The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Ric N Price - One of the best experts on this subject based on the ideXlab platform.
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diagnosis and treatment of Plasmodium vivax malaria
American Journal of Tropical Medicine and Hygiene, 2016Co-Authors: Kevin J Baird, Neena Valecha, Ric N Price, Stephan DuparcAbstract:Abstract The diagnosis and treatment of Plasmodium vivax malaria differs from that of Plasmodium falciparum malaria in fundamentally important ways. This article reviews the guiding principles, practices, and evidence underpinning the diagnosis and treatment of P. vivax malaria.
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the global public health significance of Plasmodium vivax
Advances in Parasitology, 2012Co-Authors: Katherine E Battle, Iqbal R F Elyazar, Peter W Gething, Ric N Price, Rosalind E Howes, Catherine L Moyes, Marianne E Sinka, Carlos A Guerra, Kevin J BairdAbstract:Plasmodium vivax occurs globally and thrives in both temperate and tropical climates. Here, we review the evidence of the biological limits of its contemporary distribution and the global population at risk (PAR) of the disease within endemic countries. We also review the most recent evidence for the endemic level of transmission within its range and discuss the implications for burden of disease assessments. Finally, the evidence-base for defining the contemporary distribution and PAR of P. vivax are discussed alongside a description of the vectors of human malaria within the limits of risk. This information along with recent data documenting the severe morbid and fatal consequences of P. vivax infection indicates that the public health significance of P. vivax is likely to have been seriously underestimated.
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new developments in Plasmodium vivax malaria severe disease and the rise of chloroquine resistance
Current Opinion in Infectious Diseases, 2009Co-Authors: Ric N Price, Nicholas M Douglas, Nicholas M AnsteyAbstract:Purpose of reviewUnlike Plasmodium falciparum, Plasmodium vivax rarely causes severe disease in healthy travellers or in temperate endemic regions and has been regarded as readily treatable with chloroquine. However, in tropical areas, recent reports have highlighted severe and fatal disease associa
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Plasmodium vivax trophozoites insensitive to chloroquine
Malaria Journal, 2008Co-Authors: Wesley W Sharrock, Usa Lekuthai, Anchalee Jaidee, Thomas Travers, Kanlaya Sriprawat, Michael D. Edstein, Rossarin Suwanarusk, Varakorn Kosaisavee, Ric N PriceAbstract:Background Plasmodium vivax is a major cause of malaria and is still primarily treated with chloroquine. Chloroquine inhibits the polymerization of haem to inert haemozoin. Free haem monomers are thought to catalyze oxidative damage to the Plasmodium spp. trophozoite, the stage when haemoglobin catabolism is maximal. However preliminary in vitro observations on P. vivax clinical isolates suggest that only ring stages (early trophozoites) are sensitive to chloroquine. In this study, the stage specific action of chloroquine was investigated in synchronous cryopreserved isolates of P. vivax.
Kevin J Baird - One of the best experts on this subject based on the ideXlab platform.
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diagnosis and treatment of Plasmodium vivax malaria
American Journal of Tropical Medicine and Hygiene, 2016Co-Authors: Kevin J Baird, Neena Valecha, Ric N Price, Stephan DuparcAbstract:Abstract The diagnosis and treatment of Plasmodium vivax malaria differs from that of Plasmodium falciparum malaria in fundamentally important ways. This article reviews the guiding principles, practices, and evidence underpinning the diagnosis and treatment of P. vivax malaria.
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Plasmodium vivax malaria endemicity in indonesia in 2010
PLOS ONE, 2012Co-Authors: Iqbal R F Elyazar, Peter W Gething, Anand P Patil, Hanifah Rogayah, Elvieda Sariwati, Niken W Palupi, Siti Nadia Tarmizi, Rita Kusriastuti, Kevin J BairdAbstract:Background Plasmodium vivax imposes substantial morbidity and mortality burdens in endemic zones. Detailed understanding of the contemporary spatial distribution of this parasite is needed to combat it. We used model based geostatistics (MBG) techniques to generate a contemporary map of risk of Plasmodium vivax malaria in Indonesia in 2010.
