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Query: UMLS:C0002895 (sickle cell disease)
 11,747 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the spring and summer of 1988, two separate outbreaks of an illness with a rash resembling erythema infectiosum occurred among members of the nursing staff of the Children's Hospital of Philadelphia. The sources were two adolescent patients with sickle cell disease and aplastic crisis who had unsuspected parvovirus infection. Tests for IgM and IgG antibodies to parvovirus B19 were positive in both patients, and electron microscopical examination showed parvovirus-like particles in the early serum samples. Of 40 health care workers exposed to infected patients, 12 (30 percent) were infected, 2 (5 percent) were possibly infected, 8 (20 percent) had evidence of a past infection with B19, and 18 (45 percent) remained seronegative. Attack rates among the susceptible contacts were 36 percent in the first outbreak and at least 38 percent in the second. Clinical symptoms began a mean of 12.6 days after exposure and included malaise, rash, and joint pain. We conclude that hospital workers are at risk of contracting nosocomial erythema infectiosum from patients with parvovirus-associated aplastic crisis. We recommend that all patients with hereditary hemolytic anemias who are admitted with a febrile illness be evaluated for aplasia and promptly placed in respiratory and contact isolation if aplastic crisis is suspected.
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PMID:Human parvovirus B19 infection among hospital staff members after contact with infected patients. 254 99

Discovered by chance in 1974, the human serum parvovirus B19 is at present the only recognized, autonomous, pathogenic human parvovirus. For some years following its discovery, B19 was not associated with any defined clinical syndrome; although a high titre viraemia was often noted in infected individuals they were largely asymptomatic. In 1980 the causal association between B19 infection and aplastic crisis in chronic haemolytic anaemia began to emerge with the discovery of B19 as the agent responsible for aplastic crisis in sickle cell anaemia. This fulfilled the expectation of a disease of tissue comprising a large proportion of dividing cells, namely the erythropoietic elements of the bone marrow, anticipated in autonomous parvovirus infection where viral replication is confined to dividing cells. More recently, erythema infectiosum, an illness sharing many of the clinical features of rubella, has been found to be the common result of B19 infection, although a spectrum of disease is now emerging. Much effort is currently directed toward the elucidation of the effects of maternal B19 infection on the developing fetus.
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PMID:Human parvovirus infections. 282 52

B19 virus is the first human virus to be shown to be a member of the parvovirus genus. This review is concerned with the diseases associated with B19 virus, their nature, pathogenesis and diagnosis. The virus was discovered by chance in blood donors but has been shown to be a common infection of childhood. Infection may be asymptomatic or associated with mild, non-specific symptoms. The most common specific clinical manifestation is an erythematous rash illness which often has the classical features of erythema infectiosum. Often, however, it is described simply as rubelliform and only laboratory tests can distinguish B19 and rubella virus infections. Joint involvement is the most common complication of B19 virus infection occurring especially in adult females. It often involves the joints of the hands and wrists, clears rapidly in most patients but may persist for months or years in a few. B19 virus is also the principle cause of the transient aplastic crisis which complicates chronic haemolytic anaemia. This has been demonstrated repeatedly in sickle cell anaemia and hereditary spherocytosis and in individual cases of other haemolytic anaemias. The pathogenesis of the aplastic crisis is related to the ability of B19 virus to infect and damage early erythroid progenitor cells. Volunteer studies in normal individuals have demonstrated that this is a regular event occurring about a week after infection via the respiratory tract. Rash illness and joint involvement occur 7 to 10 days later and are presumably immune mediated. Diagnosis of B19 virus infection can be achieved by detection of the viraemia (aplastic crisis) or by detection of virus specific IgM antibody (all diseases).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:B19 virus--a pathogenic human parvovirus. 284 30

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

B19 parvovirus, the cause of fifth disease and transient aplastic crisis, has been successfully propagated in suspension cultures of human erythroid bone marrow cells obtained from patients with sickle cell disease and stimulated by erythropoietin. B19 inoculation in vitro resulted in a marked decline in identifiable erythroid cells over seven to nine days of incubation. Characteristic giant early erythroid cells were seen on Wright's-Giemsa stain of infected cultures. By in situ hybridization, 30% to 40% of erythroblasts were infected at 48 hours; a similar proportion of cells showed B19 capsid protein by immunofluorescence. B19 DNA was present in erythroblasts but not in the leukocyte fraction of bone marrow. B19 replication, as determined by Southern analysis, and B19 encapsidation, as determined by sensitivity of isolated cell fractions to DNase I, were restricted to the nuclei. B19 DNA was detectable in the nuclei from infected cultures beginning at 18 hours and in the supernatant at 32 hours; B19 genome copy number was estimated at about 25,000 to 30,000/infected cell at 48 hours. Recovery of virus depended on the multiplicity of infection (moi); at low moi, approximately 200x input virus was recovered from total cultures and 50x from the culture supernatants. Virus released into the supernatant was as infectious or more infectious than virus obtained from sera of infected patients. Human erythroid bone marrow culture represents a safe in vitro system for the elucidation of the cellular and molecular biology of the pathogenic B19 parvovirus.
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PMID:Productive infection by B19 parvovirus of human erythroid bone marrow cells in vitro. 303 11

