Friday, August 26, 2016

Journal Journal of Toxicology and Environmental Health, Part A Volume 79, 2016 - Issue 16-17 Prion Research in Perspective IV CANADA BSE CWD SCRAPIE CJD TSE Prion Disease

Journal Journal of Toxicology and Environmental Health, Part A Volume 79, 2016 - Issue 16-17 Prion Research in Perspective IV

 

Volume 79, 2016 - Issue 16-17

 

Prion Research in Perspective IV

 

Submit an article Back to journal

 

editorial

 

Preface—Prion research in perspective IV

 

Neil Cashman, Shalu Darshan & Michael G. Tyshenko

 

Page 675-676 | Published online: 24 Aug 2016

 

“Prion Research in Perspective IV” is PrioNet Canada’s fourth open paper call and maintains its mandate allowing PrioNet Canada researchers, the Alberta Prion Research Institute, and other partner organizations a venue to publish their latest research.

 

The lead papers deal with stochastic models that estimate previous and future prion disease epidemics in Canada. Various risk models have been developed to estimate the number of animals incubating the disease, including bovine spongiform encephalopathy (BSE)-infected animals undetected by surveillance systems in several BSE-affected countries. The first article, by Oraby et al., presents a stochastic model to estimate the risk of BSE in Canada from importation of cattle and meat and bone meal (MBM) from high-risk countries. The model simulates the amount of imported infectivity, as well as its recycling and propagation through rendering and feeding processes. The model is used to develop a distribution of the yearly number of newly infected animals (infection incident) and the yearly cumulative number of infected cattle (prevalent cases), as well as the yearly number of cattle slaughtered for human consumption. Scenario analysis is used to investigate the sensitivity of the model predictions of the BSE risk in Canada to the choice of model parameters.

 

The second article, by Al-Arydah et al., looks at the application of mathematical modeling to manage chronic wasting disease (CWD) in wild cervids under alternative harvesting scenarios.

 

The third article, by Al-Zoughool et al., presents a different model that uses a Bayesian back-calculation method to estimate the risk of BSE in Canada during the time period from 1996–2011.

 

The forward projection models for BSE and especially CWD provide those managing the outbreaks to explore different management options, response scenarios, and mixes. The use of expert opinion in this regard is vitally important. The fourth article, by Oraby et al., and the fifth article, by Tyshenko et al., investigate the use of expert opinion for prion disease management options. Oraby et al. use three different expert opinion exercises (1, expert views of the most likely scenarios for the evolution of the CWD among cervid populations in Canada; 2, ranking analyses of the importance of direct and indirect transmission routes; and 3, rating analyses of the CWD control measures in farmed and wild cervids).

 

In the fifth article, Tyshenko et al. use a formalized expert elicitation exercise with target questions to help structure the issues surrounding CWD transmission and hence provide a rational basis for estimating some the risk factors for which evidence is currently lacking. Uncertainties for many transmission issues surrounding CWD were determined to be large by the expert group highlighting areas requiring more research. The elicited values can be used as surrogate values for management purposes until research evidence becomes available.

 

The sixth and seventh articles from Dr. Goddard’s research group (University of Alberta) investigate the economic impacts of prion disease. The sixth article, by Muringai and Goddard, considers the long-term impacts of BSE on beef risk perceptions and risk attitudes in Canada. Even though the first domestic case of BSE was reported in the year 2003, the authors found that concerns about BSE were still lingering and contributing to consumers’ risk perceptions about consuming beef several years later.

 

The seventh and final article, by Chiu et al., investigates CWD and caribou consumption in northern Canadian communities. The authors conclude with a warning that although CWD is not currently a threat to caribou populations, management efforts to minimize the spread of the transmissible spongiform encephalopathies in wild deer populations should be pursued to reduce the chance of prion disease transmission to caribou populations. CWD in caribou could have significant regional socioeconomic impacts in terms of aggregate food supply available to northern communities.

 

Collectively, the articles in this fourth and final volume once again showcase the excellent caliber of research funded and supported by PrioNet Canada.

 


 

Volume 79, 2016 - Issue 16-17

 

Prion Research in Perspective IV

 

research article

 

A stochastic model of the bovine spongiform encephalopathy epidemic in Canada

 

Tamer Oraby, Mustafa Al-Zoughool, Susie Elsaadany & Daniel Krewski

 

Page 677-689 | Published online: 24 Aug 2016

 

ABSTRACT

 

Bovine spongiform encephalopathy (BSE) appeared in the United Kingdom in the mid 1980s, and has been attributed to the use of meat and bone meal (MBM) in cattle feed contaminated with a scrapie-like agent. Import of infectious materials from a country where BSE has occurred is believed to be the major factor underlying the spread of the BSE epidemic to other countries. This study presents a new stochastic model developed to estimate risk of BSE from importation of cattle infected with the BSE agent. The model describes the propagation of the BSE agent through the Canadian cattle herd through rendering and feeding processes, following importation of cattle with infectious prions. This model was used estimate the annual number of newly infected animals each year over the period 1980–2019. Model predictions suggested that the number of BSE infections in Canada might have been approximately 40-fold greater than the actual number of clinically diagnosed cases. Under complete compliance with the 2007 ban on feeding MBM, this model further predicts that BSE is disappearing from the Canadian cattle system. A series of sensitivity analyses was also conducted to test the robustness of model predictions to alternative assumptions about factors affecting the evolution of the Canadian BSE epidemic.

 


 

Volume 79, 2016 - Issue 16-17 Prion Research in Perspective IV Submit an article Back to journal 0 Views 0 CrossRef citations 0 Altmetric be0ef6915d1b2200a248b7195d01ef22 research article Long-term impacts of bovine spongiform encephalopathy on beef risk perceptions and risk attitudes in Canada Violet Muringai Department of Resource Economics and Environmental Sociology, University of Alberta, Edmonton, Alberta, Canada & Ellen Goddard Department of Resource Economics and Environmental Sociology, University of Alberta, Edmonton, Alberta, CanadaCorrespondenceellen.goddard@ualberta.ca Page 746-761 | Published online: 24 Aug 2016 Page 746-761 Published online: 24 Aug 2016 Download citation Crossmark Select Language​▼ Translator disclaimer Full Article Figures & data References You need access

 

Metrics Reprints & Permissions Get access /doi/full/10.1080/15287394.2016.1174008?needAccess=true ABSTRACT ABSTRACT

 

In this study, the objective was to examine whether or not changes in bovine spongiform encephalopathy (BSE) concerns exert an effect on people’s risk perceptions and risk attitudes regarding consuming beef in Canada, 8 years after finding the first domestic animal with BSE. Data were collected from two surveys (2071 respondents) conducted with the same respondents in 2008 and 2011 in Canada. Data on meat consumption for the same households were also available from the Nielsen Homescan panel over the period 2002 to 2009. Based on census data, the current sample is generally not representative of the Canadian population, but the sample is unique in that the same individuals responded to two surveys and there is an ability to track their evolving household purchases of beef before the first survey and between the two surveys. In essence, alterations in beef risk perceptions are significantly influenced by changes in concerns regarding (1) feed given to livestock, (2) animal diseases and BSE, (3) trust in manufacturers, the government, and farmers, and (4) demographic characteristics. There were significant differences in beef purchases across households, with alterations to their risk perceptions and risk attitudes. In conclusion, although the first domestic incident of BSE was in 2003, concerns regarding BSE are still contributing to consumers’ risk perceptions but not to their risk attitudes with respect to consumption of beef in 2011.

 


 

Volume 79, 2016 - Issue 16-17

 

Prion Research in Perspective IV

 

Altmetric

 

research article

 

Applications of mathematical modeling in managing the spread of chronic wasting disease (CWD) in wild deer under alternative harvesting scenarios

 

M. Al-arydah, M. C. Croteau, T. Oraby, R. J. Smith? & D. Krewski

 

Page 690-699 | Published online: 24 Aug 2016

 

Volume 79, 2016 - Issue 16-17 Prion Research in Perspective IV Submit an article Back to journal 0 Views 0 CrossRef citations 0 Altmetric be0ef6915d1b2200a248b7195d01ef22 research article A Bayesian back-calculation method to estimate the risk of bovine spongiform encephalopathy (BSE) in Canada during the period 1996–2011 Mustafa Al-Zoughool Department of Community and Environmental Health, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Saudi ArabiaCorrespondencezoughoolm@ksau-hs.edu.sa, Tamer Oraby School of Mathematical and Statistical Sciences, University of Texas Rio Grande Valley, Edinburg, Texas, USA & Daniel Krewski McLaughlin Center for Population Health Risk Assessment, University of Ottawa, Ottawa, Canada Page 700-712 | Published online: 24 Aug 2016 Page 700-712 Published online: 24 Aug 2016

 

Metrics Reprints & Permissions Get access /doi/full/10.1080/15287394.2016.1174004?needAccess=true ABSTRACT ABSTRACT

 

Seventeen typical cases of bovine spongiform encephalopathy (BSE) were detected in Canada the period of 2003-2011. The clinical incidence of BSE was censored by early slaughter, death, or exportation of infected cattle due to the long incubation period of BSE disease. The aim of this study was to estimate the infection incidence of BSE in birth cohorts during 1996–2004 and project infection frequency through to 2007. An estimate of the number of asymptomatic infected cattle slaughtered for human consumption is also provided. The number of incident, asymptomatic cases was assumed to follow a Poisson process. A Bayesian back-calculation approach was used to project the risk of contracting BSE in those birth cohorts. Model parameters and inputs were taken from scientific literature and governmental data sources. The projected number of infected cattle in birth cohorts spanning the period 1996–2007 was 492, with median 95% credible interval 258–830. If the requirement to remove specified risk material (SRM) from cattle prior to entering the food chain was not in place, the predicted number of slaughtered infected in the human food chain from 1996–2010 was 298, with a 95% credible interval 156–500. The magnitude of the BSE epidemic in Canada for 1996–2007 birth cohorts was estimated to be approximately 28-fold higher than the number of clinical cases detected through to October 2011. Although some of those cattle were slaughtered for human consumption, the requirement of SRM removal may have prevented most of the infectious material from entering the food chain.

 


 

   ABSTRACT

 

The application of a recently developed mathematical model for predicting the spread of chronic wasting disease (CWD) in wild deer was assessed under different scenarios where harvesting is employed in disease management. A process-based mathematical model for CWD transmission in wild deer populations was recently developed and parameterized by Al-arydah et al. (2011) to provide a scientific basis for understanding the factors that affect spread of CWD and evaluate concomitant disease-control strategies. The impact of gender on CWD transmission was shown to have a significant influence on the spread of the disease in the wild. Our model demonstrates a range of harvesting rates in which CWD is controlled and deer populations survive. However, if harvesting rates are too low, the disease remains endemic for decades. Conversely, the Canadian deer population is eradicated if harvesting rates are excessive. Future investigation includes building the model to assess the spread of CWD under different disease-management scenarios.

 


 

Volume 79, 2016 - Issue 16-17 Prion Research in Perspective IV Submit an article Back to journal 0 Views 0 CrossRef citations 0 Altmetric be0ef6915d1b2200a248b7195d01ef22 research article Expert elicitation on the uncertainties associated with chronic wasting disease Michael G. Tyshenko McLaughlin Centre for Population Health Risk Assessment, Institute of Population Health, University of Ottawa, Ottawa, Ontario, CanadaCorrespondencemtyshenk@uottawa.ca, Tamer Oraby Department of Mathematics, University of Texas-Pan American, Edinburg, Texas, USA, Shalu Darshan McLaughlin Centre for Population Health Risk Assessment, Institute of Population Health, University of Ottawa, Ottawa, Ontario, Canada, Margit Westphal McLaughlin Centre for Population Health Risk Assessment, Institute of Population Health, University of Ottawa, Ottawa, Ontario, Canada, Maxine C. Croteau McLaughlin Centre for Population Health Risk Assessment, Institute of Population Health, University of Ottawa, Ottawa, Ontario, Canada, Willy Aspinall Aspinall and Associates, Tisbury, United Kingdom School of Earth Sciences and Cabot Institute, University of Bristol, Bristol, United Kingdom, Susie Elsaadany Professional Guidelines and Public Health Practice Division, Centre for Infectious Disease Prevention and Control, Public Health Agency of Canada, Ottawa, Ontario, Canada, Daniel Krewski McLaughlin Centre for Population Health Risk Assessment, Institute of Population Health, University of Ottawa, Ottawa, Ontario, Canada Department of Epidemiology and Community Medicine, University of Ottawa, Ottawa, Ontario, Canada & Neil Cashman Brain Research Centre, University of British Columbia, Vancouver, British Columbia, Canada Page 729-745 | Published online: 24 Aug 2016 Page 729-745 Published online: 24 Aug 2016

 

Metrics Reprints & Permissions Get access /doi/full/10.1080/15287394.2016.1174007?needAccess=true ABSTRACT ABSTRACT

 

A high degree of uncertainty exists for chronic wasting disease (CWD) transmission factors in farmed and wild cervids. Evaluating the factors is important as it helps to inform future risk management strategies. Expert opinion is often used to assist decision making in a number of health, science, and technology domains where data may be sparse or missing. Using the “Classical Model” of elicitation, a group of experts was asked to estimate the most likely values for several risk factors affecting CWD transmission. The formalized expert elicitation helped structure the issues and hence provide a rational basis for estimating some transmission risk factors for which evidence is lacking. Considered judgments regarding environmental transmission, latency of CWD transmission, management, and species barrier were provided by the experts. Uncertainties for many items were determined to be large, highlighting areas requiring more research. The elicited values may be used as surrogate values until research evidence becomes available.

 


 

Journal Journal of Toxicology and Environmental Health, Part A Volume 79, 2016 - Issue 16-17 Prion Research in Perspective IV Submit an article Back to journal 0 Views 0 CrossRef citations 0 Altmetric be0ef6915d1b2200a248b7195d01ef22 research article Caribou consumption in northern Canadian communities Angie Chiu Department of Resource Economics & Environmental Sociology, University of Alberta, Edmonton, Alberta, Canada, Ellen Goddard Department of Resource Economics & Environmental Sociology, University of Alberta, Edmonton, Alberta, CanadaCorrespondenceellen.goddard@ualberta.ca & Brenda Parlee Department of Resource Economics & Environmental Sociology/Faculty of Native Studies, University of Alberta, Edmonton, Alberta, Canada Page 762-797 | Published online: 24 Aug 2016 Page 762-797 Published online: 24 Aug 2016

 

Metrics Reprints & Permissions Get access /doi/full/10.1080/15287394.2016.1174011?needAccess=true ABSTRACT ABSTRACT

 

Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) found in both farmed and wild deer, elk, and moose in the United States and Canada. Surveillance efforts in North America identified the geographical distribution of the disease and mechanisms underlying distribution, although the possibility of transmission to other cervids, including caribou, and noncervids, including humans, is not well understood. Because of the documented importance of caribou (Rangifer tarandus) to human populations in the northern regions of Canada, a risk-management strategy for CWD requires an understanding of the extent of potential dietary exposure to CWD. Secondary 24-h dietary recalls conducted among Inuvialuit and Inuit in 4 communities in the Northwest Territories and Nunavut were employed in this study. Econometric demand systems were estimated to model the impacts of individual- and community-level socioeconomic characteristics on expenditures on caribou and other foods, in order to examine the households’ ability to consume other foods in response to changing levels of caribou consumption. Thirty-five percent of respondents reported consuming caribou in the survey period, and caribou comprised, on average, 26% of daily dietary intake by weight, or approximately 65 g/d, across individuals in the 4 communities. Consuming caribou was also shown to exert positive impacts on dietary quality, as measured by calorie intake and dietary diversity. Communities with less access to employment, income and food stores are predicted to be constrained in their ability to obtain an adequate diet in the event of scarcity of caribou meat.

 


 


 

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HOW TO FORCE FEED BSE TSE PRION AKA MAD COW TYPE DISEASE TO THE WORLD USDA FAS CFIA OIE

 

Date: 10/10/2003 GAIN Report Number: CA3065 CA3065 Canada Agricultural Situation This Week in Canadian Agriculture, Issue 37 2003 Approved by: Gary Groves U.S. Embassy Prepared by: Geroge Myles, Matthew Cahoon

 

snip...

 

GAIN Report - CA3065 Page 2 of 6

 

UNCLASSIFIED USDA Foreign Agricultural Service

 

This Week in Canadian Agriculture is a weekly review of Canadian agricultural industry developments of interest to the U.S. agricultural community. The issues summarized in this report cover a wide range of subject matter obtained from Canadian press reports, government press releases, and host country agricultural officials and representatives. Disclaimer: Any press report summaries in this report are included to bring U.S. readership closer to the pulse of Canadian developments in agriculture. In no way do the views and opinions of these sources reflect USDA’s, the U.S. Embassy’s, or any other U.S. Government agency’s point of view or official policy.

 

MORE COUNTRIES OPEN BORDERS TO CANADIAN BEEF: Antigua and Barbuda, Barbados, Jamaica, Philippines, Russia and Trinidad and Tobago have recently partially lifted their bans on Canadian products. The Canadian Food Inspection Agency is reportedly working with authorities in many of these countries on the conditions necessary for the resumption of exports. Agriculture and Agri-Food Minister Lyle Vanclief says that it demonstrates that countries are showing their confidence in the safety and quality of Canadian beef. "While our number one priority continues to be the full re-opening of the U.S. border to live Canadian cattle, we consider every step forward to be a victory for the Canadian agriculture industry." As of October 8 2003, Canada has shipped more than 44 million pounds of boxed beef, veal, processed beef products and bovine livers to the United States. Shipments to Mexico are expected to begin within days. Mr. Vanclief noted work continues on fully reopening the borders of Canada's other trading partners.

