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Journal articles on the topic 'Cerebral malaria'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 June 2024

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1

Mandala, Wilson L., Chisomo L. Msefula, Esther N. Gondwe, James J. Gilchrist, Stephen M. Graham, Paul Pensulo, Grace Mwimaniwa, et al. "Lymphocyte Perturbations in Malawian Children with Severe and Uncomplicated Malaria." Clinical and Vaccine Immunology 23, no. 2 (November 18, 2015): 95–103. http://dx.doi.org/10.1128/cvi.00564-15.

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ABSTRACTLymphocytes are implicated in immunity and pathogenesis of severe malaria. Since lymphocyte subsets vary with age, assessment of their contribution to different etiologies can be difficult. We immunophenotyped peripheral blood from Malawian children presenting with cerebral malaria, severe malarial anemia, and uncomplicated malaria (n= 113) and healthy aparasitemic children (n= 42) in Blantyre, Malawi, and investigated lymphocyte subset counts, activation, and memory status. Children with cerebral malaria were older than those with severe malarial anemia. We found panlymphopenia in children presenting with cerebral malaria (median lymphocyte count, 2,100/μl) and uncomplicated malaria (3,700/μl), which was corrected in convalescence and was absent in severe malarial anemia (5,950/μl). Median percentages of activated CD69+NK (73%) and γδ T (60%) cells were higher in cerebral malaria than in other malaria types. Median ratios of memory to naive CD4+lymphocytes were higher in cerebral malaria than in uncomplicated malaria and low in severe malarial anemia. The polarized lymphocyte subset profiles of different forms of severe malaria are independent of age. In conclusion, among Malawian children cerebral malaria is characterized by lymphocyte activation and increased memory cells, consistent with immune priming. In contrast, there are reduced memory cells and less activation in severe malaria anemia. Further studies are required to understand whether these immunological profiles indicate predisposition of some children to one or another form of severe malaria.

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Beare, Nicholas A. V., Simon J. Glover, and Malcolm Molyneux. "Malarial Retinopathy in Cerebral Malaria." American Journal of Tropical Medicine and Hygiene 80, no. 2 (February 1, 2009): 171. http://dx.doi.org/10.4269/ajtmh.2009.80.171.

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3

Pikatan, Orlando, Ellen Ferlita Tirtana, Kezia Seraphine, and Wienta Diarsvitri. "BIOMARKERS AND PROGNOSTIC SCORING IN CEREBRAL MALARIA." MNJ (Malang Neurology Journal) 8, no. 2 (July 1, 2022): 140–43. http://dx.doi.org/10.21776/ub.mnj.2022.008.02.13.

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Malaria remains a public health concern and remain the deadliest in infectious disease in the world. Cerebral malaria is a particularly severe complication of this disease and associated with high mortality. This literature review is made up from 19 literatures consisting of journals, and book. The literature review used data base www.pubmed.com, and www.scholar.google.com using “cerebral malaria and biomarker, predictor of cerebral malaria and treatment of severe malaria”. The languages for this journal are English and Indonesian. From the collection of literatures in this literature review, severe consists of cerebral malaria, blackwater fever, acute kidney injury, pulmonary edema, electrolyte disturbance, hematology disturbance, and obstetrics emergency resulting from malaria which is postpartum hemorrhage. Cerebral malaria increases the mortality of the patient, so they have to be diagnosed early and treated precisely. Patients with infection of plasmodium falciparum and GCS<11 must be suspected as cerebral malaria. Biomarker examination such as Soluble ICAM-1, Specific muscle’s protein, Angiopoetin-1 and 2, and Plasma microparticles is the most precise way to detect malarial emergency earlier Coma Acidosis Malaria score is also found to be useful in predicting the prognosis in cerebral malaria. Early diagnosis should be made as early as possible to reduce mortality from malaria and its emergencies.

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4

Burton, Adrian. "When is cerebral malaria not cerebral malaria?" Lancet Neurology 3, no. 3 (March 2004): 139. http://dx.doi.org/10.1016/s1474-4422(04)00699-4.

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Lawton, Jonathan G., Albert E. Zhou, Drissa Coulibaly, Emily M. Stucke, Antoine Dara, Matthew B. Laurens, Joana C. Silva, Mahamadou A. Thera, and Mark A. Travassos. "272 Differential expression of two Plasmodium falciparum variant surface antigen families in Malian children with cerebral malaria compared to mild malaria." Journal of Clinical and Translational Science 7, s1 (April 2023): 81–82. http://dx.doi.org/10.1017/cts.2023.330.

