Linking biodiversity and parasite transmission across spatial scales
Parasites represent one of the most conspicuous gaps in our understanding of life’s diversity. This ignorance is a liability when considered in light of the increasingly important role that parasites play in human and wildlife health. Especially troubling are indications that anthropogenic biodiversity loss could increase parasite transmission, which has been the focus of substantial research effort in disease ecology. However, a concurrent line of research makes the apparently opposite prediction that host and parasite diversity should be positively correlated. We propose that this paradox arises, in part, from the fact that relationships among host diversity, parasite diversity, and disease risk are scale-dependent. While processes like species interactions may be important in determining parasite abundance or transmission at local scales, other processes, including parasite dispersal and colonization, might override such interactions as scale increases. We test this hypothesis using two approaches: (1) by assessing the magnitude and direction of the biodiversity–disease relationship for amphibian parasites across spatial scales, using both a continental-scale dataset and a more finely resolved dataset from California and (2) by performing a manipulative, ecosystem-scale experiment to test the mechanisms underlying the biodiversity–disease relationship.
We find that species interactions are important drivers of parasite transmission at local scales, whereas large-scale processes such as dispersal and colonization govern the abundance of parasites at broader spatial scales. This results in variable relationships between biodiversity and disease at local scales (i.e., either “dilution” or “amplification”, depending on the traits of parasite and host species), and positive relationships at larger scales. In an experiment designed to test this hypothesis using natural ponds in Northern California, we have the ability to control rates of parasite colonization by manipulating the local diversity and abundance of birds, which disperse trematode parasites into aquatic habitats. Although vertebrate manipulations are challenging, preliminary results indicate that our approach is highly effective in excluding birds from ponds, and thereby simulating reductions in colonization rate for bird-transmitted trematodes. Findings from this study will help build toward a general theory on the functional relationship between biodiversity and disease. From an applied perspective, a mechanistic understanding of how community structure affects parasite transmission can help to enhance the efficacy of human and wildlife disease control programs.