Abstract

The establishment and spread of a disease within a metapopulation is influenced both by dynamics within each population and by the host and pathogen spatial processes through which they are connected. We develop a spatially explicit metapopulation model to investigate how the form of host and disease dispersal jointly influence the probability of disease establishment and invasion. We show that diseases are more likely to establish if both the host and the disease tend to disperse locally, since the former leads to the spatial aggregation of host populations in the environment while the latter facilitates the pathogen's exploitation of this spatial pattern. In contrast, local pathogen dispersal is likely to reduce the probability of subsequent disease spread because it increases the spatial segregation of infected and uninfected populations. The effects of local dispersal on disease dynamics are less pronounced when the pathogen spreads through the movement of infected hosts and more pronounced when pathogen dispersal is independent (for example through airborne viruses) though the details of host and pathogen biology can be important. These spatial effects tend to be more pronounced if the sites available for host occupation are themselves spatially aggregated.

Highlights

  • Many species are distributed across the landscape in metapopulations, ensembles of populations connected by dispersal which persist despite the limited lifespan of any of their constituents (Hanski and Gaggiotti, 2004; Clobert et al, 2004)

  • Since dispersal leads to both new patch colonisation and to disease spread in these studies, the overall effects on metapopulation persistence are complex and dependent on the detailed biology of the system

  • Structured metapopulations We ask how the initial spread of the disease is affected by metapopulation structure. To do this we explore the two limiting cases of (i) disease spread by the movement of infected hosts and (ii) disease spread by the dispersal of infectious propagules independent of host movement

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Summary

Introduction

Many species are distributed across the landscape in metapopulations, ensembles of populations connected by dispersal which persist despite the limited lifespan of any of their constituents (Hanski and Gaggiotti, 2004; Clobert et al, 2004). In a metapopulation, infected populations will tend to become clustered if the migration of infection between populations is spatially limited (Watts et al, 2005; Cross et al, 2005, 2007) This factor may slow or even prevent epidemics from occurring, suggesting that the range of dispersal may be at least as important as the rate of dispersal to pathogen dynamics in structured host populations (Keeling, 1999; Brown and Bolker, 2004; Watts et al, 2005).

Site dynamics
Site type transition rates
Population dynamics
Model and methods
The absence of disease
Disease establishment
No local spatial interactions
Disease establishment is easier in static than dynamic
Local disease migration reduces the rate of spread of the disease
Spatial structure may affect the equilibrium prevalence of the disease
Discussion
Full Text
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