UC Berkeley

Sudden Oak Death (SOD), caused by the oomycete pathogen, Phytophthora ramorum, is an introduced forest disease causing large-scale tree mortality in the oak woodlands of California. Pathogen dynamics are bound to be affected by site ecology, forest structure and composition and by interactions among sympatric pathogens. In the four chapters included in this dissertation I address various aspects of the both ecology and epidemiology of the Sudden Oak Death disease, including the competition between three sympatric species of Phytophthora, the population structure of the P.ramorum on its three main hosts, California bay laurel (Umbellularia californica), tanoak (Notholithocarpus densiflorus) and coast live oak (Quercus agrifolia), and at sites with different levels of disease incidence and the population structure of isolates found in two different substrates, soil and bay laurel leaves, in various weather conditions.

Using molecular tools coupled with an intensive multi-year field sampling approach, all within a coastal California watershed with a relatively long and uniform history of disease presence, I determined the following:

When in competition with other Phytophthora species, specifically P. nemorosa, P. ramorum prevalence increases to levels higher than those of the competing species when abundant rainfall triggers its sporulation. Despite P. nemorsa having a broader geographic range, it exhibits a narrower ecological amplitude and, in any given region, occupies fewer sites than P. ramorum. Results additionally suggest that, perhaps due to priority effects, P. nemorosa can persist at levels comparable to those of P. ramorum in ecologically suitable plots when climate favors P. ramorum dormancy.

Shifts in weather, primarily levels of rainfall are accurate predictors in the likelihood of both bay laurel and oak infection as well as transitions between dormant and active infection of the pathogen itself. Additionally site specific factors such as aspect, bay laurel density and bay laurel basal area drive differences in levels of both disease incidence and prevalence on both bay laurel and oak hosts. For oaks specifically, infection rates are greater among larger trees, yet levels of mortality are greater among smaller trees. Neighborhood effects such as proximity to infected bay laurel foliage, and surrounding bay laurel density and basal area are important factors in predicting oak infection.

Ten microsatellites were used for genetic analyses on cultures from successful isolations to determine differences in population structure between different substrates, namely populations isolated from soil versus aerial populations isolated from bay laurel leaves in various weather conditions. Migration of genotypes among sites was low and spatially limited during dry periods, but intensity and range of migration of genotypes significantly increased for leaf populations during wet periods. Only leaf genotypes persisted significantly between years, and genotypes present in different substrates were distributed differently in soil and leaves. It was concluded that epidemics start rapidly at the onset of favorable climatic conditions through highly transmissible leaf genotypes, and that soil populations are transient and may be less epidemiologically relevant than previously thought.

Population structure of the pathogen in each of the three main hosts was examined to provide evidence of contagion pathways among hosts, as well as differences in population structure in wet vs. dry years and at sites with various levels of disease incidence and prevalence. The relationships among P. ramorum populations in bay laurels, oaks and tanoaks were analyzed and structure was found to exist among hosts. It was determined that bay laurel is the source population for both tanoak and oak infection, and that tanoak contributes minimally to oak infection. In spite of their common source of inoculum, oaks and tanoaks were found to be sinks that select for different pathogen genotypes, due to the variance in selection pressure in each host type. Additionally, different sites supported a dominance of different genotypes, more genotypes overall and more persistent genotypes, when compared to other sites, and these ‘hotspots’ are likely to play a more significant epidemiological and evolutionary role for the pathogen.

Together these results help to advance the state of knowledge surrounding the ecology, epidemiology and population genetics of the Sudden Oak Death pathogen in California, add to the growing body of research on invasive plant pathogens, support theories of invasion biology and most importantly can be applied to regulatory and land management practices in attempt to mitigate the spread of this disease.

Chair Date