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OBJECTIVES/GOALS: Recent in vitro evidence suggests that diverse parasite protein families called RIFINs and STEVORs are displayed on the surface of infected red blood cells and may have a role in severe malaria, but they remain sparsely studied in natural infections. We measured the RNA expression of these antigens in Malian children with severe or mild malaria illness. METHODS/STUDY POPULATION: We collected blood samples from Malian children aged six months to five years, including 14 with cerebral malaria, 10 with severe malarial anemia, and demographic-matched controls with mild, uncomplicated malaria. We extracted total RNA from each patient and used a custom capture array to selectively enrich Plasmodium falciparum parasite RNA. We then performed Illumina next-generation RNA sequencing and reconstructed parasite transcriptomes using reference-free de novo assembly. We identified RNA encoding RIFINs and STEVORs using an in-house classifier, then measured the diversity and abundance of gene expression for each infection. Expression diversity was defined as the number of unique variants transcribed. Expression abundance was calculated as transcripts per million (TPM). RESULTS/ANTICIPATED RESULTS: Cerebral malaria cases, but not severe malarial anemia cases, had higher diversity and abundance of RIFIN expression compared to mild infections. Type A RIFINs predominated over Type B RIFINs, and the same two RIFINs were predominantly expressed in all disease phenotypes. We anticipate that predominantly expressed RIFINs share high sequence homology with variants previously shown to bind blood antigens or immune inhibitory receptors. STEVOR expression was also higher in cerebral malaria compared to mild malaria, but STEVOR transcripts were sparse overall. DISCUSSION/SIGNIFICANCE: Elevated RIFIN expression in cerebral malaria over mild malaria supports a role for these antigens in pathogenesis. Severe malarial anemia may progress through a different pathogenic mechanism. Predominantly expressed RIFIN variants may be promising targets for vaccines and therapeutics to protect children against cerebral malaria.

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6

Burté, Florence, Biobele J. Brown, Adebola E. Orimadegun, Wasiu A. Ajetunmobi, Nathaniel K. Afolabi, Francis Akinkunmi, Olayinka Kowobari, et al. "Circulatory hepcidin is associated with the anti-inflammatory response but not with iron or anemic status in childhood malaria." Blood 121, no. 15 (April 11, 2013): 3016–22. http://dx.doi.org/10.1182/blood-2012-10-461418.

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7

Aprilen, Nisa, and I. Made Bayu Indratama. "Handling cerebral malaria patient with limited resources: a case report." Jurnal Penyakit Dalam Udayana 5, no. 2 (December 20, 2021): 26–31. http://dx.doi.org/10.36216/jpd.v5i2.149.

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Cerebral malaria is an emergency condition. All patients with Plasmodium falciparum infection followed by neurological symptoms should be treated as cerebral malaria. The pathogenesis of cerebral malaria is caused by the damage of blood vessels endothelium due to parasites sequestration, production of pro-inflammatory cytokines and leakage of blood vessels which can cause brain hypoxia. The proper management is needed, however this become quiet challenging issue in the setting of limited resouces. We report a case of a 35 year old patient presenting with a loss of consciousness accompanied by shivering fever for 5 days. On examination of the peripheral blood smear, the Plasmodium falciparum was found. The patient was later diagnosed as cerebral malaria and treated with anti-malarial drugs. The fifth day of treatment the patient has fully alert. In the next day, the patient was allowed to go home. The management of cerebral malaria is challenging, particularly in the area with limited resources.

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8

Desruisseaux, Mahalia S., Fabiana S. Machado, Louis M. Weiss, Herbert B. Tanowitz, and Linnie M. Golightly. "Cerebral Malaria." American Journal of Pathology 176, no. 3 (March 2010): 1075–78. http://dx.doi.org/10.2353/ajpath.2010.091090.

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9

Cartagena, Yuliet, Carolina Monsalve, and María Eugenia Toro. "Malaria cerebral." Acta Neurológica Colombiana 37, no. 1 supl. 1 (March 1, 2021): 148–53. http://dx.doi.org/10.22379/24224022347.

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10

Mturi, Neema, Crispin O. Musumba, Betty M. Wamola, Bernhards R. Ogutu, and Charles R. J. C. Newton. "Cerebral Malaria." CNS Drugs 17, no. 3 (2003): 153–65. http://dx.doi.org/10.2165/00023210-200317030-00002.

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11

Rénia, Laurent, Shanshan Wu Howland, Carla Claser, Anne Charlotte Gruner, Rossarin Suwanarusk, Teck-Hui Teo, Bruce Russell, and Lisa F. P. Ng. "Cerebral malaria." Virulence 3, no. 2 (March 2012): 193–201. http://dx.doi.org/10.4161/viru.19013.

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12

White, N. J. "Cerebral Malaria." Practical Neurology 4, no. 1 (February 2004): 20–29. http://dx.doi.org/10.1111/j.1474-7766.2004.05-199.x.

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13

Hamer, Davidson, and David Wyler. "Cerebral Malaria." Seminars in Neurology 13, no. 02 (June 1993): 180–88. http://dx.doi.org/10.1055/s-2008-1041124.

