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From March to August 1984, 26 patients with hereditary hemolytic anemia in northeastern Ohio developed acute, profound red cell aplasia. The patients included 14 males and 12 females 2 to 23 years old, with sickle cell anemia (20 cases), hemoglobin SC-disease (4 cases), sickle-beta-thalassemia (1 case), or hereditary spherocytosis (1 case). All had an acute onset of severe reticulocytopenia and anemia and prodromal symptoms of illness including fever, abdominal symptoms, headache, and arthralgias. Twenty-two received transfusions. Reticulocytosis occurred spontaneously within 2 to 14 days of presentation. In five acute-phase sera, 10(8) to 10(12) viral particles/mL were detected by electron microscopy. Human parvovirus B19 DNA was demonstrated in high concentration by hybridization in the same five acute-phase sera and in low concentration in sera of eight additional patients. The five highly viremic sera inhibited erythroid colony formation in vitro. B19-specific IgM was detected in sera of 24/26 patients, and B19-specific IgG in 21 of 22 patients tested. Our results indicate that human parvovirus B19 was the etiologic agent in this large epidemic of life-threatening acute red cell aplasia in patients with hereditary hemolytic anemia.
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PMID:Human parvovirus B19-induced epidemic acute red cell aplasia in patients with hereditary hemolytic anemia. 300 91

A 30-year-old postpartum woman was admitted to our hospital because of progressive anemia, malaise, night sweating, headache and low grade fever which began 9 days after delivery (day 0). She had normocytic hypochromic anemia accompanied with marked decrease in reticulocytes. In addition, a temporary decrease in platelets and white blood cells especially neutrophils were observed. Bone marrow smears showed an apparent decrease in erythroid cells and the presence of giant proerythroblasts (1.2%) as well as hemophagocytes (1.2%). IgM and IgG antibody against human parvovirus B19 (HPV) was detected on day 22 of the disease although negative results were obtained on day 3. The presence of the virus in the blood on admission was confirmed by dot-blot analysis. Thus, this case was diagnosed as acute pure red cell aplasia and hemophagocytic syndrome caused by HPV infection. This patient had been given iron for iron deficiency anemia before delivery and the iron deficiency was still present after the episode of the present disease although the iron metabolism data was perturbed during the disease. These findings suggest that HPV could cause acute pure red cell aplasia not only in patients with hemolytic anemia but also in patients with iron deficiency anemia or after acute bleeding. Furthermore it is suggested that pancytopenia often observed on HPV infection could be at least partly caused by hemophagocytic syndrome.
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PMID:[Postpartum parvovirus B19-associated acute pure red cell aplasia and hemophagocytic syndrome]. 756 95

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.
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PMID:Clinical characteristics of children with hereditary hemolytic anemias and aplastic crisis: a 7-year review. 802 3

A 43-year-old female with spherocytosis was admitted to the hospital because of fever, headache, and rapidly progressive anemia. On admission, she had severe anemia (Hb 3.9 g/dl) with marked decrease in reticulocytes (0.3%). Some premature leukocytes, such as promyerocyte, were observed in the peripheral blood. Bone marrow smear revealed normocellular marrow with normal presence of erythroid cells. Anti-human parvovirus B19 IgM and IgG antibody was positive in the serum on admission. The DNA of the virus was also detected in the peripheral blood by PCR assay. Thus, this case was diagnosed as acute aplastic crisis caused by human parvovirus B19 infection. Blood transfusion was performed on day 1 and day 2. The symptoms gradually disappeared and increase in reticulocyte (11.5%) was observed on day 5. Premature leukocytes in the peripheral blood disappeared on day 2. She recovered from anemia and was discharged on day 7.
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PMID:[Human parvovirus B19-induced aplastic crisis in a case with spherocytosis]. 964 48

A 22-year-old Caucasian woman with a 6 year history of persistently active, systemic onset juvenile rheumatoid arthritis (JRA) developed symptoms of headache, dry cough, nausea, vomiting, abdominal pain, diarrhea, and dehydration associated with a high fever, elevated liver enzymes, and lymphopenia. Subsequent investigation revealed acute infection with parvovirus B19. Following clinical improvement over 10-14 days solely with supportive care, her underlying disease remained in remission for about 7 months.
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PMID:Remission of juvenile rheumatoid arthritis after infection with parvovirus B19. 1055 14

