Home Print this page Email this page Small font sizeDefault font sizeIncrease font size
Users Online: 292
Home | About us | Editorial board | Search | Ahead of print | Current issue | Archives | Submit article | Instructions | Subscribe | Contacts | Login 
     


 
 Table of Contents  
LETTER TO EDITOR
Year : 2017  |  Volume : 7  |  Issue : 1  |  Page : 47-48  

Falciparum malaria and parvovirus B19 coinfection: A rare entity


1 Department of Cardiology, IPGMER and SSKM Hospital, Kolkata, West Bengal, India
2 Department of Obstetrics and Gynaecology, IPGMER and SSKM Hospital, Kolkata, West Bengal, India
3 Department of General Medicine, IPGMER and SSKM Hospital, Kolkata, West Bengal, India

Date of Acceptance30-Nov-2016
Date of Web Publication16-Mar-2017

Correspondence Address:
Rakesh Agarwal
Department of Cardiology, IPGMER and SSKM Hospital, Kolkata, West Bengal
India
Login to access the Email id


DOI: 10.4103/2229-5070.202299

PMID: 28459015

Rights and Permissions

How to cite this article:
Agarwal R, Baid R, Datta R, Saha M, Sarkar N. Falciparum malaria and parvovirus B19 coinfection: A rare entity. Trop Parasitol 2017;7:47-8

How to cite this URL:
Agarwal R, Baid R, Datta R, Saha M, Sarkar N. Falciparum malaria and parvovirus B19 coinfection: A rare entity. Trop Parasitol [serial online] 2017 [cited 2017 Jul 28];7:47-8. Available from: http://www.tropicalparasitology.org/text.asp?2017/7/1/47/202299

Sir,

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.
Figure 1: Giant proerythroblasts

Click here to view


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.[4]

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.[2]

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.[8] A Ghanian study concluded that B19 virus was associated with malaria in cases of severe anemia.[9]

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.[10]

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.[11]

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.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Wildig J, Michon P, Siba P, Mellombo M, Ura A, Mueller I, et al. Parvovirus B19 infection contributes to severe anemia in young children in Papua New Guinea. J Infect Dis 2006;194:146-53.  Back to cited text no. 1
    
2.
Lortholary O, Eliaszewicz M, Dupont B, Courouce AM. Parvovirus B19 infection during acute Plasmodium falciparum malaria. Eur J Haematol 1992;49:219.  Back to cited text no. 2
    
3.
Gupta R, Singh T. Parvovirus B19 co-infection with falciparum malaria: a cause of severe anemia. Haematologica 2005;90 12 Suppl: ECR41.  Back to cited text no. 3
    
4.
Menendez C, Fleming AF, Alonso PL. Malaria-related anaemia. Parasitol Today 2000;16:469-76.  Back to cited text no. 4
    
5.
Urganci N, Arapoglu M, Kayaalp N. Plasmodium falciparum malaria with coexisting parvovirus B19 infection. Indian Pediatr 2003;40:369-70.  Back to cited text no. 5
    
6.
Scarlata F, Gianelli E, Miceli S, Galimberti L, Antinori S. Acute parvovirus B19 infection and anemia during Plasmodium falciparum malaria. Clin Infect Dis 2002;35:1449-51.  Back to cited text no. 6
    
7.
Ingrassia F, Gadaleta A, Maggi P, Pastore G. Plasmodium falciparum malaria and parvovirus B19; A case of acute co-infection. BMC Infect Dis 2010;10:87.  Back to cited text no. 7
    
8.
Toan NL, Sy BT, Song LH, Luong HV, Binh NT, Binh VQ, et al. Co-infection of human parvovirus B19 with Plasmodium falciparum contributes to malaria disease severity in Gabonese patients. BMC Infect Dis 2013;13:375.  Back to cited text no. 8
    
9.
Duedu KO, Sagoe KW, Ayeh-Kumi PF, Affrim RB, Adiku T. The effects of co-infection with human parvovirus B19 and Plasmodium falciparum on type and degree of anaemia in Ghanaian children. Asian Pac J Trop Biomed 2013;3:129-39.  Back to cited text no. 9
    
10.
Koduri PR. Novel cytomorphology of the giant proerythroblasts of parvovirus B19 infection. Am J Hematol 1998;58:95-9.  Back to cited text no. 10
    
11.
Ho M, Webster HK, Looareesuwan S, Supanaranond W, Phillips RE, Chanthavanich P, et al. Antigen-specific immunosuppression in human malaria due to Plasmodium falciparum. J Infect Dis 1986;153:763-71.  Back to cited text no. 11
    


    Figures

  [Figure 1]



 

Top
  
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
    References
    Article Figures

 Article Access Statistics
    Viewed568    
    Printed6    
    Emailed0    
    PDF Downloaded0    
    Comments [Add]    

Recommend this journal