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Christopher J. M. Whitty - One of the best experts on this subject based on the ideXlab platform.
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Geographical and temporal trends and seasonal relapse in Plasmodium ovale spp. and Plasmodium Malariae infections imported to the UK between 1987 and 2015
BMC Medicine, 2018Co-Authors: Laura E. B. Nabarro, Debbie Nolder, Claire Broderick, Behzad Nadjm, Valerie Smith, Marie Blaze, Anna M. Checkley, Peter L. Chiodini, Colin J. Sutherland, Christopher J. M. WhittyAbstract:Background Plasmodium ovale spp. and P. Malariae cause illness in endemic regions and returning travellers. Far less is known about these species than P. falciparum and P. vivax. Methods The UK national surveillance data, collected 1987 to 2015, were collated with the International Passenger Survey and climatic data to determine geographical, temporal and seasonal trends of imported P. ovale spp . and P. Malariae infection. Results Of 52,242 notified cases of Malaria, 6.04% (3157) were caused by P. ovale spp. and 1.61% (841) by P. Malariae ; mortality was 0.03% (1) and 0.12% (1), respectively. Almost all travellers acquired infection in West or East Africa. Infection rate per travel episode fell fivefold during the study period. The median latency of P. Malariae and P. ovale spp. was 18 and 76 days, respectively; delayed presentation occurred with both species. The latency of P. ovale spp. infection imported from West Africa was significantly shorter in those arriving in the UK during the West African peak Malarial season compared to those arriving outside it (44 days vs 94 days, p
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Geographical and temporal trends and seasonal relapse in Plasmodium ovale spp. and Plasmodium Malariae infections imported to the UK between 1987 and 2015.
BMC medicine, 2018Co-Authors: Laura E. B. Nabarro, Debbie Nolder, Claire Broderick, Behzad Nadjm, Marie Blaze, Anna M. Checkley, Peter L. Chiodini, Colin J. Sutherland, Valerie J. Smith, Christopher J. M. WhittyAbstract:Plasmodium ovale spp. and P. Malariae cause illness in endemic regions and returning travellers. Far less is known about these species than P. falciparum and P. vivax. The UK national surveillance data, collected 1987 to 2015, were collated with the International Passenger Survey and climatic data to determine geographical, temporal and seasonal trends of imported P. ovale spp. and P. Malariae infection. Of 52,242 notified cases of Malaria, 6.04% (3157) were caused by P. ovale spp. and 1.61% (841) by P. Malariae; mortality was 0.03% (1) and 0.12% (1), respectively. Almost all travellers acquired infection in West or East Africa. Infection rate per travel episode fell fivefold during the study period. The median latency of P. Malariae and P. ovale spp. was 18 and 76 days, respectively; delayed presentation occurred with both species. The latency of P. ovale spp. infection imported from West Africa was significantly shorter in those arriving in the UK during the West African peak Malarial season compared to those arriving outside it (44 days vs 94 days, p
Joachim Richter - One of the best experts on this subject based on the ideXlab platform.
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Clinical implications of a gradual dormancy concept in Malaria
Parasitology Research, 2016Co-Authors: Joachim Richter, Gabriele Franken, Martha C. Holtfreter, Susanne Walter, Alfons Labisch, Heinz MehlhornAbstract:Malaria recurrences after an initially successful therapy and Malarial fever occurring a long time after infection are well-known problems in malariology. Currently, two distinct types of Malaria recurrences are defined: recrudescence and relapse. A recrudescence is thought to originate from circulating Plasmodium blood stages which do not cause fever before a certain level of a microscopically detectable parasitemia is reached. Contrary, a relapse is thought to originate from quiescent intracellular hepatic parasite stages called hypnozoites. Recrudescences would typically occur in infections due to Plasmodium falciparum. Plasmodium knowlesi , and Plasmodium Malariae , whereas relapses would be caused exclusively by Plasmodium vivax and Plasmodium ovale. This schematic view is, however, insufficiently supported by experimental evidence. For instance, hypnozoites of P. ovale have never been experimentally documented. On the other hand, the nonfinding of P. Malariae hypnozoites turned into the proof for the nonexistence of P. Malariae hypnozoites. Clinical relapse-type recurrences have been observed in both P. ovale and P. Malariae infections, and decade-long incubation times have also been reported in P. falciparum infections. We propose a gradual hypothesis in accordance with the continuity concept of biological evolution: both, relapse and recrudescence may be potentially caused by all Plasmodium spp. We hypothesize that the difference between the various Plasmodium spp. is quantitative rather than qualitative: there are Plasmodium spp. which frequently cause relapses such as P. vivax , particularly the P.v . Chesson strain, species which cause relapses less frequently, such as P. ovale and sometimes P. Malariae , and species which may exceptionally cause relapses such as P. falciparum . All species may cause recrudescences. As clinical consequences, we propose that 8-aminquinolines may be considered in a relapse-type recrudescence regardless of the causal Plasmodium sp., whereas primaquine relapse prevention might not be routinely indicated in Malaria due to P. ovale.
