Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrophoretic variation of the enzymes glucose phosphate isomerase, 6-phosphogluconate dehydrogenase, lactate dehydrogenase and glutamate dehydrogenase (NADP-dependent) has been studied in the African murine malaria parasites Plasmodium berghei, P. yoelii, P. vinckei and P. chabaudi and their subspecies. Horizontal starch gel electrophoresis was used throughout. The number of isolates examined in each subspecies varied from 1 (P. y. nigeriensis) to 24 (P. c. chabaudi). Extensive enzyme variation was found among isolates of most of the subspecies from which more than two such isolates were available for study. It is clear that the phenomenon of enzyme polymorphism is of common occurrence among malaria parasites. With the exception of P. berghei and P. yoelii, of which all isolates share an identical electrophoretic form of lactate dehydrogenase, no enzyme forms are shared between any of the 4 species of murine plasmodia. By contrast, within each species common enzyme forms are shared among each of the subspecies. The subspecies are nevertheless, distinguished from each other by the electrophoretic forms of at least one enzyme. The distribution and reassortment of enzyme variation among isolates of a single subspecies is in accordance with the concept of malaria parasites as sexually reproducing organisms. The study of variation among parasites present in individual wild-caught rodent hosts demonstrates that natural malarial infections usually comprise genetically heterogeneous populations of parasites. Nevertheless, the number of genetically distinct types of parasite of any one species present in a single infected host appears to be small. Generally not more than 2 or 3 clones of parasite of distinct genetic constitution are present in a single infected animal.
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PMID:Studies on enzyme variation in the murine malaria parasites Plasmodium berghei, P. yoelii, P. vinckei and P. chabaudi by starch gel electrophoresis. 35 25

The simultaneous infection of mice with lactic dehydrogenase-elevating virus (LDV) and Plasmodium yoelii resulted in an exacerbated attack of malaria. Peak parasitaemia was higher and the patent infection more prolonged in doubly infected mice. The results indicate that contamination with LDV must be considered when a change in parasite virulence is observed, particularly when the parasite is maintained by blood passage in mice.
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PMID:Exacerbation of murine malaria by concurrent infection with lactic dehydrogenase-elevating virus. 71 54

A 44-year-old man developed bouts of fever (up to 40 degrees C) seven days after returning from a holiday in Kenya. Malaria prophylaxis with chloroquine had been correctly undertaken. Concentrations of lactate dehydrogenase and total bilirubin were raised (493 U/l and 3.55 mg/dl, respectively). Blood smear revealed the ring forms of Plasmodium falciparum. Thereupon the patient was given mefloquine in decreasing doses (750/500/250 mg) at intervals of 8 hours. The following night he had a circulatory collapse and complained of pain on pressure, especially in the left upper abdomen. Abdominal sonography showed a slightly enlarged spherical spleen with an echo-poor band and fluid collection in the rectovesicular pouch, indicating rupture of the spleen. A splenectomy was performed. Subsequently the number of malaria organisms in the blood smear gradually fell and signs of haemolysis disappeared. Splenic rupture is a very rare complication of acute malaria. It is presumably caused by marked stasis in the splenic sinuses with deformed parasite-containing red blood cells.
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PMID:[Spontaneous splenic rupture in acute malaria tropica]. 159 9

Procoagulant alterations and thrombocytopenia in falciparum malaria correlate with parasitemia, serum levels of tumor necrosis factor alpha (TNF alpha), and clinical severity. Thus, heparin or acetylsalicylic acid (ASA), which are used frequently to prevent thrombosis and (in the case of ASA) to control fever, could be potentially beneficial. We randomized 97 patients with falciparum malaria into three groups: 33 patients received low-dose heparin subcutaneously, 31 received ASA intravenously, and 33 did not receive either drug. All patients received appropriate antiparasitic treatment. Eighteen of 97 patients (seven receiving heparin, five receiving ASA, and 6 in the control group) had complications upon admission. During therapy, elevated TNF alpha and lactate dehydrogenase levels and decreased platelet counts returned to normal values. Except for a minimal partial thromboplastin time prolongation with heparin, heparin or ASA did not affect any laboratory parameter, duration of parasitemia, fever clearance, or the length of hospitalization. Thus, it appears that ASA and heparin do not influence the course of falciparum malaria. Hence, in view of possible side effects, these substances should not be recommended for routine use in the treatment of human malaria.
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PMID:Neither heparin nor acetylsalicylic acid influence the clinical course in human Plasmodium falciparum malaria: a prospective randomized study. 195 71

