ABO blood type is further differentiated by + or – sign. This positive or negative sign refers to the presence or absence of another blood group system antigen called Rh factor. Rh blood group system is defined on the basis of Rh factor present on the surface of RBC. This system is named Rh after Rhesus monkey because its antigen was first discovered in it by Landsteiner in 1930s.
Rh blood group system is encoded by three genes C, D and E, which occupy two tightly linked loci. Alleles of gene D occupy one locus called locus D, while genes C and E alternatively occupy the other locus. The D locus is of prime importance.
Gene D has two alleles, D and d. D is completely dominant over d. Persons having genotype DD or Dd have Rh factor on their RBC and are Rh⁺. Persons with genotype dd do not have Rh factor and are Rh⁻. Unlike the naturally occurring anti – A and anti – B antibodies of ABO system, anti – Rh antibody production requires a stimulus by the human Rh antigen itself.
An Rh⁻ person does not produce anti – Rh antibodies unless he is exposed to Rh antigen. Rh⁺ donor is totally incompatible for Rh⁻ recipient. If an Rh⁻ person receives Rh antigen through wrong Rh⁺ blood transfusion, he will begin to produce anti – Rh antibodies against Rh antigens. Rh⁻ blood, clear of any anti – Rh antibody from a donor who has never been exposed to Rh antigen can be transferred to Rh⁺ recipient.
When we talk about maternal – foetal Rh incompatibility, it results when an Rh⁻ woman, married to an Rh⁺ man conceives a child who is Rh⁺. If the man’s genotype is DD, all of their offspring will be Rh⁺. If the man’s genotype is Dd, half of their offspring will Dd genotype will be Rh⁺.
If RBC of Rh⁺ fetus cross the placental barrier and enter into Rh⁻ mother’s blood stream, the mother’s immune system reacts to the foetal Rh antigen stimulus by producing a large number of anti – Rh antibodies. When mother’s anti – Rh antibodies seep through placenta into blood circulation of foetus, they start hemolysis which results in break down/ bursting of RBC of foetus.
As this destruction continues, the foetus becomes anaemic. The anaemic foetus starts to release many immature erythroblasts into his blood stream. That is why this hemolytic disease of the new born is called erythroblastosis foetalis. This anemia may lead to abortion or still birth. Even if the pregnancy continues, the liver and spleen of the foetus swell as they rapidly produce RBC.
The breakdown product of RBC called bilirubin also accumulates in the foetus. Bilirubin damages his brain cells and turns his skin and whites of the eye yellow. This condition is jaundice. So the baby if born alive, suffer from severe hemolytic anemia and jaundice. Such baby’s blood should be immediately replaced by Rh⁻ blood free of anti – Rh antibodies.
The first Rh incompatible pregnancy may not face much problems if very few of foetal antigens cross placenta into maternal circulation and the amount of maternal antibody production is not very high.
But when placenta detaches at birth, a large number of foetal cells enter mother’s blood stream and stimulate production of large amount of anti – Rh antibodies by the mother. These anti –Rh antibodies persist in mother’s blood for a long time and are persistent risk for the next Rh⁺ foetus.
Sometimes a mild ABO incompatibility protects the baby against more severe Rh incompatibility. If O⁻ mother conceives A⁺or B⁺ baby, any foetal A or B type RBC entering the mother’s blood are quickly destroyed by her anti – A or anti – B antibodies, before she can form anti – Rh antibodies.
Rh sensitization of Rh⁻ mother can be avoided by simple therapy. She is given an injection of Rh antiserum during early pregnancy and immediately after birth. The Rh – antibodies in Rh antiserum will destroy Rh⁺ RBC of the foetus before they stimulate production of maternal anti – Rh antibodies. The injected antiserum disappears before the next pregnancy.