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Plasmodium Falciparum Infection (plasmodium + falciparum_infection)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Acalculous Cholecystitis in a Patient With Plasmodium falciparum Infection: A Case Report and Literature Review

JOURNAL OF TRAVEL MEDICINE, Issue 3 2006
Jean C. Yombi MD
Acute acalculous cholecystitis (AAC) can occur without gallstones in critically ill or injured patients and has also been associated with various infectious agents.1,4 We report here a case of AAC in a patient with Plasmodium falciparum malaria. [source]

Experimental cerebral malaria progresses independently of the Nlrp3 inflammasome

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 3 2010
Thornik Reimer
Abstract Cerebral malaria is the most severe complication of Plasmodium falciparum infection in humans and the pathogenesis is still unclear. Using the P. berghei ANKA infection model of mice, we investigated a potential involvement of Nlrp3 and the inflammasome in the pathogenesis of cerebral malaria. Nlrp3 mRNA expression was upregulated in brain endothelial cells after exposure to P. berghei ANKA. Although ,-hematin, a synthetic compound of the parasites heme polymer hemozoin, induced the release of IL-1, in macrophages through Nlrp3, we did not obtain evidence for a role of IL-1, in vivo. Nlrp3 knock-out mice displayed a delayed onset of cerebral malaria; however, mice deficient in caspase-1, the adaptor protein ASC or the IL-1 receptor succumbed as WT mice. These results indicate that the role of Nlrp3 in experimental cerebral malaria is independent of the inflammasome and the IL-1 receptor pathway. [source]

Erythrocytapheresis for Plasmodium falciparum infection complicated by cerebral malaria and hyperparasitemia

JOURNAL OF CLINICAL APHERESIS, Issue 1 2001
Y. Zhang
Abstract In malaria due to Plasmodium falciparum, life-threatening complications are in part related to the degree of parasitemia. Whole blood exchange and red blood cell exchange (RCE) have been used for the rapid removal of parasites from the circulation of patients with a high parasite load complicated by cerebral, pulmonary, and renal dysfunction. We have treated three 5,45-year-old patients with hyperparasitemia and end-organ dysfunction with red cell exchange by automated apheresis as an adjunct to specific anti-malarial chemotherapy. Parasitemia dropped more than 80% in all three patients immediately after the exchange, and all patients had an uneventful and full recovery. In combination with effective anti-malarial chemotherapy, apheresis RCE is a safe and rapid approach to treat complicated malaria due to P. falciparum. J. Clin. Apheresis. 16:15-18, 2001. © 2001 Wiley-Liss, Inc. [source]

Distinct pattern of class and subclass antibodies in immune complexes of children with cerebral malaria and severe malarial anaemia

PARASITE IMMUNOLOGY, Issue 6-7 2008
E. K. MIBEI
SUMMARY Plasmodium falciparum infection can lead to deadly complications such as severe malaria-associated anaemia (SMA) and cerebral malaria (CM). Children with severe malaria have elevated levels of circulating immune complexes (ICs). To further investigate the quantitative differences in antibody class/subclass components of ICs in SMA and CM, we enrolled 75 children with SMA and 32 children with CM from hospitals in western Kenya and matched them to 74 and 52 control children, respectively, with uncomplicated symptomatic malaria. Total IgG IC levels were always elevated in children with malaria upon enrolment, but children with CM had the highest levels of any group. Conditional logistic regression showed a borderline association between IgG4-containing IC levels and increased risk of SMA (OR = 3·11, 95% CI 1·01,9·56, P = 0·05). Total IgG ICs (OR = 2·84, 95% CI 1·08,7·46, P = 0·03) and IgE-containing ICs (OR = 6·82, OR 1·88,24·73, P , 0·01) were associated with increased risk of CM. These results point to differences in the contribution of the different antibody class and subclass components of ICs to the pathogenesis of SMA and CM and give insight into potential mechanisms of disease. [source]

Plasmodium falciparum infection of the placenta affects newborn immune responses

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2003
J. ISMAILI
SUMMARY The effects of exposure to placental malaria infection on newborn immunological responses, in particular Th1/Th2 cytokines and antigen-presenting cell (APC) function, were compared between cord blood mononuclear cells (CBMC) from parasitized and non-parasitized placentas of Gambian women. Cells were analysed in vitro for their ability to respond to mitogens [phorbol myristate acetate (PMA)/ionomycin, phytohaemagglutinin (PHA)], a malaria-unrelated test antigen [purified protein derivative of Mycobacterium tuberculin[purified protein derivative (PPD)] and Plasmodium falciparum schizont extracts. Mitogens induced strong proliferation and secretion of high concentrations of both IL-13 and sCD30 in CBMC from both groups. Conversely, significantly lower amounts of IFN- , were induced in the parasitized group in response to low doses of PHA. Protein antigens induced very low amounts of all tested cytokines, in particular IFN- ,. However, a significantly higher release of sCD30 was observed in response to schizont extracts in the parasitized group. Addition of LPS to activate APC to low doses of PHA or schizont extracts increased the IFN- , production in both groups but levels remained lower in CBMC from the parasitized group. This result correlates with the lower production of IL-12 found following lipopolysaccharide (LPS) stimulation in this group. Taken together, these data show that placental infection with P. falciparum affects Th1 differentiation and sCD30 priming of neonatal lymphocytes and that the probable mode of action is via APC. [source]