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

The primary objective of this project was to study the life cycle and ecology of Plasmodium pitheci, a malaria parasite of the orang-utan. The field work was based on the orang-utan rehabilitation centre in the Sepilok Forest Reserve of eastern Sabah. Two visits were made to Sepilok, the first in February and March, 1972, and the second (by W.P.) in January 1974. On the first visit two species of "surrogate host" were taken to Sabah, i.e. chimpanzees and Aotus monkeys for experimental work. The arboreal habitat of the orang-utan in the dipterocarp forests of eastern Sabah is described. In the Sepilok Forest Reserve dwell gibbons and leaf-monkeys, in addition to a small population of semi-domesticated and wild, free-ranging orang-utans of various ages. Although numerous species of anopheline mosquitoes have been collected in eastern Sabah, longitudinal studies are not available. Anopheles balabacensis was caught both attracted to orang-utans and to man at Sepilok. This species which is the main vector of human malaria in the north of Borneo, is suspected also of transmitting orang-utan malaria in this part of Sabah. Repeated blood examinations have been made on a number of orang-utans in the centre since 1966 and a high prevalence of infection was recorded with Plasmodium pitheci. In 1966 10 out of 19 animals had demonstrable parasitaemia. Detailed case histories are presented to show the course of parasitaemia in several orang-utans. Infections of P. pitheci were found to run a very chronic course. During the 1972 expedition a second, previously undescribed malaria parasite of the orang-utan was discovered, and was named P. silvaticum. The new parasite was successfully transmitted both by blood inoculation and, later, by sporozoite inoculation, into splenectomized chimpanzees. Although both species of malaria parasite may cause transitory signs of illness, orang-utans in general appear to be little discomforted by the infection. The animals do however suffer from other infectious diseases such as amoebic and balantidial dysentery, and melioidosis is a serious natural hazard which may have accounted for several deaths of wild orang-utans. An unidentified, intraerythrocytic structure that appeared in the blood of one chimpanzee, which had been inoculated with blood from an orang-utan, may have contributed to its death. Detailed descriptions and illustrations of P. pitheci and P. silvaticum are given. All stages of the life cycle of P. silvaticum are known (the tissue stages having been described in the liver of a "surrogate host", the chimpanzee) but only the blood and sporogonic stages of P. pitheci have been seen. This species was not infective to a chimpanzee, although there is an earlier report of a transient infection in this host by other workers. In the blood both parasites showed a tertian periodicity. From the appearance of the tissue schizonts on the seventh day it was estimated that the complete pre-erythrocytic cycle of P. silvaticum in the chimpanzee would occupy 8 days. P...
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PMID:Malaria of the orang-utan (Pongo pygmaeus) in Borneo. 1 May 89

Infections with both Epstein-Barr virus (EBV) and malaria have been implicated as causal factors in the pathogenesis of Burkitt's lymphoma (BL). Proposed trials of preventive measures for both infections are receiving serious consideration as possible means of establishing a causal relationship with BL. In this paper we examine certain models for the interaction of EBV and malaria in the induction of BL, and also review the aims of the longitudinal, population-based study being conducted in the West Nile District of Uganda. Given existing knowledge, the outcome of preventive trials, even for the most simple interaction models, is unpredictable and, under certain circumstances, trials of an EBV vaccine could actually increase the incidence of BL. It is suggested that trials of an EBV vaccine at this time would be premature and should be delayed at least until the results from the West Nile prospective study are clear.
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PMID:Epstein-Barr virus-malaria interaction models for Burkitt's lymphoma: implications for preventive trials. 17 23

Sarcomas were induced in CFW mice by the iv inoculation of simian virus 40 (SV40) in neonatal animals. Infection with murine malaria parasites, Plasmodium berghei yoelli, decreased the latency and increased the incidence and invasiveness of the tumors. All mice given both SV40 and P. berghei yoelli had sarcomas of the liver and spleen at 9 months of age. At 11 months of age, 70% of the SV40-inoculated mice had sarcomas of the liver indistinguishable from those in the group given both pathogens. Only 1 lung metastasis was seen in the SV40-treated group. The sarcomas contained SV40 T-antigen as revealed by the indirect immunofluorescence technique. Among adult CFW mice given iv injections of SV40, only 2 tumors were found at 11 or 12 months after virus inoculation. Both tumors were in the lungs; 1 was an adenoma and 1 was a papillary adenocarcinoma. Neither gave a positive reaction with the immunofluorescence test.
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PMID:Sarcomas induced by injection of simian virus 40 into neonatal CFW mice. 22 3

