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Malaria falciparum

Pathogen:Protozoa →Plasmodium falciparum
Transmission:Female mosquitoes of the Anopheles genus
Geographical range:Tropical regions
Incidence:Up to 200 million infections per year

Case history

A 30-year old man returned from a long-term business trip to central Africa and went to his general practitioner with these symptoms: fever, fatigue, headache and vomiting. On account of the man’s last travel destination, a complete blood count with WBC differential and reticulocyte analysis was performed to investigate the cause of fever.

Malaria pathophysiology and clinical course

Each year there are around half a million reported deaths due to malaria, mostly caused by Plasmodium falciparum infections (1). While malaria exists in more than 100 countries, it is mainly confined to poorer tropical areas of Africa, Asia and Latin America. More than 90% of malaria cases and the great majority of malaria deaths occur in tropical Africa.

Malaria is a parasitic infection transmitted primarily by the bite of an infected female Anopheles mosquito. Malaria may also be transmitted via blood transfusion or between mother and foetus during pregnancy. In humans, parasites multiply exponentially in the liver and, after several developmental stages, in infected red blood cells. Mosquitoes ingest parasites with a blood meal upon which the parasites undergo another reproductive phase inside the mosquito before being passed on to another human host.

Of the four species of Plasmodium that commonly infect humans (P. falciparum, P. vivax, P. ovale and P. malariae) P. falciparum accounts for the highest mortality. Infection with P. falciparum is not restricted to immature RBCs as it is with P. Vivax and therefore results in the highest levels of parasitaemia.

The parasite is protected from the body's immune system because for most of its life cycle it resides within the liver and the red blood cells. However, circulating red blood cells are destroyed in the spleen. To avoid the destruction, the P. falciparum parasite displays adhesive proteins on the surface of the infected blood cells, causing the infected red blood cells to adhere to endothelial cells of capillaries, thereby sequestering the parasite from the immune recognition in the spleen (2). In some cases infected RBCs cannot be found in peripheral blood smears because they are sequestered in the host microvasculature. Severe complications of P. falciparum infection include cerebral malaria, renal failure, pulmonary oedema and anaemia

Laboratory results

 

Case interpretation

In the presented case, a population of Plasmodium falciparum gametocytes was observed in the WDF scattergram, which triggered the appearance of the ‘pRBC?‘ flag. Without the activation of this flag, the reported results can lead to incorrect results such as false high neutrophils or eosinophils when schizonts and/or gametocytes are present. Even a small number of infected RBCs with these larger forms may have a significant impact on the differential count, as the concentration of RBCs is a thousand-fold higher than that of WBCs. Once the flag is activated, the neutrophil and eosinophil counts are corrected to the accurate values. In the WNR scattergram the ghost population consisting also of cell debris of parasitised RBCs did not interfere with the WBC population, and thus the correct WBC count is reported.

In the RET scattergram, parasitised RBCs (trophozoites) were visible as a distinct cell population with intermediate fluorescence interfering with reticulocytes. The ring-form trophozoites interfere in the area of relatively mature reticulocytes (low fluorescence reticulocytes, LFR) and lead to falsely increased values of RET and LFR parameters resulting in a falsely decreased value of immature reticulocyte fraction (IRF). The interference usually causes a pseudo-reticulocytosis with low IRF values. This combination is clinically not possible and should flag the results as unreliable. However, in the presented case – due to the low basal erythropoiesis rate – these RET channel-derived parameters are not significantly different from their normal values.

Furthermore, the patient had anaemia, moderate thrombocytopenia and leukocytosis. The reason for the increased WBC count was an abnormally high count of neutrophils, which, together with increased fluorescence of the neutrophil population (NEUT-RI = 51.8 FI, compared to the normal value of around 45 FI), indicates the possibility of a concomitant bacterial infection in the patient. The WDF scattergram also revealed the presence of immature granulocytes, which indicates depletion of the neutrophil pool in the peripheral blood during a prolonged infection. The high immature platelet fraction value (IPF) was also supporting the diagnosis of a co-infection beside the malaria infection.  

The final diagnosis of malaria was confirmed by the microscopic examination of blood film, and the bacterial infection was confirmed by a positive blood culture. 

Literature

  1. World Health Organization (2015): Malaria
    http://www.who.int/mediacentre/factsheets/fs094/en/
  2.  Tilley L, Dixon MW, Kirk K (2011): The Plasmodium falciparum-infected red blood cell. Int J Biochem Cell Biol. 43(6):839-42. 

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