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

Those who live in areas where Malaria is endemic, acquire immunity by continuous contact. This immunity cannot be acquired during a short holiday. Children in endemic areas acquire a more severe form of malaria during the period of developing immunity and more often suffer complications like acute hemolytic anemia and, in the case of plasmodium falciparum infection, cerebral malaria. This is a report of 39 cases of cerebral malaria which corresponds to an acute encephslopathy with high temperatures, generalized tonic-clonic spasms and unconsciousness. All children were between 6 months and 5 years old. Cerebral malaria at higher ages is rarely seen in Malawi. But its frequency depends on the intensity of endemic infection and the geographic distribution of the types of malaria. 11 (29%) of the 39 children died. Treatment was with chloroquine against which there was no resistance in East Africa for falciparum infections and with plasmaexpanders. In 1 case permanent neurologic changes a spastic cerebral paresis, were seen. Unconsciousness lasting more than 36 hours appears to be a bad prognostic sign. The CSF is clear and normal except for an occasional rise in protein never higher than 90 mg%.
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PMID:[Malaria in children, with special reference to cerebral malaria (author's transl)]. 110 Aug 97

In a study of neonatal malaria at the University of Benin Teaching Hospital, we documented the features of six neonates in an effort to highlight that the manifestations of malaria in the newborn cannot be readily distinguished from those of neonatal sepsis. Maternal peripartum fever, an important identifiable risk factor for neonatal sepsis, also featured prominently in the mothers of these babies. These mothers ingested pyrimethamine weekly in the course of their pregnancy. All six neonates were critically ill. Their cultures of blood, CSF and urine for bacterial pathogens yielded no growth and they were unresponsive to conventional antibiotics. The diagnosis of malaria should be considered, in spite of regular maternal ingestion of antimalarial prophylaxis with pyrimethamine, in critically ill neonates in malarious areas. All six neonates responded satisfactorily to oral doses of chloroquine. We therefore suggest that a blood film for malaria parasites be included in screening for neonatal sepsis as part of the initial work-up.
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PMID:Malaria parasitaemia in neonates with predisposing risk factors for neonatal sepsis: report of six cases. 128 46

A natural body protein is probably a major cause of the deadliest complication of malaria, a finding that could point toward new methods of treatment. Studies in an experimental model indicate that tumor necrosis factor (TNF), a protein also known as cachectin, is an essential element in highly fatal cerebral malaria. This contention is supported by the following observations. First, during the course of an infection by P. berghei ANKA strain, mice of a CM-susceptible strain express markedly elevated levels of TNF in their serum at the time that neurological signs are evident. Second, in contrast, either mice from nonsusceptible strains, susceptible strains depleted of CD4+ T lymphocytes, or susceptible mice inoculated with malaria organisms incapable of producing CM all fail to express high serum TNF activity. Third, passive immunization against mouse TNF significantly prolong the survival of P. berghei-infected CBA/Ca mice, and prevented the development of neurologic signs to an extent that was highly significant. Treatment with the anti-TNF antibody also prevents the histopathological lesions that are characteristic of CM, i.e. plugging of cerebral vessels by macrophages, lymphoid and parasitized erythrocytes. We have recently shown that this increased TNF release and macrophage accumulation are schematically made of two components, each mediated by different cytokines presumably released by stimulated CD4+ T lymphocytes: (a) a quantitative component: increased accumulation of macrophages results from the concomitant release of IL-3 and GM-CSF, and (b) a qualitative component: macrophage number has not only to be raised, but macrophages need to be activated by IFN-gamma. Thus, CM appears to be the result of a cytokine cascade mediated by the immune response. TNF might also be involved in the pathogenesis of human cerebral malaria. Indeed, we have recently shown that in african children with falciparum malaria, elevated serum concentrations of this molecule are associated with severe neurological involvement and fatal outcome. Clinical trials of treatment with monoclonal anti-TNF antibodies are presently underway in an attempt to reduce mortality and morbidity in african children with cerebral malaria.
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PMID:Essential role of tumor necrosis factor and other cytokines in the pathogenesis of cerebral malaria: experimental and clinical studies. 135 36

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

This study reflects the clinical pattern, diagnosis and management of cerebral malaria in 55 consecutive patients from Chittagong Hill Tracts. The predominant clinical features were: impaired consciousness with convulsion in a febrile patient with temporary residence in the endemic zone. Younger people were more prone to develop this condition. Thirty two patients (58.18%) were between 18-25 years. A high incidence of cerebral malaria was noted in blood group 'O' (37.5%) and group 'B' (33.33%). The malarial parasite count MPC was not proportional to the severity of the disease. Twenty four patients (43.63%) had malarial parasite count below 100% cumm. Anaemia (63.63%) and Jaundice (34.54%) were common, Splenomegaly (7.27%) was uncommon. Clinical features of cerebral oedema/raised intracranial pressure were not evident. CSF study was unremarkable except for raised pressure in 7 patients (12.65%). Response to intravenous quinine was satisfactory and yet the mortality was 11%.
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PMID:Cerebral malaria--an analysis of 55 cases. 209 10

