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<p>Synchronised multiplication of <i>Plasmodium</i> parasites within red blood cells causes periodic malaria fevers. Aligning blood stage development with the feeding-fasting rhythm of the vertebrate host facilitates within-host survival and between-host transmission. We use the rodent model <i>Plasmodium chabaudi</i> to test when, following development in the liver, the blood stage of infection begins. We find egress from the liver into the blood is aligned with the time of day of rhythmic host feeding, but only in wild type hosts, with egress occurring after a fixed period of pre-erythrocytic development in hosts without a canonical circadian clock. However, perturbing the duration over which parasites enter the bloodstream does not affect their multiplication rate in the first five intraerythrocytic development cycles, suggesting that the expected fitness benefits from timing egress anticipates rhythmic challenges or opportunities (e.g. rhythmic nutrient limitation or nutrient availability) later in the infection when parasite densities increase.</p>

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Plasmodium chabaudi malaria parasites adjust liver stage development to synchronise egressing blood stages with host daily rhythms

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  • 发表日期：

    2026年7月16日

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  • Alejandra Herbert-Mainero,
  • Petra Schneider,
  • Aidan J. O’Donnell,
  • Sarah E. Reece

摘要

Synchronised multiplication of Plasmodium parasites within red blood cells causes periodic malaria fevers. Aligning blood stage development with the feeding-fasting rhythm of the vertebrate host facilitates within-host survival and between-host transmission. We use the rodent model Plasmodium chabaudi to test when, following development in the liver, the blood stage of infection begins. We find egress from the liver into the blood is aligned with the time of day of rhythmic host feeding, but only in wild type hosts, with egress occurring after a fixed period of pre-erythrocytic development in hosts without a canonical circadian clock. However, perturbing the duration over which parasites enter the bloodstream does not affect their multiplication rate in the first five intraerythrocytic development cycles, suggesting that the expected fitness benefits from timing egress anticipates rhythmic challenges or opportunities (e.g. rhythmic nutrient limitation or nutrient availability) later in the infection when parasite densities increase.