Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral malaria (CM) is one of the severe complications of Plasmodium infection. In murine models of CM, Talphabeta cells have been implicated in the neuropathogenesis. To obtain insights into the TCRB repertoire during CM, we used high throughput CDR3 spectratyping and set up new methods and software tools to analyze data. We compared PBL and spleen repertoires of mice infected with Plasmodium berghei ANKA that developed CM (CM(+)) or not (CM(-)) to evidence modifications of the TCRB repertoire associated with neuropathology. Using distinct statistical multivariate methods, the PBL repertoires of CM(+) mice were found to be specifically altered. This alteration is partly due to recurrently expanded T cell clones. Strikingly, alteration of the PBL repertoire can be used to distinguish between CM(+) and CM(-). This study provides the first ex vivo demonstration of modifications of Talphabeta cell compartment during CM. Finally, our original approach for deciphering lymphocyte repertoires can be transposed to various pathological conditions.
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PMID:A profound alteration of blood TCRB repertoire allows prediction of cerebral malaria. 1538 90

Inflammatory cytokines play an important role in human immune responses to malarial disease. However, the role of these mediators in disease pathogenesis, and the relationship between host protection and injury remains unclear. A total of 248 cases of severe Plasmodium falciparum malaria among children aged 3 months to 14 years residing in Bandiagara, Mali, were matched to cases of uncomplicated malaria and healthy controls. Using modified World Health Organization criteria for defining severe malaria, we identified 100 cases of cerebral malaria (coma, seizure, and obtundation), 17 cases of severe anemia (hemoglobin, <5 g/dl), 18 cases combined cerebral malaria with severe anemia, and 92 cases with hyperparasitemia (asexual trophozoites, >500,000/mm3). Significantly elevated levels (given as geometric mean concentrations in picograms/milliliter) of interleukin-6 (IL-6; 485.2 versus 54.1; P = <0.001), IL-10 (1,099.3 versus 14.1; P = <0.001), tumor necrosis factor alpha (10.1 versus 7.7; P = <0.001), and IL-12(p70) (48.9 versus 31.3; P = 0.004) in serum were found in severe cases versus healthy controls. Significantly elevated levels of IL-6 (485.2 versus 141.0; P = <0.001) and IL-10 (1,099.3 versus 133.9; P = <0.001) were seen in severe malaria cases versus uncomplicated malaria controls. Cerebral malaria was associated with significantly elevated levels of IL-6 (754.5 versus 311.4; P = <0.001) and IL-10 (1,405.6 versus 868.6; P = 0.006) compared to severe malaria cases without cerebral manifestations. Conversely, lower levels of IL-6 (199.2 versus 487.6; P = 0.03) and IL-10 (391.1 versus 1,160.9; P = 0.002) were noted in children with severe anemia compared to severe malaria cases with hemoglobin at >5 g/dl. Hyperparasitemia was associated with significantly lower levels of IL-6 (336.6 versus 602.1; P = 0.002). These results illustrate the complex relationships between inflammatory cytokines and disease in P. falciparum malaria.
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PMID:Serum levels of the proinflammatory cytokines interleukin-1 beta (IL-1beta), IL-6, IL-8, IL-10, tumor necrosis factor alpha, and IL-12(p70) in Malian children with severe Plasmodium falciparum malaria and matched uncomplicated malaria or healthy controls. 1538 60

Cerebral malaria with Plasmodium vivax is uncommon. Normally Plasmodium falciparum is the cause of cerebral malaria. We report about a 18 year old patient from Pakistan with a history of intermittent fever for several months. The patient recovered within a few days; however prognosis can be severe when cerebral malaria is complicating the course of Plasmodium vivax infection.
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PMID:[Status febrilis and unconsciousness]. 1565 21

Cerebral malaria is one of the most serious complications of Plasmodium falciparum infection. Its diagnosis may sometimes be difficult. We report the case of a 63-year-old woman who presented with abdominal pain and nausea, rapidly followed by delirium and stupor, a few days after a travel in Africa. No prophylactic measures were prescribed. The main clinical features concerning cerebral malaria, diagnostic tools and therapeutic measures are discussed.
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PMID:[Imported cerebral malaria]. 1567 9

Malaria remains the most important parasitic disease worldwide. Falciparum malaria is a medical emergency and requires immediate diagnosis and treatment. Cerebral malaria is a rapidly progressive, potentially fatal complication of Plasmodium falciparum infection. This case, including post-mortem observations, histology, and laboratory diagnosis, emphasizes the necessity of appropriate advice regarding malaria prophylaxis before travel to an endemic area. Malaria should always be considered in the differential diagnosis of patients presenting with fever and/or nonspecific flu-like symptoms after traveling to endemic countries.
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PMID:Fulminant cerebral malaria in a Swiss patient. 1575 Jul 58

