Implications of Plasmodium vivax Biology for Control, Elimination, and Research.
Identifieur interne : 001491 ( PubMed/Curation ); précédent : 001490; suivant : 001492Implications of Plasmodium vivax Biology for Control, Elimination, and Research.
Auteurs : Piero L. Olliaro [Suisse] ; John W. Barnwell [Géorgie (pays)] ; Alyssa Barry [Australie] ; Kamini Mendis ; Ivo Mueller [Australie] ; John C. Reeder [Suisse] ; G Dennis Shanks [Australie] ; Georges Snounou [France] ; Chansuda Wongsrichanalai [Thaïlande]Source :
- The American journal of tropical medicine and hygiene [ 1476-1645 ] ; 2016.
Descripteurs français
- KwdFr :
- Antipaludiques (usage thérapeutique), Humains, Paludisme à Plasmodium vivax (), Paludisme à Plasmodium vivax (parasitologie), Paludisme à Plasmodium vivax (transmission), Plasmodium vivax (génétique), Plasmodium vivax (physiologie), Santé mondiale, Spécificité d'espèce, Variation génétique, Étapes du cycle de vie.
- MESH :
- génétique : Plasmodium vivax.
- parasitologie : Paludisme à Plasmodium vivax.
- physiologie : Plasmodium vivax.
- usage thérapeutique : Antipaludiques, Paludisme à Plasmodium vivax.
- Humains, Paludisme à Plasmodium vivax, Santé mondiale, Spécificité d'espèce, Variation génétique, Étapes du cycle de vie.
English descriptors
- KwdEn :
- MESH :
- chemical , therapeutic use : Antimalarials.
- genetics : Plasmodium vivax.
- parasitology : Malaria, Vivax.
- physiology : Plasmodium vivax.
- prevention & control : Malaria, Vivax.
- transmission : Malaria, Vivax.
- Genetic Variation, Global Health, Humans, Life Cycle Stages, Species Specificity.
Abstract
This paper summarizes our current understanding of the biology of Plasmodium vivax, how it differs from Plasmodium falciparum, and how these differences explain the need for P. vivax-tailored interventions. The article further pinpoints knowledge gaps where investments in research are needed to help identify and develop such specific interventions. The principal obstacles to reduce and eventually eliminate P. vivax reside in 1) its higher vectorial capacity compared with P. falciparum due to its ability to develop at lower temperature and over a shorter sporogonic cycle in the vector, allowing transmission in temperate zones and making it less sensitive to vector control measures that are otherwise effective on P. falciparum; 2) the presence of dormant liver forms (hypnozoites), sustaining multiple relapsing episodes from a single infectious bite that cannot be diagnosed and are not susceptible to any available antimalarial except primaquine, with routine deployment restricted by toxicity; 3) low parasite densities, which are difficult to detect with current diagnostics leading to missed diagnoses and delayed treatments (and protracted transmission), coupled with 4) transmission stages (gametocytes) occurring early in acute infections, before infection is diagnosed.
DOI: 10.4269/ajtmh.16-0160
PubMed: 27799636
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Kamini Mendis<affiliation><nlm:affiliation>Independent Consultant, Colombo 5. Sri Lanka.</nlm:affiliation>
<wicri:noCountry code="subField">Colombo 5</wicri:noCountry>
</affiliation>
Le document en format XML
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<front><div type="abstract" xml:lang="en">This paper summarizes our current understanding of the biology of Plasmodium vivax, how it differs from Plasmodium falciparum, and how these differences explain the need for P. vivax-tailored interventions. The article further pinpoints knowledge gaps where investments in research are needed to help identify and develop such specific interventions. The principal obstacles to reduce and eventually eliminate P. vivax reside in 1) its higher vectorial capacity compared with P. falciparum due to its ability to develop at lower temperature and over a shorter sporogonic cycle in the vector, allowing transmission in temperate zones and making it less sensitive to vector control measures that are otherwise effective on P. falciparum; 2) the presence of dormant liver forms (hypnozoites), sustaining multiple relapsing episodes from a single infectious bite that cannot be diagnosed and are not susceptible to any available antimalarial except primaquine, with routine deployment restricted by toxicity; 3) low parasite densities, which are difficult to detect with current diagnostics leading to missed diagnoses and delayed treatments (and protracted transmission), coupled with 4) transmission stages (gametocytes) occurring early in acute infections, before infection is diagnosed.</div>
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<Abstract><AbstractText>This paper summarizes our current understanding of the biology of Plasmodium vivax, how it differs from Plasmodium falciparum, and how these differences explain the need for P. vivax-tailored interventions. The article further pinpoints knowledge gaps where investments in research are needed to help identify and develop such specific interventions. The principal obstacles to reduce and eventually eliminate P. vivax reside in 1) its higher vectorial capacity compared with P. falciparum due to its ability to develop at lower temperature and over a shorter sporogonic cycle in the vector, allowing transmission in temperate zones and making it less sensitive to vector control measures that are otherwise effective on P. falciparum; 2) the presence of dormant liver forms (hypnozoites), sustaining multiple relapsing episodes from a single infectious bite that cannot be diagnosed and are not susceptible to any available antimalarial except primaquine, with routine deployment restricted by toxicity; 3) low parasite densities, which are difficult to detect with current diagnostics leading to missed diagnoses and delayed treatments (and protracted transmission), coupled with 4) transmission stages (gametocytes) occurring early in acute infections, before infection is diagnosed.</AbstractText>
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