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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liposomes containing neutral glycolipids with a terminal glucose or galactose, when injected intravenously, prevented the appearance of erythrocytic forms of malaria (Plasmodium berghei) in mice previously injected with sporozoites. Inhibitory glycolipids included glucosyl, galactosyl, or lactosyl ceramide. Inhibition was not observed with liposomes containing ceramide, phosphocholine ceramide, sulfogalactosyl ceramide (sulfatide), or ganglioside GM1. Liposomes containing glycolipids did not inhibit infection transmitted by injecting blood containing erythrocytic stages of malaria. These results may have therapeutic implications in the treatment of malaria. Analysis of the mechanism of interference with the life cycle of malaria by liposomal glycolipids may yield information about the interactions of parasites with cellular membranes.
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PMID:Sporozoite-induced malaria: therapeutic effects of glycolipids in liposomes. 38 58

The surface charge and lectin-binding capacity of isolated malaria parasites and host erythrocytes were analyzed and compared by chromatographic, electrophoretic, and cytochemical methods. Results indicated that at physiological pH values both freshly prepared and glutaraldehyde-fixed parasites and erythrocytes possess a net negative surface charge. Both cell types were strongly bound to cation-exchange resins and underwent cathode-directed electrophoretic migration. The isoelectric points for erythrocyte-free parasites and uninfected erythrocytes were approximately 3.0 and 4.0, respectively. The different effects of selective enzymatic digestion and solvent extraction on the electrophoretic mobilities of free parasites and erythrocytes suggested that the chemical constituents responsibile for the net negative surface charges on each type of cell are different. The surface charge of the free parasites seemed mainly to be a function of ionized phospholipids rather than of the ionogenic sialic acid moieties, which are the major contributors to the negative charge on erythrocytes. Results of lectin-binding studies indicated that specific glycosidimoieties (i.e., glucose, galactose, mannose, and n-acetyglucosamine), common to the erythrocyte surface, were either absent or in low concentration at the parasite's surface. These observations suggest that the normally intracellular malaria parasites have surface characteristics, differing from those of the host cell, characterized by a scarcity of lectin-binding receptors and sialic acid residues and by the major contribution of lipids to their surface charge.
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PMID:Surface properties of extracellular malaria parasites: electrophoretic and lectin-binding characteristics. 79 92

From July 1989 to February 1990, 17 non-pregnant patients with severe falciparum malaria, aged 14 years and above received an initial intravenous quinine dihydrochloride loading dose of 20 mg/kg in 500 mls of normal saline or 5% dextrose infused over 4 hours followed by 100mg/kg infused 8 hourly for at least 24 hours. Sixteen comparable controls were similarly treated but without an initial loading dose. Oral quinine bisulfate 10mg/kg 8 hourly was substituted for a total of 7 days when patients were well enough. There was no significant difference in clinical and parasitological response between the two groups. Fever clearance time in hours was 44.00 +/- 13.92 (mean +/- SD) in the study group and 51.43 +/- 19.63 (mean +/- SD) in the control group (p > 0.05). Parasite clearance time in hours was 42.40 +/- 9.75 (mean +/- SD) in the study group and 47.05 +/- 7.69 (mean +/- SD) in the control group (p > 0.05). One patient from each group died. Mild toxic effects were common in both groups. Transient partial hearing loss occurred significantly more in the study than control group (p < 0.05). Hypoglycaemia during treatment occurred in 3 (18%) patients in the study group and 1 (6%) in the control group. The mean trough and peak plasma quinine levels in 3 patients per group was persistently higher than 9mg/L after first infusion. We conclude that though fairly well tolerated, quinine loading dose appears to have no advantage over the standard treatment for severe falciparum malaria at Kenyatta National Hospital, Nairobi, Kenya.
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PMID:Quinine loading dose in severe Falciparum malaria at Kenyatta National Hospital, Kenya. 129 31

