• Title/Summary/Keyword: Cerebral malaria

Search Result 6, Processing Time 0.019 seconds

A Case of Subcortical Dementia After Cerebral Malaria (말라리아 후유증으로 초래된 피질하성 치매 1례)

  • Chung, Hyo-Kyung;Lee, Young-Ho;Chung, Young-Cho;Kim, Su-Sie;Park, Byoung-Kwan
    • Korean Journal of Biological Psychiatry
    • /
    • v.2 no.2
    • /
    • pp.301-305
    • /
    • 1995
  • Subcortical dementia may occur as a complication of cerebral malaria via deep white matter demyelination with encephalitis and diffuse small vessel vasculitis. In subcortical dementia, impairment in attention and frontal executive function are predominant. Patients are often inert, indifferent, and uninterested. They appear characteristically 'slowed up' with a marked deficit in the retrieval of information. Changes in mood, personality, and social conduct are very common. We describe a case of subcortical dementia, who has definite changes in brain MRI after cerebral malaria.

  • PDF

Possible Role of Heme Oxygenase-1 and Prostaglandins in the Pathogenesis of Cerebral Malaria: Heme Oxygenase-1 Induction by Prostaglandin $D_2$ and Metabolite by a Human Astrocyte Cell Line

  • Kuesap, Jiraporn;Na-Bangchang, Kesara
    • Parasites, Hosts and Diseases
    • /
    • v.48 no.1
    • /
    • pp.15-21
    • /
    • 2010
  • Astrocytes are the most abundant cells in the central nervous system that play roles in maintaining the blood-brain-barrier and in neural injury, including cerebral malaria, a severe complication of Plasmodium falciparum infection. Prostaglandin (PG) $D_2$ is abundantly produced in the brain and regulates the sleep response. Moreover, $PGD_2$ is a potential factor derived from P. falciparum within erythrocytes. Heme oxygenase-1 (HO-1) is catalyzing enzyme in heme breakdown process to release iron, carbon monoxide, and biliverdin/bilirubin, and may influence iron supply to the P. falciparum parasites. Here, we showed that treatment of a human astrocyte cell line, CCF-STTG1, with $PGD_2$ significantly increased the expression levels of HO-1 mRNA by RT-PCR. Western blot analysis showed that $PGD_2$ treatment increased the level of HO-1 protein, in a dose- and time-dependent manner. Thus, $PGD_2$ may be involved in the pathogenesis of cerebral malaria by inducing HO-1 expression in malaria patients.

Characterization of Plasmodium berghei Homologues of T-cell Immunomodulatory Protein as a New Potential Candidate for Protecting against Experimental Cerebral Malaria

  • Cui, Ai;Li, Yucen;Zhou, Xia;Wang, Lin;Luo, Enjie
    • Parasites, Hosts and Diseases
    • /
    • v.57 no.2
    • /
    • pp.101-115
    • /
    • 2019
  • The pathogenesis of cerebral malaria is biologically complex and involves multi-factorial mechanisms such as microvascular congestion, immunopathology by the pro-inflammatory cytokine and endothelial dysfunction. Recent data have suggested that a pleiotropic T-cell immunomodulatory protein (TIP) could effectively mediate inflammatory cytokines of mammalian immune response against acute graft-versus-host disease in animal models. In this study, we identified a conserved homologue of TIP in Plasmodium berghei (PbTIP) as a membrane protein in Plasmodium asexual stage. Compared with PBS control group, the pathology of experimental cerebral malaria (ECM) in rPbTIP intravenous injection (i.v.) group was alleviated by the downregulation of pro-inflammatory responses, and rPbTIP i.v. group elicited an expansion of regulatory T-cell response. Therefore, rPbTIP i.v. group displayed less severe brain pathology and feverish mice in rPbTIP i.v. group died from ECM. This study suggested that PbTIP may be a novel promising target to alleviate the severity of ECM.

