Cases reported "Parvoviridae Infections"

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1/26. parvovirus B19 causing leucopenia and neutropenia in a healthy adult.

    A 27-year-old healthy female presented with a prolonged and intermittent febrile illness. She was found to have leucopenia, neutropenia and thrombocytopenia, but a normal haemoglobin. The patient recovered spontaneously and convalescent serology 1 month later was positive for specific parvovirus B19 IgM and IgG. parvovirus B19 infection was confirmed by detection of viral dna by dot blot hybridization in a specimen of blood taken during the acute illness. A review of the previously reported cases of parvovirus B19-induced leucopenia in normal adults is presented. parvovirus B19 should be considered in the differential diagnosis of leucopenia and neutropenia in healthy adults.
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2/26. Pure red cell aplasia associated with parvovirus B19 infection in T-large granular lymphocyte leukemia.

    There have been few reports of large granular lymphocyte (LGL) leukemia with neutropenia complicated with pure red cell aplasia (PRCA) that developed after human parvovirus (HPV) B19 infection. We report here the case of a 35-year-old female who developed HPV B19-associated PRCA with T-LGL leukemia. LGL count of peripheral blood was lower than 2 x 10(9) l(-1), although phenotypic analysis of LGL showed CD3 , CD16-, CD56-, CD57 with double positive for CD3 and CD57, and genetic study showed the clonal rearrangement of T-cell receptor gene. Microscopically, the patient's bone marrow showed characteristic giant proerythroblasts. A serologic study of HPV B19 was positive for IgM, but negative for IgG, with a positive result on Dot-blot hybridization assay for HPV B19 dna. Severe anemia and reticulocytopenia ameliorated without treatment 10 days after the initial examination, but slight anemia, neutropenia, a moderate increase of LGL counts with rearrangement of TCR gene, and positive result of HPV B19 dna has persisted 7 months after the initial examination. We suggest that this viral infection may play an etiologic role in some patients with LGL leukemia who develop PRCA.
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3/26. Focal parvovirus B19 myocarditis in a patient with brugada syndrome.

    The brugada syndrome is characterized by a distinct ECG pattern consisting of ST segment elevation in the right precordial leads and right bundle branch block, a propensity for life-threatening arrhythmias, and an apparently structurally normal heart. The authors describe the case of a patient with an aborted sudden cardiac death and the typical ECG signs of brugada syndrome. Nevertheless, magnetic resonance imaging displayed signal enhancement in the left ventricular myocardium. Additionally, histologic examination, in-situ hybridization, and PCR revealed evidence of a locally restricted inflammation due to parvovirus B19. brugada syndrome is regarded as a primary electrical disease due to dysfunction of distinctive ion channels, but focal myocarditis may serve as a trigger for ventricular arrhythmias in this patient. Further morphologic studies will be helpful to establish the possible role of structural changes in the pathophysiology of this syndrome.
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4/26. Fatal parvovirus B19-associated myocarditis clinically mimicking ischemic heart disease: an endothelial cell-mediated disease.

    We report the case of a 34-year-old female patient who died 4 days after hospital admission of acute heart failure clinically mimicking ischemic heart disease. Microscopic examination of the heart showed severe myocarditis. Polymerase chain reaction (PCR), including quantitative real-time PCR, disclosed exclusively parvovirus B19 (PVB19), with a high viral load of 4.3x10(5) PVB19 viral genome equivalents per microg myocardial nucleic acid. Radioactive in situ hybridization detected viral genomes in endothelial cells (ECs) predominantly in the venular compartment and (to a lesser degree) in small arteries and arterioles of the heart, but not in cardiac myocytes or other tissue components. Concomitant with EC infection, marked expression of the adhesion molecule e-selectin was noted, accompanied by margination, adherence, penetration, and perivascular infiltration of T lymphocytes. We speculate that, due to the high viral load in cardiac ECs, PVB19 infection of endothelial cells was sufficient to induce impaired coronary microcirculation with secondary cardiac myocyte necrosis.
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5/26. Replicative multivirus infection with cytomegalovirus, herpes simplex virus 1, and parvovirus B19, and latent Epstein-Barr virus infection in the synovial tissue of a psoriatic arthritis patient.

    BACKGROUND: Psoriatic arthropathy occurs as complicating feature in about 5-7% of psoriasis patients. Infectious mechanisms including viral antigens have been suggested by serologic data as CD8 T cellular specifity towards viral epitopes. OBJECTIVE AND RESULTS: We here reported a case of a 32-year-old male psoriatic arthritis patient, where we could demonstrate simultaneous infection with cytomegalovirus (CMV), herpes simplex virus type I (HSV1) and parvovirus B19 (B19), as well as latent Epstein-Barr virus (EBV) infection within the synovial tissue by immunohistochemistry (CMV, parvovirus B19, HSV1, EBV-LMP) and dna-in situ-hybridization (CMV). Serologic examination revealed positive EBV and parvovirus B19-IgG-antibodies, but no antibody response to HSV1 and CMV. CONCLUSION: This case is of special interest, since replicative viral infections have not yet been demonstrated localised in the psoriatic arthritis synovia. Thus, with particular regard to the limited information of the serologic data and the possible need of immuno suppressive therapy direct synovial testing for viral antigenes may be considered in psoriatic arthritis patients.
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6/26. Autologous peripheral blood progenitor cells are a potential source of parvovirus B19 infection.

