White-tailed deer (Odocoileus virginianus) are important game mammals and potential reservoirs of diseases of domestic livestock, so diseases of deer are of great concern to wildlife managers. In many situations, models can be useful for integrating existing data, understanding disease transmission patterns, and predicting effects on host populations. Individual-based modeling (IBM) has become more commonplace in ecology as a tool to link individual behavior to population dynamics and community interactions, especially for gauging the effects of management actions. Spatially explicit IBMs are especially useful when ecological processes, such as disease transmission, are affected by the spatial composition of the environment. I developed a spatially explicit IBM, DeerLandscapeDisease (DLD), to simulate direct and indirect disease transmission in white-tailed deer. Using data from GPS-collared deer in southern Illinois, I developed methods to identify habitats and times of high contact probability. I parameterized movement models, for use in DLD, using field data from GPS-collared deer in both southern and east-central Illinois. I then used DLD to simulate deer movements and epizootiology in two different landscapes: a predominantly agricultural landscape with fragmented forest patches in east-central Illinois and a landscape dominated by forest in southern Illinois. Behavioral and demographic parameters that could not be estimated from the field data were estimated using published literature of deer ecology. I assumed that bioavailability of infectious pathogens deposited in the environment decreased exponentially. Transmission probabilities were estimated by fitting to published trends in infection prevalence, assuming that infection probability during an encounter was equal for all age classes, so infection prevalence varied with sex- and age-specific behavior. DLD simulations of chronic wasting disease epizootiology demonstrated significant effects of landscape structure, social behavior, and mode of transmission on prevalence, emphasizing the importance of spatial, temporal and behavioral heterogeneity in disease modeling. These results demonstrate the utility of IBMs in incorporating spatio-temporal variables as well as animal behavior when predicting and modeling disease spread.

A difficulty in using diffusion models to predict large-scale animal population dispersal is that individuals move differently based on local information (as opposed to gradients) in differing habitat types. This can be accommodated by using ecological diffusion. However, real environments are often spatially complex, limiting application of a direct approach. Homogenization for partial differential equations has long been applied to Fickian diffusion (in which average individual movement is organized along gradients of habitat and population density). In this work, we derive a homogenization procedure for ecological diffusion, which allows us to determine the impact of small-scale (10-100 m) habitat variability on large-scale (10-100 km) movement, and apply it to models for chronic wasting disease (CWD) in mule deer. CWD is an infectious prion disease that affects members of the Cervidae family. It is a slow-developing, fatal disease, which is rare in the free-ranging deer population of Utah. We first present a simple spatial disease model to illustrate our homogenization procedure and the use of ecological diffusion as a way to connect animal movement with disease spread. Then we develop a more disease-specific sex-structured model for the spread of CWD, incorporating both horizontal and environmental transmission pathways. We apply our homogenization technique to greatly reduce the computational load for a simulation of disease spread from the La Sal Mountains to the Abajo Mountains of Southeast Utah. We use the averaged coefficients from the homogenized model to explore asymptotic invasion speed and critical population size for portions of our study area. Lastly, we describe the estimation of motilities for the disease-specific model from GPS location data, using a continuous-time correlated random walk model.