We have studied prospectively the C-reactive protein values in the cerebrospinal fluid of 54 patients with bacterial meningitis, tuberculous meningitis, and severe malarial infection and convulsions without infections of the central nervous system. CSF CRP above 1 mg/l was observed in 23 out of 28 patients with bacterial meningitis (sensitivity of 82%). The specificity was 73% at the 1 mg/l level. Five out of 19 patients with severe malarial infection had CSF CRP levels above 1 mg/l. Two patients with TB meningitis were also studied. Both of them had CSF CRP above 1 mg/l. Five patients with febrile convulsions or sepsis without meningitis had CSF CRP below 1 mg/l. It is concluded that CSF CRP would not be used as a useful discriminatory test in areas where malaria and TB meningitis are common.
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PMID:C-reactive protein and bacterial meningitis. 246 9

A prospective study using a Latex particle agglutination test for the detection of bacterial antigens in CSF has been carried out in 91 patients in Kamuzu Central Hospital, Malawi. The antigens sought were those of Streptococcus pneumoniae, Haemophilus influenzae b, Neisseria meningitidis B/E. coli K1, and Neisseria meningitidis A,C,Y,W 135. Forty-one patients had proven bacterial meningitis, two had tuberculous meningitis, 39 had cerebral malaria, four had aseptic meningitis and five had convulsions. The sensitivity and specificity of the tests (Str. pneumoniae, 88% and 100%, H. influenzae b, 87% and 96%; N. meningitidis A,C,Y,W 135, 100% and 100%; and N. meningitidis B, 100% and 98%) were as good as those reported from developed countries. Unlike in some other parts of Africa, group B meningococci seem to predominate in cases of meningococcal meningitis in Malawi.
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PMID:Latex particle agglutination tests as an adjunct to the diagnosis of bacterial meningitis: a study from Malawi. 248 30

Evidence is presented here that tumor necrosis factor/cachectin (TNF), is of crucial importance in the pathogenesis of cerebral malaria. First, the central lesion of CM, hemorrhagic necrosis of cerebral vessels, corresponds to lesions observed during other pathological conditions associated with high serum TNF levels, such as endotoxemic shock or administration of TNF. Second, in both mouse and human, there is a close correlation between high serum TNF levels and CM. At least in mouse, high TNF levels and CM depend upon T lymphocytes of the CD4+ phenotype. Third, passive immunization against mouse TNF significantly prolongs the survival of P. berghei-infected CBA/Ca mice, and prevents the development of neurologic signs. Treatment with the anti-TNF antibody also prevents hemorrhagic necrosis of brain vessels. Fourth, in the mouse model, a cytokine cascade including at least GM-CSF, IL-3 and IFN-gamma is required for the elevation of TNF level. This cascade appears to involve two components: (a) a quantitative component: increased accumulation of macrophages results from the concomitant release of IL-3 and GM-CSF, and (b) a qualitative component: macrophage number has not only to be raised, but macrophages need to be activated by IFN-gamma. Fifth, metabolic parameters of CM and its main lesion in both mouse and human, i.e. the hemorrhagic necrosis of small brain vessels, correspond to the known properties of TNF.
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PMID:Tumor-necrosis factor and other cytokines in cerebral malaria: experimental and clinical data. 257 74

In primary Rhodesian sleeping sickness patients, parasitological diagnosis was best performed by rodent inoculation of blood (98.5%+) followed by Giemsa-stained thick blood smears (93.3%+). Parasitological diagnosis in relapse patients was sometimes impossible and clinical diagnosis based on CSF examination was necessary. Early during a disease outbreak in 1980, 89% of the infections were detected by mobile field teams, but once established in the endemic area a stationary diagnostic facility detected most of the cases. A total number of 23,751 examinations for Rhodesian sleeping sickness and malaria were made by mobile field teams during 1980-1984; 102 primary cases (0.43%) and 25 (0.10%) relapse cases were diagnosed. A total of 9339 individuals (39%) had patent malaria infections. The IFAT was positive in 89% of the primary sleeping sickness patients and 77% of the relapse patients. Seventy-nine per cent of the primary patients were positive in a CFT test, and 77% of the relapse patients were considered positive.
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PMID:Diagnosis of Rhodesian sleeping sickness in the Lambwe Valley (1980-1984). 269 86

IL-3 and granulocyte/macrophage colony stimulating factor (GM-CSF) are two cytokines released by activated T lymphocytes that stimulate the growth and differentiation of various hematopoietic cell lines, among which are macrophages. It has been shown that TNF/cachectin, another cytokine that is released mostly by activated macrophages, plays a central role in experimental cerebral malaria (CM), an acute and lethal neurological syndrome induced by Plasmodium berghei ANKA infection in CBA mice. Since CM requires functional CD4+ T lymphocytes to occur, we explored, by injecting rabbit antibodies to murine rIL-3 and/or GM-CSF, whether these cytokines are intermediates in the marked TNF release leading to CM. Treatment of infected mice with each antibody separately had no protective effect. In contrast, when both anti-rGM-CSF and anti-rIL-3 antibodies were injected together; (a) the occurrence of neurological syndrome was prevented in 90% of the cases; (b) the rise in serum TNF was prevented; and (c) macrophage accumulation in the spleen was significantly reduced. Murine CM appears to involve a cytokine cascade in which IL-3 and GM-CSF lead to the accumulation of TNF-releasing macrophages in vivo.
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PMID:Prevention of experimental cerebral malaria by anticytokine antibodies. Interleukin 3 and granulocyte macrophage colony-stimulating factor are intermediates in increased tumor necrosis factor production and macrophage accumulation. 304 13


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