Parvovirus B19 has been associated with persistent chronic anaemia and with transient aplastic crisis in children with sickle cell disease. A study involving a cohort of Jamaican patients with sickle cell disease showed that almost all cases of transient aplastic crisis were caused by Parvovirus B19 infection.(1,2)

Reports suggests that Parvovirus B19 can be transmitted through blood transfusions and plasma-derived products.(3,4) B19 is a non-enveloped virus and is resistant to high temperatures and most solvent-detergent treatments.

Despite this fact, routine screening of blood products for B19 DNA does not occur. However, many manufacturers carryout B19 PCR on plasma mini-pools to reduce high B19 viral load.

The seroprevelance of B19 in the normal population is considered to be around 70%. B19 seropositivity generally rises with age and reaches about 72% over the age of 60 years. Studies have revealed that the seroprevelance of Parvovirus B19 antibodies in the haemophiliac population is higher than in the normal population. It is generally considered that this is due to haemophiliac patients receiving products derived from plasma pools that are more likely to contain infectious B19 DNA. A study by Eis Hübinger et al revealed that haemophiliac children treated with virally inactivated clotting factor had an increased level of B19 seroprevelance at approximately 92%.(5)

The prevalence of Parvovirus B19 was reported at 1 in 3000 in non-epidemic periods. This rises to approximately 1 in 167 during an epidemic. (6) A recent recommendation by the Health Council in the Netherlands suggests that individual donors should be screened for B19 IgG and those with continually high levels of B19 IgG could be identified. The blood or plasma from these donors could then be used for any immunocompromised or other high risk patients, thereby reducing the risk of B19 infection.(7)

References

1. Outbreak of aplastic crises in sickle cell anaemia associated with Parvovirus-like agent. Lancet 1981: 2, 595-597. Serjeant, G.R., Topley, J.M., Mason, K. et al.
   
2.  Haematological response to Parvovirus B19 infection in homozygous sickle-cell disease. Lancet 2001:358, 1779-80. Serjeant, B.E., Hambleton, R.R., Kerr, S., Kilty, C.G., Serjeant, G.R.
    
3. Human Parvovirus B19 and blood products. Vox Sang 1997: 72, 1-10. Prowse, C., Ludlam, C.A., Yap, P.L.
   
4. Transmission of Parvovirus B19 by coagulation factor concentrates exposed to 100 degrees C heat after lyophilization. Transfusion 1997: 37, 517-522. Santagostino, E., Mannucci, P.M., Gringeri, A., Azzi, A., Morfini,M., Musso, R., Santoro, R., Schiavoni, M.
   
5. The prevalence of antibody to Parvovirus B19 in hemophiliacs and in the general population. Zenthl Bakteriol 1996: 284, 232-240. Eis-Hübinger, A. M., Oldenburg, J., Brackmann, H. H., Matz, B., Schneweis, K.E.
   
6. Incidence of human parvovirus B19 DNA detection in blood donors. Br J Haematol 1995: 91,1017-8 Yoto, Y., Kudoh, T., Haseyama, K., Suzuki, N., Oda, T., Katoh, T., Takahashi, T., Sekiguchi, S., Chiba, S.