Letters to the editor
Parvovirus B 19 infection during acute Plasmodium falciparum malaria To the editor: Parvovirus B19 has been well investigated as an agent responsible for erythroblastopenia in children with hemoglobin disorders (1, 2). The primary site of B19 infection in humans appears to be erythroid precursor cells (2) that are also infected by Plasmodium falciparurn (3). We report a case of Parvovirus B 19 infection during acute Plasmodiumfalciparum malaria. A 8-year-old African boy was referred to our unit for the treatment of acute Plasmodium falciparum malaria 1 day after returning from the Congo. Past medical history included a glucose-6-phosphate dehydrogenase deficiency and minor beta thalassemia. Several episodes of vomiting associated with severe parasitemia led to the prescription of intravenous quinine. On the day of admission, hemoglobin was 11.3 g/dl; white blood cell count 19 500/mm3 and platelet count 200 OOO/mm3. Blood smears were positive for P. fakiparum. After 2 d of treatment, hemoglobin was 9.4 g/dl, reticulocytes 39 000/mm3, serum lactase dehydrogenase 490 UIjl and haptoglobinemia 0.13 g/l. After 4 d of treatment, hemoglobin was 7.5 g/dl while parasitemia was no longer observed. The child received no treatment other than quinine, which does not stimulate the oxidative metabolism of glucose in the erythrocyte. Because of reticulocytopenia associated with hemolysis, the diagnosis of recent infection due to Parvovirus B19 was considered. Antigenemia B 19 was detected by counter electrophoresis (4) in the serum collected 5 d after admission, confirming a very recent viral infection. In this sample, antibodies anti-B 19 IgM and IgG were not detected by radio-immuno-assay (5). For personal reasons, the patient left our unit very soon afterwards and no further sample was available. Erythroid precursor cells represent a common target for both Parvovirus B19 and Plasmodium falciparum. A predisposing factor to viral infection could be the depression of cellular immunity induced by Plasmodium falciparum (6). Indeed, Herpes sim-
plex (7) and Herpes zoster infections (8) have been reported during acute Plasmodium falciparum malaria. In conclusion, reticulocytopenia during acute Plasmodium fakiparum malaria can be due to Parvovirus B 19 co-infection and this particular association can be a life-threatening disease. This possibility must be ruled out in cases of worsening of anemia with reticulocytopenia despite clearance of parasitemia with an effective antimalaria treatment.
References 1. RAOKRP, PATELAR, ANDERSON MJ, HODGSON J, JONES SE, PATTISONJR. Infection with parvovirus-like virus and aplastic crisis in chronic hemolytic anemia. Ann Intern Med 1983: 98: 930-932. 2. ANDERSON LJ. Human parvovirus. J Inf Dis 1990: 161: 603608. 3. ABDALLA SH, WICHRAMASINGHE SN. A study of erythroid progenitor cells in the bone marrow of gambian children with falciparum malaria. Clin Lab Haematol 1988: 10: 33-40. AM, FERCHAL F, MORINETF, eta]. Human 4. COUROUCE parvovirus infections in France. Lancet 1984: 1: 160. PP, PEREIRAMS. Diagnostic assays 5. COHENBJ, MORTIMER with monoclonal antibodies for the human serum parvoviruslike virus (SPLV). J Hyg Camb 1983: 91: 113-130. 6. H o M, WEBSTERK, LOOAREESUWAN S, et al. Antigenspecific immunosuppression in human malaria due to Plasmodiumfalciparum. J Infect Dis 1986: 153: 763-711. 7. SCOTTJG. Herpes simplex corneae in malaria. Br Med J 1944: 2: 213. 8. COOKIF. Herpes zoster in children following malaria. J Trop Med Hyg 1985: 88: 261-264.
Correspondence: 0. Lortholary, MD*, M. Eliaszewicz, MD*, B. Dupont, MD*, A.M. Courouce, PhD**, *Department of Infectious and Tropical Diseases, Pasteur Hospital, 21 1 rue de Vaugirard, 75724 Paris, Cedex 15, and **National Institute of Blood Transfusion, Paris, France.
