Mechanisms of community, structural, and functional change by the generalist pathogen Phytophthora ramorum in California coast redwood forests

Pathogens have been powerful forces shaping the composition and ecology of North American forests. Exotic pathogens have caused diseases such as chestnut blight, Dutch elm disease, and beach bark disease that altered forest community and canopy structure at the landscape scale. The pathogen Phytophthora ramorum is an exotic pathogen which causes the disease sudden oak death in California and Oregon forests. P. ramorum is a generalist with a broad host range however P. ramorum has disparate ability to sporulate or cause disease across hosts. In California forests, tanoak (Notholithocarpus densiflorus) supports sporulation and also rapidly develops disease. In contrast, several oak species (especially Quercus agrifolia) suffer mortality following infection but generally do not support sporulation. California bay laurel (Umbellularia californica ) is the most problematic of native host trees; this species supports high levels of sporulation but does not appear to have any deleterious impacts resulting from infection. In this dissertation I use six years of annual surveys across a network of 120 plots in redwood forests to understand the influences of community composition on disease dynamics and use these insights to determine the consequences of sudden oak death for community composition, canopy structure, and woody debris dynamics.;Infection in bay laurel has a 31% greater impact on tanoak mortality compared to infection in tanoak. The combination of greater killing power and the lack of deleterious impacts on bay laurel by the pathogen result in apparent competition between bay laurel and tanoak. This pattern is likely to increase bay laurel densities over time and thereby increase pathogen populations. The mortality rate of individual tanoak stems was also dependent on tree size with larger trees suffering more rapid mortality compared to small trees. Tanoak mortality was widespread in our study stands and we found no indirect evidence for pathogen resistance in our plot network however, P. ramorum infection only killed the above ground portion of infected tanoak in 43% of disease killed trees. The remaining trees develop prolific basal sprouts which are important in maintaining tanoak as a component of these forests. A combined epidemiological and population model for tanoak suggests that retention of tanoak is likely in many forests except those with very high bay laurel abundance and associated sporulation levels. In most cases tanoak will be removed from the overstory and, similarly to American chestnut, will become a species relegated to the forest understory. Stands with low densities of tanoak in a matrix of non-sporulation supporting species like Douglas-fir (Pseudotsuga menziesii) may reduce pathogen levels below those needed for disease outbreak and are potential refugia for overstory tanoak and associated ecosystem function. Some tanoak forests are likely to be protected due to geographic isolation, low densities of sporulation supporting species, or climate conditions outside the acceptable range for P. ramorum however, in most of the range of tanoak, extensive overstory mortality is likely in the coming century. The high likelihood of disease outbreak at the landscape level in combination with rapid mortality of large trees suggests a substantial pulse of carbon (C) may be released from California and Oregon forests over the course of this disease.