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From: Terry Singeltary <flounder9@verizon.net>
From: Terry Singeltary <flounder9@verizon.net>
To: william.barker@wisc.edu <william.barker@wisc.edu>; Timothy.Sullivan@usda.gov <Timothy.Sullivan@usda.gov>; robert.m.smith@usda.gov <robert.m.smith@usda.gov>; joelpedersen@wisc.edu <joelpedersen@wisc.edu>; chris625@msu.edu <chris625@msu.edu>
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Sent: Sun, Jan 3, 2021 3:33 pm
Subject: NC1209: North American interdisciplinary chronic wasting disease research consortium Singeltary Submission January 2021
Greetings NA Interdisciplinary CWD Research Consortium, Organizers, Scientist, Wildlife, and Government officials et al,
THANK YOU! THIS LOOKS EXCITING!
i have followed the mad cow follies every day since inception here in the USA and abroad since December of 1997. i lost my Mom to the Heidenhain Variant Creutzfeldt Jakob disease hvCJD sporadic/spontaneous strain. after they told me mad cow was not here not to worry, and at the same time watching my mom jerk so bad it took three grown adults to hold her down, while she was screaming what's wrong with me, why can't i stop this, and at the same time, at nights, watching Oprah on T.V. getting sued by cactus cattle here in Texas et al, and them saying it's not here, i just made a promise to Mom back then, never forget, and never let them forget. well, i tried. I wish to submit the following history and science to this Consortium on CWD...my submission will follow;
NC1209: North American interdisciplinary chronic wasting disease research consortium
Duration: 10/01/2020 to 09/30/2025
Administrative Advisor(s):
William Barker NIFA Reps:
Timothy Sullivan Robert Smith Statement of Issues and Justification Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE), or prion disease, of North American deer and elk (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. TSEs are inevitably fatal, progressive neurodegenerative diseases with long incubation periods and no known cure (Prusiner, 1982, 1998). Once believed to be isolated to the front range of the Rocky Mountains, since 2000 the known range of CWD has expanded dramatically to include 27 U.S. states, three Canadian provinces, Scandinavia, and South Korea. The range of the disease continues to expand, prevalence is increasing within endemic areas, and the disease has acquired new hosts (viz. moose and reindeer; Baeten et al. 2007, Benestad et al. 2016). In addition to affecting wild cervid populations, the occurrence of CWD in North America poses a potential risk to the agricultural industry, outdoor recreation, and human health. 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). Because the disease directly threatens North American cervid populations, it also challenges the fiscal foundations of wildlife conservation in the U.S. Sales of deer hunting licenses constitute a large proportion of annual revenue for conservation and management programs across taxa. Declines in these revenues due to CWD threatens the financial cornerstone of state fisheries and wildlife programs. Transmission to humans has not been documented, but the Centers for Disease Control and Prevention advises hunters to not consume the meat of infected animals because CWD is closely related to bovine spongiform encephalopathy, which has transmitted to humans and caused fatal human prion disease (CDC 2017). Uncertainties about human and livestock susceptibility, environmental contamination, and the ability of plants to accumulate the disease agent raise food and feed safety concerns (Hamir et al., 2011; Moore et al., 2017; Race et al 2009; 2018; Marsh et al., 2005; Pritzkow et al., 2015). Finally, emerging evidence is renewing concern that CWD may pose a risk to human health, and even perceptions that humans may become infected will have dramatic ecological and social consequences.
The infectious agent of CWD is a prion, an infectious, misfolded form of the normally benign prion protein. Misfolded prion protein accumulates in the brainstem and lymphatic tissue of infected animals, and to a lesser extent in muscle and other tissues (Sigurdson et al. 2002, Angers et al. 2006, Henderson et al. 2015a, Spraker et al. 2015, Davenport et al. 2018). The disease propagates via a process in which infectious, misfolded forms of the protein template the conformational conversion of the normal, benign form of the protein into the abnormal, disease-associated form (Prusiner, 1982;1998). This property of prions has been exploited to develop a variety of amplification assays that can be used to detect prions in tissues, secretions, excreta, and environmental samples (Haley et al. 2012, Henderson et al. 2015b, Pritzkow et al. 2015, Denkers et al. 2016, Henderson et al. 2017, Plummer et al. 2018).
Chronic wasting disease is transmitted directly through animal-to-animal contact and indirectly through contact with contaminated environments (Miller et al. 2004). Infected deer shed prions through secretions and excreta (Miller et al. 2004, Mathiason et al. 2006, Safar et al. 2008, Haley et al. 2009, Tamgüney et al. 2009), and human-facilitated movement of infected live deer or carcasses contributes to the geographic spread of CWD. Prion shedding by deer is poorly understood; shedding rate, time, and amounts need to be clarified. 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). Only the first steps have been taken towards understanding sites on the landscape where environmental transmission may occur (Plummer et al. 2018).
Prions shed into the environment remain infectious for years (Brown & Gajdusek. 1991, Miller et al. 2004, Georgsson et al. 2006, Seidel et al. 2007). Prions 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; Taylor 1999, Colby and Prusiner 2011). Some treatments are effective, at least in laboratory settings (e.g., concentrated hypochlorous acid, sodium hydroxide, peroxymonosulfate; Taylor 1999, Chesney et al. 2016, Williams et al. 2019). No cure exists 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 shed prions long before they manifest any outward signs of CWD (e.g., emaciation, disorientation, fearlessness, paralysis; Henderson et al. 2015). Therefore, reducing environmental contamination would benefit from detection and removal of diseased deer from the environment well before clinical disease signs are exhibited.
Benefit of a Multistate Effort. Chronic wasting disease is distributed widely in North America, affects multiple cervid species, and does not respect jurisdictional boundaries. Research across multiple disciplines is needed to fully address the complexities of CWD and acquire the knowledge needed to limit or eliminate its spread. A multistate CWD effort to coordinate research across jurisdictions would be beneficial for several reasons.
· The ecology of CWD is expected to differ across the regions and jurisdictions in which it occurs due to variation in species, climate, surficial geology, habitat, and land use.
· Host prion protein genotype (Prnp) distribution varies geographically. While no genotype is known to confer complete resistance to CWD, susceptibility to the disease depends on Prnp genotype (Johnson et al. 2006). Host Prnp genotype can affect management strategies.
· Prion strains vary geographically. Different strains of CWD exist and can be distinguished by the length of incubation period and Prnp polymorphism-dependent infectivity. Prion shedding into the environment by infected individuals may differ in magnitude or in dynamics by CWD strain (or host genotype). Strains may differ in their zoonotic potential and can affect management strategies.
· A multistate effort could facilitate the coordination of resources. Resources could include funding for joint research efforts, sources of negative control animals or tissues, a clearinghouse for reference samples, large-scale research facilities, and increased capacity through a human resource network.
· Jurisdictions impacted by CWD differ in their surveillance approaches. Standardization across jurisdictions would facilitate data sharing and increase epidemiological understanding of CWD dynamics.
· Jurisdictions impacted by CWD differ in their legal authorities to minimize spread and resulting policy or management responses. Multi-state research provides the opportunity to assess the effectiveness of different regulatory strategies.
· Disease management activities (or lack thereof) in one jurisdiction can affect the spread of the disease in another. Coordination across jurisdictional boundaries will improve the efficacy of disease surveillance and management and can enhance consistency and coordination between jurisdictions.
State and federal policies require public support and, frequently, funding for implementation. Given emerging research and perceptions around human health risk, as well as the growing footprint of CWD and CWD-related management, public health departments, natural resource agencies, and agricultural agencies are becoming increasingly involved with communication and public engagement regarding CWD. Understanding public attitudes, values, risk perceptions, and associated behavior will be critical for the development of socially accepted disease response strategies and effective strategies for addressing CWD. A multistate research project would facilitate sharing of data and resources, promote interdisciplinary collaboration among researchers and managers in different jurisdictions, and serve as a vehicle through which to communicate research and management priorities to national decision-makers. The multistate project would be 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. Research on and management of CWD across North America is fragmented and not coordinated leading to issues of data comparability, duplication of effort, and concerns about the validity of measurements. The proposed multistate project would directly address these issues and both accelerate and improve the quality of CWD research and management nationally.
National and Regional Priorities. On September 9 and 10, the NCDC234 Multistate Research Coordinating Committee and Information Exchange Group held a facilitated 2-day workshop at Michigan State University to define research priorities, develop a list of action items to facilitate and coordinate research across states, and discuss the formation of a Multistate Research Project focused on chronic wasting disease. The workshop brought together 46 researchers and wildlife managers from 14 universities, 7 state agencies, 3 federal agencies, 1 Canadian province, and 1 non-governmental organization to identify critical research priorities informed by the needs of state and provincial CWD managers. Participants included both disease managers and university researchers from states currently affected by CWD and were selected based on their expertise in basic prion biology, prion measurement techniques, surveillance for human prion diseases, deer ecology, soil science, quantitative ecology, disease ecology, genetics, and policy. The workshop generated much enthusiasm for a Multistate Research Project and resulted in the prioritization of research topics and several action plans.
We guided workshop participants through a structured strategic planning process to identify and flesh out research priorities and critical activities that would benefit research on and management of CWD in North America. We developed clear pathways forward for establishing a collaborative of scientists and managers with consensus around research topic areas of immediate need. We intend to build upon this successful workshop and assemble interdisciplinary teams of researchers and partner agencies to develop research proposals around these prioritized research areas. This coordination helps address a critical need for the formation of a CWD research consortium focused on conducting research across multiple disciplines and jurisdictions to address the challenges of CWD. The workshop participants built consensus around and developed the following five thematic areas:
1. Disease Transmission and Pathogenesis. Questions remain about indirect/environmental transmission of CWD prions and the persistence of prions in the environment. The structural basis for CWD prion strains is unknown. A multistate effort could help advance knowledge of CWD transmission and pathogenesis in several ways. Access to samples across regions would facilitate the characterization of strains and infectivity. A national CWD tissue and reagents bank could provide reference tissue samples to researchers across the nation to validate assays, improve comparability of inactivation studies. As the range of CWD expands, the acquisition of negative control samples is expected to become increasingly difficult. The multistate project could serve as a coordinating body for the distribution of verified negative control samples for researchers across the country. Cross-jurisdictional standardization of surveillance approaches and assays would facilitate data sharing.
2. Development of Large-scale Research Facilities. Workshop participants identified the need for facilities to conduct controlled CWD research at scales better approximating those relevant for free-ranging cervids. An opportunity exists for developing such research facilities using fenced (depopulated) deer facilities. Large-scale research facilities could be used for studies on the impact of population demographics on transmission, possible habitat management options,, and remediation of environmental contamination. A multistate project could help establish these facilities and once formed solicit research proposals for the use of such facilities to advance knowledge on CWD disease dynamics and management that would have a significant impact for all countries affected by CWD.
3. Improving Diagnostic Testing for CWD. Although assays to sensitively detect prions have improved rapidly in recent years, a rapid, inexpensive diagnostic test for live animals or environments does not exist or appear to be on the horizon, at least in the near to intermediate term (Haley and Richt. 2017). A transformative advance in the detection of prions has been the development of in vitro prion amplification assays, of which several variations have been developed. The most prominent are serial protein misfolding cyclic amplification (sPMCA) and real-time quaking-induced conversion (RT-QuIC). These assays may provide the needed foundation for advancing diagnostic testing of live animals and environments for presence of CWD prions. At present, RT-QuIC appears to be more suitable for adoption by federal and state agencies. Workshop participants identified a number of activities that could promote broader adoption of RT-QuIC and that a multistate effort could facilitate including coordination of provision of the recombinant prion protein substrate needed for the assay, providing training for laboratories wishing to adopt RT-QuIC, following up on trained personnel, certification of laboratories for diagnosis, and developing protocols for handling suspect samples.
