Chronic Wasting Disease Surveillance Plan

Chris Geremia, John Treanor, and P. J. White
March 2016

Executive Summary


Chronic wasting disease (CWD) is a contagious, fatal disease of deer, elk, and moose for which there is no vaccine or known treatment. It is transmitted by direct animal-to-animal contact or indirectly through contact with infectious particles persisting in the environment.

Deer, elk, and moose in and near Yellowstone National Park are at risk for infection by CWD because it is known to occur less than 10 miles from an infected area, the disease is spreading towards the park, and there are large concentrations of deer and elk in and near the park. There is no credible evidence that CWD constitutes a livestock or human health threat, but the possibility cannot be discounted and public concern is high.

CWD is managed as a non-native disease by the National Park Service because its distribution and prevalence were influenced by human activities (e.g., translocation of animals; artificial feeding; loss of habitat).

No strategy has been effective at eradicating CWD from areas where the disease is present. Thus, our disease management objectives will focus on early detection and monitoring.

The park will:

  • Monitor the prevalence of CWD in deer and elk by aggregating data over 5- to 10- year intervals due to the slow progression of epidemics and difficulty of obtaining samples.
  • Collaborate with state agencies to test for CWD in deer, elk, and moose killed by hunters, predators, and vehicles.
  • Identify areas within Yellowstone with increased risk for CWD based on known locations of infected deer and elk populations, soils, genetics, and movement patterns.
If CWD is detected in Yellowstone, the park will:

  • Increase visual surveillance, the investigation of carcasses and collection of samples for testing, and targeted culling and testing of animals demonstrating signs of the disease.
  • Investigate whether selective predation and scavenging remove a greater proportion of CWD-infected animals than culling or harvest and dilute environmental contamination and suppress CWD prevalence.
  • Establish 5% (males) and 2-3% (females) as thresholds in 5- to 10- year prevalence levels that would trigger an evaluation of whether active disease suppression was feasible and warranted to maintain prevalence below these thresholds (e.g., selective culling).
CWD management is a long-term commitment of personnel and funding because reducing transmission risk factors and prevalence by any conceivable approach will take many decades. Implementation of this plan could be expensive and exceed the park’s current financial capability with regards to wildlife disease management.

Background


Chronic wasting disease (CWD) is a contagious, fatal disease of cervid populations, including deer, elk, and moose for which there is no vaccine or known treatment (Williams et al. 2002, Baeten et al. 2007). CWD is from a category of diseases known as transmissible spongiform encephalopathies, which are also known as prion diseases. Other diseases in this category include mad cow disease in cattle, scrapie in goats and sheep, and Creutzfeldt-Jakob disease in humans. Prion diseases are believed to be caused by the accumulation of a misfolded variant of native prion (a protein naturally found within all mammals) which leads to neurodegeneration and, ultimately, death. Infected animals may appear normal initially, but typically lose weight, drink and urinate more frequently, drool excessively, have a wide-based stance with lowered head and ears, have a blank facial expression, lose their fear of humans and, eventually, become isolated as infection progresses. However, these signs are not specific to CWD and a definitive diagnosis is made by laboratory testing of the brain or lymph nodes collected from dead animals.

The disease course is prolonged with deer capable of transmitting infectious prions within months of exposure, and infected animals remaining alive for up to two years (Fox et al. 2006, Miller et al. 2008, Geremia et al. 2015). CWD is transmitted by direct animal-animal contact (e.g., saliva, blood) or, indirectly, through infectious particles that can persist in the environment (e.g., carcasses, antlers, soils, plants; Mathiason et al. 2006, Tamgüney et al. 2009, Pritzkow et al. 2015). The debilitating effects of CWD are progressive with minimal pathophysiological effects during the first year after exposure, followed by rapid deterioration of motor function, such as gut control, vision, and hearing. CWD reduces adult deer survival with effects increasing over time (Miller et al. 2008, Geremia et al. 2015); though some research suggests the disease does not influence survival in populations subject to intensive harvest (Magle et al. 2012). CWD is not believed to influence reproduction (Dulberger et al. 2010, Magle et al. 2012).

