Doctor of Philosophy (PhD)


Biological Sciences

Document Type



Crop pest management requires an understanding of the complex interactions among pest species that potentially damage crop yield and species that may be crucial for controlling pest species outbreaks. For example, predators, parasitoids, and pathogens are constantly interacting via their shared prey or hosts. Predators may prefer infected prey, which can be easier to catch; however, infected prey may be less nutritious or even lethal for predators. These interactions then dictate the short-term dynamics of host and pathogen as well as between prey and predator. "How these dynamics change as the species in the system change either empirically or theoretically?" is the underlying question in this dissertation.

I conducted a meta-analysis to determine the effects of virus- and fungus-infected prey on predators. Examining experiments with one predator/parasitoid and one pathogen, I quantified life-history responses of predators consuming infected prey across published studies. Predators and parasitoids responded separately to infected prey. True predators had no preference, while parasitoids preferred healthy prey. Both predators and parasitoids had reduced fitness when reared in infected hosts. For example, if the host died from infection before the parasitoid completed development, the parasitoid also died. Predators also had a reduction in fitness when consuming infected prey (i.e., shorter lifespans, fewer offspring produced). I then used lab and field studies to expand on these results.

In the lab, I reared a common agricultural predator, the spined-soldier bug (Podisus maculiventris) on a diet of either healthy or infected prey, which responded similarly to those in my meta-analysis. They suffered increased developmental time and decreased longevity. I also found that predators exhibited preference for infected prey while the prey were alive. When prey were frozen, the predators exhibited no preference for healthy or infected prey. This indicates that prey are likely easier to consume when they are infected. Field studies investigated how predators change disease transmission in their prey. I found that predators increased transmission by decreasing the prey's heterogeneity in susceptibility to the disease. That is, the spread between the least susceptible and the most susceptible host decreased, which increase overall disease transmission. This research extended the results of the meta-analysis from the individual effects to population dynamics.

Finally, I created two mathematical models to show how predators and pathogens interact across multiple generations as compared to the single generation in the field. These models compare and contrast the differences between predator response to prey and the effects the predator response has on disease dynamics. Predators that show a Holling type I response can lead to stable states, while predators exhibiting a type III response lead to cycles exemplified by boom and bust dynamics. Through a meta-analysis, field and lab studies, and a mathematical model, I explored the interactions between predators and pathogens when they attack the same prey or host species. By combining a variety of quantitative techniques to investigate a single question, my work adds important insight into how ecological interactions can help improve agricultural practices.



Committee Chair

Elderd, Bret