4. Evaluating Management Strategies across State Boundaries. Workshop participants advocated for a multistate adaptive management approach. Although scientific approaches are used to inform management decisions, science is less commonly factored into the evaluation of the impacts of management actions. Topics of interest include evaluation of how hunting and CWD regulations impacts sex and age structure of the harvest and disease dynamics (prevalence vs. spread). Participants also identified the need for standardization of data, coordination of CWD surveillance efforts, and when possible combining data for cross-jurisdictional analysis of CWD harvest surveillance and research data to increase understanding of CWD epidemiology and effects of disease management actions. 5. Enhanced Coordination, Understanding, and Communication of Social Science as it relates to CWD Research and Management (Wildlife, Agriculture, Public Health, Science Communication). Collective understanding of heterogeneous social values, motivations, and attitudes is inadequate at present to evaluate and inform disease management decision-making at local, state, and regional levels. Additionally, effective, targeted, and consistent communication strategies are critical to gain and maintain public support for necessary management interventions. A multistate effort could serve as a central scientific advisory group; increase coordination of human dimensions research; and assist federal, state and local agencies in developing effective policies and strategies to slow CWD spread as well as consistent, scientifically accurate messaging. Workshop participants identified the need to bring social scientists and communication specialists into the consortium.
All of these research themes would rely on multiple disciplines and multiple states or provinces to address critical gaps in the current understanding and management of CWD. The workshop went beyond identifying priority research themes and began to formulate plans to address some of the critical needs that can be addressed in the next year or so. Workshop participants agreed to begin laying the groundwork for a national tissue clearinghouse and to facilitate access to the substrate for RT-QuIC to promote wider adoption of this sensitive prion detection method. Additionally, participants have begun to develop the framework for evaluating management strategies across state boundaries by building support for this effort among the directors of state wildlife agencies during the recent Association of Fish and Wildlife Agencies (AFWA) meeting. In summary, the workshop produced considerable enthusiasm and generated momentum toward achieving the identified research priorities. We think that this augurs well for the success of the multistate project we propose.
Contributions of the Participating Agricultural Experiment Stations. Ten agricultural experiment stations participated in our initial workshop and a further four indicated interest in future participation. The researchers associated with these stations bring a wide range expertise to address the proposed study objectives. We expect Colorado State University (co-lead), Pennsylvania State University (co-lead), Cornell University, and University of Wisconsin – Madison to contribute strongly to Objective 1 along with Michigan State University, University of Minnesota, and University of Missouri. Objective 2 would include Texas A & M (lead), Iowa State University, Mississippi State University, and University of Tennessee. The research team for Objective 3 would encompass Cornell University (co-lead), Colorado State University (co-lead), University of Wisconsin – Madison, University of Minnesota, and Mississippi State University. Objective 4 would include University of Wisconsin – Madison (lead), Michigan State University, Cornell University, the University of Arkansas, Iowa State University, Mississippi State University, and University of Tennessee. Finally, Objective 5 would draw on the expertise of University of Minnesota (lead), Michigan State University, University of Arkansas, Iowa State University, and Cornell University. Given the breadth of relevant expertise at Michigan State University, University of Minnesota, and University of Missouri we expect that researchers from these universities will participate in all five objectives. The breadth of experiment stations engaged in multistate research on CWD through our proposed collaborative effort reflects the current need for such research to meet the challenges of this disease.
Expected Outcomes and Impacts. Research across multiple disciplines is essential 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 around the Great Lakes region alone, four large studies in different states have been initiated within the last two years to investigate the role of movement behavior in shaping epidemiological models of CWD. Furthermore, disparate methods of surveillance for the disease (e.g., no sampling or only sampling hunter harvest) has resulted in new disease outbreaks being documented with prevalence levels that indicate the disease could have been present for many years. The proposed multistate consortium would improve the coordination of research efforts and exchange of information and materials among universities and researchers with common goals, but different backgrounds and knowledge bases. Increased collaboration would improve research quality by standardizing protocols, enabling and validating sensitive methods to measure CWD prions, permit modeling of CWD across jurisdictions leading to an improved understanding of CWD epidemiology, and avoid duplication of work at a critical time when effective solutions are needed quickly.
Progress will be tracked at the subcommittee meetings and at annual meetings for the entire multistate project. Annual multistate project meetings will include time allocated for developing objectives and routes to achieve them for the coming year. Subcommittees will be tasked with drafting proposed objectives and approaches ahead of annual multistate project meetings. Annual progress reports will represent formal evaluations of progress and result.
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.
Related, Current and Previous Work The workshop participants included representatives from many of the leading CWD research groups in North America. These groups have contributed substantially to current understanding of the mechanisms of CWD transmission, trafficking, and pathogenesis; characterization of species barriers and strains; transgenic mouse modeling of prion diseases; development of in vitro prion amplification assays to detect CWD prions in biological tissues, fluids, excreta, and environmental samples; investigation of the environmental behavior of CWD prions; investigation of the role of deer ecology and management; and development of prion disease therapeutics. The objectives outlined above represent the priorities developed by this group of researchers along with wildlife ecologists and those managing CWD at the state level. Below we outline the current status of work related to the proposed objectives.
Tissue database and repository. At present, individual laboratories maintain tissue samples from past studies and may use them as reference samples in their own work. The investment required to determining prion titers in reference samples is considerable. Sharing of reference samples between research groups is currently limited. The proposed multistate project would facilitate the provision of reference samples to the CWD prion research community.
Large-scale research facilities. Contaminated pens and paddocks have provided important insights into indirect, environmental transmission of sheep scrapie and CWD (e.g., Miller et al. 2004, Georgesson et al. 2006, Gough et al. 2019). Many of these studies were the result of so-called natural experiments. Across the country, breeding facilities, game farms, and other captive facilities have been shut down due to CWD. Questions surround the re-use of such contaminated facilities for commercial purposes because the longevity of CWD prion infectivity in such environments has not been defined and the efficacy of attempts to decontaminate such facilities is uncertain. The purchase of contaminated facilities by state agencies or others presents an opportunity to conduct coordinated research on CWD ecology at a scale relevant for management of deer populations.
Diagnostic testing for CWD. The detection limits, specificity, robustness, and speed of prion detection methods have improved dramatically (prion amplification methods) over the last decade and a half (Saá et al. 2006, Wilham et al. 2010, Haley et al. 2018, Escobar et al. 2019). Adoption of these methods outside of research settings has been limited by the need for trained personnel and for access to substrate for the amplification assays. The proposed multistate project would address both these needs.
Multistate adaptive management. Chronic wasting disease does not respect state or national boundaries. Currently, management efforts across the country are fragmented with little coordination across jurisdictions. Actions taken in one state can affect CWD disease dynamics in adjacent states. The proposed multistate project would facilitate communication among state wildlife managers and the development of regional management approaches.
Human dimensions research. As judged by publication rate, research in human dimensions of CWD management has progressed at a modest pace since 2000. As noted above, workshop participants deemed understanding of social values, motivations, and attitudes is inadequate at present to evaluate and inform disease management decision-making at multiple jurisdictional levels, and effective, targeted, and consistent communication strategies need to be developed to gain and maintain public support for necessary management interventions. Research in human dimensions of CWD management, including the link between communication approaches and acceptance of disease management responses, is needed to effectively design and implement management strategies. Stakeholder attitudes towards management interventions are expected to evolve with CWD epizootics and may differ in regions with no prior experience with the disease. Two efforts related to our proposed work on human dimensions with which we intend to connect are the National Socio-Environmental Synthesis Center (SESYNC) and concurrently proposed multi-state project led by the Center for Conservation Social Sciences of Cornell University (Bruce Lauber, PI). More detail about these efforts is provided under the methods for Objective 5.
Objectives Establish a national CWD tissue database and repository with improved access for transmission and pathogenesis research and validation of CWD prion detection assays. Develop large-scale research facilities for controlled CWD research using depopulated cervid facilities where CWD has been detected. Advance diagnostic testing for CWD with a focus on facilitating adoption of the RT-QuIC assay and improved sourcing for the recombinant prion protein substrate. Develop a multistate adaptive management approach for CWD to evaluate surveillance and management strategies and how deer harvest regulatory options impact deer disease dynamics. Evaluate heterogeneous social values, motivations, attitudes, and effective communication to inform disease management decision-making at local, state, and regional levels. Methods Objective 1. Establish a national CWD tissue database and repository with improved access for transmission and pathogenesis research and validation of CWD prion detection assays. To accomplish Objective 1, we will first establish a coordinating body that will define metadata standards, storage conditions, and procedures for vetting requests for materials. One of the outcomes of the workshop held in September 2019 was to take some initial steps towards the development of such a coordinating body. We envision the tissue and reagents bank to not be a single repository, but a clearinghouse to coordinate the provision of samples to researchers. The physical storage locations would be based on geographical proximity to sources of tissue, ideally in facilities that routinely perform CWD diagnostic services for states with high sample testing numbers. Samples will be stored at –80 °C, identified with a unique bar code that is linked to the metadata associated with the sample. A metadata gap analysis will be conducted prior to collecting and storing data. An oversight committee will be assembled which will be comprised of state and federal representatives, field biologists, basic scientists, and industry representatives as deemed appropriate. This committee will determine how samples are distributed and will develop a memorandum of understanding for how data, analyses, testing, and diagnostics will be used and any assignment of fees.
Objective 2. Develop large-scale research facilities for controlled CWD research using depopulated cervid facilities where CWD has been detected. We propose to establish CWD research sites in and around captive animal facilities where CWD has been detected. Facilities in several states would be suitable for this purpose, and collaboration among efforts in different states would be valuable to ensure efficient use of resources. Ideally, sites would have a history of holding CWD-positive deer on-site, and contain several paddocks (e.g., 1-acre paddocks surrounded by 8-ft high fences to limit deer movement), animal handling facilities, and pastures varying in size from a few to hundreds of acres.
The first step will be to assess the risks and benefits of using such facilities for research. The primary risk is the maintenance or amplification of CWD prions in the environment. Risks are expected to differ among sites and be determined in part by the current level of contamination in and around the potential research site. Benefits include providing research sites where management actions to reduce the spread and prevalence of the disease can be evaluated and refined. State and federal regulatory authorities will decide if such facilities will be permitted. If regulatory authorities permit the facility, scoping meetings with local landowners and officials would be held to seek support for the facility.
Assuming a facility was permitted and obtained local support, a stake-holder advisory group would be established to raise funds to purchase the facility (if necessary) and any surrounding land necessary to fulfil research objectives and ensure biosecurity. The stake-holder group would also raise funds to (1) make the facility and research pastures secure with double fencing of at least 8 feet high and (2) maintain the research facility once it is operational. Once these steps have been completed, title would be transferred to the agency, university, or non-governmental organization responsible for the research facility, personnel would be hired, and the facility would become operational. Funding for these projects would be sought from state and federal agencies, non-governmental organizations, and private sources. A research committee would be established with representatives from each of the state wildlife agencies where facilities are located, scientists with expertise in CWD research, and representatives from important stakeholder groups such as hunters, landowners, and the captive deer industry. Projects and funding would be evaluated and paired to make the best use of each research facility and available funding.
Objective 3. Advance diagnostic testing for CWD with a focus on facilitating adoption of the RT-QuIC assay and improved sourcing for the recombinant prion protein substrate. Efforts to manage CWD are hindered by the inability of commonly used methods to detect the low levels of prions that are relevant for disease transmission. The multistate project would facilitate the adoption of the highly sensitive RT-QuIC assay (Wilham et al. 2010) by academic laboratories and state and federal agencies. This would be accomplished by coordinating provision of the recombinant prion protein substrate needed for the assay, providing training for laboratories wishing to adopt RT-QuIC, following up on trained personnel, certification of laboratories for diagnosis, and developing protocols for handling suspect samples.
