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Primary and secondary infection with human parvovirus B19 in pregnant women in South Africa.

A study of human parvovirus B19 infection in 1,967 pregnant women of all races in Johannesburg revealed an overall prevalence of 24.9% for IgG antibodies and 3.3% for IgM antibodies. Of the 64 IgM-positive sera indicating active infection, 62 were resistant to urea denaturation. No differences in the prevalence of IgG antibodies between population groups were observed, but active infections, as demonstrated by IgM antibodies, were significantly more prevalent in black than in white, coloured or Asian mothers.

Antibodies, Viral↗

B19 parvovirus-induced anemia in a normal child. Initial bone marrow erythroid hyperplasia and response to intravenous immunoglobulin.

PURPOSE: Human B19 parvovirus infection may cause severe erythroid hypoplasia in patients with an underlying hemolytic anemia. We report a case of severe parvovirus-induced anemia with initial marrow erythroid hyperplasia in a child with no underlying hematologic disorder. CONCLUSIONS: The patient's rapid hemoglobin recovery after treatment with i.v. immunoglobulin further supports this form of therapy for children with parvovirus-induced anemia.

Anemia↗

[Human Parvovirus B19 infection and aplastic crisis].

Human Parvovirus B19 (B19-virus) is the most frequent cause of aplastic crisis in patients with underlying hereditary haemolytic anaemia. B19-virus interrupts erythropoiesis by lytic damage of erythroid precursors in the bone marrow. Patients with hereditary haemolytic anaemia have a shortened red cell life span and a compensatory increased activity of the erythroid precursors in the bone marrow. Temporary interruption of erythropoiesis leads to a precipitous fall in haematocrit and absence of reticulocytes in the circulation. The symptoms of the illness are anaemia and fever. The treatment is red cell transfusion. The infection is diagnosed either by direct demonstration of B19-virus-DNA or by demonstration of specific IgM-antibodies to B19-virus. The natural infectivity of B19-virus is high, and infection is presumably followed by lasting immunity. Because the infectivity of cases of aplastic crisis caused by B19-virus is especially high, control guidelines are necessary for pregnant seronegative staff. A review of the literature is presented.

Anemia, Aplastic↗

Established fibromyalgia syndrome and parvovirus B19 infection.

OBJECTIVE: To determine the seroprevalence of prior and persistent parvovirus B19 (B19) infection in a group of patients with fibromyalgia (FS) compared with controls. METHODS: Fifteen female patients with FS who recalled a viral prodrome (+VP) preceding the onset of FS symptoms and eleven patients with FS who did not recall any such illness (-VP) were selected from a referral practice. We excluded patients with FS who described a history of trauma prior to the onset of FS symptoms. Twenty-six female medical workers served as controls. Serum IgM and IgG anti-B19 antibodies were measured by ELISA: Polymerase chain reaction (PCR) products from serum were analyzed by dot blot hybridization for B19 DNA. Fisher's 2-tailed exact test was used to compare the proportion of positive serologies in each group. RESULTS: No patient or control had positive IgM levels. For all patients with FS, the prevalence of prior B19 infection was comparable to that of healthy controls (11/26 vs 12/26, p = 1.00) and that of the general population. No significant difference was found in the prevalence of prior B19 infection in FS + VP and FS-VP patients (8/15 vs 3/11, p = 0.25). None of the patients or controls showed evidence for persistent B19 viremia, as determined by PCR analysis. CONCLUSION: Our data do not suggest that B19 plays a pathogenic role in this population of patients with FS. Testing for IgM against B19 within 2-3 months of symptom onset may prove more helpful in further defining the role of B19 in FS.

Adult↗

[Transient aplasia of the red progenitor cells manifest in a child with double heterozygote Hb SC carriership: the role of human parvovirus B19 (HPV-B19)].

Severe pure red cell anaemia due to B19 parvovirus infection is reported in a child with haemoglobin SC disease. B19 parvovirus infection was demonstrated by specific IgM. Although hypoplastic crisis occurring in SC children is usually less frequent and more benign than in sickle- cell anaemia, it necessitated several blood transfusions in our patient. The child recovered rapidly and was discharged after 12 days. This case again illustrates the role of HPV-B19 in the development of transient red cell aplasia occurring in patients with haemolytic anaemia. However, it is unusual since in the few reported children with HbSC disease and HPV-B19 infection, aregenerative anaemia remained moderate and did not generally require blood transfusions.

Anemia, Aplastic↗

[Detection of human parvovirus B19 DNA using PCR and serological test using ELISA for diagnosis of infection].

The development of a polymerase chain reaction (PCR) method for detection of human parvovirus B19 DNA and serological test of clinical specimens using ELISA is described. Of 43 serum (or plasma) samples, 29 were found to be positive for B19 DNA using the PCR, anti-IgM was detected in 16 specimens and anti-IgG in 25. In all specimens confirmed to contain B19-specific IgM, the presence of B19 DNA was demonstrated. Furthermore, B19 DNA was demonstrated in a patient with B19 infection for a longer period of time than was anti-IgM. In addition, we discuss the diagnosis of B19 infection using anti-IgG, in the acute stage and convalescent stage. In fetal infection, the PCR method provides sufficient detection of B19 DNA in cord blood, amniotic fluid, ascitic fluid, and fetal pericardial effusion and pleural effusion.

Adult↗

A report of human parvovirus B19 infection in hydrops fetalis. First Australian cases confirmed by serology and immunohistology.

OBJECTIVE: To present the first Australian cases of fetal hydrops induced by parvovirus B19. CLINICAL FEATURES: Autopsies on two cases of intrauterine fetal death with hydrops fetalis and pallor revealed evidence of myocarditis and widespread characteristic inclusion-bearing cells, predominantly erythroblasts. The diagnosis of hydrops fetalis induced by parvovirus B19 was confirmed in both cases by immunohistological localisation of the viral inclusions by means of a monoclonal antibody to the VP1 and VP2 proteins of parvovirus B19. A low level of parvovirus B19 IgM antibodies was detected in the second case. CONCLUSIONS: It is possible that our relatively small population and lack of familiarity with the histopathological features may have led to underdiagnosis rather than a true absence of fetal parvovirus B19 infection in Australia. The condition can be diagnosed and treated antenatally and therefore should be included in the differential diagnosis of causes of hydrops fetalis.

Adult↗