History of Blood Banking
devices for transfusion and became
 Discovered over a hundred years ago, but
recognized only in late 50 years
 It was not until World War 2 that blood
transfusion Science became an important
part of medical science
 1492 – blood was taken to 3 young men and
give to Pope Innocent VII
 1628 – English physician, William Harvey,
discovers the circulation of blood. Shortly
afterward, the earliest known blood
transfusion is attempted.
 1665 – The first recorded successful blood
transfusion occurs in England. Physician
Richard Lower kept dogs alive by
transfusing blood from other dogs.
 1795 – In Philadelphia, Philip Syng Physick,
an American physician, performs the first
human blood transfusion, although he did
not publish this information.
 1818 – James Blundell, a British
obstetrician, performs the first successful
transfusion of human blood to a patient for
the treatment of postpartum hemorrhage.
Using the patient’s husband as a donor, he
extracts approximately four ounces of blood
from the husband’s arm and using a
syringe, successfully transfuses the wife.
Between 1825 and 1830, he performs 10
transfusions, five of which prove beneficial
to his patients. He publishes these results.
 1869 - Attempts to find nontoxic
anticoagulant, Braxton Hicks recommended
sodium phosphate.
 1900 - `Karl Landsteiner, an Australian
physician, discovers the first three human
blood groups (A, B, and O). The fourth, AB is
added by his colleagues Decastello and
Sturli in 1902. Landsteiner receives the
Nobel Prize for Medicine for his discovery in
1930.
 Edward Lindemann – he tried appropriate
successful. HE carried out vein-vein
transfusion of blood by multiple syringes
and a special cannula.
 Unger – designed a syringe valve apparatus
that transfusion from donor to patient by
an unassisted physician became practical.
 1907 – Hektoen suggests that the safety of
transfusion might be improved by
crossmatching blood between donors and
patients to exclude
incompatible mixtures. Reuben Ottenber
performs the first blood transfusion using
typing and crossmatching in New York.
 1912 – Roger Lee demonstrates that it is
safe to give group O blood from all groups
can be given to group AB patients. The
terms “Universal Donor” and “Universal
Recipient” are coined.
 1914 –Hustin reported the used of Sodium
Citrate as an anticoagulant.
 1915 – Lewisohn determined the minimum
amount of citrate needed for
anticoagulation
 1916 – Rous & Turner introduced a citrate
dextrose solution for the preservation of
blood.
 1937 – Bernard Fantus, director of
therapeutics at the Cook county Hospital in
Chicago, establishes the first hospital blood
bank. In creating a hospital laboratory that
can preserve and store donor blood, Fantus
originates the term “blood bank”. Within a
few years, hospital and community blood
banks begin to be established across the
United States. Some of the earliest are in
San Francisco, New York, Miami, and
Cincinnati.
 1939 – The rH blood group system is
discovered by Karl Lansteiner, Alex Wiener,
Page 1 of 11
 Philip Levine and R.E. Stetson and is soon
recognized as the cause of the majority of
transfusion reaction. Identification of rh
factor takes place history as one of the
most important breakthroughs in the
history of blood banking.
 1941- Dr. Drew was appointed director of
the first American Red Cross Blood Bank
Presbyterian Hospital
 1943 Loutit & Mollison introduced the
formula for the preservative acid-citrate
 1947- Blood Banks were established in
many major cities of the United States, The
American association of Blood Banks (AABB)
is formed to promote common goals among
blood banking practitioners and the blood
donating public.
 1950- In one of the single most influential
technical developments in blood banking,
Carl Walter and W.P. Murphy Jr., introduce
the plastic bag for blood collection.
Replacing breakable glass bottles with
durable plastic bags allows for the evolution
