The evolution of host tolerance to disease and the impact of predators

In this Thesis, we focus on the effects of the evolution of tolerance to disease in a susceptible-infected-susceptible model and on the impact of including a predator species. Host defence against parasite infection can rely on two broad strategies: resistance and tolerance. While resistance strategies aim to lower parasite fitness, tolerant hosts can bear the effects of the disease without reducing its prevalence. Here, we first examine the potential for the host to drive parasites to extinction in the host-parasite system through the evolution of one or other defence mechanism. When defence comes with costs, it is impossible for the host to eliminate the infection through resistance, because costly resistance is selected against when parasites are at low prevalence. We uncover that the only path to disease clearance in the presence of costs is through tolerance. Paradoxically, however, it is by lowering tolerance -and hence increasing disease-induced mortality- that extinction can occur. We then consider how the introduction of a predator species changes both host-parasite ecological and evolutionary dynamics. At the ecological level, a key role is played by predator selectivity for either healthy or infected prey. When predators feed mainly on susceptible prey we found region of bi-stability between coexistence and parasite extinction. Conversely, when predator selection is strongly towards infected prey, total prey population density can be maximal when the three species coexist, consistent with the 'healthy herd' hypothesis. At the evolutionary level, the presence of predators allows for the evolutionary branching of tolerance, which is impossible in the host-parasite case. Predation also decreases selection for tolerance when it reaches an optimal value and increases the possibilities for parasite extinction. We found a general pattern of higher tolerance higher infection risk and low predation density.