Wildlife diseases often occur under quantifiable and consistent patterns, which can be understood to statistically predict their occurrence and spread across landscapes. Chronic wasting disease (CWD) is a neurodegenerative disease in the deer family Cervidae caused by a prion, a pathogenic and misfolded variant of a naturally occurring protein. Managing and controlling CWD is imperative for conservation of ecologically and economically important cervid species, but unclear transmission mechanisms within landscapes complicate evidence-based management. Gaps of information in the landscape ecology for CWD are particularly pronounced for areas with recent disease emergence and spread, such as within the CWD cluster in the Mid-Atlantic United States. Thus, I identified current gaps in information and sought to fill neglected areas of research, specifically focusing on landscape determinants for CWD occurrence and spread in the state of Virginia. In chapter 2, I conducted a scoping study that collected and synthesized decades of CWD research and identified trends with respect to statistical and mathematical modeling methods used, connectivity within the CWD research community, and the geographic areas from which studies were performed. In chapter 3, I investigated landscape determinants for CWD in Virginia using remote sensing landscape data and an epidemiological dataset from Virginia Department of Wildlife Resources (DWR) using diverse algorithms and model evaluation techniques. Finally, in chapter 4, I modeled landscape connectivity between confirmed CWD cases to examine potential paths and barriers to CWD spread across landscapes. My results indicate that landscape ecology was rarely incorporated throughout CWD's 50+ year history. I provide evidence that remotely-sensed landscape conditions can be used to predict the likelihood of CWD occurrence and connectivity in Virginia landscapes, suggesting plausible CWD spread. I suggest areas of future work by explicitly identifying gaps in CWD research and diagnostic methods from which models are based, and encourage further consideration of host's ecology in modeling. By integrating remotely-sensed data into my modeling framework, the workflow should be easily adaptable to new study areas or other wildlife diseases. / Master of Science / Understanding why diseases occur in some locations and not others can be a critical challenge for disease ecologists. One disease that has received significant attention from the media and scientific community is chronic wasting disease (CWD), which is caused by a misfolded protein called a prion. Virginia Department of Wildlife Resources (DWR) has identified a stark increase in the number of CWD cases since first discovered in 2009, which threatens white-tailed deer populations and a 500 million dollar industry used for conservation of Virginia wildlife species. Previous research found that CWD does not occur randomly on the landscape, but otherwise little is known about the landscape ecology of CWD. To provide insight on Virginia's CWD outbreak, I assessed methods used to investigate other CWD outbreaks in both space and time. Also, I used landscape data collected from satellites and data from CWD cases in Virginia, and applied statistical tools to identify patterns in the landscape that were linked with CWD cases. My results suggest that landscapes were rarely examined to understand CWD, and instead, researchers focused on understanding how populations will respond to the disease. I also provide evidence that, at least in Virginia, researchers can use satellite information with disease data to predict CWD on the landscape and estimate its spread. This information can be used by wildlife managers to control the disease. For example, disease surveillance can be increased in areas where CWD has been predicted, or herd sizes can be reduced in areas likely to promote disease spread. This information could also be used to tailor wildlife health regulations aimed to minimize the risk of other deer populations acquiring the disease. Ultimately, the landscape plays an important role in CWD, but research on this topic is limited; therefore, additional research is needed to understand and eventually control this disease affecting ecologically and culturally important game species.

