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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral malaria is the most important manifestation of severe Plasmodium falciparum infection. The clinical picture in South East Asian adults differs from that in African children. The children are more likely to have abnormal brain stem reflexes, signs suggestive of cerebral herniation, and raised CSF opening pressure, and to suffer persistent neurological sequelae. The mortality remains high at about 20%. The diagnosis must be considered in all patients with fever and impaired consciousness who may have been exposed to the infection. The pathophysiology of cerebral malaria may involve mechanical obstruction of the cerebral circulation by parasitized erythrocytes which have adhered to the vascular endothelium. Cytokines such as tumor necrosis factor may also contribute. The most important element of treatment is early, optimal chemotherapy with quinine, but artemisinine derivatives may prove even more effective.
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PMID:Cerebral malaria. 161 97

Out of 604 Gambian children admitted with falciparum malaria to one hospital between September and December, 1988, 308 had cerebral malaria and 203 were severely anaemic (haemoglobin less than 60 g/l). 14% of those with cerebral malaria died, as did 7.8% of those with severe anaemia. 32 (12%) of children surviving cerebral malaria had residual neurological deficit. 69 other children were admitted with clinical features strongly suggestive of cerebral malaria but with negative blood films; 16 of these died and 3 had residual neurological deficits. The commonest sequelae of cerebral malaria were hemiplegia (23 cases), cortical blindness (11), aphasia (9), and ataxia (6). Factors predisposing to sequelae included prolonged coma, protracted convulsions, severe anaemia, and a biphasic clinical course characterised by recovery of consciousness followed by recurrent convulsions and coma. At follow up 1-6 months later over half these children had made a full recovery, but a quarter were left with a major residual neurological deficit. Cerebral malaria in childhood may be an important cause of neurological handicap in the tropics.
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PMID:Neurological sequelae of cerebral malaria in children. 197 27

Cerebral malaria is a rapidly progressive encephalopathy with up to 50% mortality. A cardinal feature is the massing of red cells containing mature Plasmodium falciparum within the cerebral capillaries. Adhesion of these parasitised red cells to endothelium, an event which may initiate cerebral malaria, is being studied at the molecular level. However, the relevance of these studies to the pathophysiology and treatment of human cerebral malaria is uncertain. Although chloroquine is still widely used to treat falciparum malaria, resistance has spread to most of the endemic zone. Quinine is emerging as the only effective treatment for cerebral malaria, though resistance to this drug threatens to become a problem. Alternative drugs are urgently needed.
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PMID:Cerebral malaria in children. 167 Nov 39

Eleven patients with 14 episodes of malaria have been admitted to Kaohsiung Medical College Hospital in the past 10 years and have been evaluated in this study. All of the patients were male and had traveling history to Africa or Southeast Asia. Eight of them were suffering from falciparum malaria and three vivax malaria. Initially they were treated with chloroquine (900 mg + 300 mg x 2 d) and primaquine (15 mg x 14 d). Quinine (650 mg q8h x 7-10 d) was used in one severe and another reinfected case of falciparum malaria. Cerebral malaria was noted in two falciparum cases with good response to treatment. One severe patient who also suffered from black water fever died of acute renal failure, even though quinine had been given immediately. It is concluded that chloroquine combined with primaquine is effective and safe in the treatment of vivax and falciparum malaria in Taiwan. Quinine should be given as soon as possible in a severe case of falciparum malaria. Supportive management and basic knowledge of epidemiology is also very important in the medical treatment of malaria.
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PMID:Medical treatment of malaria. 205 64

This paper is a description of the clinical features of cerebral malaria in children, based on the author's experience in a study of this disease in Malawi, Africa. The presenting symptoms, physical signs and laboratory features are described, and the course of the illness during treatment is outlined. Cerebral malaria can resemble many other childhood illnesses; accurate diagnosis is essential if correct treatment is to be provided quickly. Even with optimal treatment the mortality is about 20%, and some children are left with neurological sequelae.
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PMID:The clinical features of cerebral malaria in children. 236 51

Three cases of cerebral malaria during pregnancy are described. One patient had intrauterine foetal death and died, one patient delivered a dead baby and the other had severe postpartum haemorrhage. Cerebral malaria worsens the outlook both for the mother and for the foetus.
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PMID:Cerebral malaria in pregnancy. 269 87