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the global public health significance of Plasmodium vivax
Advances in Parasitology, 2012Co-Authors: Katherine E Battle, Iqbal R F Elyazar, Peter W Gething, Ric N Price, Rosalind E Howes, Catherine L Moyes, Marianne E Sinka, Carlos A Guerra, Kevin J BairdAbstract:Plasmodium vivax occurs globally and thrives in both temperate and tropical climates. Here, we review the evidence of the biological limits of its contemporary distribution and the global population at risk (PAR) of the disease within endemic countries. We also review the most recent evidence for the endemic level of transmission within its range and discuss the implications for burden of disease assessments. Finally, the evidence-base for defining the contemporary distribution and PAR of P. vivax are discussed alongside a description of the vectors of human malaria within the limits of risk. This information along with recent data documenting the severe morbid and fatal consequences of P. vivax infection indicates that the public health significance of P. vivax is likely to have been seriously underestimated.
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neglect of Plasmodium vivax malaria
Trends in Parasitology, 2007Co-Authors: Kevin J BairdAbstract:Plasmodium vivax infects 130–435 million of the 2.6 billion people living at risk of infection. Recent studies suggest that vivax malaria can become lethal in a similar way to severe falciparum malaria. First-line therapies remain unchanged after 50 years. Despite evidence of failing chloroquine efficacy, little work has assessed the problem or explored alternative therapies. Primaquine treatment, the only therapeutic option against relapse, might also be failing. No licensed primary chemoprophylactic agent protects travelers from relapse. Misdiagnosis of species now affects clinical decisions resulting in inadequate therapy for P. falciparum and P. vivax . All of these factors demonstrate the lack of research on P. vivax .
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chloroquine resistance in Plasmodium vivax
Antimicrobial Agents and Chemotherapy, 2004Co-Authors: Kevin J BairdAbstract:Emerging resistance to chloroquine (CQ) by Plasmodium vivax threatens the health of the hundreds of millions of people routinely exposed to the risk of infection with this organism. CQ has been the first-line therapy for vivax malaria since 1946 (32, 115). Plasmodium falciparum developed resistance to CQ in the 1950s (110), and today it occurs globally (91). Resistance by P. vivax was unknown until 1989, when Australians repatriated from Papua New Guinea failed routine treatment (94). Subsequent reports affirmed that finding, and CQ-resistant P. vivax (CRPV) was reported from Indonesia (8, 35, 99, 100, 111). Reports from Myanmar (76, 82) and India (56, 107) followed. CRPV appeared in travelers from Guyana, South America (88). However, studies in Thailand (38, 72, 103), the Philippines (10), and Vietnam (105) revealed only CQ-sensitive P. vivax. Surveys in Indonesia revealed a low frequency of CRPV in the west (∼10%) (15, 16, 49, 50, 51, 53, 75) and a higher risk in the east (∼45%) (9, 18, 52, 81, 102, 106). This minireview summarizes the present state of knowledge of CRPV as a scientific, clinical, and public health problem. It examines the genesis of CQ therapy for P. vivax and the laboratory and clinical data underpinning the diagnosis of CRPV. The available data showing the global distribution of CRPV are listed. Finally, the clinical data on alternative therapies against CRPV are reviewed.
Chetan E. Chitnis - One of the best experts on this subject based on the ideXlab platform.
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amplification of duffy binding protein encoding gene allows Plasmodium vivax to evade host anti dbp humoral immunity
Nature Communications, 2020Co-Authors: Jean Popovici, Camille Roesch, Lenore L Carias, Amelie Vantaux, Ivo Mueller, Nimol Khim, Chetan E. Chitnis, Christopher L KingAbstract:Antigenic variation, the capacity to produce a range of variable antigens, is a well-described strategy of Plasmodium and other parasites to evade host immunity. Here, we show that gene amplification is an additional evasion mechanism used by Plasmodium vivax to escape humoral immunity targeting PvDBP, the key ligand involved in reticulocyte invasion. PvDBP gene amplification leads to increased mRNA levels and protects P. vivax in vitro against invasion inhibitory human monoclonal antibodies targeting a conserved binding domain of DBP. Patient samples suggest that parasites with increased pvdbp copy number are able to infect individuals with naturally acquired antibodies highly blocking the binding of PvDBP to the Duffy receptor. These results show that gene copy number variation affect the parasite’s ability to evade anti-PvDBP humoral immunity. Duffy binding protein (DBP) of Plasmodium vivax is important for invasion and is a potential vaccine candidate. Here, the authors show that PvDBP gene amplification protects P vivax in vitro against invasion inhibitory human monoclonal antibodies and is associated to infection of patients with PvDBP binding inhibitory antibodies.
