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ABO incompatibility disease afflicts newborns whose mothers are blood type O, and who have a baby with type A, B, or AB.
Ordinarily, the antibodies against the foreign blood types A and B that circulate in mother's bloodstream remain there, because they are of a type that is too large to pass easily across the placenta into the fetal circulation. Some fetal red cells always leak into mother's circulation across the placental barrier (mother and fetal blood theoretically do not mix, but in actuality, they do to a small degree).
These fetal red cells stimulate the formation of a smaller type of anti-A or anti-B antibody which can pass into the baby's circulation and there cause the destruction of fetal red cells. The increased rate of destruction of red cells causes a subsequent increase in waste product production. This excess waste product, bilirubin, can overwhelm the normal waste elimination processes and lead to jaundice, the presence of excess bilirubin.
Anemia sometimes becomes an issue some weeks after the initial jaundice problems are resolved. This is caused by ongoing faster than normal breakdown of the baby's fetal cells by the maternal antibodies, which linger in the baby's bloodstream for weeks after birth. For this reason, babies with ABO incompatibility disease may need to be tracked with periodic blood counts. If the anemia were to become severe, a blood transfusion might be required to restore a normal level of red blood cells in the baby's circulation. Such a transfusion would add blood to the baby's circulation to prevent possible complications of the anemia (in distinction to the exchange transfusion, which replaces the baby's red cells with adult cells). This complication is rare; I personally have yet to see a case severe enough to justify transfusion.
For reasons that are unclear, B-O incompatibility (mother type O, baby type B) seems to be in general more severe than A-O incompatiblity.