There is general uncertainty regarding how CWD epidemics will effect cervid populations because epidemics are prolonged, playing out over decades. Simulation models have predicted a variety of outcomes from limited population decline and sustained low disease prevalence to local extinction within decades of disease introduction (Gross et al. 2001, Wasserberg et al. 2009, Wild et al. 2011, Almberg et al. 2011, Jennelle et al. 2014,Monello et al. 2014, Potapov et al. 2015). Empirical studies have confirmed that under high prevalence (>20% in females) deer populations have sustained short-term declines, and CWD has been implicated as a proximal cause acting through decreases in adult female survival (Miller et al. 2008, Edmunds 2013, Devivo 2015). However, similar effects have been muted across larger spatial areas because high prevalence has remained a local phenomenon (Geremia et al. 2015). If epidemics lead to widespread population reductions in Yellowstone, CWD could indirectly alter the structure and function of this ecosystem during future decades; adversely affect species of predators and scavengers; and have serious economic effects on the recreation-based economies of the area.

The National Park Service is tasked with maintaining native plants and animals by preserving and restoring the natural abundances, diversities, dynamics, distributions, habitats, and behaviors of native plant and animal populations and the communities and ecosystems in which they occur (National Park Service 2006). The origin of CWD is unknown, but it is clear that its distribution and prevalence were influenced by human activities such as the translocation of deer and elk between game farms, research facilities, and zoological parks and, also, by concentration of wildlife through artificial feeding, loss of habitat, and changes in movement patterns due to fragmented landscapes. By causing deer and elk to increase in numbers and become more sedentary in many areas, anthropogenic actions have increased the chances of animal-to-animal transmission and exposure from a contaminated environment, which may result in a disease process that is incongruent with a naturally functioning ecosystem. Thus, it is appropriate for the National Park Service to consider CWD management actions (National Park Service 2006).

CWD has continued to spread north and west across the state of Wyoming during the past 15 years. In 2015, CWD was detected in a mule deer harvested in a hunt area approximately 9.3 miles from the southeastern boundary of Yellowstone National Park. Elk that summer in the park could commingle with deer in this area. This plan for Yellowstone National Park outlines a step-wise surveillance plan for CWD and describes what actions the park will take to suppress disease prevalence and spread if it is detected.

Surveillance


A primary purpose of Yellowstone National Park is to preserve abundant and diverse wildlife in one of the largest remaining intact ecosystems on earth. Disease management actions such as depopulation or substantial population reductions by random culling may be inappropriate for the park because they would remove many more healthy animals than infected animals, substantially reduce the prey base for predators and scavengers, and result in fewer benefits (e.g., scientific knowledge) and reduced visitor enjoyment (e.g., recreational viewing).

Yellowstone National Park provides summer range for more than 10,000 deer and elk from multiple herds. Surveillance for the majority of these populations is difficult because they are widely distributed in high mountain habitats during summer and winter at lower elevations outside the park. Also, deer and elk from different populations intermix during summer, making it impossible to differentiate animals from different target populations and difficult to define sampling units. The current abundance of moose in and near the park is unknown due to the difficulty of conducting surveys and obtaining rigorous population estimates for this species at low densities.

CWD can be confirmed through laboratory analysis of central (obex, spinal cord) or peripheral (retropharyngeal lymph node, tonsil, rectal mucosa associated lymphoid tissue) nervous system tissue. Tissue samples can be obtained by anesthetizing live animals and obtaining a biopsy of tonsil or rectal mucosa associated lymphoid tissue (Wolfe et al. 2002, 2007) or from necropsying carcasses. Current screening tests include enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry (Spraker et al. 2002), though other prion amplification methods are being evaluated (Wyckoff et al. 2015). Immunohistochemistry is currently the most reliable test for detecting CWD in animal tissues. However, it is still an imperfect test and a negative test result does not guarantee a CWD-free animal, particularly early in the disease course (Fox et al. 2006, Wolfe et al. 2007). Furthermore, pathogenesis of CWD may differ among deer and elk and within species based on composition of the prion precursor gene, especially with regards to the timing of misfolded prion deposition in different tissues (Keane et al. 2009, Spraker et al. 2009, Wolfe et al. 2014). These differences reduce the ability to detect CWD early in the disease course.