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Why do Plasmodium Malariae infections sometimes occur in spite of previous antiMalarial medication?
Parasitology Research, 2012Co-Authors: Gabriele Franken, Martha C. Holtfreter, Susanne Walter, Alfons Labisch, Heinz Mehlhorn, Irmela Müller-stöver, Dieter Häussinger, Joachim RichterAbstract:Quartan Malaria due to Plasmodium Malariae is commonly regarded as being preventable by current antiMalarials. A case of P. Malariae infection occurred in spite of previous treatment of Plasmodium falciparum Malaria 4 months earlier with a full therapy course of intravenous quinine hydrochloride and oral doxycycline followed by artemether + lumefantrine. Since the patient was not anymore exposed to agents of Malaria in the meantime, a new infection by P. Malariae after therapy is unlikely. The present observation is difficult to explain by the current view on the origin of latent P. Malariae infections and recurrences which are thought to arise from intra-erythrocytic development stages susceptible to common antiMalarials. The most likely explanation of our observation is a delayed pre-erythrocytic development. The latency between infection by P. Malariae and the quartan Malaria fever attack might have been extended further by an initial subclinical circulation of a low number of intra-erythrocytic asexual parasites in the blood stream preceeding the clinical quartan Malaria breakthrough.
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Plasmodium Malariae infection in spite of previous anti-Malarial medication
Parasitology Research, 2008Co-Authors: Irmela Müller-stöver, Jaco J. Verweij, Barbara Hoppenheit, Klaus Göbels, Dieter Häussinger, Joachim RichterAbstract:Plasmodium Malariae is regarded as usually being susceptible to all anti-Malarials whether applied for prophylaxis or treatment. We report on three cases of P. Malariae infection which occurred 12–14 weeks after anti-Malarial chemoprophylaxis or treatment with mefloquine or atovaquone/proguanil. The most likely explanation for the failure of mefloquine and atovaquone/proguanil to prevent quartan Malaria occurring some months later is the insufficient effect on the particularly long-lasting pre-erythrocytic development stages of P. Malariae .
Nicholas J White - One of the best experts on this subject based on the ideXlab platform.
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collider bias and the apparent protective effect of glucose 6 phosphate dehydrogenase deficiency on cerebral Malaria
eLife, 2019Co-Authors: Julie A Simpson, Arjen M. Dondorp, James Watson, Stije J Leopold, Nicholas J WhiteAbstract:: Case fatality rates in severe falciparum Malaria depend on the pattern and degree of vital organ dysfunction. Recent large-scale case-control analyses of pooled severe Malaria data reported that glucose-6-phosphate dehydrogenase deficiency (G6PDd) was protective against cerebral Malaria but increased the risk of severe Malarial anaemia. A novel formulation of the balancing selection hypothesis was proposed as an explanation for these findings, whereby the selective advantage is driven by the competing risks of death from cerebral Malaria and death from severe Malarial anaemia. We re-analysed these claims using causal diagrams and showed that they are subject to collider bias. A simulation based sensitivity analysis, varying the strength of the known effect of G6PDd on anaemia, showed that this bias is sufficient to explain all of the observed association. Future genetic epidemiology studies in severe Malaria would benefit from the use of causal reasoning.
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Anaemia and Malaria
Malaria Journal, 2018Co-Authors: Nicholas J WhiteAbstract:Malaria is a major cause of anaemia in tropical areas. Malaria infection causes haemolysis of infected and uninfected erythrocytes and bone marrow dyserythropoiesis which compromises rapid recovery from anaemia. In areas of high Malaria transmission Malaria nearly all infants and young children, and many older children and adults have a reduced haemoglobin concentration as a result. In these areas severe life-threatening Malarial anaemia requiring blood transfusion in young children is a major cause of hospital admission, particularly during the rainy season months when Malaria transmission is highest. In severe Malaria, the mortality rises steeply below an admission haemoglobin of 3 g/dL, but it also increases with higher haemoglobin concentrations approaching the normal range. In the management of severe Malaria transfusion thresholds remain uncertain. Prevention of Malaria by vector control, deployment of insecticide-treated bed nets, prompt and accurate diagnosis of illness and appropriate use of effective anti-Malarial drugs substantially reduces the burden of anaemia in tropical countries.
