Abstract
Infectious diseases significantly threaten many wildlife populations. Proposed treatments often fail to consider resulting impacts on natural host defense mechanisms and ongoing infection risks. We demonstrate the importance of prior knowledge of host defenses by modeling outcomes of various treatment regimes on bat populations infected with white-nose syndrome (WNS), a disease that has caused declines in multiple North American species. Despite differences in species susceptibility to the causative fungus, how hosts respond to and survive infection remains unclear. We explore three potential host-defense mechanisms: upregulation of the responsive innate or adaptive immune systems, and rapid evolution that enables evolutionary rescue. We demonstrate that treatment can accelerate extirpation (relative to inaction) if hosts are defended by responsive immunity; whereas, treatment can cause populations undergoing evolutionary rescue to regain population viability faster. We conclude that successful treatment of wildlife diseases must first consider how individuals respond to and survive infection.
Highlights
Infectious disease historically has not been considered a major cause of species’ extinction and, disease management has far remained a low priority relative to other conservation actions (Fisher et al, 2012; Pullin et al, 2013)
That the influence of infectious disease on extinction risk has been largely underestimated and that the coupled effects of anthropogenic forces on hosts and diseases will greatly contribute to our global biodiversity crisis (Smith et al, 2009; McCallum, 2012)
The evolutionary rescue model makes the conservative assumption that phenotypic robustness to white-nose syndrome (WNS) was based upon a Boolean protective genetic profile
Summary
Infectious disease historically has not been considered a major cause of species’ extinction and, disease management has far remained a low priority relative to other conservation actions (Fisher et al, 2012; Pullin et al, 2013). That the influence of infectious disease on extinction risk has been largely underestimated and that the coupled effects of anthropogenic forces on hosts and diseases will greatly contribute to our global biodiversity crisis (Smith et al, 2009; McCallum, 2012). Anthropogenic climate change and globalization have expanded the natural range of many pathogens and/or their suite of host species, releasing them from co-evolutionary forces that may have maintained lower-virulence strains (e.g., Brasier and Buck, 2001). The unprecedented frequency of disease emergence (Harvell et al, 2002; Fisher et al, 2012) and the strength of impacts on wild populations (Daszak et al, 2000), increasingly point to the importance of successful mitigation of disease in species’ conservation
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