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development of vaccines for Plasmodium vivax malaria
Vaccine, 2015Co-Authors: Ivo Mueller, Chetan E. Chitnis, Ahmad Rushdi ShakriAbstract:Plasmodium vivax continues to cause significant morbidity outside Africa with more than 50% of malaria cases in many parts of South and South-east Asia, Pacific islands, Central and South America being attributed to P. vivax infections. The unique biology of P. vivax, including its ability to form latent hypnozoites that emerge months to years later to cause blood stage infections, early appearance of gametocytes before clinical symptoms are apparent and a shorter development cycle in the vector makes elimination of P. vivax using standard control tools difficult. The availability of an effective vaccine that provides protection and prevents transmission would be a valuable tool in efforts to eliminate P. vivax. Here, we review the latest developments related to P. vivax malaria vaccines and discuss the challenges as well as directions toward the goal of developing highly efficacious vaccines against P. vivax malaria.
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targeting the Plasmodium vivax duffy binding protein
Trends in Parasitology, 2008Co-Authors: Chetan E. Chitnis, Amit SharmaAbstract:Plasmodium vivax requires interaction with the Duffy antigen receptor for chemokines (DARC) to enable its invasion of human erythrocytes. Interaction with DARC is mediated by the P. vivax Duffy-binding protein (PvDBP) and is essential for junction formation, which is a key step in the invasion process. The receptor-binding domain of PvDBP maps to a conserved cysteine-rich region, referred to as region II (PvRII). Here, we review data on the interaction of PvRII with DARC and explore the potential of targeting this crucial receptor–ligand interaction to develop new intervention strategies against P. vivax .
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Plasmodium vivax invasion of human erythrocytes inhibited by antibodies directed against the duffy binding protein
PLOS Medicine, 2007Co-Authors: Brian T Grimberg, Jia Xainli, Amy M Mchenry, Tasanee Panichakul, Jetsumon Sattabongkot, Moses J. Bockarie, John H Adams, Chetan E. Chitnis, Rachanee Udomsangpetch, Peter A ZimmermanAbstract:Background Plasmodium vivax invasion requires interaction between the human Duffy antigen on the surface of erythrocytes and the P. vivax Duffy binding protein (PvDBP) expressed by the parasite. Given that Duffy-negative individuals are resistant and that Duffy-negative heterozygotes show reduced susceptibility to blood-stage infection, we hypothesized that antibodies directed against region two of P. vivax Duffy binding protein (PvDBPII) would inhibit P. vivax invasion of human erythrocytes.
Nicholas J. White - One of the best experts on this subject based on the ideXlab platform.
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Plasmodium vivax relapse rates following Plasmodium falciparum malaria reflect previous transmission intensity
The Journal of Infectious Diseases, 2019Co-Authors: Elizabeth A Ashley, Francois Nosten, Nicholas J. White, Aung Pyae Phyo, Verena I Carrara, Kyaw Myo Tun, Frank SmithuisAbstract:From 2003 through 2009, 687 of 2885 patients (23.8%) treated for Plasmodium falciparum malaria in clinical studies in Myanmar or on the Thailand-Myanmar border had recurrent Plasmodium vivax malaria within 63 days, compared with 18 of 429 patients (4.2%) from 2010 onward (risk ratio [RR], 0.176; 95% confidence interval, .112-.278; P < .0001). Corresponding data from 42 days of follow-up revealed that 820 of 3883 patients (21.1%) had recurrent P. vivax malaria before 2010, compared with 22 of 886 (2.5%) from 2010 onward (RR, 0.117; 95% CI, .077-.177; P < .0001). This 6-fold reduction suggests a recent decline in P. vivax transmission intensity and, thus, a substantial reduction in the proportion of individuals harboring hypnozoites.
