Chronic Wasting Disease: Anthropogenic? Containable?

CHRONIC WASTING DISEASE: ANTHROPOGENIC? CONTAINABLE? From AHVMA Journal • Volume 59 Summer 2020 p. 16-18 Michael W. Fox BVetMed, PhD, DSc, MRCVS

Chronic wasting Disease (CWD) in cervids has been confirmed in at least 26 U.S. states, three Canadian provinces, South Korea, Finland, Norway, and Sweden, with a notable increase in the past 5 years.

Predator “control” and other wildlife management practices may have contributed to this increase. Coupled with human and livestock encroachment in ever-increasing numbers, dysbiosis and climate change have intensified from continent to continent.(1)

Correcting such anthropogenic health problems with vaccines, pesticides, antibiotics and other drugs, even genetic engineering biotechnologies, while ignoring preventive measures, have limited medical and veterinary progress for decades.(2).Such limitations have failed to prevent the spread of tick-borne zoonoses such as Lyme disease, and the emergence of Chronic Wasting Disease in N. America where there is sub-optimal biodiversity and lack of predators in the dystrophic ecosystems (3).

According to the U.S. Government’s Centers for Disease Control and Prevention Chronic Wasting Disease (CWD) was first identified in captive mule deer in the late 1960s in Colorado and in wild deer in 1981. By the 1990s, it had been reported in surrounding areas in northern Colorado and southern Wyoming. Since 2000, the area known to be affected by CWD in free-ranging animals has increased to at least 26 states, including states in the Midwest, Southwest, and limited areas on the East Coast. It is possible that CWD may also occur in other states without strong animal surveillance systems. Once CWD is established in an area, prions can remain for a long time in the environment. The affected areas are likely to continue to expand. (4).

Late symptoms of CWD in cervids (deer, elk, moose, caribou, reindeer and big horn sheep) are clearly neurological. Infected animals often tremble on splayed legs and have trouble standing. They drool and eat continuously but continually waste away. Many are hyper- excitable and nervous. Researchers call them “droopy droolers.”

CWD is not unlike Scrapie, a prion disease of sheep that is also naturally transmissible, while Bovine Spongiform Encephalopathy, (BSE) also caused by prions, is a transmissible zoonotic disease. BSE was spread by putting cattle remains including prion-loaded brain and spinal cord tissues into cattle feed that decimated the U.K’s cattle industry and infected people consuming contaminated meat who developed Creutzfeldt–Jakob disease. Some primate species fed CWD infected deer meat were found to develop spongiform encephalopathy brain lesions, (5) raising the legitimate issue of cross-species infection from deer and other infected cervids to human consumers.

The possibility of spread to livestock from infective deer, soil and vegetation (that could have been the original source of cervid infection decades ago) is also considerable (6).But such a possibility, without a mutation in the CWD prion, is considered unlikely (7).

Prions are self-replicating protein molecules that are present in humans and other animals, their functions being not yet fully determined beyond playing some role in normalizing neuron function. Generally speaking, prion diseases may be infectious, hereditary or occur sporadically/spontaneously. Disease arises when the normal prion protein mutates to the diseased variant, which differs from the healthy prion proteins by its change in structure. The body’s cells have difficulty in breaking down this prion protein due to its different structure, and it therefore accumulates.

What causes prions to become malformed like a mutation, has not yet been determined. Prions can be passed out in bodily fluids and are in the soil and vegetation and are resistant to conventional methods of sterilization. Mosquitoes, ticks and other insects feeding off infected cervids may spread CWD. Infective prions have been found in dust and may be spread also by wind currents. ( 8).

Practices that may facilitate CWD prion contamination and accumulation include deer and elk farming, mineral licks and planting feed for deer by private land-owning deer hunters. Normal prions can be affected by metals (9), possibly being damaged by hunters’ lead shot when ingested by deer or in their bodies after surviving after being shot. Twenty million metric tons of lead bullets were fired in the United States in the 20th century (10).

Since EMFs can damage yeast prions, (11) the electromagnetic fields and non-ionizing radiation from cell phone towers and power lines may also cause prion malformations. Also, widely used herbicides, Monsanto’s “Roundup” (glyphosate) in particular, may play a role in the genesis of spongiform encephalopathies. It is widely used in agriculture and in forest management to reduce vegetation for fire-prevention. Glyphosate chelates all cations, making them biologically unavailable, (12).

An oxide of manganese destroys prions (13). Manganese deficiency in soils, via chelation of manganese by glyphosate, may therefore serve to increase the viability and longevity of prions that cause diseases such as CWD {and other spongiform encephalopathies} in the soil. In sum, soil type and especially mineral and humus content affect the nutritive value of vegetation and therefore the health of cervids consuming same. Notably, various prions are destroyed in soils with high humic acid content (14). Prions bind to montmorillonite and whole soils, remain orally infectious, and, in most cases, increased the oral transmission of disease compared to the unbound agent. Certain soils may therefore contribute to environmental spread of CWD by increasing the transmissibility of small amounts of infectious agent in the environment. (15).

