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

Malnutrition interacting with infectious and parasitic diseases are the main causes of the appalling mortality in childhood in the tropics. The most important single safeguard against these in infancy is breast feeding and the trend now evident to abandon this is a disaster which demands urgent attention. Reasons for this trend are discussed. Efforts to control infectious diseases, other than smallpox, have had little success and the emergence and spread of dengue haemorrhagic fever in S.E. Asia have added new dimensions to the problem. Malaria is still widely prevalent in the tropics and falciparum malaria, holoendemic in much of Africa, remains a major cause of death with its most serious impact on pregnant women and children. The emergence and spread of drug resistant strains of this parasite in parts of the world is a cause for serious concern. Quartan malaria is also an insidious corruptor of health in childhood and commonly causes the nephrotic syndrome. Neonatal jaundice, often associated with G6PD deficiency, is increasing in frequency in urban areas of Africa and now constitutes a significant hazard to the newborn and requires urgent investigation. These problems in tropical paediatrics indicate the need for urgent reappraisal of our role as a profession in the affairs of the tropical developing world.
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PMID:Aspects of tropical paediatrics. 79 3

The jungle habitat of the Temuan aborigines harbors a variety of infectious diseases, the most notable being malaria. Our study of 15 genetic systems in the Temuan revealed substantial polymorphism and within-population genetic diversity. The polymorphisms for Hb beta, G6PD, and El are of interest in regard to genetic adaptation to malaria. Among the polymorphisms investigated we conclude that G6PD deficiency and elliptocytosis are likely to have malaria-resistant effects as evidenced by their low association with malarial parasitemia or their higher frequency in adults than in children. These findings suggest that the malarial habitat of the Temuans is livable in the long range sense for them because of the cluster of malaria-resistant alleles in their gene pool (G6PD)-, El, and possibly, but not tested here because of its low frequency, Hb beta E). The same condition probably holds for the Semai, the nearest aborigine neighbors of the Temuan (although the Semai have not been tested for malarial parasitemia and for these polymorphisms simultaneously), since the Semai have substantial Hb betaE, G6PD-, and El. The Temuan have a cultural identity system of rituals, beliefs, and certain aspects of language which effectively isolates them genetically from Malays and other nonaborigines. This system hinders the dilution of the malaria-resistant alleles of the Temuan gene pool with the malaria-susceptible alleles of the nonaborigine gene pools.
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PMID:Genetic factors and malaria in the Temuan. 81 97

Great streams of tourists flow every year from the Federal Republic to southern countries. The danger of infection with serious tropical diseases such as smallpox, cholera or leprosy is fairly small, statistically speaking. Even exotic parasitoses merit only individual medical interest in the majority of cases. Of greater importance are the cosmopolitan infectious diseases such as typhoid fever, paratyphoid, salmonella enteritis, poliomyelitis, viral hepatitides which are transmitted orally and altogether are imported in no small numbers. The alteration of the mode of living caused by the holiday and frequently a false confidence in the hygienic conditions favor the infection. Almost independent of the behavior of the tourists are the infections produced by insect bites, such as malaria or the leishmaniases, which often end fatally for lack of recognition. Here, a better enlightment of the travelers, the use of prophylactic agents and improvement of diagnosis must be instituted.
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PMID:[Tourism and risk of infection (author's transl)]. 82 9

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

The causes of mortality and frequency of diseases were tabulated in 304 autopsies performed at Hopital Mama Yemo, Kinshasa, between July 1973 and December 1974. 78 of these autopsies were performed on subjects who died at Hopital Mama Yemo, 36 encompassed subjects from other hospitals, and 190 were of medicolegal cases in which the cause of death was not apparent from external examination. Men comprised 63.5% of autopsied cases. The mean age was 30.19 +or- 1.31 for men and 19.84 +or- 1.76 for women. 16.8% of deaths were due to homicide, 6.3% to suicide, and 8.9% to accidents, yielding an overall prevalence for trauma of 32%. Cancer accounted for only 3% of deaths, and cardiovascular diseases 8.2%. Bacterial infections (predominantly streptococcal disease, lobar pneumonia, and pulmonary tuberculosis) represented the largest single cause of death (17.4%). Parasitic infections comprised a further 6.3% of mortality and viral infections 7.2%, giving infectious diseases a combined frequency of 30.9%. Metabolic diseases were responsible for an additional 11.8% of deaths. Obstetric causes were identified in 3.9% of fatalities, and 95% of these cases represented hemorrhagic and septic complications of illegal abortion. Neonatal deaths (4.3%) were largely due to pneumonitis from aspirated amniotic fluid. A final 5.9% of deaths were unexplained. Also analyzed were cases of sudden death occurring outside the hospitals. 31.3% of these deaths were attributed to cardiovascular diseases and 46.3% to infection (including 2.5% due to septic abortion). Finally, the frequency of major diseases in this series was tabulated. Malaria was most frequently found (41.8%), followed by intravascular erythrocytic sickling (18.3%) and hypertension (16%). 12% of females in this series (20% of those dying traumatically) showed evidence of pelvic inflammatory disease. This series is considered to overestimate the frequency of trauma because of the large number of medicolegal cases that fall in this category. This selection for trauma further led to an oversampling of adult men. Nonetheless, it represents the 1st and best qualitative estimate of disease mortality and prevalence in Zaire. The trends in mortality and morbidity identified through this study provide a basis for planning health care and health education.
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PMID:Autopsy analysis of disease frequency in Kinshasa, Republic of Zaire. 96 86

