Host-pathogen interactions under pressure: A review and meta-analysis of stress-mediated effects on disease dynamics

Human activities have increased the intensity and frequency of natural stressors and created novel stressors, altering host-pathogen interactions and changing the risk of emerging infectious diseases. Despite the ubiquity of such anthropogenic impacts, predicting the directionality of outcomes has proven challenging. Here, we conduct a review and meta-analysis to determine the primary mechanisms through which stressors affect host-pathogen interactions and to evaluate the impacts stress has on host fitness (survival and fecundity) and pathogen infectivity (prevalence and intensity). We assessed 891 effect sizes from 71 host species (representing seven taxonomic groups) and 78 parasite taxa from 98 studies. We found that infected and uninfected hosts had similar sensitivity to stressors and that responses varied according to stressor type. Specifically, limited resources compromised host fecundity and decreased pathogen intensity, while abiotic environmental stressors (e.g., temperature and salinity) decreased host survivorship and increased pathogen intensity, and pollution increased mortality but decreased pathogen prevalence. We then used our meta-analysis results to develop susceptible-infected theoretical models to illustrate scenarios where infection rates are expected to increase or decrease in response to resource limitations or environmental stress gradients. Our results carry implications for conservation and disease emergence and reveal areas for future work. Disruptions in host-pathogen interactions can negatively impact human and animal health, biodiversity conservation and ecosystem structure and function. We synthesized the current understanding of how human-induced stressors affect host-pathogen interactions by altering (1) host density, (2) host defences and (3) pathogen infectivity. We then conducted a meta-analysis of studies where impacts of host fitness (survival and fecundity) and pathogen prevalence and intensity were evaluated under control and stressful conditions (low resources, adverse environmental conditions and pollution). Responses varied according to stressor type: limited resources compromised host fecundity and decreased pathogen intensity, while environmental stressors (e.g., temperature) decreased host survivorship and increased pathogen intensity, and pollution increased mortality but decreased pathogen prevalence. To reveal scenarios where infection rates would increase or decrease in response to the simultaneous trait changes occurring over resource and environmental stress gradients, we incorporated our findings into two theoretical susceptible-infected models.image