 

JAPAN BSE NEWS WON’T IMPACT U.S. RULEMAKING PROCESS SAY CATTLEMEN: News of an eighth case of BSE found in Japan, this time in an animal that is reported to be 23 months of age won’t impact rulemaking in the U.S. to expand the list of Canadian products eligible for export, including live cattle under 30 months, says the Canadian Cattlemen’s Association (CCA). The CCA believes that the abnormal case is probably linked to high levels of infected feed in Japan at an early age. In its BSE update to members, the CCA states that the proposed U.S. rule for exporting live cattle to the U.S. has now gone to the U.S. Office of Management and Budget, which normally has up to 90 days to complete the draft rule, but may complete it sooner. Then, the draft rule will be published in the Federal Register for a comment period of a minimum of 30 days. The CCA anticipates that the soonest Canadian live cattle will begin to move to the U.S. is during the first quarter of 2004.

 

YEAR-ROUND CATTLE IMPORTS NOT YET POSSIBLE SAYS MINISTER: Canada’s Agriculture Minister Lyle Vanclief responded to questions in Parliament this week on live cattle imports saying that until risk assessment studies by the Canadian Food Inspection Agency are complete, the border will remain closed to year-round cattle imports from the United States. Canada’s cattle industry has been lobbying strenuously for regulatory change that would permit year-round imports currently prohibited under regulations pertaining to bluetongue and anaplasmosis. In recent years, U.S. feeder cattle have entered Canada during the October to March period (the non-vector period) under Canada’s Restricted Feeder Program. The CCA believes that easing the regulation to enable year-round access to U.S. feeder cattle poses minimal risk and addresses concerns related to normal trade and an open border. Trade potential is significant. During the period October 2000 to March 2001, Canadian feedlots imported more than 209,000 head of U.S. feeder cattle with an estimated value exceeding $150 million.

 


 

 Date: 12/19/2003 GAIN Report Number: KS3074 KS3074 Korea, Republic of FAIRS Product Specific Meat & Poultry Health Certificate for Korean Exports 2003 Approved by: Marcus E. Lower U.S. Embassy Prepared by: Stan Phillips / Yong Keun Ban Report Highlights: Due to the outbreak of BSE in Canada, the Republic of Korea has changed the type of FSIS health certificates required for exporting meat and processed meat products to Korea. This report provides information on the current FSIS health certificates required for exports to the Republic of Korea. Includes PSD Changes: No Includes Trade Matrix: No Unscheduled Report Seoul [KS1] [KS] USDA Foreign Agricultural Service GAIN Report Global Agriculture Information Network Template Version 2.09 GAIN Report - KS3074 Page 2 of 3 UNCLASSIFIED USDA Foreign Agricultural Service FSIS Health Certificates Required for Exporting Meat Products to the Republic of Korea Meat quarantine inspections are very strict in Korea. No meat products will clear Korean Customs without the necessary certificates and required information. Recently, new FSIS Health certificates for importing meat products from the United States have been put in place, in conjunction with the outbreak of BSE in Canada. The current FSIS Forms may undergo another revision, depending on the outcome of the comment gathering process on the draft proposal to allow live cattle imports from Canada. However, the following is the health certificates that are required for exporting meat products into the Republic of Korea at present. Red Meat Products: Red meat products must be accompanied by the following FSIS certificates (FSIS Form 9060-5 for every shipment and all or one of the FSIS form 9305-4, 9305-5 and/or 9305-6, depending on the type of meat used for producing the final product.): - FSIS Form 9060-5, Meat and Poultry Export Certificate of Wholesomeness (All meats must have this certificate) - FSIS Form 9305-4, Certificate for Export of Beef and Beef Products to the Republic of Korea (For beef and beef products) - FSIS Form 9305-5 Certificate for Export of Pork Meat to the Republic of Korea (For pork and pork products) - FSIS Form 9305-6 Certificate for Export of Sheep and Goat Meat and Sheep and Goat Meat Products to the Republic of Korea (For sheep and goat meat products) Note: Form 9305-4, 9305-5, and 9305-6 are new certificates replacing Form 9305-3. The new certificates have been required for unprocessed meat (e.g., cut meat) since October 1, 2003. The new certificates are also required for processed beef, pork, sheep and/or lamb products from December 1, 2003. If the processed product contains more than one ingredient (e.g., beef and pork), then it will be required to be accompanied by the respective certificates (e.g., in the case of beef and pork, 9060-5, 9305-4 and 9305-5). Additional Information for Processed Meat Products: Processed meat products such as sausages, hamburger patties and ground meat do not need to indicate slaughter information on the FSIS Form (9305-4, 9305-5, and 9305-6). These products are required to indicate only processing information. Livestock or Dairy Products: To get an exemption from quarantine inspection for livestock or dairy products that have undergone a pasteurization or sterilization process and meet the Korean government standards, one of following documents shall be furnished to confirm the product has been pasteurized or sterilized according to Korean standards: - Health certificate issued by exporting government - Manufacturing process verified by exporting government - Notarized verification document issued by the representative of the manufacturing company In response to the BSE issues, Korea has currently banned all ruminant animals and their products originating from 30 European nations, Japan, Israel, and Canada. Korea now requires certification that the imported ruminant or ruminant product did not originate from GAIN Report - KS3074 Page 3 of 3 UNCLASSIFIED USDA Foreign Agricultural Service the countries listed by the Korean government as BSE outbreak nations. Certification of a US product from "non-BSE origin countries" can be a statement issued by the U.S.

 


 

 Date: 8/26/2004

 

GAIN Report Number: E34050

 

E34050

 

EU-25

 

Livestock and Products

 

EFSA publishes new report on the Geographical BSE Risk Assessment

 

2004

 

Approved by:

 

Stan Cohen

 

U.S. Mission to the EU

 

Prepared by:

 

Karin Bendz

 

Report Highlights:

 

In August 2004 the European Food Safety Agency (EFSA) published new scientific reports on the GBR classifications for seven countries. The U.S. was classified in level three which means "BSE is likely but not confirmed or confirmed at a lower level".

 

The risk assessment was based on information submitted by the countries concerned, and relates in particular to imports of bovines and meat and bone meal from the UK and other BSE-risk countries.

 

Includes PSD Changes: No

 

Includes Trade Matrix: No

 

Unscheduled Report

 

Brussels USEU [BE2]

 

[E3]

 

USDA Foreign Agricultural Service

 

GAIN Report

 

Global Agriculture Information Network

 

Template Version 2.09

 

GAIN Report - E34050 Page 2 of 4

 

UNCLASSIFIED USDA Foreign Agricultural Service

 

On August 20, 2004 the European Food Safety Authority (EFSA) published up-to-date scientific reports on the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) for seven countries. The countries are Australia, Canada, Mexico, Norway, South Africa, Sweden and the United States.

 

The GBR evaluations are based on information submitted by the countries concerned in response to a European Commission recommendation in 1998, which set out the information requirements for such an assessment. The scientific reports address the GBR in a number of countries based on data covering the period 1980-2003.

 

The information concerns in particular imports of bovines and meat and bone meal (MBM) from the United Kingdom and other BSE-risk countries, rendering standards for animal byproducts, use specific risk materials (SRM’s), and feeding of meat and bone meal (MBM) to ruminants.

 

Table of the classification of the countries

 

GBR of the country/Region

 

GBR

 

level

 

Presence of one or more cattle clinically or preclinically

 

infected with the BSE agent in a

 

geographical region/country

 

Status Before Status After

 

I Highly unlikely Australia (I)

 

Norway (I) Australia (I)

 

II Unlikely but not excluded

 

Sweden (II)

 

Canada (II)

 

USA (II)

 

Sweden (II)

 

Norway (II)

 

III Likely but not confirmed or confirmed at a lower level South Africa (N/A)

 

Mexico (N/A),

 

Canada (III)

 

USA (III)

 

South Africa (III)

 

Mexico (III)

 

IV Confirmed at a higher level

 

The result of the report is that Australia and Sweden were kept at the same level as before the update, while Norway, Canada and the U.S. were classed at a higher level.

 

The EFSA concludes that the BSE agent that was found in the U.S. was probably imported into the U.S. and could have reached domestic cattle in the middle of the 1980s. Cattle imported in the mid-1980s could have been rendered in the late 1980s and therefore led to an internal challenge in the early 1990s. EFSA concludes that it is possible that MBM’s imported into the U.S. reached domestic cattle and posed a risk in the early 1990s.

 

According to the EFSA, a processing risk developed in the late 1980s and early 1990s when cattle imports from BSE-risk countries were slaughtered or died, and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid-1990s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.

 

This assessment deviates from the previous assessment (Scientific Steering Committee (SSC) opinion, 2000) because at that time several exporting countries were not considered a potential risk.

 

GAIN Report - E34050 Page 3 of 4

 

UNCLASSIFIED USDA Foreign Agricultural Service

 

It is also worth noting that the current GBR conclusions are not dependent on the large exchange of imports between the U.S. and Canada. The threat from European exports to the U.S. varied from moderate to high. These challenges indicate that it was likely that BSE infectivity was introduced into the North American continent.

 

EFSA and its Scientific Expert Working group on GBR are concerned that the inspection missions of the Food and Veterinary office (FVO – DG SANCO) conducted in member states and third countries didn’t assess the available information in light of the risk posed by BSE. They recommend including BSE-related aspects in future inspection missions.

 

Expected development of the GBR

 

As long as there are no significant changes in rendering or feeding, the stability remains very to extremely unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.

 

Canada

 

For Canada the EFSA evaluation concludes that the BSE agent was probably imported to the country in the 1980s and could have been rendered in the late 1980s and therefore posed a risk in the early 1990s. A certain risk that BSE-infected cattle entered processing in Canada, and were at least partly rendered for feed, occurred in the early 1990s when cattle imported from the UK in the mid-1980s could have been slaughtered. This risk grew significantly in the mid-1990s when domestic cattle, infected by imported MBM, reached processing. This risk increased over the years with continued imports of cattle and MBM from BSE risk countries.

 

Australia

 

The EFSA concludes that in the case of Australia, an extremely or very unstable system was exposed to a very low or negligible challenge through the import of cattle. Given the negligible level of external challenge through MBM it is highly unlikely that any internal risk occurred.

 

This report is drafted from the EFSA scientific report. The full report can be found at:

 

www.efsa.eu.int

 

GAIN Report - E34050 Page 4 of 4

 

UNCLASSIFIED USDA Foreign Agricultural Service

 

Visit our website: our website www.useu.be/agri/usda.html provides a broad range of useful information on EU import rules and food laws and allows easy access to USEU reports, trade information and other practical information.

 

E-mail: AgUSEUBrussels@usda.gov Related reports from USEU Brussels: Report Number Title Date Released E24047 Host Country BSE Response Questionnaire 2004 04/05/04 E24044 European Commissioner David Byrn’s first regular BSE report of the year 04/04/04 E24006 BSE – Potential Concerns of the European Commission 01/09/04 These reports can be accessed through our website www.useu.be/agri or through the FAS website http://www.fas.usda.gov/scriptsw/attacherep/default.asp.

 


 

Date: 9/1/2004 GAIN Report Number: CA4063 CA4063 Canada Livestock and Products Annual 2004 Approved by: Gary C. Groves U.S. Embassy Prepared by: George Myles Report Highlights: Canada’s cattle industry is formulating a made-in-Canada strategy to deal with a large surplus of cattle related to the U.S. border closure to Canadian live cattle exports following the discovery of BSE in an Alberta beef cow in May 2003. Canadian fed cattle prices are down 30-35% from their pre-BSE levels and prices for some classes of non-fed slaughter cattle are at distress levels. Since the R-Calf injunction of April 2004, hope that the U.S. border would soon be open has turned to despair among many industry participants.

 

Includes PSD Changes: Yes Includes Trade Matrix: No Annual Report Ottawa [CA1] [CA]

 

a USDA proposed rule that would amend U.S. regulations to add Canada to a category of regions that present minimal risk of introducing BSE into the United States that would permit the importation of live Canadian cattle.

 

In the three years preceding the discovery of Canada’s first case of BSE in May 2003, Canada exported an average of 1.3 million head annually of predominantly slaughter cattle into the U.S. market, a level often representing as much as a third of its slaughter-type animals. Canadian fed cattle prices are down 30-35% from their pre-BSE levels and some classes of non-fed slaughter cattle prices are at distress levels.

 

Since the R-Calf injunction of April 2004, hope that the U.S. border would soon be open has turned to despair among many industry participants. As a result, the Canadian cattle industry is formulating a made in Canada strategy to deal with a surplus of cattle. Canada’s Agriculture Minister, Andy Mitchell supports the made-in-Canada solutions, including increased slaughter capacity, matching supply of animals to capacity available and increasing access to foreign markets. He believes the Canadian cattle industry needs to reposition itself to lessen its reliance on live cattle exports.

 

Key Features of A Strategic Plan:

 

The Canadian Cattlemen’s Association (CCA) is exploring contingency plans to address a cattle inventory backlog and insufficient domestic slaughter capacity. At the CCA’s annual convention held in mid-August 2004, the association revealed it is considering a set aside style program with the support of the provinces and the federal government whereby fed cattle would be set aside on a holding ration and enrolled in a type of regulated marketing schedule to enable cattle to be slaughtered prior to 30 months of age. The plan may include government assistance funds to offset feed costs during a holding period. The CCA is hopeful that a plan will be forthcoming in the next few weeks. The industry has additional longer-term goals to increase slaughter capacity particularly for cull animals and to increase its market share of the domestic market by displacing imported product.

 

Increasing Slaughter Capacity

 

According to industry sources, existing slaughter capacity (federal and provincial) in Canada is currently about 79,000 head per week. Through expansion to existing facilities, plant conversion, and new investment, the industry is targeting to have capacity increase to 86,000 by spring 2005 and to 98,000 by 2006. The medium term solution includes recapturing the ability to process non-fed slaughter cattle that previously were exported live to plants in the United States. A major part of this strategy is to process for consumption a much greater share of Canadian domestic needs for manufacturing type beef that in recent years has been dominated by imported product. In fact, past GOC policies that encouraged the importation of manufacturing beef led, in part, to the decline in number of non-fed slaughter facilities that are so desperately needed under present circumstances. Since BSE, the GOC has responded by not issuing supplementary import permits for beef beyond Canada’s non-NAFTA tariff rate quota.

 

GAIN Report - CA4063 Page 8 of 13

 

UNCLASSIFIED USDA Foreign Agricultural Service

 

Trade

 

Imports: Canadian beef imports fell dramatically in the first half of 2004 reflecting in part, the additional supplies of domestic beef and the GOC policy to restrict supplementary import permits for non-NAFTA beef. Also, there was some development time surrounding the U.S. Beef Export Verification Program administered by the Agricultural Marketing Service of USDA to ensure that U.S. beef exports to Canada meet Canadian BSE import requirements. In the January to June period of 2004, total Canadian beef imports ran 70% below the level for the same period a year ago. All major suppliers to Canada’s beef market noted significant reductions in their sales to Canada.

 

Exports: Canadian beef exports suffered sharply in 2003 following the single case of BSE discovered in Alberta in May 2003. However, since the U.S. action on August 8, 2003 to permit imports of certain Canadian boneless beef and beef products, Canadian beef exports to the United States have recovered almost to their pre-BSE levels and beef exports to Mexico have advanced strongly beyond their pre-BSE levels. Prospects for 2005 beef exports generally rest on U.S. and Mexican markets although Macau and the Philippines are accepting Canadian beef.

 

Policy

 

The GOC continues to lobby USDA at every opportunity in its attempt to secure the reopening pf the U.S. border to Canadian live cattle. Last week, Agriculture Minister Mitchell met with U.S. Secretary of Agriculture Ann Veneman to discuss the border situation. Canada’s BSE policies including those related to the removal of Specified Risk Materials (SRM), feed bans, surveillance and imports are detailed on the following Canadian Food Inspection Agency Inspection webpage:

 


 


 

*** Last week, Agriculture Minister Mitchell met with U.S. Secretary of Agriculture Ann Veneman to discuss the border situation.

 

 a review of the mad cow debacle by USDA et al under Agriculture Secretary Ann Veneman ;

 

 US SENATOR AND STAN THE MAN SLAM USDA ''DAMNING TESTIMONY''

 

 Senator Michael Machado from California

 

 ''USDA does not know what's going on''.

 

 ''USDA is protecting the industry''.

 

 ''SHOULD the state of California step in''

 

 Stanley Prusiner

 

 ''nobody has ever ask us to comment''

 

 ''they don't want us to comment''

 

 ''they never ask''

 

 i tried to see Venemon, after Candian cow was discovered with BSE. went to see lyle. after talking with him... absolute ignorance... then thought I should see Venemon... it was clear his entire policy was to get cattle bonless beef prods across the border... nothing else mattered...

 

 his aids confirmed this... 5 times i tried to see Venemon, never worked... eventually met with carl rove the political... he is the one that arranged meeting with Venemon... just trying to give you a sense of the distance... healh public safety...

 

 was never contacted...

 

 yes i believe that prions are bad to eat and you can die from them... END

 

 Dr. Stan bashing Ann Veneman - 3 minutes

 


 

 Recall Authority and Mad Cow Disease: Is the Current System Good for Californians?

