Biodiversity loss sometimes increases disease risk or parasite transmission in humans, wildlife and plants. Some have suggested that this pattern can emerge when host species that persist throughout community disassembly show high host competence -the ability to acquire and transmit infections. Here, we briefly assess the current empirical evidence for covariance between host competence and extirpation risk, and evaluate the consequences for disease dynamics in host communities undergoing disassembly. We find evidence for such covariance, but the mechanisms for and variability around this relationship have received limited consideration. This deficit could lead to spurious assumptions about how and why disease dynamics respond to community disassembly. Using a stochastic simulation model, we demonstrate that weak covariance between competence and extirpation risk may account for inconsistent effects of host diversity on disease risk that have been observed empirically. This model highlights the predictive utility of understanding the degree to which host competence relates to extirpation risk, and the need for a better understanding of the mechanisms underlying such relationships.
Summary1. Ecologists often measure the biomass and productivity of organisms to understand the importance of populations and communities in the flow of energy through ecosystems. Despite the central role of such studies in the advancement of freshwater ecology, there has been little effort to incorporate parasites into studies of freshwater energy flow. This omission is particularly important considering the roles that parasites sometimes play in shaping community structure and ecosystem processes. 2. Using quantitative surveys and dissections of over 1600 aquatic invertebrate and amphibian hosts, we calculated the ecosystem-level biomass and productivity of trematode parasites alongside the biomass of free-living aquatic organisms in three freshwater ponds in California, USA. 3. Snails and amphibian larvae, which are both important intermediate trematode hosts, dominated the dry biomass of free-living organisms across ponds (snails = 3Á2 g m À2 ;amphibians = 3Á1 g m À2 ). An average of 33Á5% of mature snails were infected with one of six trematode taxa, amounting to a density of 13 infected snails m À2 of pond substrate.Between 18% and 33% of the combined host and parasite biomass within each infected snail consisted of larval trematode tissue, which collectively accounted for 87% of the total trematode biomass within the three ponds. Mid-summer trematode dry biomass averaged 0Á10 g m À2 , which was equal to or greater than that of the most abundant insect orders (coleoptera = 0Á10 g m À2 , odonata = 0Á08 g m À2 , hemiptera = 0Á07 g m À2 and ephemeroptera = 0Á03 g m À2 ). 4.On average, each trematode taxon produced between 14 and 1660 free-swimming larvae (cercariae) infected snail À1 24 h À1 in mid-summer. Given that infected snails release cercariae for 3-4 months a year, the pond trematode communities produced an average of 153 mg m À2 yr À1 of dry cercarial biomass (range = 70-220 mg m À2 yr À1 ). 5.Our results suggest that a significant amount of energy moves through trematode parasites in freshwater pond ecosystems, and that their contributions to ecosystem energetics may exceed those of many free-living taxa known to play key roles in structuring aquatic communities.
Pathogen transmission responds differently to host richness and abundance, two unique components of host diversity. However, the heated debate around whether biodiversity generally increases or decreases disease has not considered the relationships between host richness and abundance that may exist in natural systems. Here we use a multi-species model to study how the scaling of total host community abundance with species richness mediates diversity-disease relationships. For pathogens with density-dependent transmission, non-monotonic trends emerge between pathogen transmission and host richness when host community abundance saturates with richness. Further, host species identity drives high variability in pathogen transmission in depauperate communities, but this effect diminishes as host richness accumulates. Using simulation we show that high variability in low richness communities and the non-monotonic relationship observed with host community saturation may reduce the detectability of trends in empirical data. Our study emphasizes that understanding the patterns and predictability of host community composition and pathogen transmission mode will be crucial for predicting where and when specific diversity-disease relationships should occur in natural systems.
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