Modeling chronic wasting disease prevalence through time to investigate mechanisms of spread in deer and elk in Wyoming Active
Diseases are challenging to manage in wild ungulate populations, particularly when there are many ways the disease can spread. Wildlife management agencies often need to take action to control disease spread, but it is unclear which actions are most effective in constraining disease because the importance of different spread mechanisms is not fully understood. This project will aid state wildlife management agencies by modeling which disease transmission mechanisms most influence changes in prevalence and geographic spread of chronic wasting disease (CWD) in deer and elk. The results simulate the potential effectiveness of different management alternatives at reducing CWD spread and can contribute to the development of management strategies that constrain the disease.
Background
Chronic wasting disease, (CWD; Williams and Young, 1980, 1982, 1992; Baeten and others, 2007) a neurological illness caused by misshapen proteins in the central nervous system (prions), has gained international attention due to its potential for dramatic population-level impacts and our inability to eradicate CWD once it is established. CWD is always fatal and has been linked to substantial population declines at high prevalence in white-tailed deer, mule deer, and likely elk (Monello and others, 2014; Edmunds and others, 2016; DeVivo and others, 2017). Despite over 20 years of intensive research, no effective management prescriptions have been discovered that can control the spread or effectively lower prevalence once CWD is established. In that time, the known affected area increased dramatically both nationally (30 states in the United States) and internationally (three Canadian provinces, and three countries in Europe [Norway, Sweden, and Finland]) in free-ranging cervids, with newly affected areas discovered annually.
Although preventing spread of CWD is a national management priority (America’s Conservation Enhancement Act; S.3051; Public Law 116–188; Oct. 30, 2020), there is limited understanding of the transmission mechanisms and which mechanisms impact disease spread and containment options the most. As no disease has ever been effectively managed without fully understanding transmission, this project aims to provide clarity on the relevance and influence of different spread mechanisms. Results will provide a scientific basis for refining future data collection, testing potential management strategies, and assessing the effects of climate change on disease spread.
Study Design and Methods
To model and investigate the importance of different spread mechanisms on CWD prevalence, we are undertaking a case study. We are using hunter-killed CWD surveillance data (1997-2022) from two selected Wyoming deer Herd Units (Wyoming Game and Fish Department) where CWD has increased in prevalence through time. We developed simulation-based disease spread models (spatially explicit individual-based model; HexSim; Schumaker and Brookes 2018) to investigate the relative influence of animal-animal, and environmental prion-animal spread mechanisms. We simulated past disease spread patterns and are comparing results from different scenarios of spread pathways to better understand the potential role of environmental prions in affecting disease spread.
Future phases of work will assess the contributions of direct (animal-to-animal) and indirect (animal-to-environment-to-animal) transmission, investigate the role of density- versus frequency-dependent transmission and vertical versus horizontal transmission through time, and through climate change. Future modeling scenarios will incorporate additional aspects of animal movement (for example, anthropogenic barriers and attractants such as feed grounds), landscape features (for example, riparian areas, migration corridors, winter grounds), habitat suitability, and predator and scavenger activity, as well as several ongoing and planned management actions.
Project Outcomes
Our project aims to develop an extensible model that can be used to simulate the outcomes of alternative approaches to managing CWD in mule deer and their impacts on prion loads in the environments. The management-relevant analyses and models developed through this project can be adapted to other species and locations, and may assist other wildlife and land management agencies in refining management plans to reduce the spread of CWD prevalence and distribution.
References
Baeten LA, Powers BE, Jewell JE, Spraker TR, Miller MW. 2007. A natural case of chronic wasting disease in a free-ranging moose (Alces alces shirasi). J Wildl Dis 43:309-314.
DeVivo MT, Edmunds DR, Kauffman MJ, Schumaker BA, Binfet J, Kreeger TJ, Richards BJ, Schätzl HM, Cornish TE. 2017. Endemic chronic wasting disease causes mule deer population decline in Wyoming. PLOS ONE 12:e0186512.
Edmunds DR, Kauffman MJ, Schumaker BA, Lindzey FG, Cook WE, Kreeger TJ, Grogan RG, Cornish TE. 2016. Chronic Wasting Disease Drives Population Decline of White-Tailed Deer. PLOS ONE 11:e0161127.
Monello RJ, Powers JG, Hobbs NT, Spraker TR, Watry MK, Wild MA. 2014. Survival and population growth of a free-ranging elk population with a long history of exposure to chronic wasting disease. J Wildl Manage 78:214-223.
Schumaker NH, Brookes A. 2018. HexSim: a modeling environment for ecology and conservation. Landscape Ecol 33:197-211.
Williams ES, Young S. 1980. Chronic wasting disease of captive mule deer: A spongiform encephalopathy. J Wildl Dis 16:89-98.
Williams ES, Young S. 1982. Spongiform encephalopathy of Rocky Mountain elk. J Wildl Dis 18:465-471.
Williams ES, Young S. 1992. Spongiform encephalopathies in Cervidae. Rev Sci Tech 11:551-567.