 

 Tuesday, February 24, 2004

 

 JOINT HEARING

 

 AGRICULTURE AND WATER RESOURCES HEALTH AND HUMAN SERVICES AND SELECT COMMITTEE ON GOVERNMENT OVERSIGHT - MACHADO, ORTIZ, and SPEIER, Chairs

 

 ALL VIDEOS OF THIS HEARING HAVE BEEN REMOVED FROM THE WWW, LIKE IT NEVER HAPPENED...but we know different...TSS

 

 -------- Original Message -------- Subject: Re: Congressman Henry Waxmans's Letter to the Honorable Ann Veneman on failure by USDA/APHIS TO TEST TEXAS MAD COW Date: Wed, 9 Jun 2004 16:48:31 -0500 From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de References: 40A8CD52.1070308@wt.net

 

 ######## Bovine Spongiform Encephalopathy #########

 

 USA BSE RED BOOK

 

 October 1998

 

 BSE Red Book 2.1-36

 

snip...see full text of USDA BSE cover up here ;

 

Thursday, October 22, 2015

 

*** Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened those mad cows in Texas ***

 


 

Voluntary Report - public distribution

 

Date: 1/7/2005

 

GAIN Report Number: CA5001

 

CA5001

 

Canada

 

Agricultural Situation

 

This Week in Canadian Agriculture, Issue 1

 

2005

 

Approved by: Gary Groves

 

U.S. Embassy

 

Prepared by: Christina Patterson and George Myles

 

Report Highlights:

 

* Canada Confirms Second Case of BSE * Reactions to Minimal Risk Rule and 2nd BSE Case in Canada * Birth Date Registration Service For Cattle * Despite BSE, Canadian Agricultural Exports to U.S. Remain Strong * Manitoba Confident of Successful Defense in Swine Anti- Dumping Case * Canadian Wheat Board Election Results * Toss of the Coin Gives Canada Majority on ECC Panel * Retaliation Tariff Could Drive Bean Seed Prices Higher * Drop in Ontario Corn Acreage Forecasted * Nothing More Than an Expensive Party Includes PSD Changes: No

 

Includes Trade Matrix: No

 

Unscheduled Report

 

Ottawa [CA1]

 

[CA]

 

USDA Foreign Agricultural Service

 

GAIN Report

 

Global Agriculture Information Network

 

Template Version 2.09

 

GAIN Report - CA5001 Page 2 of 4

 

UNCLASSIFIED USDA Foreign Agricultural Service

 

This Week in Canadian Agriculture is a weekly review of Canadian agricultural industry developments of interest to the U.S. agricultural community. The issues summarized in this report cover a wide range of subject matter obtained from Canadian press reports, government press releases, and host country agricultural officials and representatives.

 

Disclaimer: Any press report summaries in this report are included to bring U.S. readership closer to the pulse of Canadian developments in agriculture. In no way do the views and opinions of these sources reflect USDA’s, the U.S. Embassy’s, or any other U.S. Government agency’s point of view or official policy.

 

CANADA CONFIRMS SECOND CASE OF BSE: One day after the December 29, 2004 announcement of USDA's BSE minimal-risk rule that proposes the resumption of imports of cattle under 30 months from Canada and additional Canadian beef and ruminant products on March 7, 2005, Canada’s Food Inspection Agency (CFIA) announced that preliminary test results identified a BSE suspect animal in Alberta. After additional laboratory testing, it was confirmed on January 2, 2005 that an older dairy cow from Alberta was positive for bovine spongiform encephalopathy (BSE). The infected animal was born in 1996, prior to the introduction of Canada’s 1997 feed ban. It is suspected that the animal became infected by contaminated feed before the feed ban. On January 4, 2005, Ron DeHaven, Administrator, Animal and Plant Health Inspection Service, announced that USDA remains confident that the animal and public health measures that Canada has in place, including the removal of specified risk material (SRMs) from the human food chain, a ruminant-to-ruminant feed ban, a national surveillance program and import restrictions, combined with existing U.S. domestic safeguards and the additional safeguards announced as part of USDA's BSE minimal-risk rule announced Dec. 29 provide the utmost protections to U.S. consumers and livestock.

 

REACTIONS TO MINIMAL RISK RULE AND 2ND BSE CASE IN CANADA: During the hearing on the nomination of Nebraska Gov. Mike Johanns as Secretary of Agriculture, Johanns listened to several appeals from members of the Senate Agriculture Committee to slow down the opening of the Canadian border to live cattle imports from the March 7, 2005 scheduled date. Gov. Johanns assured the Committee that he intended to fully participate in congressional hearings related to the minimal risk rule. R-CALF USA, the Ranchers-Cattlemen Action Legal Fund, United Stockgrowers of America, posted a fund raising appeal on its website asking members to contribute generously to a continued effort to fight the re-opening of the border to Canadian live cattle. In a statement, American Meat Institute (AMI) President and CEO J. Patrick Boyle made the following comment: "Beef trade with Canada should move forward because the measures taken by both the U.S. and Canada, to ensure that beef is safe and wholesome, are working as planned." Mark Dopp of the American Meat Association reportedly said that Canadian cattle should be allowed into the U.S., given that the two countries now have almost identical rules in place when it comes to testing for and dealing with cases of mad cow disease. Calling Canadian beef unsafe is like calling your twin sister ugly," Dopp said.

 

snip...

 

DESPITE BSE, CANADIAN AGRICULTURAL EXPORTS TO U.S. REMAIN STRONG: Despite BSE border restrictions in effect throughout 2004, Canada managed an estimated $11.5 billion worth of agricultural exports to the U.S., up more than 10% from the 2003 level and more than 11% above the pre-BSE 2002 level. Increased beef exports were partially responsible. Since August 8, 2003, when the U.S. allowed imports of Canadian boneless beef from young cattle, the Canadian beef industry has slaughtered animals that can no longer be exported as live, and has taken advantage of strong U.S. wholesale meat prices. The value of Canadian fresh or frozen beef to the U.S. in the January to October period of 2004 was almost $1.0 billion, 58% greater than during the same period of 2003 and

 

GAIN Report - CA5001 Page 3 of 4

 

UNCLASSIFIED USDA Foreign Agricultural Service almost $100 million higher than the same period of 2002- before BSE! In addition, large increases in Canadian exports of pork, live swine, frozen french fries, vegetable oils, and snack foods to the U.S. all helped to more than offset the declines in the value of live cattle trade over the last couple of years.

 


 

*** Calling Canadian beef unsafe is like calling your twin sister ugly," Dopp said.

 


 

GAIN Report Number: CA5038 CA5038 Canada Agricultural Situation This Week in Canadian Agriculture, Issue 19 2005

 

*** bovine spongiform encephalopathy (BSE) The new policy would be less restrictive than the current one.

 

GOC RELEASES CONSULTATION DOCUMENT ON NEW BSE IMPORT POLICY IN LINE WITH OIE: The Canadian Food Inspection Agency (CFIA) is inviting public comment on a proposed new Canadian Import Policy to prevent bovine spongiform encephalopathy (BSE) in bovine animals and their products. The proposed policy would bring Canada’s approach in line with new World Organization for Animal Health (OIE) standards as well as the proposed North American import standard announced on March 29, 2005. It is based on the recognition that international knowledge of bovine spongiform encephalopathy (BSE) and me asures to mitigate its transmission have advanced significantly since Canada’s existing import policy for controlling BSE was established in 1997. The new policy would be less restrictive than the current one. Canada’s current policy permits the importation of live ruminants including, cattle, sheep and goats, and products derived from them, only after the exporting country has been officially recognized as BSE-free. Current science recognizes that the “ BSE-free” requirement is unnecessarily restrictive. The draft policy is based on a proposed new OIE three-tier system for classifying bovine-trading countries based on their BSE risk management regimes. In all cases, exporting countries would also have to continue to meet other non-BSE food safety and animal health

 

GAIN Report - CA5038 Page 3 of 4

 

UNCLASSIFIED USDA Foreign Agricultural Service

 

requirements before becoming eligible to ship to Canada under any of the new BSE risk categories. A consultation period ending on July 22, 2005 is being provided to allow interested parties the opportunity to provide comments on the draft policy. Notice of this consultation is being published in the Canada Gazette.

 

*** bovine spongiform encephalopathy (BSE) The new policy would be less restrictive than the current one.

 


 

Date: 8/26/2005 GAIN Report Number: CA5056 CA5056 Canada Livestock and Products Annual 2005 Approved by: Gary C. Groves U.S. Embassy Prepared by: George Myles

 

GAIN Report - CA5056 Page 3 of 16

 

UNCLASSIFIED USDA Foreign Agricultural Service

 

Executive Summary

 

* On July 18, 2005 after the implementation of the USDA minimal risk rule, the U.S. border re-opened to certain live cattle imports from Canada for the first time in more than two years, but imports from Canada have not resumed the average levels of the pre-BSE period. Part of the Canadian cattle industry’s repositioning strategy is to become less reliant on the U.S. processing industry by expanding domestic slaughter capacity.

 

* Another Canadian cattle industry restructuring goal is to recapture the ability to domestically process non-fed cattle that previously were exported live to plants in the United States. Most of these animals are over 30 months and are ineligible for export to the United States under the USDA minimal risk rule.

 

* By the end of 2005, domestic cattle slaughter in Canada is expected to be nearly 20% above pre-BSE levels and further slaughter capacity expansion is planned. By 2006, annual Canadian beef and veal production is forecast to be almost 25% greater than during the pre- BSE period.

 

* The impact of country bans on imports of Canadian beef following the BSE case of May 2003 in Alberta was mitigated by the U.S. action to allow the entry of boneless beef from Canadian cattle under 30 months in early August 2003, less than 3 months after the Alberta BSE incident. Despite major world markets remaining closed to Canadian beef, Canada’s total beef exports have surpassed their pre-BSE level on the strength of access to the U.S. market.

 

* Increases in the Canadian hog inventory have moderated in the past two years and the July 1, 2005 survey by Statistics Canada showed only fractional growth (0.9%) compared to total hog numbers on farms on that date a year ago.

 

* Following a flat performance in 2004, Canadian pork exports rebounded during the first six months of 2005 with strong sales increases to South Korea, Japan, Romania and Australia. Canadian pork exports to the United States, the largest export market for Canadian pork continued to decline in the first half of 2005. On balance, Canadian pork exports during 2005 are forecast to exceed 1.0 million metric tons for the first time.

 

* During 2004, Canadian pork imports from the United States surpassed the 100,000 metric ton level for the first time since the late 1970s. For 2005, pork imports from the United States are on pace to register a year over year increase of approximately 30%.

 

GAIN Report - CA5056 Page 4 of 16

 

UNCLASSIFIED USDA Foreign Agricultural Service

 

Section I. Cattle and Beef

 

Canada’s cattle industry continues to be impacted by the discovery of a case of Bovine Spongiform Encephalopathy (BSE) in Alberta in May 2003. Major markets for Canadian beef remain closed, most notably Japan. Although access to the U.S. market has improved for Canadian cattle and beef, bovines older than 30 months of age, beef from older animals, and breeding stock are still banned from entering the United States. Prior to its BSE case of May 2003, the Canadian cattle industry was heavily dependent on cattle exports to the United States and Canada’s experience with BSE-related trade restrictions has prompted a repositioning strategy that has implications for future U.S./Canada beef and cattle trade. The Canadian industry is determined to become less reliant on U.S. live cattle markets and industry and government leaders equally support a more aggressive approach to increasing offshore markets for Canadian beef.

 


 

Date: 3/16/2006 GAIN Report Number: CA6012 CA6012 Canada Agricultural Situation This Week in Canadian Agriculture, Issue 8 2006 Approved by: Lisa Anderson U.S. Embassy Prepared by: George Myles

 

BSE NOT WORSENING IN NORTH AMERICA SAYS AG MINISTER: Canadian agriculture minister Chuck Strahl said in a press release that (this week’s) confirmation of bovine spongiform encephalopathy (BSE) in Alabama does not indicate an increased risk associated with American beef and live cattle. The minister stated that the most recent case, and others that may be found in the future, do not indicate that BSE in this part of the world is worsening. Rather, they are a reflection of government, industry and individual producer’s commitment, on both sides of the border, to responsibly manage the disease. Strahl said that Canadian and American officials remain in close contact and although the origin of the animal remains unconfirmed, that Canada had received no requests to conduct any tracing of Canadian animals.

 


 

*** Strahl said that Canadian and American officials remain in close contact and although the origin of the animal remains unconfirmed, that Canada had received no requests to conduct any tracing of Canadian animals. ***

 

*** 2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006 ***

 


 

Saturday, August 14, 2010

 

BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY

 

*** (see mad cow feed in COMMERCE IN ALABAMA...TSS) ***

 


 

Thursday, January 3, 2008

 

*** ANIMAL HEALTH REPORT 2006 (BSE h-BASE EVENT IN ALABAMA, Scrapie, and CWD)

 


 

Date: 8/11/2006 GAIN Report Number: CA6033 CA6033 Canada Agricultural Situation This Week in Canadian Agriculture, Issue 19 2006 Approved by: Lisa Anderson U.S. Embassy Prepared by: George Myles

 

INVESTIGATION OF MANITOBA BSE CASE COMPLETED: The Canadian Food Inspection Agency (CFIA) has concluded its epidemiological investigation of the case of bovine spongiform encephalopathy (BSE) confirmed on July 3, 2006 in a 16 year-old cow from Manitoba. According to CFIA, no part of the animal’s carcass entered the human food or animal feed chains. The advanced age of the affected animal (at least 16 years old) limited the CFIA’s capacity to collect information concerning the animal’s early history, including its birth farm. The CFIA traced 21 herdmates that had been previously purchased with the affected animal. One of these animals was still alive and tested negative for BSE. Canada’s 7th confirmed BSE case occurred about week later in a 50 month-old dairy cow from Alberta. The CFIA investigation of this most recent case of BSE, confirmed July 13, 2006, is nearing completion and the CFIA expects to summarize the findings of that investigation shortly.

 


 

Date: 9/6/2006 GAIN Report Number: CA6038 CA6038 Canada Livestock and Products Annual 2006 Approved by: Lisa Anderson U.S. Embassy Prepared by: George Myles

 

GAIN Report - CA6038 Page 7 of 13

 

UNCLASSIFIED USDA Foreign Agricultural Service

 

Per Capita Consumption

 

Eight cases of BSE detection in Canada since May 2003 have not had a major negative impact on Canadian beef and veal consumption. In fact, per capita beef consumption was higher last year than during 2002, the pre-BSE era. Canadian consumers continue to demonstrate a high level of confidence in the Canadian food inspection system.

 


 

Date: 2/28/2008 GAIN Report Number: CA8009 CA8009 Canada Livestock and Products Semi-Annual 2008 Approved by: Norval Francis U.S. Embassy Prepared by: George Myles

 

Market recovery post-BSE

 

Canada continues its attempts to regain access to world markets that were lost after the BSE case in may 2003. In May 2007, the World Organization for Animal Health, or commonly referred to as the OIE (for its French language acronym), granted Canada (and the U.S.) a “controlled” risk status for bovine spongiform encephalopathy (BSE). Hugh Lynch-Staunton, president of the Canadian Cattlemen's Association, told the Canadian Press that the Canadian cattle industry is hopeful that the OIE’s second-highest safety designation will translate into more (Canadian beef) exports. "It's a very significant step," said Lynch-Staunton. "It gives an independent, scientific assessment of the BSE situation in Canada," he said. On February 25, 2008 Gerry Ritz, Minister of Agriculture and Agri-Food announced that Mexico will allow the resumption of the importation of Canadian breeding cattle, dairy or beef, under 30 months of age. Mexico banned imports of live Canadian cattle in May 2003 after the initial detection of BSE in Alberta. Mexico reopened the market for most Canadian beef that same summer, but has kept the border closed to Canadian cattle. Canadian products now approved for export to Mexico include beef derived from animals under 30 months of age and dairy and beef breeding cattle. At the same time, the Minister also said that Barbados, which had already opened its market to Canadian beef, would now accept a full range of breeding cattle.

 

Canada Confirms 12th BSE Case With Detection In Alberta

 

On February 26, 2008, the Canadian Food Inspection Agency (CFIA) confirmed bovine spongiform encephalopathy (BSE) in a six-year-old dairy cow from Alberta. The animal's carcass is under CFIA control, and no part of it entered the human food or animal feed systems. According to the CFIA, the age and location of the infected animal are consistent with previous cases detected in Canada and the new case will not affect Canada’s Controlled Risk country status, as recognized by the World Organization for Animal Health (OIE). Based on science, the CFIA says that it does not expect that the finding should impact access to any of Canada’s current international markets for cattle and beef. The CFIA reiterated that as Canada progresses toward the eradication of BSE, the periodic detection of a small number of cases is fully expected. It said that its BSE surveillance program, which targets the highest risk animals and regions, continues to benefit from very strong producer participation and that Canada’s animal and human health safeguards prevent potentially harmful cattle tissues from entering the human food and animal feed systems. The CFIA will conduct an epidemiological investigation directed by international guidelines to identify the animal’s herdmates at the time of birth and potential pathways by which it might have become infected. Once completed, a report on the investigation will be publicly released. Canada’s last case of BSE was detected in December, 2007.