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management of relapsing Plasmodium vivax malaria
Expert Review of Anti-infective Therapy, 2016Co-Authors: Nicholas J. WhiteAbstract:ABSTRACTIntroduction: Relapses are important contributors to illness and morbidity in Plasmodium vivax and P. ovale infections. Relapse prevention (radical cure) with primaquine is required for optimal management, control and ultimately elimination of Plasmodium vivax malaria. A review was conducted with publications in English, French, Portuguese and Spanish using the search terms ‘P. vivax’ and ‘relapse’.Areas covered: Hypnozoites causing relapses may be activated weeks or months after initial infection. Incidence and temporal patterns of relapse varies geographically. Relapses derive from parasites either genetically similar or different from the primary infection indicating that some derive from previous infections. Malaria illness itself may activate relapse. Primaquine is the only widely available treatment for radical cure. However, it is often not given because of uncertainty over the risks of primaquine induced haemolysis when G6PD deficiency testing is unavailable. Recommended dosing of primaqui...
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Determinants of relapse periodicity in Plasmodium vivax malaria
Malaria Journal, 2011Co-Authors: Nicholas J. WhiteAbstract:Plasmodium vivax is a major cause of febrile illness in endemic areas of Asia, Central and South America, and the horn of Africa. Plasmodium vivax infections are characterized by relapses of malaria arising from persistent liver stages of the parasite (hypnozoites) which can be prevented only by 8-aminoquinoline anti-malarials. Tropical P. vivax relapses at three week intervals if rapidly eliminated anti-malarials are given for treatment, whereas in temperate regions and parts of the sub-tropics P. vivax infections are characterized either by a long incubation or a long-latency period between illness and relapse - in both cases approximating 8-10 months. The epidemiology of the different relapse phenotypes has not been defined adequately despite obvious relevance to malaria control and elimination. The number of sporozoites inoculated by the anopheline mosquito is an important determinant of both the timing and the number of relapses. The intervals between relapses display a remarkable periodicity which has not been explained. Evidence is presented that the proportion of patients who have successive relapses is relatively constant and that the factor which activates hypnozoites and leads to regular interval relapse in vivax malaria is the systemic febrile illness itself. It is proposed that in endemic areas a large proportion of the population harbours latent hypnozoites which can be activated by a systemic illness such as vivax or falciparum malaria. This explains the high rates of vivax following falciparum malaria, the high proportion of heterologous genotypes in relapses, the higher rates of relapse in people living in endemic areas compared with artificial infection studies, and, by facilitating recombination between different genotypes, contributes to P. vivax genetic diversity particularly in low transmission settings. Long-latency P. vivax phenotypes may be more widespread and more prevalent than currently thought. These observations have important implications for the assessment of radical treatment efficacy and for malaria control and elimination.
Daniel E Neafsey - One of the best experts on this subject based on the ideXlab platform.
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resolving the cause of recurrent Plasmodium vivax malaria probabilistically
Nature Communications, 2019Co-Authors: Aimee R Taylor, Kanokpich Puaprasert, Jureeporn Duanguppama, Daniel E Neafsey, Francois Nosten, James A Watson, Caroline O BuckeeAbstract:Relapses arising from dormant liver-stage Plasmodium vivax parasites (hypnozoites) are a major cause of vivax malaria. However, in endemic areas, a recurrent blood-stage infection following treatment can be hypnozoite-derived (relapse), a blood-stage treatment failure (recrudescence), or a newly acquired infection (reinfection). Each of these requires a different prevention strategy, but it was not previously possible to distinguish between them reliably. We show that individual vivax malaria recurrences can be characterised probabilistically by combined modelling of time-to-event and genetic data within a framework incorporating identity-by-descent. Analysis of pooled patient data on 1441 recurrent P. vivax infections in 1299 patients on the Thailand–Myanmar border observed over 1000 patient follow-up years shows that, without primaquine radical curative treatment, 3 in 4 patients relapse. In contrast, after supervised high-dose primaquine only 1 in 40 relapse. In this region of frequent relapsing P. vivax, failure rates after supervised high-dose primaquine are significantly lower (∼3%) than estimated previously. Relapse, reinfection and recrudescence can all cause recurrent infection after treatment of Plasmodium vivax malaria in endemic areas, but are difficult to distinguish. Here the authors show that they can be differentiated probabilistically and thereby demonstrate the high efficacy of primaquine treatment in preventing relapse.
