Haematology Vignettes – 16

Anaemia secondary to a parvovirus infection

A 9-month-old child presented to the Casualty Department with pallor and a maculopapular rash on the face.

A full blood count was performed and the following results noted:
Hb 84 g/L, WBC 15.5 x 109/L, Platelet count 422 x 109/L and Reticulocyte count 0.6 %.

The blood film showed a normochromic normocytic anaemia with a reticulocytopenia.

A Hb EPG was performed with no abnormality detected

A bone marrow examination revealed an erythroblastopenia together with giant proerythroblasts scattered throughout the marrow. Such findings may be associated with a parvovirus infection.

Parvovirus serology was performed:

Parvovirus B19 IgG and parvovirus B19 IgM were both positive.

Parvovirus B19 infection

Bone marrow (giant proerythroblast)

Bone marrow
(giant proerythroblast)

Bone marrow trephine (intracellular viral inclusion within a giant proerythroblast)

Bone marrow trephine
(intracellular viral inclusion within a giant proerythroblast)

The human parvovirus was discovered in 1975 in the sera of normal blood donors whilst screening for the hepatitis B virus. The term parvovirus is derived from the Latin ‘parvum’ meaning ‘small’. Parvoviruses are amongst the smallest DNA containing viruses infecting man. They are extremely stable, resisting heat inactivation at 56ºC for more than 60 minutes.

Parvovirus infection is a common infection in humans. Approximately 50% of children have detectable parvovirus B19 IgG in their blood by the age of fifteen and more than 90% of the elderly are also seropositive.

The parvovirus has an unusual predilection for rapidly growing cells, particularly red cell precursors in the bone marrow. It uses the P antigen as a receptor to enter the red cell. The P antigen is also present on granulocytes and megakaryocytes. Once inside the cell the parvovirus inhibits growth by inducing cell cycle arrest and apoptosis. This process gives rises to a severe haemolytic anaemia when the red cells are infected. When the granulocytes and megakaryocytes are infected an aplastic crisis may occur.

Parvovirus infection is also responsible for causing aplastic crises in children with a chronic haemolytic state such as hereditary spherocytosis. It can produce prolonged pancytopenia in an otherwise healthy child and frequently produces a prolonged pancytopenia in children with deficient immunity such as thalassaemia, hereditary pyropoikilocytosis, pyruvate kinase deficiency and autoimmune haemolytic anaemia.

The parvovirus is transmitted in the form of droplets. It may also enter the body via other routes including transfusion with contaminated blood products.

There is no specific treatment for patients with parvovirus B19.

Remission usually occurs within one to two weeks post infection. An increase in the number of granulocytes, platelets and finally reticulocytes indicates the return of normal bone marrow function. Severe anaemia may require transfusion of red blood cells.