Objective 4. Develop a multistate adaptive management approach for CWD to evaluate surveillance and management strategies and how deer harvest regulatory options impact deer disease dynamics. One of the difficulties in managing CWD is that affected species range across jurisdictional boundaries; yet currently, communication or coordination among management agencies regarding CWD response is limited, and unified efforts to evaluate the effectiveness of the suite of management actions that agencies have applied for disease control are lacking. Objective 4 aims to fill these gaps by leveraging information maintained by state agencies to evaluate the impacts of CWD management activities on population and disease dynamics and establishing a framework to improve coordination and information exchange. This framework will serve as the basis for the development and implementation of an adaptive management strategy for controlling CWD among state and federal wildlife management agencies. Recognizing that harvest management is the main tool available for agencies to control both deer population sizes and CWD and that its application varies dramatically across state agencies, we will investigate the impacts of harvest regulations on the realized harvest within and among states. Specifically, initial work will focus on regulation-driven changes to the size and age/sex structure of the harvest. We will begin by surveying the participating states to ascertain the (1) variety of harvest regulations they have applied pre- and post-CWD invasion; (2) availability of spatial and temporal harvest information, including license sales, harvest reporting rates, success rates and harvest sex/age composition, associated with the various regulatory frameworks; (3) methods used to collect the harvest information and estimate these rates; (4) availability of ancillary data that may help this assessment (e.g., research studies); and (5) level of precision needed on key rates to permit CWD management decisions to be made. The results of the survey will help to guide the analysis and elucidate key gaps that may hinder the collation of data across agencies and a regional assessment of regulatory impacts on deer harvest. If the survey demonstrates that enough information is currently available for analysis, we will solicit this information from each participating agency. This will entail working with each agency to ensure data are standardized and interpretable. We will employ Bayesian statistical techniques to estimate the effects of various regulations on deer harvest within and between states based on this standardized dataset. In the event that the survey reveals gaps too substantial to overcome in some states, we will convene a meeting with these agencies to develop a protocol that can be applied to capture the needed information and work to implement these practices to permit the desired evaluation in the future. The next step will be to tie the above analytical results to CWD dynamics. We will employ stochastic compartmental disease models to simulate CWD burden in populations that are parameterized using information from previous research and/or published literature. These models will be simulated under a variety of transmission scenarios (i.e., varying rates of direct and indirect transmission). We will then introduce harvest regulations and associated harvest rates into the system, based on the results from above, and measure the potential effects of harvest regulations on disease processes and outcomes. This will permit us to make recommendations on the harvest regulations most likely to have the desired outcome for managing CWD. This effort will be coordinated with existing work at Michigan State University. Finally, using the results of this modeling effort we will work with participating state agencies to implement the harvest regulations that appear most effective in their CWD-affected areas. This will require monitoring of the realized impacts of these regulations on both population sizes and disease burden. This monitoring will provide key information for assessing the effectiveness of management activities and adapting future disease control efforts. Thus, the over-arching goal of this theme is to capitalize on the breadth of management responses that agencies in the Midwest and elsewhere have made after CWD introduction to measure the impact of harvest regulations, on deer harvest and ultimately CWD. This knowledge will guide CWD management in the Midwest under an adaptive management approach.
Objective 5. Evaluate heterogeneous social values, motivations, attitudes, and effective communication to inform disease management decision-making at local, state, and regional levels. A major challenge in CWD management and control is inadequate understanding and integration of social values, motivations, and attitudes into disease management decision-making and effective communication of necessary management actions that connects stakeholders. Wildlife and cervid farming regulations can increase or decrease the spread of CWD, but their effectiveness depends on buy-in by relevant stakeholders (e.g., hunters, farmers, landowners). A need remains for improved understanding of social values, motivations, and attitudes toward CWD and the interaction between the resulting behaviors and CWD management. Equally important is the need for scientific evaluation of targeted communication strategies surrounding management and policy in their effectiveness. We intend a multidisciplinary, multiagency, multistate approach to meeting these challenges through an iterative process that includes disease and management experts, social scientists, and stakeholders. We propose to pursue two key activities for this: Activity 1. Understanding stakeholder values and motivations associated with CWD management and control. We propose to establish a formal working group that would include scientists from public health, wildlife management, epidemiology, prion, and social sciences, as well as communication specialists. The overarching goal of this group would be to prioritize communication needs and develop strategies for CWD messaging across ecological contexts (areas with varying levels of CWD) in association with control, mitigation, and public health. The group would meet quarterly in the first year to (1) refine goals and objectives developed at the September 2019 workshop (Table 1), (2) identify several key stakeholders to bring into the process early, and (3) work toward funding recruitment and support for research endeavors. Key stakeholders would include hunter organizations, cervid farmer organizations, land owners, and others groups impacted by CWD. Involving stakeholders early in the process has been identified as a critical need to ensure interests and perspectives are well represented in the prioritization of communication needs, as well as to enhance audience trust in CWD messaging through stakeholder delivery of key messages. Additionally, this kind of multidisciplinary work to explore the human dimensions of CWD, aligns well with The National Socio-Environmental Synthesis Center (SESYNC), which convenes science teams to work on broad issues of national and international relevance to find solutions to complex environmental problems. Thus, we will explore opportunities with SESYNC to leverage its support and capacity to meet our team’s objectives, particularly in relation to Aim 1 (Table 1), where the “Propose a Priority” program (https://www.sesync.org/opportunities/propose-a-pursuit) may be an opportunity to assemble human dimensions data across states and regions to summarize and conduct an analysis of human behaviors/responses to CWD under different ecological contexts (e.g., history in a region, prevalence level, management actions). These objectives align with concurrent work led by the Center for Conservation Social Sciences of Cornell University (Bruce Lauber, PI). Finally, we would facilitate the identification of research gaps in CWD human dimensions research and inform the design and implementation of new human dimensions research. Activity 2: Develop, implement, and measure the effectiveness of targeted communication strategies on CWD management and control for different audiences. The newly formed Human Dimensions working group would create a consensus document of current CWD best practices for management and control, leveraging existing efforts such as the American Fish and Wildlife Association’s Best Practices for CWD management. This document would form the basis of scientifically-informed recommendations prioritized for dissemination to different stakeholder groups. The working group, which will include communication specialists, will use results from Activity 1 to develop strategies for communicating the science on CWD that meet the needs and prioritize the values and motivations of each stakeholder group (Figure 1). This endeavor would include the development of materials on recommended CWD management actions that can be shared with policymakers at various levels. Simultaneously, the working group will design and implement a plan for measuring the impact of varying communication strategies across locations (states, regions) in garnering stakeholder trust and effecting changes in behavior and attitudes. This might include a variety of survey methods, distributed alongside the communication mechanism, as well as structured and unstructured interviews of informants from the targeted stakeholder groups. This may include metrics that reflect changes in stakeholder behavior, such as annual trends in hunting license purchases, frequency of CWD test submissions across varying hunting zones, adoption of biosecurity and CWD surveillance regulations on farms, and trends in the integration of CWD management actions and funding in policies and bills. These results will be used to refine communication strategies, including message context and delivery while maintaining the science-informed content for the intended audience (Figure 1).
Measurement of Progress and Results Outputs Objective 1. Establish a national CWD tissue database and repository with improved access for transmission and pathogenesis research and validation of CWD prion detection assays. Comments: The significance of the outputs for Objective 1 is multifold. First, a repository of CWD field isolates from a wide range of geographic locations in North America will allow, for the first time, the means to begin to assess the distribution and frequency of CWD strains in North America. Since prion strains can differ in pathogenicity and host range, these are essential data for the determination for risk of interspecies prion transmission to humans and to domestic livestock and wildlife. Second, this repository can provide uniform standardized CWD-infected and uninfected sources of tissue for diagnostic assay development, mitigation testing, and for basic research purposes. Finally, the implementation of the repository will facilitate cooperation among the various state agencies that could lead to new collaborative efforts. Objective 2. Develop large-scale research facilities for controlled CWD research using depopulated cervid facilities where CWD has been detected. Comments: This first output of this objective will include identifying potential facilities, evaluating them for use in CWD research, and working with governmental regulators and local stakeholders on permitting and acceptance of a research objective for these facilities. The second output would be to obtain funding to purchase, modify to meet research and biosecurity requirements, and manage each research facility. The third output would be research projects conceived, funded, conducted, and published. The fourth output will be graduates students trained in CWD research techniques and the ecology and management of the disease. Objective 3. Advance diagnostic testing for CWD with a focus on facilitating adoption of the RT-QuIC assay and improved sourcing for the recombinant prion protein substrate. Comments: Outputs of this objective include the training of personnel in producing substrate and in conducting the RT-QuIC assay, facilitating access to substrate for laboratories that have not yet developed the capability to generate substrate, certifying laboratories, and developing protocols for dealing with suspect samples. We anticipate training representatives from a number of groups during the first year as well as developing protocols for dealing with suspect samples of specific types. Objective 4. Develop a multistate adaptive management approach for CWD to evaluate surveillance and management strategies and how deer harvest regulatory options impact deer disease dynamics. Comments: First, we will assemble a standardized dataset related to deer harvest rates and regulations that will encompass information from wildlife management agencies across the Midwest. Secondly, we will develop mathematical models to be used to forecast the most efficacious regulations for CWD management. These models can also be used to answer additional questions related to deer and CWD management and will be made publicly available for that purpose. This theme will also create platform for enhanced communication and coordination among wildlife management agencies. Lastly, we will build and an implement an adaptive management strategy for CWD and deer management that is multijurisdictional. Objective 5. Evaluate heterogeneous social values, motivations, attitudes, and effective communication to inform disease management decision-making at local, state, and regional levels. Comments: Outputs early in the project would include the formation of a scientific team to design new, multi-state studies on values and motivations across stakeholder groups impacted by CWD and the development of strategies for communicating the science on CWD that meet the needs and prioritize the values and motivations of stakeholder groups. Plans would be design and implemented to measure the impact of varying communication strategies across locations. Ultimately, this objective will produce knowledge about best practices in designing communication strategies related to CWD. Outcomes or Projected Impacts Objective 1. Establish a national CWD tissue database and repository with improved access for transmission and pathogenesis research and validation of CWD prion detection assays. Outcomes from establishing a tissue repository or bank and an associated database will be multifold. Data from this effort will include a survey of CWD strains over a wide geographical region. Additionally, polymorphisms of the host prion protein can be determined. These data will be useful in combination with environmental and weather patterns in determining factors that may influence the distribution of prion strains and how changes in long-term weather patterns may alter this distribution. These data may be used to better predict the populations of cervids and the environments that CWD may more likely spread to. This information can be used to focus surveillance resources. Strain distribution, in conjunction with studies on how strains of CWD affect zoonotic potential, can be used to address areas where zoonotic potential of CWD is the highest to focus mitigation resources. Monitoring the strain prevalence over time will provide important information regarding CWD strain dynamics and will enable identification of novel emerging strains that may exhibit altered pathogenicity or zoonotic potential compared to currently circulating CWD strains. Objective 2. Develop large-scale research facilities for controlled CWD research using depopulated cervid facilities where CWD has been detected. Achievement of this objective will provide CWD scientists with facilities to address key aspects of CWD management and ecology that are difficult to study with current resources. Graduate students interested in studying CWD transmission, persistence, and management will have facilities to learn about these crucial aspects of the disease. State wildlife agencies, private wildlife biologists, and land owners will have knowledge they can use to manage deer in the face of CWD and thereby reduce the impacts of the disease on deer populations and wildlife conservation. Objective 3. Advance diagnostic testing for CWD with a focus on facilitating adoption of the RT-QuIC assay and improved sourcing for the recombinant prion protein substrate. Successful achievement of this objective will result in the certification of laboratories across the country for use of RT-QuIC for diagnostic purposes. State and federal agencies will be able to confidently use RT-QuIC to sensitively measure CWD prions in a variety of sample types. Objective 4. Develop a multistate adaptive management approach for CWD to evaluate surveillance and management strategies and how deer harvest regulatory options impact deer disease dynamics. The major outcome of this theme will be an improved ability to manage CWD in the Midwest and elsewhere in North America. This will be accomplished by providing managers with critical information on the use of harvest as a management tool for this disease, fostering multijurisdictional collaboration, and establishing an adaptive management strategy that will lead to regional disease response efforts. Objective 5. Evaluate heterogeneous social values, motivations, attitudes, and effective communication to inform disease management decision-making at local, state, and regional levels. Achievement of this objective will lead to sustained and broad public/stakeholder support for research and management (prevention, contamination, mitigation) of CWD that is demonstrated through behavioral changes that are responsive to management recommendations and regulations, enhanced funding support, and increased collaborations across stakeholder groups. Further outcomes include enhanced trust by the public and key stakeholder groups in management agency decisions and recommendations, implementation of science-based actions and policy rule-making by governing bodies, and effective CWD control and mitigation as evidenced by lack of new captive facility outbreaks or spread to new populations. Milestones (2020):Formalize administrative structure (including subcommittee membership), initiate research, and identify additional state organizations and researchers willing to actively contribute to each of the 5 objectives. Prepare and submit first group research proposal. Proposals will be developed in all years and research will be based on funding success. Additional milestones in the first project year include • Development of a policy on tissue distribution and a data sharing agreement with state organizations who are willing to participate in this program. Identify the sites of physical storage of CWD samples. Identify procedures for shipping and begin metadata recording of samples into a database. • Identify key personnel in cooperating states and assess available large-scale facilities. Seek regulatory approval and local stakeholder acceptance of facilities. • Develop protocols for dealing with suspect samples of specific types being analyzed by RT-QuIC.
