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Parvovirus B19 and Plasmodium falciparum coinfection are rarely reported in literature. Parvovirus B19 may be an important cause of persisting reticulocytopenia or bone marrow suppression in malaria patients. Here, we describe a case of a 21-year-old male patient who was diagnosed with P. falciparum infection but did not respond to antimalarials and was subsequently diagnosed to harbor parvovirus B19 infection. This is, in our knowledge, only the second such case report from India.
A 21-year-old male patient presented with high-grade fever, pain abdomen, and worsening jaundice for 10 days before admission. He also complained of marked lethargy, generalized weakness, and effort intolerance during the same period though there was no history of bleeding manifestations. He had no history of similar complaints in the past. There was no history of oral ulcers, arthralgias, or unprotected sexual exposure.
Physical examination revealed moderate pallor, icterus, soft hepatomegaly, and moderate splenomegaly of 5 cm below left costal margin. No lymphadenopathy or sternal tenderness was present.
A routine hemogram revealed hemoglobin (Hb): 5.2 g/dL, total leukocyte count (TLC): 1800/cu mm, differential count (DLC): N50 L44 M4 E2 B0. Platelet count was 16000/cu mm. Liver function tests revealed bilirubin: 5.8 g/dL (indirect: 5 g/dL, direct: 0.8 g/dL) and mild transaminitis. Renal and thyroid function tests were normal.
Imaging in the form of ultrasonography abdomen corroborated the physical examination findings. Direct Coombs test and antinuclear antibodies were negative. A thin peripheral smear showed P. falciparum trophozoites. Malarial parasite dual antigen tested positive for P. falciparum malaria as well. The patient was put on combination artemisinin therapy with a 3-day course of artemether-lumefantrine.
His fever subsided and by day 7 of admission, his hemogram revealed Hb: 8.1 g/dL, TLC: 2200/cu mm, and platelet count: 100,000/cu mm. However, he mounted high-grade fever again on day 11 of admission despite being managed conservatively. Blood samples sent for malaria antigen and slide tests, dengue serology, and blood cultures were negative.
The patient was put on empirical antibiotics. A hemogram obtained showed Hb: 3.4 g/dL, TLC: 750/cu mm, DLC: N28 L67 M2 E3 B0, platelets: 14000/cu mm. The patient was managed with blood and platelet transfusions, but his condition failed to improve. Seven days later, his hemogram still read: Hb: 5.1 g/dL, TLC: 794/cu mm, DLC: N20 L74 M3 E3 B0, and platelet count: 10,000/cu mm. Reticulocyte production index was <2.5.
A bone marrow biopsy revealed cellular marrow with the presence of giant proerythroblasts [Figure 1]. This clinched the diagnosis. A parvovirus B19 IgM was ordered which came out to be positive. The patient was treated with blood and platelet transfusions and aseptic precautions were taken. His counts recovered by day 30 of admission when he was discharged. At 2 months of follow-up, the patient was doing well and was asymptomatic. A repeat ELISA for B19 specific antibody 2 weeks after discharge was negative for IgM but positive for IgG antibodies.
Parvovirus B19 is the etiologic agent of erythema infectiosum or fifth disease. It has also been associated with transient aplastic anemia, usually in patients with chronic hemolytic anemias and/or in immunocompromised patients. This is due to the high affinity for the virus toward the erythroid precursor cells.[1,2,3,4,5]
Malaria is a major health problem in developing countries. Anemia in malaria has been ascribed to multiple causes including hemolysis and dyserythropoiesis.
Although both P. falciparum and parvovirus show predilection for erythroid cells, parvovirus usually infects early erythroid precursors compared to Plasmodium which infects matures red cells.
Only a few case reports have so far described the association between P. falciparum and parvovirus coinfection.[6,7] A coinfection such as this can lead to severe anemia with life-threatening consequences. A 2013 study identified frequent parvovirus B19 virus infection in Gabonese children with P. falciparum malaria and considered it as an additional diagnostic measure in malaria patients with life-threatening anemia. A Ghanian study concluded that B19 virus was associated with malaria in cases of severe anemia.
The long duration of the symptomatology despite adequate management of malaria and resolution with development of parvovirus B19 IgG antibodies signifies the involvement of parvovirus in pathology. Furthermore, the presence of giant proerythroblasts in the bone marrow is a specific finding for parvovirus infection though it is uncommonly found. At the same time, it would be difficult to attribute the bone marrow suppression to uncomplicated P. falciparum alone.
A depressed cell-mediated immunity in P. falciparum infection may favor opportunistic coinfection. However, literature on the subject is limited due to paucity of data.
This is probably only the second case report of such an association from India. In conclusion, unexplained bone marrow suppression in any patient with P. falciparum infection should alert the physician to a parvovirus B19 infection since classical findings, such as giant proerythroblasts, might not always be present.
There are no conflicts of interest.