Why Manage CWD?
Chronic Wasting Disease (CWD) has the potential to negatively impact deer herds wherever the disease occurs. CWD is always fatal and could have serious negative impacts on the state’s deer population if it became established and widely prevalent (Almberg et al. 2011).
CWD infection decreases deer survival odds and lowers total life expectancy (Miller et al. 2008; Edmunds et al. 2016). If a large percentage of the population becomes infected there could be negative impacts on the population, such as:
- A decline in doe survival, which results in an overall reduced population (Gross and Miller 2001);
- Fewer older bucks, as male animals are more likely to be infected due to specific male social and behavioral tendencies (Miller et al. 2008, Jennelle et al. 2014, Samuel et al. 2016); and
- An overall decline in population (Gross and Miller 2001, Almberg et al. 2011), as currently exhibited in Colorado and Wyoming.
- In the area of Colorado with highest CWD prevalence, mule deer numbers have plummeted by 45%, in spite of good habitat and protection from hunting (Miller et al. 2008).
- In an area of Wyoming that is known to be affected by CWD, the white-tailed deer population is experiencing a 10% annual decline. The most common causes of mortality in this population were reported to be CWD and hunting, and CWD-positive deer were more likely to be killed by hunters then non-infected deer (Edmunds et al 2016).
The Department is concerned about the impact CWD could have on Virginia’s deer herd; once CWD has become established in an area, its persistence in the environment makes eradication extremely difficult, if not impossible. Taking action to keep the percentage of infected animals low helps to prevent (or at least slow) the spread of CWD to new areas, and also helps to slow the transmission of the disease between individuals.
Understanding the Spread of CWD
CWD prions, which are the infectious proteins that cause the disease, are found in saliva, urine, feces, and blood (Mathiason et al. 2006, Mathiason et al. 2009, Haley et al. 2011). Prions can persist for years in soil and in other substances, can be taken up by grass roots from contaminated soil, and can be transmitted by infected cervids that are not yet showing symptoms of the disease (Miller et al. 2004, Mathiason et al. 2009, Pritzkow et al. 2015, Plummer et al. 2017, Davenport et al. 2018). Halting or slowing the spread of CWD is therefore a matter of reducing transmission between deer and making deer less likely to pick up prions from the environment (Mathiason et al. 2009, Grear et al. 2010, Storm et al. 2013).
Differences in animal behavior between the sexes and age classes results in different rates of disease spread.
- Bucks are more likely to become infected than does (Grear et al. 2006, Miller et al. 2008, Jennelle et al. 2014, Samuel et al. 2016).
- Higher CWD prevalence is found in older age classes of bucks, generally 3 years and older (Grear et al 2006, Samuel et al. 2016).
- Adult bucks make long excursions outside their home range, bringing them into contact with more individual deer spread across a wider area (Karns 2011).
- Young bucks are more likely to disperse from their mother’s home range and can cover many miles, thereby potentially spreading the disease across the landscape if infected with CWD (McCoy et al. 2005).
- Young bucks infected with CWD may not be indicative of established CWD presence at the location of death because they may have been killed while dispersing away from their mother’s home range.
- The detection of a CWD-positive doe suggests that CWD is established in the population from which the infected doe was killed (Grear et al. 2010, Magel et al. 2013). Does are relatively sedentary, usually spending their lives near their place of birth, and spend most of their time interacting with a related social group. Does only rarely make excursions (Kolodzinski et al. 2009, Miller et al. 2010, Grear et al. 2010).
Due to the nature of the prions which cause CWD (please see the What Are Prions? page for more information), there is no vaccine available to prevent infection and no known treatment for infected animals. However, research suggests that management of CWD should be attempted. Below are some best practices for the management of CWD.
- Objective: Minimize the transmission of CWD
- Lower deer density
- Population reduction should reduce contacts between infected and susceptible individuals and consequently reduce the disease transmission rate. Analysis of spatial data indicates that CWD is clustered on the landscape, suggesting that healthy deer whose home ranges are located in close proximity to the kill site of a CWD-positive deer are more likely to be infected (Joly et al. 2003.).
- A lower density population surrounding a location of known infection reduces the chances of deer picking up CWD prions from the environment. Research indicates that indirect transmission is just as important as animal-to-animal transmission (Storm et al. 2013), most notably in the later stages of an outbreak.
- Earn-a-Buck, currently in effect in Frederick, Warren, and Clarke Counties, is designed to reduce the overall deer population by focusing more hunting pressure on the female segment of the population.
- Ban feeding and baiting of deer in areas with CWD, including prohibiting the use of mineral licks.
- CWD prions can be found in saliva (Mathiason et al. 2009) and feed or bait piles are excellent modalities to transfer saliva between deer.