Chronic wasting disease (CWD) was detected in Saskatchewan wild deer populations in 2000 which prompted disease management actions consisting of population reduction. Little is known about population structure, health status, interactions or movement patterns of deer in Saskatchewan and these factors are important in designing a management program for CWD. As part of an ongoing study on deer movement patterns of wild deer in southern Saskatchewan, a survey was conducted to: 1) determine prevalence of CWD and selected infectious agents in mule deer (Odocoileus hemionus) and white-tailed deer (Odocoileus virginianus), and 2) identify infectious agents which could be used as a surrogate measure of the effectiveness of the adopted CWD management strategies. Tonsil biopsies, feces and blood were collected from 254 mule deer and 43 white-tailed deer during winters of 2006, 2007 and 2008. Immunohistochemical staining of tonsil biopsies for CWD revealed a prevalence of 2.4% (6/249) in mule deer and 0% (0/43) in white-tailed deer. Parasitological investigation of 253 fecal samples from mule deer identified eggs of nematodes in the superfamily Trichostrongyloidea (29.2%); and parasitic stages of the following genera: Nematodirus (7.1%), Skrjabinema (14.3%), Trichuris (0.8%), Moniezia (16.2%), Thysanosoma (12.2%), Orthostrongylus (35.2%), Eimeria (13.4%) and Giardia (0%, 0/137). A similar investigation of 42 white-tailed deer fecal samples identified parasitic stages of nematodes in the super family Trichostrongyloidea (4.8%) and in genera of Orthostrongylus (2.4%), Moniezia (2.4%) and Eimeria (2.4%). Dorsal-spined larvae were detected in 2.4% of the white-tailed deer fecal samples. In serum samples from 253 mule deer, antibodies (Ab) were detected against bovine herpesvirus1 (BoHV-1) (34.8%), parainfluenza-3 (PI-3) (56.5%), bovine virus diarrhoea virus (BVDV-1) (30.8%) and Neospora caninum (15.4%, 36/245). In serum samples from 40 white-tailed deer, Ab to BoHV-1(32.5%), PI-3 (35%), BVD-1 (12.5%) and Neospora caninum (20.5%, 8/39) was detected. Based on relative host specificity, moderate prevalence and horizontal routes of transmission, herpesvirus, parainfluenza 3, Eimeria and Skrjabinema were identified as infectious agents which could potentially be used to evaluate the effectiveness of disease management strategies, which may in turn predict the response of CWD to these same strategies. Using polymerase chain reaction (PCR) a herpesvirus was detected, in 42.1% (40/95) of retropharyngeal lymph nodes from hunter-submitted mule deer and white-tailed deer heads from Saskatchewan in 2007. DNA sequences of the partial DNA polymerase gene from this virus were 98 - 100% identical to mule deer lymphotropic herpesvirus (mule deer-LHV). A 3.6 kb contiguous sequence of mule deer-LHV genome was generated by genome walking (GenBank Accession number: HM014314). Use of a mule deer-LHV-specific PCR on buffy coat samples collected during winters of 2007 and 2008, detected mule deer-LHV in 42.1% (67/158) of mule deer and 33.3% (8/24) of white-tailed deer. Very little DNA sequence diversity in the partial sequences of glycoprotein B (gB) gene and the intergenic spacer regions between DPOL and gB gene of mule deer-LHV was observed among deer from different wildlife management zones. Mule deer-LHV is also a potential marker for evaluating the effectiveness of disease management activities because of its moderate prevalence, host specificity, ease of sample collection and the availability of a rapid and low-cost method for its detection. A variable region of the mule deer-LHV genome needs to be identified if this virus to be used as an inferential tool for studying host population structure.

Chronic wasting disease (CWD) was detected in Saskatchewan wild deer populations in 2000 which prompted disease management actions consisting of population reduction. Little is known about population structure, health status, interactions or movement patterns of deer in Saskatchewan and these factors are important in designing a management program for CWD. As part of an ongoing study on deer movement patterns of wild deer in southern Saskatchewan, a survey was conducted to: 1) determine prevalence of CWD and selected infectious agents in mule deer (Odocoileus hemionus) and white-tailed deer (Odocoileus virginianus), and 2) identify infectious agents which could be used as a surrogate measure of the effectiveness of the adopted CWD management strategies. Tonsil biopsies, feces and blood were collected from 254 mule deer and 43 white-tailed deer during winters of 2006, 2007 and 2008. Immunohistochemical staining of tonsil biopsies for CWD revealed a prevalence of 2.4% (6/249) in mule deer and 0% (0/43) in white-tailed deer. Parasitological investigation of 253 fecal samples from mule deer identified eggs of nematodes in the superfamily Trichostrongyloidea (29.2%); and parasitic stages of the following genera: Nematodirus (7.1%), Skrjabinema (14.3%), Trichuris (0.8%), Moniezia (16.2%), Thysanosoma (12.2%), Orthostrongylus (35.2%), Eimeria (13.4%) and Giardia (0%, 0/137). A similar investigation of 42 white-tailed deer fecal samples identified parasitic stages of nematodes in the super family Trichostrongyloidea (4.8%) and in genera of Orthostrongylus (2.4%), Moniezia (2.4%) and Eimeria (2.4%). Dorsal-spined larvae were detected in 2.4% of the white-tailed deer fecal samples. In serum samples from 253 mule deer, antibodies (Ab) were detected against bovine herpesvirus1 (BoHV-1) (34.8%), parainfluenza-3 (PI-3) (56.5%), bovine virus diarrhoea virus (BVDV-1) (30.8%) and Neospora caninum (15.4%, 36/245). In serum samples from 40 white-tailed deer, Ab to BoHV-1(32.5%), PI-3 (35%), BVD-1 (12.5%) and Neospora caninum (20.5%, 8/39) was detected. Based on relative host specificity, moderate prevalence and horizontal routes of transmission, herpesvirus, parainfluenza 3, Eimeria and Skrjabinema were identified as infectious agents which could potentially be used to evaluate the effectiveness of disease management strategies, which may in turn predict the response of CWD to these same strategies. Using polymerase chain reaction (PCR) a herpesvirus was detected, in 42.1% (40/95) of retropharyngeal lymph nodes from hunter-submitted mule deer and white-tailed deer heads from Saskatchewan in 2007. DNA sequences of the partial DNA polymerase gene from this virus were 98 - 100% identical to mule deer lymphotropic herpesvirus (mule deer-LHV). A 3.6 kb contiguous sequence of mule deer-LHV genome was generated by genome walking (GenBank Accession number: HM014314). Use of a mule deer-LHV-specific PCR on buffy coat samples collected during winters of 2007 and 2008, detected mule deer-LHV in 42.1% (67/158) of mule deer and 33.3% (8/24) of white-tailed deer. Very little DNA sequence diversity in the partial sequences of glycoprotein B (gB) gene and the intergenic spacer regions between DPOL and gB gene of mule deer-LHV was observed among deer from different wildlife management zones. Mule deer-LHV is also a potential marker for evaluating the effectiveness of disease management activities because of its moderate prevalence, host specificity, ease of sample collection and the availability of a rapid and low-cost method for its detection. A variable region of the mule deer-LHV genome needs to be identified if this virus to be used as an inferential tool for studying host population structure.

