Plasmodium infection and oxidative status in breeding great tits, Parus major

Plasmodium parasites may affect the oxidative status of their hosts, defined as the balance of pro-oxidant compounds and antioxidant defences in an organism. An increased energy requirement, the activation of immune functions or the parasite itself may lead to a higher production of pro-oxidants and/or an antioxidant depletion resulting in a higher oxidative stress and associated damage in infected individuals. Relatively little is known about the mechanisms underlying oxidative processes at play during host-Plasmodium interaction in the wild.

The effect of Plasmodium infection on host oxidative status was investigated in wild populations of breeding great tits, Parus major, naturally infected by Plasmodium spp. When chicks were 14 days old, the parents were blood-sampled to measure four complementary oxidative status markers: pro-oxidant production as mitochondrial superoxide production in red blood cells (RBC), antioxidant defences as plasma antioxidant capacity and oxidative damage as reactive oxygen metabolites in the plasma and RBC membrane resistance to oxidative attack.

Plasmodium-infected individuals produced more pro-oxidants compared to uninfected ones and pro-oxidant production positively correlated to infection intensity. There was also a conditional effect of reproductive effort on oxidative damage depending on Plasmodium infection status. There was no direct effect of infection on oxidative damage and no effect on antioxidant defences.

The results suggest that Plasmodium parasites may impose a cost in terms of increased oxidative stress possibly mediated via a higher energy requirement in infected hosts. This further suggests that Plasmodium parasites may modify host life history traits via an induction of oxidative stress. This study highlights that measuring several complementary oxidative status markers may enable to capture oxidative processes at play during host-Plasmodium interactions.