Severe population bottlenecks and the small size of many remnant habitats may render many bird populations prone to extinction from disease outbreaks. Bottlenecks may increase inbreeding which in turn may result in a low diversity of resistance and an immune system that is impaired or defective. Thus, bottlenecked populations may be less immunocompetent and more vulnerable to microbiological and parasitic perturbations. Few studies have assessed the effect of bottlenecks on the immunocompetence of birds. In this study, I used twelve saddleback (Philesturnus carunculatus) and two New Zealand robin (Petroica a. australis) populations, to determine if the severe bottlenecks reduce the immunocompetence of birds. When I experimentally challenged the immune system of two robin populations I found that despite the two populations having similar parasite loads, robins from the severely bottlenecked Motuara Island population exhibited a significantly lower T-cell mediated immune response than the source population (Nukuwaiata Island) suggesting that birds passing through severe population bottlenecks have a compromised immunocompetence. In the saddleback, severe bottlenecks, as well as high population densities and small island size, lead to individuals exhibiting higher stress levels and feather mite loads and lower immune function, as was evident by lower lymphocyte counts. I did not find levels of fluctuating asymmetry of saddlebacks to be directly influenced by bottleneck size. However, I did find that individuals with higher levels of fluctuating asymmetry had higher loads of hippoboscid flies and lower loads of coccidia suggesting a possible trade-off between growth and immune function. In contrast to previous studies looking at behavioural secondary sexual traits, I found no effect of founder number on the size of wattles in saddleback. I did however demonstrate that wattle size reflected the level of immune function in females as well as males, suggesting that females play a far greater role in offspring fitness than has been appreciated in traditional theories of sexual selection. Overall, my results indicate that severe bottlenecks can lead to reductions in immunocompetence in the resulting populations, especially in those populations that pass through the most severe bottlenecks. Based on the evidence from my thesis, I recommend conservation managers should aim to use at least 90 individuals to found new populations in order to reduce the deleterious effects of bottlenecks on immune function. If the costs of population bottlenecks and inbreeding are to be avoided, conservationists must adequately address the role of genetic factors in susceptibility to disease, and work towards minimising the risk of severe population bottlenecks in the management of endangered birds

Severe population bottlenecks and the small size of many remnant habitats may render many bird populations prone to extinction from disease outbreaks. Bottlenecks may increase inbreeding which in turn may result in a low diversity of resistance and an immune system that is impaired or defective. Thus, bottlenecked populations may be less immunocompetent and more vulnerable to microbiological and parasitic perturbations. Few studies have assessed the effect of bottlenecks on the immunocompetence of birds. In this study, I used twelve saddleback (Philesturnus carunculatus) and two New Zealand robin (Petroica a. australis) populations, to determine if the severe bottlenecks reduce the immunocompetence of birds. When I experimentally challenged the immune system of two robin populations I found that despite the two populations having similar parasite loads, robins from the severely bottlenecked Motuara Island population exhibited a significantly lower T-cell mediated immune response than the source population (Nukuwaiata Island) suggesting that birds passing through severe population bottlenecks have a compromised immunocompetence. In the saddleback, severe bottlenecks, as well as high population densities and small island size, lead to individuals exhibiting higher stress levels and feather mite loads and lower immune function, as was evident by lower lymphocyte counts. I did not find levels of fluctuating asymmetry of saddlebacks to be directly influenced by bottleneck size. However, I did find that individuals with higher levels of fluctuating asymmetry had higher loads of hippoboscid flies and lower loads of coccidia suggesting a possible trade-off between growth and immune function. In contrast to previous studies looking at behavioural secondary sexual traits, I found no effect of founder number on the size of wattles in saddleback. I did however demonstrate that wattle size reflected the level of immune function in females as well as males, suggesting that females play a far greater role in offspring fitness than has been appreciated in traditional theories of sexual selection. Overall, my results indicate that severe bottlenecks can lead to reductions in immunocompetence in the resulting populations, especially in those populations that pass through the most severe bottlenecks. Based on the evidence from my thesis, I recommend conservation managers should aim to use at least 90 individuals to found new populations in order to reduce the deleterious effects of bottlenecks on immune function. If the costs of population bottlenecks and inbreeding are to be avoided, conservationists must adequately address the role of genetic factors in susceptibility to disease, and work towards minimising the risk of severe population bottlenecks in the management of endangered birds