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14

DAROFF, R. B. "Cerebral malaria." Journal of Neurology, Neurosurgery & Psychiatry 70, no. 6 (June 1, 2001): 817a—818. http://dx.doi.org/10.1136/jnnp.70.6.817a.

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15

Hall, AnthonyP, Dominic Kwiatkowski, Malcolm Molyneux, Terrie Taylor, Nigel Klein, Nigel Curtis, Margot Smit, et al. "Cerebral malaria." Lancet 337, no. 8752 (May 1991): 1281–84. http://dx.doi.org/10.1016/0140-6736(91)92949-3.

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16

Warreil, D. A. "Cerebral malaria." Biomedicine & Pharmacotherapy 43, no. 10 (January 1989): 782–83. http://dx.doi.org/10.1016/0753-3322(89)90175-3.

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17

Luzolo, Ange Landela, and Dieudonné Mumba Ngoyi. "Cerebral malaria." Brain Research Bulletin 145 (February 2019): 53–58. http://dx.doi.org/10.1016/j.brainresbull.2019.01.010.

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18

Brook, M. G., W. R. C. Weir, and B. A. Bannister. "Cerebral malaria." Lancet 337, no. 8733 (January 1991): 115. http://dx.doi.org/10.1016/0140-6736(91)90773-i.

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19

Turner, Gareth. "Cerebral Malaria." Brain Pathology 7, no. 1 (January 1997): 569–82. http://dx.doi.org/10.1111/j.1750-3639.1997.tb01075.x.

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20

Sharma, Y. D., Rajiv Kant, C. R. Pillai, M. A. Ansari, and Usha Filial. "Cerebral malaria." Nature 376, no. 6539 (August 1995): 380. http://dx.doi.org/10.1038/376380b0.

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21

Birbeck, Gretchen L. "Cerebral malaria." Current Treatment Options in Neurology 6, no. 2 (April 2004): 125–37. http://dx.doi.org/10.1007/s11940-004-0022-7.

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22

Shikani, Henry J., Brandi D. Freeman, Michael P. Lisanti, Louis M. Weiss, Herbert B. Tanowitz, and Mahalia S. Desruisseaux. "Cerebral Malaria." American Journal of Pathology 181, no. 5 (November 2012): 1484–92. http://dx.doi.org/10.1016/j.ajpath.2012.08.010.

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23

Salsabila, Dinda, Alifia Mawadddah, Athalitha Andhera Nabil, Baiq Ramdhani Amelia Negara, Herdiana Nurul Utami, Indri Setiawati, and Ni Nyoman Geriputri. "Cerebral Malaria." Jurnal Biologi Tropis 23, no. 1 (November 1, 2023): 33–38. http://dx.doi.org/10.29303/jbt.v23i1.5810.

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Cerebral malaria is the worst complication of malaria caused by Plasmodium spp. This disease is spread in tropical and subtropical countries and can attack all age groups and genders. The peak incidence occurs in preschool children and very often causes death in children. The endemic areas of malaria in Indonesia include NTT, Maluku, West Papua and Papua. Every year, as much as 40% of the total global population lives in or visits endemic areas every year. Cerebral malaria can cause long-term neurocognitive complications that can reduce quality of life. The speed of treatment determines the patient's prognosis. Therefore, it is necessary to understand the signs of malaria and the complications that can arise. This article was written to discuss cerebral malaria as a whole based on existing literature.

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24

Carvalho, Leonardo J. M. "Murine cerebral malaria: how far from human cerebral malaria?" Trends in Parasitology 26, no. 6 (June 2010): 271–72. http://dx.doi.org/10.1016/j.pt.2010.03.001.

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25

Kamminana, Geetha Priyadarsini, Jyotirmayi Boddu, and Vasudev Rajapantula. "A Study of Clinical Profile and Outcome in Adults with Plasmodium vivax Malaria." Journal of Evidence Based Medicine and Healthcare 7, no. 43 (October 26, 2020): 2470–73. http://dx.doi.org/10.18410/jebmh/2020/511.

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BACKGROUND Among malarial parasites, Plasmodium vivax is most prevalent in humans. Recent studies have shown severe and fatal complications with Plasmodium vivax infection. We wanted to evaluate the clinical spectrum, complications and outcomes of adult subjects with Plasmodium vivax malaria mono-infection. METHODS This is a retrospective study involving 100 subjects RESULTS Males were more commonly affected. It was most prevalent in the second decade of life. Fever was present in all patients. The other common symptoms were headache, vomiting, and jaundice. The incidence of associated clinical findings were pallor (43 %), icterus (21%), hepatomegaly (39 %) and splenomegaly (27 %). Severe thrombocytopenia was seen in 18 %, hyper bilirubinaemia in 39 % of subjects. Cerebral malaria was observed in 3 %, acute kidney injury in 13 %, ARDS (Acute Respiratory Distress Syndrome) in 5 % cases, MODS (Multi Organ Dysfunction Syndrome) was seen in 3 % cases, with a mortality of 3 %. CONCLUSIONS Complications like ARDS, AKI (Acute Kidney Injury), cerebral malaria and MODS were observed in benign tertian malaria subjects in our study. Cerebral malaria, AKI, MODS, ARDS were associated with high degrees of mortality. KEYWORDS Plasmodium vivax, ARDS (Acute Respiratory Distress Syndrome), Cerebral Malaria, AKI (Acute Kidney Injury), MODS (Multiorgan Dysfunction Syndrome)

