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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.

7 Pág., The canker disease caused by Diplodia corticola is one of the most important emerging pathologies of cork oak (Quercus suber) in western Europe. The fungus is dispersed by borer insects, although it is also thought that the spores can be dispersed by wind and rain. The aim of this study was to evaluate the presence of airborne inoculum of D. corticola in managed cork oak stands during cork harvesting season. Semi-passive spore traps were set in eight sampling plots in Catalonia (north-eastern Spain) in summer of 2020. Traps were replaced every week and the number of D. corticolas spores per sampling event was estimated based on a specific nested-qPCR protocol. Spatial-temporal distribution of airborne inoculum accumulation along sampling areas was analyzed using generalized additive models (GAMs). The availability of airborne inoculum resulted rather low with noticeable accumulation peaks in some of the sampled areas. The fitted GAM revealed a positive effect of high air humidity during the sampling period on the availability of spores. This study represents the first attempt to model the spore release of this emerging pathogen, and it provides insights for developing D. corticola canker control strategies based on the precise timing of cork harvesting operations., This work was partially funded by the Generalitat de Catalunya, Departament d'Acció Climàtica, Alimentació i Agenda Rural (Spain). Anand B. Uppara is granted by an Industrial Pre-Doctoral Fellowship at Forest Bioengineering solutions and the Forest Sciences Center of Catalonia (CTFC) (reference: E-25-2020-0115755). Authors thank J. Heras (Generalitat de Catalunya), O. Plana (Diputació de Barcelona), A. Torrell (Forestal Catalana), and J.M. Riba for their helpful advice and support in plot selection and sampling development. Fungal strain CAA007-1 used in molecular procedures was provided by Dr. A. Alves (Universidade de Aveiro, Portugal). Authors especially thank Ajuntament de Tordera, Agents Rurals, the staff of Forestal Catalana, and forest owners for giving support in fieldwork and trap monitoring.

In forest ecosystems, habitat fragmentation negatively impacts stand structure and biodiversity; the resulting fragmented patches of forest have distinct, disturbed edge habitats that experience different environmental conditions than the interiors of the fragments. In southwest Western Australia, there is a large-scale decline of the keystone tree species Corymbia calophylla following fragmentation and land use change. These changes have altered stand structure and increased their susceptibility to an endemic fungal pathogen, Quambalaria coyrecup, which causes chronic canker disease especially along disturbed forest habitats. However, the impacts of fragmentation on belowground processes in this system are not well-understood. We examined the effects of fragmentation on abiotic soil properties and ectomycorrhizal (ECM) and arbuscular mycorrhizal (AM) fungal communities, and whether these belowground changes were drivers of disease incidence. We collected soil from 17 sites across the distribution range of C. calophylla. Soils were collected across a gradient from disturbed, diseased areas to undisturbed, disease-free areas. We analysed soil nutrients and grew C. calophylla plants as a bioassay host. Plants were harvested and roots collected after 6 months of growth. DNA was extracted from the roots, amplified using fungal specific primers and sequenced using Illumina MiSeq. Concentrations of key soil nutrients such as nitrogen, phosphorus and potassium were much higher along the disturbed, diseased edges in comparison to undisturbed areas. Disturbance altered the community composition of ECM and AM fungi; however, only ECM fungal communities had lower rarefied richness and diversity along the disturbed, diseased areas compared to undisturbed areas. Accounting for effects of disturbance, ECM fungal diversity and leaf litter depth were highly correlated with increased disease incidence in C. calophylla. In the face of global change, increased virulence of an endemic pathogen has emerged in this Mediterranean-type forest.