An account on the types of blood groups and its biochemistry along with Rh factore and its incompatibility.

1. Presented by,
Gopika Beena Chandran
RGITBT

2. Multiple Allele System
• A system in which one gene has more than
two allelic states at the same locus in different
members of the population.
• T. H. Morgan in 1910 described the first case
of multiple alleles of a gene controlling eye
colour in Drosophila during his studies on
mutation.

3. Historical context
• Czek serologist Jan Jansky
first to classify blood into 4
types (A, B, AB and O).
•Did not receive a nobel
prize. His work left
unnoticed.

4. Karl Landsteiner (1869-1943)
• ABO Blood group system first
discovered in 1900.
• Received Nobel Prize in
Physiology or medicine in
1930.

5. How he did it?
• Took blood samples from different people.
• Separated their red cells from the colourless
serum or plasma, and then mixed them up in
various ways.
• Found that the red cells derived from one sample
would mix smoothly with the serum of that
person.
• And red cells of a person is mixed with plasma of
another person,
either the two mix well or there would be
clumping of red cells.

6. • Later on Landsteiner found that human
erythrocytes carry on their surface two
distinct types of proteinaceous antigens A and
B which can stimulate the production of
specific antobodies.

7. • Bernstein in 1924 found that the blood group
antigens are controlled by an autosomal gene
designated as I (isohemaglutinin) which has 3
alleles IA , IB and IO or i .

8. • In this system, the IA and IB alleles are codominant
and are expressed equally in the IAIB
heterozygotes.
• The i allele is recessive to both the IA and IB
alleles.
• All the three alleles are found at appreciable
frequencies in human populations, thus the I gene
is said to be polymorphic.

10. How are the blood types determined?
• By the patterns of molecules (polysaccharides) on
the surface of red blood cells.
• The sugar is the antigen, which is the molecule that
the immune system recognizes.
• IA and IB alleles encode for transferase enzymes
which modifies a precursor carbohydrate to form
the A and B antigens respectively.
• IA IA / IA IO - A polysaccharide only
• IB IB / IB IO - B polysaccharide only
• IA IB - A & B polysacchrides
• IO IO – Lack both A & B polysaccharides

12. • The IA allele encodes an enzyme that adds N-
acetylgalactsamine to the precursor.
• The IB allele encodes an enzyme that adds galactose
to the precursor.
• Allele IO codes for an inactive enzyme and leaves
the precursor unmodified called the H substance.
• Other coloured sugar units are N-acetylglucosamine
and fucose

13. • AB – Universal recipient
• O - Universal donor

14. Rh Factor
• Antigen present in RBC.
• Discovered by Weiner and Lansteiner in 1940.
• First found on the surface of red blood cells of
the Indian brown monkey (Macacus rhesus).

15. How did they find Rh factor?
• Injected blood of rhesus monkey into rabbits and
guinea pigs Ab produced in blood serum of
these animals agglutinate RBC of rhesus monkey.
• When the same antiserum is added to human
blood, red cells of 85% of the persons tested
were also agglutinated.
• It was thus revealed that human blood contained
the same Rh antigen as in rhesus monkey.

16. • There are many Rh antigens.
• But only D(autosomal dominant gene) is more
antigenic in human.
• Other Ags present- C, E, c & e.
• Persons with D Ag – Rh positive
• Persons without D Ag – Rh negative
• Among Asian population, 85% are Rh +ve and
15% are Rh –ve.

17. • Different from ABO grouping as the Ag D
doesn’t have corresponding natural Ab (anti
D).
• If Rh +ve is transfused to Rh –ve – anti D is
formed.
• No risk of complications if Rh +ve receives Rh
–ve blood.

18. Inheritance of Rh Ag
• Rh factor is an inherited dominant factor.
• May be Homozygous [DD(Rh +ve) / dd(Rh -ve)]
or heterozygous [Dd(Rh +ve)].

19. Father
DD
Rh +
Mother
Dd
Rh -
Father - homozygous
Dd Dd DdDd
All offsprings are Rh + (heterozygous)

20. Father - homozygous
Father
dd
Rh -
Mother
dd
Rh -
dd dd dddd
All offsprings are Rh-

21. Father- heterozygous
Father
Dd
Rh +
Mother
dd
Rh -
Dd dd Dd Dd
50% offsprings are Rh + (heterozygous)

22. Transfusion
reactions due to
Rh
incompatibility.
No complications
But Rh antibody is produced
Rh antigen reacts with Rh antibody
Rh positive Rh negative
Agglutination
First tranfusion
Second transfusion

23. Hemolytic Disease of Fetus and
Newborn
• Disease in fetus and newborn.
• Traced by Levin in 1942.
• Characterised by abnormal hemolysis of RBCs.
• Due to Rh incompatibility ( diff. In Rh blood group
of mother and baby)
• Hemolytic disease leads to erythroblastosis
fetalis.

24. Erythroblastosis Fetalis

26. • The Rh agglutinins cause agglutination of fetal
RBCs resulting in hemolysis.
• Severe hemolysis in the fetus leads to jaundice.
• To compensate the hemolysis , rapid production
of RBCs (from bone marrow, spleen and liver).
• large and immature cells of erythroblastic stage
are released into circulation.
• Because of this, the disease is called
erythroblastosis fetalis.

27. Other complications
• Severe anaemia-results from hemolysis,infant dies in
severe anaemia.
• Hydrops Fetalis- characterised by edema,
enlargement of liver and spleen and cardiac failure.
Leads to intrauterine death of fetus.
• Kernicterus- form of brain damage( affects basal
ganglia, hippocampus, cerebellum etc due to entry of
bilirubin).

28. Prevention or Treatment
1. Anti D administered to Rh – mother at 28th
and 34th weeks of gestation as prophylactic
measure.
• Anti D should be administered to Rh – mother
within 48 hours of delivery  develops
passive immunity prevents formation of Rh
antibodies.
2. Exchange Transfusion