Adaptive phenotypic plasticity in malaria parasites is not constrained by previous responses to environmental change

BACKGROUND AND OBJECTIVES: Phenotypic plasticity enables organisms to maximize fitness by matching trait values to different environments. Such adaptive phenotypic plasticity is exhibited by parasites, which experience frequent environmental changes during their life cycle, between individual hosts and also in within-host conditions experienced during infections. Life history theory predicts that the evolution of adaptive phenotypic plasticity is limited by costs and constraints, but tests of these concepts are scarce. METHODOLOGY: Here, we induce phenotypic plasticity in malaria parasites to test whether mounting a plastic response to an environmental perturbation constrains subsequent plastic responses to further environmental change. Specifically, we perturb red blood cell resource availability to induce Plasmodium chabaudi to alter the trait values of several phenotypes underpinning within-host replication and between-host transmission. We then transfer parasites to unperturbed hosts to examine whether constraints govern the parasites’ ability to alter these phenotypes in response to their new in-host environment. RESULTS: Parasites alter trait values in response to the within-host environment they are exposed to. We do not detect negative consequences, for within-host replication or between-host transmission, of previously mounting a plastic response to a perturbed within-host environment. CONCLUSIONS AND IMPLICATIONS: We suggest that malaria parasites are highly plastic and adapted to adjusting their phenotypes in response to the frequent changes in the within-host conditions they experience during infections. Our findings support the growing body of evidence that medical interventions, such as anti-parasite drugs, induce plastic responses that are adaptive and can facilitate the survival and potentially, drug resistance of parasites. LAY SUMMARY: Malaria parasites have evolved flexible strategies to cope with the changing conditions they experience during infections. We show that using such flexible strategies does not impact upon the parasites’ ability to grow (resulting in disease symptoms) or transmit (spreading the disease).