    BACKGROUND: parvovirus B19 is a cause of delayed red blood cell (RBC) engraftment after marrow transplantation (BMT). The diagnosis of parvovirus infection requires serologic and dna testing in the context of clinical disease and characteristic marrow morphologic findings; however, the source of infection is often difficult to determine. STUDY DESIGN AND methods: Investigation of a case of delayed RBC engraftment and pure RBC aplasia (PRCA) occurring 3 months after autologous peripheral blood progenitor cell (PBPC) transplantation in a patient with high-risk diffuse large B-cell lymphoma. dna testing of serum and of a sample of cryopreserved PBPCs was performed. RESULTS: Marrow morphology showed a maturational arrest of erythroid cells with giant proerythroblasts. polymerase chain reaction and nucleic acid hybridization confirmed the presence of parvovirus dna in the serum and in a sample of sequestered PBPCs saved at the time of PBPC harvest. PRCA resolved after the administration of intravenous immune globulin. CONCLUSION: Autologous PBPCs are a potential source of parvovirus infection, which may cause significant disease after autologous BMT.
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7/26. parvovirus B19 infection of the fetus. histology and in situ hybridization.

    Fetal tissues from 16 spontaneous abortions, two terminations, and one perinatal death, 18 of which were associated with maternal human parvovirus B19 infection, were examined for B19 infection by histology and in situ hybridization using a digoxigenin-labeled B19-dna probe. In 15 spontaneous abortions and one termination, erythroblasts with intranuclear inclusions (lantern cells) reacted with B19-dna by in situ hybridization. No internal or external fetal malformations were observed. Because 13 (86.7%) spontaneous abortions with lantern cells occurred between the 20th and 28th weeks of gestation, it is postulated that B19 infection may be a particular threat to the fetus during this stage of gestation.
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8/26. Manifestations and treatment of human parvovirus B19 infection in immunocompromised patients.

    We diagnosed infections from human parvovirus B19 in three patients by using dot-blot hybridization and a polymerase chain reaction to detect B19 dna and using an enzyme immunoassay to detect IgG and IgM to B19. For 5 months a 5-year-old boy with acute lymphoblastic leukemia in remission had anemia without reticulocytes or bone marrow erythrocyte precursors. His serum lacked IgG and IgM to B19 but contained B19 dna. He received gamma globulin intravenously (0.4 gm/kg/day for 5 days); his viremia promptly cleared and reticulocytosis developed. A 14-year-old boy with acute lymphoblastic leukemia in remission had fever, rash, neutropenia (less than 300 leukocytes/mm3), and a hemophagocytic syndrome lasting 3 weeks. His serum contained IgM to B19 and B19 dna. Without therapy, IgG to B19 developed; although low levels of B19 dna persisted, the leukocyte count returned to normal. In a 19-year-old patient with systemic lupus erythematosus and hemolytic anemia, an aplastic crisis lasted 2 weeks. Her serum lacked IgG and IgM to B19 but contained B19 dna. Without therapy, IgG and IgM to B19 appeared, viremia diminished, and reticulocytosis occurred. These patients illustrate the varied manifestations of chronic B19 infections, the importance of dna detection for diagnosis, and the possible efficacy of gamma globulin therapy.
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9/26. cordocentesis for the diagnosis and treatment of human fetal parvovirus infection.

    Human parvovirus B-19 infection was diagnosed by dna hybridization in blood obtained by cordocentesis from two hydropic fetuses at 22 and 26 weeks' gestation; B-19-specific immunoglobulin m (IgM) in fetal blood was negative in both cases. Hematologic studies demonstrated severe anemia, which was treated by intravascular fetal blood transfusions. The hydrops resolved and healthy infants were delivered at term. The pathophysiology of hydrops in fetal parvovirus infection is discussed.
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10/26. Persistent B19 parvovirus infection in patients infected with human immunodeficiency virus type 1 (hiv-1): a treatable cause of anemia in AIDS.

    OBJECTIVE: To determine the role of B19 parvovirus in red cell aplasia of patients infected with human immunodeficiency virus type 1 (hiv-1). DESIGN: Uncontrolled clinical trial, with assay of serum, peripheral blood cells, and bone marrow for virus using dna hybridization and immunocytochemistry techniques; these assays were then correlated with clinical findings, results of immunoassays for antivirus antibodies, and with immunoglobulin (Ig) therapy. SETTING: government medical referral center, and university and private hospitals. patients: Seven patients with pure red cell aplasia and serologic evidence of infection with hiv-1. MEASUREMENTS AND MAIN RESULTS: All patients had giant pronormoblasts in the bone marrow (present in transient aplastic crisis caused by acute B19 parvovirus infection). High concentrations of B19 parvovirus were demonstrated in sera, in several cases in samples separated by weeks or months. Viral dna and capsid protein were present in the bone marrow of three patients studied, and active viral replication was detected by southern analysis. There was no antivirus IgG in capture immunoassay and no or very low levels of antivirus IgM. The patients did not have symptoms of fifth disease, the illness caused by this virus in immunologically normal persons. Six patients were treated with a regimen of intravenous commercial immunoglobulin. In all cases, this therapy resulted in rapid reduction in serum virus concentrations and full recovery of erythropoiesis. Relapses in two cases were predicted by dna hybridization studies, and these cases were successfully retreated. CONCLUSIONS: The B19 parvovirus is a remediable cause of severe chronic anemia in HIV-infected patients. Recognition of and therapy for parvovirus in this population will avoid erythrocyte transfusion and should prevent transmission of the virus to other persons, including immunosuppressed persons and women of child-bearing age.
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