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Parvovirus B 19 infection during acute Plasmodium falciparum malaria To the editor: Parvovirus B19 has been well investigated as an agent responsible for erythroblastopenia in children with hemoglobin disorders (1, 2). The primary site of B19 infection in humans appears to be erythroid precursor cells (2) that are also infected by Plasmodium falciparurn (3). We report a case of Parvovirus B 19 infection during acute Plasmodiumfalciparum malaria. A 8-year-old African boy was referred to our unit for the treatment of acute Plasmodium falciparum malaria 1 day after returning from the Congo. Past medical history included a glucose-6-phosphate dehydrogenase deficiency and minor beta thalassemia. Several episodes of vomiting associated with severe parasitemia led to the prescription of intravenous quinine. On the day of admission, hemoglobin was 11.3 g/dl; white blood cell count 19 500/mm3 and platelet count 200 OOO/mm3. Blood smears were positive for P. fakiparum. After 2 d of treatment, hemoglobin was 9.4 g/dl, reticulocytes 39 000/mm3, serum lactase dehydrogenase 490 UIjl and haptoglobinemia 0.13 g/l. After 4 d of treatment, hemoglobin was 7.5 g/dl while parasitemia was no longer observed. The child received no treatment other than quinine, which does not stimulate the oxidative metabolism of glucose in the erythrocyte. Because of reticulocytopenia associated with hemolysis, the diagnosis of recent infection due to Parvovirus B19 was considered. Antigenemia B 19 was detected by counter electrophoresis (4) in the serum collected 5 d after admission, confirming a very recent viral infection. In this sample, antibodies anti-B 19 IgM and IgG were not detected by radio-immuno-assay (5). For personal reasons, the patient left our unit very soon afterwards and no further sample was available. Erythroid precursor cells represent a common target for both Parvovirus B19 and Plasmodium falciparum. A predisposing factor to viral infection could be the depression of cellular immunity induced by Plasmodium falciparum (6). Indeed, Herpes sim-
plex (7) and Herpes zoster infections (8) have been reported during acute Plasmodium falciparum malaria. In conclusion, reticulocytopenia during acute Plasmodium fakiparum malaria can be due to Parvovirus B 19 co-infection and this particular association can be a life-threatening disease. This possibility must be ruled out in cases of worsening of anemia with reticulocytopenia despite clearance of parasitemia with an effective antimalaria treatment.
References 1. RAOKRP, PATELAR, ANDERSON MJ, HODGSON J, JONES SE, PATTISONJR. Infection with parvovirus-like virus and aplastic crisis in chronic hemolytic anemia. Ann Intern Med 1983: 98: 930-932. 2. ANDERSON LJ. Human parvovirus. J Inf Dis 1990: 161: 603608. 3. ABDALLA SH, WICHRAMASINGHE SN. A study of erythroid progenitor cells in the bone marrow of gambian children with falciparum malaria. Clin Lab Haematol 1988: 10: 33-40. AM, FERCHAL F, MORINETF, eta]. Human 4. COUROUCE parvovirus infections in France. Lancet 1984: 1: 160. PP, PEREIRAMS. Diagnostic assays 5. COHENBJ, MORTIMER with monoclonal antibodies for the human serum parvoviruslike virus (SPLV). J Hyg Camb 1983: 91: 113-130. 6. H o M, WEBSTERK, LOOAREESUWAN S, et al. Antigenspecific immunosuppression in human malaria due to Plasmodiumfalciparum. J Infect Dis 1986: 153: 763-711. 7. SCOTTJG. Herpes simplex corneae in malaria. Br Med J 1944: 2: 213. 8. COOKIF. Herpes zoster in children following malaria. J Trop Med Hyg 1985: 88: 261-264.
Correspondence: 0. Lortholary, MD*, M. Eliaszewicz, MD*, B. Dupont, MD*, A.M. Courouce, PhD**, *Department of Infectious and Tropical Diseases, Pasteur Hospital, 21 1 rue de Vaugirard, 75724 Paris, Cedex 15, and **National Institute of Blood Transfusion, Paris, France.
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