Abstract
Metapopulation structure plays a fundamental role in the persistence of wildlife populations. It can also drive the spread of infectious diseases and transmissible cancers such as the Tasmanian devil facial tumour disease (DFTD). While disrupting this structure can reduce disease spread, it can also impair host resilience by disrupting gene flow and colonisation dynamics. Using an individual-based metapopulation model we investigated the synergistic effects of host dispersal, disease transmission rate and inter-individual contact distance for transmission, on the spread and persistence of DFTD from local to regional scales. Disease spread, and the ensuing population declines, are synergistically determined by individuals’ dispersal, disease transmission rate and within-population mixing. Transmission rates can be magnified by high dispersal and inter-individual transmission distance. The isolation of local populations effectively reduced metapopulation-level disease prevalence but caused severe declines in metapopulation size and genetic diversity. The relative position of managed (i.e., isolated) local populations had a significant effect on disease prevalence, highlighting the importance of considering metapopulation structure when implementing metapopulation-scale disease control measures. Our findings suggest that population isolation is not an ideal management method for preventing disease spread in species inhabiting already fragmented landscapes, where genetic diversity and extinction risk are already a concern.
Highlights
Infectious diseases are a major threat to the long-term survival of wildlife populations across many taxa [1]
Disease Spread Is Driven by the Interplay between Local Transmission and Population size decreased as dispersal rate (γ0 ) increased across all values of transmission rate (β) and contact distance (δ)
We developed an individual-based metapopulation model that allowed us to investigate the synergistic effects of local-scale disease transmission processes and population dynamics, and landscapescale metapopulation processes, on the spread of a transmissible cancer in Tasmanian devil populations, with the consequences for population abundances that ensue
Summary
Infectious diseases are a major threat to the long-term survival of wildlife populations across many taxa [1]. Infectious cancers in wildlife are nowadays recognised as a major conservation problem, for endangered species and populations with restricted distribution [2,3]. Increased host movement has been shown to drive both the regional spread of disease [13,14,20] and host extinction risk from disease in theoretical metapopulations (i.e., collections of local populations connected via dispersal corridors) [14,21]. Restricting the movement of individual animals in order to reduce the spread of disease is tempting, but it could result in great ecological costs, such as disrupting migratory patterns and reducing gene flow between populations, as barriers that reduce disease spread have been shown to shape landscape genetics [24]. While increasing connectivity may facilitate efficient disease spread and disease-induced host population decline, reduced population connectivity may disrupt vital patch colonization dynamics and the maintenance of host genetic diversity [21,25]
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