of a collection system capable of safe and
easy preparation of multiple blood
components from a single unit of blood.
 Invention of the refrigerated centrifuge the
following year further expedites blood
component therapy.
 1955- In response to the heightened
demand to create an open heart surgery
and advance in trauma care, blood use
enters its most explosive growth period.
 1960- Blood testing advances help to
prevent Hemolytic disease through
immunization. Through this, Rh positive and
negative blood testing is done to protect
pregnant mothers and their babies against
getting blood that doesn’t match. In
emergencies, pregnant women will receive
the blood they need on the Rh factor and
no harm will be done to mother or child.
 1979 - The anticoagulant preservative
CPDA-1 is introduced. This extends the shelf
life of blood and facilities resources-sharing
among blood banks.
 2005 - All donated blood in the United
States is screened for HIV, Hepatitis B and
C, HTLV-1 and 2, West Nile Virus and
Treponema Pallidum.
 2006 - Roughly 15 million units of blood are
transfused each year in the United States.
Blood Banking
GENETIC BACKGROUND OF BLOOD GROUP
SYSTEM
 Blood group system
 Series of antigens exhibiting similar
serological and physiological characteristics,
and inherited according to a specific
pattern.
ANTIGEN
 A substance recognized by the body as
being foreign, which can cause an immune
response.
ANTIBODY
 A protein substance secreted by plasma
cells that are developed in response to and
interacting specifically with an antigen.
Page 2 of 11
INHERITANCE TERMINOLOGIES
GENE
 Determines specific inherited trait (e.g. blood
type)
CHROMOSOME
 Unit of inheritance
 Carries genes
 23 pairs of chromosomes per person, carrying
many genes
 One chromosome inherited from mother, one
from father.
LOCUS
 Site on chromosome where specific gene is
located
ALLELE
 Alternate choice of genes at a locus (ex. A or
B; C or c, Lewis a or Lewis b)
 The different forms of a gene. Y and y are
different alleles of the gene that determines
seed color. Alleles occupy the same locus, or
position on chromosomes
HOMOZYGOUS
 Alleles are the same for any given trait on
both chromosome (ex. A/A)
 Both alleles for a trait are the same in an
individual. They can be homozygous
dominant (YY), or homozygous recessive (yy).
HETEROZYGOUS
 Alleles for a given trait that are different on
each chromosome (ex. A/B or A/O)
 Differing alleles for a trait in an individual,
such as Yy.
PHENOTYPE
 Observed inherited trait (ex. Group A or Rh
positive)
 The physical appearance of an organism with
respect to a trait, i.e, yellow (Y) or green (y)
seeds in garden peas. The dominant trait is
normally represented with a capital letter,
and the recessive trait with the same lower
case letter
GENOTYPE
 Actual genetic information for a trait carried
on each chromosome (ex. O/O or A/O)
 The genetic constitution of an organism with
respect to a trait (homozygous etc.)
DOMINANT
 The expressed characteristic on one
chromosome takes precedence over the
characteristic determined on the other
chromosome (ex. A/O types as A)
 A trait expressed preferentially over another
trait
CO-DOMINANT
 The characteristics determined by the genes
on both chromosomes are both expressed-
neither is dominant over the other (ex. A/B
types as AB)
RECESSIVE
 The characteristic determined by the allele
will only be expressed if the same allele is on
the other chromosome also (ex. Can type as O
only when genotype is O/O)
AMORPH GENE
 Genes that does not express or detected
*picture (3)
Page 3 of 11
INHERITANCE PATTERN OFFSPRING POSSIBILITIES
 A/A parent can only pass along A gene Mother’s Genes Father’s Genes
 A/O parent can pass along either A or O gene B O
 B/B parent can only pass along B gene A AB AO
 B/O parent can pass along either B or O gene O BO OO
 O/O parent can only pass along O gene
 AB parent can pass along either A or B gene Mother’s Genes Father’s Genes
B B
A AB AB
A AB AB

