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Background  Severe anaemia can develop in the aftermath of  Plasmodium falciparum  malaria because of protracted bone marrow suppression, possibly due to residual subpatent parasites.    Materials and methods  Blood was collected from patients with recent malaria and negative malaria microscopy. Detection of the  Plasmodium  antigens, lactate dehydrogenase (Optimal ® ), aldolase and histidine rich protein 2 (Now malaria ® ) were used to differentiate between patients with (1) no malaria, (2) recent cleared malaria, (3) persistent  P. falciparum  infection. Red cell distribution width (RDW), plasma levels of soluble transferrin receptor (sTfR) and erythropoietin (EPO) were measured as markers of erythropoiesis. Interleukin (IL) 10 and tumour necrosis factor (TNF)α were used as inflammation markers.    Results  EPO was correlated with haemoglobin, irrespective of malaria (R = -0.36, P < 0.001). Persistent  P. falciparum  infection, but not recent malaria without residual parasites, was associated with bone marrow suppression i.e., low RDW (P < 0.001 vs. P = 0.56) and sTfR (P = 0.02 vs. P = 0.36). TNF-α and IL-10 levels were not associated with bone marrow suppression.    Conclusion  In the treatment of malaria, complete eradication of parasites may prevent subsequent development of anaemia. Severely anaemic children may benefit from antimalarial treatment if antigen tests are positive, even when no parasites can be demonstrated by microscopy.

malaria journal

Bone marrow suppression and severe anaemia associated with persistent Plasmodium falciparum infection in African children with microscopically undetectable parasitaemia