Parasite prevalence is determined by infection state- and risk-dependent dispersal of the host.

The spread of parasites and the emergence of disease are currently threatening global biodiversity and human welfare. To address this threat, we need to better understand those factors that determine parasite persistence and prevalence. It is known that dispersal is central to the spatial dynamics of host-parasite systems. Yet past studies have typically assumed that dispersal is a species-level constant, despite a growing body of empirical evidence that dispersal varies with ecological context, including the risk of infection and aspects of host state such as infection status (parasite-dependent dispersal; PDD). Here, we develop a metapopulation model to understand how different forms of PDD shape the prevalence of a directly transmitted parasite. We show that increasing host dispersal rate can increase, decrease or cause a non-monotonic change in regional parasite prevalence, depending on the type of PDD and characteristics of the host-parasite system (transmission rate, virulence, and dispersal mortality). This result contrasts with previous studies with parasite-independent dispersal which concluded that prevalence increases with host dispersal rate. We argue that accounting for host dispersal responses to parasites is necessary for a complete understanding of host-parasite dynamics and for predicting how parasite prevalence will respond to changes such as human alteration of landscape connectivity. This article is part of the theme issue 'Diversity-dependence of dispersal: interspecific interactions determine spatial dynamics'.

Impact of State-Dependent Dispersal on Disease Prevalence.

Based on a susceptible-infected-susceptible patch model, we study the influence of dispersal on the disease prevalence of an individual patch and all patches at the endemic equilibrium. Specifically, we estimate the disease prevalence of each patch and obtain a weak order-preserving result that correlated the patch reproduction number with the patch disease prevalence. Then we assume that dispersal rates of the susceptible and infected populations are proportional and derive the overall disease prevalence, or equivalently, the total infection size at no dispersal or infinite dispersal as well as the right derivative of the total infection size at no dispersal. Furthermore, for the two-patch submodel, two complete classifications of the model parameter space are given: one addressing when dispersal leads to higher or lower overall disease prevalence than no dispersal, and the other concerning how the overall disease prevalence varies with dispersal rate. Numerical simulations are performed to further investigate the effect of movement on disease prevalence.

Parasite infection drives the evolution of state-dependent dispersal of the host.

Dispersal plays a fundamental role in shaping the ecological processes such as host-parasite interactions, and the understanding of host dispersal tendency leads to that of parasites. Here, we present the result of our study on how the evolutionarily stable dispersal of a host would depend on parasite infection, considering kin competition among neighbours. We show that the evolving dispersal rate might be higher for susceptible than for infected individuals (S-biased dispersal) or vice versa (I-biased dispersal). S-biased dispersal is favoured by strong virulence affecting competitive ability, by high rate of parasite release during dispersal, and by low virulence for infected emigrants (i.e. low virulence affecting dispersal ability), whereas I-biased dispersal is favoured in the opposite situation. We also discuss population structure or between-deme genetic differentiation of the host measured with Wright's FST. In I-biased dispersal, between-deme genetic differentiation decreases with the infection rate, while in S-biased dispersal, genetic differentiation increases with infection rate.