scholarly journals Lipidome profiles of plasma microvesicles differ in experimental cerebral malaria, compared to malaria without neurological complications

2020 ◽  
Author(s):  
Amani M Batarseh ◽  
Fatemeh Vafaee ◽  
Elham Hosseini-Beheshti ◽  
Alex Chen ◽  
Amy Cohen ◽  
...  
Keyword(s):  
Cerebral Malaria ◽  
Neurological Complications ◽  
Sub Saharan Africa ◽  
South East Asia ◽  
Fatal Complication ◽  
Experimental Cerebral Malaria ◽  
Lipid Species ◽  
Experimental Mouse Model ◽  
Experimental Mouse ◽  
Sub Saharan

ABSTRACTCerebral malaria (CM), a fatal complication of Plasmodium infection that affects children in sub-Saharan Africa and adults in South-East Asia, results from incompletely understood pathogenetic mechanisms, which include an excessive release of microvesicles (MV). Plasma MV levels have been found elevated in CM patients and in the experimental mouse model.We compared lipid profiles in circulating MV purified from CBA mice infected with P. berghei ANKA (PbA), which causes CM, to those from P. yoelii (Py), which does not. Here we show that plasma MV produced at the time of CM differed dramatically from those from non-CM mice, in spite of identical levels of parasitaemia. Using high-resolution LCMS, we identified over 300 lipid species within 12 lipid classes. Total lysophosphatidylethanolamine (LPE) levels were significantly lower in PbA infection compared to uninfected mice, while they were unchanged in Py MV, and lysophosphatidylcholine (LPC) was more significantly reduced in PbA mice compared to the other two groups. These results suggest, for the time, that experimental CM is characterised by specific changes in lipid composition of circulating MV, pointing towards triglycerides (TG) especially docosahexaenoic acid (DHA 22:6) containing species, phosphatidylethanolamine (PE), LPC, LPE, and diacylglycerol (DG) as potential important players in CM pathogenesis.

scholarly journals Molecular Correlates of Experimental Cerebral Malaria Detectable in Whole Blood

2010 ◽  
Vol 79 (3) ◽  
pp. 1244-1253 ◽  
Author(s):  
Miranda S. Oakley ◽  
Vivek Anantharaman ◽  
Thiago M. Venancio ◽  
Hong Zheng ◽  
Babita Mahajan ◽  
...  
Keyword(s):  
Cerebral Malaria ◽  
Whole Blood ◽  
Cell Receptor ◽  
Sub Saharan Africa ◽  
Molecular Signature ◽  
Receptor Protein ◽  
Pcr Analysis ◽  
Data Set ◽  
Experimental Cerebral Malaria ◽  
Sub Saharan

ABSTRACTCerebral malaria (CM) is a primary cause of deaths caused byPlasmodium falciparumin young children in sub-Saharan Africa. Laboratory tests based on early detection of host biomarkers in patient blood would help in the prognosis and differential diagnosis of CM. Using thePlasmodium bergheiANKA murine model of experimental cerebral malaria (ECM), we have identified over 300 putative diagnostic biomarkers of ECM in the circulation by comparing the whole-blood transcriptional profiles of resistant mice (BALB/c) to those of two susceptible strains (C57BL/6 and CBA/CaJ). Our results suggest that the transcriptional profile of whole blood captures the molecular and immunological events associated with the pathogenesis of disease. We find that during ECM, erythropoiesis is dysfunctional, thrombocytopenia is evident, and glycosylation of cell surface components may be modified. Furthermore, analysis of immunity-related genes suggests that slightly distinct mechanisms of immunopathogenesis may operate in susceptible C57BL/6 and CBA/CaJ mice. Furthermore, our data set has allowed us to create a molecular signature of ECM composed of a subset of circulatory markers. Complement component C1q, β-chain, nonspecific cytotoxic cell receptor protein 1, prostate stem cell antigen, DnaJC, member 15, glutathioneS-transferase omega-1, and thymidine kinase 1 were overexpressed in blood during the symptomatic phase of ECM, as measured by quantitative real-time PCR analysis. These studies provide the first host transcriptome database that is uniquely altered during the pathogenesis of ECM in blood. A subset of these mediators of ECM warrant validation inP. falciparum-infected young African children as diagnostic markers of CM.

scholarly journals Plasmodium vivax cerebral malaria in an adult patient in Sudan

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Maowia M. Mukhtar ◽  
Omer A. Eisawi ◽  
Seth A. Amanfo ◽  
Elwaleed M. Elamin ◽  
Zeinab S. Imam ◽  
...  
Keyword(s):  
Plasmodium Vivax ◽  
Cerebral Malaria ◽  
Blood Film ◽  
Sub Saharan Africa ◽  
Measured Temperature ◽  
Neck Stiffness ◽  
The Pacific ◽  
High Parasitaemia ◽  
Brain Ct Scan ◽  
Sub Saharan

