The Science Behind CWD Management
Why Manage CWD?
Chronic Wasting Disease (CWD) has the potential to negatively impact deer herds wherever the disease occurs. CWD is always fatal and while there have only been 13 cases detected in Virginia, as of February 2016, CWD 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). If a large percentage of the population were to become infected there could be negative impacts for the population, including:
- A decline in doe survival, which results in an overall reduced population (Gross and Miller 2001);
- Fewer older bucks, as male animals may be more likely to be infected due to specific male social and behavioral tendencies (Miller et al. 2008, Jennelle et al. 2014); and
- An overall decline in population (Gross and Miller 2001, Almberg et al. 2011), as exhibited in Colorado and Wyoming.
- In an area of Colorado with high CWD prevalence, mule deer numbers have plummeted by 45%, in spite of good habitat and protection from human hunting (Miller et al. 2008).
- In Wyoming a monitored infected population experienced a 10.4% annual decline, with CWD-positive animals having a higher mortality rate than non-infected deer (Edmunds et al 2016).
DGIF is concerned about the impact CWD could have on Virginia’s deer herd; once CWD has become well 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). They can persist for years outside the body, in soil and in other substances, can be taken up by grass roots from contaminated soil, and can be transmitted by animals that are not yet showing symptoms of the disease (Miller et al. 2004, Mathiason et al. 2009, Pritzkow et al. 2015). 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 behavior make tracking the spread of CWD different between does and bucks and between younger and older adults.
- Bucks are more likely to become infected, for reasons that are not well understood (Grear et al. 2006, Miller et al. 2008, Jennelle et al. 2014).
- Higher CWD prevalence is found in older age classes of bucks (Grear et al 2006).
- Adult bucks make long excursions outside their home range, bringing them into contact with a wider area and more individual deer (Karns 2011).
- Young bucks are more likely to disperse from their mother’s home range and can cover many kilometers, thereby potentially spreading the disease across the landscape (McCoy et al. 2005).
- Young bucks infected with CWD may not be indicative of established CWD presence at the location they were killed because the buck may have been traveling.
- Does are relatively sedentary, usually spending their lives near their place of birth and with a related social group. Does only rarely make excursions (Kolodzinski et al. 2009, Miller et al. 2010, Grear et al. 2010).
- Locations where infected does are found are likely to be a source of further infected deer (Grear et al. 2010, Magel et al. 2013).
- An infected doe suggests that CWD is established in the population where that doe was killed (Grear et al. 2010, Magel et al. 2013).
Of Virginia’s thirteen infected deer (as of February 2016), just four were does. Of the nine infected bucks, seven were harvested within just a few miles of the does, suggesting a small cluster of infection. The last two bucks were killed several miles from the cluster. The fact that these two outliers were young bucks makes it likely, though not certain, that these individuals were on the move, dispersing from their birth places.
Due to the nature of the prions which cause CWD (please see the What Are Prions page for more information), treatment of diseased animals is not an option. Research suggests that there is some hope of managing CWD, and that the best methods available are:
- Decreasing transmission opportunity by:
- Lowering the density of the deer population
- A lower density population surrounding a location of known infection reduces the chances of deer picking up CWD prions from the environment, or from each other. Research indicates that indirect transmission is just as important as animal-to-animal transmission (Storm et al. 2013).
- Population reduction could 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, from which one could infer that deer near CWD-positive deer are more likely to be infected (Joly et al. 2003.)
- Earn-a-Buck, currently in effect in Frederick, Warren, and Clarke Counties (the cluster of infected deer is located in Frederick County), is designed to reduce the overall deer population by focusing more hunting pressure on the female segment of the population.
- Banning feeding or baiting of deer in areas with CWD
- CWD prions can be found saliva (Mathiason et al. 2009), and feed or bait piles are excellent modalities to transfer saliva between deer.
- Feed and bite piles also artificially congregate deer, thereby facilitating transmission through urine and feces.
- Lowering the density of the deer population
- Prevent the introduction of CWD prions into new areas:
- VDGIF prohibits the movement of deer carcasses out of the CWD Containment Area until after they have been processed according to guidelines described in Transporting Carcasses Within and Out of the Containment Area.
- VDGIF prohibits the transport of carcasses from states/provinces listed as CWD Carcass Restriction Zones into Virginia unless they have already been processed according to these guidelines.
- VDGIF prohibits the possession and use of attractants made from real deer urine or other natural body fluids from deer while afield.
- 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 live animal test for CWD that is approved by the USDA, therefore deer farms producing and bottling urine cannot guarantee that they are collecting urine from healthy animals.
- There is no economically viable way to test urine for CWD after collection.
Doing nothing to manage CWD is not a satisfactory option, as 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, (a) testing harvested animals for CWD and using hunters to reduce herds in CWD areas were acceptable strategies, (b) agencies taking no action and allowing CWD to take its natural course were considered unacceptable, and (c) using agency staff to reduce herds in CWD areas was controversial. Hunters also generally supported efforts to minimize spread of CWD and eliminate the disease from animal herds (Vaske 2010). A VDGIF survey conducted following the discovery of CWD in Frederick County in 2009 concluded that respondents supported five 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 (VDGIF 2010, unpublished data). Respondents did not support the use of sharpshooting to reduce localized deer populations (42% opposed, 36% supported, 22% were neutral), but the strongest opposition was recorded for the option that described a complete lack of effort or attempt to manage CWD (79 % opposed, 8% supported).
- 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
- 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.
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- 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. J. 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.
- 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.
- VDGIF. 2010. 2010 Virginia deer, bear, and turkey hunter survey. Richmond, VA.