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

Post-malaria neurological syndrome (PMNS) defined by a post-infective encephalopathy occurring within 2 months after an episode of Plasmodium falciparum infection is still a debated entity. We describe 2 cases of PMNS in 2 patients of African origin, born and living in France. Both patients had severe P. falciparum infection, followed by PMNS. They recovered with no sequelae. These are the first-reported cases of PMNS in patients of African ethnicity and living in France.
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PMID:Post-malaria neurological syndrome--two cases in patients of African origin. 1845 99

Certain distinctive components of the severe systemic inflammatory syndrome are now well-recognized to be common to malaria, sepsis, viral infections, and post-trauma illness. While their connection with cytokines has been appreciated for some time, the constellation of changes that comprise the syndrome has simply been accepted as an empirical observation, with no theory to explain why they should coexist. New data on the effects of the main pro-inflammatory cytokines on the genetic control of sickness behaviour can be extended to provide a rationale for why this syndrome contains many of its accustomed components, such as reversible encephalopathy, gene silencing, dyserythropoiesis, seizures, coagulopathy, hypoalbuminaemia and hypertriglyceridaemia. It is thus proposed that the pattern of pathology that comprises much of the systemic inflammatory syndrome occurs when one of the usually advantageous roles of pro-inflammatory cytokines--generating sickness behaviour by moderately repressing genes (Dbp, Tef, Hlf, Per1, Per2 and Per3, and the nuclear receptor Rev-erbalpha) that control circadian rhythm--becomes excessive. Although reversible encephalopathy and gene silencing are severe events with potentially fatal consequences, they can be viewed as having survival advantages through lowering energy demand. In contrast, dyserythropoiesis, seizures, coagulopathy, hypoalbuminaemia and hypertriglyceridaemia may best be viewed as unfortunate consequences of extreme repression of these same genetic controls when the pro-inflammatory cytokines that cause sickness behaviour are produced excessively. As well as casting a new light on the previously unrationalized coexistence of these aspects of systemic inflammatory diseases, this concept is consistent with the case for a primary role for inflammatory cytokines in their pathogenesis across this range of diseases.
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PMID:Sickness behaviour pushed too far--the basis of the syndrome seen in severe protozoal, bacterial and viral diseases and post-trauma. 1885 46

The neurologic symptoms in malaria are usually associated with a severe infection by Plasmodium falciparum. Less frequently, the presence of impaired consciousness, seizures and visual and auditory deficits is related with hypoglycemia (by malaria or quinine) or with the toxicity of anti-malarial drugs. In the last years, it was recognized a rare neurologic complication after the efficient treatment of Plasmodium falciparum malaria - post-malaria neurologic syndrome (PMNS). PMNS occurs days to weeks after the parasite clearance, presenting as an encephalopathy of variable severity. The pathogenic mechanisms involved in PMNS are not well understood, being admitted a possible immunological cause. We describe a case of a 61-year-old man presenting with a severe encephalopathy (delirium, cerebellar ataxia and ophthalmoparesis ), 2 days after complete recovery from Plasmodium falciparum malaria. Peripheral blood smears were repeatedly negative for malaria parasites. MRI during acute phase showed extensive multifocal white matter abnormalities. He was treated with high-dose methylprednisolone with complete resolution of neurological deficits. After 9 months the MRI showed minimal residual lesions.
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PMID:[Post-malaria neurologic syndrome]. 1909 16

Two cases of a one and 4 year old child of plasmodium vivax malaria are reported in association with CNS complications. Both presented with encephalopathy and seizures. One had severe thrombocytopenia, massive intracranial bleed and hydrocephalus requiring shunt surgery while the other had gastrointestinal manifestations, encephalopathy and hydrocephalus. Both responded to quinine but are left with sequelae.
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PMID:Plasmodium vivax malaria presenting with severe thrombocytopenia, cerebral complications and hydrocephalus. 1939 Jul 98

Cerebral malaria is a diffuse encephalopathy associated with seizures and status epilepticus which can occur in up to one-third of patients with severe malaria, particularly that caused by Plasmodium falciparum. In this article, we report three cases of Plasmodium vivax malaria (all adult male patients) complicated by seizures and symptoms of diffuse meningoencephalitis. Two patients had predominantly meningeal signs, while in the third patient the features were purely of encephalitis All cases were treated with artesunate. Usually, cerebral malaria is caused by P. falciparum, and rarely, cerebral malaria is a presenting complication or occurs during the course of P. vivax infection.
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PMID:Cerebral malaria caused by Plasmodium vivax in adult subjects. 1974 68

