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Population bottlenecks and avian immunity: implications for conservation

The study of immune function in the bottlenecked endemic New Zealand robin, presented by Hale & Briskie (2007), is a timely and informative addition to the growing body of literature on the effects that passing through genetic bottlenecks can have on bird species, and the resulting implications for their population management, recovery and longterm resilience. In a critical review of the implications of this work for conservation of both this species and bottlenecked populations in general, however, three key questions need to be asked. Is there sufficient evidence that bottlenecks cause reduced immune function? Does such a reduction actually impact on the resilience and long-term viability of such species? If there is indeed an issue, can it be addressed by management? Is there sufficient evidence that bottlenecks cause reduced immune function? Hale & Briskie (2007) conclude ‘Our results confirm that severe bottlenecks reduce the immunocompetence of birds . . .’ In support of this statement, their work has demonstrated that two measures of immune function are significantly lower in a recently bottlenecked population of the New Zealand robin compared with its source population. Although trade-offs in the different branches of the immune system may occur, lower levels of function in two different measures are generally taken as good evidence for a meaningful reduction in immune function (Norris & Evans, 2000; Lindström et al., 2004; Tompkins, Mitchell & Bryant, 2006). However, results from a single bottlenecked population versus a single source population do not demonstrate that the bottleneck caused the reduction – other confounding factors may be involved. Although this study alone does not confirm a bottleneck/ immune function link, the accumulated evidence in the literature, as Hale & Briskie (2007) note, is heavily in favour of there being such a link. For conservation purposes, I would argue that the weight of evidence is sufficient for these considerations to be taken into account in species management programmes – definitive proof for such a link (requiring long-term manipulations at the population scale) may never be obtained, avoidable losses of species may occur while waiting for such proof. Having made such a recommendation, however, there are two further considerations that may inform any management undertaken, and hence need to be taken into account. First, there is no evidence that immune function reductions linked to bottlenecks are not just relatively short-term transient effects. All studies to date have focused on time points relatively soon after bottleneck events. Repeated observations on subsequently expanding populations are thus required to demonstrate that reductions in immune function are maintained and, hence, are a long-term concern to population viability. Second, due to the complex lifehistory interactions of immunity (Norris & Evans, 2000), reductions in such functions may not be a simple direct consequence of loss of genetic variation. For example, a potential alternative mechanism is that the more frequent failure to breed successfully in bottlenecked populations (Briskie & Mackintosh, 2004) may be energetically costly, drawing resources away from immunocompetence. Whether reduced immune function is directly or indirectly caused by bottlenecks has implications for its management. Does such a reduction actually impact on the resilience and long-term viability of such species? As many studies have documented, including Hale & Briskie (2007), temporal changes in measures of immune function in birds are common. Such changes are hypothesized as being due to either immune components being adapted to cope with a greater impact of parasites at certain times (Møller, Erritzoe & Saino, 2003), as a consequence of an increased need for wound-healing and resisting infection capabilities during periods when the likelihood of injury is greater (Zuk & Johnsen, 1998), lymphatic organ size peaking in relation to winter conditions (Nelson &Demas, 1996), or (related to the point made above) lack of resource availability due to the demands of reproduction and increased investments in other aspects of immunity (Zuk & Johnsen, 1998; Norris & Evans, 2000). Regardless of the cause, however, such changes