Genetic factors associated with development of cerebral malaria and fibrotic schistosomiasis

  • Hirayama, Kenji
    • Parasites, Hosts and Diseases
    • /
    • v.40 no.4
    • /
    • pp.165-172
    • /
    • 2002
  • Collaborative studies have identified some genetic factors contributing to the development of severe forms of malaria and schistosomiasis. In Thailand, the $TNF-{\alpha}{\;}5'-flanking$ region shows biallelic polymorphic sites at nucleotides -238, -308, -857, -863, and -1031, and seven alleles have been identified in patients from Myanmar. We found that the TNF promoter (TNFP)-D allele was significantly associated with cerebral malaria in populations from Karen (P < 0.0001. OR = 124.86) and ethnic Burma (P < 0.0001, OR = 34.50) . In China, we have identified two major genes related to the severity of liver fibrosis, one an HLA class II gene, and the other the IL-13 gene. The frequency of the HLA- DRB5*0101 allele and that of the IL-13 promoter A/A (IL- l3P- A/A) genotype were elevated in fibrotic patients, although the two genes are located on different chromosomes, chromosomes 6p and 5q, respectively Subjects with both genotypes had odds ratios (OR = 24.5) much higher than the sum of the ratios for each individual genotype (OR = 5.1,95% Confidence Interval 1.3-24.7 for HLA-DRB5*0101, OR = 3.1 95% CI 1.5 - 6.5 for IL-l3P-A/A). That the effects of the two susceptibility markers are synergistic rather than additive, strongly suggests that the pathogenic Th2 response directly influences the prognosis of post-schistosomal liver fibrosis.

Two Cases of Falciparum Malaria with Acute Respiratory Distress Syndrome (중증 열대열 말라리아에 동반된 급성호흡곤란증후군 2예)

  • Park, Joo-Hun;Shin, Eun-Sug;Woo, Jun-Hee;Kim, Yeun-Ok;Bae, In-Gyu;Jang, Jae-Jeong;Chi, Hyun-Sook;Koh, Youn-Suck
    • Tuberculosis and Respiratory Diseases
    • /
    • v.45 no.4
    • /
    • pp.888-895
    • /
    • 1998
  • Malaria is one of the most common infectious diseases in the world. Plasmodium falciparum, accounting for nearly all malaria mortality, kills an estimated 1 to 2 million persons yearly and has several features that make it deadlist of malarias. While cerebral malaria is the most common presentation of severe disease, acute lung injury associated with malaria is uncommon but serious and fatal complication. We report two cases of severe malaria with ARDS and multi-organ failure. All two patients traveled to foreign countries, Kenya, Papua New Guinea where choroquine-resistant malaria is distributed. The first case, which developed cerebral malaria, hypoglycemia, multi-organ failure, and ARDS, treated with quinine and mechanical ventilator, but expired due to oxygenation failure. Autopsy showed acute necrotizing infiltration, diffuse eosinophilic fibrinoid deposits along the alveolar space, and alveolar macrophage with malaria pigment The second case also developed multi-organ failure, followed by ARDS, and was treated with quinine, exchange transfusion, plasmapheresis, and mechanical ventilator. He recovered with residual restrictive lung change after treatment.

  • PDF

Age-Related $CD4^+CD25^+Foxp3^+$ Regulatory T-Cell Responses During Plasmodium berghei ANKA Infection in Mice Susceptible or Resistant to Cerebral Malaria

  • Shan, Ying;Liu, Jun;Pan, Yan-Yan;Jiang, Yong-Jun;Shang, Hong;Cao, Ya-Ming
    • Parasites, Hosts and Diseases
    • /
    • v.51 no.3
    • /
    • pp.289-295
    • /
    • 2013
  • Different functions have been attributed to $CD4^+CD25^+Foxp3^+$ regulatory T-cells (Tregs) during malaria infection. Herein, we describe the disparity in Treg response and pro- and anti-inflammatory cytokines during infection with Plasmodium berghei ANKA between young (3-week-old) and middle-aged (8-month-old) C57BL/6 mice. Young mice were susceptible to cerebral malaria (CM), while the middle-aged mice were resistant to CM and succumbed to hyperparasitemia and severe anemia. The levels of pro-inflammatory cytokines, such as TNF-${\alpha}$, in young CM-susceptible mice were markedly higher than in middle-aged CM-resistant mice. An increased absolute number of Tregs 3-5 days post-inoculation, co-occurring with elevated IL-10 levels, was observed in middle-aged CM-resistant mice but not in young CM-susceptible mice. Our findings suggest that Treg proliferation might be associated with the suppression of excessive pro-inflammatory Th1 response during early malaria infection, leading to resistance to CM in the middle-aged mice, possibly in an IL-10-dependent manner.