 


 

August 15, 2008

 

CANADA CONFIRMS 14TH CASE OF BSE: On August 15, 2008, the Canadian Food Inspection Agency (CFIA) confirmed bovine spongiform encephalopathy (BSE) in a six-year-old beef cow from Alberta. It was Alberta’s 10th case. There were three in British Columbia and one in Manitoba. The animal’s birth farm has been identified, and an investigation is underway. The CFIA is tracing the animal's herdmates and e xamining possible sources of infection. According to the CFIA, the age and location of the infected animal are consistent with previous cases detected in Canada. The case was detected through the Canada’s BSE surveillance program and the CFIA said that n o part of the animal’s carcass entered the human food or animal feed systems. Canada is a Controlled Risk country for BSE, a designation it received in May 2007 by the World Organization for Animal Health (OIE). The finding of this latest case is not expected to affect exports of Canadian cattle or beef.

 


 

Date: 5/22/2008 GAIN Report Number: CA8034 CA8034 Canada Agricultural Situation This Week in Canadian Agriculture, Issue #14 2008 Approved by: Lisa Anderson U.S. Embassy Prepared by: Darlene Dessureault, George Myles

 

BSE FIVE YEARS LATER; BEEF EXPORTS 30% LOWER: Five years ago this week, May 20, 2003, Canada’s first case of Bovine Spongiform E ncephalopathy (BSE) was detected in a beef cow in Alberta. In the years prior to the incident, Canada’s cattle industry was in an expansion phase, exporting more than 60% of its production to the United States and overseas markets. Following BSE detection, Canada’s trading partners shut their borders to Canadian cattle and beef and the subsequent loss of international markets was devastating to the industry. Loss estimates in the first two years were in the $5-7 billion range. The Canadian government responded with financial aid upwards of $500 million. The market disruption altered the U.S./Canada trade flow of cattle and beef that had evolved into an integrated market. By late 2007, Canadian market access to the U.S. beef market was in large part back to where it was prior to BSE following U.S. action to harmonize cattle and beef trade with Canada in line with International Animal Health Standards. However, despite renewed access to the U.S., and several other markets, Canada’s beef industry has had difficulty restoring exports to the pre-BSE level although it continues to make efforts to re-open blocked markets such as South Korea. According to official trade data, total Canadian product weight exports of beef and veal (fresh, frozen, and prepared) during 2007 reached 326,723 MT. The level was up from 2003 when the first BSE detection resulted in exports declining to 295,085 MT, but remained 30% below the 469,490 MT exported during 2002, the full calendar year prior to the BSE finding. Canadian live cattle exports to the United States which reached 1.7 million head in 2002, fell to zero in 2004, rebounded to 1.4 million head after access to the U.S. market for live cattle normalized in two stages in 2005 and 2007 after USDA categorized Canada as a minimal risk region for BSE.

 

GAIN Report - CA8034 Page 3 of 5 UNCLASSIFIED USDA Foreign Agricultural Service

 

WHAT NOW FOR CANADIAN BEEF EXPORTS?: Even with BSE essentially behind them, there is nor shortage of current concern among Canadian cattle producers. Faced with a glut of cattle after BSE, the industry has worked the inventory down to the point where slaughter plant capacity is underutilized. Also, new difficulties including higher feed prices, a stronger Canadian dollar, and low market prices for cattle have been stressing the industry. Given the challenges ahead, many in the Canadian beef industry feel the need to be pro-active in order to preserve both profitability and competitiveness. In this regard, at least two industry/producer initiated strategies have emerged to tackle the issue of market development for an industry so heavily dependent on exports. One such initiative is the Canadian Beef Advantage, an ongoing market strategy embraced by The Canadian Cattlemen Market Development Council, the Beef Information Centre, the industry’s domestic promotional arm, a nd the Canadian Beef Export Federation, the industry’s export promotion arm. The cornerstone of the Canadian Beef Advantage is the development of a global branding strategy for Canadian beef and cattle genetics. The sponsoring groups believe they can promote the advantages of Canadian beef drawing on Canada’s grading system (quality criteria), Canada’s regulatory and food safety standards, and the country’s reputation as a “natural” environment. Another initiative is the Canada Gold Beef concept, a grass roots effort in western Canada that also wants to produce and sell a family of branded beef products with environmental, animal husbandry, and strict food safety requirements to meet the demands of local and international customers. That group wants to s tart its own Alberta based slaughter plant to compete with the U.S. players in Alberta, Tyson and Cargill. Comment: A similar, producer run plant called Rancher’s Beef, which began operation during the BSE crisis, went bankrupt within two years. Whatever the outcome, it appears that the Canadian beef industry realizes that beef marketing in the post-BSE era needs to be different. The new realities of international beef marketing, whether they be adjusting to the upcoming U.S. Country of Origin Labeling regulations or facing increased competition in world markets from other global beef suppliers, are likely to be reflected in both industry and government future policies directed at Canada’s beef industry.

 


 

Date: 11/21/2008 GAIN Report Number: CA8083 CA8083 Canada Agricultural Situation This Week in Canadian Agriculture: Issue 34 2008 Approved by: Robin Tilsworth U.S. Embassy Prepared by: George Myles & Darlene Dessureault

 

CANADA’S 15TH CASE OF BSE CONFIRMED IN BRITISH COLUMBIA: On November 18, 2008 the Canadian Food Inspection Agency (CFIA) confirmed bovine spongiform encephalopathy (BSE) in a seven-year-old dairy cow from British Columbia. No part of the animal’s carcass entered the human food or animal feed systems. The animal’s birth farm has been identified, and an investigation is underway. The CFIA is tracing the animal's herdmates at the time of birth and examining possible sources of infection. This case was detected through Canada’s BSE surveillance program. The CFIA said that the program continues to play an important role in Canada’s strategy to manage BSE. Canada remains a Controlled Risk country for BSE, as recognized by the World Organization for Animal Health (OIE). According to the CFIA, the latest case should not affect exports of Canadian cattle or beef.

 


 

Date: 3/27/2009 GAIN Report Number: CA9016 CA9016 Canada Agricultural Situation This Week in Canadian Agriculture, Issue 12 2009 Approved by: Robin Tilsworth U.S. Embassy Prepared by: George Myles & Darlene Dessureault

 

GAIN Report - CA9016 Page 2 of 3

 

UNCLASSIFIED USDA Foreign Agricultural Service

 

This Week in Canadian Agriculture is a weekly review of Canadian agricultural industry developments of interest to the U.S. agricultural community. The issues summarized in this report cover a wide range of subject matter obtained from Canadian press reports, government press releases, and host country agricultural officials and representatives. Disclaimer: Any press report summaries in this report are included to bring U.S. readership closer to the pulse of Canadian developments in agriculture. In no way do the views and opinions of these sources reflect USDA’s, the U.S. Embassy’s, or any other U.S. Government agency’s point of view or official policy.

 

RITZ DELIVERS BLUNT MESSAGE TO SOUTH KOREA ON ACCEPTANCE OF CANADIAN BEEF: Following his trade mission to Seoul, Canada Agriculture Minister Gerry Ritz spoke to the media by telephone late last week and said he told South Korean Trade Minister Kim Jong-hoon and Agriculture Minister Chang Tae-pyong that unless the Asian country lifted its ban on Canadian beef soon that Canada would initiate a WTO challenge. Ritz told reporters, "We left the Koreans with no illusion that the FTA is on hold until we get this beef issue worked through and resolved to Canadian producers' benefit," Ritz told reporters in a conference call. "It makes it very difficult to move forward when they want to just hive off a very significant part of our exports and hold it in abeyance while we move forward with all smiles and chuckles. I'm not prepared to do that . . . the (Canadian) government in Ottawa is not prepared to do that." Ritz said he thinks South Korea's refusal to accept Canadian beef stems from protectionism of its own industry. Comment: South Korea banned all Canadian beef and cattle following Canada’s initial detection of BSE in May, 2003. During 2002, the full year prior to international BSE bans on Canadian beef, South Korea was the third most important export market for Canadian beef. Exports in 2002 totaled almost 12,500 metric tons valued at C$45 million. Canadian beef exports have not yet recovered to their pre-BSE level and renewed access to the South Korean beef market would be welcome news for the Canadian beef industry. South Korea agreed to accept U.S. beef about a year ago (see USDA release 0106.08) and Canadian beef exporters thought that a South Korea/Canada beef agreement would soon follow. Canada and South Korea launched free trade agreement negotiations in July 2005.

 

CANADA BEEF EXPORT FEDERATION CONGRATULATES MINISTER RITZ ON TRADE MISSION TO KOREA: In a press release, the Canada Beef Export Federation (CBEF) has congratulated Agriculture Minister Gerry Ritz on his recent trade mission to Seoul, South Korea. “We congratulate Minister Ritz and support him in his efforts to pursue access for Canadian beef and veal in this very important market,” said Gib Drury, Board Chair of the Canada Beef Export Federation. “In traveling to Korea and directly engaging with senior Korean Government officials, Minister Ritz has demonstrated the very serious intent of the Canadian Government to resolve this impasse in a non confrontational manner. Our Korea office reports that all of the importer representatives who met with Minister Ritz were very impressed with the Minister’s assertive and business-friendly attitude. This will stand our industry in good stead upon our return.” According to Drury, the CBEF believes that South Korea will only resume trade in Canadian beef if Canada takes the steps of increasing pressure by initiating WTO dispute settlement consultations. In this light, CBEF believes that Canada must initiate the consultations - a process that can be halted should Korea agree to the resumption of trade. Drury said that Canada's strategy must be dedicated to the goal of resuming trade in all edible beef and veal products derived from cattle less than 30 months of age in the spring of 2009. Comment: The CBEF is the non-profit export promotional agency for Canada’s beef industry. It is headquartered in Calgary, Alberta and has overseas offices in Japan, South Korea, Taiwan, China, Hong Kong and Mexico.

 


 

Date: 3/16/2009 GAIN Report Number: HK9007 HK9007 Hong Kong Livestock and Products Hong Kong Opens Market to Certain Canadian Bone-In Beef Cuts 2009 Approved by: Philip A. Shull American Consulate General Prepared by: Caroline Yuen Report Highlights: The Hong Kong Government (HKG) announced on March 9, 2009 that it was opening its market to most Canadian bone-in beef cuts (the exception being vertebral column cuts) from cattle less than 30 months old. The HKG cited Canada’s implementation of enhanced control measures as the reason for its decision. All Canadian plants currently approved for boneless exports to Hong Kong are cleared to ship bone-in cuts. U.S. bone-in cuts remain banned. Includes PSD Changes: No Includes Trade Matrix: No Trade Report Hong Kong [HK1] [HK] GAIN Report - HK9007 Page 2 of 2 UNCLASSIFIED USDA Foreign Agricultural Service The Hong Kong government (HKG) issued a press release on March 9, 2009 announcing that the Center of Food Safety (CFS) will resume processing import applications for Canadian bone-in beef with immediate effect. All non-vertebral (e.g. rib and shoulder cuts) bone-in cuts from cattle less than 30 months old are allowed to be imported from Canada. The press release stated that Hong Kong is taking this decision as a result of Canada's implementation of enhanced control measures against Bovine Spongiform Encephalopathy (BSE). All Canadian plants which are currently cleared to export boneless beef to Hong Kong are automatically eligible to export bone-in beef to Hong Kong. Unlike the Canadian press release that was issued on January 16, 2009 on this subject, the Hong Kong statement did not discuss subsequent phases of the market opening that would include offals and vertebral column cuts. It simply said "We will closely monitor the situation and review our import requirements as and when necessary." The HKG banned the entry of Canadian beef since May 2003, after the detection of a case of BSE in Alberta, Canada. The ban on import of boneless beef from Canada was lifted in November 2004. The HKG conducted a plant audit visit in September 2007 as part of its requirement to open its market to Canadian bone-in beef. Following the Canadian Agriculture Minister’s visit to Hong Kong in January 2009, the Canadian government issued a press release on January 16 announcing that Canada and Hong Kong reached an agreement in-principle that would open the market to Canadian bone-in beef in three phases. According to the statement, phase I expands access from the current “boneless under 30 months (UTM)” to allow entry of all bone-in beef from cattle UTM, except vertebral column cuts (i.e. T-bones). Phase I will be concluded following successful shipments of a minimum of twelve consignments and twelve tons, and a minimum of two-to-four months. Phase II eliminates age restrictions on ribs and boneless beef, and also grants access to offals from cattle of any age. Following a three-to-six month period of smooth imports of Phase II products, the Phase III addition of T-bones from animals UTM will be added. Despite Canada having more recent and more numerous cases of BSE than the U.S, the Hong Kong market remains closed to all U.S. bone-in beef.

 


 

Date: GAIN Report Number: Post: Report Categories: Approved By: Prepared By: Report Highlights: BSE Case in United States Will Not Affect Trade, States Canadian Food Inspection Agency * Health Canada Moves to Close Fortified Snack and Beverage Loophole * Canadian Food Inspection Agency Publishes Notice of Intent with Respect to Importer Licensing Regime * Canadian Grain Sector Shakeup Expected with Potential Foreign Acquisition of Canadian Grain Company Darlene Dessureault Robin Gray Agriculture in the News This Week in Canadian Agriculture - Issue 7 Ottawa Canada CA12016 4/25/2012 Public Voluntary 2

 

This Week in Canadian Agriculture is a review of Canadian agricultural industry developments of interest to the U.S. agricultural community. The issues summarized in this report cover a wide range of subject matter obtained from Canadian press reports, government press releases, and host country agricultural officials and representatives. Disclaimer: Any press article summaries in this report are included to bring U.S. readership closer to the pulse of Canadian developments in agriculture. In no way do the views and opinions of these sources reflect USDA’s, the U.S. Embassy’s, or any other U.S. Government agency’s point of view or official policy.

 

BSE Case in United States Will Not Affect Trade, States Canadian Food Inspection Agency On April 25, 2012, the Canadian Food Inspection Agency (CFIA) issued a press release stating that the bovine spongiform encephalopathy (BSE) finding in a U.S. dairy cow sent for rendering in California will not affect trade between the United States and Canada as both countries have implemented science-based measures to protect animal and human health. These science-based measures include prohibiting specified risk materials from entering the human food system and animal feed chains and testing cattle for BSE. U.S. officials, who made their announcement on April 24, 2012, have made clear that the BSE finding will not affect the country's "controlled risk" status for BSE (bovine spongiform encephalopathy) at the World Organization for Animal Health (OIE), nor is it expected to affect U.S. beef or dairy exports to any nations following OIE standards. USDA officials explained that the animal in question tested positive for atypical BSE, a form of the disease not generally associated with an animal consuming infected feed. U.S. officials have also confirmed that no part of the animal`s carcass entered the food system. The statement from CFIA can be found at the following URL address: http://www.inspection.gc.ca/about-the-cfia/newsroom/news-releases/bse/eng/1335311345275/1335311647373

 


 

force feeding TSE Prions aka mad cow disease to the public, and how to make them like it $$$

 

Center for North American Studies CNAS 2005-1 Food Chain Disruptions and Trade: The Case of North American Animal and Meat Trade March 2005

 


 

CRS REPORT FOR CONGRESS

 

Order Code RS21709 Updated December 6, 2006 Mad Cow Disease and U.S. Beef Trade Charles E. Hanrahan and Geoffrey S. Becker Senior Specialist and Specialist in Agricultural Policy Resources, Science, and Industry Division

 

Summary

 

The 110th Congress is expected to monitor closely U.S. efforts to regain foreign markets that banned U.S. beef when a cow in Washington state tested positive for bovine spongiform encephalopathy (BSE, or mad cow disease) in December 2003. Rebuilding foreign confidence in the safety of U.S. beef and cattle has been impeded by two other confirmed U.S. cases of BSE, announced June 2005 and March 2006. The four major U.S. beef export markets, Canada, Mexico, Japan, and Korea, are again accepting U.S. product. Resumption of beef trade with Japan and Korea has not gone smoothly. Japan temporarily suspended all U.S. exports when prohibited materials were discovered in a shipment, but trade has now resumed. Korea rejected some shipments with bone fragments, but has not prohibited all export trade. This report will be updated.1

 

U.S. Beef Trade

 

In 2003, the United States exported about 1.1 million metric tons (MMT) of beef, veal and beef variety meats, valued at $3.9 billion. This was equivalent to approximately 10% of the farm value of U.S. cattle and calves. U.S. beef exports had grown rapidly during the decade beginning in 1992, increasing by 85%, while domestic beef consumption grew by just 14%.2

 

1 For additional details and background see CRS Report RS22345, BSE (“Mad Cow Disease:): A Brief Overview, and CRS Report RL32199, Bovine Spongiform Encephalopathy (BSE, or “Mad Cow Disease”): Current and Proposed Safeguards.

 

2 Trade data sources are primarily USDA, Foreign Agricultural Service (FAS), World Markets and Trade: Dairy, Poultry and Livestock, various issues; and FASonline’s U.S. Trade Internet System at [http://www.fas.usda.gov/ustrade/]. Unless noted, other data are from the USDA Economic Research Service (ERS) website at [http://www.ers.usda.gov/features/bse/index.htm].

 

After USDA’s 2003 BSE announcement, most countries banned or restricted some or all imports of U.S. beef and cattle products. These included Japan, South Korea, Mexico, and Canada, which together had purchased approximately 90% of U.S. beef

 

CRS-2

 

3 For the latest list and specifics on country bans, see the USDA/APHIS trade ban status website at [http://www.aphis.usda.gov/newsroom/hot_issues/bse/bse_trade_ban_status.shtml].

 

4 Center for Agricultural and Rural Development, Iowa Ag Review, summer 2003, at [http://www. card.iastate.edu/iowa_ag_review/summer_03/article4.aspx]. Canadian cattle imports resumed in 2005; see “Canada Situation.”

