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At least 487 records · Page 27Linked to original sources
PubMed1991

Symptomatic diagnosis of Plasmodium falciparum malaria in field conditions.

This paper examines the relationship between clinical manifestations and parasitaemia in relation to malaria endemicity. Discriminant analysis, showed that fever alone can detect 74.4% of the parasite positive cases and the inclusion of other symptoms like headache, vomiting, nausea, bodyache and diarrhoea marginally increases the efficiency of discrimination (i.e., from 74.4% to 74.7%). It was observed that the association of symptoms with parasitaemia varies with the degree of malaria endemicity. The percentage of correct classification of parasite carriers varied from 45.7% in the immune population to 80.6% in the non-immune population. A significant difference was observed in the density grades between symptom positive and symptom negative cases. Slide examination in hyperendemic area does not give any advantage over the clinical examination and the data obtained from the slides collected during fever surveys tend to overestimate the malaria incidence in hyperendemic area.

Animals↗
PubMed1995

Response of Plasmodium falciparum to chloroquine and Fansidar in vivo and chloroquine and amodiaquine in vitro in Uganda.

The response of P. falciparum to chloroquine and pyrimethamine-sulfadoxine in vivo and chloroquine and amodiaquine in vitro was investigated in parasitaemic school children from six locations. Mean parasite sensitivity to chloroquine at day 7 was 74% (range 61-97) with parasite clearance rates between 2-3 days and complete defervescence in 85% of febrile children. Sensitivity declined in the four sites followed up to day 14 to 45% (range 37-53). Parasites were significantly more sensitive to pyrimethamine/sulfadoxine at 5/6 sites (100% day 7) but 5% of subjects became parasitaemic by day 14. In vitro isolates were significantly less sensitive to chloroquine than to amodiaquine with a mean 99% effective concentration of 348 mumol/L compared to 6.44 mumol/L. Clearly the role of chloroquine as the primary therapy for uncomplicated P. falciparum malaria should be reconsidered especially in the light of increasing disease severity and resurgence. Amodiaquine may be suitable alternative with pyrimethamine/sulfadoxine as second line and for more severe malaria prior to referral. The cost of alternative antimalarials and the dynamic and deteriorating pattern of resistance are powerful arguments for more objective slide diagnosis to minimise drug pressure and a regular drug sensitivity surveillance system. We believe that the latter should concentrate on measuring clinical drug efficacy in symptomatic outpatients rather than in asymptomatic children while the former needs more pragmatic and economical strategies possibly centred on seasonality and risk.

Amodiaquine↗
PubMed1993

[Soluble antigens of intra-erythrocyte stages of Plasmodium falciparum: diagnostic and vaccinal value].

A wide variety of soluble antigens also called exoantigens or excretory-secretory antigens are released by asexual blood stages of P. falciparum at the time of schizont burst and subsequent merozoite invasion. At present, most of these soluble malarial proteins have been purified and have had their genes cloned; the primary sequence displays considerable polymorphism upon tandem repeats. However, its function and the relevance of the polymorphism for the induction of host immune response, predominantly IgM and T-cell-independent type, has yet to be determined. The potential of P. falciparum exoantigens as immunodiagnostic tools has been the focus of numerous studies. Enzyme immunoassays or radioimmunoassays for the detection of malarial antigens in blood of suspected peoples have been reported. Their development requires increasing both specificity and sensitivity. Recently, some P. falciparum exoantigens have been proposed as candidates for inclusion in an anti-disease vaccine which induces a clinical but not parasiticidal immunity against malaria. There is much interest in this concept and their efficiency remains to be confirmed, as new strategies are needed in the prevention of malaria.

Animals↗
PubMed1995

Localized permanent epidemics: the genesis of chloroquine resistance in Plasmodium falciparum.

Localized permanent epidemics occur when, for an indefinite period of time, there is a temporary but continuous introduction of unprotected non-immunes into the same locality of a hyperendemic area. The main epidemiological factors involved in the genesis of localized permanent epidemics were encountered in Pailin (Cambodia) the epicenter of drug resistance in Southeast Asia: a very efficient vector, Anopheles dirus, exophilic and of limited distribution with, therefore, adjacent hyperendemic and non-endemic areas; a permanent pole of attraction in the hyperendemic area: Pailin's sapphires and rubies; a temporary but continuous influx of non-immunes into the pole of attraction: continuous influx of non-immunes into the Pailin gem mining area. In the gem-mining Pailin village drug pressure was considerable: mass drug administration, a medicated salt project and permanent self-medication with very high doses, much higher doses being required to cure non-immunes with heavy infections and severe clinical attacks in epidemic situations. It appears, therefore, that the emergence of chloroquine resistance in Southeast Asia was the consequence of the localized permanent epidemics in Païlin. High level resistance was the result of continuous and intensive serial passages of P. falciparum in the non-immune subjects, large numbers of parasites being exposed to a high level of drug pressure at each passage. Similar epidemiological conditions are encountered in some parts of South America where the exophilic vector is An. nuneztovari. In Colombia, whose eastern mountains bordering Venezuela yield the most highly prized emeralds in the world, chloroquine resistance was detected at about the same time as in Southeast Asia.(ABSTRACT TRUNCATED AT 250 WORDS)

Africa↗
PubMed1997

Quinoline resistance mechanisms in Plasmodium falciparum: the debate goes on.

