Abstract

In animal populations, males are commonly more susceptible to disease-induced mortality than females. However, three competing mechanisms can cause this sex bias: weak males may simultaneously be more prone to exposure to infection and mortality; being ‘male’ may be an imperfect proxy for the underlying driver of disease-induced mortality; or males may experience increased severity of disease-induced effects compared with females. Here, we infer the drivers of sex-specific epidemiology by decomposing fixed mortality rates into mortality trajectories and comparing their parameters. We applied Bayesian survival trajectory analysis to a 22-year longitudinal study of a population of badgers (Meles meles) naturally infected with bovine tuberculosis (bTB). At the point of infection, infected male and female badgers had equal mortality risk, refuting the hypothesis that acquisition of infection occurs in males with coincidentally high mortality. Males and females exhibited similar levels of heterogeneity in mortality risk, refuting the hypothesis that maleness is only a proxy for disease susceptibility. Instead, sex differences were caused by a more rapid increase in male mortality rates following infection. Males are indeed more susceptible to bTB, probably due to immunological differences between the sexes. We recommend this mortality trajectory approach for the study of infection in animal populations.

Highlights

  • There is increasing epidemiological evidence of sex-related differences in host– pathogen interactions in animal populations

  • Sex differences in epidemiological traits have been observed in bovine tuberculosis (bTB)-infected badgers, with males suffering increased mortality during early disease stages and faster progression into advanced diseased states [14], where they experience double the rate of disease-induced mortality when compared with females [14,15]

  • While increased mortality due to bTB infection is already known to occur in male badgers [14,15], we have located where in the infection process these sex-related differences arise, and can begin to infer the mechanisms that might generate this variation

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Summary

Introduction

There is increasing epidemiological evidence of sex-related differences in host– pathogen interactions in animal populations. Sex differences in epidemiological traits have been observed in bTB-infected badgers, with males suffering increased mortality during early disease stages and faster progression into advanced diseased states [14], where they experience double the rate of disease-induced mortality when compared with females [14,15].

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