 

Japan 37% Korea 24% Mexico 20% Canada 10% Others 9% 2003 U.S. Beef Export Markets

 

exports. Canada and Mexico resumed importing some U.S. beef in 2004. Japan and Korea reopened their markets in July and November 2006, respectively.3 In 2003, the United States was the world’s third largest beef/veal exporter, claiming 18% of the world beef/veal market. Australia and Brazil ranked one and two, with 1.3 MMT and 1.2 MMT in exports, respectively. U.S. market share plummeted to 3% in 2004 (209,000 MT) and has climbed to 7% (523,000 MT) in 2006. Meanwhile, Brazil has become the top beef/veal exporter in 2006 with 28% of the world market share, followed by Australia with 20%. Imports have represented about 13% of total beef consumption in the United States, the largest world beef importer. Imports from Canada (and Mexico) reflected an integrated North American market. Prior to its own May 2003 BSE event, Canada was the United States’ major source of beef and cattle imports. In 2002 Canada sent about 1.7 million cattle to the United States, where large feeding and slaughter capacity readily absorbed them.4 Live cattle imports from Canada in 2006 were more than 730,000 head (January-September).

 

U.S. Beef Exports to Japan

 

After months of negotiations, the United States and Japan announced on October 23, 2004, that the United States would establish, with Japanese concurrence, an interim marketing program — a modified version of its Beef Export Verification (BEV) Program — enabling a resumption of some U.S. exports to Japan. BEV would certify that only beef products from cattle of 20 months or younger are shipped. Also, the United States agreed to an expanded definition of cattle parts that have a higher risk of harboring the BSE agent. These “specified risk materials” (SRMs) include — for cattle of all ages — the entire head except tongues and cheek meat; tonsils; spinal cords; distal ileum; and part of the vertebral column. This is broader than the U.S. SRM definition, which applies mainly to cattle over 30 months old.

 

The United States also agreed to permit Japanese beef into its market following relevant domestic rule-making. USDA’s Animal and Plant Health Inspection Service (APHIS) published a final rule on December 14, 2005, permitting such imports (whole

 

CRS-3

 

5 70 Federal Register, pp. 48494-484500 and pp. 73905-73919. 6 See U.S. Dept. of Agriculture, Foreign Agricultural Service, Japan: Livestock and Products Annual Report 2006 at [http://www.fas.usda.gov/gainfiles/200608/146208801.pdf]. 7 Ibid, p. 4.

 

boneless beef cuts under specified conditions).5 Prior to imposition of a U.S. ban on Japanese beef imports due to animal disease (including BSE) outbreaks there, that country exported an annual average of less than 9 tons of primarily specialty beef (Kobe and other Wagyu).

 

Japan did not finalize its decision to permit U.S. beef imports until December 2005, following a final report from its independent Food Safety Commission (FSC) certifying the adequacy of U.S. safeguards, at which point shipments resumed. However, the Japanese abruptly halted imports from all U.S. importers again on January 20, 2006, after they found vertebral column bones in several boxes of veal from one U.S. processor. Following Japan’s review of the eligibility of U.S. slaughter facilities to export beef to Japan, the market reopened for U.S. beef on July 27, 2006.

 

Recapturing more of the Japanese market for U.S. beef will not be easy. U.S. beef exports to Japan confront several constraints: consumer beef safety concerns, strict port scrutiny of U.S. shipments, currently high U.S. offer prices, uncertainty about supplies of specific cuts under the BEV system, a shift in consumer choice of protein from beef to pork, and competition for the Japanese market from Australia, a BSE-free exporter.6 Australia currently provides about 88% of Japanese imports of chilled and frozen beef. Another potential constraint to expanding U.S. beef exports to Japan is potential imposition of the beef import safeguard (a 50% tariff) should imports in 2007 exceed trigger levels.7

 

In Congress. During the 109th Congress, many Members expressed deep frustration with the Japanese situation. Introduced in March 2005 were H.Res. 137 and S.Res. 87, calling for economic sanctions against Japan if it does not permit U.S. beef. Also, S. 1922/H.R. 4179, introduced in October 2005, would have imposed $3.14 billion in retaliatory tariffs on Japanese imports if Japan did not lift the beef ban by December 15, 2005. Elsewhere, a Senate floor amendment to the FY2006 USDA appropriation (H.R. 2744), which would have blocked a new U.S. rule to permit some Japanese beef imports unless Japan lifted its own ban, was deleted from the final conference agreement (H.Rept. 109-255, P.L. 109-97). Legislative initiatives in the 110th Congress will depend in large part on the pace of resumption of U.S. beef imports by Japan.

 

U.S. Beef Exports to Korea

 

Korea’s prohibition on U.S. beef, which had been in place since December 2003, was lifted on September 11, 2006. Resumption of U.S. beef exports to Korea, the United States second largest export destination for beef in 2003, is expected to proceed slowly for the same reasons that will slow Japan’s resumption of beef imports. Strict quarantine inspection requirements in Korean ports have already resulted in the rejection of three shipments of U.S. beef because of the presence of bone fragments.

 

CRS-4

 

8 See also CRS Report RL32932, Bovine Spongiform Encephalopathy (BSE, or “Mad Cow Disease”) in North America: A Chronology of Selected Events.

 

Canada Situation

 

After Canada’s first BSE-infected cow (from Alberta) was announced in May 2003, USDA published an interim final rule banning all Canadian ruminant and product imports. In August 2003, USDA partially lifted the ban by permitting (without publishing a rule) imports of boneless beef from animals 30 months or younger, among other products. On November 4, 2003, USDA published a proposed rule to permit other Canadian ruminant imports, including younger live cattle. However, USDA already had been expanding the types of Canadian beef permitted without formal rulemaking. In April 2004, in response to a lawsuit by Ranchers-Cattlemen Action Legal Fund USA (RCALF), a federal judge blocked this expansion, citing concerns about food safety and improper rulemaking procedures. Further expansion in Canadian imports (beyond products announced August 2003) was halted until the October 2003 rule was finalized.8 APHIS’s final rule in the January 4, 2005 Federal Register permits, among other things, imports of live cattle under 30 months old. Specifically, the rule creates a new category of “minimal risk” BSE regions — including those in which BSE-infected animals have been diagnosed but where sufficient regulatory measures have been in place to ensure that the introduction of BSE into the United States is unlikely. The rule further classifies Canada in this category, the first such region to qualify, based on what USDA declared was “a thorough risk analysis.”

 

Five days before the March 7, 2005, effective date for the rule, a Montana federal judge ordered a delay until he could hold a trial on the merits of a new R-CALF lawsuit, charging that USDA had made several procedural and substantive mistakes in this rulemaking. A federal appeals court overruled the Montana judge’s decision in July 2005, and cattle imports from Canada soon resumed (see below).

 

USDA had unveiled the final rule as Canada (in early January 2005) confirmed it had two more BSE cases, in an Alberta dairy cow born before a 1997 ban on feeding most ruminant materials back to ruminants was published, and in an Alberta beef cow born in March 1998 after the feed ban. Another case was reported by Canada in January 2006, in an Alberta crossbreed cow born in 2000, also after the feed ban. Canadian officials said use of contaminated feed was the most likely cause in all cases. Canadian and U.S. government teams had each conducted a review of the Canadian feed ban, and in March 2005 both reported that the ban was effective. Still, critics have questioned those assessments, given that several Canadian cases were born and contracted the disease after the feed ban.

 

A number of producers and others continue to oppose the entry of Canadian beef and particularly live cattle. Many say they remain worried about the impact on U.S. farm prices as large numbers of cattle again cross the border from Canada, which has reported eight BSE cases, five of them in 2006. Some also argue that opening the border to what they believe are potentially risky Canadian animals undermines efforts to regain the Japanese and Korean markets. Others counter that moving forward with the Canada rule was necessary for the United States to convince other countries that North American beef

 

CRS-5

 

is safe, that U.S. and Canadian safeguards are sound, and that all countries should, like the United States, base their import policies on thorough, scientific risk assessments. Canada historically has exported around 60% of its beef production, and the United States has taken 80%-90% of such exports. Canadian fed steer (slaughter-ready steer) prices had declined substantially from the high US$70s per cwt. before the May 2003 BSE announcement to the mid-US$30s shortly afterward. Canadian producers were losing between $100 and $200, and in some cases, $300 per head, according to Cattle- Fax, a marketing information service associated with the industry. Cattle prices climbed through fall 2003, but generally were in the US$50-$60 per cwt. range during much of 2004. They reached US$70s per cwt. during 2005.

 

Canadian cattle inventory numbers had increased after May 2003, because producers were not permitted to export live animals to the United States and lacked adequate capacity to slaughter them, Cattle-Fax and USDA had observed. Canada then added 30,000 head per week to its total slaughter capacity, a 22% increase in 2004 alone, two meat industry officials told the House Agriculture Committee at a March 1, 2005, hearing. This increase is likely to be permanent and place U.S.-based packers at a competitive disadvantage, because they will not have access to the cattle that Canada will kill rather than export to their plants, meat industry and USDA officials argued.

 

After the ban on younger Canadian cattle was lifted in July, the United States imported 558,000 head in 2005. A recent report (September 2006) by the FAS agricultural attache in Canada has estimated that 2006 live cattle imports would be 910,000 head — lower than earlier forecast, due partly to increased slaughter capacity in Canada and partly to weaker demand in the United States.

 

In 2006, USDA has been preparing a proposed rule to permit imports of Canadian cattle over 30 months old. This so-called “Minimal Risk Rule #2” purportedly was slowed while USDA reviewed Canada’s latest BSE case, which occurred in a cow born long after Canada’s own 1997 “feed ban.” Increased Canadian access to U.S. markets for live, older cattle would seem to depend in part on adoption of this rule. Expanded exports of live cattle that would ensue from this rule change could result in additional declines in Canadian slaughter rates.

 

In Congress. In the 109th Congress, the Senate passed a resolution (S.J.Res. 4) to disapprove the 2005 Canada import rule, by a vote of 52-46. A related resolution (H.J.Res. 23) did not reach the House floor for a vote in 2005. Other bills addressing the 2005 rule included H.R. 187, to prohibit the rule “unless United States access to major markets for United States exports of cattle and beef products is equivalent or better than the access status accorded such exports as of January 1, 2003”; and H.R. 384/S. 108, to prohibit the Canada rule unless mandatory retail country-of-origin labeling (COOL) is implemented. The current statutorily set deadline for COOL for fresh meats is September 30, 2008 (see CRS Report 97-508, Country-of-Origin Labeling for Foods). S. 294 would have prohibited imports (from a minimal risk region like Canada) of meat, meat byproducts, and meat food products from bovines over 30 months old unless the Secretary reports to Congress that the region “is in full compliance with a ruminant feed ban and other [BSE] safeguards.” New bills are possible in the 100th Congress.

 

CRS-6 9 Sources for this section include USDA/ERS, Livestock, Dairy, and Poultry Outlook, various issues, the ERS website (see footnote 2), and ERS, U.S. 2003 and 2004 Livestock and Poultry Trade Influenced by Animal Disease and Trade Restrictions (LDPM-120-01), July 2004. 10 The Kansas State study can be found at [http://www.agmanager.info/livestock/marketing/bulletins%5F2/industry/demand/EconomicImpactofBSEonUSBeefIndustry.pdf].

 

Related U.S. Price and Trade Impacts9

 

Industry analysts believe that the BSE expe rience has been much less devastating economically in the United States than it has been in other countries. One reason is that the United States, learning from Europe, was able to put BSE safeguards into place prior to its own first case. Also, the U.S. beef industry is much less dependent on export demand than the Canadians, cushioning the price effects. Before the BSE events, Canada exported 37% of its beef production, whereas the United States exported 9%.

 

In 2003, the U.S. ban on Canadian beef and cattle, coupled with already tight U.S. supplies and strong demand, had driven up U.S. beef and cattle prices substantially. After the December 2003 BSE case was announced, cattle prices fell. However, they had stabilized by early January 2004. Industry analysts reported that U.S. domestic demand (both retail and restaurant, including fast-food hamburger sales) appeared to be holding steady. That, combined with lower U.S. cattle inventories due in part to widespread drought in cattle country, kept cattle and beef prices high during 2004, helping to offset the effects of the BSE-related foreign bans. USDA reported that average U.S. fed steer (i.e., slaughter-ready cattle) prices were nearly $85 per cwt. for all of 2004, compared with average fed steer prices of $85 in 2003 and $67 in 2002.

 

Nonetheless, foreign import bans mean the domestic market had to absorb some 23 million more pounds of beef weekly or 1.2 billion pounds annually due to lost exports, according to Cattle-Fax. Exports of by-products like collagen, sausage casings, brains, other organs, tongue, tails, and tendons (all adding value to each animal) also were affected by the bans on U.S. beef products. In Japan, as noted, other countries, particularly Australia, have filled U.S. lost market share.

 

A study by researchers at Kansas State University of the impact that BSE has had on the U.S. beef industry found that average U.S. wholesale boxed beef prices during 2004 were 12 to 17 cents per pound lower than they would have been if all the export markets had been open. The loss of beef export markets also meant that by-product prices were lower than they would have been. The total estimated U.S. beef industry losses attributable to the loss of beef and by-product exports in 2004 ranged from $3.2 to $4.7 billion, according to the study.10

 

USDA’s November 2006 outlook and situation reports estimate that U.S. beef and veal exports have climbed from 209,000 MT and 3% of world market share in 2004, to 523,000 MT and 7% of world market share in 2006. Cattle prices averaged more than $85 per cwt. in 2006, and were predicted to be $82-$88 per cwt. in 2007.

 


 

CANADA BSE TSE PRION

 

 Confirmed Cases of Bovine Spongiform Encephalopathy (BSE) in 2015

 

 BSE is a reportable disease under the Health of Animals Regulations. This means that all suspected cases must be reported to the CFIA.

 

 Current as of: 2015-11-30

 

 The following table lists individual animals confirmed to be infected with BSE in Canada in 2015.

 

 Date confirmed

 

 Location

 

 Animal type infected

 

 Age of Animal

 

 February 11 Alberta Beef cow 70 months

 


 

 Monday, November 30, 2015

 

 *** Report on the Investigation of the Nineteenth Case of Bovine Spongiform Encephalopathy (BSE) in Canada November 2015 ***

 


 

 Herds infected with Chronic Wasting Disease in Canada in 2015

 

 The CFIA works with provincial governments and industry to conduct regular Chronic Wasting Disease (CWD) surveillance. Ongoing provincial surveillance for CWD varies with each particular province's perceived threat and infection status. Testing is mandatory in Manitoba, Saskatchewan, Alberta and the Yukon; it is voluntary, completed by random submission, or organized through policy in other provinces and territories.

 

 In addition, CWD is a reportable disease under the Health of Animals Regulations. This means that all suspected cases must be reported to the CFIA.

 

 Current as of: 2015-11-30

 

 Domestic cervid herds confirmed to be infected with CWD in Canada in 2015

 

 Date confirmed

 

 Location

 

 Animal type infected

 

 November 25 Saskatchewan Deer

 

 July 16 Alberta Elk

 

 June 11 Saskatchewan Elk

 

 April 9 Saskatchewan Deer

 

 March 19 Saskatchewan Elk

 

 January 16 Alberta Elk

 


 

 Flocks infected with Scrapie in Canada in 2015

 

 The CFIA, in co-operation with provincial governments and industry, launched a national scrapie surveillance program in 2005. Under the program, producers are encouraged to report animals that die on the farm or exhibit symptoms of the disease.

 

 In addition, scrapie is a reportable disease under the Health of Animals Regulations. This means that all suspected cases must be reported to the CFIA.

 

 Current as of: 2015-11-30

 

 Sheep flocks and/or goat herds confirmed to be infected with classical scrapie in Canada in 2015

 

 Date confirmed

 

 Location

 

 Animal type infected

 

 January 5 Ontario Goat

 

 May 22 Quebec Sheep

 

 June 16 Ontario Sheep

 


 

 Friday, July 10, 2015

 

 CANADA TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION UPDATE

 


 

 Monday, February 23, 2015

 

 20th BSE Case Raises New Concerns about Canada's Feeding Practices and Voluntary Testing Program; Highlights Importance of COOL

 


 

 Friday, February 20, 2015

 

 A BSE CANADIAN COW MAD COW UPDATE Transcript - Briefing (February 18, 2015)

 


 

 Saturday, February 14, 2015

 

 Canadian Food Inspection Agency Confirms Bovine Spongiform Encephalopathy (BSE) in Alberta

 


 

 SNIP...see more TSE prion stats from Canada with CJD update as well...

 

 Friday, July 10, 2015

 

 CANADA TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION UPDATE

 


 

 EDMONTON - Some of former Alberta premier Ralph Klein's most colourful quotes — and the reactions they elicited:

 

 SNIP...

 

 "This all came about through the discovery of a single, isolated case of mad cow disease in one Alberta cow on May 20th. The farmer — I think he was a Louisiana fish farmer who knew nothing about cattle ranching. I guess any self-respecting rancher would have shot, shovelled and shut up, but he didn't do that." — Klein recalls how the mad cow crisis started and rancher Marwyn Peaster's role. The premier was speaking at the Western Governors Association meeting in Big Sky, Mont. September 2004.

 

 "The premier meant that in an ironic or almost a sarcastic way." — Klein spokesman Gordon Turtle.

 

 ---

 

 "You would have to eat 10 billion meals of brains, spinal cords, ganglia, eyeballs and tonsils." — Klein speaking in Montreal in January 2005 on the risk of humans contracting mad cow disease.