Although partial resistance (RI) of Plasmodium falciparum to quinine is common in some areas of the world, failure to obtain an initial response (RII or RIII) is unusual. Furthermore, emergence of quinine resistance during therapy of malaria infections in humans and animals is uncommon. In the current study, exposure of the Panama II strain of P. falciparum in Aotus monkeys to subcurative quinine therapy during six serial passages over 6 months resulted in a shift in the quinine responsiveness of the strain from mild insensitivity to quinine to uniform resistance of a marked degree. Treatment with quinine for 14 days of infections in 12 monkeys with the original isolate resulted in cure in 8 monkeys and RI resistance in 4. Infections with the resistant isolate (selected under quinine pressure) were uniformly resistant to cure by 14 days of quinine; resistance to quinine was RIII in 4 of 12 monkeys and was RII in 5. These results suggest that extensive usage of quinine or related drugs (e.g., mefloquine) in the field may result in decreasing sensitivity of falciparum malaria to quinine.
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PMID:Selection of increased quinine resistance in Plasmodium falciparum in Aotus monkeys. 41 28

Malaria infection in young rats is characterized by high parasitemia, severe anemia, and death. Parasitemia is lower in older rats, and the rats usually survive. This study was designed to investigate the immunological basis of this difference. T cell numbers in the thymuses and spleens of young (4 weeks old) and in adult (18 weeks old) infected and control rats were determined by killing with anti-theta serum and complement. The number of complement receptor lymphocytes (B cells) in spleens was determined after these cells had formed rosettes with sensitized, complement-coated sheep erythrocytes. Infection in young rats was characterized by progressive and severe thymic involution and by decreasing numbers of T and B cells in the spleen. In 18-week-old rats, T cell numbers in the spleen were slightly below those of controls early in infection but exceeded normal values by day 15. Progressive thymic involution was not a feature of infection in adult rats. The number of complement receptor lymphocytes in the spleens of adult rats decreased dramatically early in infection but were nearly normal by day 15. Severity of malarial infection in young rats is related to the inability of their lymphocytes to respond to Plasmodium berghei antigens early in infection in a way that leads to immunity.
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PMID:T and B cell population changes in young and in adult rats infected with Plasmodium berghei. 78 Feb 72

Rhesus monkey erythrocytes when incubated in vitro under similar conditions to those used for the cultivation of Plasmodium knowlesi-infected erythrocytes in vitro, exhibit an increase both in their osmotic fragility and in the activity of their acetylthiocholinesterase. No effect was observed on the catabolism of glucose through the glycolytic pathway or through the primary dehydrogenases of the pentose phosphate pathway. The ATP content of normal monkey erythrocytes was also unchanged during incubation in vitro. These observations indicate that incubation of erythrocytes in vitro primarily causes membrane changes. Infection of normal erythrocytes by P. knowlesi was reduced markedly by preincubation in vitro at 37 degrees C for 24 and 48 h. These results suggest that the maintenance of integrity of the surface of the erythrocyte in vitro is a necessary prerequisite for an efficient culture system for the malaria parasite.
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PMID:The effect of incubation in vitro on the susceptibility of monkey erythrocytes to invasion by Plasmodium knowlesi. 82 5

A lipid analysis was performed on the avian malaria parasite Plasmodium lophurae, freed from duckling erythrocytes by immune hemolysis, and on the erythrocytes and plasmas of normal and P. lophurae-infected ducklings. Major lipids of normal erythrocytes were: phosphatidylcholine (40% of total lipids), phosphatidylethanolamine (20%), cholesterol (20%), sphingomyelin (11%), and glycosphingolipids (5%). Major fatty acids of erythrocyte total phospholipids (74% of total lipids) were 16:0 (22%), 18:2 (n-6) (21%), 18.1 (n-7, n-9) (18%), 18:0 (9%), 20:4 (n-6) (9%), 22:6 (n-3) (5%). Erythrocyte phosphatidylcholine was greater than 90% the diacyl form, while phosphatidylethanolamine was approximately 44% alkoxy forms and phosphatidylinositol approximately 11% alkoxy forms. Major fatty aldehydes of phosphatidylethanolamine were 16:0 (47%), 18:1 (23%), 18:0 (14%), and 14:0 (12%). The lipid composition of P. lophurae (plus the parasitophorous vacuole membrane) was qualitatively and quantitatively different from that of the duckling erythrocyte in a number of respects. Major lipids were phosphatidylcholine (40%), phosphatidylethanolamine (36%), cholesterol (8%), phosphatidylinostol (4%), 1,2-diacylglycerols (3%), sphingomyelin (2%), and glycosphingolipids (2%). Diphosphatidylglycerol (approximately 1%) was also detected. The major fatty acids of parasite total phospholipids (86% of total lipids) were more saturated than those of the erythrocyte, and octadecenoic acids were notably elevated: 18:1 (33%), 16:0 (26%), 18:0 (16%), 18:2 (12%), 20:4 (3%), and 22:6 (3%). Parasite phosphatidylcholine and phosphatidylethanolamine were greater than 93% the diacyl form and phosphatidylinositol was approximately 25% alkoxy forms. Major fatty aldehydes of the phosphatidylethanolamine were 14:0 (62%), unidentified long chain forms (24%), 16:0 (7%), 18:0 (4%), 18:1 (3%). The lipid composition of the infected erythrocyte reflected the separate contributions of the erythrocyte and parasite. The major lipids of normal duckling plasma were phosphatidylcholine (33%), triacylglycerols (22%), cholesterol esters (20%), cholesterol (12%), phosphatidylethanolamine (5%), and sphingomyelin (2%). The fatty acids of plasma total lipids were 18:1 (26%), 16:0 (26%), 18:2 (12%), 20:4 (12%), 18:0 (9%), 22:6 (3%). Plasma phosphoglycerides were remarkably lower in C18 unsaturated fatty acids and higher in 20:4 than the erythrocyte phosphoglycerides. Infection of ducklings with P. lophurae caused increases in plasma unesterified fatty acids, triacylglycerols and cholesterol esters, and a notable rise in the 18:1 content of all fatty acid-containing plasma neutral lipids. These findings are compared with those reported for other species of Plasmodium infecting other avian and mammalian hosts.
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PMID:Lipids of Plasmodium lophurae, and of erythrocytes and plasma of normal and P. lophurae-infected Pekin ducklings. 84 41