The human parvovirus B19 causes aplastic crises in sickle cell anemia patients and the disease erythema infectiosum. So far, it has not been possible to grow B19 virus in cultured cells. Here we report the use of in vitro transcription in HeLa cell extracts and transient expression of cloned DNA transfected into HeLa cells to detect and map a strong transcriptional promoter on the B19 genome. The promoter is located near the left end of the B19 genome, at position 6 map units in the clone pYT103 (approximately 280 bp upstream of the first HindIII site), and directs transcription to the right. These results suggest that the strictly limited host range of B19 does not operate at the level of transcription from the promoter at the left end of the genome.
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PMID:A transcriptional promoter of the human parvovirus B19 active in vitro and in vivo. 382 10

Viruses have been shown to cause bone marrow aplasia in animals and have been implicated in bone marrow failure in man; however, until recently, a specific link between human viral infection and bone marrow failure has not been proven. In 1975 Cossart and colleagues found a serum parvovirus-like virus (SPLV, sometimes referred to as B19) in human serum. Antibody to this virus is present in the sera of 30-45% of healthy adults (Y. E. Cossart, P. P. Mortimer, unpublished observations). However, evidence for a direct link came from work by Pattison et al. who found five children with transient aplastic crisis of sickle cell disease and evidence of active infection with SPLV. This association was later confirmed in a large series of children with sickle cell disease and aplastic crisis in Jamaica. We have studied the effects of virus-containing material on haematopoiesis, using in vitro colony-forming assays to look for direct evidence for a role of SPLV in bone marrow aplasia. We show here that SPLV-containing sera inhibit erythropoiesis in culture. Moreover, in a child with hereditary spherocytosis who developed transient aplastic crisis, a strong inhibitory effect of the patient's serum on erythropoiesis correlated with the presence of virus.
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PMID:A human parvovirus-like virus inhibits haematopoietic colony formation in vitro. 683 76

Human parvovirus B19 has been associated with several diseases. Aplastic crisis in patients with chronic hemolytic anemia, erythema infectiosum, hydrops fetalis and arthritis are among the common diseases caused by this virus infection. In the period between July, 1991, and March, 1992, 48 patients with aplastic crises were hospitalized at Saudi Aramco-Dhahran Health Center, Dhahran, Saudi Arabia. Forty-six patients had homozygous sickle cell disease, one had hemoglobin H disease and one had hereditary elliptocytosis. Evidence of recent human parvovirus infection was present in 91% of the cases. Leukopenia was present in 21%, neutropenia in 27% and thrombocytopenia in 42%. This differs from previous reports in which red blood cell aplasia causing anemia was the only hematologic finding reported in most patients. There were no cases of erythema infectiosum in either the patients or the community during the epidemic and the reason for this phenomenon is not obvious. The almost limited occurrence of aplastic crisis in patients with sickle cell disease in a population with a high incidence of other types of chronic hemolytic anemias is of interest.
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PMID:An epidemic of aplastic crisis caused by human parvovirus B19. 771 86

We studied the epidemiology of human parvovirus B19 infection in 308 children with homozygous sickle cell (SS) disease and 239 controls with a normal haemoglobin (AA) genotype followed from birth in a cohort study. Annual serum samples identified the time and frequency of B19 infection, which did not differ between SS and AA children, about 40% of each group developing specific IgG by age 15. B19 infection followed an epidemic pattern similar to that observed for aplastic crises; accounted for all 91 aplastic crises that occurred; and was found in an additional 23 SS patients, of whom 10 showed mild haematological changes and 13 no changes. The magnitude or duration of IgG response did not differ between these groups. No patient had 2 attacks of aplasia and no patient nor control had 2 attacks of B19 infection. Following B19 infection, serial specific IgG concentrations remained high after 5 years in only 45% of SS patients, although the rarity of recurrent aplasia suggests lifelong immunity. B19 infection accounts for most if not all aplastic crises in SS disease, but at least 20% of infections do not result in aplasia. An effective vaccine against B19 might make an important contribution to the management of sickle cell disease.
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PMID:Human parvovirus infection in homozygous sickle cell disease. 810 Mar 15

This paper describes clinical findings in subjects heterozygous for hemoglobin C and in compound heterozygotes SC. Most of our patients were coming from lands bordering the Guinea Gulf, on the inside of the loop made by the river Niger and from Haiti, which was populated by African slaves coming mainly from the Golden Coast (actually Ghana). Heterozygotes are asymptomatic and do not suffer from anemia. Age at diagnosis is higher than for SCA, although one of our cases was diagnosed at age one. Overwhelming infections or major anemia were not observed. Basal hemolysis remained moderate. HbF levels were not increased as they may be in sickle cell anemia. Splenomegaly was observed in 2/5 patients. Among severe complications we encountered, we must mention one case of foetal death, one tibial infarct, one case of pure red cell aplasia caused by parvovirus B19 infection, and one case of proliferative retinopathy.
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PMID:[Hemoglobin C (alpha 2 beta 2 6Glu-->lys). Study of 19 heterozygote AC carriers and of 5 cases of double hemoglobinopathy SC]. 829 38


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