A Rhesus-negative woman () who did not receive anti-Rh immunoglobulin therapy after giving birth to her first Rhesus-positive child is expecting a second child. The father is Rhesus-positive (), but his mother was Rhesus-negative (). What is the probability that this second child will suffer from erythroblastosis fetalis, and what physiological mechanism triggers this medical condition?
- 50%, because maternal anti-Rh IgG antibodies produced after sensitization during the first delivery cross the placenta and destroy red blood cells if the second fetus inherits the Rhesus-positive allele ().Answer
- B100%, because all offspring of a Rhesus-positive father and Rhesus-negative mother inherit the dominant Rhesus antigen, guaranteeing erythroblastosis fetalis in all subsequent pregnancies.
- C25%, because Rhesus antigens exhibit codominance with ABO blood group alleles, requiring homozygous recessive inheritance of maternal antibody genes to trigger agglutination.
- D50%, because the mother's immune system acquired Rhesus-positive genes during her first pregnancy and directly passes these acquired genetic adaptations to her second offspring.
Answer
The probability is 50%, occurring because maternal anti-Rh IgG antibodies cross the placenta and agglutinate fetal red cells if the fetus inherits the Rhesus-positive allele.
The father is heterozygous () because his mother was Rhesus-negative (). A cross between a Rhesus-negative mother () and a heterozygous father () gives a 50% chance of producing a Rhesus-positive () child. Because the mother was sensitized during her first pregnancy with a Rhesus-positive child, her immune system contains anti-Rh IgG antibodies. In a second Rhesus-positive pregnancy, these IgG antibodies cross the placenta and lyse fetal red blood cells, causing erythroblastosis fetalis.
Step-by-Step Solution
Key Concept
Rhesus Factor Incompatibility and Erythroblastosis Fetalis
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