Date of Award

January 2025

Document Type

Thesis

Degree Name

Master of Science (MS)

Department

Biology

First Advisor

Susan N. Ellis-Felege

Abstract

Wildlife diseases have become a critical factor in the management of animal populations across the globe. Such diseases can compromise individual health, reduce population sizes, and disrupt ecosystem biodiversity. As a result, there can be a loss in recreational opportunities which, in turn, can cause economic losses for communities relying on these populations. Effective wildlife disease management not only requires the ability to respond to outbreaks but also the capacity to predict how diseases interact with populations and ecosystems. Due to the complexity of disease dynamics, a multidisciplinary approach is essential for gaining a comprehensive understanding of these systems. In recent years, genetic epidemiology has emerged as a valuable tool for investigating and mitigating the effects of disease in wildlife. In North Dakota, where white-tailed deer (Odocoileus virginianus) and mule deer (O. hemionus) are at increasing risk of chronic wasting disease (CWD) and epizootic hemorrhagic disease (EHD), examination of genetic variation in genes influencing these diseases could inform management decisions. Thus, we created a study to evaluate the genetic variation in the prion protein gene (PRNP) and the toll-like receptor 3 gene (TLR3), which are associated with CWD and EHD, respectively. Our study resulted in the spatial assessment of variants in both genes across North Dakota.Samples from 1,018 deer were assessed (797 white-tailed and 221 mule deer) across North Dakota, and quality control filtering resulted in a final dataset of 749 individuals (702 white-tailed and 47 mule deer) for PRNP sequencing. The average read length for PRNP was 537 base pairs, covering nucleotide positions 214–750. Genetic variation in the PRNP gene revealed differences between species. Mule deer exhibited very low variability, with no polymorphism at codon 225 detected. In contrast, white-tailed deer showed greater genetic diversity, including 14 polymorphic sites across 13 haplotypes. Polymorphisms at codons 95, 96, 116, and 226 associated with slower disease progression were detected, but at lower relative frequencies compared to other white-tailed deer studies. However, these polymorphisms were present in 83% of hunting units across the state, with some regions showing elevated mutation frequencies. We conducted TLR3 sequencing on exon two, which spanned 444 base pairs. We sequenced 844 individuals (789 white-tailed and 55 mule deer). For the TLR3 gene, both species showed low variability across exon two. White-tailed deer displayed five polymorphic sites (four synonymous, one nonsynonymous at nucleotide position 39), while mule deer exhibited a single synonymous mutation. Polymorphisms at codons 59 and 116 previously associated with EHD susceptibility were not detected. The wild haplotype occurred in 90% of chromosomes, with only three other haplotypes exceeding a 2% frequency threshold. No novel mutations were observed. North Dakota deer exhibit limited genetic variation within both genes. The absence of TLR3 variation at codons 59 and 116 suggests deer populations across North Dakota remain susceptible to EHD outbreaks and other climactic, vector, or genetic factors influence the historic geographic distribution of previous outbreaks. Meanwhile, PRNP polymorphisms in white-tailed deer throughout the state could lead to accelerated CWD spread across North Dakota. Our findings reveal population health implications in white-tailed deer and mule deer and demonstrate how spatial genetic variation may contribute to CWD and EHD in North Dakota.

Download

Share

COinS