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Reports on aseptic meningitis caused by human parvovirus B19 are extremely rare. A case of aseptic meningitis is described in which human parvovirus B19 DNA was detected in the acute phase in cerebrospinal fluid by the polymerase chain reaction.
A 2 year old boy developed acute cerebellar ataxia in association with erythema infectiosum. During the disease, genomic DNA and antibodies against human parvovirus B19 were detected in serum but not in cerebrospinal fluid. Parvovirus B19 associated acute cerebellar ataxia might occur due to transient vascular reaction in the cerebellum during infection.
A 59 year old woman presented with an influenza-like illness preceding signs and symptoms strongly suggestive of systemic lupus erythematosus (SLE), which progressed over several months. Owing to these influenza-like symptoms, a viral cause of her illness was sought. Human parvovirus B19 serology was positive and antibodies to DNA were detected by two different methods. This patient is believed to be the first report of human parvovirus B19 infection coinciding with the onset of SLE. The evidence for B19 virus and the part it plays in autoimmunity and arthritis is discussed.
OBJECTIVES: To determine whether parvovirus B19 (B19) infection is associated with rheumatoid arthritis (RA). METHODS: The polymerase chain reaction was applied to serum, cells isolated from synovial fluid, and synovial fluid. Enzyme immunoassay technique was used to detect antibodies against B19. RESULTS: Of 142 patients with early RA (onset of disease under one year) and 67 control patients, serological evidence of recent parvoviral infection was found in 4/135 and 2/62, respectively. However, no evidence for the presence of parvoviral DNA was observed in 18 synovial fluids, 21 samples of synovial fluid granulocytes or 40 sera, all obtained from 65 patients diagnosed with early RA. CONCLUSION: Although there is published evidence of chronic rheumatoid-like arthropathy following acute parvovirus infection, our findings do not support the involvement of B19 in the aetiopathogenesis of RA.
AIMS: To compare the use of biotinylated and digoxigenin labelled probes for diagnosis of human fetal parvovirus B19 infection in formalin fixed, paraffin wax embedded tissues; and to assess the cellular distribution of the virus in positive cases. METHODS: Sections of lung tissue from 23 cases of anatomically normal non-immune fetal hydrops presenting between 1984 and 1989, and from 13 control cases of hydrops due to chromosomal abnormality were probed for B19 DNA by in situ hybridisation using both biotinylated and digoxigenin labelled probes. The distribution of the virus was then investigated in all cases of fetal B19 infection confirmed in this laboratory to date (n = 11) by combining in situ hybridisation for viral DNA (using the digoxigenin system) with immunohistological labelling for a range of cellular antigens. RESULTS: Five unequivocal cases of B19 infection were identified among the 23 fetuses with unexplained hydrops using both probe labels. When combined with data from previous studies of the period 1974-1983, the results indicate that B19 infection was responsible for 27% of cases of anatomically normal non-immune hydrops and 8% of all cases, of non-immune hydrops presenting to this hospital over 15 years. False positive signal was seen in an additional three cases, using biotinylated probes. Digoxigenin labelled probes gave greater specificity and permitted detailed investigation of tissues high in endogenous biotin. Though most cells containing B19 DNA colabelled as erythroid precursors, viral DNA was frequently detected within mononuclear-phagocytic cells. In three cases viral signal was also found within occasional myocardial cells labelled by antibody to desmin. CONCLUSIONS: A relatively high proportion of cases of anatomically normal, non-immune hydrops are caused by B19 infection. Digoxigenin is a more reliable probe label than biotin for in situ hybridisation in archival fetal tissues. Double labelling for cellular antigens and viral nucleic acid is a powerful technique for investigating virus-host cell interactions, and provides evidence that cell types other than those of erythroid lineage may have a role in human fetal parvovirus infection.
AIMS--To compare the sensitivity, specificity, and practicality of recombinant proteins in serological tests for the detection of human parvovirus B19 IgG and IgM. METHODS--Indirect enzyme linked immunosorbent assays using B19 structural proteins expressed in Escherichia coli were developed for the detection of B19 specific IgG and IgM (rELISA-G and rELISA-M). Cells infected with baculovirus expressing B19 structural proteins were also used in an indirect immunofluorescence assay for IgG and IgM antibodies (IFA-G and IFA-M). Antibody capture radioimmunoassays for IgG and IgM (GACRIA and MACRIA) were used as comparative assays. RESULTS--Twenty nine pools of intravenous immunoglobulin were clearly positive for B19 IgG by rELISA-G and contained low IgG titres by GACRIA. From 113 samples tested by all methods, sensitivities of 92% (77/84) and 97% (68/70) were obtained for ELISA and immunofluorescence, respectively, when compared with GACRIA. One hundred and sixteen samples from patients presenting with rash or arthralgia were compared by MACRIA, rELISA-M, and IFA-M. Sensitivities of both recombinant tests were more than 95%. Despite pretreatment to remove IgG or rheumatoid factor, false positive results were a problem in the rELISA-M but were not seen with the IFA-M. CONCLUSIONS--The limited supply of native antigen has severely restricted the wide application of serology for parvovirus B19. The use of recombinant antigens permitted the introduction of local screening tests which had many advantages, including quicker results and relief of the burden on the Reference Laboratory. The use of rELISA-M for sensitivity and IFA-M for specificity and confirmation proved a useful and practical combination for diagnosis of recent infection with B19, and rELISA-G allowed the immune response to be determined in selected populations.
