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Theory predicts that hosts should evolve highly specific immune defences when there are significant fitness costs associated with parasitic infection. Historically, mechanistic studies have defined invertebrate immunity as innate and non-specific. However, recent evidence from ecological studies challenges this view by finding a high degree of specificity between host and parasite and evidence of immune priming, that are indicative of a more complex system. Critics of the ecological perspective assert that without mechanistic evidence, there is no sound reason to assume that these phenomena are generated by innate immunity. To begin bridging the gap between mechanistic and ecological fields of innate immunity, I have examined the molecular basis of specificity and priming in the model Bombus-Crithidia host-parasite system. My studies show that immune gene expression mirrors the interaction effect found with indirect, ecological measures of immunity, providing unequivocal evidence of innate immune specificity in invertebrates. A similar examination of immune priming suggested that the genes I analysed were not involved in this phenomenom and is most likely to be indicative of the relative importance of different arms of immunity in the primed immune response. Finally, I examined more general aspects of the immune response to Crithidia by characterising the temporal dynamics of immune gene expression throughout infection for the first time in this model host-parasite system. I also confirmed that the assumed link between virulence and intensity of Crithidia infection is valid. To conclude, my studies have shown that integration of molecular knowledge into natural host-parasite systems can only serve to enrich our understanding of the wider capabilities of invertebrate innate immunity.

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How host and habitat heterogeneity affects the distribution of ticks in the Scottish upland environment was examined, and the prevalence of two important tick-borne diseases in questing, field-collected ticks was investigated.  This data was used to test the predictions of an influential model of louping-ill virus. Both hosts and habitat were found to be important predictors of <i>Ixodes ricinus </i>nymph abundance.  In general, the highest nymph numbers were collected from areas of heather habitat, and lowest numbers from areas of boggy ground.  Nymph numbers increased with increasing red deer density, but were negatively associated with increasing both mountain hare and red grouse density. A total of 1063 field collected, questing ticks were individually tested for louping-ill virus, of which 621 were also tested for <i>Borrelia burgdorferi </i>sensu lato.  Louping-ill RNA was detected in 7.8 % of all ticks tested.  The percentage of ticks positive for louping-ill virus did not vary with tick stage, collection site, month, or vegetation type, and was not correlated with host density of host seroprevalence.  <i>B. burgdorferi </i>was detected in 1.4 % of the ticks.  No simultaneous infections of louping ill virus and <i>Borrelia spp. </i>were detected. Field data on tick abundance and pathogen prevalence collected during this study was used to challenge an influential model of louping-ill virus dynamics.  The model proved relatively successful at predicting tick abundance, but underestimated the extent of louping-ill virus.  The single patch model was adapted to form a two-patch modelling allowing red deer movement between the two patches.  Allowing the movement of deer between two patches with different host densities shifted the threshold for louping-ill virus persistence, allowing its persistence in almost all red deer-grouse-hare scenarios.

Infestation of commercially reared salmonids with the salmon louse Lepeophtheirus salmonis, is a large problem for the fish farming industries in Scotland, Ireland and Norway. Lice infestations cause high fish mortalities and losses in revenue for the fish farmer. Conventional treatment of lice infestation involves the use of organophosphate insecticides which are limited in their efficacy against lice, as well as being highly toxic to the flora and fauna which surround the sea cages. We have investigated the possibility of producing a recombinant vaccine against L. salmonis based on immunisation of farmed salmonids with 'concealed' antigens from lice. Murine monoclonal antibodies were raised against L. salmonis antigens using standard cell fusion techniques. The antibodies were screened by immunohistochemistry in order to establish the location of the recognised antigen in L. salmonis sections. We used the monoclonal antibodies to screen L. salmonis DNA libraries constructed in gt11 and ZAP in order to isolate the DNA coding for each recognised antigen. A monoclonal antibody was produced which showed strong immunoreactivity with cuticle-associated areas in lice sections. This antibody was subsequently shown to recognise the enzyme chitinase from L. salmonis. We have expressed recombinant proteins from the isolated phage which have been used in immunisation trials on the Atlantic salmon (Salmo salar). Lice feeding on fish immunised with three of the recombinant antigens, displayed abnormal egg development and an overall decrease in egg number. We are currently retesting these antigens in a larger immunisation trial. We have also used polymerase chain reaction technology to look for known genes in L. salmonis and have identified a member of the wnt gene family, wnt-5a.