Predators and pathogens exert strong forces on the population dynamics of prey. Interactions between predators and pathogens are common in agricultural and natural communities. Predators may remove pathogens from the environment by acting as incompetent hosts or may mechanically spread virus to novel hosts. Additionally, predators may be negatively impacted by pathogen-infected prey. To test interactions between predators and pathogens when attacking a shared host, we used a crop pest caterpillar Pseudoplusia includens, a generalist predator Podisus maculiventris, and a generalist pathogen Anticarsia gemmatalis multicapsid nuclear polyhedravirus (AcMNPV). We tested three hypotheses, 1) predators have reduced fitness parameters when consuming infected prey, 2) predators prefer healthy prey, and 3) predators negatively influence disease transmission in their prey. For fitness parameters, we reared predators on healthy or infected prey and measured the number of eggs produced by females, the lifespan from adulthood to death, and the developmental time from hatch to adult. We tested preference by offering predators infected alongside healthy caterpillars in petri dishes. Finally, to test disease transmission, we used soybean plants in the field and applied virus (one of three viral densities) and predator treatments (predator, non-consumptive predator, and no predator).
Results/Conclusions
We found that P. maculiventris exhibited preference for live infected P. includens (P = 0.037), but did not have preference when prey were already dead (P = 0.35). Predators were negatively influenced when consuming infected prey compared to healthy prey. Predators took 30.7 days to develop on infected prey and 24.1 days to develop on healthy prey (P < 0.001). Predators reared on healthy prey lived for 56.1 days compared to 38.2 days on infected prey (P = 0.042). There was no significant difference in the number of eggs laid between the two treatments (P = 0.10). We tested several models for the effects of predation on disease transmission. The best model separated predators and the combined no predator and non-consumptive predator treatments (AICwt = 0.26). Predators increased virus transmission at high virus densities. In all models, predator treatments had higher virus transmission at high virus densities than no predator treatments. These models suggest that predators may decrease heterogeneity of viral transmission rates in their prey. Our results suggest that predators are negatively influenced by consuming infected prey but increase virus transmission. This work highlights the importance of indirect effects of predators on pathogens and vice-versa.