Having just found out that my pregnant daughter-in-law is Rh negative, I began to wonder about that. She will have some injections (I think the drug they will use is called Rhogam, if I heard correctly over a noisy phone line) that is supposed to prevent her from making antibodies). But I wonder why, given the reproductive disadvantage, the rhesus factor doesn’t spread throughout the population. Is there any selective advantage to being Rh negative? If there is, why did Rh positive become the most prevalent somatype? And, while I raising these questions, I am curious why Rh incompatibility is a problem, while A or B incompatiibility is not. My son, like all the rest of us, is A positive, while his wife is B negative, but she will not make A antigens or, if she did, it would not harm subsequent fetuses. And why does the Rh antigen harm the baby anway, since there is no direct mixing of maternal and fetal blood?
IANAD, but here goes anyway.
The Rh factor is usually only an issue for second and later births. During the first pregnancy, the Rh negative mother’s body may start making antibodies to an Rh positive fetus’s Rh factor, but usually not soon enough to make a difference to the baby. If she later carries a second Rh positive child, there are already antibodies present, which can start to affect the child. For each successive pregnancy the possiblility of a serious problem increases.
Aaah, there may not be mixing of maternal and fetal blood, but antibodies can cross barriers (in the human type of plancentation, not for all animals) and enter the fetal circulation. Not to mention that antibodies are secreted in breastmilk (colostrum), and pass on to the newborn, whose digestive system is capable of taking the antibodies without destroying them first.
So to answer your last question, no, you don’t need direct mixing of blood to cause a problem, you just need the mother’s antibodies to reach fetal (or newborn) circulation. And like the previous poster said, it is mostly a problem in later pregnancies, not the first one.
Regarding selection, note that the selection is not against Rh negative but against Rh positive genotypes. Rh disease is only a problem when you have a cross-mating, specifically a negative mother and a positive father. Rh negative means the individual lacks the Rh antigen; Rh positive means he or she has it. Rh negative individuals will produce antibodies against the Rh antigen; there is no corresponding reaction in the other direction. Rh disease occurs when an Rh- mother produces antigens in response to an Rh+ fetus, with detrimental effects on the latter.
Although the maternal and fetal blood supplies are separate, small ruptures can occur allowing some mixing. There is usually no problem with the first Rh+ pregnancy. After this the mother may have become sensitized due to the first pregnancy, and subsequent pregnancies can be at risk.
Rh+ is dominant, that is, a single dose of the allele makes you Rh+. If both parents are positive, there will be no problem. Likewise, if both are negative, there will also be no problem, since an Rh- male can’t produce an Rh+ offspring. If the male has only one Rh+ allele, half the pregnancies will be Rh+. If the male has two Rh+ alleles, all will be.
KarlGrenze, sorry, but there can be mixing of maternal and fetal blood. It’s only a tiny amount, but even one Rh pos fetal cell in the maternal blood will cause the mother’s body to attack the fetal tissue. The first pregnancy isn’t usually a problem, because the mother hasn’t been exposed to the +Rh factor, so has no antibodies. Even so, Rhogam, aka, Rh immunoglobulin, is given in week 28, when the placenta can begin to leak fetal cells into the maternal blood.
As long as the mother gets the imunoglobulin with each pregnancy, her children should have no problem with hemolysis.
One reason Rh factor hasn’t disappeared is that prior to the use of Rhogam, Rh pos women whose mates were negative, could still have one or more Rh neg children before they began to produce antibodies.
Today, where Rhogam is used routinely, the incidence of fetal hemolysis approaches zero.
I’m going to leave the ABO compatibility to someone smarted.
picunurse, thanks. I wasn’t sure if there was actual mixing or not (and rereading the rest of my paragraph makes sense if there IS mixing, although a very small amount, to account for the production of antibodies).
You mean Rh negative women whose mates were positives, right?
Landsteiner worked out the ABO system in 1901 and won the Nobel Prize. Someone with type A blood, for example, has blood that contains A antigen. At about six months of age, people develop antibodies to antigens not in their blood – someone with type A blood would develop anti-B antigen as a natural process.
The Rh, or Rhesus, system was first detected in 1940 by Landsteiner and Wiener when they injected blood from rhesus monkeys into guinea pigs and rabbits. More than 50 antigens have since been discovered that belong to this system, making it the most complex red blood cell antigen system. In routine blood typing and cross-matching tests, only one of these 50 antigens, the D antigen, also known as the Rh factor or Rho[D], is tested for. If the D antigen is present, that person is Rh-positive; if the D antigen is absent, that person is Rh-negative. Other important antigens in the Rh system are C, c, E, and e. These antigens are not usually tested for in routine blood typing tests. Testing for the presence of these antigens, however, is useful in paternity testing.
Unlike the ABO system, antibodies to Rh antigens don’t develop naturally. They develop only as an immune response after a transfusion or during pregnancy. Incompatibility may occur when an Rh-negative mother and an Rh-positive father have an Rh-positive baby. Cells from the baby can cross the placenta and enter the mother’s bloodstream, causing the mother to make anti-D antibodies. Unlike ABO antibodies, the structure of anti-D antibodies makes it likely that they will cross the placenta and enter the baby’s bloodstream. There, they can destroy the baby’s red blood cells, causing a severe or fatal anemia.
So, to answer your question, it depends on the structure of the antibody, and the fact that ABO antibodies develop naturally without pregnancy. But there are lots of other antibodies and antigens apart from ABO and Rh which also have to be accounted for in blood typing.
I am not a hematologist, nor expert. I do not know what is different about the structure of rhesus D antibodies which makes them more likely to cross the placenta.
Anti-A and anti-B antibodies are mostly IgM, with a small amount of IgG as well. IgG antibodies readily cross the placenta, but IgM antibodies don’t, as they exist as a pentomer.
Vlad/Igor
:smack: Of course, Thank you.