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 limitation or environmental stress gradients. Our results carry implications for conservation and disease emergence and reveal areas for future work.

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 systematic 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 893 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 limitation or environmental stress gradients. Our results carry implications for conservation and disease emergence and reveal areas for future work.

Agrochemical use is predicted to increase 2-5 fold by 2050 to meet food demand. Evidence suggests that agrochemical pollution could increase snails that transmit the disease schistosomiasis to 250 million people, but most agrochemicals remain unexamined. Here we quantify the relative effects of fertilizer, six insecticides, and six herbicides on snail genera responsible for 90% of global schistosomiasis cases. We identified fertilizers and 4 of 6 insecticides as high risk for increasing snail biomass by increasing snail habitat (aquatic vegetation) or food (periphyton) and reducing snail predators, respectively. Herbicides generally had negative effects on snails by reducing habitat, with two herbicides increasing snails in the absence of aquatic vegetation. Parasite production, which reflects human infection risk, scaled positively to snail biomass. Our findings suggest that fertilizers and insecticides present higher chances of increasing human schistosomiasis than herbicides, and revealed several low risk agrochemicals might help increase crop production without increasing schistosomiasis.

Conventional wisdom suggests any effort to control pests and parasites is better than none. However, growing evidence demonstrates weak or moderate effort can backfire, fail, and potentially worsen outcomes versus doing nothing. A central challenge is anticipating these potential failures before inducing environmental damage. We built a resource-explicit individual-based model of human schistosome and snail host transmission to evaluate biocontrol effort by simulating 22 predator stocking densities of native prawns. We test two host mortality scenarios and show intense biocontrol effort can succeed. However, weak to moderate effort can backfire by allowing large, prolific hosts to escape predation and drive overcompensation due to three interacting ecological mechanisms—resource competition among hosts, resource-dependent infectiousness, and predator gape limits. Ultimately, integrating physiology, ecology, and epidemiology can identify the risks of weak or moderate control effort when evaluating potential ‘do or do not’ control designs for future management of wildlife pests and diseases.