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In this paper, we aim to understand how both parasite transmission and infection tolerance can influence the host's migratory behaviour.

We constructed a model that incorporates two host strategies (migration and tolerance) to understand whether allowing for tolerance affects the proportion of the population that migrates at equilibrium in response to infection.

We show that the benefits of tolerance can either decrease or increase the host's migration. Also, if the benefit of migration is great, then individuals are more likely to migrate regardless of the presence of tolerance. Finally, we find that the transmission rate of parasite infection can either decrease or increase the tolerant host's migration, depending on the cost of migration.

These findings highlight that adopting two defence strategies is not always beneficial to the hosts. Instead, a single strategy is often better, depending on the costs and benefits of the strategies and infection pressures. Our work further suggests that multiple host‐defence strategies as a potential explanation for the evolution of migration to minimize the parasite infection. Moreover, migration can also affect the ecological and evolutionary dynamics of parasite–host interactions.

Here, we focus on two infection‐related mechanisms that can favour migration: moving to escape versus recover from infection. By directly comparing the evolution of migration in response to each mechanism, we can evaluate the likely importance of changing abiotic conditions (linked to migratory recovery) with changing social conditions (linked to migratory escape) in terms of infection‐driven migration.

We built a mathematical model and analysed it using numerically simulated adaptive dynamics to determine when migration should evolve for each migratory recovery and social migratory escape.

We found that a higher fraction of the population migrated under migratory recovery than under social migratory escape. We also found that two distinct migratory strategies (e.g. some individuals always migrate and others only occasionally migrate) sometimes coexisted within populations with social migratory escape, but never with migratory recovery.

Our results suggest that migratory recovery is more likely to promote the evolution of migratory behaviour, rather than escape from infected conspecifics (social migratory escape).

Here, we aim to understand when parasites favour the evolution of migration.

We develop a general model which enables us to explore a broad range of biological conditions and to capture population and infection dynamics over both ecological and evolutionary time‐scales.

We show that when migration evolves depends on whether the costs of migration and infection are paid in reduced fecundity or survival. Also important are the parasite transmission mode and spatiotemporal dynamics of infection and recovery (if it occurs). Finally, we find that partial migration (where only a fraction of the population migrates) can evolve but only when parasite transmission is density‐dependent.

Our results highlight the critical, if overlooked, role of parasites in shaping long‐distance movement patterns, and suggest that infection should be considered alongside more traditional drivers of migration in both empirical and theoretical studies.

We simulated individual movement trajectories for wildlife populations using a home range‐like movement model, creating full location datasets and corresponding ‘complete’ networks. To mimic telemetry data, we created ‘sample’ networks by subsampling the population (10%–100% of individuals) with a range of sampling intervals (every minute to every 3 days). We varied the definition of contact for sample networks, using either spatiotemporal or spatial overlap, and varied the spatial configuration of populations (random, lattice or clustered). To compare complete and sample networks, we calculated seven network metrics important for disease transmission and assessed mean ranked correlation coefficients and percent error between complete and sample network metrics.

Telemetry sampling severely reduced our ability to calculate global node‐level network metrics, but had less impact on local and network‐level metrics. Even so, in populations with infrequent associations, high intensity telemetry sampling may still be necessary. Defining contact in terms of spatial overlap generally resulted in overly connected networks, but in some instances, could compensate for otherwise coarse telemetry data.

By synthesizing movement and disease ecology with computational approaches, we characterized trade‐offs important for using wildlife telemetry data beyond ecological studies of individual movement, and found that careful use of telemetry data has the potential to inform network models. Thus, with informed application of telemetry data, we can make significant advances in leveraging its use for a better understanding and management of wildlife infectious disease.

Feline immunodeficiency virus (FIV) is a lentivirus affecting domestic and wild cat species, forming species‐specific viral–host associations. FIV infection is common in populations of puma (Puma concolor), yet uncertainty remains over transmission parameters and the significance of FIV infection for puma mortality. In this study, the age‐specific FOI of FIV in pumas was estimated from prevalence data, and the evidence for disease‐associated mortality was assessed.

We fitted candidate models to FIV prevalence data and adopted a maximum likelihood method to estimate parameter values in each model. The models with the best fit were determined to infer the most likely FOI curves. We applied this strategy for female and male pumas from California, Colorado, and Florida.

When splitting the data by sex and area, our FOI modeling revealed no evidence of disease‐associated mortality in any population. Both sex and location were found to influence the FOI, which was generally higher for male pumas than for females. For female pumas at all sites, and male pumas from California and Colorado, the FOI did not vary with puma age, implying FIV transmission can happen throughout life; this result supports the idea that transmission can occur from mothers to cubs and also throughout adult life. For Florida males, the FOI was a decreasing function of puma age, indicating an increased risk of infection in the early years, and a decreased risk at older ages.

This research provides critical insight into pathogen transmission and impact in a secretive and solitary carnivore. Our findings shed light on the debate on whether FIV causes mortality in wild felids like puma, and our approach may be adopted for other diseases and species. The methodology we present can be used for identifying likely transmission routes of a pathogen and also estimating any disease‐associated mortality, both of which can be difficult to establish for wildlife diseases in particular.