Common Factors Drive Disease and Coarse Woody Debr

Authors: Richard C Cobb Maggie N Chan Ross K Meentemeyer David M Rizzo

Publish Date: 2011/12/10

Volume: 15, Issue: 2, Pages: 242-255

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Abstract

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 224 Mg ha−1 of standing dead tanoak snags and 115 Mg ha−1 in logs compared to 027 and 116 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 predisease 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 pathogensRC and RM conceived and designed study performed research analyzed data designed methods and models and wrote the paper MC performed research analyzed data designed methods and models and wrote the paper DR conceived and designed study analyzed data designed methods and models and wrote the paperH 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 NSFNIH Ecology of Infectious Diseases program EF0622770 the Gordon and Betty Moore Foundation and the USDA Pacific Southwest Research Station

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