A central challenge to studying emerging infectious diseases (EIDs) is a landscape dilemma: Our best empirical understanding of disease dynamics occurs at local scales, whereas pathogen invasions and management occur over broad spatial extents. The burgeoning field of landscape epidemiology integrates concepts and approaches from disease ecology with the macroscale lens of landscape ecology, enabling examination of disease across spatiotemporal scales in complex environmental settings. We review the state of the field and describe analytical frontiers that show promise for advancement, focusing on natural and human-altered ecosystems. Concepts fundamental to practicing landscape epidemiology are discussed, including spatial scale, static versus dynamic modeling, spatially implicit versus explicit approaches, selection of ecologically meaningful variables, and inference versus prediction. We highlight studies that have advanced the field by incorporating multiscale analyses, landscape connectivity, and dynamic modeling. Future research directions include understanding disease as a component of interacting ecological disturbances, scaling up the ecological impacts of disease, and examining disease dynamics as a coupled human-natural system.

Abstract. Illuminating the ecological and evolutionary dynamics of parasites is one of the most pressing issues facing modern science, and is critical for basic science, the global economy, and human health. Extremely important to this effort are data on the diseasecausing organisms of wild animal hosts (including viruses, bacteria, protozoa, helminths, arthropods, and fungi). Here we present an updated version of the Global Mammal Parasite Database, a database of the parasites of wild ungulates (artiodactyls and perissodactyls), carnivores, and primates, and make it available for download as complete flat files. The updated database has more than 24,000 entries in the main data file alone, representing data from over 2700 literature sources. We include data on sampling method and sample sizes when reported, as well as both "reported" and "corrected" (i.e., standardized) binomials for each host and parasite species. Also included are current higher taxonomies and data on transmission modes used by the majority of species of parasites in the database. In the associated metadata we describe the methods used to identify sources and extract data from the primary literature, how entries were checked for errors, methods used to georeference entries, and how host and parasite taxonomies were standardized across the database. We also provide definitions of the data fields in each of the four files that users can download.

Empirical evidence suggests that biodiversity loss can increase disease transmission, yet our understanding of the 'diversity-disease hypothesis' for generalist pathogens in natural ecosystems is limited. We used a landscape epidemiological approach to examine two scenarios regarding diversity effects on the emerging plant pathogen Phytophthora ramorum across a broad, heterogeneous ecoregion: (1) an amplification effect exists where disease risk is greater in areas with higher plant diversity due to the pathogen's wide host range, or (2) a dilution effect where risk is reduced with increasing diversity due to lower competency of alternative hosts. We found evidence for pathogen dilution, whereby disease risk was lower in sites with higher species diversity, after accounting for potentially confounding effects of host density and landscape heterogeneity. Our results suggest that although nearly all plants in the ecosystem are hosts, alternative hosts may dilute disease transmission by competent hosts, thereby buffering forest health from infectious disease.

Despite a century of research into the factors that generate and maintain biodiversity, we know remarkably little about the drivers of parasite diversity. To identify the mechanisms governing parasite diversity, we combined surveys of 8,100 amphibian hosts with an outdoor experiment that tested theory developed for free-living species. Our analyses revealed that parasite diversity increased consistently with host diversity due to habitat (i.e., host) heterogeneity, with secondary contributions from parasite colonization and host abundance. Results of the experiment, in which host diversity was manipulated while parasite colonization and host abundance were fixed, further reinforced this conclusion. Finally, the coefficient of host diversity on parasite diversity increased with spatial grain, which was driven by differences in their species-area curves: while host richness quickly saturated, parasite richness continued to increase with neighborhood size. These results offer mechanistic insights into drivers of parasite diversity and provide a hierarchical framework for multi-scale disease research.

Forest pathogens are important drivers of tree mortality across the globe, but it is exceptionally challenging to gather and build unbiased quantitative models of their impacts. Here we harness the rare data set matching the spatial scale of pathogen invasion, host, and disease heterogeneity to estimate infection and mortality for the four most susceptible host species of Phytophthora ramorum, an invasive pathogen that drives the most important biological cause of tree mortality in a broad geographic region of coastal California and southwest Oregon. As of 2012, the most current field survey year, we estimate 17.5 (±4.6, 95% CI [confidence interval]) million tanoak (Notholithocarpus densiflorus) stems were pathogen killed with an additional 71 (±21.5) million infected. We estimated 9.0 million (±2.2) coast live oak (Quercus agrifolia) and 1.7 million (±0.5) California black oak (Quercus kelloggii) stems are disease impacted (mortality and infection combined). Lastly, our estimates suggest infection in 95.2 million (±8.6) California bay laurel (Umbellularia californica), which does not suffer mortality from infection and represents a critical source of continued spread. Prevalent infection as of 2012 suggests the cumulative number of disease‐killed stems likely increased from 20.8 to 42.8 million between 2012 and 2019 for all species. While these impacts are substantial, most host populations occur in a yet to be invaded region of northern California indicating that the disease will intensify in the coming decades.