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LETTERS
Year : 2018  |  Volume : 64  |  Issue : 2  |  Page : 129-130

A imported case of Plasmodium malariae


1 Department of Internal Medicine, Baby Memorial Hospital, Calicut, Kerala, India
2 Department of Pathology, Baby Memorial Hospital, Calicut, Kerala, India

Date of Web Publication23-Apr-2018

Correspondence Address:
K V Patil
Department of Internal Medicine, Baby Memorial Hospital, Calicut, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jpgm.JPGM_358_17

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How to cite this article:
Bhargavan P V, Patil K V, Imandi H P, Mampilly N. A imported case of Plasmodium malariae. J Postgrad Med 2018;64:129-30

How to cite this URL:
Bhargavan P V, Patil K V, Imandi H P, Mampilly N. A imported case of Plasmodium malariae. J Postgrad Med [serial online] 2018 [cited 2019 Nov 18];64:129-30. Available from: http://www.jpgmonline.com/text.asp?2018/64/2/129/231107




Plasmodium malariae is an uncommonly reported infection in India.[1] It differs from other species causing malaria, in that it causes quartan fever and has important diagnostic and clinical implications.

We present a case of P. malariae, who was infected in Kenya and was diagnosed after coming to India.

A 40-year-old businessman, originally a resident of Calicut, Kerala, and settled in Mombasa, Kenya for the past 20 years, presented with intermittent spikes of high-grade fever and chills of 3-weeks- duration. He had returned to India 4 days before the admission. Fever spike occurred each 4th day. He was asymptomatic in between the fever spikes except for the malaise and tiredness. There was no history of jaundice. He was initially evaluated by a local practitioner in Calicut and was prescribed oral doxycycline, 3 days before the admission. Rapid malarial antigen test done that time was negative.

On examination, he had a fever (temperature: 104 F), tachycardia (pulse: 114/min), and conjunctival congestion. The systemic examination was within normal limits.

Hemoglobin was 12.1 g/dl, red blood cell count - 4.14 million/mm 3, packed cell volume - 35.9%, white blood cell count - 4500/mm 3 with 85% neutrophils and marginally decreased platelet count (131,000/mm 3). Erythrocyte sedimentation rate was raised (45 mm/1st h). Liver function tests, renal function tests, and urine examination were normal.

As suggested from the history, thick and thin smears for malarial parasite were sent. Initially reported as Plasmodium vivax, on review, it was confirmed to be P. malariae with smear showing characteristic band forms [Figure 1].
Figure 1: Band form of Plasmodium malariae seen (arrow) on peripheral blood smear examination

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Although the rapid diagnostic test for Plasmodium falciparum was negative he was treated with artesunate +sulfadoxine-pyrimethamine for 3 days as coinfection with Plasmodium falciparum is common in Africa.[2] A single dose of primaquine 45 mg was also given. He was discharged in a stable condition after 5 days of in hospital management.

P. malariae is relatively common in Kenya.[3] In India, though there are possible areas with transmission of P. malariae, P. malariae infection maybe underreported as early ring forms of P. malariae are difficult to differentiate from those of P. vivax.[1]

P. malariae is difficult to differentiate from P. vivax and Plasmodium knowlesi on microscopy. There are few differences as compared to vivax. P. malariae infects old erythrocytes, ring form is thicker and stains more intensely, infected erythrocytes are normal or small sized and rarely Ziemann's stippling may be seen. However, most unique feature of P. malariae is the presence of band forms which are late trophozoites stretching across the erythrocyte. In our case, band forms were noted by the pathologist.

Although P. malariae does not produce hepatic hypnozoites, the blood infection may persist for very long duration in untreated cases. The recrudescence maybe seen up to 50 years after the initial infection (in contrast to up to 1–2 years in case of P. falciparum). P. malariae can infect mosquitoes over a long period which sustains its transmission.[4]

In conclusion, we wish to stress the importance of accurate diagnosis of this infection, which is likely to be misdiagnosed as P. vivax and which may present with pathologically different and irreversible form of nephropathy and can cause recrudescence decades after initial infection. The diagnosis may be missed by standard rapid diagnostic tests as they have very low sensitivity for detecting P. malariae, which highlights the importance of skilled technicians and pathologists.[5] Considering the demographics of migrating population in today's world such cases may prove to be of significant public health importance.

Declaration of patient consent

The authors certify that appropriate patient consent was obtained.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
 :: References Top

1.
Mohapatra PK, Prakash A, Bhattacharyya DR, Goswami BK, Ahmed A, Sarmah B, et al. Detection and molecular confirmation of a focus of Plasmodium malariae in Arunachal Pradesh, India. Indian J Med Res 2008;128:52-6.  Back to cited text no. 1
[PUBMED]  [Full text]  
2.
Collins WE, Jeffery GM. Plasmodium malariae: Parasite and disease. Clin Microbiol Rev 2007;20:579-92.  Back to cited text no. 2
    
3.
Zhou G, Afrane YA, Vardo-Zalik AM, Atieli H, Zhong D, Wamae P, et al. Changing patterns of malaria epidemiology between 2002 and 2010 in Western Kenya: The fall and rise of malaria. PLoS One 2011;6:e20318.  Back to cited text no. 3
    
4.
Savargaonkar D, Shah N, Das MK, Srivastava B, Valecha N. Plasmodium malariae infection: A case of missed diagnosis. J Vector Borne Dis 2014;51:149-51.  Back to cited text no. 4
[PUBMED]  [Full text]  
5.
Moody A. Rapid diagnostic tests for malaria parasites. Clin Microbiol Rev 2002;15:66-78.  Back to cited text no. 5
    


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2004 - Journal of Postgraduate Medicine
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