Peripheral Microscopic Localization of Plasmodium falciparum Garnham Body in an Immature Stage-III Gametocyte in Fatal Cerebral Malaria

2019 ◽  
Vol 4 (2) ◽  
pp. 27-30
Author(s):  
Akshaya Kumar Mohanty ◽  
Sanghamitra Satpathi ◽  
Krishna Pramanik ◽  
Sanjib Mohanty ◽  
Praveen Kishore Sahu
Keyword(s):  
Plasmodium Falciparum ◽  
Cerebral Malaria ◽  
Immature Stage ◽  
Stage Iii ◽  
Microscopic Localization

scholarly journals Malaria parasites both repress host CXCL10 and use it as a cue for growth acceleration

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yifat Ofir-Birin ◽  
Hila Ben Ami Pilo ◽  
Abel Cruz Camacho ◽  
Ariel Rudik ◽  
Anna Rivkin ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Life Cycle ◽  
Cerebral Malaria ◽  
Survival Strategy ◽  
Parasitic Disease ◽  
Malaria Parasites ◽  
Sensing System ◽  
Rich Domain ◽  
Cargo Delivery ◽  
Low Levels

AbstractPathogens are thought to use host molecular cues to control when to initiate life-cycle transitions, but these signals are mostly unknown, particularly for the parasitic disease malaria caused by Plasmodium falciparum. The chemokine CXCL10 is present at high levels in fatal cases of cerebral malaria patients, but is reduced in patients who survive and do not have complications. Here we show a Pf ‘decision-sensing-system’ controlled by CXCL10 concentration. High CXCL10 expression prompts P. falciparum to initiate a survival strategy via growth acceleration. Remarkably, P. falciparum inhibits CXCL10 synthesis in monocytes by disrupting the association of host ribosomes with CXCL10 transcripts. The underlying inhibition cascade involves RNA cargo delivery into monocytes that triggers RIG-I, which leads to HUR1 binding to an AU-rich domain of the CXCL10 3’UTR. These data indicate that when the parasite can no longer keep CXCL10 at low levels, it can exploit the chemokine as a cue to shift tactics and escape.

scholarly journals IgG acquisition against PfEMP1 PF11_0521 domain cassette DC13, DBLβ3_D4 domain, and peptides located within these constructs in children with cerebral malaria

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Cyril Badaut ◽  
Pimnitah Visitdesotrakul ◽  
Aurélie Chabry ◽  
Pascal Bigey ◽  
Bernard Tornyigah ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Membrane Protein ◽  
Hospital Admission ◽  
Cerebral Malaria ◽  
Erythrocyte Membrane ◽  
Uncomplicated Malaria ◽  
Clinical Status ◽  
Severe Anemia ◽  
Specific Interactions ◽  
Time Of Admission

AbstractThe Plasmodium falciparum erythrocyte-membrane-protein-1 (PF3D7_1150400/PF11_0521) contains both domain cassette DC13 and DBLβ3 domain binding to EPCR and ICAM-1 receptors, respectively. This type of PfEMP1 proteins with dual binding specificity mediate specific interactions with brain micro-vessels endothelium leading to the development of cerebral malaria (CM). Using plasma collected from children at time of hospital admission and after 30 days, we study an acquisition of IgG response to PF3D7_1150400/PF11_0521 DC13 and DBLβ3_D4 recombinant constructs, and five peptides located within these constructs, specifically in DBLα1.7_D2 and DBLβ3_D4 domains. We found significant IgG responses against the entire DC13, PF11_0521_DBLβ3_D4 domain, and peptides. The responses varied against different peptides and depended on the clinical status of children. The response was stronger at day 30, and mostly did not differ between CM and uncomplicated malaria (UM) groups. Specifically, the DBLβ3 B3-34 peptide that contains essential residues involved in the interaction between PF11_0521 DBLβ3_D4 domain and ICAM-1 receptor demonstrated significant increase in reactivity to IgG1 and IgG3 antibodies at convalescence. Further, IgG reactivity in CM group at time of admission against functionally active (ICAM-1-binding) PF11_0521 DBLβ3_D4 domain was associated with protection against severe anemia. These results support development of vaccine based on the PF3D7_1150400/PF11_0521 structures to prevent CM.

scholarly journals Plasmodium falciparum cytoadherence to ICAM-1 is associated with cerebral malaria

2010 ◽  
Vol 9 (S2) ◽  
Author(s):  
Lucy B Ochola ◽  
Bethsheba R Siddondo ◽  
Harold Ocholla ◽  
Siana Nyka ◽  
Eva N Kimani ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Cerebral Malaria

scholarly journals Epidemiological, clinical and therapeutic aspects of cerebral malaria imported in Albania

2016 ◽  
Vol 10 (02) ◽  
pp. 190-194 ◽  
Author(s):  
Arben Ndreu ◽  
Diana Hajdari ◽  
Anduena Ndoni ◽  
Klodiana Shkurti ◽  
Dhimiter Kraja ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Case Report ◽  
West Africa ◽  
Cerebral Malaria ◽  
Early Treatment ◽  
West African ◽  
First Episode ◽  
African Countries ◽  
Disease Episode

