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

The tumor necrosis factor (TNF-alpha) is a cytokine known as a mediator of inflammation and immunity. The genes coding the tumor necrosis factors alpha and beta are considered part of class III major histocompatability complex. The 2 involved genes have been mapped to chromosome 6. Certain mutations in the TNF-alpha gene are believed to be causative for increased production of the cytokine. In this respect, the most common variant is the TNF2 allele, a single nucleotide substitution of guanine by adenine at position -308 relative to the promoter transcription site of the gene. Elevated production of TNF-alpha has been found to be associated with several infectious diseases including malaria. Elevated levels of TNF-alpha have also been observed to associate with increased risk of preterm delivery, chorioamnionitis and fetal morbidity including encephalopathy. The present article reviews the genetics of the cytokine TNF-alpha and discusses its suitability as a candidate marker for assessment of increased risk of preterm delivery and fetal morbidity.
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PMID:The cytokine TNF-alpha. Genetics and suitability for prenatal risks assessment. 1496 5

Malaria represents a continuing and major global health challenge and our understanding of how the Plasmodium parasite causes severe disease and death remains poor. One serious complication of the infection is cerebral malaria, a clinically complex syndrome of coma and potentially reversible encephalopathy, associated with a high mortality rate and increasingly recognised long-term sequelae in survivors. Research into the pathophysiology of cerebral malaria, using a combination of clinical and pathological studies, animal models and in vitro cell culture work, has focussed attention on the blood-brain barrier (BBB). This represents the key interface between the brain parenchyma and the parasite, which develops within an infected red cell but remains inside the vascular space. Studies of BBB function in cerebral malaria have provided some evidence for parasite-induced changes secondary to sequestration of parasitised red blood cells and host leukocytes within the cerebral microvasculature, such as redistribution of endothelial cell intercellular junction proteins and intracellular signaling. However, the evidence for a generalised increase in BBB permeability, leading to cerebral oedema, is conflicting. As well as direct cell adhesion-dependent effects, local adhesion-independent effects may activate and damage cerebral endothelial cells and perivascular cells, such as decreased blood flow, hypoxia or the effects of parasite toxins such as pigment. Finally, a number of systemic mechanisms could influence the BBB during malaria, such as the metabolic and inflammatory complications of severe disease acting 'at a distance'. This review will summarise evidence for these mechanisms from human studies of cerebral malaria and discuss the possible role for BBB dysfunction in this complex and challenging disease.
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PMID:Human cerebral malaria and the blood-brain barrier. 1661 45

Cerebral malaria is a diffuse encephalopathy associated with seizures and status epilepticus which can occur in up to one-third of children with severe malaria, particularly that caused by Plasmodium falciparum. We report a unique case of P. vivax infection complicated by status epilepticus. A 4-year-old boy was admitted to the emergency outpatient clinic with intractable seizures for the previous hour. During resuscitation, two episodes of left-focal tonic convulsions occurred and he received phenytoin. Because of a history of P. vivax infection in the family 3 months previously, a blood slide for malaria was undertaken. Thin blood smears demonstrated P. vivax. He was treated with chloroquine and primaquine. An initial EEG was normal but after 3 months of follow-up a second EEG showed generalised epileptic activity. Rarely, cerebral malaria is a presenting complication or occurs during the course of P. vivax infection. In endemic areas such as Turkey, the possibility of cerebral malaria should be considered.
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PMID:Cerebral malaria owing to Plasmodium vivax: case report. 1670 34

Certain arthropod-borne infections are common in tropical regions because of favorable climatic conditions. Water-borne infections like leptospirosis are common due to contamination of water especially during the monsoon floods. Infections like malaria, leptospirosis, dengue fever and typhus sometimes cause life threatening organ dysfunction and have several overlapping features. Most patients present with classicial clinical syndromes: fever and thrombocytopenia are common in dengue, malaria and leptospirosis; coagulopathy is frequent in leptospirosis and viral hepatitis. Hepatorenal syndrome is seen in leptospirosis, falciparum malaria and scrub typhus. The pulmonary renal syndrome is caused by falciparium malaria, leptospirosis, Hantavirus infection and scrub typhus. Fever with altered mental status is produced by bacterial meningitis, Japanese B encephalitis, cerebral malarial, typhoid encephalopathy and fulminant hepatic failure due to viral hepatitis. Subtle differences in features of the organ failure exist among these infections. The diagnosis in some of these diseases is made by demonstration of antibodies in serum, and these may be negative in the first week of the illness. Hence empiric therapy for more than one disorder may be justified in a small proportion of cases. In addition to specific anti-infective therapy, management of organ dysfunction includes use of mechanical ventilation, vasopressor drugs, continuous renal replacement therapy and blood products. Timely transfer of these patients to well-equipped ICUs with experience in managing these cases can considerably decrease mortality and morbidity.
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PMID:Tropical infections in the ICU. 1694 13