Mother’s Genes Father’s Genes

B O
A AB AO
A AB AO
The A, B and O alleles
 There are three different alleles for human
blood type: Mother’s Genes Father’s Genes
Blood types For simplicity, we call O O
these A AO AO
A
I A A AO AO
B
I B
i O
ABO PHENOTYPES AND GENOTYPES
 Group A phenotype = A/A or A/O genotype Mother’s Genes Father’s Genes
 Group B phenotype = B/B or B/O genotype O O
 Group O phenotype = O/O genotype A AO AO
 Group AB phenotype = A/B genotype B BO BO

SIX DIFFERENT GENOTYPES AT THE HUMAN PROBLEM:

ABO GENETIC LOCUS Could a man with type
Allele from Allele from Genotype Blood types B blood and a woman
Parent 1 Parent 2 of offspring of offspring with type AB produce a
A A AA A child with type O
A B AB* AB blood?
A O AO A
B A AB* AB
B B BB B
B O BO B
O O OO O

Page 4 of 11

BIOCHEMISTRY OF THE ABO BLOOD GROUP
SYSTEM
 ABO antigens are terminal sugars found at
the end of long sugar chains
(oligosaccharides)
 The A and B antigens are the last sugar
added to the chain
 The “O” antigen is the lack of A or B antigen
but it does have the most amount of next to
the last terminal that is called the H antigen
PRODUCTION OF A, B, AND H
 Controlled by the action of transferases
 TRANSFERASES are enzymes that catalyse
addition of specific sugars to the
oligosaccharide chain.
 The H, A, or B genes each produce a
different transferase, which adds a different
specific sugar to the oligosaccharide chain.
ABO BLOOD GROUP SYSTEM
 ABO system is the most important blood
type system
 The associated anti-A antibodies and Anti-B
antibodies are usually IgM antibodies,
which are usually produced in the first years
of life by sensitization to environmental
substances such as food, bacteria, and
viruses
 IgM are cold reacting, binds to complement
and do not cross the placenta.
NOMENCLATURE
 Number of ABO blood group antigens: 4
 ISBT symbol: ABO
 ISBT number: 001
 Gene symbol: ABO
 Gene name: ABO blood group (A
transferase, a1,3-N-
acetylgalactosaminyltransferase; B
transferase, a1,3-galactosyltransferase)
HISTORICAL PERSPECTIVE
 Discovered by the Austrian scientist Karl
Landsteiner, who found three different
blood types in 1901
 He was awarded the Nobel Prize in
Physiology or Medicine in 1930 for his work
 First to perform forward and reverse
grouping
Page 5 of 11
FORWARD GROUPING (Antigen Typing on
DONOR’S CELL and PATIENT’S CELL)
Blood being tested Serum

Anti A Anti B
Type AB (contains + (for + (for
agglutinogens A agglutination) agglutination)
and B)
REVERSE GROUPING
Type B (contains - +
REVERSE RESULT
agglutinogen B)
Patient SERA/ known cells
Type A (contains + -
agglutinogen A)
A Cells B Cells
Type O (contains - -
- + A
no agglutinogens)
+ - B
- - AB
+ + O

BLOOD GROUP ANTIGEN ANTIBODY

A A Anti-B
B B Anti-A
AB A and B Neither
O Neither anti-A or Anti-A,B
anti-B

ABO Antigen A Antigen B Antibody Antibody

Blood anti-A anti-B
type

A Yes No No Yes
B No Yes Yes No
O No No Yes Yes
AB Yes Yes No No

Page 6 of 11
 1902- Sturle and von Descatello discovered
the fourth ABO group- Type AB
 AB individuals does not agglutinate group A
or group B cells, indicating the absence of
antibodies to both A and B

 Incidence (%) of ABO Blood Groups

ABO Group Whites Blacks
O 45% 49%
A 40% 27%
B 11% 20%
AB 4% 4%

FREQUENCY
 A and O are the most common blood types
 AB is the rarest
 Blood Group O is a Universal Donor
 Blood Group AB is the Universal Recipient

Importance in Transfusion Reaction

 Individuals with type A blood can receive
blood from donors of type A and Type O
blood.
 Individuals with type B blood can receive
blood from donors of type B and Type O
blood.
 Individuals with type AB blood can receive
blood from donors of type A, type B, type
AB, or type O blood. Type AB blood is called
the universal recipient.
 Individuals with type O blood can receive
blood from donors of only type O.
 Individuals of type A, B, AB and O blood can
receive blood from donors of type O blood.
Type O blood is called the universal donor.

INHERITANCE OF ABO GROUPINGS

 ABO blood types are inherited through
genes on chromosome 9, and they do not
change as a result of environmental
influences during life.

Page 7 of 11
 An individual’s ABO type is determined by
the inheritance of 1 of 3 alleles (A, B, or O)
from each parent.

THE FORMATION OF ABO ANTIGENS

 ABO produce specific glycosyl transferases
that add sugars to a basic precursor
substance on the RBC
 A “donor” nucleotide derivative supplies
the sugar that confers ABH specificity
 Formation of ABH antigens results from the
interaction of ABO genes
 A, B, H antigens are formed from basic
precursor material which is itself a genetic
product
 H antigens are found in greatest
concentration on red cells of O group
 The basic material has a glycoprotein or
glycolipid backbone to which sugars are
attached in response to specific enzyme
transferases elicited by inherited gene
 ABH glycoplipid antigens are built upon a
common carbohydrate residue Donor Nucleotides & Immunodominant Sugar
 ABO antigens are terminal sugars found at Responsible for H, A & B Antigen
the end of long sugar chains Gene Glycosyltransferas Nucleotide Immunodominant Ag
(oligosaccharides) that are attached to e (Sugar donor) sugar

lipids on the red cell membrane

 The A and B antigens are the last sugar
added to the chain H Alpha-2- Guanosine L-Fucose H
 The “O” antigen is the lack of A or B Lfucosyltrans diphosphate – L-
antigens but it does have the most amount ferase fucose (GDP-
of next to last terminal sugar that is called fucose)
the H antigen. A Alpha-3-N- Uridine N-acetyl A
acetylgalacto diphosphate N- galactosamine
saminyltransf acetyl-D-
erase galactosamine
(UDP-GalNac)
B Alpha-3-D- UDP- Galactose D-galactose B
galactosyltra
nsferase

