Journal of Infection (I984) 9, 298-300 CASE REPORT Human parvovirus infection and aplastic crisis in hereditary spherocytosis R. J. Davidson,* T. Brownt and D. Wiseman *Haematology Unit and tRegional Virus Laboratory, Medical School, Foresterhill, Aberdeen and Netherton House, Auchenblae, Kincardineshire Accepted for publication I9 June I984 Summary This report records an episode of parvovirus-induced bone-marrow aplasia in a child with hereditary spherocytosis and arising during a local outbreak of erythema infectiosum (fifth disease or 'slapped-cheek syndrome'). Inapparent infection was found in two haematologically normal family contacts. Introduction Parvoviruses are distributed widely throughout the animal kingdom where they may give rise to such diverse conditions as panleucopenia in cats and generalised arteritis in Aleutian mink. The human parvovirus was first and fortuitously detected in I9731 in the serum of blood donors being screened for hepatitis B antigen but it is only recently that retrospective and prospective studies have revealed its association with erythema infectiosum. 2, 3 The causal role of the virus in the aplastic crisis of sickle-cell anaemia is now firmly established, 4 and its implication in the aplastic or hypoplastic crises of some other haemolytic disorders, hereditary spherocytosis5, 6 and pyruvate kinase deficiency,7 is now also being recognised. Case report A 4-year-old boy was admitted on i2 February I984 to the Royal Aberdeen Children's Hospital with a 6-day history of listlessness, malaise and thirst. Previously he had been an apparently healthy child except for mild neonatal jaundice. Clinically, he was extremely pale, slightly icteric and pyrexial (38 °C). There was significant enlargement of cervical and inguinal lymph nodes and 3 cm enlargement of both liver and spleen. The relevant haematological indices from serial Coulter S Plus profiles are recorded in Table I. Microscopy of the stained blood film revealed prominent microspherocytosis and confirmed the marked neutrophilia and thrombocytosis, both of reactive type. The serum bilirubin concentration was 23 ~tmol/1 (normal, < 26 lamol/1). Clinical im- provement followed the administration of 35o ml packed red cells and, despite the transfusion, reticulocytes peaked (I 1% ) 3 days later. Prophylactic folic acid (5 mg b.d.), was commenced. The child was discharged from hospital 6 days oi63-4453/84/o6o298 +03 $02.00/0 © I984 The British Society for the Study of Infection