Foals with the Ca blood group antigen on their RBC were given colostrum with anti-Ca antibodies (6 foals) or colostrum without anti-Ca antibodies (6 foals). The PVC were determined at birth and 2, 4, and 6 days after birth for the foals in each group. Significant differences were not observed for the PCV between the 2 groups, indicating that foals were not adversely affected by ingesting colostrum with the anti-Ca antibody. Standardbred mares without the Aa blood group antigen were evaluated to determine whether production of anti-Ca antibodies influenced production of anti-Aa antibodies. Of 266 mares without the Aa antigen, 3 of 61 (5%) mares without the Ca blood group antigen produced anti-Aa antibodies and 43 of 205 (21%) with the Ca blood group antigen produced anti-Aa antibodies. These 2 groups of mares were significantly (p = 0.006) different; Ca-negative mares were less likely to produce antibodies to Aa than were mares with the Ca blood group antigen. This observation was consistent with a hypothesis of antibody-mediated immunosuppression of immune response to the As blood group antigen by antibodies to the Ca blood group antigen, ie, when a mare is exposed to her foal's RBC and already has antibodies to the Ca blood group antigen on the foal's RBC, then she is less likely to initiate an immune response to the Aa blood group antigen also on the foal's RBC.

Using radioimmunoassay methods, quality control criteria were applied to monoclonal antibodies produced to measure porcine immunoglobulins by quantitative ELISA. Porcine IgM and IgA were purified to homogeneity and were used to produce murine hybridomas that secreted antibodies against IgM, IgA, and immunoglobulin light chains. A competitive ELISA was developed to measure IgM, and a sandwich ELISA was to quantify IgA in serum and colostrum. Both ELISA were tested for specificity, accuracy, sensitivity, and precision. Monoclonal antibodies were specific for porcine IgM or IgA in serum and colostrum, and competitive and sandwich ELISA fulfilled all validation criteria.

Primigravid swine were vaccinated orally with a live enterotoxigenic Escherichia coli (ETEC) strain that produces pilus antigen K99. The titers of K99 antibody in colostrum and milk of vaccinates remained higher than those of nonvaccinated controls through the first lactation after vaccination (4 weeks). Some control swine had low titers of K99 antibody in colostrum or developed low titers of K99 antibody in milk during lactation. Lacteal K99 antibody titers of vaccinates dropped to control levels during the second lactation, 6 months after vaccination. Pigs suckling vaccinates and controls were equally susceptible to challenge exposure to K99+ ETEC during the second lactation. Orally vaccinated swine given a parenteral booster vaccination (with killed K99+ ETEC) during their second gestation had K99 antibody in milk through their second lactation. During the second lactation, these orally vaccinated parenterally revaccinated swine had higher titers of K99 antibody in postcolostral milk than did nonvaccinated controls, controls given only the parenteral booster injection, or controls vaccinated parenterally during both gestations.