Of 65 serum samples submitted for diagnostic purposes which proved to be anti-complementary by complement fixation test, 49 were parvovirus B19 IgM positive. Forty four of the 49 serum samples were from patients with arthropathy. Acute parvovirus B19 infection should be suspected when a patient has symptoms of disease of the joints and the serum is anticomplementary.
AIMS: Parvovirus B19 has been demonstrated in testes of patients with germ cell tumours but not in controls, raising the possibility that the virus has an aetiological role in these tumours. The aims of this study were to investigate the association of the virus with germ cell tumours and to localise the virus histologically. METHODS: DNA was extracted from paraffin wax embedded sections of testes from 10 seminomas, eight teratomas, two mixed seminoma/teratomas, and 10 testes showing benign histology. Polymerase chain reaction (PCR) amplification of three regions within the NS and VP1/2 genes was carried out in duplicate on all samples. One PCR positive case (seminoma/teratoma) was examined by microdissection of histologically defined tissue components followed by PCR amplification of parvoviral sequences. Samples from PCR positive patients were immunostained using a B19 specific monoclonal antibody. RESULTS: Seven cases were PCR positive, these comprised two of 10 seminomas, one of two mixed tumours, none of eight teratomas, and four of 10 benign controls. PCR analysis of the material microdissected from the seminoma/teratoma showed the presence of the virus in regions of seminoma, teratoma, intratubular germ cell neoplasia, normal tubules, and connective tissue. All patient samples studied immunohistochemically were negative. CONCLUSIONS: This confirms the presence of parvovirus B19 in a proportion of germ cell tumours; however, in one patient, the virus was widespread in the tissue components and not confined to tumour cells. In addition, the virus was present in control benign testes. These data suggest that B19 might not be of aetiological importance in germ cell tumours of testis.
Canine parvovirus isolates from clinical cases of enteritis were obtained from the United Kingdom, Germany and the USA and differentiated by restriction enzyme analysis into three groups, namely CPV2, CPV2a and CPV2b. The three groups were readily identified by their HphI restriction profile. CPV2 was not prevalent in cases of canine parvovirus disease after 1986. Only two CPV2 strains (original type) were found among 110 strains isolated after 1980. In Europe the frequency of isolation of the CPV2a and CPV2b field strains was similar whereas in the USA the CPV2b strain predominated. Dogs inoculated with a vaccine strain were resistant to infection after challenge with UK isolates of CPV2a and CPV2b.
Rapid immunomigration on a membrane was applied to the diagnosis of canine parvovirus (CPV) in 128 samples of faeces containing four strains of parvovirus (two CPV-2a strains, including one vaccine strain, and two CPV-2b strains). The results were compared with the results of haemagglutination and ELISA sandwich techniques. The new test was quick and easy to use, and made it possible to identify both the CPV-2a and CPV-2b strains. Its detection thresholds per gram of faeces corresponded to specific haemagglutination titres of between 320 and 640 and a virus titre of between 10(4) and 10(5) CCID50 (dose required to infect 50 per cent of cell cultures).
Canine parvovirus type 2a (CPV-2a) and type 2b (CPV-2b) have recently been isolated from cats throughout the world, and CPV-2b strain FP84 has been reported to be virulent in domestic cats. Although live feline panleucopenia virus (FPLV) vaccines protect domestic cats from CPV infection, the efficacy of inactivated FPLV vaccines has not been established. In this study, two domestic cats were vaccinated with a commercial inactivated FPLV vaccine and challenged with CPV-2b strain FP84 isolated from a domestic cat. The cats were protected against CPV-2b strain FP84 infection and their clinical signs were suppressed, although the two unvaccinated cats showed the typical clinical signs of parvovirus infection.
