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.