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26

White, Nicholas J. "Cerebral perfusion in cerebral malaria." Critical Care Medicine 27, no. 3 (March 1999): 478–79. http://dx.doi.org/10.1097/00003246-199903000-00020.

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27

Thiam, Alassane, Sabrina Baaklini, Babacar Mbengue, Samia Nisar, Maryam Diarra, Sandrine Marquet, Mouhamadou Mansour Fall, et al. "NCR3 polymorphism, haematological parameters, and severe malaria in Senegalese patients." PeerJ 6 (December 3, 2018): e6048. http://dx.doi.org/10.7717/peerj.6048.

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Background Host factors, including host genetic variation, have been shown to influence the outcome of Plasmodium falciparum infection. Genome-wide linkage studies have mapped mild malaria resistance genes on chromosome 6p21, whereas NCR3-412 polymorphism (rs2736191) lying within this region was found to be associated with mild malaria. Methods Blood samples were taken from 188 Plasmodium falciparum malaria patients (76 mild malaria patients, 85 cerebral malaria patients, and 27 severe non-cerebral malaria patients). NCR3-412 (rs2736191) was analysed by sequencing, and haematological parameters were measured. Finally, their association with clinical phenotypes was assessed. Results We evidenced an association of thrombocytopenia with both cerebral malaria and severe non-cerebral malaria, and of an association of high leukocyte count with cerebral malaria. Additionally, we found no association of NCR3-412 with either cerebral malaria, severe non-cerebral malaria, or severe malaria after grouping cerebral malaria and severe non-cerebral malaria patients. Conclusions Our results suggest that NCR3 genetic variation has no effect, or only a small effect on the occurrence of severe malaria, although it has been strongly associated with mild malaria. We discuss the biological meaning of these results. Besides, we confirmed the association of thrombocytopenia and high leukocyte count with severe malaria phenotypes.

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Guenther, Geoffrey, Daniel Muller, Dominic Moyo, and Douglas Postels. "Pediatric Cerebral Malaria." Current Tropical Medicine Reports 8, no. 2 (January 25, 2021): 69–80. http://dx.doi.org/10.1007/s40475-021-00227-4.

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29

Aikawa, Masamichi. "Human Cerebral Malaria *." American Journal of Tropical Medicine and Hygiene 39, no. 1 (July 1, 1988): 3–10. http://dx.doi.org/10.4269/ajtmh.1988.39.3.

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30

John, Chandy C. "Cerebral Malaria Pathogenesis." American Journal of Pathology 171, no. 6 (December 2007): 1729–32. http://dx.doi.org/10.2353/ajpath.2007.070917.

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31

Wyler, DavidJ, and AnthonyP Hall. "Treating cerebral malaria." Lancet 337, no. 8738 (February 1991): 433–34. http://dx.doi.org/10.1016/0140-6736(91)91216-h.

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Brook, M. G., W. R. C. Weir, and B. A. Bannister. "Treating cerebral malaria." Lancet 337, no. 8745 (April 1991): 851. http://dx.doi.org/10.1016/0140-6736(91)92557-i.

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33

Wijdicks, Eelco F. M., and John G. Park. "Surviving cerebral malaria." Neurology 91, no. 21 (November 19, 2018): 978–79. http://dx.doi.org/10.1212/wnl.0000000000006557.

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34

Sachdev, H. S., and M. Mohan. "Vivax Cerebral Malaria." Journal of Tropical Pediatrics 31, no. 4 (August 1, 1985): 213–15. http://dx.doi.org/10.1093/tropej/31.4.213.

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35

OO, MAUNG MAUNG, MASAMICHI AIKAWA, THAN THAN, TIN MAUNG AYE, PE THAN MYINT, IKUO IGARASHI, and WILLIAM C. SCHOENE. "Human Cerebral Malaria." Journal of Neuropathology and Experimental Neurology 46, no. 2 (March 1987): 223–31. http://dx.doi.org/10.1097/00005072-198703000-00009.

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36

Guenther, Geoffrey, Alexuse M. Saidi, Rima Izem, Karl Seydel, and Douglas G. Postels. "Post-Malaria Anemia Is Rare in Malawian Children with Cerebral Malaria." American Journal of Tropical Medicine and Hygiene 104, no. 6 (June 2, 2021): 2146–51. http://dx.doi.org/10.4269/ajtmh.20-1668.