Wolves, Mountain lions, Grizzly bears, Lynx and Coyote packs, probably immune after generations of co-evolution, could help control this disease by killing diseased cervids. These apex predators have been persecuted and exterminated for many decades. Their protection and reintroduction across states and provinces where CWD has been found would help reduce this epidemic (16, 17) and best serve the public interest, and also with Lyme and other tick-borne disease mitigation (18). Restoration and maintenance of healthy biodiversity calls for protection of predators large and small (19) especially from being killed by hunters, trappers, State wildlife “game” management for deer and elk hunters and by the livestock industry.

CWD is not going to go away and is most likely a product of over-stocking of selected cervids for hunters coupled with centuries of land uses causing ecological damage, reducing natural disease-controls of optimal biodiversity (20). Practices that facilitate CWD prion contamination and accumulation include deer and elk farming, interstate transportation of infected cervids, mineral licks and planting feed for deer on private land and hunting preserves all need to be curtailed.

According to the Coloradoan newspaper (21) veterinarian Dr. Mike Miller, Colorado Parks and Wildlife’s Wildlife Health Program Leader said “the best hope now is managing the disease so it doesn’t kill deer and elk in such large numbers that herds are reduced to sizes too low to allow hunting.” But in my opinion extensive degradation of wildlands coupled with wildlife management practices have contributed to the spread of insect-borne diseases such as Lyme and West Nile, and to Chronic Wasting Disease in deer, moose and elk now all spreading across much of the U.S. and in Canada along with other zoonotic and “emergent” diseases ( 22). Selective culling of CWD infected and exposed animals in contaminated areas and investing in vaccine development may not suffice without effective protection of large predators and restoration and recovery of disease-containing and suppressing biodiversity. ********************************** The Coloradoan published the following timeline of the spread from what some believe to be the epicenter at Colorado State University’s Foothills Campus outside Fort Collins because research was also going on with sheep infected with a similar prion disease called Scrapie, and had been in the same pen as the research-held mule deer who developed CWD. The infective prions might or might not have crossed the species barrier. The mule deer could have already been infected before they were brought to the facility from various parts of Colorado.

Chronic wasting disease timeline

1967: Wasting syndrome is observed in captive mule deer at the Colorado State University wildlife research facility in west Fort Collins. 1975−81: Wasting syndrome is observed in Toronto Zoo mule deer transferred from the Denver Zoo. 1979: Recognized in captive mule deer at Wyoming wildlife research facility. 1981: Detected in wild elk in Colorado. 1985: Detected in wild mule deer in Colorado and Wyoming. 1996: Detected in a captive elk farm in Saskatchewan; 38 other linked farms eventually found positive. 1997: Detected in captive elk facilities in South Dakota. 1998: Detected in captive elk facilities in Montana and Oklahoma. 1999: World Health Organization indicates no evidence CWD is transmissible to humans, but advises that exposure should be avoided. 2000: Detected in wild mule deer in Nebraska and Saskatchewan. 2002: Colorado establishes guidelines to minimize transport of high-risk carcass materials. First International CWD Symposium is held in Denver. 2002: Detected in captive elk in Minnesota, wild and captive white-tailed deer in Wisconsin and Illinois, mule deer in New Mexico and elk in South Dakota. 2003: Detected in wild mule deer in Utah. 2004: Detected in wild elk in New Mexico. 2005: Detected in moose in Colorado. 2008: Research indicates CWD may be a plausible explanation for local deer population declines in Colorado. 2010: Detected in captive white-tailed deer in Missouri and wild white-tailed deer in North Dakota and Virginia. 2016: Detected in wild elk and white-tailed deer in Arkansas and wild reindeer in Norway.


In an up-date, “CWD spreading, sometimes long before discovery” in the Journal of the American Veterinary Medical Association ( Vol 286, p 747-748, 2008) half of all adult deer killed by hunters in southern Wisconsin where infected with CWD and 30% of all adult females. Efforts to control the disease in infected herds by culling were blocked in some states by political opposition. Since CWD prions can persist in top soil for several years, this cervid plague has now become endemic and the question if and when humans become infected remains open.

Can wolves guard Yellowstone’s gates against CWD?