Parvovirus B19, the only known human pathogenic parvovirus, is associated with a wide range of disease manifestations. In healthy individuals, the major presentation of B19 infection is erythema infectiosum. In patients with underlying hemolytic disorders, infection is the primary cause of transient aplastic crisis. In immunosuppressed patients, persistent infection may develop that presents as pure red cell aplasia and chronic anemia. In utero infection may result in hydrops fetalis or congenital anemia. Diagnosis is based on examination of bone marrow and virologic studies. Much is known of the pathophysiology of the virus, and studies are in progress to develop a vaccine to prevent this widespread infection.
Transfer of viruses between hosts to create a new self-sustaining epidemic is rare; however, those new viruses can cause severe outbreaks. Examples of such viruses include three pandemic human influenza A viruses and canine parvovirus in dogs. In each case one virus made the original transfer and spread worldwide, and then further adaptation resulted in the emergence of variants worldwide. For the influenza viruses several changes were required for growth and spread between humans, and the emergence of human H2N2 and H3N2 strains in 1957 and 1968 involved the acquisition of three or two new genomic segments, respectively. Adaptation to humans involved several viral genes including the hemagglutinin, the neuraminidase, and the replication proteins. The canine adaptation of the parvoviruses involved capsid protein changes altering the recognition of the host transferrin receptors, allowing canine transferrin receptor binding and its use as a receptor for cell infection.
A 33-year-old primigravida at 26 weeks gestation presented with fetal hydrops and fetal anemia following prior parvovirus B19 infection. The fetus required two intrauterine transfusions of packed red cells. At 35 weeks gestation, a cesarean section was performed for obstetric reasons. As a consequence of a prenatal bowel perforation, the neonate developed meconium peritonitis, for which she needed laparotomy. This case demonstrates that there may be an association between intrauterine parvovirus infection and meconium peritonitis, the latter possibly caused by vascular injury in fetal life.
We report a successful treatment of a B19 parvovirus-induced fetal hydrops diagnosed at 16 weeks of gestation. This disease could be corrected by means of a unique intraperitoneal blood transfusion performed at 18 weeks, once diagnosis was established. The delivery occurred at 36 weeks, leading to the birth of a healthy baby. This case suggests that transfusion should be attempted, as the spontaneous fetal recovery remains uncertain and shows that intraperitoneal blood transfusion is an effective therapeutic option of the B19 parvovirus-induced anemia, in the absence of a viral myocarditis.
Transplacental transmission of human parvovirus B19 (B19 virus) to the fetus is an important cause of intrauterine death, abortion, stillbirth, and nonimmune hydrops fetalis. Adverse outcome of pregnancy can occur after symptomatic and asymptomatic maternal infection. Only rare cases of congenital malformations and fetal disease in live-born infants have been associated with intrauterine B19 virus infection. Laboratory results obtained from paired maternal and fetal cord blood samples indicate that a reliable diagnosis of fetal B19 virus infection should be based on detection of parvovirus B19 DNA.
The hematologic data and symptoms of 7 patients seropositive for parvovirus B19 IgM antibody after gynecologic surgery were analysed. Parvovirus may have been transmitted by fibrin glue prepared from heat-treated human plasma and used for hemostasis during surgery. The peripheral blood neutrophil count decreased to below 1 x 10(9)/l between postoperative day (POD) 10 and 18, but recovered spontaneously to within the normal range. G-CSF injection was effective in preventing neutropenia or obtaining a prompt recovery. The reticulocyte count fell below 10 x 10(9)/l between POD 13 and 19, and also recovered spontaneously. A slapped-cheek rash was not observed in any of the 7 patients.
Erythroid lineage cells are target cells for human parvovirus B19, and a natural infection often results in transient anemia. To determine whether recombinant B19 capsid proteins (VP1/VP2) also inhibit human hematopoietic progenitor growth, a model system was set up. The B19 capsids were inoculated into primary cultures of hematopoietic stem cells derived from human fetal liver, resulting in a 70-95% reduction of BFU-E (burst-forming unit erythroid cells) as compared with the medium control. A similar effect was seen in human hematopoietic stem cell cultures derived from cord blood and adult bone marrow. Preincubation of the B19 capsids with either a monoclonal antibody to the virus or with B19 IgG positive human sera reduced the inhibitory effect. Furthermore, the inhibitory effect could be reduced by preincubating the target cells with a monoclonal antibody to the cellular receptor for the virus, the P antigen. These findings thus show that the inhibition of colony formation of human hematopoietic stem cells can occur in the absence of parvovirus B19 nonstructural proteins. We speculate that B19 capsid could provide a possible strategy to downregulate indigenous hematopoiesis in fetal stem cell transplantations.