1. Hypoglycaemia and lactic acidosis are important manifestations of severe falciparum malaria. To investigate hepatic gluconeogenesis in acute falciparum malaria, liver blood flow and galactose clearance were estimated in seven adult patients with moderately severe infection and seven patients with severe infection (three of whom died later). Nine patients were restudied in convalescence. 2. Liver blood flow, determined from the plasma clearance of Indocyanine Green, was lower in acute illness than in convalescence [16.1 (7.0) versus 23.9 (7.2) ml min-1 kg-1, mean (SD)], but this difference was not statistically significant (P = 0.15). There was a significant inverse correlation between admission venous plasma lactate concentrations and the liver blood flow estimated from the clearance of Indocyanine Green (rs = 0.71, P = 0.004). 3. The plasma clearance of galactose after intravenous injection was similar in the acute [15.4 (4.90) ml min-1 kg-1] and convalescent study [12.8 (2.1) ml min-1 kg-1]. The ratio of galactose clearance to Indocyanine Green clearance was significantly higher in acute disease [1.41 (0.51)] than in convalescence [0.70 (0.34)], largely because of the elevated ratios in severely ill patients [1.48 (0.50)]. 4. The rise in blood glucose concentration after galactose administration was significantly higher during acute illness [1.48 (0.72) mmol/l] than in convalescence [0.67 (0.41) mmol/l, P = 0.022], but the insulin response was similar, indicating reduced tissue insulin sensitivity. There was no significant change in the plasma concentrations of other metabolites (lactate, pyruvate, alanine and triacylglycerol) in either study. 5. These results suggest that the segment of the glycolytic pathway between galactose and glucose is unimpaired in patients with severe falciparum malaria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatic blood flow and metabolism in severe falciparum malaria: clearance of intravenously administered galactose. 131 Sep 19

This study investigates protein glycosylation in the asexual intraerythrocytic stage of the malaria parasite, Plasmodium falciparum, and the presence in the infected erythrocyte of the respective precursors. In in vitro cultures, P. falciparum can be metabolically labeled with radioactive sugars, and its multiplication can be affected by glycosylation inhibitors, suggesting the capability of the parasite to perform protein-glycosylation reactions. Gel-filtration analysis of sugar-labeled malarial proteins before and after specific cleavage of N-glycans or O-glycans, respectively, revealed the majority of the protein-bound sugar label to be incorporated into O-glycans, but only little (7-12% of the glucosamine label) or no N-glycans were found. Analysis of the nucleotide sugar and sugar-phosphate fraction showed that radioactive galactose, glucosamine, fucose and ethanolamine were converted to their activated derivatives required for incorporation into protein. Mannose was mainly recovered as a bisphosphate, whereas the level of radiolabeled GDP-mannose was below the detection limit. The analysis of organic-solvent extracts of sugar-labeled cultures showed no evidence for the formation by the parasite of dolichol cycle intermediates, the dedicated precursors in protein N-glycosylation. Consistently, the amount of UDP-N-acetylglucosamine formed did not seem to be affected by the presence of tunicamycin in the culture. Oligosaccharyl-transferase activity was not detectable in a lysate of P. falciparum, using exogenous glycosyl donors and acceptors. Our studies show that O-glycosylation is the major form of protein glycosylation in intraerythrocytic P. falciparum, whereas there is little or no protein N-glycosylation. A part of these studies has been published in abstract form [Dieckmann-Schuppert, A., Hensel, J. and Schwarz, R. T. (1991) Biol. Chem. Hoppe-Seyler 372, 645].
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PMID:Apparent lack of N-glycosylation in the asexual intraerythrocytic stage of Plasmodium falciparum. 137 32

Classification, management and prevention of seizures in children are summarized for clinicians in Papua New Guinea. Seizures are classified as febrile with or without underlying brain pathology, and afebrile, including neonatal fits, infantile spasms, myoclonic jerks, akinetic seizures, tonic clonic fits, petit mal, benign focal, and psychomotor seizures. In all cases the first step is to secure the airway, then do a fingerstick and treat hypoglycemia, and finally stop the fit if it is prolonged with paraldehyde, diazepam, phenobarbitone or phenytoin. A cause for the seizure should be sought: physical exam, especially tympanic membranes and throat, blood slide for malaria, lumbar puncture for signs of meningitis, blood culture, serum calcium, and other chemistries. Some empirical treatments to use for negative findings include: dextrose, calcium gluconate, magnesium SO4, pyridoxine, quinine and Fansidar. Hyperthermia in a febrile child can be reversed with cool sponging. The author recommends prescribing phenobarbitone to prevent subsequent simple febrile seizures if the child has 3 or more, then slowly withdrawing the drug if the child is seizure free for a year. Drug therapy for the various other types of seizures available in Papua New Guinea include sodium valproate by special order, and phenobarbitone, phenytoin, carbamazepine, nitrazepam, ethosuximide, and prednisolone. A table is provided to help select the drug for each seizure type, e.g. ethosuximide for petit mal, prednisolone for infantile spasms, and carbamazepine for various types of focal and psychomotor seizures.
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PMID:Convulsions in children. 150 14

