Temperature dependence of plasmodium falciparum erythrocytic stage development

Plasmodium falciparum infection causes febrile illness and severe disease with multiple organ failure and death when treatment is delayed. Antipyretic treatment is standard, and inducing hypothermia has been proposed to protect the brain in cerebral malaria. Here, we investigated the temperature dep...

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Main Authors: Singhaboot, Y, Keayarsa, S, Piaraksa, N, Phumratanaprapin, W, Kunawut, P, Dondorp, A, Chotivanich, K
Format: Journal article
Language:English
Published: American Journal of Tropical Medicine and Hygiene 2019
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author Singhaboot, Y
Keayarsa, S
Piaraksa, N
Phumratanaprapin, W
Kunawut, P
Dondorp, A
Chotivanich, K
author_facet Singhaboot, Y
Keayarsa, S
Piaraksa, N
Phumratanaprapin, W
Kunawut, P
Dondorp, A
Chotivanich, K
author_sort Singhaboot, Y
collection OXFORD
description Plasmodium falciparum infection causes febrile illness and severe disease with multiple organ failure and death when treatment is delayed. Antipyretic treatment is standard, and inducing hypothermia has been proposed to protect the brain in cerebral malaria. Here, we investigated the temperature dependence of asexual-stage parasite development and parasite multiplication in vitro. Plasmodium falciparum laboratory strain TM267 was incubated for 2 hours (short exposure) or 48 hours (continuous exposure) at different temperatures (32°C, 34°C, 35°C, 38°C, 39°C, and 40°C). The starting parasite developmental stage (ring, trophozoite, or schizont) varied between experiments. The parasite multiplication rate (PMR) was reduced under both hyper- and hypothermic conditions; after continuous exposure, the mean PMR ± SD was 9.1 ± 1.2 at 37°C compared with 2.4 ± 1.8 at 32°C, 2.3 ± 0.4 at 34°C, and 0.4 ± 0.1 at 40°C (P < 0.01). Changes in PMR were not significant after 2-hour exposure at temperatures ranging from 32°C to 40°C. Morphological changes in parasite cytoplasm and nucleus could be observed after long exposure to low or high temperature. After 48-hour incubation, rosette formation (≥ 2 uninfected red blood cells bound to infected red blood cells) was decreased at 34°C or 39°C compared with that at 37°C. In conclusion, both hyper- and hypothermia reduce PMR and delay erythrocytic stage development of P. falciparum, subsequently reducing rosette formation.
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spelling oxford-uuid:93d27c01-f90e-4c5a-8302-99ccbecc5a972022-03-26T23:34:57ZTemperature dependence of plasmodium falciparum erythrocytic stage developmentJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:93d27c01-f90e-4c5a-8302-99ccbecc5a97EnglishSymplectic Elements at OxfordAmerican Journal of Tropical Medicine and Hygiene2019Singhaboot, YKeayarsa, SPiaraksa, NPhumratanaprapin, WKunawut, PDondorp, AChotivanich, KPlasmodium falciparum infection causes febrile illness and severe disease with multiple organ failure and death when treatment is delayed. Antipyretic treatment is standard, and inducing hypothermia has been proposed to protect the brain in cerebral malaria. Here, we investigated the temperature dependence of asexual-stage parasite development and parasite multiplication in vitro. Plasmodium falciparum laboratory strain TM267 was incubated for 2 hours (short exposure) or 48 hours (continuous exposure) at different temperatures (32°C, 34°C, 35°C, 38°C, 39°C, and 40°C). The starting parasite developmental stage (ring, trophozoite, or schizont) varied between experiments. The parasite multiplication rate (PMR) was reduced under both hyper- and hypothermic conditions; after continuous exposure, the mean PMR ± SD was 9.1 ± 1.2 at 37°C compared with 2.4 ± 1.8 at 32°C, 2.3 ± 0.4 at 34°C, and 0.4 ± 0.1 at 40°C (P < 0.01). Changes in PMR were not significant after 2-hour exposure at temperatures ranging from 32°C to 40°C. Morphological changes in parasite cytoplasm and nucleus could be observed after long exposure to low or high temperature. After 48-hour incubation, rosette formation (≥ 2 uninfected red blood cells bound to infected red blood cells) was decreased at 34°C or 39°C compared with that at 37°C. In conclusion, both hyper- and hypothermia reduce PMR and delay erythrocytic stage development of P. falciparum, subsequently reducing rosette formation.
spellingShingle Singhaboot, Y
Keayarsa, S
Piaraksa, N
Phumratanaprapin, W
Kunawut, P
Dondorp, A
Chotivanich, K
Temperature dependence of plasmodium falciparum erythrocytic stage development
title Temperature dependence of plasmodium falciparum erythrocytic stage development
title_full Temperature dependence of plasmodium falciparum erythrocytic stage development
title_fullStr Temperature dependence of plasmodium falciparum erythrocytic stage development
title_full_unstemmed Temperature dependence of plasmodium falciparum erythrocytic stage development
title_short Temperature dependence of plasmodium falciparum erythrocytic stage development
title_sort temperature dependence of plasmodium falciparum erythrocytic stage development
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AT kunawutp temperaturedependenceofplasmodiumfalciparumerythrocyticstagedevelopment
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