The phospholipid and fatty acid compositions of the host infected erythrocyte plasma membrane (IEPM) have been determined for erythrocytes infected with the human malaria parasite Plasmodium falciparum. IEPM were prepared by selective lysis of the host erythrocyte (but not of the parasite membranes) with 0.1% saponin, followed by differential centrifugation. The purity of the IEPM was determined by measuring the membrane-specific enzyme markers acetylcholinesterase, glutamate dehydrogenase and lactate dehydrogenase, and by immunoelectron microscopy using monoclonal antibodies specific for human erythrocyte glycophorin A (4E7) and for a 195 kDa parasite membrane glycoprotein (Pf6 3B10.1). Both approaches demonstrated that the host erythrocyte plasma membrane preparation was free from contamination by parasite membranes. During intra-erythrocytic development of the parasite, the phospholipid composition of the erythrocyte membrane was strikingly altered. IEPM contained more phosphatidylcholine (38.7% versus 31.7%) and phosphatidylinositol (2.1% versus 0.8%) and less sphingomyelin (14.6% versus 28.0%) than normal uninfected erythrocytes. Similar alterations in phospholipid composition were determined for erythrocyte membranes of parasitized cells isolated by an alternative method utilizing polycationic polyacrylamide microbeads (Affigel 731). The total fatty acid compositions of the major phospholipids in IEPM were determined by g.l.c. The percentage of polyunsaturated fatty acids in normal erythrocyte phospholipids (39.4%) was much higher than in phospholipids from purified parasites (23.3%) or IEPM (24.0%). The unsaturation index of phospholipids in IEPM was considerably lower than in uninfected erythrocytes (107.5 versus 161.0) and was very similar to that in purified parasites (107.5 versus 98.5). Large increases in palmitic acid (C16:0) (from 21.88% to 31.21%) and in oleic acid (C18:1) (from 14.64% to 24.60%), and major decreases in arachidonic acid (C20:4) (from 17.36% to 7.85%) and in docosahexaenoic acid (C22:6) (from 4.34% to 1.8%) occurred as a result of infection. The fatty acid profiles of individual phospholipid classes from IEPM resembled in many instances the fatty acid profiles of parasite phospholipids rather than those of uninfected erythrocytes. Analysis of IEPM from P. falciparum-infected erythrocytes (trophozoite stage) revealed that, during intra-erythrocytic maturation of the parasite, the host erythrocyte phospholipid composition was markedly refashioned. These alterations were not dependent on the method used to isolate the IEPM, with similar results obtained using either a saponin-lysis method or binding to Affigel beads. Since mature erythrocytes have negligible lipid synthesis and metabolism, these alterations must occur as a result of parasite-directed metabolism of erythrocyte lipids and/or trafficking of lipids between the parasite and erythrocyte membranes.
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PMID:Modification of host cell membrane lipid composition by the intra-erythrocytic human malaria parasite Plasmodium falciparum. 200 Dec 27

185 isolates of Plasmodium vivax were collected from patients visiting the malaria clinic run by the National Malaria Eradication Programme, Delhi, India. Percoll gradient centrifugation was used to concentrate P. vivax parasites from 0.4 to 0.5 ml of blood collected by finger prick. The parasite concentrate from each isolate was electrophoretically analysed for lactate dehydrogenase (LDH), NADP-dependent glutamate dehydrogenase (GDH), glucose phosphate isomerase (GPI) and adenosine deaminase (ADA). Variations were observed in GPI, GDH and ADA systems. Four electrophoretic forms of GPI and 5 each of GDH and ADA were observed. Electrophoretic mobilities of the different isoenzymic forms in P. vivax were identical to those reported for P. falciparum, indicating that the 2 species cannot be differentiated on the basis of electrophoretic patterns of the 4 enzyme systems studied.
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PMID:Plasmodium vivax: enzyme polymorphism in isolates of Indian origin. 269 26

