Thermal mismatch in high latitude host-parasite interactions

Emerging infectious diseases and climate change are urgent wildlife threats responsible for many population reductions and extinctions, but their synergistic effects can be hard to predict, as temperature shifts influence host-parasite dynamics in complex ways. The thermal mismatch hypothesis predicts that cold-adapted hosts will become increasingly susceptible to parasites as temperatures rise. However, temperature effects on host-parasite interactions in high latitudes remain understudied. My thesis investigates the role of temperature and thermal adaptations in shaping host-parasite interactions in high latitudes. For this, I use amphibians and their fungal parasite Batrachochytrium dendrobatidis (Bd), and perform experimental infections in different temperatures, followed by analysis of the survival, growth and gene expression of each host. The fungus Bd causes the disease chytridiomycosis, which has decimated amphibian populations worldwide and is a global conservation concern, with its severity varying between hosts, populations, Bd strains and environmental conditions.In paper I, I analyse the transcriptomic responses of two populations of common toads to infection with two Bd strains of different origin and uncover tissue differences in gene expression. In paper II, I look at the effects of temperature on the survival and growth of four amphibian species from southern Sweden. I discover that the two more cold-adapted species have higher survival and growth when infected with Bd at low temperatures compared to one of the warm-adapted ones, that the second warm adapted species is not at all affected by Bd infection and that the Bd strain I used appears to tolerate high temperature less well than expected. In paper III, I make comparisons between the cold-adapted southern species and individuals of the same species from northern Sweden, and find that northern populations may be less susceptible to Bd infection despite their overall lower survival. In paper IV, I look at the transcriptomic responses of the two cold-adapted species from both populations and find that immune system activity is increased in infected hosts, especially in lower temperatures, but is not always associated with higher survival.