No description available.

No description available.

The study involved Indigenous communities of Saskatchewan and Alberta which are adversely impacted by industrial activities in their traditional territory. The overall goal of this study is: the assessment of social media in risk studies among Indigenous communities of western Canada. The methods used were: interviews, focus group discussion (FGD), and net-mapping. Results showed that the majority of youths communicated around risk using new social media (NSM) in event of risk outbreak, while Indigenous Elders, communicated face-to-face and via cell-phone. Results also showed that youths use Traditional Knowledge learnt from the Elders to understand Chronic wasting disease (CWD) risk, interpret, communicate and mobilize around mitigation. The study concluded that the use of NSM is becoming increasingly important for scoping information around wildlife decline and emergency in these Indigenous communities.

Chronic wasting disease (CWD) is a fatal pathogen affecting white-tailed and mule deer in east-central Alberta, and I addressed two current limitations of CWD management. First, to improve precision and accuracy of density estimates obtained from aerial surveys, I evaluated alternative survey designs and developed a model to correct for undetected deer due to low snow cover, small group sizes, and deer inactivity. Surveys stratified by resource selection functions showed the greatest improvement in precision compared to currently employed designs. Second, I addressed how density and landscape features affect contact rates among deer, a major component of CWD transmission. Contact rates increased as a saturating function of density, and were highest in regions where deer habitat was limited. My results will allow managers to better plan and evaluate management actions such as herd reductions, and underscore the need for developing spatially-explicit models to understand CWD spread in heterogeneous environments. / Ecology

This thesis utilizes input-output analysis to calculate the economic impacts from potential prion diseases outbreaks in Alberta and Canada. Both chronic wasting disease and bovine spongiform encephalopathy have the capacity to not only affect the farmed cervid and cattle industries, but to impact all industries with direct and indirect links to these sectors. Cervid sector shocks consistently yield small spillover effects on the economy in all models. In contrast, the cattle sector generates larger multiplier effects. A worst-case scenario that reduces cervid sector output to zero yields total economic losses of $11.5 million in Alberta, and $43.7 million in Canada. A reduction of cattle sector output to zero results in total economic losses of $6.4 billion in Alberta, and $34.9 billion in Canada. / Agricultural and Resource Economics