Host Dispersal Responses to Resource Supplementation Determine Pathogen Spread in Wildlife Metapopulations

Abstract

Many wildlife species occupy landscapes that vary in the distribution, abundance, and quality of food resources. Increasingly, urbanized and agricultural habitats provide supplemental food resources that can have profound consequences for host distributions, movement patterns, and pathogen exposure. Understanding how host and pathogen dispersal across landscapes is affected by the spatial extent of food-supplemented habitats is therefore important for predicting the consequences for pathogen spread and impacts on host occupancy. Here we develop a generalizable metapopulation model to understand how the relative abundance of provisioned habitats across the landscape and how the host dispersal responses to provisioning and infection influence patch occupancy by hosts and their pathogens. We find that pathogen invasion and landscape-level infection prevalence are greatest when provisioning increases patch attractiveness and disperser production and when infection has minimal costs on dispersal success. Alternatively, if provisioning promotes site fidelity or reduces disperser production, increasing the fraction of food-supplemented habitats can reduce landscape-scale infection prevalence and minimize disease-induced declines in host occupancy. This work highlights the importance of considering how resources and infection jointly influence host dispersal for predicting how changing resource distributions influence the spread of infectious diseases.

Infection in patchy populations: Contrasting pathogen invasion success and dispersal at varying times since host colonization

“…This result mirrors theory on the role of patch quality in host metapopulations. Here, high-quality or resource rich patches both attract and support greater host and pathogen densities, facilitating a constant supply of infected carriers across a landscape (e.g., Leach et al 2016;Becker et al 2018). In contrast, Civitello et al (2013) found that pathogens are more likely to invade populations of intermediate density, as foraging interference limits transmission at higher host densities.…”

Comparative landscape genetics reveals differential effects of environment on host and pathogen genetic structure in Tasmanian devils (Sarcophilus harrisii) and their transmissible tumour

“…Despite the apparent decoupling of host and pathogen gene flow herein, host connectivity generally plays a significant role in wildlife disease dynamics. Higher connectivity among habitat patches and increased host movements increase rates of pathogen spread, prevalence and persistence in the landscape (Becker, Snedden, Altizer, & Hall, 2018;Wilber, Johnson, & Briggs, 2020). However, wildlife populations themselves benefit similarly from increased connectivity, which is critical for maintaining genetic diversity and facilitating demographic rescue (Brown & Kodric-Brown, 1977;Keyghobadi, 2007;Whiteley, Fitzpatrick, Funk, & Tallmon, 2015).…”

Can pathogens optimize both transmission and dispersal by exploiting sexual dimorphism in their hosts?

“…Predictions for pathogen evolution in a patchy landscape often centre on a pathogen's dispersal ability relative to that of a generic host [7,8], implying that there is one optimal dispersal strategy. In nature, however, hosts commonly vary in their dispersal capacity and provided resources, with one common source of host heterogeneity being sexual dimorphism.…”