Journal
ECOLOGY LETTERS
Volume 24, Issue 1, Pages 130-148Publisher
WILEY
DOI: 10.1111/ele.13621
Keywords
Chytridiomycosis; compensatory recruitment; density-dependent transmission; environmental refugia; host-pathogen; management; population persistence; population recovery; resistance; tolerance
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Funding
- Griffith University International Workshop Award
- Australian Research Council [DE180101395, DP180101415]
- National Science Foundation [DEB-1336290, DEB-1115895, DEB-1717498]
- Australian Research Council [DE180101395] Funding Source: Australian Research Council
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The study examined mechanisms enabling host persistence and the impact on conservation management strategies. The majority of species' mechanisms for persistence remain unidentified, highlighting the importance of understanding mechanisms of host persistence.
Emerging infectious diseases have caused many species declines, changes in communities and even extinctions. There are also many species that persist following devastating declines due to disease. The broad mechanisms that enable host persistence following declines include evolution of resistance or tolerance, changes in immunity and behaviour, compensatory recruitment, pathogen attenuation, environmental refugia, density-dependent transmission and changes in community composition. Here we examine the case of chytridiomycosis, the most important wildlife disease of the past century. We review the full breadth of mechanisms allowing host persistence, and synthesise research on host, pathogen, environmental and community factors driving persistence following chytridiomycosis-related declines and overview the current evidence and the information required to support each mechanism. We found that for most species the mechanisms facilitating persistence have not been identified. We illustrate how the mechanisms that drive long-term host population dynamics determine the most effective conservation management strategies. Therefore, understanding mechanisms of host persistence is important because many species continue to be threatened by disease, some of which will require intervention. The conceptual framework we describe is broadly applicable to other novel disease systems.
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