Hearing loss: a possible consequence of malaria.
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More than 200 million people worldwide contract malaria from mosquito bites. In sub-Saharan Africa, 100 million clinical cases of malaria are reported every year, resulting in almost one million deaths. Malaria has been implicated in the causation of deafness in several studies in the West Africa subregion. This paper examines the association between malaria and deafness, and considers which factors may be involved in the causation of deafness. Although age, immunity, the type of malaria parasite, fever, complications of malaria, and complications resulting from the drug treatment of malaria may contribute to the development of deafness in malaria, the actual mechanism of causation is not clearly understood. Deafness in malaria is associated with P. falciparum parasitic infection. The author is certain that the high fever in malaria, leading to febrile convulsions and cerebral involvement, can result in deafness. Further investigation is needed to determine whether the presence of untreated malaria parasites in the blood causes deafness.Keywords:
Cerebral Malaria
Causation
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Background The main processes in the pathogenesis of cerebral malaria caused by Plasmodium falciparum involved sequestration of parasitized red blood cells and immunopathological responses. Among immune factors, IgG autoantibodies to brain antigens are increased in P. falciparum infected patients and correlate with disease severity in African children. Nevertheless, their role in the pathophysiology of cerebral malaria (CM) is not fully defined. We extended our analysis to an Indian population with genetic backgrounds and endemic and environmental status different from Africa to determine if these autoantibodies could be either a biomarker or a risk factor of developing CM.
Parasitology
Cerebral Malaria
Tropical Medicine
Medical microbiology
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Over the past 5 years, 1620 comatosed patients of both sexes aged 1-75 years were screened for cerebral malaria. Of these, 505 (31.2%) were positive for Plasmodium falciparum. During this period frequency of malaria increased from 22.1% in 1991 to 44.4% in 1995. Sixty-four percent cases of cerebral malaria were seen in children and thirty-six percent in adults. Mortality was also higher (41%) in children than in adults (25%). As cerebral malaria is particularly prevalent in Pakistan and is a major community problem, accurate and easier methods of its diagnosis are needed at primary health care level, in all febrile comatose patients, without focal neurological findings.
Cerebral Malaria
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SUMMARY Plasmodium falciparum malaria is responsible for over 250 million clinical cases every year worldwide. Severe malaria cases might present with a range of disease syndromes including acute respiratory distress, metabolic acidosis, hypoglycaemia, renal failure, anaemia, pulmonary oedema, cerebral malaria (CM) and placental malaria (PM) in pregnant women. Two main determinants of severe malaria have been identified: sequestration of parasitized red blood cells and strong pro-inflammatory responses. Increasing evidence from human studies and malaria infection animal models revealed the presence of host leucocytes at the site of parasite sequestration in brain blood vessels as well as placental tissue in complicated malaria cases. These observations suggested that apart from secreting cytokines, leucocytes might also contribute to disease by migrating to the site of parasite sequestration thereby exacerbating organ-specific inflammation. This evidence attracted substantial interest in identifying trafficking pathways by which inflammatory leucocytes are recruited to target organs during severe malaria syndromes. Chemo-attractant cytokines or chemokines are the key regulators of leucocyte trafficking and their potential contribution to disease has recently received considerable attention. This review summarizes the main findings to date, investigating the role of chemokines in severe malaria and the implication of these responses for the induction of pathogenesis and immunity to infection.
Cerebral Malaria
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In Thai patients with Plasmodium falciparum malaria, IgG and IgM values were elevated, whereas IgA levels were within normal ranges. No association of Ig values with parasitaemia was noted. IFA-IgM antibody levels were lower in cerebral malaria (CM) than in the non cerebral malaria (NCM) group. IFA-IgG antibodies were present in all patients. The mean C3 and C4 values were similar among patients from the CM and NCM groups. Interferon like activity was detected in all CM and NCM patients, and no correlation was found with either antimalarial antibodies, complement or parasitaemia.