In most areas and especially during the early phases of CWD epidemics, CWD is likely to occur at low prevalence that is difficult to detect (Samuel et al. 2003). As an example, for surveillance to reliably provide early detection of CWD, sample sizes must be sufficient to detect relatively low infection rates with considerable confidence. At a disease prevalence of 1%, we would need to sample a minimum of 450 animals from a population of approximately 10,000 animals to be 99% confident of detecting one animal with CWD.

Given these challenges, we propose a stepwise surveillance program. Initially, we will implement targeted surveillance aimed to opportunistically test deer and elk that are more likely to be infected with CWD. In these deer, the CWD-detection probability per animal sampled would be higher than other, more random methods of surveillance (e.g., harvests) and, as a result, fewer samples should be needed to detect a CWD-positive animal (Walsh 2012). In general, prevalence tends to be twice as high in males compared to females (Miller and Conner 2005, Jennelle et al. 2014). Also, prevalence is higher in mule deer compared to elk or white-tailed deer living in the same area. In addition to targeting species and demographics, we will:

  1. Collect tissue samples from deer, elk, or moose killed in vehicle collisions in or near Yellowstone. CWD-infected deer may be more vulnerable to vehicle collisions than otherwise healthy deer in the same populations (Krumm et al. 2005).
  2. Collect tissue samples from recently killed deer, elk, and moose in central and northern Yellowstone as part of ongoing ungulate and wolf programs. Wolves are highly selective for elk throughout the year and bears are highly selective of neonatal elk during summer. CWD-infected deer have been shown to be more susceptible to mountain lion predation (Miller et al. 2008, Krumm et al. 2010).
  3. Collaborate with state agencies to collect tissue samples from harvested deer and elk at game check stations. Data from harvested mule deer in Colorado suggests that CWD-infected individuals may be more vulnerable to harvest (Conner et al. 2000), though similar effects were not found in a white-tailed deer population subject to intensive harvest (Grear et al. 2006). In cooperation with other federal and state agencies, we will continue targeted sampling of deer, elk, and moose that are more likely to be infected with CWD (e.g., deer killed by hunters, predators, and vehicles).
If CWD is detected in the park, we will:

  1. Respond to reports of “sick” deer, elk, and moose to evaluate them for signs of CWD and cull animals exhibiting clinical signs. We will collaborate with state and federal agencies to provide training to park personnel to help them identify the signs of disease.
  2. As possible, dispose of carcasses of known-infected animals. Carcasses and samples submitted to diagnostic laboratories for testing will be individually identified and appropriately processed and stored until they are submitted for testing. All CWD-positive samples will be incinerated following analysis. All carcasses with CWD-negative test results will be placed in municipal solid waste landfills. Carcasses of predator-killed animals will be left in place once samples are removed. Carcasses of vehicle-killed animals will be moved to established areas in the immediate vicinity where predators and scavengers can facilitate quick decomposition.
  3. As funding and collaborations allow, begin random sampling of mule deer and elk populations on wintering ranges in and near Yellowstone. Use live-animal testing (Wolfe et al. 2002, 2007) procedures to collect tissue samples from deer and elk captured as part of existing long-term monitoring programs in and near the park.
  4. Conduct research on the potential for predators and scavengers to remove a greater proportion of CWD-infected animals than culling or harvest and dilute environmental contamination and suppress CWD prevalence. Yellowstone supports a robust large-predator complex and scavenger guild that rapidly remove debilitated animals and carcasses. Selective predation and scavenging could remove a greater proportion of CWD-infected animals than culling or harvest and dilute environmental contamination and suppress CWD prevalence.
  5. Establish 5% (males) and 2-3% (females) as thresholds in 5- to 10- year prevalence levels that would trigger an evaluation of whether active disease suppression was feasible and warranted. We would consider the science and technology available at the time to decide whether to implement actions to maintain prevalence below these thresholds, which may include practices such as selective culling.
We will measure CWD prevalence over 5- to 10- year horizons given the slow progression of CWD epidemics, difficulty of obtaining enough samples to identify the presence of CWD and, if it is found, accurately estimate prevalence. Tissue samples will be tested using ELISA as an initial screening and any samples testing positive will be reevaluated using immunohistochemistry.

Risk Mapping


Laboratory studies have shown that prions bind to clay minerals and clay-laden whole soils with dramatic increases on infectivity (Johnson et al. 2006, 2007). Cervids ingest soil both deliberatively and inadvertently during foraging and grooming. Prions propagated in lymphoid tissue of the oropharynx and gut may bind to ingested soil particles enhancing infectivity both within and outside the host (Johnson et al. 2006, 2007; Walter et al. 2011).