Preliminary results of a study in Yellowstone National Park suggest that the park’s wolf packs are helping prevent chronic wasting disease outbreaks in wild deer and other cervids by killing sick animals before they spread the prions that cause CWD, says study leader Ellen Brandell, a doctoral student in wildlife ecology at Pennsylvania State University. Natural predation probably won’t make a difference where CWD is already endemic, but predators could prevent it from establishing itself elsewhere, Brandell says. Full Story: The New York Times (tiered subscription model) (1113)

10 deer at Minn. farm had CWD The National Veterinary Services Laboratories found chronic wasting disease in five does and four bucks from a Houston County, Minn., white-tailed deer farm that was depopulated when CWD was found in another deer in October. The farm had been double-fenced since 2017 and the owner was in compliance with regulations, which shows how difficult it is to detect and control CWD, says Minnesota Board of Animal Health Assistant Director Linda Glaser. Full Story: KSTP-TV (Minneapolis) (2/22/2021)

References 1. Khasnis A.A, Nettleman M.D. Global warming and infectious disease. Arch. Med. Res.2005; 36: 689–96 2. Fox M.W. The One Health: Human Disease, Veterinary Responsibilities and Our Animal and Environmental Relationships. J Am Holist Vet Med Assoc. 2018;53:26-31. 3. Levi T., Kilpatrick, A. M., Mangel, M. and Wilmers, C.C. Deer, predators, and the emergence of Lyme disease Proc Natl Acad Sci U S A. 2012 Jul 3; 109(27): 10942–10947. 4. For more details visit 5., Race, B., Meade-White, K.D., Phillips, K., et al Chronic Wasting Disease Agents in Nonhuman Primates . Emerg Infect Dis 2014 May; 20(5): 833–837. doi: 10.3201/eid2005.130778 6. Osterholm M.T., Anderson, C.J.. Zabel,,M.D., et al Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species American Society for Microbiology Journal. 2019.DOI: 10.1128/mBio.01091-19 7. Williams E. S., O’Toole, D. Miller, M.W. Kreeger, T.J., and Jewell, T.J., Cattle (Bos Taurus) resist Chronic Wasting Disease following oral inoculation challenge or ten years natural exposure in contaminated environments. 2018. Journal of Wildlife Diseases 54 (3) 460-470”. 8. Zabel, M and Aimee Ortega, A. The Ecology of Prions. Microbiology and Molecular Biology Reviews May 2017, 81 (3) e00001-17; DOI: 10.1128/MMBR.00001-17 9. Singh N, Das D, Singh A, Mohan ML. Prion Protein and Metal Interaction: Physiological and Pathological Implications. In Tatzelt J.2010 The Prion Protein. Savanna Press. ISBN 978-0954333522. 10. Virginia Tech. “Do Lead Bullets Continue To Be A Hazard After They Land?”. ScienceDaily, 5 November 2004. . 11. Lian H.Y., Lin, K-W., Yang, C and Cai, P. Generation and propagation of yeast prion [URE3] are elevated under electromagnetic field. Cell Stress Chaperones. 2018 Jul;23(4):581-594. doi: 10.1007/s12192-017-0867-9. Epub 2017 Dec 6 12. Mertens M., Hoss, S., Neumann, G., Afzal, J and Reichenbecher, W. Glyphosate, a chelating agent—relevant for ecological risk assessment? Environ Sci Pollut Res Int. 2018; 25(6): 5298–5317. 13. Russo F., Johnson C.J, McKenzie D, Aiken J.M, Pedersen J.A. Pathogenic Prion Protein Is Degraded by a Manganese Oxide Mineral Found in Soils Journal of General Virology 2009 90(Pt 1):275-80 14. Kuznetsova A., Cullingham, C., McKenzie, D and Aiken, J.M. Soil humic acids degrade CWD prions and reduce infectivity PLoS Pathog. 2018 Nov. 29, 15.. Johnson C.J. Pedersen, J.A., Chappell, R,J., McKenzie, D. and Aiken, J.M., Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles PLoS Pathog. 2007 Jul; 3(7): e93.Published online 2007 Jul 6. doi: 10.1371/journal.ppat.0030093 16. Krumm C.E., Conner M.M, Hobbs N.T, Hunter D.O, and Miller M.W. Mountain lions prey selectively on prion-infected mule deer. Biol Lett. 2010 Apr 23;6(2):209-11. doi: 10.1098/rsbl.2009.0742. Epub 2009 Oct 28. 17. Hobbs N. T., A Model Analysis of Effects of Wolf Predation on Prevalence of Chronic Wasting Disease in Elk Populations of Rocky Mountain National Park 4/12/2006 18.Hofmeester T.R., Jansen, P.A., Hendrikus al Cascading effects of predator activity on tick-borne disease risk. Proc. R. Soc. B 2017 284: 20170453. 19.Farnsworth M..L.,Wolfe,,L.L., Hobbs, N.T., et al Human Land Use Influences Chronic Wasting Disease Prevalence in Mule Deer. Ecological Applications 2005 15: 119–126. 20. Wild, M. A., Hobbs N.T, Graham M.S, and Miller M.W. The Role of Predation in Disease Control: A Comparison of Selective and Nonselective Removal on Prion Disease Dynamics in Deer. Journal of Wildlife Diseases 2011 47(1):78–93. 21. Blumhardt, M. Chronic wasting disease linked to Fort Collins for 50 years. Fort Collins Coloradoan, August 23, 2018. 22. Fox M.W. The One Health: Human Disease, Veterinary Responsibilities and Our Animal and Environmental Relationships. J Am Holist Vet Med Assoc. 2018;53:26-31