Page 565 - Review of Medical Microbiology and Immunology ( PDFDrive )

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mebooksfree.com mebooksfree.com mebooksfree.com TABLE 64–4 Rh Status and Hemolytic Disease of the mebooksfree.com
PART VII Immunology
554
that type O blood has A and B antibodies. Therefore when
type O blood is given to a person with type A, B, or AB
Newborn
blood, you might expect a reaction to occur. A clinically
Rh Status
detectable reaction does not occur because the donor anti-
body is rapidly diluted below a significant level. Persons
1
Hemolysis
Father
Child
Mother
with group AB blood have neither A nor B antibody and
thus are universal recipients.
No (1st child)
++
–
++
In addition to red blood cells, the A and B antigens
Yes (2nd child and subsequent

appear on the cells of many tissues. Furthermore, these ++ ++ ++ or – No children)

mebooksfree.com mebooksfree.com mebooksfree.com 1 hemolytic disease will therefore not occur. Yes indicates that hemolysis of the new- mebooksfree.com
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antigens can be secreted in saliva and other body fluids.
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No
++
–
–
Secretion is controlled by a secretor gene. Approximately
85% of people carry the dominant form of the gene, which
++ or –
No
–
+++
allows secretion to occur.
–
–
No
–
ABO blood group differences can lead to neonatal jaun-
No indicates that hemolysis of the newborn’s red cells will not occur and that
dice and anemia, but the effects on the fetus are usually less
severe than those seen in Rh incompatibility (see next sec-
born’s red cells is likely to occur and that symptoms of hemolytic disease will there-
fore probably occur.
tion). For example, mothers with blood group O have anti-
bodies against both A and B antigens. These IgG antibodies
can pass the placenta and, if the fetus is blood group A or
they lack the gene for the Rh(D) protein.
B, cause lysis of fetal red cells. Mothers with either blood
The Rh status of parents is clinically important because
group A or B have a lower risk of having a neonate with
a specific combination can result in hemolytic disease of
jaundice because these mothers produce antibodies to Rh-positive. The remaining 15% are Rh-negative, that is,
the newborn (erythroblastosis fetalis). When an Rh-
either B or A antigens, respectively, that are primarily IgM,
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negative woman has an Rh-positive fetus (the D gene
and IgM does not pass the placenta.
being inherited from the father), the Rh(D) antigen on the
Rh Blood Type & Hemolytic Disease of
bodies in the mother (Table 64–4). This occurs most often
the Newborn
when the Rh(D) erythrocytes of the fetus leak into the
maternal circulation during delivery of the first Rh(D)
About 85% of humans have erythrocytes that express the
child (Figure 64–13).
Rh(D) antigen on their surface. They are said to be
–
+
Rh mother
in blood
of Rh child
Placenta breaks Late in second pregnancy Erythroblasts
away
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mebooksfree.com mebooksfree.com Anti-Rh antibody Second Rh fetus mebooksfree.com mebooksfree.com mebooksfree.com
Rh factor
on RBCs
+
Rh fetus
+
+
First Rh fetus
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FIGURE 64–13
Hemolytic disease of the newborn (erythroblastosis fetalis). Left panel: Fetal red cells (RBCs) bearing the Rh antigen
enter the mother’s blood when the placenta separates during the birth of the first Rh-positive child. IgG antibodies to Rh antigen are then pro-
duced by the mother. Center panel: During a second pregnancy with an Rh-positive fetus, IgG antibodies pass from the mother into the fetus
via the placenta. The antibodies bind to the fetal red cells, complement is activated, and the membrane attack complex lyses the fetal red cells.
Right panel: Anemia and jaundice occur in the fetus/newborn. As a result of the anemia, large numbers of erythroblasts are produced by the
bone marrow and are seen in the blood of the newborn. (Reproduced with permission from Cowan MK, Talaro KP, eds. Microbiology: A Systems Approach. New York:
McGraw-Hill; 2009.)
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