 

 ---

 

 "I would offer $5 billion to have a Japanese person to come over here and eat nothing but Alberta beef for a year. And if he gets mad cow disease, I would be glad to give him $5 billion — make it $10 billion — Canadian." — Klein speaking after Japan closed its borders to Canadian beef.

 

 ---

 


 


 

 Increased Atypical Scrapie Detections

 

Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.

 


 

Thursday, March 29, 2012

 

atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012

 

NIAA Annual Conference April 11-14, 2011San Antonio, Texas

 


 


 

 Thursday, February 10, 2011

 

 TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31

 


 

 Wednesday, August 11, 2010

 

 REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA

 


 

 Thursday, August 19, 2010

 

 REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA

 


 

 Friday, March 4, 2011

 

 Alberta dairy cow found with mad cow disease

 


 

Sunday, May 27, 2012

 

CANADA PLANS TO IMPRISON ANYONE SPEAKING ABOUT MAD COW or ANY OTHER DISEASE OUTBREAK, CENSORSHIP IS A TERRIBLE THING

 


 

 Tuesday, October 2, 2012

 

Canadian veterinarian fined after approving banned BSE high risk cattle for export to U.S.A.

 


 

Sunday, December 2, 2012

 

CANADA 19 cases of mad cow disease SCENARIO 4: ‘WE HAD OUR CHANCE AND WE BLEW IT’

 


 

Thursday, January 17, 2013

 

Canada, U.S. agree on animal-disease measures to protect trade, while reducing human and animal health protection

 


 

 Tuesday, May 21, 2013

 

 Canada, USA, Bad feed, mad cows: Why we know three BSE cases had a common origin and why the SSS policy is in full force $$$

 


 

Saturday, September 12, 2015

 

The Canadian Management of Bovine Spongiform Encephalopathy in Historical and Scientific Perspective, 1990-2014

 

>>>We propose that Canadian policies largely ignored the implicit medical nature of BSE, treating it as a purely agricultural and veterinary issue. In this way, policies to protect Canadians were often delayed and incomplete, in a manner disturbingly reminiscent of Britain’s failed management of BSE. Despite assurances to the contrary, it is premature to conclude that BSE (and with it the risk of variant Creutzfeldt-Jakob disease) is a thing of Canada’s past: BSE remains very much an issue in Canada’s present. <<<

 


 

Friday, January 10, 2014

 

USDA AUDIT ON CANADA'S MEAT INSPECTION DISTURBING (pot calling kettle black again) US audit finds Canada's meat inspections wanting

 

 Canada's food inspection agency received the lowest possible passing grade—"adequate"—from the US Department of Agriculture (USDA) in its latest audit of practices surrounding meat, poultry, and eggs, according to a Food Safety News (FSN) story today.

 

 The Canadian Food Inspection Agency (CFIA) needs to improve its oversight of practices at meat facilities concerning hazard analysis and critical control points (HACCP) and of sanitation and humane animal handling. The CFIA said it has taken corrective action after being informed of the report, FSN report.

 

 The USDA's Food Safety and Inspection Service (FSIS) conducted the audit from Oct 22 to Nov 9, 2012, but the USDA released the report just last month.

 

 FSIS inspectors visited two red-meat slaughterhouses, four meat-processing facilities that produce ready-to-eat meat products, and an egg-processing facility. Inspectors also visited five Canadian government food safety agencies and two private laboratories.

 

 The inspectors found a lack of HACCP compliance and noted concerns over sanitation and humane handling at a beef slaughter plant that was involved in an expansive recall in 2010. They also found poor sanitation practices at a pig slaughterhouse.

 

 Because of the results of the audit, food imported to the United States from Canada will be subject to closer scrutiny than food from countries with higher-rated food safety systems, FSN reported.

 

 Jan 8 FSN story

 


 

Full USDA audit report

 


 


 

Current as of: 2015-01-31 Sheep flocks and/or goat herds confirmed to be infected with classical scrapie in Canada in 2015 Date confirmed Location Animal type infected January 5 Ontario Goat

 


 


 

CANADA SRM

 


 


 


 

Working Group Report on

 

the Assessment of the Geographical BSE-Risk (GBR) of

 

CANADA

 

2004

 

snip...

 

- 2 -

 

2. EXTERNAL CHALLENGES

 

2.1 Import of cattle from BSE-Risk2 countries

 

An overview of the data on live cattle imports is presented in table 1 and is based on

 

data as provided in the country dossier (CD) and corresponding data on relevant exports

 

as available from BSE risk countries that exported to Canada. Only data from risk

 

periods are indicated, i.e. those periods when exports from a BSE risk country already

 

represented an external challenge, according to the SSC opinion on the GBR (SSC July

 

2000 and updated January 2002).

 

• According to the CD, 231 cattle were imported from UK during the years 1980 to

 

1990 and no cattle imports from UK were recorded after 1990.

 

• According to Eurostat, altogether 198 cattle have been imported from the UK during

 

the years 1980 to 1990, Additionally 500 were recorded in 1993; this import is

 

1 For the purpose of the GBR assessment the abbreviation "MBM" refers to rendering products, in particular

 

the commodities Meat and Bone Meal as such; Meat Meal; Bone Meal; and Greaves. With regard to imports

 

it refers to the customs code 230110 "flours, meals and pellets, made from meat or offal, not fit for human

 

2 BSE-Risk countries are all countries already assessed as GBR III or IV or with at least one confirmed

 

Annex to the EFSA Scientific Report (2004) 2, 1-14 on the Assessment of the

 

Geographical BSE Risk of Canada

 

- 3 -

 

mentioned in Eurostat and the updated UK export statistic as male calves, but not

 

mentioned in the original UK export statistics. According to the CD, detailed

 

investigations were carried out and it is very unlikely that the 500 calves have been

 

imported. Therefore, they were not taken into account.

 

• According to the CD, in 1990 all cattle imported from UK and Ireland since 1982

 

were placed in a monitoring program.

 

• Following the occurrence of the BSE index case in 1993 (imported from UK in 1987

 

at the age of 6 months), an attempt was made to trace all other cattle imported from

 

UK between 1982 and 1990.

 

• Of the 231 cattle imported from the UK between 1980 and 1990, 108 animals had

 

been slaughtered and 9 had died. From the remaining, 37 were exported, 76 were

 

sent to incineration and one was buried; these were not entering the rendering system

 

and therefore not taken into account.

 

• According to the CD, 16 cattle were imported from Ireland (according to Eurostat

 

20), of which 9 were slaughtered, 3 died. The remaining 4 were incinerated and did

 

therefore not enter the rendering system. According to the CD, the 6 animals which

 

were imported in 1990 according to Eurostat, were never imported.

 

• Moreover 22 cattle have been imported from Japan (through USA), of which 4 were

 

exported (excluded from the table) and 14 were destroyed and therefore not entering

 

the rendering system, 4 were slaughtered.

 

• Of 28 imported bovines from Denmark, 1 was destroyed and 1 was exported. Of the

 

19 buffalos imported in 2000, 1 was incinerated and the others were ordered to be

 

destroyed.

 

• Additionally in total 264 cattle according to the CD (276 according to other sources)

 

were imported from Austria, France, Germany, Hungary, Italy, The Netherlands and

 

Switzerland.

 

• The numbers imported according to the CD and Eurostat are very similar. Some

 

discrepancies in the year of import can be explained by an extended quarantine;

 

therefore it is likely that imports according to Eurostat in 1980 and imports

 

according to the CD in 1981 are referring to the same animals.

 

• Additionally, between 16.000 and 340.000 bovines have annually been imported

 

from US, almost all are steers and heifers. In total, between 1981 and 2003,

 

according to the CD more than 2.3 million, according to other sources 1.5 million

 

cattle have been imported.

 

• According to the CD, feeder/slaughter cattle represent typically more than 90% of

 

the imported cattle from the USA; therefore, only 10% of the imported cattle have

 

been taken into account.

 

snip...

 

Annex to the EFSA Scientific Report (2004) 2, 1-15 on the Assessment of the

 

Geographical BSE Risk of Canada

 

2.2 Import of MBM or MBM-containing feedstuffs from BSE-Risk

 

countries

 

An overview of the data on MBM imports is presented in table 2 and is based on data

 

provided in the country dossier (CD) and corresponding data on relevant exports as

 

available from BSE risk countries that exported to Canada. Only data from risk periods

 

are indicated, i.e. those periods when exports from a BSE risk country already

 

represented an external challenge, according to the SSC opinion on the GBR (SSC, July

 

2000 and updated January 2002).

 

According to the CD, no imports of MBM took place from UK since 1978 (initially

 

because of FMD regulations).

 

• According to Eurostat data, Canada imported 149 tons MBM from the UK in the

 

period of 1993 to 2001. According to up-dated MBM statistics from UK (August

 

2001) no mammalian MBM was exported to Canada from 1993 – 1996. As it was

 

illegal to export mammalian meat meal, bone meal and MBM from UK since

 

27/03/1996, exports indicated after that date should only have included nonmammalian

 

MBM. Therefore, these imports were not taken into account.

 

• According to the CD, imports of MBM have taken place from Denmark, Germany,

 

France, Japan and US.

 

• According to Eurostat Canada imported MBM from Denmark, Belgium, France and

 

Ireland.

 

• According to the CD further investigations concluded that all imported MBM from

 

Denmark consisted of pork and poultry origin and was directly imported for

 

aquaculture, the imported MBM from France was feather meal, the imported MBM

 

from Germany was poultry meal for aquaculture and the imported MBM from

 

Belgium was haemoglobin; therefore these imports were not taken into account.

 

• The main imports of MBM were of US origin, according to the CD around 250.000

 

tons, according to other sources around 310.000 tons between 1988 and 2003.

 

snip...

 

2.3 Overall assessment of the external challenge

 

The level of the external challenge that has to be met by the BSE/cattle system is

 

estimated according to the guidance given by the SSC in its final opinion on the GBR of

 

July 2000 (as updated in January 2002).

 

Live cattle imports:

 

In total the country imported according to the CD more than 2.3 million, according to

 

other data 1.5 million live cattle from BSE risk countries, of which 231 (CD)

 

respectively 698 (other sources) came from the UK. The numbers shown in table 1 are

 

the raw import figures and are not reflecting the adjusted imports for the assessment of

 

the external challenge. Broken down to 5 year periods the resulting external challenge is

 

as given in table 3. This assessment takes into account the different aspects discussed

 

above that allow to assume that certain imported cattle did not enter the domestic

 

BSE/cattle system, i.e. were not rendered into feed. In the case of Canada, the 500 cattle

 

imported from UK according to Eurostat were not taken into account and it is assumed

 

that all incinerated, buried, exported animals and the animals still alive did not enter the

 

rendering system and were therefore excluded from the external challenge.

 

MBM imports:

 

In total the country imported according to the CD around 300.000 tons, according to

 

other sources nearly 360.000 tons of MBM from BSE risk countries, of which 149 tons

 

came from the UK. The majority consisted of MBM imported from the US. The

 

numbers shown in table 2 are the raw import figures and are not reflecting the adjusted

 

imports for the assessment of the external challenge. Broken down to 5 year periods the

 

resulting external challenge is as given in table 3. This assessment takes into account

 

the different aspects discussed above that allow to assume that certain imported MBM

 

did not enter the domestic BSE/cattle system or did not represent an external challenge

 

for other reasons. As it was illegal to export mammalian meat meal, bone meal and

 

MBM from UK since 27/03/1996, exports indicated after that date should only have

 

included non-mammalian MBM. In the case of Canada all imported MBM from UK,

 

Germany, Belgium, Denmark and France was not taken into account.

 

snip...

 

3. STABILITY

 

3.1 Overall appreciation of the ability to avoid recycling of BSE

 

infectivity, should it enter processing

 

Feeding

 

The annual Canadian production of MBM is approximately 575,000 tons of which

 

approx. 40,000 tons are exported each year, mainly to USA.

 

Use of MBM in cattle feed

 

• Before the feed ban, dairy cattle received supplementary feed containing MBM

 

during their productive life (maximum 200-400 g MBM per day). Beef cattle in the

 

western part of the country do not usually receive complementary feed. Beef cattle

 

in the eastern part receive normally no supplement protein but the calves could have

 

access to creep feeds containing MBM, after weaning the ratios may have contained

 

supplemental protein containing MBM (100-400 g per day).

 

• According to the CD, MBM is mainly fed to pigs and poultry and included in pet

 

food.

 

• According to the CD, only a proportion of dairy cattle may have received MBM.

 

Feed bans

 

• Before 1997, there was no legal restriction to include MBM into cattle feed.

 

• An MBM-ban was introduced in August 1997; it is forbidden since to feed

 

mammalian MBM to ruminants except if of pure porcine, equine and non

 

mammalian origin, i.e. in practice a ruminant-to-ruminant ban (RMBM-ban).

 

Annex to the EFSA Scientific Report (2004) 2, 1-15 on the Assessment of the

 

Geographical BSE Risk of Canada

 

- 9 -

 

Potential for cross-contamination and measures taken against

 

• Cross-contamination in the about 600 feed mills is assumed to be possible as long as

 

cattle and pig feed is produced in the same production lines, and premises.

 

• Cross-contamination during transport is possible, particularly if the same trucks are

 

used for transporting ruminant MBM (RMBM) and non-ruminant MBM (porcine or

 

poultry MBM which still might be included into cattle feed) or for transporting

 

pig/poultry feed and cattle feed.

 

• On-farm cross-contamination is regarded to be possible.

 

• Cross-contamination of cattle feed with RMBM can not be excluded. Hence, as

 

reasonable worst case scenario, it has to be assumed that cattle, in particular dairy

 

cattle, can still be exposed to RMBM and hence to BSE-infectivity, should it enter

 

the feed chain.

 

Control of Feed bans and cross-contamination

 

• With the introduction of the RMBM ban (1997) the feed mills (approximately 600)

 

were checked for compliance with the ban, including good manufacturing practices

 

(GMP) and record keeping, i.e. the separation in production of MBM containing

 

ruminant material (RMBM) from non-ruminant MBM.

 

• The feed mills had previously – since 1983 – been regularly checked in relation to

 

production of medicated feed.

 

• No examinations are performed to assess cross-contamination with RMBM of the

 

protein (e.g. non ruminant MBM) that enters cattle feed. Differentiation would

 

anyway be difficult.

 

Rendering

 

Raw material used for rendering

 

• Ruminant material is rendered together with material from other species, but

 

according to the CD only in the production of MBM prohibited for use in ruminant

 

feeds.

 

• Slaughter by-products, including specified risk material (SRM) and fallen stock are

 

rendered.

 

• The country expert estimated that 20% of the rendering plants, processing 20% of

 

the total amount of raw material, are connected to slaughterhouses. Their raw

 

material is more than 98 % animal waste from these slaughterhouses while less than

 

2 % is fallen stock. No estimation was given for the remaining 80% of the rendering

 

capacity.

 

• There are 32 rendering plants of which 3 are processing blood exclusively.

 

Rendering processes

 

• The rendering systems (parameters) were specified for 6 plants producing mixed

 

MBM, none of these fulfilled the 133/20/3 standard. Of these, 5 have dedicated

 

facilities to produce products for use in ruminant feed and products not permitted for

 

use in ruminant feed.

 

• The remaining plants process porcine or poultry material exclusively.

 

SRM and fallen stock

 

• There is an SRM ban for human food in place since 2003.

 

Annex to the EFSA Scientific Report (2004) 2, 1-15 on the Assessment of the

 

Geographical BSE Risk of Canada

 

- 10 -

 

• However, SRM are rendered together with other slaughter waste and fallen stock.

 

However, according to the CD, MBM with SRM is not permitted to be fed to

 

ruminants.

 

Conclusion on the ability to avoid recycling

 

• Between 1980 and 1997 the Canadian system would not have been able to avoid

 

recycling of the BSE-agent to any measurable extent. If the BSE-agent was

 

introduced into the feed chain, it could have reached cattle.

 

• Since 1997 this ability gradually improved with the introduction of the ruminant

 

MBM ban and its implementation.

 

• Since cross-contamination cannot be excluded, and as SRM is still rendered by

 

processes unable to significantly reduce BSE-infectivity, the system is still unable to

 

avoid recycling of BSE-infectivity already present in the system or incoming.

 

3.2 Overall appreciation of the ability to identify BSE-cases and to

 

eliminate animals at risk of being infected before they are processed

 

Cattle population structure

 

• Cattle population: 12.15 Million in 1988 increasing to 14.6 Million in 2001;

 

• Of the total cattle population, 2.2 million are dairy cattle and 12.4 million are beef.

 

• The cattle population above 24 months of age: approx. 6.0 Million.

 

• Of the approximately 2.2 Million dairy cattle 2 Million are located in the two eastern

 

provinces Ontario and Quebec.

 

• Mixed farming (cattle and mono-gastric species) is usually not practiced; the

 

country expert estimated the proportion of mixed farming to be less than 1%.

 

• Individual regions traditionally have ID systems under provincial authorities. Brand

 

inspectors are present when cattle are assembled. It is estimated by the Canadians

 

that the level of a national, uniform ID for cattle is less than 10%; most of those

 

individual pedigree animals. Mandatory ID for the milk-fed veal sector was

 

implemented in Quebec in 1996, but does not contain information on the herd of

 

origin. An agreement of the relevant industries to develop a national cattle ID and

 

trace back strategy was reached on 1 May 1998 (starting in 2001).Since 2002, a

 

national identification program is existing. Al cattle leaving any farm premises must

 

be uniquely identified by ear tag.

