Stressors modulate host density
A key assumption of many infectious disease models is that contact rates between infected and uninfected individuals increase as population density increases (Anderson et al. 1986; McCallum et al.2001). Therefore, if stressors depress host population growth, via reduced fecundity, increased mortality, or emigration, pathogens will be less frequently transmitted, and prevalence is expected to decline. This reasoning justifies culling campaigns, where infection rates are reduced, or pathogens are extirpated by reducing host density below a critical transmission threshold (Lafferty & Holt 2003). For example, population control of badgers (Meles meles ) in the UK decreased bovine tuberculosis infection rates (Donnelly et al. 2007). However, culling campaigns have also backfired (Prentice et al.2019), like vampire bats (Desmodus rotundus ) and rabies virus. Rather than targeting naïve susceptible individuals, bat culling efforts reduced the number of recovered seroconverted individuals and surviving individuals spread rabies to new bat colonies (Streicker et al.2012). Such examples demonstrate that a simplistic approach (e.g., reducing population density) may not necessarily yield intended results if other dynamic properties of wild populations are not considered (e.g., susceptibility to infections and animal movements).
Alternatively, stressors may contribute to increased local host density without increasing fecundity. For instance, behavioral responses to stressors, such as changes in migration patterns (Satterfield et al. 2018; Sánchez et al. 2020), foraging behaviors (Epsteinet al. 2006), and aggregations in low-quality food-provisioned sites (intentional or unintentional) (Becker et al. 2015), have been associated with increased host density. Consequently, higher local density may intensify disease transmission via increased contact rates, as illustrated by theoretical models (Becker & Hall 2014).
Finally, stressors may affect the fitness of infected and uninfected hosts differently. It has been shown that infection increases sensitivity to other stressors, possibly because infected hosts are more energetically constrained (Marcogliese & Pietrock 2011). Such a combined effect of stress (i.e., climate change) and infection (i.e., chytrid fungus) may be responsible for the rapid global amphibian decline (Hof et al. 2011). Despite the many examples of the synergistic toll that stressors and pathogens have on host fitness, few efforts have tested whether such stressors have a differential impact on the fitness of infected compared to uninfected hosts (Marcogliese & Pietrock 2011; Beldomenico & Begon 2016).