Model predictions
Using our dynamical models (Box 1 and Box 2), we evaluated whether the
patterns of trait sensitivity to stressors we documented in the
meta-analysis reduce or increase infection prevalence across stress
gradients and how stressors ultimately impact host population densities.
The SI-Resource model predicts that a decrease in resource productivity
decreases infection prevalence (Fig. 5A), in part because host densities
also decrease with limited resources (Fig. 5C). Once a pathogen
establishes in a population, there is stabilizing feedback, where
pathogens suppress host density, increasing resources, and further
increasing transmission (Fig. S11). Therefore, in all scenarios of
sensitivity of pathogen transmissibility to resources (smaller values of
the half-saturation transmission constant (ht) increase
sensitivity of transmission rate (β) to resources), the model reaches
the same prevalence equilibrium. However, although population density
also stabilizes, impacts on host density are different for each
scenario: populations more sensitive to resources available will reach
smaller population sizes compared to less sensitive populations (Fig.
5C)
The SI-Environmental stress gradient models revealed that population
density decreases regardless of effects of stress on hosts
susceptibility due to increased mortality. But it exponentially
decreases host populations when transmission rate is sensitive to the
environmental factor (Fig. 5B and D). Specifically, when stress
increases host susceptibility (i.e., greater values of
βE), infection prevalence will increase rapidly (Fig.
5B) but at the cost of increasing host mortality (Fig. 5D). Therefore,
infection prevalence will have a maximum at intermediate stress level
but will drop as population densities are too low to sustain
transmission. In contrast, as transmission is more negatively affected
by stressors (i.e., pathogens are negatively affected by stressors),
infection prevalence will quickly reach zero with increasing
environmental stress (Fig. 5B). But as stress increases and persists,
populations will decline after pathogen extirpation (Fig. 5D).
Importantly, our models suggest that high pathogen prevalence and/or
stressors can result in host population extinction.
Our models illustrate that consequences of stress gradients on disease
can depend on the sensitivity that host traits, such as births and
deaths, and shared host-pathogen traits, such as transmission (i.e., β)
have to stressors. Interestingly, and consistent with Lafferty & Holt
(2003) simulations, our models showed that increased environmental
stress generally decreased disease, mainly driven by host density
reductions. Although stress can make hosts more likely to become
infected at the individual level, at the population level, negative
impacts on host survival and reproduction may be driving pathogen and
host local extinctions (Lafferty & Holt 2003).