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Abstract.Artesunate therapy for severe malaria syndromes has been associated with post-treatment hemolysis and anemia. We defined post-malaria anemia as any decrease in hematocrit between the index hospitalization for severe malaria and 1 month after. We determined the incidence and severity of post-malaria anemia in Malawian children surviving cerebral malaria (CM) by analyzing hospital and follow-up data from a long-standing study of CM pathogenesis. Children enrolled before 2014 and treated with quinine (N = 258) were compared with those admitted in 2014 and after, and treated with artesunate (N = 235). The last hematocrit value obtained during hospitalization was compared with the 1-month post-hospitalization hematocrit value. The overall rate of a post-hospitalization decrease in hematocrit in children surviving CM was 5.3% (11 of 235 or 4.7% for quinine, 15 of 258 or 5.8% for artesunate; odds ratio, 3.23 [0.88, 18.38]); no patients with a decrease in hematocrit were symptomatic, and none required transfusion after hospitalization. Of the 26 children who had a decrease in hematocrit 1 month after hospitalization, 23.1% had evidence of a new malaria infection. When children treated with quinine and artesunate were combined, a higher hematocrit level on admission, lower quantitative histidine-rich protein level, and splenomegaly were associated independently with post-malaria anemia. In African survivors of CM, post-malaria anemia is rare, mild, and unassociated with the anti-malarial treatment received.

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Pradhan, Subal Ku, Pawan Mutalik, Tirumal Subudhi, Arakhita Swain, and Niranjan Mohanty. "Outcomes of paediatric malarial hepatopathy: a study from Eastern India." Paediatrica Indonesiana 54, no. 5 (October 30, 2014): 256. http://dx.doi.org/10.14238/pi54.5.2014.256-9.

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Background Severe malaria causes multi-organ involvement ,including hepatic dysfunction.Jaundice in severe malaria is foundmore commonly in adults than in children. It is important toassess the factors associated with malarial hepatopathy, the variedclinical presentations, as well as the complications in order toinitiate early interventional measures. There are a limited numberof studies in the pediatric population on malarial hepatopathy.Objective To assess the factors associated with malarialhepatopathy, the varied clinical presentations, as well as itscomplications.Methods This prospective study was conducted in the Departmentof Paediatrics, Sardar Vallabh Bhai Patel Post Graduate Institute ofPaediatrics (SVPPGIP), Cuttack, Odisha, India from January 20 10to June 2013, and included 70 children with malaria and jaundice,aged 6 months to 14 years. Malaria was confirmed by microscopicexamination of blood smears. Detailed clinical evaluations andinvestigation s were carried out to find multi-organ afflictions,with a special emphasis on hepatic involvement.Results Of218 children with malaria admitted during this period,70 (32%) children had fever and jaundice on presentation. Allchildren who had both Plasmodium faldparum and vivax infectionhad malarial hepatopathy. Complications, including acutekidney injury (AKI), disseminated intravascular coagulation(DIC), cerebral malaria, and mortality, were significantlyhigher among children with malarial hepatopathy compared tochildren without hepatopathy. Howevei; there was no significantdifference of hypoglycemia, respiratory distress syndrome (RDS),convulsions or severe anemia, between children with and withouthepatopathy.Conclusion Hepatopathy is more common with mixed malariainfections. The incidence of AKI, DIC, cerebral malaria, andmortality are significantly higher in patients with hepatopathy.Malarial hepatopathy should be considered in patients presentingwith acute febrile illness and jaundice so that specific treatmentcan be initiated early to prevent increased morbidity and mortality.

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Lyke, K. E., R. Burges, Y. Cissoko, L. Sangare, M. Dao, I. Diarra, A. Kone, et al. "Serum Levels of the Proinflammatory Cytokines Interleukin-1 Beta (IL-1β), 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." Infection and Immunity 72, no. 10 (October 2004): 5630–37. http://dx.doi.org/10.1128/iai.72.10.5630-5637.2004.

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ABSTRACT 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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Willimann, K., H. Matile, N. A. Weiss, and B. A. Imhof. "In vivo sequestration of Plasmodium falciparum-infected human erythrocytes: a severe combined immunodeficiency mouse model for cerebral malaria." Journal of Experimental Medicine 182, no. 3 (September 1, 1995): 643–53. http://dx.doi.org/10.1084/jem.182.3.643.

