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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

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

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

Infections with parasitic protozoa have always been problems for the developing world and are becoming of greater importance to the developed world in this age of easy international travel. The major human protozoal diseases are summarised with an emphasis on their presentation in normal hosts and in immunocompromised individuals and current US drug treatment recommendations are discussed. Present antiprotozoal regimens are based either on a pharmacokinetic rationale or on clinical trial and error. Regimens based on trial and error include amphotericin B against leishmaniasis and arsenic against African trypanosomiasis. Regimens which are to some extent driven by pharmacokinetic or biochemical considerations include paromomycin and metronidazole against amoebiasis, sodium stibogluconate against leishmaniasis, halofantrine and mefloquine against malaria, dihydrofolate reductase (DHFR) inhibitors against Pneumocystis carinii and toxoplasmosis and aerosolised pentamidine against P. carinii pneumonia. The majority of pharmacokinetic studies have been performed only on agents which have some therapeutic activity against other diseases of the developed world. Despite the trend toward rational treatment regimens, no studies have been performed that permit optimisation of antiprotozoal treatment regimens on the basis of clinical conditions such as renal failure.
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PMID:Pharmacokinetic justification of antiprotozoal therapy. A US perspective. 178 41

The acquired immune deficiency syndrome (AIDS) is fundamentally the same disease in all parts of the world, but the prevalence of microorganisms in an environment governs the patterns of disease arising from reactivated latent infections, invading pathogens and opportunistic infections. AIDS in Africa has certain characteristic presentations. Enteropathic AIDS is most common: Cryptosporidium and Isospora belli are identified in up to 60% of patients, but it is uncertain whether they are the causes of diarrhoea. Pneumocystis carinii pneumonia is rare. Tuberculosis, both pulmonary and extrapulmonary, is the supreme complicating infection. Herpes zoster is frequently the first clinical presentation, and has a 95% positive predictive value for HIV positivity. Measles may be more frequent in infants born to HIV-infected mothers, and appears to be worse in HIV-infected children. There is accelerated progress of both diseases in patients infected by HIV and Mycobacterium leprae. Salmonellosis is frequent. There is no direct interaction between malaria and HIV, but, by being a potent cause of anaemia, malaria enhances transmission of HIV to children through blood transfusion. HIV-positive subjects are liable to new or reactivated visceral leishmaniasis with dissemination to unusual sites. Cerebral toxoplasmosis is common. There are no apparent interactions between HIV and helminths, although there is one report of hyperinfection with Strongyloides stercoralis. Cryptococcal meningitis has high frequency. Infections with Histoplasma encapsulatum are common in tropical America, but there has been no increase of frequency of H. duboisii in Africa since the advent of AIDS.
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PMID:Opportunistic infections in AIDS in developed and developing countries. 220 Nov 7

A retrospective survey was carried out on adult medical admissions to Kamuzu Central Hospital, Lilongwe, Malawi during the period January to December 1986, and results compared with those obtained in Queen Elizabeth Central Hospital, Blantyre in 1973. There were 4700 admissions which was more than twice the number seen in Blantyre. However, the age distribution, the pattern of disease and the overall hospital mortality were similar. Infections (malaria, pneumonia, tuberculosis, gastroenteritis/dysentery and meningitis) were the most common cause of admission, and the major causes of death were still tuberculosis, pneumonia and meningitis. Smoking related diseases were uncommon, and there was no documented case of ischaemic heart disease. The reasons for the importance of periodic surveys, such as the present study, are discussed.
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PMID:Medical admissions to Kamuzu Central Hospital, Lilongwe, Malawi in 1986: comparison with admissions to Queen Elizabeth Central Hospital, Blantyre in 1973. 229 37

Infections with the human malaria parasite Plasmodium falciparum are characterized by sequestration of erythrocytes infected with mature forms of the parasite. Sequestration of infected erythrocytes appears to be critical for survival of the parasite and to mediate immunopathological abnormalities in severe malaria. A leukocyte differentiation antigen (CD36) was previously suggested to have a role in sequestration of malaria-infected erythrocytes. CD36 was purified from platelets, where it is known as GPIV, and was shown to be a receptor for binding of infected erythrocytes. Infected erythrocytes adhered to CD36 immobilized on plastic; purified CD36 exhibited saturable, specific binding to infected erythrocytes; and purified CD36 or antibodies to CD36 inhibited and reversed binding of infected erythrocytes to cultured endothelial cells and melanoma cells in vitro. The portion of the CD36 molecule that reverses cytoadherence may be useful therapeutically for rapid reversal of sequestration in cerebral malaria.
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PMID:Identification of a platelet membrane glycoprotein as a falciparum malaria sequestration receptor. 268 26

Infections with the human malaria Plasmodium falciparum are characterized by the retention of parasitized erythrocytes in tissue capillaries and venules. Erythrocytes containing trophozoites and schizonts attach to the endothelial cells that line these vessels by means of structurally identifiable excrescences present on the surface of the infected cell. Such excrescences, commonly called knobs, are visible by means of scanning or transmission electron microscopy. The biochemical mechanisms responsible for erythrocyte adherence to the endothelial cell are still undefined. In an attempt to identify the cytoadhesive molecule on the surface of the infected cell, we have prepared monoclonal antibodies to knob-bearing erythrocytes infected with the FCR-3 strain of P. falciparum. One of these monoclonal antibodies, designed 4A3, is an IgM that reacts (by means of immunofluorescence) with the surface of unfixed erythrocytes bearing mature parasites of the knobby line; it does not react with knobless lines or uninfected erythrocytes. By immunoelectron microscopy the monoclonal antibody 4A3 was localized to the knob region. In an in vitro cytoadherence assay, the monoclonal antibody partially blocked the binding of knob-bearing cells (FCR-3 strain) to formalin-fixed amelanotic melanoma cells. The monoclonal antibody was used to immunoprecipitate a protein from extracts of knobby erythrocytes that had been previously surface iodinated. By a two-dimensional peptide mapping technique, the antigen recognized by the monoclonal antibody was found to be structurally related to band 3 protein, the human erythrocyte anion transporter.
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PMID:Characterization of a modified red cell membrane protein expressed on erythrocytes infected with the human malaria parasite Plasmodium falciparum: possible role as a cytoadherent mediating protein. 264 11

Parasitaemias and loss of natural antibody to Plasmodium falciparum were studied in 104 infants in a highly endemic area of Papua New Guinea. There were 4 cases of congenital infection. Most infants lost malaria-specific immunoglobulin G (IgG) between 4 and 7 months (median = 21 weeks). 73% of heavy infections developed in infants without detectable antimalarial IgG. Infections in the presence of antimalarial IgG were asymptomatic and had scanty parasitaemias.
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PMID:A seroepidemiological study to evaluate the role of passive maternal immunity to malaria in infants. 269 54


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