(2021):Prepare presentations and publications based on previous years' activities and research. Additional milestones in the second project year include • Certify first set of laboratories for using RT-QuIC for diagnostic purposes. • Secure funding to acquire and operate permitted large-scale facilities.
(2022):Prepare presentations and publications based on previous years' activities and research. Additional milestones in the third project year include • Secure funding to acquire and operate permitted large-scale facilities. • Completed analysis of deer harvest regulation packages on CWD growth and spread.
(2023):Prepare presentations and publications based on previous years' activities and research. Additional milestones in the fourth project year include • Initiate operations and start CWD research at the large-scale facilities. • Develop and then work with interested states to implement and test an adaptive management framework for deer harvest frameworks with the explicit purpose of controlling spread and growth of CWD
(2024):Prepare presentations and publications based on previous years' activities and research. Additional milestones in the fifth project year include. • Submit final report for the multistate project and proposal for second 5-year period of the project provided sufficient support exists.
Projected Participation View Appendix E: Participation Outreach Plan Our project will generate multiple peer-reviewed publications in disciplinary and impactful journals. We will also produce shorter communications for the public in professional magazines (e.g., The Wildlife Professional), on partnering agency websites, and through respective land-grant university extension communications. Research presentations will be targeted to regional, national, and international conferences. Participants with an outreach and extension role will further disseminate progress and results to agency wildlife managers and the public. Given the national importance of CWD, we anticipate project participants communicating results to state and federal agencies and legislatures.
Organization/Governance Membership in the proposed multistate project will be open to SAES scientists, other public and private sector scientists, extension professionals, administrative advisors, CSREES representatives, and others who are in a position to contribute to the proposed activities. Voting members will consist of one representative from each member SAES. Voting membership may be extended to other members not affiliated with a SAES upon a majority vote of the voting members. In addition to conducting the agreed-upon research collaboration, project members are responsible for reporting progress, contributing to the ongoing progress of project activities, and communicating their accomplishments to the committee members and their respective employing institutions.
All voting members of the committee are eligible for office, regardless of sponsoring agency affiliation. The executive committee consists of the officers: Past chair: The past chair will prepare the annual report for the year in which s/he served as chair. The past chair will assist the chair to ensure a smooth transition. The past chair will serve as chair in the absence of both the elected chair and vice-chair.
Chair: In consultation with the administrative adviser, notifies the committee members of the time and place of meetings, prepares the agenda, presides at meetings of the committee and the executive committee. The chair is responsible for preparing or supervising the preparation of the annual report of the project. The chair will serve a one-year term.
Vice-chair: Succeeds the chair and is expected to carry out duties assigned by the chair. The chair-elect serves as the chair in the absence of the elected chair. The chair-elect will serve a one-year term and will succeed to the chair the following year.
Secretary: records the minutes and performs other duties assigned to him/r by the committee or the administrative advisor. The secretary shall prepare and e-mail the minutes of any official meeting to committee members within 4 weeks after the end of the meeting. The secretary shall be responsible for assisting the chair to prepare official communications to the administrative advisor, NIMSS, and other external parties. The secretary will serve a one-year term and succeed to the vice-chair the following year.
Subcommittees will be named by the chair as needed for specific assignments. This may include subcommittees to develop procedures, manuals, and phases of the regional project; to review work assignments; to develop research methods; and to prepare publications. One of the outcomes of the September 2019 workshop was the initial formation of subcommittees associated with each of the project objectives.
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Attachments File Tables and Figures for Multistate Project.pdf Land Grant Participating States/Institutions AR, IA, MI, MN, MO, MS, NY, TN, WI, WY Non Land Grant Participating States/Institutions Case Western Reserve University, Colorado State University, Creighton University, Idaho Fish and Game, Iowa Department of Natural Resources, Michigan Department of Natural Resources, State of Minnesota, Texas A&M University - Kingsville, The University of Texas Health Science Center at Houston, University of Alberta, University of Georgia, USDA Forest Service, USDA-APHIS, USDA/APHIS/WS/National Wildlife Research Center, USGS, Wisconsin Department of Natural Resources
October 26th, 2020
Dear Colleagues,
As members of the NC1209: North American interdisciplinary chronic wasting disease research consortium we wanted to provide the group with quarterly updates on the progress of the objectives and to communicate relevant information. Thank you for your continued efforts in moving the objectives forward. To document the benefit of this interdisciplinary group, we would like to collect information regarding publications, grant submissions, etc. that have been a result of the interactions of the members of this group. To facilitate the data collection, we have generated a google doc (https://docs.google.com/forms/d/e/1FAIpQLSf7hSbINk7u_MRqQ82vOroeHdrooyltlBO9 q32XGMIMASoy3g/viewform). We intend to hold the next consortium meeting during fall 2021. As the course of the pandemic becomes clearer, we will follow up on potential dates and location. Objective 1. Establish a national CWD tissue database and repository with improved access for transmission and pathogenesis research and validation of CWD prion detection assays.
NC1209: North American interdisciplinary chronic wasting disease research consortium Singeltary Submission
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018
Greetings APHIS, USDA, Dr. Tracy Nichols, et al,
I wish to kindly submit my comments on the Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards please. i have submitted online and sent a hard copy to Dr. Nichols via email. i know that my concern may not be the same concern as others, but ramifications from cwd tse prion can be long lasting, and science is still emerging. however, the science today warrants immediate and further actions be taken, especially about zoonosis potential for cwd tse prion, if it has not happened already. my comments, with reference materials, are as follows, and will be formatted in such a way, i will address issues by numbers 1-10, and under each one of my comments by each number, i will reference my comments with science to back up what i am stating/asking...thank you kindly, terry
1. I believe that immediately, there should be a 'DECLARATION OF EXTRAORDINARY EMERGENCY FOR FOREIGN ANIMAL DISEASE OF THE United States of America USA' due to Chronic Wasting Disease CWD Transmissible Spongiform Encephalopathy TSE Prion disease. All Intercontinental, International, Interstate movements of cervid should be banned immediately from the USA, and documented CWD TSE Prion Countries. ...snip...see full text Singeltary Submission for references.
2. Voluntary Chronic Wasting Disease Herd Certification Program should be made MANDATORY immediately, OR NO PERMIT TO FARM DEER OR ELK, PERIOD! you don't want to join, then fine, you don't farm cervid and or any product there from...see full text Singeltary Submission for references.
3. INDEMNITY, NO MORE Federal indemnity program, or what i call, ENTITLEMENT PROGRAM for game farm industry. NO MORE BAIL OUTS FROM TAX PAYERS. if the captive industry can't buy insurance to protect not only themselves, but also their customers, and especially the STATE, from Chronic Wasting Disease CWD TSE Prion or what some call mad deer disease and harm therefrom, IF they can't afford to buy that insurance that will cover all of it, then they DO NOT GET A PERMIT to have a game farm for anything. This CWD TSE Prion can/could/has caused property values to fall from some reports in some places. roll the dice, how much is a state willing to lose?...see full text Singeltary Submission for references.
4. QUARANTINE OF ALL CAPTIVE, BREEDERS, URINE, ANTLER, VELVET, SPERM, OR ANY FACILITY that has been confirmed to have Chronic Wasting Disease CWD TSE Prion, the QUARANTINE should be for 21 years due to science showing what scrapie can do. 5 years is NOT enough. see; Infectious agent of sheep scrapie may persist in the environment for at least 16 years...snip...see full text Singeltary Submission for references.
PLEASE SEE Singeltary 5 - 10 comoments, and full text file DOWNLOAD ON GOVERNMENT SITE, OR GO TO THIS URL LINK FOR FULL TEXT OF SINGELTARY SUBMISSION TO Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018, PLEASE SEE;
FRIDAY, MARCH 30, 2018
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018
***> Transmissible Spongiform Encephalopathy TSE Prion End of Year Report 2020 Singeltary Submission <***CJD FOUNDATION VIRTUAL CONFERENCE CJD Foundation Research Grant Recipient Reports Panel 2 Nov 3, 2020zoonotic potential of PMCA-adapted CWD PrP 96SS inoculum4 different CWD strains, and these 4 strains have different potential to induce any folding of the human prion protein.***> PIGS, WILD BOAR, CWD <******> POPULATIONS OF WILD BOARS IN THE UNITED STATES INCREASING SUPSTANTUALLY AND IN MANY AREAS WE CAN SEE A HIGH DENSITY OF WILD BOARS AND HIGH INCIDENT OF CHRONIC WASTING DISEASEHYPOTHOSIS AND SPECIFIC AIMSHYPOTHOSISBSE, SCRAPIE, AND CWD, EXPOSED DOMESTIC PIGS ACCUMULATE DIFFERENT QUANTITIES AND STRAINS OF PRIONS IN PERIPHERAL TISSUES, EACH ONE OF THEM WITH PARTICULAR ZOONOTIC POTENTIALSFinal Report – CJD Foundation Grant Program A.Project Title: Systematic evaluation of the zoonotic potential of different CWD isolates. Principal Investigator: Rodrigo Morales, PhD.Systematic evaluation of the zoonotic potential of different CWD isolates. Rodrigo Morales, PhD Assistant Professor Protein Misfolding Disorders lab Mitchell Center for Alzheimer’s disease and Related Brain Disorders Department of Neurology University of Texas Health Science Center at Houston Washington DC. July 14th, 2018Conclusions and Future Directions • We have developed a highly sensitive and specific CWD-PMCA platform to be used as a diagnostic tool. • Current PMCA set up allow us to mimic relevant prion inter-species transmission events. • Polymorphic changes at position 96 of the prion protein apparently alter strain properties and, consequently, the zoonotic potential of CWD isolates. • Inter-species and inter-polymorphic PrPC → PrPSc conversions further increase the spectrum of CWD isolates possibly present in nature. • CWD prions generated in 96SS PrPC substrate apparently have greater inter-species transmission potentials. • Future experiments will explore the zoonotic potential of CWD prions along different adaptation scenarios, including inter-species and inter-polymorphic.Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion ResearchTitle: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting diseaseAuthor item MOORE, SARAH - Orise Fellow item Kunkle, Robert item KONDRU, NAVEEN - Iowa State University item MANNE, SIREESHA - Iowa State University item SMITH, JODI - Iowa State University item KANTHASAMY, ANUMANTHA - Iowa State University item WEST GREENLEE, M - Iowa State University item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 month challenge groups). The remaining pigs (>6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion ResearchTitle: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNPAuthor item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018 Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44.Interpretive Summary:Technical Abstract: We have previously shown that the chronic wasting disease (CWD) agent from white-tailed deer can be transmitted to domestic pigs via intracranial or oral inoculation although with low attack rates and restricted PrPSc accumulation. The objective of this study was to assess the potential for cross-species transmission of pig-passaged CWD using bioassay in transgenic mice. Transgenic mice expressing human (Tg40), bovine (TgBovXV) or porcine (Tg002) PRNP were inoculated intracranially with 1% brain homogenate from a pig that had been intracranially inoculated with a pool of CWD from white-tailed deer. This pig developed neurological clinical signs, was euthanized at 64 months post-inoculation, and PrPSc was detected in the brain. Mice were monitored daily for clinical signs of disease until the end of the study. Mice were considered positive if PrPSc was detected in the brain using an enzyme immunoassay (EIA). In transgenic mice expressing porcine prion protein the average incubation period was 167 days post-inoculation (dpi) and 3/27 mice were EIA positive (attack rate = 11%). All 3 mice were found dead and clinical signs were not noted prior to death. One transgenic mouse expressing bovine prion protein was euthanized due to excessive scratching at 617 dpi and 2 mice culled at the end of the study at 700 dpi were EIA positive resulting in an overall attack rate of 3/16 (19%). None of the transgenic mice expressing human prion protein that died or were euthanized up to 769 dpi were EIA positive and at study end point at 800 dpi 2 mice had positive EIA results (overall attack rate = 2/20 = 10%). The EIA optical density (OD) readings for all positive mice were at the lower end of the reference range (positive mice range, OD = 0.266-0.438; test positive reference range, OD = 0.250-4.000). To the authors’ knowledge, cervid-derived CWD isolates have not been successfully transmitted to transgenic mice expressing human prion protein. The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.cwd scrapie pigs oral routes***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <******> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.cwd to pig, orally ;Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIESLocation: Virus and Prion ResearchTitle: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting diseaseAuthor item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, JustinSubmitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.CONFIDENTIALEXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHYWhile this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...CONFIDENTIALwe cannot rule out the possibility that unrecognized subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....snip...see much more here ;WEDNESDAY, APRIL 05, 2017Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting diseaseTUESDAY, APRIL 18, 2017*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***TUESDAY, MARCH 28, 2017*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***
Friday, December 14, 2012DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012snip.....In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include:1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES.It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.snip.....36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).snip.....In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip..... In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.snip.....Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.snip.....***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are;BSE TESTING (failed terribly and proven to be a sham)BSE SURVEILLANCE (failed terribly and proven to be a sham)BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham)these are facts folks. trump et al just admitted it with the feed ban.see;FDA Reports on VFD ComplianceJohn MadayAugust 30, 2019 09:46 AM VFD-Form 007 (640x427)Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.SUNDAY, SEPTEMBER 1, 2019***> FDA Reports on VFD Compliance***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.
