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The effects of human parvovirus B19 and cytomegalovirus during pregnancy.

Human parvovirus B19 and cytomegalovirus (CMV) are two common viruses that can have significant and devastating effects on a fetus. Maternal infection may lead to vertical transmission of the virus to the fetus. Parvovirus infection in the fetus may cause miscarriage, nonimmune hydrops, or demise. Fetal CMV infection can cause a number of problems, including nonimmune hydrops and neurosensory disabilities. Nurses who are knowledgeable about possible viral effects during pregnancy can collaborate in the management of these patients, particularly in the areas of patient assessment, education, and support.

Cytomegalovirus Infections↗

Intrauterine parvovirus B19 infection may cause an asymptomatic or recurrent postnatal infection.

Although infection with parvovirus B19 (B19) during pregnancy may cause fetal demise, the true incidence of intrauterine infection is unknown. For 19 women with serologically confirmed B19 infections between 4 and 38 weeks of gestation, we performed follow-up examinations of their infants. Serial sonograms of the 19 fetuses showed that none developed hydrops. All 19 women delivered healthy term infants. Cord sera of four infants were tested for IgM to B19 and three were positive. Between 3 and 21 months of age, all 19 infants had normal physical examinations, developmental evaluations and hematocrits; and 16 lacked IgG to B19. One infant who was IgM-positive to B19 at birth was IgM-positive at age 7 months when he also had an IgG titer to B19 of 1:500,000 (mother's concurrent titer, 1:10,000), and had B19 DNA in serum detected by polymerase chain reaction. The other two infants who were IgM-positive at birth were IgM- and IgG-negative by 11 and 16 months of age. These results suggest that intrauterine B19 infection may be frequent and occasionally cause an asymptomatic postnatal infection.

Antibodies, Viral↗

Serologic and virologic evidence for frequent intrauterine transmission of human parvovirus B19 with a primary maternal infection during pregnancy.

OBJECTIVE: To define the intrauterine viral transmission rate during primary maternal parvovirus B19 infection and identify factors that may influence this rate. METHODS: Forty-three pregnant women at two medical centers were identified with a primary B19 infection and followed to delivery. At delivery maternal and infant (umbilical cord) blood was obtained for B19 serologic and virologic PCR testing. RESULTS: All of the women delivered healthy infants at term and none was hydropic. Overall 22 (51%) of the 43 infants had some evidence of a congenital B19 infection. B19-specific IgM was detected in 11 infants at delivery, B19 IgA was detected in 10 and B19 DNA was detectable by PCR in 11 infants. One infant was negative at birth but became positive for IgM, IgA and PCR at 6 weeks of age. No association was found between the likelihood of intrauterine infection and: maternal age; symptomatic maternal infection; method of delivery; maternal IgG titer at delivery; maternal IgG avidity at delivery; or maternal viremia at delivery. Intrauterine infection was associated with maternal IgM positivity at delivery; this association may have been a result of maternal infection occurring later in gestation. CONCLUSION: Although the incidence of intrauterine hydrops and fetal demise after maternal infection is low, there is a high rate of intrauterine viral infection that occurs throughout gestation and yields newborns who, although infected in utero, are asymptomatic at birth.

Antibodies, Viral↗

Clinical characteristics of children with hereditary hemolytic anemias and aplastic crisis: a 7-year review.

We reviewed the clinical courses of children < or = 16 years of age with hereditary hemolytic anemias who were admitted to the University of Mississippi Medical Center for aplastic crisis. Constitutional signs, gastrointestinal complaints, and headache were the most frequent findings. Statistically significant decreases in hemoglobin levels, hematocrit, and reticulocyte counts, but not total white blood cell or platelet counts, were found on admission when compared to other times of determination. For 27 of 49 patients, IgM antibody determinations to human parvovirus (B19) were available, and 15 (56%) had positive values. We conclude that erythroid (but not other) blood cell lines are helpful in establishing a clinical diagnosis, and that both acute and convalescent titers are necessary to assess the immune response to the infection. Physicians should continue to search for agents other than B19 parvovirus in patients in whom B19 antibodies cannot be found.

