Interestingly, however, in spite of higher check details parasitaemia, iNOS-inhibited birds did not pay a higher cost of infection because

haematocrit values were similar for iNOS-inhibited and control birds. This result parallels those reported for Plasmodium chabaudi-infected mice and suggests that the cost of higher parasitaemia in iNOS-inhibited birds might be compensated by a reduced cost of immunopathology. Overall, these results also point towards a possible trade-off between resistance and tolerance. As mentioned above, the control of the acute proliferation of asexual malaria parasites relies on several inflammatory effectors. Up-regulating the inflammatory response however adds a potential immunopathology toll to the overall cost of infection. Breaking down immunological tolerance therefore constitutes a possible mechanism underpinning a physiological trade-off between resistance and tolerance. A pending important question is now how parasites do adapt to hosts depending on the defence strategy (resistance vs. tolerance) and the possible trade-off between strategies. Again insight into the possible evolutionary trajectory followed by parasites experiencing particular immune environments comes from studies on rodent malaria, where Plasmodium chabaudi serially passaged in vaccinated mice

evolved to become a more serious threat to their host [59]. The reason for increased virulence of parasites evolving in vaccinated host lies on the relaxed cost of virulence. selleck screening library Vaccinated hosts are protected from infection-induced mortality but they still contribute to parasite transmission [60]. Therefore, rapidly growing parasites are favoured Alectinib in vaccinated hosts and can

be highly pathogenic in nonvaccinated hosts. Evidence in support to parasite evolution as a function of host immunity [61] also comes from a recent study involving Plasmodium relictum-infected canaries. Cornet et al. [62] assessed the infection dynamics and the cost of infection in canaries facing two diets. Birds enjoying a protein- and vitamin-enriched food were better able to control parasite growth (they had lower parasitaemia, and peak parasitaemia was reached earlier than for control, nonsupplemented hosts). Protein and vitamins are important environmental determinants of immune competence as shown in several organisms, including humans [63, 64]. Therefore, reduced parasitaemia in food-supplemented birds is consistent with an improved resistance. Nevertheless, food-supplemented birds also paid the highest per-parasite cost of infection (Figure 2a). In a follow-up experiment, parasites grown in food-supplemented and control hosts were inoculated in another group of hosts following a fully factorial design (parasites grown in food-supplemented hosts passaged in food-supplemented and in control hosts; parasites grown in control hosts passaged in food-supplemented and in control hosts) [62].