An outline is given of the pattern of communicable disease in the South Pacific, as far as it is known. Surveillance and research are imcomplete and the World Health Organization is assisting in carrying these out. Reporting and laboratory diagnosis of communicable disease are inadequate and sometimes inaccurate. This is being improved. Medical checks for intending migrants from the South Pacific are, in a number of cases, inadequately performed in the country of origin and this situation should be altered. The risks to surrounding developed countries from migrants, temporary workers and returning travellers are not tremendous but they cannot be neglected and vigilance has to be maintained. Tuberculosis importation does present risks, as does that of typhoid. Malaria importation carries risks for Northern Australia. Leprosy poses little real risk to Australia or New Zealand and neither does filariasis. Cholera would have to be watched for closely should there ever be a South Pacific outbreak, but the developed countries around the South Pacific which are cholera-non-receptive can control occasional cases. Other than malaria, tuberculosis, typhoid and possibly dengue, problems are thus mainly in the diagnosis and treatment of individuals.
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PMID:Communicable disease in the South Pacific Islands, 1. 100 33

A prospective study was made in 283 patients who attended IMAN's Children's Hospital, with fever the main symptom. A clinical and paraclinical procedure was designed for the study of each patient. 112 patients were eliminated because they did not follow the established criteria. All patients had acute infectious diseases considered trivial; 85% were 3 weeks to 2 years of age. They all had an antibacterial treatment without precise diagnosis. It was considered that on admission the patients showed a normal course in the natural history of the basic disease. The study group included 171 patients 2 months to 13 years of age; 62.5% had fever due to infection, 12.2% to collagenopathies, 7% to neoplasias 5.2% to miscellaneous causes and 12.8% were not diagnosed. The most common infectious causes for prolonged fever were tuberculosis, upper respiratory infections, amoebic liver abscess, typhoid fever and malaria. Careful questioning and clinical examination were enough to enlighten diagnosis in more than 80% of the patients.
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PMID:[Prospective study of patients with prolonged fever]. 108 38

A hypothesis which explains disease prevalence among different socio-economic groups following early infantile modulation of cell-mediated immunity by infection and nutrition related stress is presented. Wealthy populations living under highly hygienic circumstances can develop their cell-mediated immunity to genetic expectation while their humoral systems remains unstimulated. Primitive populations protect the infant's immune development by breast feeding and suffer from temporary cell-mediated immune deficiencies due to intercurrent infectious disease and famine later on. Intermediary populations harbour a small percentage of people, whose cell-mediated immune system has been permanently damaged by infection in early childhood, leading to a high incidence of diseases linked to cell-mediated immune deficiency. The possible cocarcinogenesis of the cell-mediated immune deficiency following repeated gastroenteritis and persistent stimulation of B cells, leading to alpha heavy chain disease and primary intestinal lymphoma, or due to falciparum malaria in newborns and its impact on the EB virus genome in development of Burkitt's lymphoma, are discussed.
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PMID:Immune modulation and disease patterns in population groups. 122 70

Recent investigations indicate that Burkitt's lymphoma consists of several subtypes, defined by their clinical and molecular features. Each geographical region so far studied appears to consist of a different mixture of subtypes. Interestingly, there appear to be geographic 'gradients' with respect to the fraction of tumors associated with EBV and the type of 8;14 chromosomal translocation. The rate of EBV association is highest in Equatorial Africa, lowest in North America and intermediate in South America. The fraction of tumors with breakpoints far upstream of the c-myc gene follows a similar pattern. These findings strongly suggest that the subtypes of Burkitt's lymphoma are environmentally determined, and we propose that the pattern of infection (e.g. malaria) to which the young child is exposed influences the tumor subtype distribution by altering the relative and absolute numbers of various B cell precursors at sites of B cell ontogeny (the bone marrow, and possibly mesentery). These B cell precursors are the cells which are susceptible to the specific chromosomal translocations associated with Burkitt's lymphoma. We further propose that immunoglobulin enhancers (recognized and unrecognized) both influence the likelihood of the translocation occurring, and in at least a fraction of cases, contribute to the deregulation of a c-myc. EBV, via EBNA-1, the only invariably expressed latent-gene in Burkitt's lymphoma, probably influences c-myc expression in Burkitt's lymphoma by increasing immunoglobulin enhancer function. Thus, in effect, EBV collaborates with the translocations associated with Burkitt's lymphoma in causing c-myc deregulation. This collaboration is independent of the breakpoint location. While other molecular abnormalities must be able to contribute to myc deregulation in the same way, EBV association in Burkitt's lymphoma is probably determined by the age at which EBV infection occurs (being more likely when infection occurs in very young children) and perhaps also by other infectious diseases that numerically influence the fraction, and predominant stage of differentiation (and hence translocation breakpoint sites) of immature B cells infected by EBV. The presence of EBV in many such cells greatly increases the incidence rate of Burkitt's lymphoma, since one of the genetic lesions needed to deregulate c-myc is already present.
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PMID:Epstein-Barr virus and Burkitt's lymphoma. 133 92


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