Fifth disease after immunoglobulin administration in an AIDS patient with parvovirus-induced red cell aplasia.
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Parvovirus B19 infection in the fetus is associated with anemia and hydrops and can result in fetal death. Fetal transfusion has been used in an attempt to improve outcome; however, it is associated with its own perinatal morbidity. We report two cases of fetal parvovirus B19 infection that were confirmed by polymerase chain reaction for parvovirus B19 deoxyribonucleic acid in umbilical cord blood. Ultrasonographic signs of compromise were observed at 30 and 24 weeks of gestation. Both fetuses were hydropic and one fetus was also anemic. Serial sonograms demonstrated that the hydrops resolved spontaneously over 3 to 5 weeks after diagnosis. One infant was delivered at 32 weeks of gestation as a result of idiopathic preterm labor. The other infant was delivered at term. Both infants appeared relatively normal at birth and have developed normally in the first year of life. Thus fetal hydrops in association with parvovirus B19 infection does not always lead to poor long-term outcome. A conservative approach without in utero therapy may be appropriate for the management of some of these fetuses.
OBJECTIVE: Nonimmune hydrops fetalis is a potentially lethal condition reflecting the clinical manifestation of several pathologic processes. Recently maternal infection by human parvovirus B19 has been reported to result in nonimmune fetal hydrops. We sought to develop a rapid and sensitive test to detect the presence of this agent in utero. STUDY DESIGN: Using a cloned isolate of the virus, we developed an assay based on enzymatic amplification of a segment of the human parvovirus B19 genome that allows direct detection of this agent in samples of fetal blood and amniotic fluid. RESULTS: The method detected as few as 100,000 genome equivalences and was specific for the viral genome alone. We used this assay to evaluate nine fetuses initially seen with nonimmune hydrops. Three cases were found to be positive for the human parvovirus B19 genome. CONCLUSION: The method is powerful in that it is rapid, sensitive, and simple. This assay may have general applicability in evaluation of nonimmune hydrops and in documentation of the natural history of fetal human parvovirus infections.
A nurse (index case) at a rehabilitation hospital was diagnosed with acute parvovirus B19 infection. A 2-year-old male patient was identified as the source patient. The epidemiological investigation focused on 15 individuals with symptomatic disease or risk factors for complications of parvovirus B19 infection. Serologic testing confirmed parvovirus B19 infection in the index case and source patient and identified a second health care worker who possibly contracted acute parvovirus B19 infection through nosocomial transmission. Parvovirus B19 infection can cause serious complications in pregnant women, persons with chronic hemolytic anemia, and persons with immunodeficiencies. Measures to control the transmission of parvovirus B19 infection should be part of the infection control plan at rehabilitation hospitals.
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Three children with homozygous sickle cell disease, 22 months and 8 and 10 years of age, had clinical and hematologic manifestations of aplastic and splenic sequestration crisis simultaneously. They had an acute drop in hemoglobin level (16, 20, and 45 gm/L), reticulocytopenia (0.1%, 0.6%, and 0.3%), and sudden splenic enlargement. Evidence of recent parvovirus infection was demonstrated.
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There are striking similarities between human parvovirus B19 (HPV-B19) infection and systemic lupus erythematosus (SLE): both may present with malar rash, fever, arthropathy, myalgia, cytopenia, hypocomplementemia, anti-DNA, and antinuclear antibodies (ANA). Therefore, it is difficult at times to differentiate HPV-B19 infection from SLE presentation or exacerbation. We report 4 cases of HPV-B19 infection mimicking SLE and review 10 other reported cases, all of whom were women. The similarity to a typical SLE presentation was indeed striking: most patients presented with rash, arthropathy, myalgia, fever, and positive ANA. In some cases, HPV-B19 infection seemed to exacerbate SLE rather then resemble it, and differentiation was difficult. Nearly all patients improved within several weeks. However, a few patients had symptoms and laboratory abnormalities lasting more than 6 months. The possibility of HPV-B19 infection should be entertained in patients presenting with SLE-like features.
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We report three children with congenital anaemia after intrauterine infection with B19 parvovirus. All the fetuses developed hydrops fetalis that was treated by blood transfusion. After delivery the infants had hypogammaglobulinaemia. In all three, sera lacked B19 but viral DNA was found in bone marrow. All were treated with immunoglobulin. One child died and B19 was found in various tissues. In the other two cases, virus could no longer be detected after therapy but the patients remain persistently anaemic. Persistent B19 infection should be suspected in infants with congenital red-cell aplasia.
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A transfusional B19 parvovirus infection may have severe consequences in immunocompromised hosts. The presence of B19 DNA was investigated with a polymerase chain reaction (PCR) assay in 30 batches of solvent/detergent-treated clotting factor concentrates (12 batches of factor VIII, 16 batches of factor IX, 1 batch of factor VII, and 1 batch of PPSB). B19 DNA was detected in 6 (20%) batches, including 3 factor VIII and 3 factor IX concentrates. Because of the frequency of B19 DNA in batches of clotting factors, measures to prevent transfusional risk of B19 infection via these blood products are justified, especially in recipients immunocompromised by HIV infection.
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We describe three patients who had infection with human parvovirus B19 in association with new-onset systemic necrotising vasculitis syndromes, two with features of polyarteritis nodosa and one with features of Wegener's granulomatosis. Chronic B19 infection, lasting 5 months to more than 3 years, was shown by enzyme immunoassay for IgG and IgM antibodies to B19 and polymerase chain reaction for B19 DNA in serum and tissue samples. The patients had atypical serological responses to the B19 infection, although none had a recognisable immunodeficiency disorder. Treatment with corticosteroids and cyclophosphamide did not control vasculitis. Intravenous immunoglobulin (IVIG) therapy led to rapid improvement of the systemic vascultis manifestations, clearing of the chronic parvovirus infection, and long-term remission. These observations suggest an aetiological relation between parvovirus B19 infection and systemic necrotising vasculitis in these patients and indicate a potentially curative role for IVIG in such disorders.
Because parvovirus B19 occasionally causes some of the features typical of Kawasaki disease, we investigated B19 involvement in 15 children with Kawasaki disease. Active or recent B19 infection, as shown by B19-DNAaemia, positive B19-specific IgM antibodies, or both, was diagnosed in 10 patients (67%). A high frequency of all major criteria for diagnosis of Kawasaki disease (60%), anaemia (60%), coronary aneurysms (30%), and arthropathy (30%) was found in children with B19-associated Kawasaki disease. Thus B19 may have a pathogenic role in the development of Kawasaki disease, with other predisposing factors.