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Parvovirus B19 Yvonne Cossart, an Australian virologist working in London in the mid-1970s

. Parvovirus B19 Yvonne Cossart, an Australian virologist working in London in the mid-1970s the name comes from parvum, the Latin word for small contains a genome consisting of single-stranded DNA Leili Chamani.MD.,MPH specialist in infectious diseases.

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Parvovirus B19 Yvonne Cossart, an Australian virologist working in London in the mid-1970s

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  1. . ParvovirusB19 • Yvonne Cossart, an Australian virologist working in London inthe mid-1970s • the namecomes from parvum, the Latin word for small • contains agenome consisting of single-stranded DNA Leili Chamani.MD.,MPH specialist in infectious diseases

  2. The virusis spread by respiratory droplets, and secondary infection ratesamong household contacts are very high.Nosocomial infectionhas been described. • ParvovirusB19 has also been transmittedby blood products, especially pooled factor VIII and factorIX concentrates.

  3. Most cases of parvovirus B19 infection are asymptomatic. • Themost common clinical presentation of infection is erythema infectiosum,or fifth disease, a childhood exanthem characterized by a "slappedcheek" rash • Fever and nonspecificinfluenza-like symptoms occurres early in adults, particularly middle-agedwomen, the infection may cause clinically significant arthropathy. • The later onset of a cutaneous eruption and rheumaticsymptoms, about two weeks after the initial infection, correspondedto the appearance of antiviral antibodies. It is likely thatthese symptoms of parvovirusB19 infection are due to the formationand deposition of immune complexes in the skin and elsewhere.Serologic testing at this stage of infection generally showsseroconversion, IgM antibodies, or the new presence of IgG antibodiesto parvovirus.

  4. ParvovirusB19 infection in a pregnant woman, followed by transplacentaltransmission to the fetus, can lead to miscarriage or hydropsfetalis The swollen appearance in hydrops is the result of severe anemiaand perhaps also myocarditis, both of which contribute to congestiveheart failure. Thrombocytopenia may accompany severe anemia. the United States,7 the estimated risk of transplacental infection among women who are infected with parvovirusB19 during pregnancy is 30 percent, with a 5 to 9 percent risk of fetal loss. Infection during the second trimester poses the greatest risk of hydrops fetalis ParvovirusB19 probably accounts for 10 to 20 percent of all cases of nonimmune hydrops fetalis. Approximately 8 percent of intrauterine fetal deaths were blamed on parvovirusB19 in a Swedish survey. The risk of infection is highest in epidemic years and is correlated with the extent of contact the pregnant woman had with children.

  5. Most parvovirusB19 infections during pregnancy do not leadto loss of the fetus. The few reported cases of developmentalanomalies in the eyes or nervous system of infants with in uteroexposure may be coincidental. However, severe anemia at birthwith bone marrow morphologic features that are consistent withconstitutional pure red-cell aplasia (Diamond–Blackfananemia) or congenital dyserythropoietic anemia may be due totransplacental transmission of parvovirusB19 infection.76

  6. Immunity • Humoral Pathophysiology • The only known natural host cell of parvovirusB19 is the humanerythroid progenitor • Small amounts of parvovirusB19 dramaticallyinhibit colony formation by early and especially by late erythroidprogenitors without affecting myeloid colony • Globoside, a neutral glycolipid that acts as a cellular receptor,accounts for the tropism of the virus for erythroid cells. Thepresence of globoside in the placenta and in fetal myocardium— mainly on the surface of erythroid precursors and redcells but also on some megakaryocytes and endothelial cells— is consistent with the clinical effects of parvovirusB19 infection.

  7. Dx • serologicand DNA tests • propagating the virus in standard tissueculture is difficult • IgM antibodies are detected in almost all cases of fifth diseaseat the time of presentation, and they appear within a few daysafter the onset of transient aplastic crisis; these antibodiespersist for two to three months after acute infection • DNA assays are required to diagnose persistentinfection, since antibody production is absent or minimal. ParvovirusDNA can also be found in serum early in the course of a transientaplastic crisis. • Virus can be detected in amniotic fluid, and both virus andIgM antibodies to parvovirusB19 are detectable in umbilical-cordblood; maternal serum will show seroconversion during pregnancy,but tests for maternal IgM antibodies may be negative at theonset of hydrops fetalis.

  8. Treatment • Most cases of parvovirus infection in children and adults donot require specific therapy. • Isolation of infected personsis impractical, with the exception of hospitalized patients. • Pure red-cell aplasia and the underlying persistent parvovirusB19 infection may be terminated rapidly by discontinuing immunosuppressivetherapy, or by instituting antiretroviral drug therapy in patientswith AIDS. • Commercial immune globulins are a good source ofantibodies against parvovirus; Immune globulin therapy can precipitate the rash and joint symptomsof fifth disease. • Hydrops fetalis may resolve spontaneously,but intrauterine blood transfusions have been used with apparentsuccess. • Chronic arthropathy has been treatedsymptomatically with antiinflammatory drugs.

  9. Prevention • Vaccine Development (The recombinant immunogen) • Such a vaccine could prevent transientaplastic crisis in patients with sickle cell disease or otherhemolytic anemias and pure red-cell aplasia in some immunodeficientpersons, as well as hydrops fetalis, if seronegative women wereinoculated early in pregnancy.

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