Diseases are challenging to manage in wild ungulate populations, particularly when there are many ways the disease can spread. Wildlife management agencies often need to take action to control disease spread, but it is unclear which actions are most effective in constraining disease because the importance of different spread mechanisms is not fully understood. This project will aid state wildlife management agencies by modeling which disease transmission mechanisms most influence changes in prevalence and geographic spread of chronic wasting disease (CWD) in deer and elk. The results simulate the potential effectiveness of different management alternatives at reducing CWD spread and can contribute to the development of management strategies that constrain the disease.
Background
Chronic wasting disease, (CWD; Williams and Young, 1980, 1982, 1992; Baeten and others, 2007) a neurological illness caused by misshapen proteins in the central nervous system (prions), has gained international attention due to its potential for dramatic population-level impacts and our inability to eradicate CWD once it is established. CWD is always fatal and has been linked to substantial population declines at high prevalence in white-tailed deer, mule deer, and likely elk (Monello and others, 2014; Edmunds and others, 2016; DeVivo and others, 2017). Despite over 20 years of intensive research, no effective management prescriptions have been discovered that can control the spread or effectively lower prevalence once CWD is established. In that time, the known affected area increased dramatically both nationally (30 states in the United States) and internationally (three Canadian provinces, and three countries in Europe [Norway, Sweden, and Finland]) in free-ranging cervids, with newly affected areas discovered annually.
Although preventing spread of CWD is a national management priority (America’s Conservation Enhancement Act; S.3051; Public Law 116–188; Oct. 30, 2020), there is limited understanding of the transmission mechanisms and which mechanisms impact disease spread and containment options the most. As no disease has ever been effectively managed without fully understanding transmission, this project aims to provide clarity on the relevance and influence of different spread mechanisms. Results will provide a scientific basis for refining future data collection, testing potential management strategies, and assessing the effects of climate change on disease spread.
Study Design and Methods
To model and investigate the importance of different spread mechanisms on CWD prevalence, we are undertaking a case study. We are using hunter-killed CWD surveillance data (1997-2022) from two selected Wyoming deer Herd Units (Wyoming Game and Fish Department) where CWD has increased in prevalence through time. We developed simulation-based disease spread models (spatially explicit individual-based model; HexSim; Schumaker and Brookes 2018) to investigate the relative influence of animal-animal, and environmental prion-animal spread mechanisms. We simulated past disease spread patterns and are comparing results from different scenarios of spread pathways to better understand the potential role of environmental prions in affecting disease spread.
Future phases of work will assess the contributions of direct (animal-to-animal) and indirect (animal-to-environment-to-animal) transmission, investigate the role of density- versus frequency-dependent transmission and vertical versus horizontal transmission through time, and through climate change. Future modeling scenarios will incorporate additional aspects of animal movement (for example, anthropogenic barriers and attractants such as feed grounds), landscape features (for example, riparian areas, migration corridors, winter grounds), habitat suitability, and predator and scavenger activity, as well as several ongoing and planned management actions.
Project Outcomes
Our project aims to develop an extensible model that can be used to simulate the outcomes of alternative approaches to managing CWD in mule deer and their impacts on prion loads in the environments. The management-relevant analyses and models developed through this project can be adapted to other species and locations, and may assist other wildlife and land management agencies in refining management plans to reduce the spread of CWD prevalence and distribution.
References
Baeten LA, Powers BE, Jewell JE, Spraker TR, Miller MW. 2007. A natural case of chronic wasting disease in a free-ranging moose (Alces alces shirasi). J Wildl Dis 43:309-314.
DeVivo MT, Edmunds DR, Kauffman MJ, Schumaker BA, Binfet J, Kreeger TJ, Richards BJ, Schätzl HM, Cornish TE. 2017. Endemic chronic wasting disease causes mule deer population decline in Wyoming. PLOS ONE 12:e0186512.
Edmunds DR, Kauffman MJ, Schumaker BA, Lindzey FG, Cook WE, Kreeger TJ, Grogan RG, Cornish TE. 2016. Chronic Wasting Disease Drives Population Decline of White-Tailed Deer. PLOS ONE 11:e0161127.
Monello RJ, Powers JG, Hobbs NT, Spraker TR, Watry MK, Wild MA. 2014. Survival and population growth of a free-ranging elk population with a long history of exposure to chronic wasting disease. J Wildl Manage 78:214-223.
Schumaker NH, Brookes A. 2018. HexSim: a modeling environment for ecology and conservation. Landscape Ecol 33:197-211.
Williams ES, Young S. 1980. Chronic wasting disease of captive mule deer: A spongiform encephalopathy. J Wildl Dis 16:89-98.
Williams ES, Young S. 1982. Spongiform encephalopathy of Rocky Mountain elk. J Wildl Dis 18:465-471.
Williams ES, Young S. 1992. Spongiform encephalopathies in Cervidae. Rev Sci Tech 11:551-567.