The structure of the prion precursor (PRNP) gene within hosts may afford some general protection against infection. A nucleotide substitution in the 225th codon of mule deer PRNP leads to an amino acid phenylalanine (F) for serine (S) substitution (Jewell et al. 2005). This amino acid change may disrupt or slow prion propagation, such that the 225F/S substitution has been associated with slower disease progression in mule deer (Fox et al. 2006, Wolfe et al. 2014). Similar non-synonymous nucleotide substitutions in white-tailed deer (O’Rourke et al. 2004, Johnson et al. 2006) and elk (Green et al. 2008) have been associated with longer incubation or reduced prevalence in individuals possessing the rarer allele.

We will begin risk mapping for CWD based on soils, genetics, and movement patterns of deer and elk inside Yellowstone, and distances to known infected deer and elk populations outside the park. We will collaborate with other agencies and researchers currently studying elk, mule deer, and CWD in and near Yellowstone to unify existing information to (1) identify deer and elk movement patterns and identify spatial population structure, (2) characterize deer and elk PRNP genotypes and soil conditions at population and subpopulation scales, (3) integrate soil, PRNP, and population structure information with known distances to CWD to predict areas more likely for CWD introduction, and (4) develop stepped-up surveillance strategies if CWD is detected in the park.

Disease Management


We will establish 5% (males) and 2-3% (females) as thresholds in 5- to 10- year prevalence levels that would trigger an evaluation of whether active disease suppression was feasible and warranted. This decision was based on several important aspects of CWD epidemiology and management:
  1. CWD epidemics are prolonged and prevalence generally remains at low levels for years and perhaps decades after disease introduction.
  2. Empirical evidence suggests that CWD prevalence below these thresholds does not induce population decreases (Monello et al. 2014, Geremia et al. 2015). At low prevalence, CWD effects are limited to the individual-level, with little to no effects on population dynamics.
  3. Predators have been shown to selectively kill CWD-infected animals (Krumm et al. 2010) and simulation studies have predicted that selective removal by predators could retard CWD epidemics (Wild et al. 2011). Yellowstone supports a robust large-predator complex and scavenger guild that could rapidly remove CWD-infected animals and suppress CWD prevalence.
  4. There is equivocal evidence that active disease management given current technologies suppresses or eradicates CWD epidemics. CWD prevalence in mule deer populations with a long history of CWD was unaffected by 1-3 year-long efforts of population control to lower abundance and selectively remove likely infected individuals (Conner et al. 2007). Reevaluation of prevalence in these deer populations a decade later suggested declines in prevalence. However, it is unknown whether declines were a delayed response to management or the natural course of epidemics (Geremia et al. 2015). Localized culling, such as an attempt to kill all deer in a predetermined area, may stabilize CWD prevalence at low levels, but not eradicate disease (Manjerovic et al. 2014). Nonselective hunting may also reduce prevalence, but to a lesser degree than culling (Wasserberg et al. 2009, Manjerovic et al. 2014, Potapov et al. 2014).
There is equivocal evidence that active disease management given current technologies suppresses or eradicates CWD epidemics. CWD prevalence in mule deer populations with a long history of CWD was unaffected by 1-3 year-long efforts of population control to lower abundance and selectively remove likely infected individuals (Conner et al. 2007). Reevaluation of prevalence in these deer populations a decade later suggested declines in prevalence. However, it is unknown whether declines were a delayed response to management or the natural course of epidemics (Geremia et al. 2015). Localized culling, such as an attempt to kill all deer in a predetermined area, may stabilize CWD prevalence at low levels, but not eradicate disease (Manjerovic et al. 2014). Nonselective hunting may also reduce prevalence, but to a lesser degree than culling (Wasserberg et al. 2009, Manjerovic et al. 2014, Potapov et al. 2014).

If prevalence reaches 5% (males) or 2-3% (females), we would evaluate the science and technology at the time and consider implementing disease management actions (e.g., selective culling) to maintain prevalence below these thresholds.