https://www.nature.com/articles/srep11573O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populationsEmmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=3131601: J Infect Dis 1980 Aug;142(2):205-8Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.snip...The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.PMID: 6997404http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=AbstractRecently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the scrapie problem urgent if the sheep industry is not to suffer grievously.snip...76/10.12/4.6Nature. 1972 Mar 10;236(5341):73-4.Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).Gibbs CJ Jr, Gajdusek DC.Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)C. J. GIBBS jun. & D. C. GAJDUSEKNational Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, MarylandSCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).Wednesday, February 16, 2011IN CONFIDENCESCRAPIE TRANSMISSION TO CHIMPANZEESIN CONFIDENCETHURSDAY, AUGUST 20, 2020***> Why is USDA "only" BSE TSE Prion testing 25,000 samples a year? <***MONDAY, DECEMBER 14, 2020Experimental oral transmission of chronic wasting disease to sika deer (Cervus nippon)***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.
https://www.nature.com/articles/srep11573O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populationsEmmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=3131601: J Infect Dis 1980 Aug;142(2):205-8Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.snip...The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.PMID: 6997404http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=AbstractRecently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.snip...76/10.12/4.6Nature. 1972 Mar 10;236(5341):73-4.Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).Gibbs CJ Jr, Gajdusek DC.Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)C. J. GIBBS jun. & D. C. GAJDUSEKNational Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, MarylandSCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).Wednesday, February 16, 2011IN CONFIDENCESCRAPIE TRANSMISSION TO CHIMPANZEESIN CONFIDENCECHRONIC WASTING DISEASE ZOONOSIS ZOONOTIC> However, to date, no CWD infections have been reported in people.key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ****** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***Chronic Wasting Disease CWD TSE Prion aka mad deer disease zoonosisWe hypothesize that:(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;(3) Reliable essays can be established to detect CWD infection in humans; and(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATEPrion 2017 ConferenceFirst evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/GoettingenThis is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERSPRION 2018 CONFERENCEOral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic miceHermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years.After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate.The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.
Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD..***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***Prion Conference 2018READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United StatesAbrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA..SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD
states.AND ANOTHER STUDY;P172 Peripheral Neuropathy in Patients with Prion DiseaseWang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio..IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017,ANDincluded 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%),ANDTHAT The Majority of cases were male (60%), AND half of them had exposure to wild game.snip…see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below…terryPrion 2018 Conference***> 8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.International Conference on Emerging Diseases, Outbreaks & Case Studies & 16th Annual Meeting on Influenza March 28-29, 2018 | Orlando, USAQingzhong KongCase Western Reserve University School of Medicine, USAZoonotic potential of chronic wasting disease prions from cervidsChronic wasting disease (CWD) is the prion disease in cervids (mule deer, white-tailed deer, American elk, moose, and reindeer). It has become an epidemic in North America, and it has been detected in the Europe (Norway) since 2016. The widespread CWD and popular hunting and consumption of cervid meat and other products raise serious public health concerns, but questions remain on human susceptibility to CWD prions, especially on the potential difference in zoonotic potential among the various CWD prion strains. We have been working to address this critical question for well over a decade. We used CWD samples from various cervid species to inoculate transgenic mice expressing human or elk prion protein (PrP). We found infectious prions in the spleen or brain in a small fraction of CWD-inoculated transgenic mice expressing human PrP, indicating that humans are not completely resistant to CWD prions; this finding has significant ramifications on the public health impact of CWD prions. The influence of cervid PrP polymorphisms, the prion strain dependence of CWD-to-human transmission barrier, and the characterization of experimental human CWD prions will be discussed.Speaker Biography Qingzhong Kong has completed his PhD from the University of Massachusetts at Amherst and Post-doctoral studies at Yale University. He is currently an Associate Professor of Pathology, Neurology and Regenerative Medicine. He has published over 50 original research papers in reputable journals (including Science Translational Medicine, JCI, PNAS and Cell Reports) and has been serving as an Editorial Board Member on seven scientific journals. He has multiple research interests, including public health risks of animal prions (CWD of cervids and atypical BSE of cattle), animal modeling of human prion diseases, mechanisms of prion replication and pathogenesis, etiology of sporadic Creutzfeldt-Jacob disease (CJD) in humans, normal cellular PrP in the biology and pathology of multiple brain and peripheral diseases, proteins responsible for the α-cleavage of cellular PrP, as well as gene therapy and DNA vaccination.SATURDAY, FEBRUARY 23, 2019Chronic Wasting Disease CWD TSE Prion and THE FEAST 2003 CDC an updated review of the science 2019TUESDAY, NOVEMBER 04, 2014Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011Authors, though, acknowledged the study was limited in geography and sample size and so it couldn't draw a conclusion about the risk to humans. They recommended more study. Dr. Ermias Belay was the report's principal author but he said New York and Oneida County officials are following the proper course by not launching a study. "There's really nothing to monitor presently. No one's sick," Belay said, noting the disease's incubation period in deer and elk is measured in years. "Transmission StudiesMule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSSresulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.snip....Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author AffiliationsIn mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.Prions in Skeletal Muscles of Deer with Chronic Wasting DiseaseHere bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”From: TSSSubject: CWD aka MAD DEER/ELK TO HUMANS ???Date: September 30, 2002 at 7:06 am PSTFrom: "Belay, Ermias"To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"Sent: Monday, September 30, 2002 9:22 AMSubject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERSDear Sir/Madam,In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.Ermias Belay, M.D. Centers for Disease Control and Prevention-----Original Message-----From: Sent: Sunday, September 29, 2002 10:15 AMSubject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERSSunday, November 10, 2002 6:26 PM .......snip........end..............TSSThursday, April 03, 2008A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.snip...*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,snip... full text ;*** I urge everyone to watch this video closely...terry*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ****** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.> However, to date, no CWD infections have been reported in people.sporadic, spontaneous CJD, 85%+ of all human TSE, just not just happen. never in scientific literature has this been proven.if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;sporadic = 54,983 hits https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadicspontaneous = 325,650 hits https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneouskey word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ****** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***CWD TSE PRION AND ZOONOTIC, ZOONOSIS, POTENTIALSubject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDYDate: Fri, 18 Oct 2002 23:12:22 +0100From: Steve DeallerReply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online memberTo: BSE-L@ References: <3daf5023 .4080804="" wt.net="">Dear Terry,An excellent piece of review as this literature is desparately difficult to get back from Government sites.What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!Steve Dealler ===============BSE Inquiry Steve DeallerManagement In ConfidenceBSE: Private Submission of Bovine Brain Deallersnip...see full text;MONDAY, FEBRUARY 25, 2019***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019***********CJD REPORT 1994 increased risk for consumption of veal and venison and lamb***********CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD…tss)These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. …Table 9 presents the results of an analysis of these data.There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).snip…It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = 0.05).snip…In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. …snip…In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???…TSS)snip…see full report ;http://web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdfThursday, October 10, 2013*************CJD REPORT 1994 increased risk for consumption of veal and venison and lamb**************CJD9/10022October 1994Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZDear Mr Elmhirst,CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORTThank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
THURSDAY, DECEMBER 17, 2020***> Exposure Risk of Chronic Wasting Disease in Humans <****** IF CWD is not a risk factor for humans, then I guess the FDA et al recalled all this CWD tainted elk tenderloin (2009 Exotic Meats USA of San Antonio, TX) for the welfare and safety of the dead elk. ...tssExotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have Chronic Wasting DiseaseContact: Exotic Meats USA 1-800-680-4375FOR IMMEDIATE RELEASE -- February 9, 2009 -- Exotic Meats USA of San Antonio, TX is initiating a voluntary recall of Elk Tenderloin because it may contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD). The meat with production dates of December 29, 30 and 31, 2008 was purchased from Sierra Meat Company in Reno, NV. The infected elk came from Elk Farm LLC in Pine Island, MN and was among animals slaughtered and processed at USDA facility Noah’s Ark Processors LLC.Chronic Wasting Disease (CWD) is a fatal brain and nervous system disease found in elk and deer. The disease is caused by an abnormally shaped protein called a prion, which can damage the brain and nerves of animals in the deer family. Currently, it is believed that the prion responsible for causing CWD in deer and elk is not capable of infecting humans who eat deer or elk contaminated with the prion, but the observation of animal-to-human transmission of other prion-mediated diseases, such as bovine spongiform encephalopathy (BSE), has raised a theoretical concern regarding the transmission of CWD from deer or elk to humans. At the present time, FDA believes the risk of becoming ill from eating CWD-positive elk or deer meat is remote. However, FDA strongly advises consumers to return the product to the place of purchase, rather than disposing of it themselves, due to environmental concerns.Exotic Meats USA purchased 1 case of Elk Tenderloins weighing 16.9 lbs. The Elk Tenderloin was sold from January 16 – 27, 2009. The Elk Tenderloins was packaged in individual vacuum packs weighing approximately 3 pounds each. A total of six packs of the Elk Tenderloins were sold to the public at the Exotic Meats USA retail store. Consumers who still have the Elk Tenderloins should return the product to Exotic Meats USA at 1003 NE Loop 410, San Antonio, TX 78209. Customers with concerns or questions about the Voluntary Elk Recall can call 1-800-680-4375. The safety of our customer has always been and always will be our number one priority.Exotic Meats USA requests that for those customers who have products with the production dates in question, do not consume or sell them and return them to the point of purchase. Customers should return the product to the vendor. The vendor should return it to the distributor and the distributor should work with the state to decide upon how best to dispose. If the consumer is disposing of the product he/she should consult with the local state EPA office.#RSS Feed for FDA Recalls Information11 [what's this?12]TUESDAY, DECEMBER 29, 2020Chronic Wasting Disease: Can Science Save Our Dear Deer?WEDNESDAY, DECEMBER 30, 2020Mississippi CWD TSE Prion 71 Confirmed Cases Since February 2018THURSDAY, DECEMBER 31, 2020Mississippi CWD TSE Prion Detected in Tippah and Alcorn Counties
FRIDAY, DECEMBER 18, 2020Wyoming WGFD Elk Tests Positive for Chronic Wasting Disease in Grand Teton National ParkTHURSDAY, DECEMBER 24, 2020Montana Whitetail Deer tests positive for Chronic Wasting Disease (CWD) on Blackfeet reservationWEDNESDAY, DECEMBER 23, 2020Virginia CWD has been confirmed for the first time in a hunter-harvested deer from Madison CountyFRIDAY, DECEMBER 18, 2020Wyoming WGFD Elk Tests Positive for Chronic Wasting Disease in Grand Teton National ParkTHURSDAY, DECEMBER 17, 2020Wisconsin DNR CONFIRMS CWD DETECTED IN WASHINGTON COUNTY; NEW BAITING AND FEEDING BAN NOW FOR OZAUKEE COUNTYTUESDAY, DECEMBER 15, 2020OHIO TISSUE SAMPLE CONFIRMED POSITIVE FOR CHRONIC WASTING DISEASE IN ONE WILD DEER Thursday, December 10, 2020TUESDAY, DECEMBER 15, 2020COMBATTING CHRONIC WASTING DISEASE IN PENNSYLVANIA DECEMBER 2020 PENNSYLVANIA CHRONIC WASTING DISEASE TASK FORCESATURDAY, DECEMBER 12, 2020Montana CWD results continue to come in from general season with 316 positives confirmed in total to dateMONDAY, NOVEMBER 23, 2020***> Chronic Wasting Disease CWD TSE Prion Cervid State by State and Global Update November 2020MONDAY, DECEMBER 21, 2020BSE TSE Prion in zoo animals, exotic ruminants, domestic cats, and CPD Camel Prion Disease, a review 2020MONDAY, NOVEMBER 16, 2020North America coyotes or pumas can serve as a vehicle for prions contributing to the spread of the infectious agent in the environmentFRIDAY, OCTOBER 04, 2019Inactivation of chronic wasting disease prions using sodium hypochlorite
i think some hunters that don't read this carefully are going to think this is a cure all for cwd tse contamination. IT'S NOT!
