Chronic Wasting Disease: Anthropogenic? Containable?

March 3, 2019
By: 
By Michael W. Fox BVetMed, PhD, DSc, MRCVS

From the perspective of One Health (1) dysfunctional ecosystems with wild animal and plant species imbalances and sub-optimal regulatory biodiversity (2) can put public health and the health of domestic animals at risk (3). Predator “control” and other wildlife management practices, coupled with human and livestock encroachment in ever-increasing numbers, have intensified dysbiosis and climate change from continent to continent.(4) 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.(5).Such limitations have failed to prevent the spread of zoonoses such as Lyme disease, and the emergence of Chronic Wasting Disease in N. America in particular where there is sub-optimal biodiversity and lack of predators ( 6) and insectivores in the dystrophic ecosystems.  

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 24 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, the risk can remain for a long time in the environment. The affected areas are likely to continue to expand. (7). Late symptoms of CWD in cervids (deer, elk, moose and big horn sheep) are horrific. 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.” Deer farms may be a major source of this disease, once a rare disease of Colorado mule deer.

It is not unlike the Mad Cow disease which 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. “It is probable that human cases of CWD associated with the consumption of contaminated meat will be documented in the years ahead,” Michael Osterholm, director of the University of Minnesota’s Center for Infectious Disease and Research Prevention, warned lawmakers at the Minnesota Capitol Feb 7, 2019. Some primate species fed CWD infected deer meat were found to develop spongioform encepalopathy brain lesions, (8) raising the legitimate fear 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.

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 them to become malformed like a mutation, has not yet been determined. They are passed out in bodily fluids and are in the soil and vegetation and are resistant to conventional methods of sterilization. Crows and ravens, being carrion-eaters, could spread CWD along with blood sucking mosquitoes, ticks and other insects feeding off infected cervids. Infective prions have been found in dust and may be spread also by wind currents.  

Practices that 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 cause prion damage (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, which is a chelating agent (12), may damage prions (13) and influence the bioavailability of manganese (14), an oxide of which destroys prions (15). This could facilitate prion survival and multiplication in contaminated soils. Notably, various prions are destroyed in soils with high humic acid content (16). 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. (17). Livestock feed high in manganese and soils high in manganese and low in copper and zinc, along with other environmental have been proposed as potential factors in the genesis of bovine encephalopathy and related CJ disease in humans (18)

Wolves, Mountain lions, Grizzly bears 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 centuries. Their protection and reintroduction across states and provinces where CWD has been found would help reduce this epidemic (19, 20) and best serve the public interest, and also with Lyme disease mitigation (21). CWD is not going to go away and is most likely a product of centuries of land uses causing ecological damage, reducing natural disease-controls of optimal biodiversity (22). Practices that facilitate CWD prion contamination and accumulation include deer and elk farming, mineral licks and planting feed for deer on private land and hunting preserves all need to be curtailed. Restoration and maintenance of healthy biodiversity calls for protection of predators large and small (23) especially from being killed by hunters, trappers, State wildlife “game” management for deer and elk hunters and by the non-sustainable livestock industry.

According to the Coloradoan newspaper (24) 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 as a veterinarian, extensive degradation of wildlands coupled with ecological mismanagement 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 ( 25). Drastic culling of CWD infected and exposed animals in contaminated areas and investing in vaccine development go in the wrong direction. The open season and no-license needed in Minnesota and other states to kill coyotes, weasels, skunks, other small mammals, carrion-eaters like crows, and seasonal killing of insectivorous “game” birds and hunting and trapping of “small game and furbearers”--- mink, pine marten, fisher, beaver, otter, bobcat, raccoon, red and grey fox, bear and badger---should all be closed to allow the recovery of disease-containing and suppressing biodiversity. It is recognized that pathogens generally become less virulent or are destroyed after passage through resistant hosts, ---adapted, immunocompetent species and individuals---and this may hold true as well for prions.

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The newspaper 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.

 

Postscript 2/25/19

Minn. lawmakers propose bills to better contain CWD

In Minnesota, the state animal health board quarantines captive cervid farms where chronic wasting disease is found, then the USDA usually buys and depopulates the herd, but farms are not required to sell to the USDA, says Minnesota Board of Animal Health veterinarian Mackenzie Reberg. An infected wild deer was found near a farm that had refused to depopulate, prompting state lawmakers to propose several bills aimed at strengthening CWD containment.

Minnesota Public Radio (2/22) 

References

1. See  www.onehealthinitiative.com and www.onehealthcommission.org )

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5. Fox, M.W., The One Health: Human Disease, Veterinary Responsibilities and Our Animal and Environmental Relationships. AHVMA Journal, 2018, 53: 26-31.

6. Levi, Taal, et al.  Deer, predators, and the emergence of Lyme disease  Proc Natl Acad Sci U S A. 2012 Jul 3; 109(27): 10942–10947.

7. For more details visit https://www.cdc.gov/prions/cwd/occurrence.html See also USGS. 2018. Distribution of Chronic Wasting Disease in North America. February 2018. https://www.usgs.gov/media/images/distribution-chronic-wasting-disease-north-america-february-2018.

 8. Race, Brent et al Chronic Wasting Disease Agents in Nonhuman Primates .    Emerg Infect Dis. 2014 May; 20(5): 833–837. doi: 10.3201/eid2005.130778

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. <www.sciencedaily.com/releases/2004/11/041104005801.htm>.

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15. Russo, F., et al Pathogenic Prion Protein Is Degraded by a Manganese Oxide Mineral Found in Soils Journal of General Virology 90(Pt 1):275-80 · January 2009

16. Kuznetsova,A. et al Soil humic acids degrade CWD prions and reduce infectivity PLoS Pathog. Nov. 29,2018 https://doi.org/10.1371/journal.ppat.1007414

17.. Johnson, C.J.  et al 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

18. Purdy https://www.ourcivilisation.com/madcow/index.htm ”Mad Cow” Disease by Mark Purdey, accessed March 1st 2019

19. Krumm CE, Conner MM, Hobbs NT, Hunter DO, Miller MW. 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.

20. 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

files.cfc.umt.edu/cesu/NPS/CSU/2005/Hobbs_wolf%20cwd%20report.pdf

21.Hofmeester TR, Jansen PA, Wijnen HJ, Coipan EC, Fonville M, Prins HHT, Sprong H, van Wieren SE. 2017 Cascading effects of predator activity on tick-borne disease risk. Proc. R. Soc. B 284: 20170453. http://dx.doi.org/10.1098/rspb.2017.0453

22.Farnsworth, M.L., L.L. Wolfe, N.T. Hobbs, K.P. Burnham, E.S. Williams, D.M Theobald, M.M. Conner, and M.W. Miller. 2005. Human Land Use Influences Chronic Wasting Disease Prevalence in Mule Deer. Ecological Applications 15: 119–126.

23. Wild, Margaret A., N. Thompson Hobbs, Mark S. Graham, and Michael 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(1):78–93.

24. https://www.coloradoan.com/story/news/2018/08/23/cdc-tse-mad-cow-chronic-wasting-disease-linked-fort-collins/878097002/

25. Fox, M.W., 2018. The One Health: Human Disease, Veterinary Responsibilities and Our Animal and Environmental Relationships. AHVMA Journal, 53: 26-31.