A new electrophoretic variant of glucose phosphate isomerase (GPI), which we now denote GPI-3, has been found in isolates of Plasmodium falciparum from 6 patients, all of whom acquired the infection in the same region (in or near Prachinburi province) of Thailand. In other regions, from which 453 isolates have been tested, only GPI-1 and/or GPI-2 have been found. Two isolates of P. malariae from patients at Kanchanaburi showed a band of GPI activity on cellulose acetate gels at a cathodal position quite distinct from that of any previously known GPI variants in other human malaria parasites. Thirty-nine isolates of P. vivax from 3 regions of Thailand have been examined for variants of GPI and lactate dehydrogenase (LDH). Three forms of GPI were found, corresponding approximately in band positions to GPI-1, 2 and 3 of P. falciparum. The position of the band of LDH activity in P. vivax was the same in all the isolates examined, and different from that of LDH-1 in P. falciparum.
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PMID:Electrophoretic variants of enzymes in isolates of Plasmodium falciparum, P. malariae and P. vivax from Thailand. 269 98

RNA was isolated from trophozoites, schizonts and mixed populations of Plasmodium falciparum. 5% of the total was poly(A+) message, of average length 1.2 kb (10-12 kb maximum) and a poly(A) content of 10%. The mRNA fractions could be translated in vitro by reticulocyte lysates supplemented either with exogenous or P. falciparum tRNA. The patterns from two independent isolates, one cloned (T9-94) and one uncloned (K1) were virtually identical. Major translation products from 16-230 kDa have been measured. The most abundant is lactate dehydrogenase (34.8 kDa). Trophozoite mRNA codes principally for proteins of less than or equal to 93 kDa, while schizont mRNA codes for additional proteins of higher molecular mass. There are marked similarities between the in vitro translation products and proteins synthesised in vivo in synchronous cultures. A number of schizont mRNA translation products (principally those of 230, 203, 185, 170, 115, 101 and 71 kDa) are specifically precipitated without post-translational modification by sera from humans exposed to malaria. A cDNA library has been constructed in phage lambda from total poly(A+) RNA and partially characterised. About 10% of the clones derive from abundant mRNA sequences. Putative actin clones have been isolated from this library and the parasite actin mRNA sized at approx. 2.8 kb.
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PMID:Characterisation and translation studies of messenger RNA from the human malaria parasite Plasmodium falciparum and construction of a cDNA library. 620 36

The involvement of the brain, lungs and kidneys was studied in a lethal rat malaria. Lewis inbred rats were infected with Plasmodium berghei K173. The disease proved fatal within 10-14 days. Parasitaemia showed an increase of up to 43% parasitised red blood cells on Day 10 p.i. The haematocrit decreased from 50% to 12%. The systolic blood pressure dropped from 99 to 56 mmHg. The lactate dehydrogenase activity rose to 2,543 U/l. BUN and serum creatinine doubled during the course of the disease. The transaminases increased tenfold and the cholinesterase decreased from 943 U/l to 271 U/l. Morphologically the kidneys showed an immune complex glomerulo-nephritis with a normal tubulo-interstitial system. The brain, heart and lungs were normal by light microscopic examination. Marked anaemia and shock were the main causes of death in the above-mentioned specimen rat, showing that the course of the disease is significantly different from lethal infections in humans with Plasmodium falciparum who show severe pulmonary, renal and cerebral complications.
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PMID:Causes of death in lethal rat malaria. 661 21

To try to find effects of malaria on clinical serum activity of certain enzymes, 3 groups of infants--malarial, asymptomatic carrier and normal controls--have been designed. Parasitologic data have been compared with serum concentration of lactate dehydrogenase (LDH), Hydroxybutyrate dehydrogenase (HBDH) alanine aminotransferase (ALT), gamma glutamyl transferase (GGT) and 5'nucleotidase (5'Nu). Results show that only LDH and HBDH are significantly increased. Respective coefficients of correlation r = 0.32 (p < 0.05) and r = 0.39 (p < 0.01) show that increasing in LDH and HBDH are linked to malarial parasite density. LDH and HBDH increasing might therefore constitute a marker of malaria.
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PMID:[Aspects of the enzymatic evaluation in Plasmodium falciparum malaria infection]. 784 Jun 86


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