Abstract
Microvascular sequestration of Plasmodium falciparum underlies cerebral malaria. Despite suggestive ex vivo evidence, this phenomenon has not been convincingly demonstrated in coma complicating Plasmodium vivax malaria. Severely-ill Papua New Guinean children with mixed P. falciparum/P. vivax infections are more likely to develop cerebral malaria and die than those with P. falciparum alone, possibly reflecting P. vivax sequestration. Nested PCR was performed on post mortem brain tissue from three such children dying from cerebral malaria due to mixed-species infections. No P. vivax DNA was detected. These findings do not support the hypothesis that P. vivax sequestration occurs in human brain.
Highlights
Plasmodium vivax accounts for nearly half of all malaria infections and is recognized as a cause of complications and death [1]
There was no evidence for cerebral sequestration of P. vivax in any of the three cases despite microscopic and/or molecular confirmation that this parasite was present in peripheral blood at presentation
This suggests that she had a synchronous infection with either maturing parasite forms starting to cytoadhere, or maturation and rupture of schizonts just before presentation
Summary
Plasmodium vivax accounts for nearly half of all malaria infections and is recognized as a cause of complications and death [1]. There is no convincing evidence of a similar phenomenon in post mortem brain specimens from patients with P. vivax, but available data are few and from studies in which interpretation of the histopathologic features is confounded by issues such as the possibility of unrecognized mixed-species infections [5]. Cerebral malaria was defined as a Blantyre Coma Score ≤2 with Plasmodium DNA detected in peripheral blood by nPCR [2], irrespective of the presence and/or species of asexual parasites by microscopy.
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