There is no evidence that CWD poses a risk to human health, but a related animal disease, bovine spongiform encephalopathy (mad cow disease), has been causally linked to the human form of that disease known as variant Creutzfeldt-Jakob disease. This has raised concerns about the possibility of CWD crossing the species barrier and infecting humans that consume meat from infected elk and deer. While current evidence indicates that the differences between mad cow disease, Creutzfeldt-Jakob disease, and CWD are significant, there is still ongoing research to establish whether CWD can cross the human species barrier. Thus, health experts warn that no part or product of any animal with evidence of CWD should be fed to any species (human or any domestic or captive animal). At this time, Yellowstone does not plan to donate meat from predator or vehicle killed animals or to local food banks or those in need.

For public safety and resource protection, the Superintendent’s Compendium (Yellowstone National Park 2014; 36 CFR 1.6(a), 1.5(a)(2)) prohibits the transport of heads and spinal cords from deer, elk, or moose through the park if they were harvested in a state or province with CWD diagnosed in their wildlife populations, except for the following portions of the carcass:

  • Meat that is cut or wrapped either commercially or privately.
  • Quarters or other portions of meat with no part of the spinal column or head attached.
  • Meat that has not been boned out.
  • Hides with no heads attached.
  • Clean (no meat or tissue attached) skull plates with antlers attached.
  • Antlers with no meat or tissue attached.
  • Upper canine teeth, also known as “buglers,” “whistlers,” or “ivories.”
  • Finished taxidermy heads.
Currently, those states and provinces include Arkansas, Colorado, Illinois, Iowa, Kansas, Maryland, Michigan, Minnesota, Missouri, Nebraska, New Mexico, New York, North Dakota, Ohio (hunting preserve), Pennsylvania, South Dakota, Texas, Utah, Virginia, West Virginia, Wisconsin, Wyoming, Alberta, and Saskatchewan.
 

Literature Cited


Almberg, A. S., P. C. Cross, C. J. Johnson, D. M. Heisey, and B. J. Richards. 2011. Modeling routes of chronic wasting disease transmission: Environmental prion persistence promotes deer population decline and extinction. PLoSONE e19896, doi:10.1371/journal.pone.0019896.

Baeten, L. A., B. E. Powers, J. E. Jewell, T. R. Spraker, and M.W. Miller. 2007. A natural case of chronic wasting disease in a free-ranging moose (Alces alces shirasi). Journal of Wildlife Diseases 43:309-314.
Conner, M. M., C. W. McCarty, and M. W. Miller. 2000. Detection of bias in harvest-based estimates of chronic wasting disease prevalence in mule deer. Journal of Wildlife Diseases 36:691-699.

Conner, M. M., M. W. Miller, M. R. Ebinger, and K. P. Burnham, K. P. 2007. A meta-BACI approach for evaluating management intervention on chronic wasting disease in mule deer. Ecological Applications 17:140-153.

DeVivo, M. T. 2015. Chronic wasting disease ecology and epidemiology of mule deer in Wyoming. Dissertation, University of Wyoming, Laramie.
Dulberger J., N. T. Hobbs, H. M. Swanson, C. J. Bishop, and M. W. Miller. 2010. Estimating chronic wasting disease effects on mule deer recruitment and population growth. Journal of Wildlife Diseases 46:1086-1095.

Edmunds, D. R. 2013. Chronic wasting disease ecology and epidemiology of white-tailed deer in Wyoming. Dissertation, University of Wyoming, Laramie.

Fox, K. A., J. E. Jewell, E. S. Williams, and M. W. Miller. 2006. Patterns of PrPCWD accumulation during the course of chronic wasting disease infection in orally inoculated mule deer (Odocoileus hemonious). Journal of General Virology 87:3451-3461.

Geremia, C., M. W. Miller, J. A. Hoeting, M. F. Antolin, and N. T. Hobbs. 2015. Bayesian modeling of prion disease dynamics in mule deer using population monitoring and capture-recapture data. PLoSONE 10:e0140687. doi:10.1371/journal.pone.0140687.

Grear, D. A., M. D. Samuel, J. A. Langenberg, and D. Keane. 2006. Demographic patterns and harvest vulnerability of chronic wasting disease infected white-tailed deer in Wisconsin. Journal of Wildlife Management 70:546-553.

