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Concentrations of immunoglobulins (Ig)A1, and IgA2, IgD, IgE, IgG, and IgM have been determined in cord blood, amniotic fluid, and maternal serum in a group of patients with a history of prematurely ruptured membranes (PRM) prior to the onset of labor and in a control group of patients undergoing normal delivery and without a history of infection during pregnancy. IgA and IgD were determined by sensitive hemagglutination-inhibition tests; IgG and IgM, by radial immunodiffusion; IgE, by a radioimmunoassay. There was evidence for an immune response in 10 of 16 cases of PRM: five of 16 had increased IgA but normal IgM; three of 16 had increased IgA and IgM; two of 16 had high IgM and normal IgA in cord blood. In patients with significantly increased levels of either IgA or IgM or both, there was a decreased level of IgD. These changes are most likely the result of the immune response to ascending infection from the maternal genitals. The sensitive testing method employed could demonstrate the presence of IgD in 53 per cent of normal cord blood samples and 72 per cent of amniotic fluid samples obtained at term. IgE was found in all normal cord blood and amniotic fluid samples tested. By concentrating the amniotic fluid up to 180-fold, IgM was demonstrated in all normal samples tested. The potential importance of IgA determinations in cord blood in addition to IgM determination for detection of intrauterine infections is stressed.

Cord blood and maternal sera were studied in a series of 227 cases of prematurely ruptured membranes (PRM) with respect to: (1) fetal immunoglobulin (lg) synthesis associated with PRM, (2) the interrelationship between different lg classes during infection, and (3) the relationship between lg values and the duration of PRM prior to the onset of labor. A preliminary report from this laboratory, which indicated that a humorla fetal immune response occurred in some but not all cases of PRM, and that significant increases in either IgA or IgM could be found, was confirmed. There was both clinical and immunologic evidence of one peak of infection one to 12 hours after onset of PRM and another after 72 hours after onset of PRM, suggesting that some patients were infected before the clinical onset of PRM symptomatology. Increased IgA and/or IgM was found in 16.3% of infants with clinical evidence of infection. This was comparable to the 18.5% of patients with PRM who had elevated IgA and/or IgM without clinical evidence of infection. Further, there was no correlation between the severity of infection and the presence of lg elevation. Based on the data in the present series, lg determination in cord blood cannot be used to distinguish cases of PRM with and without fetal infection.

Presented is a retrospective study of the newborn infants of mothers who were treated with ethanol in order to arrest premature labor, in comparison with matched control infants. In regard to neonatal mortality, there was no statistical difference between the study and the control infants. However, infants born within 12 hours after administration of ethanol had a significantly lower 1-minute Apgar score and a higher incidence of respiratory distress syndrome. This indicates that treatment with ethanol should be discontinued as soon as it becomes evident that labor cannot be arrested.

This study reports the immunohistologic detection of SSAV/GaLV type C retrovirus p30-related antigen in unfixed cryostat sections of normal human term placentas by the indirect immunofluorescence method. Goat anti-SSAV p28 serum reacted specifically with 10 of 10 anatomic specimens of human placenta. Goat anti-GaLV p29 serum reacted similarly with 8 of 10 specimens. Goat anti-BaEV p28, anti-RD-114 p28, anti-FeLV p27, anti-R-MuLV p30, and anti-MPMV p27 gave no specific reaction with placenta. The anti-SSAV p28 and anti-GaLV p29 reactive antigen was located in the placenta mainly at the basal aspect of syncytiotrophoblast near the underlying trophoblastic basement membrane where type C retroviruslike particles have been found electronmicroscopically. The specific antibody activity of anti-SSAV p28 serum against placenta was removed by critical absorption with disrupted SSAV or GaLV but not RD-114 or MuLV. These results suggest the presence in human placenta of a putative type C retroviral protein which cross-reacts with the p30 protein of the SSAV/GaLV type C retrovirus group.