Despite considerable therapeutic success with the antimalarial 4-aminoquinolines such as chloroquine, there is serious doubt about the future of this drug class due mainly to the development and spread of parasite resistance throughout endemic areas. In this article we review the possible biochemical and molecular basis of resistance. Based on our current understanding we have considered the possibility of developing strategies which may allow the aminoquinolines to once again be used effectively against P. falciparum. Our conclusions are that drug resistance is the result of a reduced rate of drug uptake which in turn reduces the amount of drug available to bind the target. The basis for this reduced accumulation could be an altered pH gradient making the food vacuole more alkaline or the parasite cytosol more acidic, an efflux pump removing drug directly from the membrane or any other process which will reduce the rate of drug uptake. Central to the effectiveness of this resistance mechanism is the transient availability of a high affinity, low capacity drug binding site (possibly haem) within the parasite. Resistance reversers such as verapamil influence the apparent Ka for this drug binding phenomenon via an increased drug uptake rate. We demonstrate that by chemical modification of the aminoquinolines, producing predictable alterations in their physicochemical properties, that it is possible to minimise the verapamil sensitive component of resistance and reduce significantly cross-resistance patterns without loss in absolute activity. Based on these views we suggest that the aminoquinoline antimalarials still have a role to play in the cheap, safe and effective chemotherapy of falciparum malaria.

Aminoquinolines↗
PubMed1997

[Specific antibodies against Plasmodium falciparum antigens in immune subjects: I. Comparison of detection/titration methods].

We report a comparative study of specific antibody levels to the blood stages of P. falciparum in individuals living in two different areas with different transmission levels of malaria. We have compared 2 techniques for the detection/titration of antibodies i.e. ELISA and IFI, ELISA being particularly suitable for immuno-epidemiological related studies. A schizont lysate from P. falciparum infected red blood cells from FUP/CB Marburg strain as antigen proved usefullness, as compared with an antigen extracted from a local strain recently adapted to in vitro culture. Using these techniques, high specific antibody responses were found in the villagers' sera and mean levels of antibodies increased with age. Levels of specific IgG were comparable between those two locations, in spite of a ten fold higher level of transmission between the two villages. In contrast, a significantly higher level of IgM in adults living in holoendemic.

Adolescent↗
PubMed2000

Two Plasmodium falciparum genes express merozoite proteins that are related to Plasmodium vivax and Plasmodium yoelii adhesive proteins involved in host cell selection and invasion.

Two related Plasmodium falciparum genes and their encoded proteins have been identified by comparative analyses with Plasmodium vivax reticulocyte binding protein 2 (PvRBP-2). The P. falciparum genes have a structure which suggests that they may be the result of an evolutionary duplication event, as they share more than 8 kb of closely related nucleotide sequence but then have quite divergent unique 3' ends. Between these shared and unique regions is a complex set of repeats, the nature and number of which differs between the two genes, as well as between different P. falciparum strains. Both genes encode large hydrophilic proteins, which are concentrated at the invasive apical end of the merozoite and are predicted to be more than 350 kDa, with an N-terminal signal sequence and a single transmembrane domain near their C termini. Importantly, they also share gene structure and amino acid homology with the Plasmodium yoelii 235-kDa rhoptry protein family, which is also related to PvRBP-2. Together these Plasmodium proteins define an extended family of proteins that appear to function in erythrocyte selection and invasion. As such, they may prove to be essential components of malaria vaccine preparations.

Amino Acid Motifs↗
PubMed2000

Linkage disequilibrium between two chromosomally distinct loci associated with increased resistance to chloroquine in Plasmodium falciparum.

Chloroquine-resistance in Plasmodium falciparum is associated with polymorphisms in a locus on or near the cg2 gene on chromosome 7, and in the pfmdr1 gene on chromosome 5. In this study we typed P. falciparum DNA from uncomplicated malaria cases in The Gambia in 1990, 1995 and 1996 for size polymorphism in the omega repeat of cg2, for sequence polymorphisms in pfmdr1 at codons 86 and 184, in dhfr at codon 108 and in the msp2 gene. Chloroquine sensitivity tests were conducted in vitro. A significant but incomplete association was found between the presence of the cg2 Dd2-like omega repeat size polymorphism and in vitro resistance, and between the tyr-86 allele of pfmdr1 and in vitro resistance. Furthermore there was strong linkage disequilibrium between the pfmdr1 asn-86 allele and the cg2 not Dd2-like omega repeat allele located on different chromosomes. In contrast, no linkage disequilibrium was found between these alleles and either the dhfr ser-108 allele or the msp2 IC sequence polymorphism. No significant linkage was measured between pfmdr1 asn-86 and phe-184 although these loci are separated only by 296 base pairs. Our results suggest that genetic elements linked to the cg2 and the pfmdr1 genes are important determinants of chloroquine resistance. It can be concluded that the observed linkage disequilibrium is maintained epistatically through selection by chloroquine.

ATP-Binding Cassette Transporters↗