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Cerebral malaria is a fatal complication of infection by Plasmodium falciparum in man. The neurological symptoms that characterize this form of malarial disease are accompanied by the adhesion of infected erythrocytes to the vasculature of the brain. To study this phenomenon in vivo, an acute phase severe combined immunodeficiency (SCID) mouse model was developed in which sequestration of P. falciparum-infected human erythrocytes took place. During acute cerebral malaria in humans, the expression of intercellular adhesion molecule-1 (ICAM-1) is induced in vascular endothelium by inflammatory reactions. Acute phase ICAM-1 expression can also be obtained in SCID mice. The endothelium of the midbrain region was the most responsive to such inflammatory stimulus. It is noteworthy that the reticular formation in the midbrain controls the level of consciousness, and loss of consciousness is a symptom of cerebral malaria. We found that infected human erythrocytes were retained 24 times more than normal erythrocytes in ICAM-1-positive mouse brain. Sequestration to the brain was reduced by anti-ICAM-1 antibodies. These in vivo results were confirmed by the binding of P. falciparum-infected erythrocytes to the ICAM-1-positive endothelium in tissue sections of mouse brain. We conclude that the SCID mouse serves as a versatile in vivo model that allows the study of P. falciparum-infected erythrocyte adhesion as it occurs in human cerebral malaria. Upregulation of ICAM-1 expression in the region of the midbrain correlates with increased retention of malaria-infected erythrocytes and with the symptoms of cerebral malaria.

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White, Valerie A. "Malaria in Malawi: Inside a Research Autopsy Study of Pediatric Cerebral Malaria." Archives of Pathology & Laboratory Medicine 135, no. 2 (February 1, 2011): 220–26. http://dx.doi.org/10.5858/135.2.220.

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Abstract Context.—Malaria is still a major cause of death in sub-Saharan Africa. Objectives.—To describe my participation as a pathologist in a research autopsy study in Malawi and to examine retinal pathologic findings in cerebral malaria and correlate them with those in the brain. To describe the challenges of conducting a research study in sub-Saharan Africa and the personal and scientific benefits resulting from this. Design.—Children with coma are admitted to the pediatric research ward, classified according to the clinical definition of severe malaria or another cause of coma, evaluated, and treated systematically. The eyes are examined by indirect ophthalmoscopy after dilatation. If a child dies and permission is given, a standardized autopsy is carried out. The patients' condition is then reclassified pathologically. Results.—Ninety autopsies have been completed, with the cause of death confirmed as cerebral malaria in 64 cases (71.1%). These patients showed heavy parasite sequestration and often extravascular pathologic findings in the brain, retina, gastrointestinal tract, and subcutaneous fat. Clinical and pathologic findings in the retina correlated with those in the brain, and ophthalmoscopy has become a useful tool in the diagnosis and prognosis of children with cerebral malaria. Twenty-eight percent of patients clinically classified as having cerebral malaria showed another cause of death and no malarial pathologic process or retinopathy. Conclusions.—The human, financial, and transportation resources and organization required for this autopsy project are substantial. The scientific benefits are now becoming evident after sufficient autopsies have been completed for detailed comparisons. Personal benefits include the opportunity to work and travel in an African setting and to develop collaborations world-wide.

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Joste, Valentin, Laurine Maurice, Gwladys I. Bertin, Agnès Aubouy, Farid Boumédiène, Sandrine Houzé, Daniel Ajzenberg, et al. "Identification of Plasmodium falciparum and host factors associated with cerebral malaria: description of the protocol for a prospective, case-control study in Benin (NeuroCM)." BMJ Open 9, no. 5 (May 2019): e027378. http://dx.doi.org/10.1136/bmjopen-2018-027378.

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IntroductionIn 2016, an estimated 216 million cases and 445 000 deaths of malaria occurred worldwide, in 91 countries. In Benin, malaria causes 26.8% of consultation and hospitalisation motif in the general population and 20.9% in children under 5 years old.The goal of the NeuroCM project is to identify the causative factors of neuroinflammation in the context of cerebral malaria. There are currently very few systematic data from West Africa on the aetiologies and management of non-malarial non-traumatic coma in small children, and NeuroCM will help to fill this gap. We postulate that an accurate understanding of molecular and cellular mechanisms involved in neuroinflammation may help to define efficient strategies to prevent and manage cerebral malaria.Methods and analysisThis is a prospective, case-control study comparing cerebral malaria to uncomplicated malaria and non-malarial non-traumatic coma. This study takes place in Benin, precisely in Cotonou for children with coma and in Sô-Ava district for children with uncomplicated malaria. We aim to include 300 children aged between 24 and 71 months and divided in three different clinical groups during 12 months (from December 2017 to November 2018) with a 21 to 28 days follow-up for coma. Study data, including clinical, biological and research results will be collected and managed using CSOnline-Ennov Clinical.Ethics and disseminationEthics approval for the NeuroCM study has been obtained fromComité National d’Ethique pour la Recherche en santéof Benin (n°67/MS/DC/SGM/DRFMT/CNERS/SA; 10/17/2017). NeuroCM study has also been approved byComité consultatif de déontologie et d’éthiqueof Institut de Recherche pour le Développement (IRD; 10/24/2017). The study results will be disseminated through the direct consultations with the WHO’s Multilateral Initiative on Malaria (TDR-MIM) and Roll Back Malaria programme, through scientific meetings and peer-reviewed publications in scientific or medical journals, and through guidelines and booklets.

