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Cerebral malaria is an unusual and treatable cause of stupor and coma, and it can present suddenly in a healthy person. It is diagnosed by finding parasites on a blood smear and is treated either with chloroquine or with quinine, pyrimethamine, and sulfadiazine.
BACKGROUNDFeatures of consumptive coagulopathy and thromboinflammation are prominent in cerebral malaria (CM). We hypothesized that thrombogenic autoantibodies contribute to a procoagulant state in CM.METHODSPlasma from children with uncomplicated malaria (UM) (n = 124) and CM (n = 136) was analyzed by ELISA for a panel of 8 autoantibodies including anti-platelet factor 4/polyanion (anti-PF4/P), anti-phospholipid, anti-phosphatidylserine, anti-myeloperoxidase, anti-proteinase 3, anti-dsDNA, anti-β-2-glycoprotein I, and anti-cardiolipin. Plasma samples from individuals with nonmalarial coma (NMC) (n = 49) and healthy controls (HCs) (n = 56) were assayed for comparison. Associations with clinical and immune biomarkers were determined using univariate and logistic regression analyses.RESULTSMedian anti-PF4/P and anti-PS IgG levels were elevated in individuals with malaria infection relative to levels in HCs (P < 0.001) and patients with NMC (PF4/P: P < 0.001). Anti-PF4/P IgG levels were elevated in children with CM (median = 0.27, IQR: 0.19-0.41) compared with those with UM (median = 0.19, IQR: 0.14-0.22, P < 0.0001). Anti-PS IgG levels did not differ between patients with UM and those with CM (P = 0.39). When patients with CM were stratified by malaria retinopathy (Ret) status, the levels of anti-PF4/P IgG correlated negatively with the peripheral platelet count in patients with Ret+ CM (Spearman's rho [Rs] = 0.201, P = 0.04) and associated positively with mortality (OR = 15.2, 95% CI: 1.02-275, P = 0.048). Plasma from patients with CM induced greater platelet activation in an ex vivo assay relative to plasma from patients with UM (P = 0.02), and the observed platelet activation was associated with anti-PF4/P IgG levels (Rs= 0.293, P = 0.035).CONCLUSIONSThrombosis mediated by elevated anti-PF4/P autoantibodies may be one mechanism contributing to the clinical complications of CM.
Neuropathologic examination of 19 fatal cases of cerebral malaria and a review of the literature showed that the epidemiologic, clinical, and pathologic features of this entity suggest consideration of cerebral malaria as a form of disseminated vasculomyelinopathy, a hyperegic reaction of the CNS to the antigenic challenge of Plasmodium falciparum infection. Experimental evidence also substantiates this view The initial event seems to be vasculopathy, with alteration of the endothelial permeability, followed by brain edema, perivascular infiltrates and ring hemorrhages, perivascular demyelination, and gliosis (malarial granuloma) in the late stages. This chain of events could be interrupted early in its course by corticosteroids. Parenteral dexamethasone should then be seriously considered at the first signs of involvement of the CNS during P falciparum malaria along with the standard forms of antimalarial therapy.
In an outbreak of Plasmodium falciparum malaria following refeeding after famine cerebral malaria was restricted to children eating grain. Nomad children consuming a predominantly milk diet were free of this complication despite an equivalent incidence of uncomplicated malaria. Freedom of nomads from cerebral complications may be due to inhibition by the milk diet of rapid division of the parasite combined with delayed recovery after famine of T cell function.
Transmission and scanning electron microscopy of hamster cerebral malaria show that haemorrhages occur following vessel necrosis in animals with low parasitaemias. There is no concurrent thrombosis nor packing of capillaries with parasitised erythrocytes. Small vessels contain numerous monocytes which have phagocytosed erythrocytes and smaller particles of similar electron density. The monocytes attach to and migrate through the endothelium but then remain in close proximity to the vessels. Irregular dense deposits are present in the basement membrane of some animals 14 days after infection. These may be immune complexes. The pathogenesis of cerebral malaria is discussed in relation to these findings.
A patient with cerebral malaria complicated by full-blown DIC, after failing to respond to other forms of treatment, was successfully treated by exchange transfusion. To the best of the authors' knowledge, this may be first reported case of full-blown DIC in malaria successfully treated by exchange transfusion.
Report and comments on one case of cerebral malaria with myocardial infarction, icterus and renal insufficiency, and of another one with a black-water-like syndrome with complete recovery under quinine treatment.
Report of a typical case of cerebral malaria with coma during 3 days, pneumopathy and renal insufficiency with failure of concentration. The delivery of a dead foetus has been started by prostaglandines.
The authors report the results of indirect immunofluorescent technique used for detecting malarial antibodies in the cerebrospinal fluid and serum of 126 African patients suspected of cerebral malaria from infection with Plasmodium falciparum. Almost all of them were less than 15 years old and were living in urban unstable hypoendemic areas. Malarial antibodies, mainly IgG, were found in about 25 0/0 of cerebrospinal fluid samples, whether the patients were admitted for malaria or for any other disease. Malarial antibodies were more frequently found in cerebrospinal fluid of patients over 2 years old and in those not treated with antimalarial drugs before hospitalization. No correlation was found between serum antibody level, parasitemia, splenomegaly, clinical form, precocity of blood collection and malarial antibodies in the cerebrospinal fluid. The results concerning serum antibodies corroborate previous works.
Four fatal cases of cerebral Plasmodium falciparum malaria in English travellers returning from Africa have been seen in the last 13 years. The haemorrhages, accumulations of microglia, and destruction of cerebral white matter around small veins as a result of blockage of cortical capillaries by parasitised red blood corpuscles resemble the effect of fat embolism. Microglia in the lesions is demonstrated by special neuropathological techniques. Attention is drawn to the need for a prompt recognition of malaria since appropriate treatment can be successful.
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The authors report one case of transfusion induced falciparum cerebral malaria. Among the parasites responsible for transfusion malaria, Plasmodium falciparum is rarely implicated, but may be accompanied by serious complications. Different ways of artificial transmission of the parasites are reported. Clinical findings are few, so the examination of blood films is essential for diagnostic. The dangerous blood donor must be identified by immunofluorescent methods. The specific treatment is quinine for cerebral malaria or chloroquine in other cases.