Disease invasion in Yellowstone: Exploring the effects of wolf social organization and trophic interactions
Open Access
- Author:
- Brandell, Ellen
- Graduate Program:
- Ecology
- Degree:
- Doctor of Philosophy
- Document Type:
- Dissertation
- Date of Defense:
- November 30, 2020
- Committee Members:
- P Hudson, Dissertation Advisor/Co-Advisor
W. David Walter, Committee Chair/Co-Chair
Nita Bharti, Committee Member
David Peter Hughes, Committee Member
W. David Walter, Outside Member
Jason Philip Kaye, Program Head/Chair - Keywords:
- infectious disease
wolf
Canis lupus
Yellowstone
ecology
social groups
transmission
predator-prey
serology
Sarcoptic mange - Abstract:
- There is a tension between pathogen persistence and the potential for transmission among social, group-living hosts. Social species have high rates of contact within groups and lower contact rates among members of different groups; this poses a challenge for pathogen transmission such that a pathogen must survive within a group until an inter-group interaction occurs. In this dissertation, I explored the spatial and metapopulation dynamics of groups infected with pathogens spanning biological scales: within-groups, groups comprising a population, and across populations. Additionally, I examined the tritrophic interactions of predators, prey, and pathogens. The gray wolf (Canis lupus) and elk (Cervus canadensis) populations residing in Yellowstone National Park were the genesis of this research, yet I expanded beyond Yellowstone in order to comprehensively address the dissertation objectives. In particular, I focused on the invasion of canine distemper and the consequences of distemper outbreaks on host populations. The dynamics and consequences of pathogen infections in social groups are not fully understood. I first developed mathematical models that elucidate infection host demographics and infection dynamics at three nested scales: within groups, among groups, and all groups comprising a population (Chapter 2). Incorporating pathogens into the models reduced the size of the host population by reducing the number of social groups; average group size responded in more subtle ways (e.g., group size can increase when a reduction in the number of groups leads to decreases in rates of intraspecific aggression). I then assessed how viral epidemics influence the space use and spatial connectivity of territorial, social carnivores by comparing and contrasting Serengeti lions with Yellowstone wolves (Chapter 3). Generalized additive models identified significant predictors of group territory size and overlap and helped elucidate that lions constrict their territory size and reduce overlap with neighboring prides, following canine distemper epidemics. Together, these two chapters emphasize how social organization influences pathogen transmission, as well as how pathogen infection influences spatial organization. In Chapter 4, I broadened the scope of my work from Yellowstone National Park to the North American continent and identified the drivers and patterns of pathogen exposure in wolves. Even as one of the most widely distributed carnivores, little is known about the distribution of pathogens infecting wolves, pathogen prevalence, or temporal and spatial dynamics. I compiled a serological database of 17 wolf populations, and wolf samples were screened for six common pathogens: canine adenovirus, canine parvovirus, canine distemper virus, canine herpesvirus, Neospora caninum, and Toxoplasma gondii. Using these data, I tested the hypothesis that there is a latitudinal gradient of pathogen exposure in North American wolves. I constructed and analyzed generalized linear mixed models and found that latitude was only a strong predictor of N. caninum exposure, and instead, probability of exposure varied predictably by region: Great Lakes populations had a higher risk of parasite infection, whereas Rocky Mountain populations had a higher risk of viral infection. Wolf age, wolf density, and human density were positive predictors of infection, the latter suggesting that synanthropic species or dogs may host pathogens affecting wildlife. This project demonstrates that individual host characteristics as well as inherent features of ecosystems determine pathogen infection risk. While Chapters 2-4 focused mainly on wolf hosts and the pathogens infecting wolves, Chapter 5 has a multi-species trophic approach where I assessed how predators may control a newly introduced pathogen in a prey population. Here I constructed a tritrophic model: predator-host-chronic wasting disease. The predator-prey systems modeled include cougar-deer and wolf-elk, mimicking predation dynamics in the Yellowstone Ecosystem. Importantly, I found that predators were able to reduce chronic wasting disease (CWD) outbreak size appreciably, and in certain plausible circumstances, extirpate CWD. The ability of predators to remove infected adult prey was crucial in reducing CWD infections because adults are responsible for the vast majority of new CWD transmission events. My results highlight the need for integrating ecology into predator management. This dissertation advances our understanding of the relationship between social living and infectious disease transmission and subsequent consequences. These results and implications are both system-specific and applicable to many species and social organizations. Additionally, I concluded by identifying future areas of disease ecology research that would help untangle the complexities of social living, infectious disease transmission, biological scale, and trophic relationships.