- Feed and bite piles artificially congregate deer, thereby facilitating both direct transmission between sick and healthy deer and indirect transmission through exposure to contaminated urine and feces.
- Mineral licks can act as reservoirs of CWD (Plummer et al. 2018).
- Lower deer density
- Objective: Prevent the introduction of CWD into new areas
- Prohibit the movement of deer carcasses out of areas known to be affected by CWD
- Prions The Department prohibits the movement of deer carcasses out of the CWD Containment Area and from other states and provinces known to be affected by CWD until after they have been processed to minimize the potential for translocation of CWD prions via movement of an infected carcass.
- Prohibit the use of lures and attractants that contain natural deer urine, scent gland secretions, or other bodily fluids.
- CWD prions may be found in the urine of infected deer even if the deer is not showing symptoms (John et al. 2013).
- There is no commercially available test to check deer bodily fluids for CWD prions.
- Link: Use of Natural Deer Lures and Attractants in Virginia
- Prohibit the movement of deer carcasses out of areas known to be affected by CWD
Doing nothing to manage CWD is not a satisfactory option! This has been shown by a number of studies that have examined hunters’ attitudes toward current and potential strategies for managing CWD (Vaske 2010). Among hunters in most states and studies these were the predominant three opinions:
(A) Testing harvested animals for CWD and using hunters to reduce herds in CWD areas were acceptable strategies.
(B) Taking no action and allowing CWD to run its course were unacceptable strategies.
(C) Using agency staff to reduce herds in CWD areas was a controversial strategy.
Hunters also generally supported efforts to minimize the spread of CWD and eliminate the disease from animal herds (Vaske 2010). A survey conducted in Virginia following the discovery of CWD in Frederick County in 2009 concluded that respondents supported five out of seven potential strategies to control CWD in affected areas, including mandatory disease testing of hunter-killed deer, deer feeding prohibitions, deer carcass movement restrictions, restrictions on deer rehabilitation, and reduction of deer populations using hunters (Virginia Department of Game and Inland Fisheries 2010, unpublished data). The strongest opposition was recorded for the option to attempt nothing in order to manage CWD (79 % opposed, 8% supported). Additionally, respondents did not support the use of sharpshooting to reduce localized deer populations (42% opposed, 36% supported, 22% were neutral).
- Almberg, E. S., P. C. Cross, C. J. Johnson, D. M. Heisey, B. J. Richards. 2011. Modeling Routes of Chronic Wasting Disease Transmission: Environmental Prion persistence Promotes Deer Population Decline and Extinction. PLoS ONE 6: e19896. doi:10.1371/journal.pone.0019896
- Davenport, K. A, B. A. Mosher, B. M. Brost, D. M. Henderson, N. D. Denkers, A. V. Nalls, E. McNulty, C. K. Mathiason, E. A. Hoover. 2018. Assessment of Chronic Wasting Disease Prion Shedding in Deer Saliva with Occupancy Modeling. Journal of Clinical Microbiology. 56:e01243-17
- Edmunds, D. R., M. J. Kauffman, B. A. Schumaker, F. G. Lindzey, W. E. Cook, T. J. Kreeger, R. G. Grogan, T. E. Cornish. 2016. Chronic Wasting Disease Drive Population Decline of White-tailed Deer. PLoS ONE 11(8):e0161127.
- Grear, D. A., M. D. Samuel, J. A. Langenberg, D. Keane. 2006. Demographic Patterns and Harvest Vulnerability of Chronic Wasting Disease Infected White-tailed Deer in Wisconsin. Journal of Wildlife Management. 20:546-553
- Grear, D. A., M. D. Samuel, K. T. Scribner, B. V. Weckworth, J. A. Langenberg. 2010. Influence of Genetic Relatedness and Spatial Proximity on Chronic Wasting Disease Infection Among Female White-tailed Deer. Journal of Applied Ecology. 47:532-540.
- 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.
- Haley, N. J., C. K. Mathiason, S. Carver, M. Zabel, G. C. Telling, E. A. Hoover. 2011. Detection of Chronic Wasting Disease Prions in Salivary, Urinary, and Intestinal Tissues, of Deer: Potential Mechanisms of Prion Shedding and Transmission. Journal of Virology. 85: 6309-6318.
- Jennee, C. S., V. Henaux, G. Wasserberg, B. Thiagarajan , R. E. Rolley, M. D. Samuel. 2014. Transmission of Chronic Wasting Disease in Wisconsin White-Tailed Deer: Implications for Disease Spread and Management. PLoS ONE 9: e91043. doi:10.1371/journal.pone.0091043
- John, T. R., H. M. Schatzl, S. Gilch. 2013. Early detection of chronic wasting disease prions in urins of pre-symptomatic deer by real-time quaking-induced conversion assay. Prion. 7:253-258.
