Common Factors Drive Disease and Coarse Woody Debris Dynamics in Forests Impacted by Sudden Oak Death
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Disease ecology has made important steps in describing how epidemiological processes control the impact of pathogens on populations and communities but fewer field or theoretical studies address disease effects at the ecosystem level. We demonstrate that the same epidemiological mechanisms drive disease intensity and coarse woody debris (CWD) dynamics in natural forest ecosystems impacted by an emerging disease. Sudden oak death (causal agent, Phytophthora ramorum) has caused mortality of tanoak (Notholithocarpus densiflorus) on a spatial scale and rate comparable to other major North American forest diseases caused by invasive pathogens. In pathogen invaded stands, mean CWD masses were 22.4 Mg ha−1 of standing dead tanoak (snags) and 11.5 Mg ha−1 in logs compared to 0.27 and 1.16 Mg ha−1 of snags and logs in an uninvaded stand. Within invaded stands variation in CWD mass and accumulation rates were largely driven by the distribution of pre-disease tanoak biomass and the densities of infected tanoak and California bay laurel (Umbellularia californica) which jointly determine P. ramorum sporulation and disease emergence rates. In a narrow range of community and host characteristics sudden oak death can result in woody debris dynamics similar to discrete disturbances such as fire and forest harvest but it is more common to have lower maximum amounts with slower rates of accumulation than these better studied disturbances. Our results indicate that models of CWD dynamics need to integrate epidemiological processes to predict realistic ecosystem impacts and lead to management applications for forest pathogens.
KeywordsPhytophthora ramorum emerging infectious disease disease ecology tanoak coarse woody debris decomposition
H. Mehl, S. Lynch, A. Westbrook, K. Ireland, C. DeLong, C. Shoemaker, and A. Oguchi provided field and laboratory support for this research. We thank two anonymous reviewers, Margaret Metz, Val Eviner, Gary Lovett, and Faith Fogel for helpful comments on earlier versions of this paper. Additionally, we are grateful to the California State Parks and the Marin Municipal Water District for granting access to the study sites. This research was funded by the NSF-NIH Ecology of Infectious Diseases program EF-0622770, the Gordon and Betty Moore Foundation, and the USDA Pacific Southwest Research Station.
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