Cerebral malaria is thought to involve specific attachment of Plasmodium falciparum-infected knobby red cells to venular endothelium. The nature of surface ligands on host endothelial cells that may mediate cytoadherence is poorly understood. We have investigated the effects of soluble thrombospondin, rabbit antiserum raised against thrombospondin, and human immune serum on cytoadherence of parasitized erythrocytes in ex vivo mesocecum vasculature. Preincubation of infected red cells with soluble thrombospondin or human immune serum inhibits binding of infected red cells to rat venular endothelium. Infusion of the microcirculatory preparation with rabbit antithrombospondin antibodies before perfusion of parasitized erythrocytes also resulted in decreased cytoadherence. In addition, incubation of infected cells with human immune sera obtained from malaria patients significantly inhibited the observed cytoadherence. Our results indicate that thrombospondin mediates binding of infected red cells to venular endothelium and may thus be involved in the pathogenesis of cerebral malaria.
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PMID:Thrombospondin mediates the cytoadherence of Plasmodium falciparum-infected red cells to vascular endothelium in shear flow conditions. 327 76

Cerebral malaria is a major form of complicated malaria consequent upon cerebral damage associated with endothelial cell necrosis. We have used assays of Plasmodium falciparum growth inhibition in vitro to study serum inhibitory factors in patients with cerebral malaria. Serum from children with cerebral malaria inhibited parasite growth in a non-synchronised 72-hour assay to a greater extent than did sera from immune adults or asymptomatic children (p less than 0.001). The high level of non-specific inhibition of parasite growth was particularly evident when sera were tested against three P. falciparum isolates, and contrasted with the inhibitory effect of sera from non-malaria febrile controls. In this study, serum from patients with cerebral malaria was more inhibitory than serum from the other groups (p less than 0.001) and its between-isolate variation, when tested against a panel of P. falciparum isolates in growth assays, was significantly less than that of the other groups tested (p less than 0.005). These results are consistent with the hypothesis of toxin-induced endothelial cell damage, with the sequence of pathogenic events involving host-derived serum factors capable of damaging P. falciparum.
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PMID:Characterisation of the host response to Plasmodium falciparum infection. I. Cerebral malaria. 353 66

Cerebral malaria with psychosomatic manifestations is one aspect of malaria which may be mistaken for mental illness. However, the psychosomatic aspects of the disease also relate to the biological, psychological and social influences which may determine changes in disease incidence and distribution. The history of the Global Malaria Eradication Campaign and the resurgence of malaria in many countries of the world have influenced attitudes and the professional milieu in which present day malaria control programmes seek to operate. The individual in a malarious area may obstruct malaria control operations by refusing to allow indoor spraying or to take prophylactic medication. Cultural beliefs often described the history of malaria in a community and the way in which the community had come to terms with this disease. Socio-economic development and population movement may disturb this equilibrium and result in a rise in malaria incidence. Behavioural habits may increase malaria risk and the degree to which the community is prepared to become involved in malaria control may influence its experience with the disease.
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PMID:Psychosomatics of malaria. 693 66

Cerebral malaria is a fatal complication of infection by Plasmodium falciparum in man. The neurological symptoms that characterize this form of malarial disease are accompanied by the adhesion of infected erythrocytes to the vasculature of the brain. To study this phenomenon in vivo, an acute phase severe combined immunodeficiency (SCID) mouse model was developed in which sequestration of P. falciparum-infected human erythrocytes took place. During acute cerebral malaria in humans, the expression of intercellular adhesion molecule-1 (ICAM-1) is induced in vascular endothelium by inflammatory reactions. Acute phase ICAM-1 expression can also be obtained in SCID mice. The endothelium of the midbrain region was the most responsive to such inflammatory stimulus. It is noteworthy that the reticular formation in the midbrain controls the level of consciousness, and loss of consciousness is a symptom of cerebral malaria. We found that infected human erythrocytes were retained 24 times more than normal erythrocytes in ICAM-1-positive mouse brain. Sequestration to the brain was reduced by anti-ICAM-1 antibodies. These in vivo results were confirmed by the binding of P. falciparum-infected erythrocytes to the ICAM-1-positive endothelium in tissue sections of mouse brain. We conclude that the SCID mouse serves as a versatile in vivo model that allows the study of P. falciparum-infected erythrocyte adhesion as it occurs in human cerebral malaria. Upregulation of ICAM-1 expression in the region of the midbrain correlates with increased retention of malaria-infected erythrocytes and with the symptoms of cerebral malaria.
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PMID:In vivo sequestration of Plasmodium falciparum-infected human erythrocytes: a severe combined immunodeficiency mouse model for cerebral malaria. 765 Apr 76


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