Q2: Sensitivity of host fitness and infectivity responses
to stress
We contrasted the fitness and infectivity effects of stressors on
infected hosts. The full model, including stressor type, response trait,
and their interaction, was also the model with the lowest AICc score
(Table S3). In this model, the interaction arises not only due to the
differential sensitivity of fecundity and survivorship responses to
stressor type but also because the direction of infectivity responses
only aligned with fitness responses in the case of endogenous
environmental stressors (Table S4; Fig. 3). Perturbation of the
endogenous environment tended to have negative consequences for hosts,
both in terms of survival and pathogen intensity (Table S4; Fig. 3, all
infectivity vs. fitness contrasts p > 0.05; however,
survivorship vs. prevalence: p = 0.057). In contrast, the effects of
resource limitation differed significantly 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 S4; Fig. 3). Finally, the
effects of chemical pollution were more negative on survivorship than on
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 S4).
We obtained a similar pattern of interaction among stressors and fitness
and infectivity responses when the RVE was used to account for the
non-independence of sampling errors (Fig. S3). Despite these contrasting
effects of moderators, heterogeneity remained high (total
I2 = 91.33%), both between (I2 =
55.86%) and within (I2 = 35.47%) experiments.