Quinine is widely used for the treatment of severe and complicated malaria, although resistant strains of Plasmodium falciparum may occur. The drug has been incriminated as a cause of hypoglycaemia in some malaria patients. To determine if quinine has untoward metabolic effects during treatment of severe and complicated malaria we have studied the effects of quinine on blood glucose and intermediary metabolites, serum insulin, C-peptide, plasma glucagon and non-esterified fatty acids in 97 children with severe malaria in Dar es Salaam. All patients responded clinically. No patient developed hypoglycaemia while on quinine therapy given as 10 mg/kg in 10 ml/kg of 5% dextrose infused over 4 h every 8 h. Endogenous insulin secretion, as reflected by C-peptide levels, increased after 4 h but insulin levels did not change significantly. Blood lactate, 3-hydroxybutyrate, plasma non-esterified fatty acids and plasma glucagon all fell appropriately during treatment. We conclude that quinine, when administered at the recommended dose and rate, does not disrupt blood glucose homeostasis, and is still the drug of choice for severe and complicated malaria in children.
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PMID:The metabolic effects of quinine in children with severe and complicated Plasmodium falciparum malaria in Dar es Salaam. 129 76

We report a case of severe hyponatraemia and hypoglycaemia in a patient with complicated falciparum malaria. The use of large volumes of intravenous dextrose as a diluent for quinine may lead to fluid overload and exacerbate hyponatraemia.
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PMID:Severe hyponatraemia in malaria. 188 20

Because hypoglycaemia is common in severe malaria, intravenous glucose is often given empirically to patients on admission to hospital. To investigate the metabolic response to rapid glucose injection in acute malaria, 50 ml of 50% w/v (25 g) dextrose was given over 5 min to 10 adult patients (7 males, 3 females; mean age 30 years) with acute falciparum malaria. Five patients with severe infections were studied between doses of intravenous quinine; 5 cases were uncomplicated and previously untreated. The patients with severe malaria had lower pre-injection plasma glucose concentrations than patients with uncomplicated infections (mean +/- standard deviation, 4.2 +/- 0.9 vs 5.8 +/- 1.1 mmol/litre, 2P less than 0.015). However, peak glucose concentrations (18.6 +/- 4.8 vs 17.0 +/- 2.4 mmol/litre) and integrated responses (AUC0-245 min) were similar in the groups (2P greater than 0.1 in each case), and pre- and post-injection plasma insulin concentrations and AUC0-245 min values were also not significantly different (2P greater than 0.05 in each case). No 'rebound' hypoglycaemia was observed. The patients with severe malaria had higher peak plasma lactate concentrations than the uncomplicated patients (2.5 +/- 0.7 vs 1.5 +/- 0.9 mmol/litre, 2P less than 0.05), but the highest plasma lactate achieved and the greatest maximum post-injection rise were only 3.8 and 0.8 mmol/litre respectively. The average maximum reduction in plasma potassium after injection was 0.2 mmol/litre at 35 min. These data suggest that injections of hypertonic dextrose given empirically in conventional doses to non-acidotic patients with acute, severe malaria are not harmful, but the metabolic response in patients with an established acidosis remains unknown.
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PMID:The metabolic response to rapid intravenous glucose injection in acute falciparum malaria. 188 67

Recently introduced chloroquine resistant malaria has altered the clinical picture and complicated the overall management of malaria. 113 adults with proved malaria admitted at Harare Central Hospital, Zimbabwe, were evaluated to determine the incidence, nature, relationship to morbidity and mortality and response to treatment of the complications due to malaria. 47.7 pc (52 of 109) patients had relatively chloroquine resistant malaria. 87.4 pc (99 of 113) had complications whose percentage frequency of occurrence were: Anaemia 51.2 pc, diarrhoea and/or vomiting 42.2 pc, cerebral malaria +/- fits 39.2 pc, renal insufficiency +/- hyperkalaemia 26.4 pc, hypoglycaemia 15.6 pc, jaundice 15.2 pc, neuro-psychiatric 15.0 pc, shock 10.6 pc, concurrent sepsis 8.9 pc, pulmonary oedema 3.5 pc and hyperpyrexia 1.7 pc. Multiple complications in the same patient were common. The combination of cerebral malaria and renal insufficiency had the worst mortality (p less than 0.001). All patients dialysed, however, survived. Non-iron deficiency anaemia, 91.7 pc (51 of 55) and diarrhoea and/or vomiting, were common, worsened morbidity but not mortality (p = 0.555). A seriously-ill patient with malaria should be suspected of having complications and chloroquine resistance and should be referred promptly to a centre with facilities for dialysis. Anti-malaria drugs should be mixed in a dextrose solution and iron supplements should not be given routinely.
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PMID:Complications of seasonal adult malaria at a central hospital. 209 79


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