Human parvovirus B19 infection can cause erythema infectiosum (EI) and several other clinical presentations. Central nervous system (CNS) involvement is rare, and only a few reports of encephalitis and aseptic meningitis have been published. Here, we describe 2 cases of B19 infection in a family presenting different clinical features. A 30 year old female with a 7-day history of headache, malaise, myalgias, joint pains, and rash was seen. Physical examination revealed a maculopapular rash on the patient's body, and arthritis of the hands. She completely recovered in 1 week. Two days before, her 6 year old son had been admitted to a clinic with a 1-day history of fever, headache, abdominal pain and vomiting. On admission, he was alert, and physical examination revealed neck stiffness, Kerning and Brudzinski signs, and a petechial rash on his trunk and extremities. Cerebrospinal fluid analysis was normal. He completely recovered in 5 days. Acute and convalescent sera of both patients were positive for specific IgM antibody to B19. Human parvovirus B19 should be considered in the differential diagnosis of aseptic meningitis, particularly during outbreaks of erythema infectiosum. The disease may mimic meningococcemia and bacterial meningitis.
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PMID:Two family members with a syndrome of headache and rash caused by human parvovirus B19. 1129 Mar 13

A 7-year-old male presented sudden-onset left hemiparesis, left-sided paresthesia, central paralysis of the left VII cranial nerve, and subsequent headache. Magnetic resonance scans were obtained 24 hours after admission. T(2)-weighted images disclosed hyperintensities located mainly in the posterior portion of the lenticular nucleus and in the head and body of the right caudate nucleus. A diagnosis of ischaemic stroke was made on the basis of neuroradiologic findings. Laboratory tests undertaken to establish the cause of stroke revealed parvovirus B19 infection preceding the neurologic abnormalities. In the absence of other known risk factors for stroke the possibility of parvovirus B19's being correlated with stroke onset is discussed.
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PMID:Case of stroke in a 7-year-old male after parvovirus B19 infection. 1265 25

Human parvovirus B19 infection has been associated with various clinical manifestations of a rheumatic nature such as arthritis, fatigue, and chronic fatigue syndrome (CFS), which can persist for years after the acute phase. The authors have demonstrated recently that acute B19 infection is accompanied by raised circulating levels of IL-1b, IL-6, TNF-a, and IFN-g and that raised circulating levels of TNF-a and IFN-g persist and are accompanied by MCP-1 in those patients who develop CFS. A resolution of clinical symptoms and cytokine dysregulation after intravenous immunoglobulin (IVIG) therapy, which is the only specific treatment for parvovirus B19 infection, also has been reported. Although CFS may be caused by various microbial and other triggers, that triggered by B19 virus is clinically indistinguishable from idiopathic CFS and exhibits similar cytokine abnormalities and may represent an accessible model for the study of CFS.
Curr Pain Headache Rep 2003 Oct
PMID:Cytokines in parvovirus B19 infection as an aid to understanding chronic fatigue syndrome. 1294 85

A Japanese woman developed prolonged fatigue, neck and shoulder pain, headache, pyrexia, insomnia, anorexia, lymphadenopathy, and diarrhea for two months. She had experienced various stressors before these symptoms developed. Serological test demonstrated that she had acute parvovirus B19 infection. Major depressive disorder was also diagnosed by a psychiatrist. Her symptoms disappeared after administration of selective serotonin reuptake inhibitors and oriental herbs, although human parvovirus B19 viral genome has been present in her serum for nine months. These findings suggest that parvovirus B19 causes clinical features similar to those of chronic fatigue syndrome in cases who have prior life stressors.
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PMID:Acute parvovirus B19 infection mimicking chronic fatigue syndrome. 1451 87

In June 1994 have been seen 16 patients with HPV B19 infection. The diagnosis was based on a positive E.L.I.S.A. test for IgM antibodies against HPV B19. No one of the patients had hematologic manifestations. Only one patient had fever, arthralgia and headache without skin involvement. The other 15 patients had skin lesion: rubella like rush in 11 cases, haemorragic exanthema in 2 and erythema infectious in 2 cases. Two children had liver involvement and one kidney involvement. The authors of this study remark the broad spectrum of clinical manifestations of HBV B19 infection and suppose a large diffusion of this disease, even in the symptomatic form.
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PMID:[Not Available]. 1497 83


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