Experimental investigations into the effects of Schistocephalus solidus on the reproductive biology of sticklebacks

Parasitism involves two distinct organisms, the parasite and the host. Parasite interactions add to the complexity of hosts’ biology. Parasites frequently reduce reproductive success of hosts, often explained by simple energy theft. However, increasing evidence suggests parasitism causes altered host phenotypes in other ways. Changes have been categorised as; 1) direct manipulation of the host, 2) defensive adaptations by the host, or 3) side effects from infection. The effect of Schistocephalus solidus infections on the three-spined stickleback’s ability to undergo sexual development varies greatly. The mechanisms underlying this are still relatively unknown. In laboratory conditions, with unlimited food sources, effects of infection vary across populations. Suggesting adverse outcomes are not solely down to resource availability, and other factors are controlling fish development. Different populations of fish have been coexisting with the parasite for varying timescales; the level of adaptation to overcoming them is likely to differ. Variation between S. solidus could lead to different responses from their hosts. Fish may be able to overcome negative effects of infections from parasites of their own locations, but not if infected by parasites from other locations. Alternatively, some parasite populations may have the ability manipulate their fish host so could have a greater impact on them. The main aim is to investigate the mechanisms by which parasites alter host reproduction in the stickleback–Schistocephalus model; specifically focusing on differences observed between populations. The effect of the timing of infection and food supply on the sexual development of stickleback hosts is also investigated. The clear outcome of this thesis is that variation between populations exists. The population background of the parasite plays an important role in determining the outcome of infections. Parasites from Carsington Water (CRS) have detrimental effects on male stickleback’s nesting behaviour. This effect was seen in both wild-caught and lab bred males from all studied populations. Other parasite populations did not show this effect. The cross infections indicate that different mechanisms may be occurring. Fish and parasites were treated the same but differences in fish response are still observed. Analysis of the CO1 gene revealed genetic variation between parasite populations, microsatellite data showed high numbers of null alleles in CRS parasites, indicating greater mutation rates in the CRS genome, thus manipulation genes may develop. The second outcome shows effects of parasitism on development and gene expression of key genes involved in reproductive development. Infections at key time points during the year showed younger fish are compromised to a greater extent. Kiss2 expression was compared between infected fish with unlimited food and those on a low ration. Surprisingly Kiss2 expression significantly increased in fish on limited diets. No change in expression was found in infected fish. Similar expression levels of Kiss2 might be expected between ration fed and infected fish if the same mechanism between low nutrition and energy drains were in place.