Neurologic morbidities seen in the children's emergency facility of the University of Benin Teaching Hospital, Nigeria, over a five-year period (July 1996-June 2001) was evaluated to determine the pattern and outcome. Notes and ward records of patients with neurologic morbidities were retrieved. Data obtained from these sources include age, sex principal diagnosis, duration of stay and outcome. Six-hundred-four out of 3,868 patients (15.6%) had neurologic morbidity. Children five years of age and under were 466 (77.2%), and modal age group was 1-2 years. Febrile convulsion was the most common neurologic morbidity seen (35.1%) followed by cerebral malaria (28.0%) and then meningitis (27.0%). An increased incidence of cases occurred during the rainy season. Sixty-four out of 406 with complete records (15.8%) died. Forty-seven (67.2%) died within 24 hours of admission. Cerebral malaria and meningitis accounted for all the deaths. Preventable infectious diseases are the major causes of emergency neurologic morbidities and mortality. The majority die within 24 hours largely due to a delay in presentation to the hospital. Effective malaria control and prevention of meningitis would reduce the incidence of neurologic morbidities and, if this is coupled with health education of the populace on the importance of attending health facility early, mortality from these causes would be greatly reduced.
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PMID:Pattern of emergency neurologic morbidities in children. 1587 Nov 44

Cerebral malaria is an important cause of morbidity and mortality in many parts of the world. It has been suggested that cerebral malaria is associated with reduced perfusion due to the blockage of blood vessels by parasitized erythrocytes; although, no quantitative validation of this has been done. We infected C57BL/6 mice with the ANKA strain of Plasmodium berghei and on day 6 of infection we investigated alterations in brain function using arterial spin labeling MRI and proton MRS. MR images did not demonstrate signs of damage. However, there was a significant reduction in cerebral blood flow (P<0.012) and the ratio of N-acetyl-aspartate (NAA) to creatine (Cr) (P<0.01) relative to non-infected mice. The NAA/Cr ratios were significantly correlated with cerebral perfusion (r=0.87) suggesting a relationship between impaired oxygen delivery and neuronal dysfunction. Pathological examination revealed accumulations of damaged axons providing a correlate for the decreased NAA/Cr ratio in infected mice. This murine model will permit non-invasive studies of neurologic function during malarial infection.
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PMID:Reduced cerebral blood flow and N-acetyl aspartate in a murine model of cerebral malaria. 1591 69

Cerebral malaria occurs in 2% of patients infected by Plasmodium falciparum. Magnetic resonance imaging findings of small white matter infarcts due to cerebral malaria have been previously reported, however nonspecific. Since diffusion-weighted imaging can differentiate acute embolic infarcts from other chronic or nonspecific white matter lesions, it may aid diagnosis of this illness in patients who travel to endemic areas.
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PMID:Diffusion-weighted imaging of cerebral malaria. 1595 12

Several neurological complications are associated with severe falciparum malaria. Cerebral malaria is one of the most life-threatening complications. A few patients may experience a neurological syndrome after complete recovery from Plasmodium falciparum infection. In the literature especially the postmalaria neurological syndrome (PMNS), acute disseminated encephalomyelitis (ADEM) and delayed cerebellar ataxia have been reported. We describe a case of a 53-year-old woman who was readmitted after an adequately treated P. falciparum infection with word-finding difficulties, confusion and tremor. Peripheral blood smears were repeatedly negative for malarial parasites. The clinical features best fitted a PMNS. Because of the severity of the syndrome she was treated with high-dose prednisone. She recovered completely. The possibility of ADEM is also discussed. Aetiology of these syndromes is still unknown, but it could be mediated by an immunological mechanism. PMNS or ADEM must be considered when neurological signs and symptoms occur after recovery from a P. falciparum infection.
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PMID:Neurological complications following Plasmodium falciparum infection. 1595 88

Sequestration of malaria-parasite-infected erythrocytes in the microvasculature of organs is thought to be a significant cause of pathology. Cerebral malaria (CM) is a major complication of Plasmodium falciparum infections, and PfEMP1-mediated sequestration of infected red blood cells has been considered to be the major feature leading to CM-related pathology. We report a system for the real-time in vivo imaging of sequestration using transgenic luciferase-expressing parasites of the rodent malaria parasite Plasmodium berghei. These studies revealed that: (i) as expected, lung tissue is a major site, but, unexpectedly, adipose tissue contributes significantly to sequestration, and (ii) the class II scavenger-receptor CD36 to which PfEMP1 can bind is also the major receptor for P. berghei sequestration, indicating a role for alternative parasite ligands, because orthologues of PfEMP1 are absent from rodent malaria parasites, and, importantly, (iii) cerebral complications still develop in the absence of CD36-mediated sequestration, dissociating parasite sequestration from CM-associated pathology. Real-time in vivo imaging of parasitic processes may be used to evaluate the molecular basis of pathology and develop strategies to prevent pathology.
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PMID:Murine malaria parasite sequestration: CD36 is the major receptor, but cerebral pathology is unlinked to sequestration. 1605 2


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