Cerebral Malaria
Humoral immunity
Cellular immunity
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SUMMARY IL-10 is a monocyte/lymphocyte derived cytokine which has been shown to inhibit certain cellular immune responses such as delayed hypersensitivity. In particular, the production of tumour necrosis factor (TNF), IL-I and IL-6, which are involved in malaria pathology, are strongly inhibited by IL-10. Accordingly, we examined whether IL-10 could be involved in a human acute parasitic infection such as Plasmodium falciparum malaria. Human IL-10 levels in plasma were determined by two-site ELISA method, taking care to avoid non-specific reactions due to autoantibodies. Fourteen cerebral, 11 severe, and 20 mild malaria cases had mean IL-10 levels of 2812, 2882 and 913 pg/ml, respectively, while 98% of healthy individuals had undetectable (less than 100 pg/ml) circulating IL-10. Thirteen of the 25 cerebral/severe cases had >2000 pg/ml. In 11 hospitalized patients, circulating IL-10 levels were found to return to virtually normal levels 7 days after antimalarial chemotherapy when biological and clinical malaria features had disappeared (mean levels fell from 3880 to 333 pg/ml). Further studies are required to determine whether these elevated levels of IL-10 play a beneficial role by reducing the parasite-induced inflammatory response, or a detrimental one by decreasing the cellular immune responses.
Cerebral Malaria
Monocyte
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Malaria infection leads to the formation of circulating immune complexes. However, it is unclear whether these complexes play a role in the pathogenesis of complicated Plasmodium falciparum malaria. This study aimed at determining if there are differences in the levels of immune complexes between children with severe malaria-associated anemia and cerebral malaria and between each of these two groups and their respective uncomplicated symptomatic malaria or healthy asymptomatic controls. Children with severe malaria-associated anemia and cerebral malaria had significantly higher immune complex levels than their respective controls, but there were no significant differences in the levels between the two severe malaria groups. In addition, there was an inverse relationship between the hemoglobin levels and immune complex levels in the severe anemia controls, suggesting that immune complexes may contribute to erythrocyte destruction in these children. These results suggest that immune complex levels alone cannot account for the differences in the distinct clinical presentation between severe malaria-associated anemia and cerebral malaria.
Cerebral Malaria
Pathogenesis
Immune complex
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We studied thrombocytopenia during acute Plasmodium falciparum malaria in 64 traveller children from Paris (France), 85 children from Dakar (Senegal) with an intermittent exposure (69 with severe attack or cerebral malaria), and 81 children from Libreville (Gabon) with a perennial exposure (43 with severe attack or cerebral malaria). Initial thrombocytopenia was present in 43-58% of children with P falciparum malaria but was not more frequent in severe outcome or cerebral malaria. Low parasitaemia may lead to the misdiagnosis of malaria and delayed treatment when there is associated thrombocytopenia
Cerebral Malaria
Severe Malaria
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Neutralizing antibodies to glycosylphosphatidylinositols (GPIs), which are Plasmodium falciparum surface protein anchor molecules implicated in malaria pathogenesis, are thought to protect against symptomatic malaria. Index cases of severe malaria in Malian children 3 months to 14 years of age were matched by age and residence to uncomplicated malaria and healthy controls. Serum antibodies to GPI (IgM and IgG) were measured at the time of severe malaria and after the malaria transmission season. The mean optical density values for IgM and IgG antibodies were higher in children with severe or uncomplicated malaria compared with healthy controls. Similarly, higher percentages of children with IgM and IgG antibodies to GPI were observed in the severe malaria group compared with matched healthy controls. IgG antibody levels to GPI were highest among children with cerebral malaria and children who died. The IgG antibody levels to GPI peaked during periods of malaria transmission and decreased after malaria transmission ended. A direct correlation between age and parasitemia and IgG antibodies to GPI was observed. In summary, higher levels of IgM and IgG antibodies to GPI in young children were associated with disease severity and were short-lived.
Cerebral Malaria
Pathogenesis
Immunoglobulin M
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Cerebral Malaria
Severe Malaria
Pathophysiology
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ABSTRACT. We used a protein microarray featuring Plasmodium falciparum field variants of a merozoite surface antigen to examine malaria exposure in Malian children with different severe malaria syndromes. Unlike children with cerebral malaria alone or severe malarial anemia alone, those with concurrent cerebral malaria and severe malarial anemia had serologic responses demonstrating a broader prior parasite exposure pattern than matched controls with uncomplicated disease. Comparison of levels of malaria-related cytokines revealed that children with the concurrent phenotype had elevated levels of interleukin (IL)-6, IL-8, and IL-10. Our results suggest that the pathophysiology of this severe subtype is unique and merits further investigation.
Cerebral Malaria
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