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TPDN 1989, Vol. 49, No. 14
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reticulocytes in the peripheral smear approxi-
mately seven to ten days after their disappear-
ance. TAC may require transfusion and hospi-
talization and can be fatal if not treated promptly.
B19 Infection in Immunodeficient Patients
A B19-related severe chronic anemia associated
with red cell aplasia has been described in
patients on maintenance chemotherapy for acute
lymphocytic leukemia, patients with congenital
immunodeficiencics, and patients with human
immunodeficiency virus (HIV)-related immu-
nodeficiency. It is not yet known how often B19
causes chronic anemia in immunodeficient pa-
tients or which patients are most susceptible to
this complication of infection. Chronic B19
infection should, however, be included in the
differential diagnosis of chronic anemia in the
immunodeficient patient.
Infection in the Pregnant Woman
Intrauterine infection and fetal death
In most of the reported B19 infections
occurring during pregnancy, the fetus has not
been adversely affected. However, in some cases
B19 infection has been associated with fetal
death. The risk of fetal death attributable to
parvovirus infection following documented ma-
ternal infection (B19 IgM-antibody-positive) is
not known, but preliminary results of one study
from the United Kingdom suggest that it is <10%.
Antibody studies of liveborn infants and
hybridization studies of fetal tissues indicate
that less than one third of maternal infections
arc associated with fetal infection in this study.
Results from an ongoing study in the United
States also suggest that B19-attributable fetal
deaths are infrequent (CDC, unpublished data).
In this study, fetal loss has so far occurred in
two (4.1%) of 49 women followed to term. It is
not known whether the two fetal deaths were
caused by B19 infection.
When the antibody status of the woman is
unknown, estimates of the risk of fetal death
after exposure must take into account the rate
of susceptibility in the population and the risk
of infection after the exposure. For example, by
taking these factors into account, the upper limit
estimate of the risk of fetal death would be <2.5%
after exposure to household members with
documented infection (<0.1 risk of fetal death x
0.5 rate of susceptibility x 0.5 rate of infection
x 100; see sections on Epidemiologic Features of
B19 Infection: Prevalence and Transmission)
and <1.5% after prolonged exposure at schools
with widespread El among students (<0.1 risk of
fetal death x 0.5 rate of susceptibility x 0.3 rate
of infection x 100). The upper limit risk estimate
of fetal death after other types of exposure (eg,
schools with limited El among students) is likely
to be substantially less.
Congenital anomalies
Since some of the animal parvoviruses are
teratogens, the possibility that infection may
also be associated with congenital anomalies in
humans is a concern. However, there is no
evidence that the rate of congenital anomalies
following B19 infection exceeds background
rates. 1319-associated congenital anomalies have
not been reported among several hundred live-
born infants of B19-infected mothers. One
aborted fetus with eye anomalies and histologic
evidence of damage to multiple tissues born
to a 1319-infected woman has been reported.
An anencephalic fetus was reported in a 1319-
infected woman, but the timing of infection
made it unlikely that B19 contributed to the
defect.
PATHOGENESIS
The pathogenesis of the rash in El is unknown,
but the rash may be immune-complex-mediated.
The other, more serious manifestations of B19
infection are related to the propensity of the
virus to infect and lyse crythroid precursor cells
and interrupt normal red cell production. In a
person with normal hematopoicsis, B19 infec-
tion produces a self-limited red cell aplasia
that is clinically inapparent. Transient leuko-
penia, lymphocytopenia, and thrombocytopenia
have also been reported with B19 infection in the
normal host.
In patients who have increased rates of red
cell destruction or loss and who depend on
compensatory increases in red cell production to
maintain stable red cell indices, B19 infection
may lead to TAC. Patients at risk for TAC
include those with chronic hemolytic anemias
and those with anemias associated with acute or
chronic blood loss. In immunodeficient persons,
B19 infection may persist, causing chronic red
cell aplasia, which results in chronic anemia;
chronic neutropenia has also been described.
B19 DNA-positive
in 20 fetal deaths;
pathologic findings
tissues have been reported
in all 17 cases in which
were described, the fetuses
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