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Letters to the Editor

Indian Pediatrics 2003; 40:369-370

Plasmodium Falciparum Malaria with Coexisting Parvovirus B19 Infection


Erythroid precursor cells represent a common target for both Parvovirus B19 and Plasmodium falciparum(1). Parvovirus B19 may cause acute aplastic crisis when asso-ciated with acquired or congenital hemolytic disorders, such as sickle cell anemia, here-ditary spherocytosis or rarely malaria(2-4). We present a case of Plasmodium falciparum malaria and simultaneous Parvovirus B19 infection in a patient with fever and anemia.

A 9-year-old boy was admitted with complaints of fever, faigue and abdominal pain for the past 7 days. On physical examination axillary temperature was 38.5ºC; pallor and hepatosplenomegaly was noted. Laboratory studies revealed a white blood cell count of 5200/mm3, with 20% neutrophils, 33% lymphocytes, 47% monocytes; hemo-globin, 8.2 g/dL; hematocrit, 0.24; platelet count, 122,000/mm3; reticulocyte, 0.8%; and erythrocyte sedimentation rate, 130 mm/h. Serological assays for typhoid fever, brucella and leishmania, and Epstein-Barr antibodies, urine and stools were negative, as were cytomegalovirus and Epstein-Barr anti-bodies, anti-HCV and anti-HBs antibodies. Tuberculosis was also ruled out. Malaria could not be identified on initial thick and thin blood films. Bone marrow aspirate showed moderate erythroid hypoplasia. Antiparvo-virus IgM was positive and antiparvovirus IgG was negative by radioimmunoassay. Diagnosis of an infection due to Parvovirus B19 was considered. However, three days later, hemoglobin was measured 6.8 g/dL reticulocyte 1%, and platelet count was 132,000/mm3. Blood smears for malaria were repeated every 12 hours and tropho-zoites were identified on the third day.

Plasmodium falciparum malaria was the diagnosis and chloroquine treatment was started. Fever subsided in two days and blood smears for malaria were negative on the third day. Hemoglobin value was 7.1 g/dL and reticulocyte count was 1% in the week follow-ing treatment. One month later the child was well with no complaints. Antiparvovirus IgM and antiparvovirus IgG were both positive. Hemoglobin was 9.4 g/dL. Five months later, hemoglobin was 11.3 g/dL hepato-splenomegaly was not noted, antiparvovirus IgM was negative and antiparvovirus IgG was positive.

Parvovirus B19 infection has a wide variety of disease manifestations, depending on the imunological and hematological status of the host. In case of a coexisting hemolytic disorder, patients with Parvovirus infection may present with severe anemia and reticulo-cytopenia(2,5). Our patient also revealed worsening anemia, reticulocytopenia, and erythroid hypoplasia in bone marrow. In suspicion of a coexisting disorder, repeated blood smears were investigated for the final diagnosis of malaria. Even after the start of the treatment for malaria, the patient’s hemo-globin values did not rise as expected and reticulocyte response was still not present because of the coexisting Parvovirus infec-tion. The symptoms subsided after chloro-quine treatment, however; while parasitemia was no longer observed only a little rise in hemoglobulin value was noticed. With resolution of Parvovirus infection, anemia also resolved.

Malaria continues to be a principal health problem in many parts of the world. Since these two infections can coexist in a patient, Parvovirus B19 infection should be ruled out in patients with malaria when worsening of anemia with reticulocytopenia is noted despite effective antimalarial treatment.

N. Urganci,
M. Arapoglu,
N. Kayaalp,

Department of Pediatrics,
Sisli Etfal Hospital,
Istanbul 80630, Turkey.
E-mail: [email protected]

References


 

1. Lortholary O, Eliaszewicz M, Dupont B, Courouce AM. Parvovirus B19 infection during acute Plasmodium falciparum malaria. Eur J Hematol 1992; 49: 219.

2. Mahmoud MM, McClain KL. Diverse Hematologic Effects of Parvovirus B19 Infection. In: Buchanan GR, editor. The Pediatric Clinics of North America. Pediatric Hematology. Philadelphia: WB Saunders. 1996. p. 809-821.

3. Pattison JR, Jones SE, Hodgson J, Davis LR, White JM, Stroud LE, et al. Parvovirus infections and hypoplastic crises in sickle cell anemia (letter). Lancet. 1981; 1: 664-665.

4. Jones P, Pickett L, Anderson M. Human parvovirus infection in children and severe anemia seen in an area endemic for malaria. J Trop Med Hyg. 1990; 93: 67-70.

5. Brown KE. Parvovirus B19. In: Mandell GL, Bennett JE, Dolin R, editors, Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Disease. 5th ed. Philadelphia: Churchill Livingstone; 2000. p. 1685-1693.

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