- Joly, D. O., C.. A. Ribic, J. A. Langenberg, K. Beheler, C. A. Batha, B. J. Dhuey, R. E. Rolley, G. Bartelt, T. R. Van Deelen, and M. D. Samuel. 2003. Chronic wasting disease in free-ranging Wisconsin white-tailed deer. Emerging Infectious Diseases 9:599-560.
- Karns, G. R., R. A. Lancia, C. S. DePerno, M. C. Conner. 2011. Investigation of Adult Male White-tailed Deer Excursions Outside Their Home Range. Southeast Naturalist. 10:39-52.
- Kolodzinski, J. J., L. V. Tennenbaum, L. I. Muller, D. A. Osborn, K. A. Aadams, M. C. Conner, W. M. Ford, K. V. Miller. 2009. Excursive Behaviors by Female White-tailed Deer During Estrus at two Mid-Atlantic Sites. Am. Mid. Nat. 163:366-373.
- Magel, S. B., M. S. Samuel, T. R. Van Deelen, S. J. Robinson, N. E. Mathews. 2013. Evaluating Spatial Overlap and Relatedness of White-tailed Deer in a Chronic Wasting Disease Management Zone. PLoS ONE 8: e56568. doi:10.1371/journal.pone.0056568
- Mathiason, C. K., J. G. Powers, S. J. Dahmes, D. A Osborn, K. V. Miller, R. Warren, G. L. Mason, S. A. Hays, J. Hayes-Klug, D. M. Seelig, M. A. Wild, L. L. Wolfe, T. R. Spraker, M. W. Miller, C. J. Sigurdson, G. C. Telling, E. A. Hoover. 2006. Infectious Prions in the Saliva and Blood of Deer with Chronic Wasting Disease. Science. 314:133-136.
- Mathiason, C. K., S. A. Hayes, J. Powers, J. Hayes-Klug, J. Langenberg, S. J. Dahmes, D. A. Osborn, K. V. Miller, R. J. Warren, G. L. Mason, E. A. Hoover. 2009. Infectious Prions in Pre-Clinical Deer and Transmission of Chronic Wasting Disease Solely by Environmental Exposure. PLosOne 4: e5916. doi:10.1371/journal.pone.0005916
- McCoy, J. E., D. G. Hewitt. F. C. Bryant. 2005. Dispersal by yearling Male White-tailed Deer and Implications for Management. Journal of Wildlife Management. 69:366-376.
- Miller, M. W., H. M. Swanson, L. L. Wolfe, F. G. Quartarone, S. L. Huwer, C. H. Southwick, P. M. Lukacs. 2008. Lion and Prions and Deer Demise. PLoS ONE 3: e4019. doi:10.1371/journal.pone.0004019
- Miller, B. F., R. W. Deyoung, T. A. Campbell, B. R. Laseter, W. M. Ford. 2010. Fine Scale Genetic and Social Structuring in a Central Appalachian White-tailed Deer Herd. USDA National Wildlife Research Center – Staff Publications. Paper 964.
- Plummer, I. H., S. D. Wright, C. D. Johnson, J. A. Pedersen, M. D. Samuel. 2017. Temporal Patterns of Chronic Wasting Disease Prion Excretion in Three Cervid Species. Journal of General Virology. 98:1932-1942.
- Plummer, I. H., C. D. Johnson, A. R. Chesney, J. A. Pedersen, M. D. Samuel. 2018. Mineral Licks as Environmental Reservoirs of Chronic Wasting Disease Prions. PLoS ONE 13(5): e0196745. https://doi.org/10.1371/journal.pone.0196745
- Pritzkow, S., R. Morales, F. Moda, U. Khan, G. C. Telling, E. Hoover, C. Soto. 2015. Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions. Cell Reports. 11:1168-1175
- Samuel, M. D., D. J. Storm. 2016. Chronic Wasting Disease in White-tailed Deer: Infection, Mortality, and Implications for Heterogeneous Transmission. Ecology. 97:3195-3205.
- Storm, D. J., M. D. Samuel, R. E. Rolley, P. Shelton, N. S. Keuler, B. J. Richards, and T. R. Van Deelen. 2013. Deer density and disease prevalence influence transmission of chronic wasting disease in white-tailed deer. Ecosphere 4:10. http://dx.doi.org/10.1890/ES12-00141.1
- Vaske, J. J. 2010. Lessons learned from Human Dimensions of Chronic Wasting Disease Research.” Human Dimensions of Wildlife. 15:165-179.
- Virginia Department of Game and Inland Fisheries. 2010 Virginia deer, bear, and turkey hunter survey. Richmond, Virginia.