Green, K. M., S. R. Browning, T. S. Seward, J. E. Jewell, D. L. Ross, M. A. Green, E. S. Williams, E. Hoover, and G. C. Telling. 2008. The elk PRNP codon 132 polymorphism controls cervid and scrapie prion propagation. Journal of General Virology 89:598-608.

Gross, J. E., and M. W. Miller. 2001. Chronic wasting disease in mule deer: Disease dynamics and control. Journal of Wildlife Management 65:205-215.

Jennelle, C. S., V. Henaux, G. Wasserberg, B. Thiagarajan, R. E. Rolley, and M. D. Samuel. 2014. Transmission of chronic wasting disease in Wisconsin white-tailed deer: Implications for disease spread and management. PloSONE 9, e91043.

Jewell, J. E., M. M. Conner, L. L. Wolfe, L. L., M. W. Miller, and E. S. Williams. 2005. Low frequency of PrP genotype 225SF among free-ranging mule deer (Odocoileus hemionus) with chronic wasting disease. Journal of General Virology 86:2127-2134.

Johnson, C. J., J. A. Pedersen, R. J. Chappell, D. McKenzie, and J. M. Aiken. 2007. Oral transmissibility of prion disease is enhanced by binding to soil particles. PLoS Pathogens 3, e93.

Johnson, C. J., K. E. Phillips, P. T. Schramm, D. McKenzie, J. M. Aiken, and J. A. Pedersen. 2006. Prions adhere to soil minerals and remain infectious. PLoS Pathogens 2, e32.

Keane, D., D. Barr, R. Osborn, J. Langenberg, K. O’Rourke, D. Schneider, and P. Bochsler. 2009. Validation of use of rectoanal mucosa-associated lymphoid tissue for immunohistochemical diagnosis of chronic wasting disease in white-tailed deer (Odocoileus virginianus). Journal of Clinical Microbiology 57:1412-1417.

Krumm, C.E., M.M. Conner, and M.W. Miller. 2005. Relative vulnerability of chronic wasting disease infected mule deer to vehicle collisions. Journal of Wildlife Diseases 41:503-511.

Magle, S. B., J. C. Chamberlin, and N. E. Mathews. 2012. Survival of white-tailed deer in Wisconsin's chronic wasting disease zone. Northeastern Naturalist 19:67-76.

Manjerovic, M. B., M. L. Green, N. Mateus-Pinilla, and J. Novakofski. 2014. The importance of localized culling in stabilizing chronic wasting disease prevalence in white-tailed deer populations. Preventative Veterinary Medicine 113:139-145.

Mathiason, C.K., J.G. Powers, S.J. Dahmes, D.A. Osborn, K.V. Miller, R.J. Warren, G.L. Mason, S.A. Hayes, J. Hayes-Klug, D.M. Seelig, M.A. Wild, L.L. Wolfe, T.R. Spraker, M.W.

Miller, C.J. Sigurdson, G.C. Telling, and E.A. Hoover. 2006. Infectious prions in the saliva and blood of deer with chronic wasting disease. Science 314:133-136.

Miller M. W., and M. M. Conner. 2005. Epidemiology of chronic wasting disease in free-ranging mule deer: spatial, temporal, and demographic influences on observed prevalence patterns. Journal of Wildlife Diseases 4:275-290.

Miller, M. W., H. M. Swanson, L. L. Wolfe, F. G. Quartarone, S. L. Huwer, C. H. Southwick, and P. M. Lukacs. 2008. Lions and prions and deer demise. PLosONE 3:e4019.

Monello, R. J., J. Powers, N. T. Hobbs, T. R. Spraker, M. W. Watry, and M. A. Wild. 2014. Survival and population growth of a free-ranging elk population with a long history of exposure to chronic wasting disease. Journal of Wildlife Management 78:214-223.
National Park Service. 2006. Management policies 2006. U.S. Department of the Interior, Washington, D.C.

O'Rourke, K. I., T. R. Spraker, L. K. Hamburg, T. E. Besser, K. A. Brayton, and D. P. Knowles. 2004. Polymorphisms in the prion precursor functional gene but not the pseudogene are associated with susceptibility to chronic wasting disease in white-tailed deer. Journal of General Virology 85:1339-1346.

Potapov, A., E. Merrill, M. Pybus, and M. A. Lewis. 2016. Chronic wasting disease: transmission mechanisms and the possibility of harvest management. PloSONE 11, e0151039.

