Ganoderma species are well-documented pathogens of a wide range of woody hosts. Recently, Ganoderma adspersum has been observed to be associated with wood decay and tree failure in California almond orchards. The purpose of this study was to investigate the pathogenicity, infectivity, and transmission of G. adspersum associated with increasing tree failure in California’s Central Valley. To date, no studies have investigated the pathogenicity of Ganoderma species in agricultural and native trees in California. Pathogenicity tests were conducted to determine the pathogenicity of G. adspersum and G. brownii (a native Ganoderma species in California) on almond, walnut, pistachio, and oak trees. Inoculations were made by coring into the sapwood of the saplings’ basal stem and pipetting Ganoderma spore solutions into the wounds. In two greenhouse trials, 10 months post-inoculation, trees had no visual, external symptoms of disease, although there were differences in the extent of internal wood decay and xylem discoloration. Ganoderma adspersum caused extensive discoloration and was reisolated from Nemaguard and Viking rootstock cultivars. The data suggest that these Ganoderma species were pathogens capable of infecting healthy sapwood of almond. Disease surveys in almond orchards revealed substantial tree losses associated with G. adspersum. In one case, tree losses resulted in early removal of a 19-20-year-old orchard. A two-year long spore survey in almond orchards revealed that the majority of spores were trapped during increased temperatures and almond harvest from August to September. These findings suggest the need to assess management practices to reduce dust production and G. adspersum spore transmission in California orchards. In field conditions, G. adspersum was often associated with bacterial colonization of Agrobacterium tumefaciens, causal agent of crown gall. The high co-incidence of the fungal and bacterial pathogens suggests potential synergystic effects in pathogenesis. However, co-inoculation assays have shown that the pathogens do not significantly interact with each other nor promote increased initial disease development. The rise of multi-pathogen diseases in almonds likely results from the rapid adoption of high-density planting, mechanized harvesting, and increased inputs of irrigation and fertilization, which create an environment that facilitates the infection and establishment of multiple pathogens.

Global losses of biodiversity alter interactions amongst hosts and pathogens, and in turn, affect disease dynamics. Uncovering the mechanisms underlying relationships between diversity and disease risk is essential for predicting and managing emerging outbreaks. It is also critical to assess how decisions that researchers make, such as how to measure disease risk, affect inference in diversity-disease patterns. In my dissertation, I broadly sought to understand why diversity (sometimes) limits disease risk by focusing on two pathosystems.

The first system I examined is a forest disease sudden oak death, caused by Phytophthora ramorum, a generalist oomycete pathogen that has killed millions of tanoak and oak trees along the coast of California and southwestern Oregon. Studying the biology of natural disease systems is powerful for understanding linkages among community composition, host competence (i.e. the ability to acquire infections and contribute to transmission), and various metrics of disease. In chapter 1, I quantified the sporulation potential of common plant species inhabiting the Big Sur region of coastal California. These lab-based competence assays indicated that bay laurel and tanoak produced large quantities of sporangia; all remaining species produced much less. In chapter 2, I studied natural forests infested by sudden oak death to empirically evaluate hypotheses underlying previously observed negative diversity-disease relationships (i.e. 'dilution effect'). In order to understand how the whole host community might contribute to transmission risk, I leveraged data from the sporulation assays and augmented it to plant community and disease field data from a large forest monitoring plot network. I demonstrated that aggregating disease observations at the community-level can lead to misinterpretations of dilution mechanisms, bias towards a negative diversity-disease relationship, and through review of the dilution effect literature, I found that this oversight is surprisingly common.

I also relied on a tractable model system consisting of crop seedlings and an agricultural fungal pathogen, Rhizoctonia solani. In chapter 3, I planted and inoculated experimental mesocosms in a greenhouse to test how variation in overall species densities and species loss order along a richness gradient affects disease risk. Consistent with theoretical expectations, richness only limited disease when species loss order negatively correlated with host competence and overall species density remained constant with richness. When species density positively correlated with richness or species loss order was random, richness had either a positive or negligible association with disease.

Returning to my overarching question, I found that diversity is more likely to limit disease risk under specific patterns of community assembly and when disease risk is measured as community prevalence. These results present areas ripe for continued research, such as documenting how communities naturally (dis)assemble. They also raise points for discussion, including whether community prevalence--which captures overall disease burden rather than risk of acquiring disease--should be considered under the dilution effect purview. This work adds to the rich and rapidly progressing research focused on uncovering why biodiversity alters disease dynamics.

Invasive Phytophthora species can potentially be destabilizing to whole ecosystems with detrimental effects on biodiversity and on ecosystem services. Studies have shown that Phytophthora species may be introduced into natural areas through outplanting of infested native plant nursery stock. The Angeles National Forest (ANF), located in Southern California, utilizes thousands of nursery-grown native plants for landscape restoration of heavily disturbed areas. Previous pathogen testing performed on ANF restoration sites detected several Phytophthora species. Little is known about the ecology and biology of Phytophthora species in drier regions of the world, thus a baseline of Phytophthora distribution and diversity is needed in ANF lands. Between 2018-2021 forty sites were selected, and soil samples were taken from plant rhizospheres, riverbeds and off-road vehicle tracks in chaparral and oak woodland areas. From these surveys, fourteen species of Phytophthora were detected, including three undescribed species and one hybrid species. Phytophthora species were found in both chaparral and oak woodland areas with a higher frequency in riparian areas. Selfing species (homothallic), capable of readily producing oospores, were more abundant in drier chaparral areas. Phytophthora species were also detected in off-road tracks, dirt trails, and riverbeds, indicating potential natural and anthropogenic-associated routes of dispersal. Pathogenicity tests were conducted to test theaggressiveness of detected Phytophthora species towards common chaparral plant species. Phytophthora cactorum, P. multivora, P. crassamura and P. chlamydospora, were all capable of causing disease on Adenostoma fasciculatum, Eriogonum fasciculatum, Salvia mellifera and Eriodictyon crassifolium. A. fasciculatum was determined to be the most susceptible plant species, especially to P. multivora and P. cactorum. Although the Angeles National Forest is among the driest and most fire prone areas in the United States, these Mediterranean areas harbor a large diversity of Phytophthora species indicating a potential risk for the native and endemic Californian chaparral vegetation. The long-term consequences of the presence of Phytophthora species in these locations still needs to be understood.

“Sudden oak death” refers to a complex set of symptoms that has already culminated in the death of tens of thousands of California oak trees. Now confirmed in seven coastal counties, SOD attacks California tanoak, coast live oak and California black oak. Although several fungal species and the western oak bark beetle and ambrosia beetles have been associated with the syndrome, we now have solid evidence that a newly discovered Phytophthora species is the primary causal agent. This Phytophthora species was recently isolated in rhododendron as well; it may be the same species that was isolated, but not described, on rhododendrons in Germany in 1993. The discovery of SOD on rhododendron has serious implications. The disease may well be present at the ecosystem scale, and its appearance on an ornamental plant suggests the possibility of wider dissemination. A team of UC scientists has developed an integrated approach to managing this disease, including practices to enhance tree health. Early disease detection and targeted chemical treatment may also hold some promise for disease management. In addition, we have developed a molecular probe that will enable rapid identification of SOD from any infected part of the plant. Ultimately, the fate of the oak species affected by SOD will be determined by the levels of disease resistance present in natural populations of these trees.