Remember that the anti-Rh serum will only agglutinate the positive D factor. There are technically three positive genes called C, D and E. The negative alleles for these three genes are usually denoted by small case c, d and e. This is an example of multiple gene (polygenic) inheritance which is explained in more detail at the following URL:

Anti-Rh (immune-type) antibodies can readily pass through the placental capillary membranes. A serious potential problem called maternal-fetal blood incompatibility or Rh Disease could occur with a pregnant Rh negative mother who carries an Rh positive fetus. Leakage of fetal red blood cells (RBCs) into the mother's system through minute lesions in the placenta may cause her to produce anti-Rh antibodies. This could occur during the latter months of pregnancy or when the baby is delivered. Because of the time interval involved in producing a concentration (titre) of antibodies, the first Rh positive child may not be adversely affected. However, a subsequent Rh positive child may be at risk because the mother's anti-Rh can pass through the placenta, thus entering the fetal circulatory system and clumping fetal RBCs.

The medical term for this maternal-fetal condition is "erythroblastosis fetalis" because of the presence of nucleated, immature RBCs called erythrobasts in the fetal circulatory system. The fetus bone marrow releases immature erythroblasts because of the destruction of mature RBCs (erythrocytes) by the mother's anti-Rh antibodies. RhoGamŪ, a serum containing anti-Rh antibodies, is now given to Rh negative woman within 72 hours after giving birth to their Rh positive baby. The RhoGamŪ enters the mother's circulatory system and destroys any residual fetal positive RBCs that may be present in her system. This prevents her from producing anti-Rh antibodies. RhoGamŪ must be given after each Rh positive baby. In this scenario of erythroblastosis fetalis, the fetus must be Rh positive, the mother Rh negative and the father Rh positive. You can easily determine the exact genotype of the mother and fetus, but the father's genotype could be homozygous or heterozygous Rh positive. Rh incompatibility is summarized in the following table:

There are also reported cases of maternal-fetal blood incompatibility with the A-B-O blood groups; however, the Rh factor appears to be much more common. The larger anti-A and anti-B antibodies (IgM type) with molecular weights of 950,000, apparently don't penetrate the placental membranes as readily. In the case of A-B-O blood incompatibility, the anti-A and anti-B antibodies of a type O mother may enter the circulatory system of a Type A or Type B fetus, thus causing agglutination of the fetal RBCs. If the fetal blood cells just happened to be Rh positive and entered the mother's circulatory system, they would be destroyed by the mother's anti-A or anti-B antibodies before her system began to produce anti-Rh immune-type (IgG) antibodies. In this latter case, the anti-A or anti-B antibodies would actually serve as a natural immunity to Rh maternal-fetal blood incompatibility.