Abstract Background Plasmodium vivax infection is rising in sub-Saharan Africa, where Plasmodium falciparum is responsible for more than 90% of malaria cases. While P. vivax is identified as a major cause of severe and cerebral malaria in South east Asia, the Pacific and South America, most of the severe and cerebral cases in Africa were attributed to P. falciparum. Cases of severe malaria due to P. vivax are emerging in Africa. A few severe P. vivax cases were reported in Eastern Sudan and they were underestimated due to the lack of accurate diagnosis, low parasitaemia and seldom use of rapid diagnostic tests (RDTs). Case presentation A 60-year-old Sudanese male presented to the Al Kuwaiti hospital in the Sudan capital Khartoum. On admission, the patient was complaining of fever (measured temperature was 38 °C), sweating, chills, vomiting and confusion in the past 2 days prior to his admission. He rapidly deteriorated into a coma state within 48 h of the admission, with significant neck stiffness. He was admitted to the intensive care unit and was suspected of meningitis. Lumbar puncture was not performed since the patient was suffering from spinal cord disc. Brain CT scan was unremarkable. Several biochemical, haematological tests, and blood film for malaria were performed. The results of the laboratory tests were within the normal range except of mild elevation of the total white blood cell count and a significant decrease in the platelets count. Malaria parasites were seen in the blood film with high parasitaemia (quantified as 3 +++). The patient was diagnosed as P. vivax cerebral malaria based on the positive blood film and the amplification of P. vivax specific 499 bp amplicon using Plasmodium multi-species multiplex Polymerase Chain Reaction (PCR). The patient was treated with quinine 10 mg/kg body weight for 10 days followed by primaquine 15 mg/days PO for 2 weeks. The symptoms subsided within 48 h and the patients was cured and released from the hospital. Conclusions Plasmodium vivax is an emerging cause of cerebral malaria in adults in Sudan and should be considered in the differential diagnosis of cerebral malaria for proper management of patients.

Tracking Development in South-East Asia and sub-Saharan Africa: The Primacy of Policy

2012 ◽  
Vol 30 ◽  
pp. s5-s24 ◽  
Author(s):  
Jan Kees van Donge ◽  
David Henley ◽  
Peter Lewis
Keyword(s):  
East Asia ◽  
Sub Saharan Africa ◽  
South East Asia ◽  
Sub Saharan

scholarly journals Malarial Related Myopathies: A Rhabdomyolysis Story

2020 ◽  
pp. 39-51
Author(s):  
Forman Erwin Siagian
Keyword(s):  
Deleterious Effect ◽  
Management Strategy ◽  
Best Practice ◽  
Sub Saharan Africa ◽  
South East Asia ◽  
Severe Anemia ◽  
Vulnerable Group ◽  
Protozoan Infections ◽  
Sub Saharan ◽  
Muscle Capillaries

Malaria is amongst the most prevalent and epidemiologically relevant global parasitic protozoan infections. It is infecting millions of people annually, especially in south east Asia and sub Saharan Africa. Its morbidity and mortality still cannot be controlled entirely and elimination is still far away. Children and pregnant women are among the most vulnerable group in the population. Its pathobiology have related to cause direct or indirect deleterious effect on the patient’s skeletal muscle, named rhabdomyolysis. Eventhough it is very rare, but potentially fatal and lethal. Three mechanism of malaria related rhabdomyolysis are very intense inflammatory response, extensive red cells sequestration in muscle capillaries due to severe anemia and the parasite toxin’s, will  lead to or add risks of complication. Derangement of specific type of muscle, named the skeletal and cardiac, is amongst the earliest sign of severe malaria. Further study need to be conducted in the future, especially on important topics about mechanism and its effect, signaling pathways, best practice on laboratory approach and management strategy best practice.

scholarly journals Snake-Bite with Disseminated Intravascular Coagulation (DIC) and Stage II Hypertension

2017 ◽  
Vol 1 (5) ◽  
Author(s):  
Hendra Subroto ◽  
Leni Lismayanti
Keyword(s):  
Snake Bite ◽  
Sub Saharan Africa ◽  
Medical Emergency ◽  
Coagulation System ◽  
South East Asia ◽  
Emergency Case ◽  
Snake Bites ◽  
Laboratory Results ◽  
Sub Saharan ◽  
D Dimer

Snake-bite is an important medical emergency case and caused of many hospitaladmission especially in the rural area, forests, plantations and swamps. Despite its importance,there have been fewer proper data of snake-bite incidence in Indonesia. World HealthOrganization estimate that at least 421,000 envenomings and 20,000 deaths from snakebitesoccur each year, especially in South and South East Asia and sub-Saharan Africa. The authorsreport a case of a 76-year-old man came to Hasan Sadikin Hospital with chief complaint woundin his right hand and right forearm from snake-bite. Snake-bites can cause DIC because thevenom activates the coagulation system and cause fibrinolysis which occurs in less than 24hours. Laboratory results, we found abnormalities such as anemia, thrombocytopenia,hypofibrinogenemia, and increased levels of D-dimer. Patients were treated for 8 days and thenallowed to go home. Snake-bite is an occupational disease of farmers, plantation workers,herdsmen, fishermen, other. Snake bite cases require prompt and comprehensive managementso as to minimize the possibility of disability and death.Keywords: snake bite, DIC, hypertension

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