 

BSE surveillance

 

• BSE was made notifiable in 1990.

 

• Every cow over one year of age exhibiting central nervous system signs suggestive

 

of BSE submitted to a laboratory or presented at an abattoir is subjected to a BSE

 

laboratory diagnostic test (histology and over the past years also PrPSc-based

 

laboratory tests).

 

• In addition, cattle submitted for rabies examination and found rabies negative are

 

examined for BSE. Samples are prepared immediately upon arrival to the federal

 

laboratory responsible for the rabies diagnostic for possible later BSE examination,

 

i.e. formalin fixation.

 

• Since the 1940’s, a rabies control program has been in place, where farmers,

 

veterinarians and the general public are well educated about this neurological

 

Annex to the EFSA Scientific Report (2004) 2, 1-15 on the Assessment of the

 

Geographical BSE Risk of Canada

 

- 11 -

 

disease. In 1990, when BSE was made notifiable, this awareness was extended to

 

suspicions of BSE.

 

• Since 1993 the number of brains examined per year did exceed the number

 

recommended by OIE (300 - 336 for countries with a cattle population over 24

 

months of age of 5.0 to 7.0 Million) in all years, except in 1995 (table 4).

 

year 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003

 

samples 225 645 426 269 454 759 940 895 1´020 1´581 3´377 3´361

 

Table 4: Number of bovine brains annually examined for CNS diseases, including BSE.

 

• According to the CD approx. 98% of the examined cattle were older than 24 months

 

and approx. 90% exhibited neurological symptoms. Although the identification

 

system of Canada does not document the birth date or age of the animals, according

 

to the CD, examination of the dentition is used to ascertain the maturity of the

 

animals.

 

• The list of neurological differential diagnoses for the 754 brains examined in 1997

 

included encephalitis (70 cases), encephalomalacia (19), hemophilus (7),

 

hemorrhage (2), listeriosis (38), meningoencephalitis (36), rabies (22), tumors (2),

 

other conditions (135) and no significant findings (423).

 

• Compensation is paid for suspect BSE cases as well as for animals ordered to be

 

destroyed (90-95% of market value with a maximum of 2,500 Can$ per cow).

 

• Diagnostic criteria developed in the United Kingdom are followed at ADRI,

 

Nepean. According to the very detailed protocol for the collection, fixation and

 

submission of Bovine Spongiform Encephalopathy (BSE) specimens at abattoirs

 

under inspection by the Canadian Food Inspection Agency, the specimen shall be

 

shipped to National Center for Foreign Animal Disease, Winnipeg, Manitoba.

 

• In 2003, around 3000 animals from risk populations have been tested.

 

• According to the CD, it is aimed to test a minimum of 8000 risk animals (animals

 

with clinical signs consistent with BSE, downer cows, animals died on farm animals

 

diseased or euthanized because of serious illness) in 2004 and then continue to

 

progressively increase the level of testing to 30,000.

 

• In May 2003, Canada reported its first case of domestic BSE. A second case was

 

detected in the US on 23 December 2003 and traced back to Canadian origin. Both

 

were born before the feed ban and originated from Western Canada.

 

3.3 Overall assessment of the stability

 

For the overall assessment of the stability, the impact of the three main stability factors

 

(i.e. feeding, rendering and SRM-removal) and of the additional stability factor,

 

surveillance, has to be estimated. Again, the guidance provided by the SSC in its

 

opinion on the GBR of July 2000 (as updated January 2002) is applied.

 

Feeding

 

Until 1997, it was legally possible to feed ruminant MBM to cattle and a certain fraction of

 

cattle feed (for calves and dairy cattle) is assumed to have contained MBM. Therefore

 

feeding was "Not OK". In August 1997 a ruminant MBM ban was introduced but feeding

 

of non-ruminant MBM to cattle remained legal as well as feeding of ruminant MBM to

 

non-ruminant animals. This makes control of the feed ban very difficult because laboratory

 

differentiation between ruminant and non ruminant MBM is difficult if not impossible.

 

Annex to the EFSA Scientific Report (2004) 2, 1-15 on the Assessment of the

 

Geographical BSE Risk of Canada

 

Due to the highly specialised production system in Canada, various mammalian MBM

 

streams can be separated. Such a feed ban would therefore be assessed as "reasonably

 

OK", for all regions where this highly specialised system exists. However, several areas

 

in Canada do have mixed farming and mixed feed mills, and in such regions, an RMBM

 

ban would not suffice. Additionally, official controls for cattle feeds to control for the

 

compliance with the ban were not started until the end of 2003. Thus, for the whole

 

country, the assessment of the feeding after 1997 remains "Not OK".

 

Rendering

 

The rendering industry is operating with processes that are not known to reduce infectivity.

 

It is therefore concluded that the rendering was and is "Not OK".

 

SRM-removal

 

SRM and fallen stock were and are rendered for feed. Therefore SRM-removal is assessed

 

as "Not OK"

 

snip...

 

4.2 Risk that BSE infectivity entered processing

 

A certain risk that BSE-infected cattle entered processing in Canada, and were at least

 

partly rendered for feed, occurred in the early 1990s when cattle imported from UK in

 

the mid 80s could have been slaughtered. This risk continued to exist, and grew

 

significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached

 

processing. Given the low stability of the system, the risk increased over the years with

 

continued imports of cattle and MBM from BSE risk countries.

 

4.3 Risk that BSE infectivity was recycled and propagated

 

A risk that BSE-infectivity was recycled and propagated exists since a processing risk

 

first appeared; i.e. in the early 90s. Until today this risk persists and increases fast

 

because of the extremely unstable BSE/cattle system in Canada.

 

5. CONCLUSION ON THE GEOGRAPHICAL BSE-RISK

 

5.1 The current GBR as function of the past stability and challenge

 

The current geographical BSE-risk (GBR) level is III, i.e. it is confirmed at a lower level

 

that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent.

 

This assessment deviates from the previous assessment (SSC opinion, 2000) because at

 

that time several exporting countries were not considered a potential risk.

 

snip...

 

full text;

 


 

 EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of the United States of America (USA) Publication date: 20 August 2004 Adopted July 2004 (Question N° EFSA-Q-2003-083)

 

 Report

 

 Summary Summary of the Scientific Report

 

The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.

 

The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.

 

A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.

 

EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.

 


 

SUMMARY

 

Summary of Scientific Report http://www.efsa.eu.int 1 of 1 Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE-Risk (GBR) of United States of America (USA) Question N° EFSA-Q-2003-083 Adopted July 2004 Summary of scientific report The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003. The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties. A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries. EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases. Key words: BSE, geographical risk assessment, GBR, USA, third countries

 


 

REPORT (6 PAGES)

 

snip...

 

EFSA Scientific Report (2004) 3, 1-6 on the Assessment of the Geographical BSE Risk of Conclusions The European Food Safety Authority concludes: 1. The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. This cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that meat and bone meal (MBM) imported into the USA reached domestic cattle and lead to an internal challenge in the early nineties. 2. A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries. 3. The current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. 4. This assessment deviates from the previous assessment (SSC opinion, 2000) because at that time several exporting countries were not considered a potential risk. 5. It is also worth noting that the current GBR conclusions are not dependent on the large exchange of imports between USA and Canada. External challenge due to exports to the USA from European countries varied from moderate to high. These challenges indicate that it was likely that BSE infectivity was introduced into the North American continent. 6. EFSA and its Scientific Expert Working group on GBR are concerned that the available information was not confirmed by inspection missions as performed by the Food and Veterinary office (FVO – DG SANCO) in Member States and other third countries. They recommend including, as far as feasible, BSE-related aspects in future inspection missions. Expected development of the GBR As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases. A table summarising the reasons for the current assessment is given in the table below

 

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EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of Mexico Last updated: 08 September 2004 Adopted July 2004 (Question N° EFSA-Q-2003-083)

 

 Report

 

http://www.efsa.eu.int 3 of 6 Conclusions The European Food Safety Authority concludes: 1. The BSE agent was probably imported into Mexico and could have reached domestic cattle. These cattle imported could have been rendered and therefore led to an internal EFSA Scientific Report (2004) 4, 1-6 on the Assessment of the Geographical BSE Risk of challenge in the mid to late 1990’s. It is possible that imported MBM into Mexico reached domestic cattle and leads to an internal challenge around 1993. 2. It is likely that BSE infectivity entered processing at the time of imported ‘at - risk’ MBM (1993) and at the time of slaughter of imported live ‘at - risk’ cattle (mid to late 1990s). The high level of external challenge is maintained throughout the reference period, and the system has not been made stable. Thus it is likely that BSE infectivity was recycled and propagated from approximately 1993. The risk has since grown consistently due to a maintained internal and external challenge and lack of a stable system. 3. The current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. 4. EFSA and its Scientific Expert Working group on GBR are concerned that the available information was not confirmed by inspection missions as performed by the Food and Veterinary office (FVO – DG SANCO) in Member States and other third countries. They recommend including, as far as feasible, BSE-related aspects in future inspection missions.

 


 

 Summary

 

Summary of Scientific Report http://www.efsa.eu.int 1 of 2 Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE-Risk (GBR) of MEXICO Question N° EFSA-Q-2003-083 Adopted July 2004 SUMMARY OF SCIENTIFIC REPORT The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in Mexico, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Mexico. This scientific report addresses the GBR of Mexico as assessed in 2004 based on data covering the period 1980-2003. The BSE agent was probably imported into Mexico and could have reached domestic cattle. These cattle imported could have been rendered and therefore led to an internal challenge in the mid to late 1990s. It is possible that imported meat and bone meal (MBM) into Mexico reached domestic cattle and leads to an internal challenge around 1993. It is likely that BSE infectivity entered processing at the time of imported ‘at - risk’ MBM (1993) and at the time of slaughter of imported live ‘at - risk’ cattle (mid to late 1990s). The high level of external challenge is maintained throughout the reference period, and the system has not been made stable. Thus it is likely that BSE infectivity was recycled and propagated from approximately 1993. The risk has since grown consistently due to a maintained internal and external challenge and lack of a stable system. EFSA concludes that the current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSEagent. The GBR is likely to increase due to continued internal and external challenge, coupled with a very unstable system. Key words: BSE, geographical risk assessment, GBR, Mexico, third countries Summary of Scientific Report http://www.efsa.eu.int 2 of 2

 


 

Summary of the Scientific Report

 

The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in Mexico, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Mexico. This scientific report addresses the GBR of Mexico as assessed in 2004 based on data covering the period 1980-2003.

 

The BSE agent was probably imported into Mexico and could have reached domestic cattle. These cattle imported could have been rendered and therefore led to an internal challenge in the mid to late 1990s. It is possible that imported meat and bone meal (MBM) into Mexico reached domestic cattle and leads to an internal challenge around 1993.

 

It is likely that BSE infectivity entered processing at the time of imported ‘at - risk’ MBM (1993) and at the time of slaughter of imported live ‘at - risk’ cattle (mid to late 1990s). The high level of external challenge is maintained throughout the reference period, and the system has not been made stable. Thus it is likely that BSE infectivity was recycled and propagated from approximately 1993. The risk has since grown consistently due to a maintained internal and external challenge and lack of a stable system.

 

EFSA concludes that the current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. The GBR is likely to increase due to continued internal and external challenge, coupled with a very unstable system.

 


 

Thursday, January 17, 2013

 

CANADA MBM LIVE CATTLE BSE TSE PRION TO USA

 

Date: Sat, 14 Jun 2003 02:23:12 +0200

 

Reply-To: Bovine Spongiform Encephalopathy

 

Sender: Bovine Spongiform Encephalopathy

 


 

Tuesday, February 10, 2015

 

Alberta Canada First case of chronic wasting disease found in farm elk since 2002

 


 

 

 

 O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations

 

 Emmanuel Comoy, Jacqueline Mikol, Val erie 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 longe 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.

 

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 ***thus questioning the origin of human sporadic cases...TSS

 

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 ***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.

 

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 Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

 

 *** Title: Transmission of scrapie prions to primate after an extended silent incubation period

 

 Authors

 

 item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire, Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron, Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item Deslys, Jean-Philippe -

 

 Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015 Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E., Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C., Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J. 2015. Transmission of scrapie prions to primate after an extended silent incubation period. Scientific Reports. 5:11573.

 

 Interpretive Summary:

 

 The transmissible spongiform encephalopathies (also called prion diseases) are fatal neurodegenerative diseases that affect animals and humans. The agent of prion diseases is a misfolded form of the prion protein that is resistant to breakdown by the host cells. Since all mammals express prion protein on the surface of various cells such as neurons, all mammals are, in theory, capable of replicating prion diseases. One example of a prion disease, bovine spongiform encephalopathy (BSE; also called mad cow disease), has been shown to infect cattle, sheep, exotic undulates, cats, non-human primates, and humans when the new host is exposed to feeds or foods contaminated with the disease agent. The purpose of this study was to test whether non-human primates (cynomologous macaque) are susceptible to the agent of sheep scrapie. After an incubation period of approximately 10 years a macaque developed progressive clinical signs suggestive of neurologic disease. Upon postmortem examination and microscopic examination of tissues, there was a widespread distribution of lesions consistent with a transmissible spongiform encephalopathy. This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.

 

 Technical Abstract:

 

 Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the past decades, c-BSE's zoonotic potential has been the driving force in establishing extensive protective measures for animal and human health. 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.

 



 
Tuesday, December 16, 2014
 
Evidence for zoonotic potential of ovine scrapie prions
 
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics
 
Abstract
 
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human ​prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE. The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
 
Subject terms: Biological sciences• Medical research At a glance
 
 
*** 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.
 
 
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
 
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
 
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
 
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France
 
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.
 
To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
 
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.
 
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.
 
 
 
why do we not want to do TSE transmission studies on chimpanzees $
 
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
 
snip...
 
R. BRADLEY
 
 
SCRAPIE AND CWD ZOONOSIS
 
PRION 2016 CONFERENCE 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
 
 
Transmission of scrapie prions to primate after an extended silent incubation period
 
***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.***
 
 
Wednesday, June 29, 2016
 
CWD, SCRAPIE, ZOONOSIS, it’s for real folks, the risk factors have increased greatly, and science has spoken, cwd and scrapie to humans as sporadic cjd may have already happened.
 
Transmission of scrapie prions to primate after an extended silent incubation period
 
Emmanuel E. Comoy , Jacqueline Mikol , Sophie Luccantoni-Freire , Evelyne Correia , Nathalie Lescoutra-Etchegaray , Valérie Durand , Capucine Dehen , Olivier Andreoletti , Cristina Casalone , Juergen A. Richt , Justin J. Greenlee , Thierry Baron , Sylvie L. Benestad , Paul Brown & Jean-Philippe Deslys
 
Abstract
 
Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.
 
snip...
 
In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free. 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.
 
***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.***
 
 
 
 
PRION 2016 TOKYO
 
Zoonotic Potential of CWD Prions: An Update
 
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6
 
1Department of Pathology, 3National Prion Disease Pathology Surveillance Center, 5Department of Neurology, 6National Center for Regenerative Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.
 
4Department of Biological Sciences and Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,
 
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
 
Chronic wasting disease (CWD) is a widespread and highly transmissible prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern, but the susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. We reported earlier that peripheral and CNS infections were detected in transgenic mice expressing human PrP129M or PrP129V. Here we will present an update on this project, including evidence for strain dependence and influence of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of experimental human CWD prions.
 
PRION 2016 TOKYO
 
In Conjunction with Asia Pacific Prion Symposium 2016
 
PRION 2016 Tokyo
 
Prion 2016
 
 
Prion 2016
 
Purchase options Price * Issue Purchase USD 198.00
 
 
Cervid to human prion transmission
 
Kong, Qingzhong
 
Case Western Reserve University, Cleveland, OH, United States
 
Abstract
 
Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. We 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.
 
Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of "humanized" Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental "human CWD" samples will also be generated for Aim 3.
 
Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1.
 
Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental "human CWD" samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
 
Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.
 
Public Health Relevance There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.
 
Funding Agency Agency National Institute of Health (NIH)
 
Institute National Institute of Neurological Disorders and Stroke (NINDS)
 
Type Research Project (R01)
 
Project # 1R01NS088604-01A1
 
Application # 9037884
 
Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)
 
Program Officer Wong, May
 
Project Start 2015-09-30
 
Project End 2019-07-31
 
Budget Start 2015-09-30
 
Budget End 2016-07-31
 
Support Year 1
 
Fiscal Year 2015
 
Total Cost $337,507
 
Indirect Cost $118,756
 
Institution
 
Name Case Western Reserve University
 
Department Pathology
 
Type Schools of Medicine
 
DUNS # 077758407
 
City Cleveland
 
State OH
 
Country United States
 
Zip Code 44106
 
 
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We 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.
 
============================================================
 
Key Molecular Mechanisms of TSEs
 
Zabel, Mark D.
 