first off, it would take a strong bleach type sodium hypochlorite, that is NOT your moms bleach she uses in her clothes, and store bought stuff.
Concentrated bleach is an 8.25 percent solution of sodium hypochlorite, up from the “regular bleach” concentration of 5.25 percent.Nov 1, 2013 https://waterandhealth.org/disinfect/high-strength-bleach-2/
second off, the study states plainly;
''We found that a five-minute treatment with a 40% dilution of household bleach was effective at inactivating CWD seeding activity from stainless-steel wires and CWD-infected brain homogenates. However, bleach was not able to inactivate CWD seeding activity from solid tissues in our studies.''
''We initially tested brains from two CWD-infected mice and one uninfected mouse using 40% bleach for 5 minutes. The results from these experiments showed almost no elimination of prion seeding activity (Table 4). We then increased the treatment time to 30 minutes and tested 40% and 100% bleach treatments. Again, the results were disappointing and showed less than a 10-fold decrease in CWD-seeding activity (Table 4). Clearly, bleach is not able to inactivate prions effectively from small brain pieces under the conditions tested here.''
''We found that both the concentration of bleach and the time of treatment are critical for inactivation of CWD prions. A 40% bleach treatment for 5 minutes successfully eliminated detectable prion seeding activity from both CWD-positive brain homogenate and stainless-steel wires bound with CWD. However, even small solid pieces of CWD-infected brain were not successfully decontaminated with the use of bleach.''
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0223659
https://chronic-wasting-disease.blogspot.com/2019/10/inactivation-of-chronic-wasting-disease.html
i think with all the fear from recent studies, and there are many, of potential, or likelihood of zoonosis, if it has not already happened as scjd, i think this study came out to help out on some of that fear, that maybe something will help, but the study plainly states it's for sure not a cure all for exposure and contamination of the cwd tse prion on surface materials. imo...terryHUNTERS, CWD TSE PRION, THIS SHOULD A WAKE UP CALL TO ALL OF YOU GUTTING AND BONING OUT YOUR KILL IN THE FIELD, AND YOUR TOOLS YOU USE...* 1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.Laboratory of Central Nervous System Studies, National Institute ofNeurological Disorders and Stroke, National Institutes of Health,Bethesda, MD 20892.Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.PMID: 8006664 [PubMed - indexed for MEDLINE]Wednesday, September 11, 2019Is the re-use of sterilized implant abutments safe enough? (Implant abutment safety) iatrogenic TSE Prion172. Establishment of PrPCWD extraction and detection methods in the farm soil
Kyung Je Park, Hoo Chang Park, In Soon Roh, Hyo Jin Kim, Hae-Eun Kang and Hyun Joo SohnForeign Animal Disease Division, Animal and Plant Quarantine Agency, Gimcheon, Gyeongsangbuk-do, KoreaABSTRACTIntroduction: Transmissible spongiform encephalopathy (TSE) is a fatal neurodegenerative disorder, which is so-called as prion diseases due to the causative agents (PrPSc). TSEs are believed to be due to the template-directed accumulation of disease-associated prion protein, generally designated PrPSc. Chronic wasting disease (CWD) is the prion disease that is known spread horizontally. CWD has confirmed last in Republic of Korea in 2016 since first outbreak of CWD in 2001. The environmental reservoirs mediate the transmission of this disease. The significant levels of infectivity have been detected in the saliva, urine, and faeces of TSE-infected animals. Soil can serve as a stable reservoir for infectious prion proteins. We found that PrPCWD can be extracted and detected in CWD contaminated soil which has kept at room temperature until 4 years after 0.001 ~ 1% CWD exposure and natural CWD-affected farm soil through PBS washing and sPMCAb.Materials and Methods: Procedure of serial PMCAb. CWD contaminated soil which has kept at room temperature (RT) for 1 ~ 4 year after 0.001%~1% CWD brain homogenates exposure for 4 months collected 0.14 g. The soil was collected by the same method once of year until 4 year after stop CWD exposure. We had conducted the two steps. There are two kinds of 10 times washing step and one amplification step. The washing step was detached PrPSc from contaminated soil by strong vortex with maximum rpm. We harvest supernatant every time by 10 times. As the other washing step, the Washed soil was made by washing 10 times soil using slow rotator and then harvest resuspended PBS for removing large impurity material. Last step was prion amplification step for detection of PrPCWD in soil supernatant and the washed soil by sPMCAb. Normal brain homogenate (NBH) was prepared by homogenization of brains with glass dounce in 9 volumes of cold PBS with TritonX-100, 5 mM EDTA, 150 mM NaCl and 0.05% Digitonin (sigma) plus Complete mini protease inhibitors (Roche) to a final concentration of 5%(w/v) NBHs were centrifuged at 2000 g for 1 min, and supernatant removed and frozen at −70 C for use. CWD consisted of brain from natural case in Korea and was prepared as 10%(w/v) homogenate. Positive sample was diluted to a final dilution 1:1000 in NBH, with serial 3:7 dilutions in NBH. Sonication was performed with a Misonix 4000 sonicator with amplitude set to level 70, generating an average output of 160W with two teflon beads during each cycle. One round consisted of 56 cycles of 30 s of sonication followed 9 min 30 s of 37°C incubation. Western Blotting (WB) for PrPSc detection. The samples (20 µL) after each round of amplification were mixed with proteinase K (2 mg/ml) and incubated 37°C for 1 h. Samples were separated by SDS-PAGE and transferred onto PVDF membrane. After blocking, the membrane was incubated for 1 h with 1st antibody S1 anti rabbit serum (APQA, 1:3000) and developed with enhanced chemiluminescence detection system.Results: We excluded from first to third supernatant in view of sample contamination. It was confirmed abnormal PrP amplification in all soil supernatants from fourth to tenth. From 0.01% to 1% contaminated washed soils were identified as abnormal prions. 0.001% contaminated washed soil did not show PrP specific band (Fig 1). The soil was collected by the same method once of year until 4 year after stop CWD exposure. After sPMCAb, there were no PrPCWD band in from second to fourth year 0.001% washed soil. but It was confirmed that the abnormal prion was amplified in the washing supernatant which was not amplified in the washed soil. we have decided to use soil supernatant for soil testing (Fig. 2). After third rounds of amplification, PrPSc signals observed in three out of four sites from CWD positive farm playground. No signals were observed in all soil samples from four CWD negative farm (Fig. 3).Conclusions: Our studies showed that PrPCWD persist in 0.001% CWD contaminated soil for at least 4 year and natural CWD-affected farm soil. When cervid reintroduced into CWD outbreak farm, the strict decontamination procedures of the infectious agent should be performed in the environment of CWD-affected cervid habitat.===186. Serial detection of hematogenous prions in CWD-infected deer
Amy V. Nalls, Erin E. McNulty, Nathaniel D. Denkers, Edward A. Hoover and Candace K. MathiasonDepartment of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO, USACONTACT Amy V. Nalls amy.nalls@colostate.eduABSTRACTBlood contains the infectious agent associated with prion disease affecting several mammalian species, including humans, cervids, sheep, and cattle. It has been confirmed that sufficient prion agent is present in the blood of both symptomatic and asymptomatic carriers to initiate the amyloid templating and accumulation process that results in this fatal neurodegenerative disease. Yet, to date, the ability to detect blood-borne prions by in vitro methods remains difficult.We have capitalized on blood samples collected from longitudinal chronic wasting disease (CWD) studies in the native white-tailed deer host to examine hematogenous prion load in blood collected minutes, days, weeks and months post exposure. Our work has focused on refinement of the amplification methods RT-QuIC and PMCA. We demonstrate enhanced in vitro detection of amyloid seeding activity (prions) in blood cell fractions harvested from deer orally-exposed to 300 ng CWD positive brain or saliva.These findings permit assessment of the role hematogenous prions play in the pathogenesis of CWD and provide tools to assess the same for prion diseases of other mammalian species.Considering the oral secretion of prions, saliva from CWD-infected deer was shown to transmit disease to other susceptible naïve deer when harvested from the animals in both theand preclinical stages69of infection, albeit within relatively large volumes of saliva (50 ml). In sheep with preclinical, natural scrapie infections, sPMCA facilitated the detection of PrPSc within buccal swabs throughout most of the incubation period of the disease with an apparent peak in prion secretion around the mid-term of disease progression.70The amounts of prion present in saliva are likely to be low as indicated by CWD-infected saliva producing prolonged incubation periods and incomplete attack rates within the transgenic mouse bioassay.41snip...Indeed, it has also been shown that the scrapie and CWD prions are excreted in urine, feces and saliva and are likely to be excreted from skin. While levels of prion within these excreta/secreta are very low, they are produced throughout long periods of preclinical disease as well as clinical disease. Furthermore, the levels of prion in such materials are likely to be increased by concurrent inflammatory conditions affecting the relevant secretory organ or site. Such dissemination of prion into the environment is very likely to facilitate the repeat exposure of flockmates to low levels of the disease agent, possibly over years.snip...Given the results with scrapie-contaminated milk and CWD-contaminated saliva, it seems very likely that these low levels of prion in different secreta/excreta are capable of transmitting disease upon prolonged exposure, either through direct animal-to-animal contact or through environmental reservoirs of infectivity.the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.***>>> Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.========================Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.HUNTERS, CWD TSE PRION, THIS SHOULD A WAKE UP CALL TO ALL OF YOU GUTTING AND BONING OUT YOUR KILL IN THE FIELD, AND YOUR TOOLS YOU USE...* 1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.Laboratory of Central Nervous System Studies, National Institute ofNeurological Disorders and Stroke, National Institutes of Health,Bethesda, MD 20892.Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.PMID: 8006664 [PubMed - indexed for MEDLINE]Wednesday, September 11, 2019Is the re-use of sterilized implant abutments safe enough? (Implant abutment safety) iatrogenic TSE PrionSATURDAY, MARCH 16, 2019Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices) Guidance for Industry and Food and Drug Administration Staff Document issued on March 15, 2019 Singeltary SubmissionTHURSDAY, SEPTEMBER 27, 2018***> Estimating the impact on food and edible materials of changing scrapie control measures: The scrapie control modelTHE tse prion aka mad cow type disease is not your normal pathogen.The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.you cannot cook the TSE prion disease out of meat.you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.the TSE prion agent also survives Simulated Wastewater Treatment Processes.IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.you can bury it and it will not go away.The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.it’s not your ordinary pathogen you can just cook it out and be done with.***> that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8***> Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.Laboratory of Central Nervous System Studies, National Institute ofNeurological Disorders and Stroke, National Institutes of Health,Bethesda, MD 20892.Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.PMID: 8006664 [PubMed - indexed for MEDLINE]2018 - 2019***> This is very likely to have parallels with control efforts for CWD in cervids.Rapid recontamination of a farm building occurs after attempted prion removalKevin Christopher Gough, BSc (Hons), PhD1, Claire Alison Baker, BSc (Hons)2, Steve Hawkins, MIBiol3, Hugh Simmons, BVSc, MRCVS, MBA, MA3, Timm Konold, DrMedVet, PhD, MRCVS3 and Ben Charles Maddison, BSc (Hons), PhD2AbstractThe transmissible spongiform encephalopathy scrapie of sheep/goats and chronic wasting disease of cervids are associated with environmental reservoirs of infectivity.Preventing environmental prions acting as a source of infectivity to healthy animals is of major concern to farms that have had outbreaks of scrapie and also to the health management of wild and farmed cervids.Here, an efficient scrapie decontamination protocol was applied to a farm with high levels of environmental contamination with the scrapie agent.Post-decontamination, no prion material was detected within samples taken from the farm buildings as determined using a sensitive in vitro replication assay (sPMCA).A bioassay consisting of 25 newborn lambs of highly susceptible prion protein genotype VRQ/VRQ introduced into this decontaminated barn was carried out in addition to sampling and analysis of dust samples that were collected during the bioassay.Twenty-four of the animals examined by immunohistochemical analysis of lymphatic tissues were scrapie-positive during the bioassay, samples of dust collected within the barn were positive by month 3.The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.snip...As in the authors' previous study,12 the decontamination of this sheep barn was not effective at removing scrapie infectivity, and despite the extra measures brought into this study (more effective chemical treatment and removal of sources of dust) the overall rates of disease transmission mirror previous results on this farm. With such apparently effective decontamination (assuming that at least some sPMCA seeding ability is coincident with infectivity), how was infectivity able to persist within the environment and where does infectivity reside? Dust samples were collected in both the bioassay barn and also a barn subject to the same decontamination regime within the same farm (but remaining unoccupied). Within both of these barns dust had accumulated for three months that was able to seed sPMCA, indicating the accumulation of scrapie-containing material that was independent of the presence of sheep that may have been incubating and possibly shedding low amounts of infectivity.This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.Acknowledgements The authors thank the APHA farm staff, Tony Duarte, Olly Roberts and Margaret Newlands for preparation of the sheep pens and animal husbandry during the study. The authors also thank the APHA pathology team for RAMALT and postmortem examination.Funding This study was funded by DEFRA within project SE1865.Competing interests None declared.Saturday, January 5, 2019Rapid recontamination of a farm building occurs after attempted prion removalTHURSDAY, FEBRUARY 28, 2019BSE infectivity survives burial for five years with only limited spread***> CONGRESSIONAL ABSTRACTS PRION CONFERENCE 2018P69 Experimental transmission of CWD from white-tailed deer to co-housed reindeerMitchell G (1), Walther I (1), Staskevicius A (1), Soutyrine A (1), Balachandran A (1)(1) National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada.Chronic wasting disease (CWD) continues to be detected in wild and farmed cervid populations of North America, affecting predominantly white-tailed deer, mule deer and elk. Extensive herds of wild caribou exist in northern regions of Canada, although surveillance has not detected the presence of CWD in this population. Oral experimental transmission has demonstrated that reindeer, a species closely related to caribou, are susceptible to CWD. Recently, CWD was detected for the first time in Europe, in wild Norwegian reindeer, advancing the possibility that caribou in North America could also become infected. Given the potential overlap in habitat between wild CWD-infected cervids and wild caribou herds in Canada, we sought to investigate the horizontal transmissibility of CWD from white-tailed deer to reindeer.Two white-tailed deer were orally inoculated with a brain homogenate prepared from a farmed Canadian white-tailed deer previously diagnosed with CWD. Two reindeer, with no history of exposure to CWD, were housed in the same enclosure as the white-tailed deer, 3.5 months after the deer were orally inoculated. The white-tailed deer developed clinical signs consistent with CWD beginning at 15.2 and 21 months post-inoculation (mpi), and were euthanized at 18.7 and 23.1 mpi, respectively. Confirmatory testing by immunohistochemistry (IHC) and western blot demonstrated widespread aggregates of pathological prion protein (PrPCWD) in the central nervous system and lymphoid tissues of both inoculated white-tailed deer. Both reindeer were subjected to recto-anal mucosal associated lymphoid tissue (RAMALT) biopsy at 20 months post-exposure (mpe) to the white-tailed deer. The biopsy from one reindeer contained PrPCWD confirmed by IHC. This reindeer displayed only subtle clinical evidence of disease prior to a rapid decline in condition requiring euthanasia at 22.5 mpe. Analysis of tissues from this reindeer by IHC revealed widespread PrPCWD deposition, predominantly in central nervous system and lymphoreticular tissues. Western blot molecular profiles were similar between both orally inoculated white-tailed deer and the CWD positive reindeer. Despite sharing the same enclosure, the other reindeer was RAMALT negative at 20 mpe, and PrPCWD was not detected in brainstem and lymphoid tissues following necropsy at 35 mpe. Sequencing of the prion protein gene from both reindeer revealed differences at several codons, which may have influenced susceptibility to infection.Natural transmission of CWD occurs relatively efficiently amongst cervids, supporting the expanding geographic distribution of disease and the potential for transmission to previously naive populations. The efficient horizontal transmission of CWD from white-tailed deer to reindeer observed here highlights the potential for reindeer to become infected if exposed to other cervids or environments infected with CWD.***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded.Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3CorrespondenceGudmundur Georgsson ggeorgs@hi.is1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland3 Bethesda, Maryland, USAReceived 7 March 2006 Accepted 6 August 2006In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION*** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSIONSEE;Back around 2000, 2001, or so, I was corresponding with officials abroad during the bse inquiry, passing info back and forth, and some officials from here inside USDA aphis FSIS et al. In fact helped me get into the USA 50 state emergency BSE conference call way back. That one was a doozy. But I always remember what “deep throat” I never knew who they were, but I never forgot;Some unofficial information from a source on the inside looking out -Confidential!!!!As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!---end personal email---end...tssInfectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).Dr. Paul Brown Scrapie Soil Test BSE Inquiry DocumentTHURSDAY, FEBRUARY 28, 2019BSE infectivity survives burial for five years with only limited spreadUsing in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.=========================***>>> Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.========================Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replicationPrion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel ProductionDetection of protease-resistant cervid prion protein in water from a CWD-endemic areaA Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During ProcessingRapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone mealsPPo4-4:Survival and Limited Spread of TSE Infectivity after BurialDiscussion Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20).Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22).Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing.Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building.Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9).The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture.When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep.Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease.It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled.Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases.Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA.Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice.In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals.In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions).As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay.False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28).This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm.This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc.In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc.Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing.The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material.In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12).A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30).This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model.Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination.These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplificationWednesday, December 16, 2015*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***THURSDAY, DECEMBER 31, 2020Autoclave treatment of the classical scrapie agent US No. 13-7 and experimental inoculation to susceptible VRQ/ARQ sheep via the oral route results in decreased transmission efficiencyWEDNESDAY, MAY 29, 2019Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures USDA HERE'S YOUR SIGN!