Adolescent↗

Parvovirus B19 infection in pediatric transplant patients.

Evidence of recent parvovirus virus infection (as determined by the presence of a positive IgM antibody titer) without other identified causes of anemia was found in 5 of 26 pediatric solid-organ transplant recipients evaluated for moderate-to-severe anemia between June 1990 and July 1991. Anemia tended to be chronic (median duration of anemia at the time of diagnosis was 12 weeks) and was associated with normal red blood cell indices in the absence of reticulocytes. The median age of the children at the time of presentation with anemia due to parvovirus was 1.8 years at a median time of 8 months after transplantation. Four of the 5 children were treated with i.v. immunoglobulin because of persistence of anemia requiring blood transfusions. A response characterized by an increase in reticulocyte count and normalization of hemoglobin was seen in each of these patients 2-4 weeks after treatment. The remaining patient experienced a spontaneous recovery from her anemia. Parvovirus infection should be included in the differential diagnosis of solid-organ transplant recipients presenting with severe anemia associated with low or absent reticulocytes.

Anemia↗

B19 parvovirus infection and transient aplastic crisis in a child with sickle cell anemia.

Transient aplastic crisis is reported in a young child with sickle cell anemia with acute B19 parvovirus infection. She also developed acute chest syndrome and bone marrow/bone infarction involving the right ilium. The clinically unsuspected bone marrow infarction in this patient may have contributed to acute chest syndrome secondary to pulmonary fat embolism. Transient cessation of erythropoiesis as a result of B19 parvovirus infection, and not the localized bone marrow infarction, was the probable cause of reticulocytopenia and worsening of anemia in this child.

Acute Disease↗

Acute transient hemolytic anemia with a positive Donath-Landsteiner test following parvovirus B19 infection.

PURPOSE: A case of childhood acute hemolytic anemia following parvovirus infection provided an hypothesis for the high frequency of Donath-Landsteiner antibodies and inappropriately low reticulocyte counts in this disease. PATIENTS AND METHODS: A 3-year-old boy with hematuria and jaundice was found to have autoimmune hemolytic anemia due to a biphasic IgG Donath-Landsteiner antibody. Despite profound anemia (hematocrit 14.5%), the reticulocyte count was low (1.0%) and examination of his normocellular bone marrow showed erythroid hypoplasia. RESULTS: A clinical diagnosis 2 weeks earlier of acute parvovirus B19 was serologically confirmed as the associated antecedent infection. Hemolytic anemia resolved with packed red cell transfusion, and intravenous immune globulin and steroid treatment. CONCLUSIONS: The high-frequency red cell P antigen is both the unusual specificity of Donath-Landsteiner antibody and the viral receptor for parvovirus infection of red cell precursors. We speculate that interaction of the virus with its receptor may change antigenicity such that anti-P autoantibody forms. Parvovirus B19 may be a primary cause of reticulocytopenic postinfectious hemolytic anemia in children.

Acute Disease↗

Clinical presentation of parvovirus B19 infection in children with aplastic crisis.

The records of 22 children with parvovirus B19-induced aplastic crisis were reviewed. The group consisted of 16 children with sickle cell hemoglobinopathies and 6 with hereditary spherocytosis. Children presented to the hospital 0.5 to 8 days (mean, 2.4 days) after the onset of symptoms. The children with sickle-cell disease presented earlier (mean, 1.4 days) than did children with hereditary spherocytosis (mean, 5 days; P = 0.02. Fever was the most common symptom, occurring in 73% of children. Rash did not occur in either group. Reticulocyte counts began to rise 1 week after onset of illness associated with a rise in parvovirus B19-specific IgG antibody. These data suggest that parvovirus B19 infection in children with sickle-cell hemoglobinopathies and heredity spherocytosis differs from infection in normal children.

Adolescent↗