| Summary: | Investment in immunity is costly: one way in which hosts can ameliorate these costs is through immune priming, whereby hosts develop increased protection to future infection following previous exposure to a parasite or immune elicitor. Priming offers hosts a more efficient way of managing immune insult by allowing for a stronger and faster response to an immune insult. As well as investing in physiological immune defences, hosts can also leverage behavioural responses to reduce the costs of infection. Group-living in insects offers several benefits, such as predator avoidance. However, it can be costly in terms of increasing the risks of exposure to parasites. Group facilitation of disease resistance through a variety of processes collectively known as 'social immunity' is well established in the eusocial insects. Many gregarious insects share several features of their ecology with eusocial species, and should thus be predisposed to many of the same risks of infection, and the same evolved processes that mitigate these risks. A form of immune priming known 'social immunisation' has recently been described in eusocial insects, whereby immunologically naïve individuals exhibit enhanced immunity against infection after being housed with infected nestmates. Whether similar mechanisms exist in gregarious but non-social insects is unknown, and it is this premise that forms the conceptual basis of this thesis. I investigated whether a non-social but gregarious insect, the mealworm beetle (Tenebrio molitor), altered its immune investment following cohabitation with an immunestimulated conspecific. I examined the potential role of both physiological and behavioural defences in offering prophylactic protection against perceived pathogenic threat. I also investigated the potential mechanisms of such an form of immunisation by examining immune responses induced by cohabitation with conspecifics challenged by a live (and transmissible) bacterial infection and those challenged by either heat-killed bacteria or an artificial antigen (both non-transmissible). Finally, I examined the role of host behaviour in affecting immunisation, quantifying behavioural changes in immune-stimulated hosts (referred to as 'sickness behaviours') to try and identify visual or behavioural cues which may be utilised by naïve hosts to stimulate prophylactic defences, There was no robust evidence for a parsimonious process of gregarious immunisation. However, there were differences between the sexes in their immune responses to infection threat, as well as in their induction of sickness behaviours following infection. Whilst there was little evidence for an upregulation of immunity in naïve females, females appeared to exhibit enhanced tolerance of infection following cohabitation with a 'sick' conspecific, as they suffered no decrease in longevity despite the presence of relatively high parasite loads. Males showed the opposite pattern to that predicted by gregarious immunisation, decreasing their investment in physiological defence following exposure to 'sick' conspecifics. Despite finding no clear evidence for enhanced resistance through a straightforward process of gregarious immunisation, these data suggest that naïve T. mollitor may be able detect social cues of infection produced by parasitised conspecifics. I propose that the immune responses displayed by both males and females constitute tolerance strategies which help hosts to minimise the costs of parasitism. Due to intrinsic differences in the life-history trajectories of the sexes, females are predicted to invest in immunological tolerance mechanisms aimed at self-preservation in order to preserve their capacity for future reproduction, whereas males are predicted to terminally invest in reproduction in order to maximise their fitness.
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