In October 1988, a project was implemented for assessing the malaria chemoprophylactic efficacy of weekly chloroquine (CQ) and daily proguanil (PROG) during pregnancy in Muheza-Tanzania. Resultant CQ and PROG-cohorts of infants were followed up for prompt diagnosis and treatment of malaria. Infections were primarily treated with 25 mg base amodiaquine/kg over 3 days. By September 1990, 49 and 60 infants from PROG and CQ cohorts respectively had completed one year follow up. Thirty-five (71%) infants of PROG and 44 (73%) for CQ-cohort were infected with malaria before 3 months of age. The one year mean infection episode rates were 7 (PROG-cohort) and 6.6 (CQ-cohort). Amodiaquine cleared 209 (80%) of PROG's total infections and 224 (81%) for CQ-cohort, and significantly reduced the infection load among clearance failures. Clearance failures had high pre-treatment parasite densities whilst post-treatment densities were higher in the CQ-cohort than PROG-cohort. Low malaria immunity and chloroquine's long residence time could explain these differences. We conclude that early infancy malaria is common and should always be suspected, looked for and adequately treated. Amodiaquine is better than chloroquine for malaria primary therapy during infancy and early childhood.
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PMID:Malaria in infants whose mothers received chemoprophylaxis: response to amodiaquine therapy. 129 36

All 110 patients seen in North East Scotland after contracting malaria from foreign travel were treated in the Regional Infection Unit in Aberdeen. Those patients managed there from January 1980 to March 1991 are described. There were 54 episodes of Plasmodium falciparum malaria (49%) and 26 episodes (23%) of Plasmodium vivax malaria. The remainder had either mixed infection or were diagnosed as malaria on high clinical probability. The majority of the patients were male (80%) and under 40 years of age (84%). Most patients were either caucasians born in the UK (69%) or native Africans (23%) who were students recently arrived for further education or who had returned from visiting their country of origin for summer holidays. The British residents acquired infection either while on oil related business in West or Central Africa (46%) or after travelling on holiday (30%). The peak incidence of presentation was August and September. 93.5% of patients with falciparum malaria had returned or originated from Africa. 42% with vivax malaria had visited Africa and 27% Papua New Guinea. 70% had been prescribed antimalarial prophylaxis but less than half of these took their medication correctly. The majority of patients with falciparum malaria presented within two weeks of arrival in Britain while patients with vivax malaria presented at varying (but generally longer) intervals, 42% being diagnosed more than three months after exposure. Falciparum infection was more severe although there have been no deaths in the unit from malaria. Our experience seemed of interest and worth reporting because of the number of patients whose infection reflected travel related to the off shore oil industry, which is centred in Aberdeen.
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PMID:Malaria in Aberdeen: an audit of 110 patients admitted between 1980-1991. 141 77

Infection of the squirrel monkey, Saimiri sciureus, with several strains of Plasmodium falciparum leads in a proportion of animals to neurological symptoms with a fatal outcome. This first simian model for human cerebral malaria was studied with three strains of parasites, the uncloned Palo Alto(FUP-1) strain, the Palo AltoPLF3 clone MHB11, and the recently monkey-adapted P. falciparum strain IPC/RAY. Cerebral malaria could develop during primo infection of monkeys, whether the animals had been splenectomized or not. It did not occur in all animals and the appearance of neurological symptoms could not be predicted, as it was not related to the degree of parasitemia or duration of parasite infections.
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PMID:Experimental Plasmodium falciparum cerebral malaria in the squirrel monkey Saimiri sciureus. 149 71


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