Cerebral malaria is an acute encephalopathy evolving from an infection with Plasmodium falciparum which kills more than one million people each year. Brain tissues from patients who died with cerebral malaria revealed multifocal capillary obstruction by parasitised red blood cells, platelets, and leukocytes. Many studies are unified in their proposal of two major hypotheses consisting of cell adhesion to the brain endothelium and excessive immune stimulation resulting in further vascular inflammation, prothrombotic cell activation, mechanical obstruction of cerebral capillaries and, consequently, blood-brain barrier disruption. Platelets and endothelial cells communicate on multiple levels. Infection-induced changes in platelets and endothelial cells occur in cerebral malaria, resulting in their concomitant activation, increased interactions between these two cell types, and a secondary procoagulant or hypercoagulable state. Here we review evidence for these mechanisms and highlight the possible role of platelets as effectors of endothelial damage in cerebral malaria. A better understanding of the complex regulation of these various interactions between brain endothelial cells and platelets in the context of cerebral malaria may prove useful in the development of new approaches to the treatment of this disease.
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PMID:Platelet-endothelial cell interactions in cerebral malaria: the end of a cordial understanding. 1996 39

In January 2007, an outbreak of Rift Valley fever (RVF) was detected among humans in northern Tanzania districts. By the end of the outbreak in June, 2007, 511 suspect RVF cases had been recorded from 10 of the 21 regions of Tanzania, with laboratory confirmation of 186 cases and another 123 probable cases. All confirmed RVF cases were located in the north-central and southern regions of the country, with an eventual fatality rate of 28.2% (N = 144). All suspected cases had fever; 89% had encephalopathy, 10% hemorrhage, and 3% retinopathy. A total of 169 (55%) of the 309 confirmed or probable cases were also positive for malaria as detected by peripheral blood smear. In a cohort of 20 RVF cases with known outcome that were also positive for human immunodeficiency virus, 15 (75%) died. Contact with sick animals and animal products, including blood, meat, and milk, were identified as major risk factors of acquiring RVF.
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PMID:Epidemiologic and clinical aspects of a Rift Valley fever outbreak in humans in Tanzania, 2007. 2068 2

We report a case of a 37-year-old patient with Plasmodium falciparum infestation who developed posterior reversible encephalopathy. In cerebral malaria, microscopic studies have shown endothelial dysfunction and disruption of the blood-brain barrier. Data from the literature show that one of the mechanisms of posterior reversible encephalopathy may be capillary leakage and acute disruption of the blood-brain barrier. Our case supports the theory of blood-brain barrier disruption being a key factor in the causation of cerebral malaria.
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PMID:Posterior reversible encephalopathy syndrome in neuro-malaria. 2104 44

A common clinical presentation of Plasmodium falciparum is parasitemia, complicated by an encephalopathy for which other explanations cannot be found, termed cerebral malaria-an important cause of death in young children in endemic areas. Our objective was to study hepatic histopathology in Malawian children with fatal encephalopathy, with and without P falciparum parasitemia, to assess the contributions of severe malaria. We report autopsy results from a series of 87 Malawian children who died between 1996 and 2008. Among 75 cases with P falciparum parasitemia, 51 had intracerebral sequestered parasites, whereas 24 without sequestered parasites had other causes of death revealed by autopsy including 4 patients with clinicopathologic findings which may represent Reye syndrome. Hepatic histology in parasitemic cases revealed very limited sequestration of parasites in hepatic sinusoids, even in cases with extensive sequestration elsewhere, but increased numbers of hemozoin-laden Kupffer cells were invariably present with a strong association with histologic evidence of cerebral malaria by quantitative analysis. Of 12 patients who were consistently aparasitemic during their fatal illness, 5 had clinicopathologic findings which may represent Reye syndrome. Hepatic sequestration of parasitized erythrocytes is not a feature of fatal malaria in Malawian children, and there is no structural damage in the liver. Reye syndrome may be an important cause of fatal encephalopathy in children in Malawi with and without peripheral parasitemia and warrants close scrutiny of aspirin use in malaria-endemic areas.
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PMID:Liver pathology in Malawian children with fatal encephalopathy. 2139 81

Accurate diagnosis of cerebral malaria (CM) is important for patient management, epidemiological and end point surveillance, and enrolling patients with CM in studies of pathogenesis or therapeutic trials. In malaria-endemic areas, where asymptomatic Plasmodium falciparum parasitemia is common, a positive blood film in a comatose individual does not prove that the coma is due to malaria. A retinopathy consisting of two unique features - patchy retinal whitening and focal changes of vessel color - is highly specific for encephalopathy of malarial etiology. White-centered retinal hemorrhages are a common but less specific feature. Either indirect or direct ophthalmoscopy can be used to identify the changes, and both procedures can be learned and practiced by nonspecialist clinicians. In view of its important contributions to both clinical care and research, examination of the retina should become a routine component of the assessment of a comatose child or adult when CM is a possible diagnosis.
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PMID:Redefining cerebral malaria by including malaria retinopathy. 2144 44


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