We have recorded the systemic and mammary/mucosal immune responses of women following natural infection with RS virus during the second and third trimesters of pregnancy. Anti-RS virus IgG antibody levels in the sera of women collected in the first trimester of pregnancy showed a bimodal distribution with high and low antibody groups. Antibody levels increased after exposure to the winter RS virus epidemic in the second trimester of pregnancy, probably as a result of infection but only for women in the low antibody group. Despite the increases, antibody levels for these women remained well below those of the high antibody group. There was no rise in mean antibody levels after exposure in the third trimester, even among women with low antibody, suggesting a degree of immunosuppression in late pregnancy. There was no evidence that infection during pregnancy was associated with adverse consequences for the infant. Exposure to RS virus in the first two trimesters, but not the third, was associated with high colostral IgA antibody levels that were maintained in the milk throughout the first 7 weeks of lactation. There was a significant correlation between colostral and maternal nasal IgA antibody levels at delivery. Levels of blood or colostral lymphocyte transformation responses at delivery were unaffected by exposure to RS virus in pregnancy. These observations upon natural infection suggest that vaccination during pregnancy is likely to achieve only marginal effects upon serum antibody levels but boost maternal mammary/mucosal immunity.
The effect of milk feeding on the ontogeny of serum IgA in breast and cow milk formula fed neonates was studied. There was a rise in serum IgA concentrations from the 2nd week in both groups, but no difference in rate of appearance or concentrations in relation to age, gestation or sex. The ingestion of RSV antibody‐rich colostrum was associated with a rise in serum anti‐RSV IgA in 2 preterm infants during the perinatal period. We suggest that there are 2 mechanisms which regulate the ontogeny of circulating IgA: an early but small intestinal uptake of colostral IgA, and a later endogenous production, which in this study was not influenced by composition of feeds.
A retrospective study using an obstetric risk score protocol was applied to a stratified sequential sample of 843 singleton livebirths, occurring in the Royal Hospital for Women, Sydney, over a 12-month period (March, 1985-February, 1986). Data collection included 53 prenatal factors, 41 intrapartum factors and 37 neonatal factors. The study was comprised of 346 women admitted to the hospital birth centre and 497 women admitted to labour ward. In labour ward admitted women there was a significant association between high prenatal scores, high intrapartum scores and high neonatal morbidity scores. Women admitted to the birth centre were subjected to a screening procedure which resulted in low prenatal and relatively low intrapartum risk scores. However, neonatal morbidity scores were similar for both groups. The risk scoring protocol used in this study requires further revision to allow the adequate selection of low risk women delivering infants with a low risk of neonatal morbidity in a low risk obstetric setting.
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