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CLARK, C. J., R. S. PHILLIPS, R. B. McMILLAN, I. O. MONTGOMERY, and T. W. STONE. "Differences in the neurochemical characteristics of the cortex and striatum of mice with cerebral malaria." Parasitology 130, no. 1 (December 13, 2004): 23–29. http://dx.doi.org/10.1017/s0031182004006237.

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Fatal murine cerebral malaria is an encephalitis and not simply a local manifestation in the brain of a systemic process. Histopathologically, murine cerebral malaria has been characterized by monocyte adherence to the endothelium of the microvasculature, activation of microglial cells, swelling of endothelial cell nuclei, microvasculature damage, and breakdown of the blood-brain barrier with cerebral oedema. Brain parenchymal cells have been proposed to be actively involved in the pathogenesis of murine cerebral malaria. We, therefore, compared the neurochemical characteristics ofPlasmodium bergheiANKA-infected mice with controls to determine whether cerebral malarial infection significantly impairs specific neuronal populations. Between 6 and 7 days after infection, we found a significant loss of neurones containing substance P, with preservation of cells containing somatostatin, neuropeptide Y and calbindin in the striatum of infected mice compared with controls. In the cortex of infected mice, we found a significant reduction in the number of cells containing substance P, somatostatin and neuropeptide Y. The number of calbindin-containing neurones was unchanged. This study found significant changes in the neurochemical characteristics of the cortex and striatum of mice infected withP. bergheiANKA, which may contribute to their cerebral symptoms.

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Medhi, N., S. B. Das, R. R. Das, S. Medhi, P. Sarma, R. Duwara, P. Das, and R. Saikia. "MRI Findings of Cerebral Malaria." Neuroradiology Journal 22, no. 4 (August 2009): 407–12. http://dx.doi.org/10.1177/197140090902200408.

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Cerebral malaria is a protozoal disease affecting the brain caused by Plasmodium falciparum. The hallmark of cerebral malaria is progressive decline in the sensorium leading to coma and in some cases death. MR findings reported in cerebral malaria are diffuse cerebral swelling / edema, bilateral nearly symmetrical T2 hyperintense lesions in basal ganglia and similar lesions in thalamus, pons and cerebellum. The imaging findings of cerebral malaria depend on the duration of the illness and time of MR examination. We describe two patients of cerebral malaria having mixed Plasmodium falciparum and Plasmodium vivex infestation showing bilateral basal ganglia infarcts with cerebral swelling in one patient and bilateral basal ganglia and cerebellar lesions in the other.

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Beare, Nicholas AV, Susan Lewallen, Terrie E. Taylor, and Malcolm E. Molyneux. "Redefining cerebral malaria by including malaria retinopathy." Future Microbiology 6, no. 3 (March 2011): 349–55. http://dx.doi.org/10.2217/fmb.11.3.

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Ahmad, Sohaib, Nadia Shirazi, Nowneet Kumar Bhat, Minakshi Dhar, Garima Mittal, Manish Mittal, Nidhi Kaeley, and Manoj Kumar. "A HOSPITAL-BASED RETROSPECTIVE COMPARATIVE STUDY OF COMPLICATIONS, OUTCOMES, CLINICAL AND LABORATORY PARAMETERS OF MALARIA WITH AND WITHOUT NEUROLOGICAL INVOLVEMENT." Mediterranean Journal of Hematology and Infectious Diseases 9, no. 1 (December 26, 2016): e2017006. http://dx.doi.org/10.4084/mjhid.2017.006.

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Background & Objectives: Classically associated with Plasmodium falciparum, neurological complications in severe malaria is associated with increased morbidity and mortality. However, reports implicate the long considered benign Plasmodium vivax for causing severe malaria as well. We aimed to analyze the cerebral complications in malaria, and study if there is a specie-related difference in the presentation and outcomes.Methods: We retrospectively compared patients of malaria hospitalised from 2009-15, with (n=105) and without (n=1155) neurological involvement in terms of outcomes, complications, demographic attributes, clinical features, and laboratory parameters. Subsequently, the same parameters were studied in those with cerebral malaria due to mono-infections of vivax or falciparum and their co-infection.Results: Cerebral malaria was observed in 8.3% (58/696), 7.4% (38/513) and 17.6% (6/51) of vivax, falciparum and combined plasmodial infections respectively. Those with cerebral malaria had significantly (p<0.05) longer hospitalization, delayed defervescence, required mechanical ventilatory support and dialysis despite comparable levels of azotemia and renal insufficiency, and adverse outcomes compared to non-cerebral malaria. Severe thrombocytopenia, respiratory distress and mechanical ventilation were significantly (p<0.05) associated with P. vivax cerebral malaria.Conclusions:The plasmodial species were comparable in clinical and laboratory parameters and outcomes in cerebral malaria in isolation and in combination (p>0.05). P. vivax emerged as the predominant cause of cerebral malaria and its virulence was comparable to P. falciparum.

