Spatial scale drives process and pattern: Support for a classic hypothesis in macroecology
Humans are presently contributing to unprecedented rates of infectious disease emergence, climate change, and homogenization of the environment, altering the distribution and abundance of organisms. A classic but untested hypothesis in ecology – that the influence of environmental drivers on species distributions is scale-dependent – poses a serious challenge to understanding and addressing these daunting problems. Ecologists have traditionally hypothesized that biotic processes (e.g., species interactions) control distribution patterns at small scales and abiotic processes (e.g., environmental filtering) do so at larger scales, suggesting that the outcomes of single-scale analyses might misrepresent the true consequences of natural and human-induced changes to the environment. However, scale hypotheses were difficult to test before the recent availability of large-scale species distribution datasets and advancements in computing power. Here, we used species distribution models to examine how the environment, human-assisted dispersal, and host richness control the distribution of pathogens responsible for three emerging diseases (West Nile virus, amphibian chytrid fungus, and Lyme disease) across seven spatial scales ranging from a few kilometers to entire regions in the US.
We found consistent effects of scale on the importance of processes controlling the distribution of all three pathogens. Host richness, a proxy for species interactions, was only a significant predictor of pathogen distributions at small scales, while abiotic factors (representing mean temperature, temperature variability, and precipitation) were only significant at large scales. Human population density, a proxy for human-mediated dispersal, was significant at scales larger than those where host richness was important, although the extent of this varied between pathogens. Additionally, our results suggest that intermediate scales may be inadequate to detect the effects of all drivers of species distributions because there was little overlap between the scales at which different processes were significant. Broadly, single-scale analyses might fail to identify processes controlling disease patterns, the spread of non-native species, or distributions of vulnerable species if the ecological processes tested operate at different scales. As humans continue to modify species composition, dispersal, and the climate across scales, it is critical that we fully understand all of the consequences of these changes. Without thorough multi-scale analyses, scientists are likely to misestimate the impacts of anthropogenic modifications on biodiversity and the environment.