Pathogenesis of neonatal group B streptococcal infections.
Infections of the neonate due to the group B Streptococcus have been recognized since the 1930s, but it was during the 1970s that their incidence grew alarmingly throughout the world. A research effort stimulated by this problem has yielded significant new information about many facets of the pathogenesis of these infections. Immunologic investigations have pinpointed a lack of transplacentally acquired antibody as a significant risk factor. In the laboratory, assays of antibody which have a functional endpoint have demonstrated that the type-specific carbohydrate antigens play a major role in stimulating the development of protective antibody. These assays have been shown to correlate with certain tests of primary antigen-antibody interaction which do not have a functional endpoint, but are simpler to use in larger scale epidemiologic studies. These tools may be useful in filling the gaps in our current knowledge of the pathogenesis of this infection.
D000907:Antibodies, Bacterial / Q000276:immunology; D000937:Antigen-Antibody Reactions; D000942:Antigens, Bacterial / Q000276:immunology; D005260:Female; D006801:Humans; D007112:Immunity, Maternally-Acquired; D007118:Immunoassay; D007231:Infant, Newborn; D007232:Infant, Newborn, Diseases / Q000276:immunology*; D009895:Opsonin Proteins / Q000032:analysis; D011135:Polysaccharides, Bacterial / Q000276:immunology; D013290:Streptococcal Infections / Q000276:immunology*; D013292:Streptococcus agalactiae / Q000276:immunology
D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D009895:Opsonin Proteins; D011135:Polysaccharides, Bacterial