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Amoako-Sakyi, Daniel, Selorme Adukpo, Kwadwo A. Kusi, Daniel Dodoo, Michael F. Ofori, George O. Adjei, Dominic E. Edoh, et al. "A STAT6 Intronic Single-Nucleotide Polymorphism is Associated with Clinical Malaria in Ghanaian Children." Genetics & Epigenetics 8 (January 2016): GEG.S38307. http://dx.doi.org/10.4137/geg.s38307.

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Malaria pathogenesis may be influenced by IgE responses and cytokine cross-regulation. Several mutations in the IL-4/STAT6 signaling pathway can alter cytokine cross-regulation and IgE responses during a Plasmodium falciparum malarial infection. This study investigated the relationship between a STAT6 intronic single-nucleotide polymorphism (rs3024974), total IgE, cytokines, and malaria severity in 238 Ghanaian children aged between 0.5 and 13 years. Total IgE and cytokine levels were measured by ELISA, while genotyping was done by polymerase chain reaction-restriction fragment length polymorphism (RFLP). Compared with healthy controls, heterozygosity protected against clinical malaria: uncomplicated malaria (odds ratios [OR] = 0.13, P < 0.001), severe malarial anemia (OR = 0.18, P < 0.001), and cerebral malaria (OR = 0.39, P = 0.022). Levels of total IgE significantly differed among malaria phenotypes (P = 0.044) and rs3024974 genotypes (P = 0.037). Neither cytokine levels nor IL-6/IL-10 ratios were associated with malaria phenotypes or rs3024974 genotypes. This study suggests a role for rs3024974 in malaria pathogenesis and offers further insights into an IL-4/STAT6 pathway mutation in malaria pathogenesis.

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Gunawan, Chandra, I. Wayan Suranadi, I. Putu Agus Surya Panji, and Tjokorda Gde Agung Senapathi. "Case Report: Managing the Coinfection of Cerebral Malaria and Dengue in the Intensive Care Unit." JAI (Jurnal Anestesiologi Indonesia) 16, no. 1 (February 2, 2024): 115–26. http://dx.doi.org/10.14710/jai.v0i0.59397.

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Background: Dengue and malaria are the two most common arthropod-borne illnesses, but cases of multiple infections are extremely uncommon. The mortality rate for individuals with dengue and malaria was higher than the death rate for those with malaria alone.Case: An intubated 53-year-old male was referred from a class B hospital because of severe malaria with suspected cerebral malaria, dengue fever (day-11), septic shock and acute kidney injury. His initial laboratory investigation showed increasing pattern of WBC, thrombocyte, anemia, peripheral blood smear normochromic normocytic erythrocyte, poikilocytosis (ovalocytes (+), teardrop cells (+)), normoblasts (+), presence of Plasmodium malariae trophozoite and schizont stage parasites, positive result of IgM and IgG anti dengue, increased liver function test, increased BUN and creatinine serum levels, hyperbilirubinemia, hypoalbuminemia, and normal result of blood gas analysis. On the sixth day of ICU admission, the patient gradually regained consciousness with appropriate responsiveness and showed clinical improvement. The patient was discharged after one month of hospital care with the last peripheral blood smear showing no parasites detected.Discussion: Mono-infection with malaria and dengue, two mosquito-borne diseases endemic to tropical and subtropical regions, often carries a high risk of fatality. The risk becomes even more pronounced when co-infection occurs. The early diagnosis and management in the ICU are crucial for cases of coinfection involving cerebral malaria and dengue. The primary focus is on both definitive and supportive therapies.Conclusion: The prognosis for coinfection of cerebral malaria and dengue is generally poor, but in this case, the patient showed improvement and was able to be discharged without any sequelae.

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Wilairatana, Polrat, Sornchai Looareesuwan, and Douglas S. Walsh. "Chemotherapy of Cerebral Malaria." CNS Drugs 7, no. 5 (May 1997): 366–80. http://dx.doi.org/10.2165/00023210-199707050-00004.

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Enwere, Godwin, Michael Boele Van Hensbroek, Richard Adegbola, Ayo Palmer, Emeka Onyiora, Martin Weber, and Brian Greenwood. "Bacteraemia in cerebral malaria." Annals of Tropical Paediatrics 18, no. 4 (December 1998): 275–78. http://dx.doi.org/10.1080/02724936.1998.11747959.

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Genton, Blaise, Fadwa AI-Yaman, Charles S. Mgone, Neal Alexander, Michael M. Paniu, Michael P. Alpers, and David Mokela. "Ovalocytosis and cerebral malaria." Nature 378, no. 6557 (December 1995): 564–65. http://dx.doi.org/10.1038/378564a0.

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