Abstract

Wildlife hosts are important reservoirs of a wide range of human and livestock infections worldwide, and in some instances, wildlife populations are threatened by disease. Yet wildlife diseases are difficult to monitor, and we often lack an understanding of basic epidemiological parameters that might inform disease management and the design of targeted interventions. The impacts of disease on host survival are generally associated with age, yet traditional epidemiological models tend to use simplistic categories of host age. Mortality trajectory analysis provides the opportunity to understand age-specific impacts of disease and uncover epidemiological patterns across complete life histories. Here, we use Bayesian survival trajectory analysis (BaSTA) software to analyse capture-mark-recapture data from a population of wild badgers Meles meles naturally infected with Mycobacterium bovis, the causative agent of tuberculosis in badgers and cattle. We reveal non-constant mortality trajectories, and show that infection exaggerates an age-dependent increase in late-life mortality. This study provides evidence for actuarial senescence in badgers, a species previously believed to display constant mortality throughout life. Our case study demonstrates the application of mortality trajectory analysis in wildlife disease research, but also highlights important limitations. We recommend BaSTA for mortality trajectory analysis in epidemiological research, but also suggest combining approaches that can include diagnostic uncertainty and the movement of hosts between disease states as they age. We recommend future combinations of multi-state and multi-event modelling frameworks for complex systems incorporating age-varying disease states.

Highlights

  • We reveal important limitations of standard mortality trajectory analysis for epidemiological research, including age-dependent predictors and diagnostic uncertainty

  • The Siler model is the sum of three different mortality models: the first describing a decrease in mortality over the initial phase of life, with ea0 being the initial level and a1 modelling the rate of decrease

  • Deviance information criterion (DIC) values are given for each model, as well as corresponding differences (∆deviance information (DIC)) with respect to the “best” model

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Summary

Introduction

Investigating the epidemiology of any disease in wild populations is challenging because of the practical difficulties in monitoring both infections and their wild hosts [1], yet wild animals are important contributors to many emergent and widespread infections of humans and livestock worldwide [2].any improvements in our understanding of wildlife disease epidemiology can be beneficial to human health, animal welfare and productivity, as well as to biodiversity conservation [1,3].Disease-related mortality is a critical parameter in any epidemiological model [4] and methods for its estimation, developed for the study of human populations, are commonly used in studies of Diversity 2019, 11, 182; doi:10.3390/d11100182 www.mdpi.com/journal/diversityDiversity 2019, 11, 182 wildlife [5]. Investigating the epidemiology of any disease in wild populations is challenging because of the practical difficulties in monitoring both infections and their wild hosts [1], yet wild animals are important contributors to many emergent and widespread infections of humans and livestock worldwide [2]. Disease-related mortality is a critical parameter in any epidemiological model [4] and methods for its estimation, developed for the study of human populations, are commonly used in studies of Diversity 2019, 11, 182; doi:10.3390/d11100182 www.mdpi.com/journal/diversity. Disease-induced mortality is commonly modelled as a simple increase in otherwise fixed mortality rates at particular life stages [10,11] but the reality can be much more complex. Mortality trajectories reveal patterns in age-specific mortality that are often missed when using fixed rates in discrete age classes, yet the inclusion of these trajectories in epidemiological models is rare. We show that the inclusion of disease status, alongside full mortality trajectory analysis, can reveal disease-induced changes in the shape of lifetime schedules of mortality

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