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The role of anti-Malarial drugs in eliminating Malaria
Malaria Journal, 2008Co-Authors: Nicholas J WhiteAbstract:Effective anti-Malarial drug treatment reduces Malaria transmission. This alone can reduce the incidence and prevalence of Malaria, although the effects are greater in areas of low transmission where a greater proportion of the infectious reservoir is symptomatic and receives anti-Malarial treatment. Effective treatment has greater effects on the transmission of falciparum Malaria, where gametocytogenesis is delayed, compared with the other human Malarias in which peak gametocytaemia and transmissibility coincides with peak asexual parasite densities. Mature Plasmodium falciparum gametocytes are more drug resistant and affected only by artemisinins and 8-aminoquinolines. The key operational question now is whether primaquine should be added to artemisinin combination treatments for the treatment of falciparum Malaria to reduce further the transmissibility of the treated infection. Radical treatment with primaquine plays a key role in the eradication of vivax and ovale Malaria. More evidence is needed on the safety of primaquine when administered without screening for G6PD deficiency to inform individual and mass treatment approaches in the context of Malaria elimination programmes.
Laura E. B. Nabarro - One of the best experts on this subject based on the ideXlab platform.
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Geographical and temporal trends and seasonal relapse in Plasmodium ovale spp. and Plasmodium Malariae infections imported to the UK between 1987 and 2015
BMC Medicine, 2018Co-Authors: Laura E. B. Nabarro, Debbie Nolder, Claire Broderick, Behzad Nadjm, Valerie Smith, Marie Blaze, Anna M. Checkley, Peter L. Chiodini, Colin J. Sutherland, Christopher J. M. WhittyAbstract:Background Plasmodium ovale spp. and P. Malariae cause illness in endemic regions and returning travellers. Far less is known about these species than P. falciparum and P. vivax. Methods The UK national surveillance data, collected 1987 to 2015, were collated with the International Passenger Survey and climatic data to determine geographical, temporal and seasonal trends of imported P. ovale spp . and P. Malariae infection. Results Of 52,242 notified cases of Malaria, 6.04% (3157) were caused by P. ovale spp. and 1.61% (841) by P. Malariae ; mortality was 0.03% (1) and 0.12% (1), respectively. Almost all travellers acquired infection in West or East Africa. Infection rate per travel episode fell fivefold during the study period. The median latency of P. Malariae and P. ovale spp. was 18 and 76 days, respectively; delayed presentation occurred with both species. The latency of P. ovale spp. infection imported from West Africa was significantly shorter in those arriving in the UK during the West African peak Malarial season compared to those arriving outside it (44 days vs 94 days, p
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Geographical and temporal trends and seasonal relapse in Plasmodium ovale spp. and Plasmodium Malariae infections imported to the UK between 1987 and 2015.
BMC medicine, 2018Co-Authors: Laura E. B. Nabarro, Debbie Nolder, Claire Broderick, Behzad Nadjm, Marie Blaze, Anna M. Checkley, Peter L. Chiodini, Colin J. Sutherland, Valerie J. Smith, Christopher J. M. WhittyAbstract:Plasmodium ovale spp. and P. Malariae cause illness in endemic regions and returning travellers. Far less is known about these species than P. falciparum and P. vivax. The UK national surveillance data, collected 1987 to 2015, were collated with the International Passenger Survey and climatic data to determine geographical, temporal and seasonal trends of imported P. ovale spp. and P. Malariae infection. Of 52,242 notified cases of Malaria, 6.04% (3157) were caused by P. ovale spp. and 1.61% (841) by P. Malariae; mortality was 0.03% (1) and 0.12% (1), respectively. Almost all travellers acquired infection in West or East Africa. Infection rate per travel episode fell fivefold during the study period. The median latency of P. Malariae and P. ovale spp. was 18 and 76 days, respectively; delayed presentation occurred with both species. The latency of P. ovale spp. infection imported from West Africa was significantly shorter in those arriving in the UK during the West African peak Malarial season compared to those arriving outside it (44 days vs 94 days, p
Dominic P Kwiatkowski - One of the best experts on this subject based on the ideXlab platform.
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severe Malarial anemia and cerebral Malaria are associated with different tumor necrosis factor promoter alleles
The Journal of Infectious Diseases, 1999Co-Authors: William Mcguire, Julian C Knight, Adrian V S Hill, Catherine E M Allsopp, B M Greenwood, Dominic P KwiatkowskiAbstract:Experimental evidence implicates tumor necrosis factor (TNF) in the pathogenesis of Malarial anemia, but there are few data relating to this hypothesis. This study found that severely anemic children with Plasmodium falciparum infection have low plasma TNF levels, in contrast to the high levels found in cerebral Malaria. A previous case-control study in The Gambia found cerebral Malaria, but not severe Malarial anemia, was associated with the TNF-308 A allele. This study found that in the same population, severe Malarial anemia was associated with the TNF-238 A allele, with an odds ratio of 2.5 (P<.001) after stratification for HLA type. These findings suggest that severe Malarial anemia and cerebral Malaria are influenced by separate genetic factors situated near the TNF gene.
