Q2: Sensitivity of host fitness and infectivity responses
to stress
We contrasted fitness and infectivity effects of stressors on infected
hosts. The full model, including stressor type, response trait, and
their interaction, had the lowest AICc score (Table S4). In this model,
the interaction arose not only due to differential sensitivity of
fecundity and survivorship responses to stressor type but also because
the direction of infectivity responses only aligned with fitness
responses for endogenous environmental stressors (Table S5; Fig. 3).
Effects of resource limitation differed between response variables
(fecundity vs. intensity: p < 0.001; fecundity vs. prevalence:
p = 0.006; survivorship vs. infection intensity: p = 0.010; and
survivorship vs. prevalence: p > 0.05). When resources were
limited, not only was host fecundity reduced (as noted in Q1), but
infection intensity was also reduced (Table S5; Fig. 3). In contrast,
chemical pollution impacted survivorship more than either proxy of
infectivity (survivorship vs. infection intensity: p = 0.024,
survivorship vs. prevalence: p = 0.018). We found that pollution
decreased both host survival and pathogen prevalence (Table S5).
Finally, perturbation of the endogenous environment tended to decrease
host survival and increase pathogen intensity, both of which had
negative consequences for host fitness and health (Table S5; Fig. 3, all
infectivity vs. fitness contrasts p > 0.05; however,
survivorship vs. prevalence: p = 0.057).
We obtained a similar pattern of interaction among stressors and fitness
and infectivity responses when the RVE was used to account for
non-independence of sampling errors (Fig. S6). Despite these contrasting
effects of moderators, heterogeneity remained high (total
I2 = 90.26%), both between (I2 =
64.11%) and within (I2 = 25.15%) experiments.
Effects of stressors on host fitness and infectivity traits also
depended on environment and mode of pathogen transmission. While the
negative effect of resource limitation on host fecundity was consistent
in both environments, resource limitation only lowered pathogen
intensity for aquatic hosts (Table S6; Fig. S7). Similarly, chemical
pollution reduced pathogen prevalence, and endogenous environmental
stressors reduced host survivorship and increased infection intensity in
aquatic but not terrestrial hosts (Table S6; Fig. S7). For host-pathogen
systems with indirect transmission modes, resource limitation decreased
host fecundity and pathogen intensity, and chemical pollution reduced
host survival and pathogen prevalence (Table S7; Fig. S8). While effects
of endogenous environmental stressors were generally consistent between
transmission modes, mortality was more pronounced in hosts exposed to
pathogens with direct transmission (Table S7; Fig. S8). Although our
results show potential distinctions and similarities between
environments and transmission modes, we note that most effects were from
aquatic (495 of 686) and indirect transmission (509 of 686) systems,
possibly biasing our findings towards these systems.