular antibody in pregnant women, including high OPA titres, could protect against rectovaginal colonization during the latter half of pregnancy.
Group B Streptococcus (GBS) rectovaginal colonization in pregnant women is associated with invasive GBS disease in newborns, preterm delivery and stillbirths. We studied the association of GBS serotype-specific capsular polysaccharide (CPS) antibody on new acquisition and clearance of rectovaginal GBS colonization in pregnant women from 20 weeks until 37 to 40 weeks' gestation. Serum serotype-specific CPS IgG antibody concentration was measured by multiplex enzyme-linked immunosorbent assay and opsonophagocytic activity (OPA) titres. Rectovaginal swabs were evaluated for GBS colonization, using standard culture methods and serotyping by latex agglutination, at five to six weekly intervals. Higher serotype III CPS antibody concentration was associated with lower risk of rectovaginal acquisition of serotype III during pregnancy (p 0.009). Furthermore, serotype-specific OPA titres to Ia and III were higher in women who remained free of GBS colonization throughout the study compared to those who acquired the homotypic serotype (p <0.001 for both serotypes). Serum CPS IgG values of ≥1μg/mL for serotype V and ≥3μg/mL for serotypes Ia and III were significantly associated with protection against rectovaginal acquisition of the homotypic serotype. A GBS vaccine that induces sufficient capsular antibody in pregnant women, including high OPA titres, could protect against rectovaginal colonization during the latter half of pregnancy.
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