This is a case-report of two patients with cerebral malaria (CM) imported from West-African countries. Notably, this form of malaria was developed as a second disease episode, while the first episode was experienced in West Africa. These findings suggest that the second episode of malaria was caused by a different strain of Plasmodium falciparum as compared to the first one. They are the first cerebral malaria cases imported in Albania after the eradication and absence of Plasmodium for five decades. Early treatment of cerebral malaria is decisive on the duration of coma and disease’s outcome.

scholarly journals Thrombospondin mediates the cytoadherence of Plasmodium falciparum- infected red cells to vascular endothelium in shear flow conditions

Blood ◽  
1988 ◽  
Vol 71 (1) ◽  
pp. 71-75
Author(s):  
EP Rock ◽  
EF Jr Roth ◽  
RR Rojas-Corona ◽  
JA Sherwood ◽  
RL Nagel ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Cerebral Malaria ◽  
Ex Vivo ◽  
Rabbit Antiserum ◽  
Immune Serum ◽  
Red Cells ◽  
Specific Attachment ◽  
Infected Cells ◽  
Human Immune ◽  
Venular Endothelium

Cerebral malaria is thought to involve specific attachment of Plasmodium falciparum-infected knobby red cells to venular endothelium. The nature of surface ligands on host endothelial cells that may mediate cytoadherence is poorly understood. We have investigated the effects of soluble thrombospondin, rabbit antiserum raised against thrombospondin, and human immune serum on cytoadherence of parasitized erythrocytes in ex vivo mesocecum vasculature. Preincubation of infected red cells with soluble thrombospondin or human immune serum inhibits binding of infected red cells to rat venular endothelium. Infusion of the microcirculatory preparation with rabbit antithrombospondin antibodies before perfusion of parasitized erythrocytes also resulted in decreased cytoadherence. In addition, incubation of infected cells with human immune sera obtained from malaria patients significantly inhibited the observed cytoadherence. Our results indicate that thrombospondin mediates binding of infected red cells to venular endothelium and may thus be involved in the pathogenesis of cerebral malaria.

Severe stridor and profound weakness after cerebral malaria

2021 ◽  
Vol 14 (4) ◽  
pp. e237681
Author(s):  
Charlotte Fuller ◽  
Gavin Wooldridge ◽  
Alice Liomba ◽  
Stephen Thomas James Ray
Keyword(s):  
Plasmodium Falciparum ◽  
Intensive Care ◽  
Cerebral Malaria ◽  
Acute Illness ◽  
Diagnostic Dilemma ◽  
Intensive Care Admission ◽  
Neurological Sequelae ◽  
Vocal Cord Paresis ◽  
Intensive Physiotherapy

Cerebral malaria (CM) is defined by WHO as coma (Blantyre Coma Score 2 or less) in a patient with Plasmodium falciparum parasitaemia and no alternative cause of coma identified. Mortality is approximately 15%–30% in African children and up to one-third of survivors have neurological sequelae. We present a patient with severe stridor and prolonged profound weakness during an intensive care admission with CM. These complications initially presented a diagnostic dilemma in our limited resourced setting. The stridor failed to improve with empiric steroids and a subsequent opportunistic ENT consult diagnosed vocal cord paresis. The weakness was so profound that the patient was unable to lift his head during the acute illness. The child received intensive physiotherapy, and at 1-month follow-up, the stridor and weakness had resolved.

Eugenol disrupts Plasmodium falciparum intracellular development during the erythrocytic cycle and protects against cerebral malaria

2021 ◽  
Vol 1865 (3) ◽  
pp. 129813
Author(s):  
Kesley A.O. Pontes ◽  
Leandro S. Silva ◽  
Edgleyson C. Santos ◽  
Alessandro S. Pinheiro ◽  
Douglas E. Teixeira ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Cerebral Malaria ◽  
Erythrocytic Cycle

scholarly journals Differential var gene transcription in Plasmodium falciparum isolates from patients with cerebral malaria compared to hyperparasitaemia

2006 ◽  
Vol 150 (2) ◽  
pp. 211-218 ◽  
Author(s):  
Helen M. Kyriacou ◽  
Graham N. Stone ◽  
Richard J. Challis ◽  
Ahmed Raza ◽  
Kirsten E. Lyke ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Cerebral Malaria ◽  
Gene Transcription ◽  
Var Gene

scholarly journals Light microscopic detection of Plasmodium falciparum in vitro through Pf histidine rich protein 2 (HRP 2) gold conjugate labeling: Rapid diagnosis of cerebral malaria in humans

2014 ◽  
Vol 13 (8) ◽  
pp. 978-982
Author(s):  
Olalekan Michael Ogundele ◽  
Sabiu Saheed ◽  
Adeshina Oloruntoba Adekeye ◽  
Philip Adeyemi Adeniyi ◽  
Oluwatosin Olalekan Ogedengbe ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Cerebral Malaria ◽  
Rapid Diagnosis ◽  
Microscopic Detection ◽  
Gold Conjugate

Plasmodium falciparum delayed cerebellar ataxia and late cerebral malaria

2005 ◽  
Vol 20 (8) ◽  
pp. 1087-1088
Author(s):  
Mahavir D. Mohire
Keyword(s):  
Plasmodium Falciparum ◽  
Cerebral Malaria ◽  
Cerebellar Ataxia
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