Cerebral malaria is the most common cause of non-traumatic encephalopathy in the world. The mainstay of therapy is either quinine or artemisinin, both of which are effective antimalarials. The clinical picture of cerebral malaria may persist or even become worse in spite of the clearance of parasites from blood. The death rate is unacceptably high even with effective antimalarials in tertiary care hospitals. The mortality increases in presence of multi organ failure (renal failure, jaundice, respiratory distress, severe anaemia, lactic acidosis, etc.). The pathogenesis of cerebral malaria is multifactorial and includes clogging, sequestration, rosette formation, release of cytokines, cerebral oedema, increased intracranial hypertension, etc. Attempts are made to use adjuvant therapy which will act through alternate mechanisms and address one or more of the pathogenetic processes. In this review, we have discussed the role of corticosteroids, pentoxifylline, desferrioxamine, mannitol and newer agents in the treatment of cerebral malaria. Though the literature on adjuvant therapy in cerebral malaria is large enough, there are a number of shortcomings in the clinical trials, many being open and non randomized or of very small sample size. Further research is of utmost importance through large multicentric, double-blind controlled trials to show the efficacy of any of these drugs.
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PMID:Adjuvant therapy in cerebral malaria. 1733 64

In malaria-endemic areas, it is difficult to differentiate between cerebral malaria (CM), bacterial meningitis, and viral encephalitis. We examined the cerebrospinal fluid of 49 children who fulfilled the World Health Organization's (WHO) definition of CM and in 47 encephalopathic children, without malaria, looking for viruses with polymerase chain reaction. In the children with CM, four (9%) had evidence of Herpes simplex virus 1 in the cerebrospinal fluid, whereas in the encephalopathy group without malaria, six (12%) were positive. A significant proportion of children who fulfil the WHO clinical definition of CM may have viral encephalitis.
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PMID:Role of viruses in Kenyan children presenting with acute encephalopathy in a malaria-endemic area. 1717 83

Post-malaria neurological syndrome (PMNS) is a rare complication of malaria. It follows recovery from an episode of Plasmodium falciparum malaria and is characterised by symptoms and signs of encephalopathy. Patients usually improve without any specific treatment. The pathogenesis is unknown, but it is probably immunologically mediated. The objective of this case study is to describe the first Italian patient with PMNS. A 60-year-old Italian man developed acute P. falciparum malaria after a stay in French Guinea. Twenty days after recovering from malaria, he became confused, developed generalised weakness, limb tremors, shivering and dizziness. These symptoms continued for three days, then resolved spontaneously. Neuroimaging was normal. Cerebrospinal fluid analysis revealed breakdown of the blood/brain barrier, without oligoclonal bands and normal IgG index. Our patient presented a mild diffuse encephalopathy suggestive of a generic activation of the immune system without any specific reaction against antigens within the CNS.
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PMID:Post-malaria neurological syndrome: clinical and laboratory findings in one patient. 1720 33

Several neurological complications are associated with severe falciparum malaria. Indeed, some patients experience a neurological syndrome after complete recovery from Plasmodium falciparum infection. Particularly, postmalaria neurological syndrome (PMNS) is a self-limiting post-infective encephalopathy that occurs within 2 months after an episode of P. falciparum infection. We describe the case of a 54-year-old Japanese man who was readmitted to our hospital with incoherent speech and markedly disturbed and uncooperative behavior after a high-grade fever that occurred after an earlier adequately treated severe P. falciparum infection. Peripheral blood smears were repeatedly negative for malaria parasites, no organisms were detected in the cerebrospinal fluid, and no hallmark lesions of acute disseminated encephalomyelitis were depicted by brain magnetic resonance imaging. The neuropsychiatric symptoms were thought to be due to PMNS. The etiology of PMNS remains unclear, but it could be mediated by an immunological mechanism and could possibly be caused by mefloquine treatment. PMNS must be considered when characteristic neurological signs and symptoms such as psychotic or acute confusional episodes, general convulsions, and tremor occur after recovery from severe P. falciparum infection treated with oral mefloquine. This is the first reported case of suspected PMNS in Japan.
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PMID:A case of postmalaria neurological syndrome in Japan. 1723 48

Renal failure and uremic encephalopathy are rare findings in Plasmodium vivax malaria. Thrombocytopenia is also an unusual manifestation of P. vivax malaria. This report highlights the occurrence of these rare manifestations in an 8-year-old boy who presented to us with fever, rash and progressive deterioration of renal functions.
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PMID:Unusual presentation of Plasmodium vivax malaria with severe thrombocytopenia and acute renal failure. 1726 56

We report four cases of encephalopathy admitted with fever, hypercyanosis, breathlessness, deep coma and convulsions considered of interest because these children had cyanotic heart diseases and concomitant cerebral malaria. Their presenting clinical features, which suggested cerebral malaria (decreased level of consciousness ranging in severity from drowsiness and severe headache to confusion, delirium and even deep coma) may equally characterise hypercyanotic episodes among children with uncorrected cyanotic cardiac defects. We also inferred that children with cyanotic cardiac defects may be prone to cerebral malaria and that those residing in the tropics may benefit from anti-malarial prophylaxis.
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PMID:Cerebral malaria in children with cyanotic heart diseases: the need for a closer look. 1837 54


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