Studies Investigating the Outcome of a Host-Parasite Interaction Using the Stickleback-Schistocephalus Model System

This thesis firstly investigates the effect of the cestode parasite Schistocephalus solidus on the reproduction of its intermediate host, the three spined stickleback. The results indicated that the parasite reduced host reproduction and the physiological basis behind this was established. In males, parasite infection reduced the fish’s ability to produce 11-ketotestosterone which resulted in reduced reproductive behaviour and sexual development. In infected females, vitellogenin production was reduced which prevented egg maturation. The adaptive nature of these changes seemed to be variable among different populations. This variation may result from genetic differences in the host or parasite population, co-evolutionary processes or reflect differences in the environmental conditions experienced by populations. The second part of this thesis investigates the effect of two types of anthropogenic stressors – endocrine disrupting chemicals and temperature change as an outcome of global climate change – on disease progression in the stickleback-Schistocephalus system. The results indicated that the natural steroid 17β estradiol (E2) had a significant impact on disease progression in a sex and dose dependent manner, with males exposed to the high 100ngLˉ¹ E2 treatment harbouring significantly larger parasites compared to females in this treatment and fish from the lower E2 and solvent control treatment. Elevated temperatures were also found to significantly increase parasite growth and reduce host growth. In addition, a behavioural study showed that fish harbouring infective parasites seek out high temperatures which could be adaptive on the part of the parasite as it would allow them to grow faster and potentially increase their reproductive output. The clear outcome of this thesis is that anthropogenic stressors increase disease progression in the stickleback-Schistocephalus system and this is likely to lead to reduced host reproduction and increased parasite transmission and reproduction, potentially leading to the evolution of higher virulence in this host-parasite interaction.