Duration: 08/26/2018 to 09/30/2020

Administrative Advisor(s):

NIFA Reps:

Non-Technical Summary

Statement of Issues and Justification

The occurrence of chronic wasting disease (CWD) in North America poses a potential risk to the agricultural industry, outdoor recreation and human health. Evidence of primate and livestock susceptibility, environmental contamination, and the ability of plants to take up the disease agent threatens food safety for both humans and livestock. The disease also challenges the fiscal foundations of wildlife conservation as it threatens the financial cornerstone of fisheries and wildlife programs because sales of deer hunting licenses represent a large proportion of annual revenue for these programs. Emerging evidence is renewing concern that CWD may pose a risk to human health. 

Chronic wasting disease is a transmissible spongiform encephalopathy (TSE) that primarily infects North American cervids (Williams 2005). Other TSEs include Creutzfeldt-Jakob disease in humans, bovine spongiform encephalopathy (“mad cow” disease) in cattle, and scrapie in sheep and goats. The infectious agent of CWD is referred to as a prion and is a misfolded form of the normally benign prion protein. Misfolded prion protein accumulates in the brainstem and lymphatic tissue of infected animals and results in neurodegeneration and eventual death. In states where CWD is established it has emerged as a major threat, reducing the health of deer populations and causing long-term population decline (Edmunds et al. 2016, Gross and Miller 2001, Manjerovic et al. 2014). There is no documented risk to humans, but the Centers for Disease Control and Prevention advises hunters not to consume meat of infected deer because CWD is closely related to bovine spongiform encephalopathy, which is fatal to humans (CDC 2017). Interim results from ongoing, and as yet unpublished, suggest that macaques can become infected after consuming meat from CWD-infected animals (Czub et al. 2017). Macaques are the non-human primate evolutionarily closest to humans that have been tested for susceptibility to CWD infection. We note that studies conducted by others using different dosing regimes have not found evidence of transmission of CWD to macaques (Race et al. 2018). 

Chronic wasting disease is transmitted directly through animal contact and indirectly through contact with contaminated environments (Miller et al. 2004). Infectious deer shed prions through bodily fluids and excreta (Miller et al. 2004, Mathiason et al. 2006, Safar et al. 2008, Haley et al. 2009), and human-facilitated movement of infected live deer or carcasses also contributes to the geographic spread of CWD. Shed prions persist in the environment and remain infectious for numerous years (Miller et al. 2004, Georgsson et al. 2006, Seidel et al. 2007). Prions are nonobligatory pathogens that are remarkably resistant to most inactivation procedures that are effective against conventional infectious agents (e.g., many chemical disinfectants, autoclaving under conventional conductions, ionizing radiation, desiccation; Colby and Prusiner 2011). Some treatments are effective, at least in laboratory settings (e.g., concentrated hypochlorous acid or sodium hydroxide, peroxymonosulfate; Taylor 1999, Chesney et al. 2016). There is no cure for CWD (Smith et al. 2011, Xu et al. 2013), and vaccine development has proven difficult because the misfolded form of host-derived prion protein is not identified by the adaptive immune system as foreign (Goni et al. 2015). Deer are infectious before they show any outward signs of CWD (e.g., emaciation, disorientation, fearlessness, paralysis; Henderson et al. 2015). Therefore, diseased deer must be removed from the environment well before clinical disease signs are exhibited. 

Although research has been conducted on CWD for multiple decades, many unknowns remain. For example, transmission rates and mode (i.e., frequency- versus density-dependence transmission) for CWD have not been determined (Almberg et al. 2011).  Epidemiological models specific to CWD and deer in highly productive habitats of the Midwest and Northeast are in early stages (Williams et al. 2014). While there is no known immunity, susceptibility to the disease depends on Prnp genotype (Johnson et al. 2006). Prion shedding by deer is poorly understood; shedding rate, time, and amounts need to be clarified. Only the first steps have been taken towards understanding sites on the landscape where environmental transmission may occur (Plummer et al. 2018). Assay techniques to detect prions are improving but there is no rapid, inexpensive diagnostic test for live animals or environments (Haley and Richt 2017). These fundamental gaps in knowledge have limited the ability of natural resource managers to effectively control the disease. The potential risks associated with CWD and all of the uncertainties about those risks have created deep concern for economic implications (Bishop 2004, Seidl and Koontz 2004).

Possible basis for forming a Multistate Research Project: Research across multiple disciplines is needed to fully address the complexities of CWD and acquire the knowledge needed to limit or eliminate its spread. Research programs are emerging and maturing at multiple universities and government agencies. These are developing in parallel with little coordination. For example, within institutions of higher education located in the Midwest alone, three large studies have been initiated within the last two years to investigate the role of movement behavior in shaping epidemiological models of CWD. Our intent is to form a multistate consortium designed to improve information exchange among universities and researchers with common goals, but different backgrounds and knowledge bases. Increased collaboration would improve research quality and avoid duplication of work at a critical time when effective solutions are needed quickly. Potential members of the proposed Multistate Research Project are listed below.

Potential duplication of efforts in existing committees: We found no active projects related to chronic wasting disease in the NIMSS database. There is no indication that the proposed consortium will duplicate the effort of any existing committee. 

Potential members of the proposed Multistate Research Project

Case Western Reserve University (Wen-Quan Zou, Chingzhong Kong)

Colorado State University (Ed Hoover, Davin Henderson, Glen Telling, Mark Zabel, N. Thompson Hobbs)

Creighton University (Jason Bartz, Anthony Kincaid)

Iowa State University (Julie Blanchong)

Michigan State University (William Porter, Sonja Christensen)

National Institutes of Health, Rocky Mountain Laboratories (Byron Caughey)

Pennsylvania State University (Duane Diefenbach, David Walter)

USDA-APHIS, Ft. Collins, CO (Tracy Nichols)

USDA-ARS, Ames, IA (Eric Nicholson)

University of Alberta (Judd M. Aiken, Debbie McKenzie)

University of Calgary (Herman Schätzl)

University of Georgia (Mark Ruder, John Fischer, Gino D’Angelo)

University of Illinois Urbana Champaign (Michelle Green, Jan Novakofski)

University of Maryland (Ilia Baskakov)

University of Texas Health Science Center (Rodrigo Morales, Claudio Soto)

University of Wisconsin – Madison (Joel A. Pedersen, Alison Ketz)

Objectives

Procedures and Activities

Expected Outcomes and Impacts

Projected Participation

View Appendix E: Participation

Educational Plan

Organization/Governance

Literature Cited

Attachments

Land Grant Participating States/Institutions

AR, IA, MI, MN, MO, MS, NY, TN, WI

Non Land Grant Participating States/Institutions

Case Western Reserve University, Iowa State University, Johns Hopkins University, University of Minnesota, USDA-ARS/Iowa, USGS