1-In 1667, in France, a 15-year-old boy was stricken with fever. His family cons

Question

1-In 1667, in France, a 15-year-old boy was stricken with fever. His family consulted local physicians, who prescribed bleeding by leeches – a common treatment at the time for many ailments. After 20 leech treatments, his family consulted Dr. Jean-Baptiste Denys (physician to King Louis XIV). Dr. Denys decided that the boy was overbled and would only live with a blood transfusion. He transfused several ounces (exact # unknown, probably only a few) of blood from a sheep into the boy and the boy lived. He repeated this several times with mixed success, including an attempt in 1668 to a man with a “harmless form of insanity”. (It was thought that transfusing the blood of a lamb would help soothe the temperament of the recipient.)

Refer back to the background preamble to your lab protocol and propose a reason, complete with background physiology, about why this might have worked. (Hint: today, blood transfusions are usually given 1 unit – about 1 pint – at a time.)

2-A baby’s blood type is typically not known until after it is born. If the mother has Rh(-) blood, she may receive an injection of a drug called Rhogam to prevent her immune system from seeing the baby’s blood (and as a consequence, the entire baby) as a foreign entity.

In this case, why might her body see the baby as a foreign entity?

Does this matter more for the first child or subsequent children? Why?

If the mother’s blood and baby’s blood are incompatible, what would happen to the baby after it is born (assuming it makes it to term)? (Tell me the name of the disease, briefly how it works, and what symptoms you might see in the newborn.)

Explanation / Answer

Answer:

2) This is a classic case of Rh incompatibility. This occurs due to the absence of the Rh(Rhesus) factor(Rh -ve) in the mother's blood(RBC) who carries an Rh positive baby. Rh+ve individuals carry D antigen in their blood but do not have anti-D Antibody. Both Rh antigen and anti-D antibody are absent in Rh -ve individuals as well but it can be seen in those who get exposed to blood containing Rh D antigen.

In such cases, the Rh -ve mother receives immunoglobulin D(Rhogam) as an injection during gestation and after the delivery of the baby to protect her and her baby from developing symptoms of Rh incompatibility.

Why is the mother seeing her own baby as a foreign entity?

Which child does this matter more to?First or second?

Ans.1. In normal Rh +ve individuals, they carry only Rh agglutinogen in their blood. And if in case antibodies are present in the same individual against this antigen, the body will initiate a severe immune response hence the immune cells start attacking the antigen located on the RBC membrane and cause lysis or hemolysis in the person, leading him to his death. This is precisely why we do not have antibodies against the same antigen in our own blood. This is also the reason why blood compatibility is mandatory before transfusing.

So, here the Rh -ve mother who does not have a D antigen or antibody in her blood, throughout the course of her pregnancy, is exposed to fetal RBCs which are Rh +ve with D antigen which is even more during parturition, causing her body to produce Anti-D antibody and the body starts to see the fetus as a foreign body and initiates an immune response and seeks to destroy by crossing the placenta and entering the fetal bloodstream and causing hemolysis in the baby by lysing the RBCs( since they carry the D antigen).

Ans.2) This affects the second Rh +ve child than the first; due to the prevailing anti-D antibody circulating in the mother's blood already from her first pregnancy causing her body to elicit an immune response against the baby, considering as a foreign body.

The consequences:

This could either cause the death of the baby in the uterus; the baby will not make it to full term. Or, In milder cases, the fetus is born alive but with severe hemolytic anemia called the Hemolytic Disease Of the Newborn(HBN) or Erythroblastosis fetalis.

The child has low Hb% and has nucleated RBCs circulating in the blood. This is because due to severe anemia, the body signals bone marrow to produce more and more RBCs to that extent that immature fetal RBCs starts getting released in the blood. Nucleated RBCs are called erythroblasts and hence this disease is named as erythroblastosis fetalis.

There will be marked jaundice due to hemolysis and kernicterus can develop due to deposition of bilirubin in the basal ganglia of the brain and in neonates unconjugated bilirubin can cross the blood-brain barrier which also contributes to kernicterus.

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