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Resolving the cause of recurrent Plasmodium vivax malaria probabilistically
'Springer Science and Business Media LLC', 2019Co-Authors: Ar Taylor, Daniel E Neafsey, Caroline O Buckee, Nosten F., Ja Watson, Cs Chu, Puaprasert K, Duanguppama J, Day Npj, Imwong MAbstract:Relapses arising from dormant liver-stage Plasmodium vivax parasites (hypnozoites) are a major cause of vivax malaria. However, in endemic areas, a recurrent blood-stage infection following treatment can be hypnozoite-derived (relapse), a blood-stage treatment failure (recrudescence), or a newly acquired infection (reinfection). Each of these requires a different prevention strategy, but it was not previously possible to distinguish between them reliably. We show that individual vivax malaria recurrences can be characterised probabilistically by combined modelling of time-to-event and genetic data within a framework incorporating identity-by-descent. Analysis of pooled patient data on 1441 recurrent P. vivax infections in 1299 patients on the Thailand-Myanmar border observed over 1000 patient follow-up years shows that, without primaquine radical curative treatment, 3 in 4 patients relapse. In contrast, after supervised high-dose primaquine only 1 in 40 relapse. In this region of frequent relapsing P. vivax, failure rates after supervised high-dose primaquine are significantly lower (∼3%) than estimated previously
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genome scale protein microarray comparison of human antibody responses in Plasmodium vivax relapse and reinfection
American Journal of Tropical Medicine and Hygiene, 2015Co-Authors: Raul Chuquiyauri, Alejandro Llanoscuentas, Douglas M Molina, Eli L Moss, Ruobing Wang, Malcolm J Gardner, Kimberly C Brouwer, Sonia Torres, Robert H Gilman, Daniel E NeafseyAbstract:Abstract. Large scale antibody responses in Plasmodium vivax malaria remains unexplored in the endemic setting. Protein microarray analysis of asexual-stage P. vivax was used to identify antigens recognized in sera from residents of hypoendemic Peruvian Amazon. Over 24 months, of 106 participants, 91 had two symptomatic P. vivax malaria episodes, 11 had three episodes, 3 had four episodes, and 1 had five episodes. Plasmodium vivax relapse was distinguished from reinfection by a merozoite surface protein-3α restriction fragment length polymorphism polymerase chain reaction (MSP3α PCR-RFLP) assay. Notably, P. vivax reinfection subjects did not have higher reactivity to the entire set of recognized P. vivax blood-stage antigens than relapse subjects, regardless of the number of malaria episodes. The most highly recognized P. vivax proteins were MSP 4, 7, 8, and 10 (PVX_003775, PVX_082650, PVX_097625, and PVX_114145); sexual-stage antigen s16 (PVX_000930); early transcribed membrane protein (PVX_090230); tryptophan-rich antigen (Pv-fam-a) (PVX_092995); apical merozoite antigen 1 (PVX_092275); and proteins of unknown function (PVX_081830, PVX_117680, PVX_118705, PVX_121935, PVX_097730, PVX_110935, PVX_115450, and PVX_082475). Genes encoding reactive proteins exhibited a significant enrichment of non-synonymous nucleotide variation, an observation suggesting immune selection. These data identify candidates for seroepidemiological tools to support malaria elimination efforts in P. vivax-endemic regions.
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the malaria parasite Plasmodium vivax exhibits greater genetic diversity than Plasmodium falciparum
Nature Genetics, 2012Co-Authors: Daniel E Neafsey, Kevin Galinsky, Rays H Y Jiang, Lauren Young, Sean M Sykes, Sakina Saif, Sharvari Gujja, Jonathan M Goldberg, Sarah Young, Qiandong ZengAbstract:Jane Carlton and colleagues report the genome sequencing, de novo assembly and annotation of four Plasmodium vivax reference strains from diverse geographic locations. Their cross-species comparisons show that P. vivax has greater genetic diversity than Plasmodium falciparum.