Page 8 of 11
 Weak Subgroups
 A3
 Ax
 A end
 Am
 Ay
 A el
 Infrequently present, recognized in ABO
discrepancy

 The production of A, B and H antigens are
controlled by the action of transferases
 These transferases are enzymes that
catalyze (or control) addition of specific
sugars to the oligosaccharide chain
 The H, A, or B genes each produce a
different transferase, which adds a different
specific sugar to the oligosaccharide chain
Fluids in which A, B, and H Substances can be
Detected in Secretors
 Saliva
 Tears
 Urine
 Digestive juices
 Bile
 Milk
 Amniotic fluid
 Pathologic fluids, pleural, peritoneal,
pericardial, ovarian cyst
ABO SUBGROUPS
 A1 and A2
 The A blood type contains about twenty
subgroups, of which A1 and A2 are the most
common (over 99%)
 A1 (A&A1) makes up about 80% of all A-
type blood, with A2 (only one antigen)
making up the rest.
 These two subgroups are interchangeable
as far as transfusion is concerned, but
complications can sometimes arise in rare
cases when typing the blood.
 Inheritance of A1 gene elicit production of
high concentration of the enzyme alpha-3-
N- acetylgalactosaminyltransferase which
converts all of the H precursor structure to
A1
 B SUBGROUPS AND WEAK B SUBGROUPS
Very rare and less frequent than A
subgroups
 B3
 Bx
 Bm
 B el

Page 9 of 11
 BOMBAY BLOOD GROUP (HH OR HNULL)
 Individuals with the rare Bombay
phenotype do not express antigen H on
their red blood cells
 As H antigen serves as precursors for
producing A and B antigens, the absence of
H antigen means the individuals do not
have A or B antigens as well (similar to O
blood group)
 However, unlike O group, the H antigens is
absent, hence the individuals produce
isoantibodies to antigen H as well as to both
A and B antigens. In case they receive blood
from O blood group, the anti-H antibodies
will bind to H antigen on RBC of donor
blood and destroy the RBCs by
complement-mediated lysis.
 Bombay phenotype can receive blood only
from other hh donors (although they can
donate as though they were type O)
ABO DISCREPANCIES
 Occur when the expected 2 positive and 2
negative reactions are not observed and are
usually technical in nature
 (see common sources of technical errors
Resulting in ABO discrepancies)
GROUP 1 DISCREPANCY
 Due to weakly reacting or missing
antibodies due to missing or weak
isoagglutinatinins due to depressed Ab
production or cannot produce ABO Ab’s
 Newborns
 Elderly patients
 Patients with leukemia
 Patients with lymphomas
 Patients taking immunosuppresives that
yield hypogammaglobulinemia
 Patients with immunodeficiency disease
 Bone marrow transplant
Resolution of Group 1 discrepancies
 Enhance reverse group reaction by
incubating the patient serum with reagent
A1 and B-cells at room temperature for 15-
30 minutes
 No reaction, incubate at 4C for 15-30
minutes
Group II discrepancies
 Due to weakly reacting or missing antigens
 Subgroups of A & B maybe present
 Leukemias that may yield weakened A and
B antigens
 Hodgkin’s disease
 Excess amount of BGSS (Blood Group
Specific Soluble Substances)
 Acquired B phenomena which results from
malignancy from the stomach
Page 10 of 11
 Resolution Resolution
 Enhanced incubation of test mixture at  Polyagglutination (RBC agglutinating with
room temperature up to 30 minutes to human sera) can occur due bacterial or
increase association of antibody with genetic inheritance, resolve by testing with
antigen several lectins
 RBC can be pretreated with enzymes then  Patients RBC should be incubated at 37C for
retested with antisera a short period
 Or maybe treated with DTT (dithiothreitol
Group III discrepancies to disperse IgM related agglutination
 Caused by protein and plasma
abnormalities and result from rouleaux
formation
 Elevated levels of globulin due to certain
disease such as multiply myeloma
 Elevated levels of fibrinogen
 Presence of plasm expanders such as
dextran and polyvinyl pyrollidone (PVP)
 Presence of Wharton’s jelly

Resolution of group III

 Washed the patient red cell several times
with saline solution
 Washing cord cells 6-8 times

Group IV discrepancies
 Polyagglutination
 Cold reactive antibodies
 Warm antibodies
 Unexpected antibodies
 Antibodies other than anti-A and anti-B
 Weak A and B antigens

Page 11 of 11