WEDNESDAY, MARCH 13, 2019CWD, TSE, PRION, MATERNAL mother to offspring, testes, epididymis, seminal fluid, and bloodSubject: Prion 2019 ConferenceSee full Prion 2019 Conference Abstractssee scientific program and follow the cwd studies here;Thursday, May 23, 2019Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and AbstractsMONDAY, NOVEMBER 30, 2020***> REPORT OF THE MEETING OF THE OIE SCIENTIFIC COMMISSION FOR ANIMAL DISEASES Paris, 9–13 September 2019 BSE, TSE, PRIONsee updated concerns with atypical BSE from feed and zoonosis...terryWEDNESDAY, DECEMBER 23, 2020BSE research project final report 2005 to 2008 SE1796 SID5THURSDAY, DECEMBER 17, 2020THE MAD COW BSE TSE PRION THAT STOLE CHRISTMAS DECEMBER 2003, WHAT REALLY HAPPENED, A REVIEW 2020*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;IBNC Tauopathy or TSE Prion disease, it appears, no one is sureTerry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT
WEDNESDAY, DECEMBER 23, 2020Idiopathic Brainstem Neuronal Chromatolysis IBNC BSE TSE Prion a Review 2020Monday, November 30, 2020Tunisia has become the second country after Algeria to detect a case of Camel Prion Disease CPD within a yearTUESDAY, NOVEMBER 17, 2020The European Union summary report on surveillance for the presence of transmissible spongiform encephalopathies (TSE) in 2019 First published 17 November 2020WEDNESDAY, OCTOBER 28, 2020EFSA Annual report of the Scientific Network on BSE-TSE 2020 Singeltary SubmissionWEDNESDAY, DECEMBER 2, 2020EFSA Evaluation of public and animal health risks in case of a delayed post-mortem inspection in ungulates EFSA Panel on Biological Hazards (BIOHAZ) ADOPTED: 21 October 2020i wonder if a 7 month delay on a suspect BSE case in Texas is too long, on a 48 hour turnaround, asking for a friend???WEDNESDAY, JULY 31, 2019The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-LTHURSDAY, SEPTEMBER 24, 2020The emergence of classical BSE from atypical/ Nor98 scrapieSUNDAY, OCTOBER 11, 2020Bovine adapted transmissible mink encephalopathy is similar to L-BSE after passage through sheep with the VRQ/VRQ genotype but not VRQ/ARQSUNDAY, OCTOBER 4, 2020Cattle Meat and Offal Imported from the United States of America, Canada and Ireland to Japan (Prions) Food Safety Commission of JapanTUESDAY, SEPTEMBER 29, 2020ISO's Updated 22442 Animal Tissue Standards — What Changed? TSE Prion!TUESDAY, SEPTEMBER 22, 2020APHIS USDA MORE SCRAPIE ATYPICAL Nor-98 Confirmed USA September 15 202017 cases of the Nor98 in the USA to date, location, unknown...tss17 Nor98-like cases since the beginning of RSSS.***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.P-088 Transmission of experimental CH1641-like scrapie to bovine PrP overexpression miceKohtaro Miyazawa1, Kentaro Masujin1, Hiroyuki Okada1, Yuichi Matsuura1, Takashi Yokoyama21Influenza and Prion Disease Research Center, National Institute of Animal Health, NARO, Japan; 2Department of Planning and General Administration, National Institute of Animal Health, NAROIntroduction: Scrapie is a prion disease in sheep and goats. CH1641-lke scrapie is characterized by a lower molecular mass of the unglycosylated form of abnormal prion protein (PrpSc) compared to that of classical scrapie. It is worthy of attention because of the biochemical similarities of the Prpsc from CH1641-like and BSE affected sheep. We have reported that experimental CH1641-like scrapie is transmissible to bovine PrP overexpression (TgBoPrP) mice (Yokoyama et al. 2010). We report here the further details of this transmission study and compare the biological and biochemical properties to those of classical scrapie affected TgBoPrP mice.Methods: The details of sheep brain homogenates used in this study are described in our previous report (Yokoyama et al. 2010). TgBoPrP mice were intracerebrally inoculated with a 10% brain homogenate of each scrapie strain. The brains of mice were subjected to histopathological and biochemical analyses.Results: Prpsc banding pattern of CH1641-like scrapie affected TgBoPrP mice was similar to that of classical scrapie affected mice. Mean survival period of CH1641-like scrapie affected TgBoPrP mice was 170 days at the 3rd passage and it was significantly shorter than that of classical scrapie affected mice (439 days). Lesion profiles and Prpsc distributions in the brains also differed between CH1641-like and classical scrapie affected mice.Conclusion: We succeeded in stable transmission of CH1641-like scrapie to TgBoPrP mice. Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.snip...In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.CH1641 TSE PrionTitle: White-Tailed Deer Susceptible to Scrapie by Natural Route of InfectionAuthor item Greenlee, Justin item Smith, Jodi item Kunkle, RobertSubmitted to: American College of Veterinary Pathologists MeetingPublication Type: Abstract OnlyPublication Acceptance Date: 10/30/2010Publication Date: 10/30/2010Citation: Greenlee, J.J., Smith, J.D., Kunkle, R.A. 2010. White-tailed deer susceptible to scrapie by natural route of infection [abstract]. American College of Veterinary Pathologists. Paper No. 81.Interpretive Summary:Technical Abstract: Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. Previous experiments demonstrated that white-tailed deer are susceptible to sheep-derived scrapie by intracranial inoculation. The purpose of an ongoing study is to determine susceptibility of white-tailed deer to scrapie after a natural route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep clinically affected with scrapie. Non-inoculated deer were maintained as negative controls. All deer are observed daily for clinical signs. Deer are euthanized and necropsied when neurologic disease is evident. One animal was euthanized 15 months post-inoculation (MPI) due to an injury. At that time, examination of brain and lymphoid tissues by immunohistochemistry (IHC) and western blot (WB) were negative. A second deer developed pneumonia and was necropsied at 28 MPI. Tissues from this deer were positive for scrapie by IHC and WB. Tissues with PrPd immunoreactivity included brainstem and various lymphoid tissues including tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. The remaining deer are under observation for clinical signs.This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.We inoculated white-tailed deer with the scrapie agent from ARQ/ARQ sheep, which resulted in 100% attack rates by either the intracranial or oronasal route of inoculation.While scrapie is not known to occur in free-ranging populations of white-tailed deer, experimental cases are difficult to differentiate from CWD. This work raises the potential concern that scrapie infected deer could serve as a confounding factor to scrapie eradication programs as scrapie from deer seems to be transmissible to sheep by the oronasal route.This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.what about cwd and cattle?***In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research, however, suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD is affecting wild and farmed cervid populations in endemic areas with some deer populations decreasing as a result.SNIP...see also cwd to cattle ;Monday, April 04, 2016*** Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle ***
WEDNESDAY, APRIL 24, 2019USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019WEDNESDAY, JULY 31, 2019The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-LTHURSDAY, AUGUST 20, 2020Why is USDA "only" BSE TSE Prion testing 25,000 samples a year?Diagnosis and Reporting of Creutzfeldt-Jakob DiseaseSingeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA Diagnosis and Reporting of Creutzfeldt-Jakob Disease To the Editor:In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.. Terry S. Singeltary, Sr Bacliff, Tex1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.doi:10.1016/S1473-3099(03)00715-1 Copyright © 2003 Published by Elsevier Ltd. NewsdeskTracking spongiform encephalopathies in North AmericaXavier BoschAvailable online 29 July 2003.Volume 3, Issue 8, August 2003, Page 463“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem..”January 28, 2003; 60 (2) VIEWS & REVIEWSRE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States Terry S. Singeltary, retired (medically)Published March 26, 200326 March 2003Terry S. Singeltary, retired (medically) CJD WATCHI lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?re-Human Prion Diseases in the United States
Posted by flounder on 01 Jan 2010 at 18:11 GMT
SPORADIC CJD LAYING ODDS SingeltaryIn briefBMJ 2000; 320 doi: https://doi.org/10.1136/bmj.320.7226.8/b (Published 01 January 2000)Cite this as: BMJ 2000;320:8Rapid Response:02 January 2000Terry S SingeltaryretiredU.S. Scientist should be concerned with a CJD epidemic in the U.S., as well... In reading your short article about 'Scientist warn of CJD epidemic' news in brief Jan. 1, 2000. I find the findings in the PNAS old news, made famous again. Why is the U.S. still sitting on their butts, ignoring the facts? We have the beginning of a CJD epidemic in the U.S., and the U.S. Gov. is doing everything in it's power to conceal it.The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.Something else I find odd, page 16;"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."A few more factors to consider, page 15;"Figure 26 compares animal protein production for the two countries. The calculations are based on slaughter numbers, fallen stock estimates, and product yield coefficients. This approach is used due to variation of up to 80 percent from different reported sources. At 3.6 million tons, the United States produces 8 times more animal rendered product than the United Kingdom.""The risk of introducing the BSE agent through sheep meat and bone meal is more acute in both relative and absolute terms in the United Kingdom (Figures 27 and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in the United States. For sheep greater than 1 year, this is less than one-tenth of one percent of the United States supply.""The potential risk of amplification of the BSE agent through cattle meat and bone meal is much greater in the United States where it accounts for 59 percent of total product or almost 5 times more than the total amount of rendered product in the United Kingdom."Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow.Considering all this, the sheep to cow ration is meaningless. As I said, it's 24 pages of B.S.e.To be continued...Terry S. Singeltary Sr.Bacliff, Texas USACompeting interests: No competing interestsRapid response to:US scientists develop a possible test for BSE15 November 1999Terry S SingeltaryNABMJ 1999; 319 doi: https://doi.org/10.1136/bmj.319.7220.1312b (Published 13 November 1999)Cite this as: BMJ 1999;319:1312Article Related content Article metricsRapid responsesResponse Rapid Response: Re: vCJD in the USA * BSE in U.S. In reading the recent article in the BMJ about the potential BSE tests being developed in the U.S. and Bart Van Everbroeck reply. It does not surprize me, that the U.S. has been concealing vCJD. There have been people dying from CJD, with all the symptoms and pathological findings that resemble U.K. vCJD for some time. It just seems that when there is one found, they seem to change the clarical classification of the disease, to fit their agenda. I have several autopsies, stating kuru type amyloid plaques, one of the victims was 41 years of age. Also, my Mom died a most hideous death, Heidenhain Variant Creutzfeldt Jakob disease. Her symptoms resemble that of all the U.K. vCJD victims. She would jerk so bad at times, it would take 3 of us to hold her down, while she screamed "God, what's wrong with me, why can't I stop this." 1st of symptoms to death, 10 weeks, she went blind in the first few weeks. But, then they told me that this was just another strain of sporadic CJD. They can call it what ever they want, but I know what I saw, and what she went through. Sporadic, simply means, they do not know. My neighbors Mom also died from CJD. She had been taking a nutritional supplement which contained the following; vacuum dried bovine BRAIN, bone meal, bovine EYE, veal bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach. As I said, this woman taking these nutritional supplements, died from CJD. The particular batch of pills that was located, in which she was taking, was tested. From what I have heard, they came up negative, for the prion protein. But, in the same breath, they said their testing, may not have been strong enough to pick up the infectivity. Plus, she had been taking these type pills for years, so, could it have come from another batch?CWD is just a small piece of a very big puzzle. I have seen while deer hunting, deer, squirrels and birds, eating from cattle feed troughs where they feed cattle, the high protein cattle by products, at least up until Aug. 4, 1997.So why would it be so hard to believe that this is how they might become infected with a TSE. Or, even by potentially infected land. It's been well documented that it could be possible, from scrapie. Cats becoming infected with a TSE. Have you ever read the ingredients on the labels of cat and dog food? But, they do not put these tissues from these animals in pharmaceuticals, cosmetics, nutritional supplements, hGH, hPG, blood products, heart valves, and the many more products that come from bovine, ovine, or porcine tissues and organs. So, as I said, this CWD would be a small piece of a very big puzzle. But, it is here, and it most likely has killed. You see, greed is what caused this catastrophe, rendering and feeding practices. But, once Pandora's box was opened, the potential routes of infection became endless.No BSE in the U.S.A.? I would not be so sure of that considering that since 1990;Since 1990 the U.S. has raised 1,250,880,700 cattle;Since 1990 the U.S. has ONLY checked 8,881 cattle brains for BSE, as of Oct. 4, 1999;There are apprx. 100,000 DOWNER cattle annually in the U.S., that up until Aug. 4, 1997 went to the renders for feed;Scrapie running rampant for years in the U.S., 950 infected FLOCKS, as of Aug. 1999;Our feeding and rendering practices have mirrored that of the U.K. for years, some say it was worse. Everything from the downer cattle, to those scrapie infected sheep, to any roadkill, including the city police horse and the circus elephant went to the renders for feed and other products for consumption. Then they only implemented a partial feed ban on Aug. 4, 1997, but pigs, chickens, dogs, and cats, and humans were exempt from that ban. So they can still feed pigs and chickens those potentially TSE tainted by-products, and then they can still feed those by-products back to the cows. I believe it was Dr. Joe Gibbs, that said, the prion protein, can survive the digestinal track. So you have stopped nothing. It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses. Speaking of autopsies, I have a stack of them, from CJD victims. You would be surprised of the number of them, who ate cow brains, elk brains, deer brains, or hog brains.I believe all these TSE's are going to be related, and originally caused by the same greedy Industries, and they will be many. Not just the Renders, but you now see, that they are re-using medical devices that were meant for disposal. Some medical institutions do not follow proper auto- claving procedures (even Olympus has put out a medical warning on their endescopes about CJD, and the fact you cannot properly clean these instruments from TSE's), and this is just one product. Another route of infection.Regardless what the Federal Government in the U.S. says. It's here, I have seen it, and the longer they keep sweeping it under the rug and denying the fact that we have a serious problem, one that could surpass aids (not now, but in the years to come, due to the incubation period), they will be responsible for the continued spreading of this deadly disease.It's their move, it's CHECK, but once CHECKMATE has been called, how many thousands or millions, will be at risk or infected or even dead. You can't play around with these TSE's. I cannot stress that enough. They are only looking at body bags, and the fact the count is so low. But, then you have to look at the fact it is not a reportable disease in most states, mis-diagnosis, no autopsies performed. The fact that their one-in-a- million theory is a crude survey done about 5 years ago, that's a joke, under the above circumstances. A bad joke indeed........The truth will come, but how many more have to die such a hideous death. It's the Government's call, and they need to make a serious move, soon. This problem, potential epidemic, is not going away, by itself.Terry S. Singeltary Sr.Bacliff, Texas 77518 USAflounder@wt.netCompeting interests: No competing interests
TUESDAY, DECEMBER 01, 2020Sporadic Creutzfeldt Jakob Disease sCJD and Human TSE Prion Annual Report December 14, 2020WEDNESDAY, OCTOBER 21, 2020Human Prion Disease Surveillance in Washington State, 2006-2017Sunday, December 27, 2020First autopsy proven case of VPSPr: Variably protease‐sensitive prionopathy in Japan
TUESDAY, DECEMBER 01, 2020Sporadic Creutzfeldt Jakob Disease sCJD and Human TSE Prion Annual Report December 14, 2020Wednesday, December 16, 2020Expanding spectrum of prion diseases Prusiner et al
Terry S. Singeltary Sr.Bacliff, Texas USA 77518
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