Primary parvovirus B19 infection usually occurs during childhood. Normal in
dividuals either remain free of hematological abnormalities or develop a tr
ansient and moderate impairment in bone marrow function responsible for ret
iculocytopenia (without significant anemia), leukopenia, and thrombocytopen
ia. In patients with inherited chronic hemolytic anemias, most notably sick
le cell anemia, hereditary syherocytosis, and thalassemia, acute parvovirus
B19 infection is responsible for transient erythroblastopenia manifesting
as a further hemoglobin decrease that frequently requires blood transfusion
therapy. The diagnosis is suggested by the low reticulocyte count and conf
irmed by the detection of IgM antibody to parvovirus B19. Patients who fail
to mount an adequate humoral immune response because of a congenital condi
tion (congenital immune deficiencies, fetus) or an acquired disease (HIV in
fection, chemotherapy, transplantation) can develop chronic erythroblastope
nia. Polyvalent immunoglobulin therapy is effective in correcting the anemi
a, although repeated injections are usually necessary to maintain this effe
ct. Parvovirus B19 infection has also been shown to be associated with idio
pathic thrombocytopenia purpura and autoimmune neutropenia of childhood. Pa
rvovirus B19 has been reported to cause hemophagocytosis syndrome in normal
individuals and in patients with immune deficiencies or chronic hemolysis.