Pritzkow, S., R. Morales, F. Moda, U. Kahn, G. C. Telling, E. Hoover, and C. Soto. 2015. Grass plants bind, retain, uptake, and transport infectious prions. Cell Reports 11:1168-1175.

Samuel, M. D., D. O. Joly, M. A. Wild, S. D. Wright, D. L. Otis, R. W. Werge, and M. W. Miller. 2003. Surveillance strategies for detecting chronic wasting disease in free-ranging deer and elk. National Wildlife Health Center, U.S. Geological Survey, Madison, Wisconsin.

Spraker, T., K. O’Rourke, Z. Balachandran, R. Zink, B. Cummings, M. Miller, and E. Powers. 2002. Validation of monoclonal antibody F99/97.6.1 for immunohistochemical staining of brain and tonsil in mule deer (Odocoileus hemionus) with chronic wasting disease. Journal of Veterinary Diagnostic Investigation 14:3-7.

Spraker, T., K. VerCauteren, T. Gidlewski, D. Schneider, R. Munger, A. Balachandran, and K. O’Rourke. 2009. Antemortem detection of PrPCWD in preclinical, ranch-raised Rocky Mountain elk (Cervus Elaphus nelson) by biopsy of the rectal mucosa. Journal of Veterinary Diagnostic Investigation 21:15-24.

Tamgüney G., M. W. Miller, L. L. Wolfe, T. M. Sirochman, D. V. Glidden, C. Palmer, A. Lemus, S. J. DeAmond, and S. B. Prusiner. 2009. Asymptomatic deer excrete infectious prions in faeces. Nature 461:529-532.

Walsh, D. P. 2012. Enhanced surveillance strategies for detecting and monitoring chronic wasting disease in free-ranging cervids. U.S. Department of the Interior and U.S. Geological Survey. Open File Report 2012-1036.

Walter, W. D., D. P. Walsh, M. L. Farnsworth, D. L. Winkelman, and M. W. Miller. 2011. Soil clay content underlies prion infection odds. Nature communications 2:200.

Wasserberg, G., E. E. Osnas, R. E. Rolley, and M. D. Samuel. 2009. Host culling as an adaptive management tool for chronic wasting disease in white-tailed deer: A modelling study. Journal of Applied Ecology 46:457-466.

Wild, M. A., N. T. Hobbs, M. S. Graham, and M. W. Miller. 2011. The role of predation in disease control: A comparison of selective and nonselective removal on prion disease dynamics in deer. Journal of Wildlife Diseases 47:78-93.

Williams, E. S., M. W. Miller, T. J. Kreeger, R. H. Kahn, and E. T. Thorne. 2002. Chronic wasting disease of deer and elk: A review with recommendations for management. Journal of Wildlife Management 66:551-563.

Wolfe, L. L., M. Conner, T. Baker, V. Dreitz, K. Burnham, E. Williams, N. Hobbs, and M. Miller. 2002. Evaluation of ante mortem sampling to estimate chronic wasting disease prevalence in free-ranging mule deer. Journal of Wildlife Management 66:564-573.

Wolfe, L. L., K. A. Fox, and M. W. Miller. 2014. Atypical chronic wasting disease in PRNP genotype 225FF mule deer. Journal of Wildlife Diseases 50:660-665.

Wolfe, L. L., T. R. Spraker, L. Gonzalez, M. P. Dagleish, T. M. Sirochman, J. C. Brown, M. Jeffrey, and M. W. Miller. 2007. PrPCWD in rectal lymphoid tissue of deer (Odocoileus spp.). Journal of General Virology 88:2078-2082.

Wycoff, A., N. Galloway, C. Meyerett-Reid, J. Powers, T. Spraker, R. Monello, B. Pulford, M. Wild, M. Antolin, K. VerCauteren, and M. Zabel. 2015. Prion amplification and hierarchical Bayesian modeling refine detection of prion infection. Scientific reports 5.

Yellowstone National Park. 2014. Superintendent’s compendium of designations, closures, permit requirements and other restrictions imposed under discretionary authority. National Park Service, Yellowstone National Park, Mammoth, Wyoming.

Last updated: December 1, 2016

Contact the Park

Mailing Address:

PO Box 168
Yellowstone National Park, WY 82190-0168

Phone:

307-344-7381

Contact Us