| Popis: |
Changes in host species richness can alter infection risk and disease levels in communities. I review theoretical predictions for direct and environmental transmission pathogens about the effects of host additions (or removals) on three common disease metrics: the pathogen community reproduction number (ℛ0) and the proportion (i.e., infection prevalence) and density of infected individuals in a focal host. To help explain why predictions differ between studies and between metrics, I analyze an SIR-type model of an environmentally transmitted pathogen and multiple host species that compete for resources. I use local sensitivity analysis to explore and compare how variation in an added host’s ability to transmit a pathogen, its density, and the pathogen transmission mechanism affect each disease metric. I find that if an added host species is a weak interspecific competitor, then each metric typically increases or decreases, respectively, when the added host has a high or low ability to transmit the pathogen. However, if the added host species is a strong interspecific competitor, then the response of each metric can be strengthened, weakened, or reversed depending on how the competitive effects of the added host propagate through the community and alter the densities of all host species in the community. The three metrics often respond in the same direction, but the metrics can respond in different directions for three reasons: (1) strong density-mediated feedbacks driven by high disease-induced mortality; (2) host additions or removals cause large changes in focal host density via competition or disease-induced mortality; and (3) the metrics use different quantities to define a host’s ability to transmit disease: the quantities for infection prevalence and infected density depend on the instantaneous production rates of infectious propagules whereas the quantities for ℛ0depend on lifetime production of infectious propagules. This study provides a framework that unifies prior theoretical studies and identifies rules governing the context-dependent relationships between host species richness and the three metrics of disease. |
