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A method has been developed for the detection in human sera of antibodies to surface antigens of group B streptococci (GBS), types Ia, Ib, or III. The sera were absorbed with GBS type II and then added to a suspension of GBS of the type against which antibodies were to be measured. After incubation and washing of the bacteria, the antibodies present on the surface of the cells were quantitated with radiolabelled protein A. Antibodies of IgG class were detected, probably specific for types Ia, Ib, or III, with the exception that the Ib GBS suspension used could detect some antibodies to type Ia. With this method it was found that 6/7 mothers to infants with GBS septicemia had low levels of serum antibodies to the infant's type of GBS. Urogenital carriers of GBS, giving birth to neonatally healthy infants, had higher serum antibody levels against the colonizing type.

Thirty-eight infants admitted to a neonatal intensive care unit because of pneumonia (14 patients) and pulmonary maladaption syndrome (PMA) (24 patients) were included in the study. Samples of potentially pathogenic, facultatively anaerobic bacteria were taken from the external ear, blood, throat, nasopharynx, umbilicus and gastric aspirates of the children, and from urethra and cervix of the mothers. Group B streptococci (GBS) and Escherichia coli were the only potentially pathogenic bacteria isolated from the infants. Out of 14 infants with pneumonia 11 (79%) harboured one of these bacteria, in contrast to 3 out of 24 (13%) with PMA (P less than 0.001). GBS was found in 8/14 infants with pneumonia and in 1/24 infants with PMA (P less than 0.001). The respective frequencies for Escherichia coli were 3/14 and 2/24 (not significant). The infant and/or the mother in 10/14 pneumonia cases harboured GBS, in contrast to 4/24 pairs in the PMA group (P less than 0.001). The levels of antibodies against GBS in sera of mothers to infants with pneumonia did not differ from the antibody levels in control sera (parturient GBS-carriers giving birth to healthy infants). The results gave evidence for an important manifestation of neonatal GBS-infection: pneumonia without septicemia. The incidence of the disease is estimated to be 1:25 parturient GBS-carriers. Finally, maternal fever, gestational age above 42 weeks, more severe respiratory difficulties and the occurrence of severe changes in fetal heart rate during the first stage of labour were found to be typical characteristics of pneumonia, as compared to PMA.

Serum antibodies against various carbohydrate antigens were studied in 16 mothers of infants with serious infections caused by group B streptococci (GBS) (the study group), and compared with a control group of 29 urogenital carriers of GBS who gave birth to neonatally healthy infants. Using a radioimmunoassay for the determination of antibodies to GBS types Ia, Ib, II and III, it was found that the study group had significantly lower levels of IgG antibodies to each of the 4 GBS types than the control group. The IgG levels against Salmonella BO and DO, Yersinia enterocolitica 03, Francisella tularense and Streptococcus pneumonia types 3, 6, 9, 19 and 23 purified carbohydrate antigens were determined using an ELISA technique. Significantly more individuals in the study group than in the control group had low levels of IgG antibodies against 8 of 9 carbohydrate antigens. No difference was found in IgM levels against 3 of 4 antigens studied, while the study group showed significantly more IgM antibodies against Salmonella DO than the controls. These results indicate that mothers of GBS-infected infants might be poor IgG antibody responders to bacterial carbohydrate antigens in general.

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A method was designed for quantitation of serum antibodies to R protein in group B streptococci (GBS). Four sera from mothers of infants with neonatal septicemia caused by type II, R+ GBS showed a binding range from 400 to 740 cpm in contrast to a range of 690–1,220 cpm in 5 parturients carrying type II, R+ strains in the urogenital tract giving birth to healthy infants (p < 0.05). The range of antibodies in sera from 8 mothers to infants infected with GBS type III, R+ was 370–750 cpm, whereas the range in sera from 10 carriers of type IIIR+ giving birth to healthy infants varied between 510 and 1,280 cpm (p < 0.01). These findings indicate that R protein is an important virulence factor in neonatal GBS septicemia/meningitis.