Colorado State University-Fort Collins, Fort Collins, CO, United States Abstract Prion diseases, or transmissible spongiform encephalopathies (TSEs), are fatal neurodegenerative diseases affecting humans, cervids, bovids, and ovids. The absolute requirement of PrPC expression to generate prion diseases and the lack of instructional nucleic acid define prions as unique infectious agents. Prions exhibit species-specific tropism, inferring that unique prion strains exist that preferentially infct certain host species and confront transmission barriers to heterologous host species. However, transmission barriers are not absolute. Scientific consensus agrees that the sheep TSE scrapie probably breached the transmission barrier to cattle causing bovine spongiform encephalopathy that subsequently breached the human transmission barrier and likely caused several hundred deaths by a new-variant form of the human TSE Creutzfeldt-Jakob disease in the UK and Europe. The impact to human health, emotion and economies can still be felt in areas like farming, blood and organ donations and the threat of a latent TSE epidemic. This precedent raises the real possibility of other TSEs, like chronic wasting disease of cervids, overcoming similar human transmission barriers. A groundbreaking discovery made last year revealed that mice infected with heterologous prion strains facing significant transmission barriers replicated prions far more readily in spleens than brains6. Furthermore, these splenic prions exhibited weakened transmission barriers and expanded host ranges compared to neurogenic prions. These data question conventional wisdom of avoiding neural tissue to avoid prion xenotransmission, when more promiscuous prions may lurk in extraneural tissues. Data derived from work previously funded by NIH demonstrate that Complement receptors CD21/35 bind prions and high density PrPC and differentially impact prion disease depending on the prion isolate or strain used. Recent advances in live animal and whole organ imaging have led us to generate preliminary data to support novel, innovative approaches to assessing prion capture and transport. We plan to test our unifying hypothesis for this proposal that CD21/35 control the processes of peripheral prion capture, transport, strain selection and xenotransmission in the following specific aims. 1. Assess the role of CD21/35 in splenic prion strain selection and host range expansion. 2. Determine whether CD21/35 and C1q differentially bind distinct prion strains 3. Monitor the effects of CD21/35 on prion trafficking in real time and space 4. Assess the role of CD21/35 in incunabular prion trafficking
 
Public Health Relevance Transmissible spongiform encephalopathies, or prion diseases, are devastating illnesses that greatly impact public health, agriculture and wildlife in North America and around the world. The impact to human health, emotion and economies can still be felt in areas like farming, blood and organ donations and the threat of a latent TSE epidemic. This precedent raises the real possibility of other TSEs, like chronic wasting disease (CWD) of cervids, overcoming similar human transmission barriers. Early this year Canada reported its first case of BSE in over a decade audits first case of CWD in farmed elk in three years, underscoring the need for continued vigilance and research. Identifying mechanisms of transmission and zoonoses remains an extremely important and intense area of research that will benefit human and other animal populations.
 
Funding Agency Agency National Institute of Health (NIH)
 
Institute National Institute of Allergy and Infectious Diseases (NIAID)
 
Type High Priority, Short Term Project Award (R56)
 
Project # 1R56AI122273-01A1
 
Application # 9211114
 
Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)
 
Program Officer Beisel, Christopher E
 
Project Start 2016-02-16
 
Project End 2017-01-31
 
Budget Start 2016-02-16
 
Budget End 2017-01-31
 
Support Year 1
 
Fiscal Year 2016
 
Total Cost
 
Indirect Cost Institution Name Colorado State University-Fort Collins
 
Department Microbiology/Immun/Virology
 
Type Schools of Veterinary Medicine
 
DUNS # 785979618 City Fort Collins
 
State CO
 
Country United States
 
Zip Code 80523
 
 
PMCA Detection of CWD Infection in Cervid and Non-Cervid Species
 
Hoover, Edward Arthur
 
Colorado State University-Fort Collins, Fort Collins, CO, United States Abstract Chronic wasting disease (CWD) of deer and elk is an emerging highly transmissible prion disease now recognized in 18 States, 2 Canadian provinces, and Korea. We have shown that Infected deer harbor and shed high levels of infectious prions in saliva, blood, urine, and feces, and in the tissues generating those body fluids and excreta, thereby leading to facile transmission by direct contact and environmental contamination. We have also shown that CWD can infect some non-cervid species, thus the potential risk CWD represents to domestic animal species and to humans remains unknown. Whether prions borne in blood, saliva, nasal fluids, milk, or excreta are generated or modified in the proximate peripheral tissue sites, may differ in subtle ways from those generated in brain, or may be adapted for mucosal infection remain open questions. The increasing parallels in the pathogenesis between prion diseases and human neurodegenerative conditions, such as Alzheimer's and Parkinson's diseases, add relevance to CWD as a transmissible protein misfolding disease. The overall goal of this work is to elucidate the process of CWD prion transmission from mucosal secretory and excretory tissue sites by addressing these questions: (a) What are the kinetics and magnitude of CWD prion shedding post-exposure? (b) Are excreted prions biochemically distinct, or not, from those in the CNS? (c) Are peripheral epithelial or CNS tissues, or both, the source of excreted prions? and (d) Are excreted prions adapted for horizontal transmission via natural/trans-mucosal routes? The specific aims of this proposal are: (1) To determine the onset and consistency of CWD prion shedding in deer and cervidized mice; (2); To compare the biochemical and biophysical properties of excretory vs. CNS prions; (3) To determine the capacity of peripheral tissues to support replication of CWD prions; (4) To determine the protease- sensitive infectious fraction of excreted vs. CNS prions; and (5) To compare the mucosal infectivity of excretory vs. CNS prions. Understanding the mechanisms that enable efficient prion dissemination and shedding will help elucidate how horizontally transmissible prions evolve and succeed, and is the basis of this proposal. Understanding how infectious misfolded proteins (prions) are generated, trafficked, shed, and transmitted will aid in preventing, treating, and managing the risks associated with these agents and the diseases they cause.
 
Public Health Relevance Chronic wasting disease (CWD) of deer and elk is an emergent highly transmissible prion disease now recognized throughout the USA as well as in Canada and Korea. We have shown that infected deer harbor and shed high levels of infectious prions in saliva, blood, urine, and feces thereby leading to transmission by direct contact and environmental contamination. In that our studies have also shown that CWD can infect some non-cervid species, the potential risk CWD may represents to domestic animal species and humans remains unknown. The increasing parallels in the development of major human neurodegenerative conditions, such as Alzheimer's and Parkinson's diseases, and prion diseases add relevance to CWD as a model of a transmissible protein misfolding disease. Understanding how infectious misfolded proteins (prions) are generated and transmitted will aid in interrupting, treating, and managing the risks associated with these agents and the diseases they cause.
 
Funding Agency Agency National Institute of Health (NIH)
 
Institute National Institute of Neurological Disorders and Stroke (NINDS)
 
Type Research Project (R01)
 
Project # 4R01NS061902-07
 
Application # 9010980
 
Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)
 
Program Officer Wong, May Project Start 2009-09-30
 
Project End 2018-02-28
 
Budget Start 2016-03-01
 
Budget End 2017-02-28
 
Support Year 7
 
Fiscal Year 2016
 
Total Cost $409,868
 
Indirect Cost $134,234 Institution Name Colorado State University-Fort Collins
 
Department Microbiology/Immun/Virology
 
Type Schools of Veterinary Medicine
 
DUNS # 785979618 City Fort Collins
 
State CO
 
Country United States
 
Zip Code 80523
 
 
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).***
 
 
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
 
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
 
O18
 
Zoonotic Potential of CWD Prions
 
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA
 
*** These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.
 
==================
 
***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***
 
==================
 
P.105: RT-QuIC models trans-species prion transmission
 
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA
 
Conversely, FSE maintained sufficient BSE characteristics to more efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was competent for conversion by CWD and fCWD.
 
***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.
 
================
 
***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***
 
================
 
 
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
 
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
 
*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.
 
*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
 
 
 
*** 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).***
 
 
*** 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.
 
 
***********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 1994
 
Consumption 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 for all exposures), while the other exposures ceased to be 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 ;
 
 
CJD9/10022
 
October 1994
 
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ
 
Dear Mr Elmhirst,
 
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
 
Thank 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.
 
 
Monday, May 02, 2016
 
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
 
 
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
 
 
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
 
*** Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP,
 
*** indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains.
 
PPo2-27:
 
Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions
 
*** Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.
 
PPo2-7:
 
Biochemical and Biophysical Characterization of Different CWD Isolates
 
*** The data presented here substantiate and expand previous reports on the existence of different CWD strains.
 
 
Envt.07:
 
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease
 
***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.
 
 
>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO CONVERSION OF THE HUMAN PRION PROTEIN<<<
 
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
 
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
 
Wednesday, January 01, 2014
 
Molecular Barriers to Zoonotic Transmission of Prions
 
*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.
 
*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
 
 
 
Thursday, August 25, 2016
 
TPWD Action Disease Detection and Response – Chronic Wasting Disease TPW Commission Adopts New CWD Zones, Deer Movement Rules August 25, 2016 This map shows the recently imposed Surveillance Zone for CWD in portions of Bandera, Medina and Uvalde counties.
 
 
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
 
 
Monday, May 02, 2016
 
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
 
 
======================================================
 
Wednesday, June 29, 2016
 
*** NIH awards $11 million to UTHealth researchers to study deadly CWD prion diseases Claudio Soto, Ph.D. ***
 
Public Release: 29-Jun-2016
 
 
Tuesday, December 16, 2014
 
Evidence for zoonotic potential of ovine scrapie prions
 
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics
 
Abstract
 
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human ​prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE. The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
 
Subject terms: Biological sciences• Medical research At a glance
 
 
*** 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.
 
 
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
 
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
 
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
 
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France
 
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.
 
To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
 
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.
 
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.
 
 
 
why do we not want to do TSE transmission studies on chimpanzees $
 
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
 
snip...
 
R. BRADLEY
 
 
SCRAPIE AND CWD ZOONOSIS
 
PRION 2016 CONFERENCE 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
 
 
Transmission of scrapie prions to primate after an extended silent incubation period
 
***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.***
 
 
 
 
WS-02
 
Scrapie in swine: A diagnostic challenge
 
Justin J Greenlee1, Robert A Kunkle1, Jodi D Smith1, Heather W. Greenlee2
 
1National Animal Disease Center, US Dept. of Agriculture, Agricultural Research Service, United States; 2Iowa State University College of Veterinary Medicine
 
A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested.
 
Since swine can be fed rations containing ruminant derived components in the United States and many other countries, we conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Scrapie inoculum was a pooled 10% (w/v) homogenate derived from the brains of clinically ill sheep from the 4th passage of a serial passage study of the U.S scrapie agent (No. 13-7) through susceptible sheep that were homozygous ARQ at prion protein residues 136, 154, and 171, respectively. Pigs were inoculated intracranially (n=19) with a single 0.75 ml dose or orally (n=24) with 15 ml repeated on 4 consecutive days. Necropsies were done on a subset of animals at approximately six months post inoculation (PI), at the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of TSE until study termination at 80 months PI or when removed due to intercurrent disease (primarily lameness). Brain samples were examined by immunohistochemistry (IHC), western blot (WB), and enzyme-linked immunosorbent assay (ELISA). Brain tissue from a subset of pigs in each inoculation group was used for bioassay in mice expressing porcine PRNP.
 
At six-months PI, no evidence of scrapie infection was noted by any diagnostic method. However, at 51 months of incubation or greater, 5 animals were positive by one or more methods: IHC (n=4), WB (n=3), or ELISA (n=5). Interestingly, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study).
 
Swine inoculated with the agent of scrapie by the intracranial and oral routes do not accumulate abnormal prion protein (PrPSc) to a level detectable by IHC or WB by the time they reach typical market age and weight. However, strong support for the fact that swine are potential hosts for the agent of scrapie comes from positive bioassay from both intracranially and orally inoculated pigs and multiple diagnostic methods demonstrating abnormal prion protein in intracranially inoculated pigs with long incubation times.
 
Curriculum Vitae
 
Dr. Greenlee is Research Veterinary Medical Officer in the Virus and Prion Research Unit at the National Animal Disease Center, US Department of Agriculture, Agricultural Research Service. He applies his specialty in veterinary anatomic pathology to focused research on the intra- and interspecies transmission of prion diseases in livestock and the development of antemortem diagnostic assays for prion diseases. In addition, knockout and transgenic mouse models are used to complement ongoing experiments in livestock species. Dr. Greenlee has publications in a number of topic areas including prion agent decontamination, effects of PRNP genotype on susceptibility to the agent of sheep scrapie, characterization of US scrapie strains, transmission of chronic wasting disease to cervids and cattle, features of H-BSE associated with the E211 K polymorphism, and the development of retinal assessment for antemortem screening for prion diseases in sheep and cattle. Dr. Greenlee obtained his DVM degree and completed the PhD/residency program in Veterinary Pathology at Iowa State University. He is a Diplomate of the American College of Veterinary Pathologists.
 
 
Prion
 
Volume 9, Issue 4, 2015
 
Porcine prion protein amyloid
 
DOI:10.1080/19336896.2015.1065373Per Hammarströma & Sofie Nyströma*
 
pages 266-277
 
Received: 1 Jun 2015 Accepted: 17 Jun 2015 Accepted author version posted online: 28 Jul 2015
 
© 2015 The Author(s). Published with license by Taylor & Francis Group, LLC Additional license information
 
ABSTRACT
 
Mammalian prions are composed of misfolded aggregated prion protein (PrP) with amyloid-like features. Prions are zoonotic disease agents that infect a wide variety of mammalian species including humans. Mammals and by-products thereof which are frequently encountered in daily life are most important for human health. It is established that bovine prions (BSE) can infect humans while there is no such evidence for any other prion susceptible species in the human food chain (sheep, goat, elk, deer) and largely prion resistant species (pig) or susceptible and resistant pets (cat and dogs, respectively). PrPs from these species have been characterized using biochemistry, biophysics and neurobiology. Recently we studied PrPs from several mammals in vitro and found evidence for generic amyloidogenicity as well as cross-seeding fibril formation activity of all PrPs on the human PrP sequence regardless if the original species was resistant or susceptible to prion disease. Porcine PrP amyloidogenicity was among the studied. Experimentally inoculated pigs as well as transgenic mouse lines overexpressing porcine PrP have, in the past, been used to investigate the possibility of prion transmission in pigs. The pig is a species with extraordinarily wide use within human daily life with over a billion pigs harvested for human consumption each year. Here we discuss the possibility that the largely prion disease resistant pig can be a clinically silent carrier of replicating prions.
 
SNIP...
 
CONCLUDING REMARKS Should the topic of porcine PrP amyloid be more of a worry than of mere academic interest? Well perhaps. Prions are particularly insidious pathogens. A recent outbreak of peripheral neuropathy in human, suggests that exposure to aerosolized porcine brain is deleterious for human health.43,44 Aerosolization is a known vector for prions at least under experimental conditions.45-47 where a mere single exposure was enough for transmission in transgenic mice. HuPrP is seedable with BoPrP seeds and even more so with PoPrP seed (Fig. 1), indicating that humans could be infected by porcine APrP prions while neurotoxicity associated with spongiform encephalopathy if such a disease existed is even less clear. Importantly transgenic mice over-expressing PoPrP are susceptible to BSE and BSE passaged through domestic pigs implicating that efficient downstream neurotoxicity pathways in the mouse, a susceptible host for prion disease neurotoxicity is augmenting the TSE phenotype.25,26 Prions in silent carrier hosts can be infectious to a third species. Data from Collinge and coworkers.21 propose that species considered to be prion free may be carriers of replicating prions. Especially this may be of concern for promiscuous prion strains such as BSE.19,48 It is rather established that prions can exist in both replicating and neurotoxic conformations.49,50 and this can alter the way in which new host organisms can react upon cross-species transmission.51 The na€ıve host can either be totally resistant to prion infection as well as remain non-infectious, become a silent non-symptomatic but infectious carrier of disease or be afflicted by disease with short or long incubation time. The host can harbor and/or propagate the donor strain or convert the strain conformation to adapt it to the na€ıve host species. The latter would facilitate infection and shorten the incubation time in a consecutive event of intra-species transmission. It may be advisable to avoid procedures and exposure without proper biosafety precautions as the knowledge of silence carrier species is poor. One case of iatrogenic CJD in recipient of porcine dura mater graft has been reported in the literature.52 The significance of this finding is still unknown. The low public awareness in this matter is exemplified by the practice of using proteolytic peptide mixtures prepared from porcine brains (Cerebrolysin) as a nootropic drug. While Cerebrolysin may be beneficial for treatment of severe diseases such as vascular dementia,53 a long term follow-up of such a product for recreational use is recommended.
 
 
Friday, August 21, 2015
 
Porcine prion protein amyloid or mad pig disease PSE Porcine Spongiform Encephalopathy ?
 
 
 
 

CANADA CJD
CJD DEATHS REPORTED BY CJDSS, 1994-2016 AS OF JULY 31, 2016 Cases
 
 
image

 
INCIDENCE OF CJD DEATHS REPORTED BY CJDSS IN CANADA AS OF JULY 31, 2016
 
 
image
 
 

REFERRALS OF SUSPECTED CJD REPORTED BY CJDSS, 1997-2016 AS OF JULY 31, 2016
 
 
image
 
 
 

Referrals of Suspected CJD Reported by CJDSS, 1997-2015
As of October 31, 2015
 
Year of Reporting Number of Referrals
1997 4
1998 43
1999 63
2000 82
2001 101
2002 103
2003 75
2004 90
2005 97
2006 80
2007 101
2008 100
2009 104
2010 76
2011 102
2012 103
2013 99
2014 99
2015 80
Total 1602

CJD Deaths Reported by CJDSS, 1994-2015
As of October 31, 2015
 
Deaths of Definite and Probable CJD
Year Sporadic Iatrogenic Familial GSS FFI vCJD Total
Cases with definite & probable diagnosis to date.
1994 2 0 0 1 0 0 3
1995 3 0 0 0 0 0 3
1996 13 0 0 0 0 0 13
1997 16 0 1 1 0 0 18
1998 22 1 0 1 0 0 24
1999 27 2 2 1 0 0 32
2000 32 0 0 3 0 0 35
2001 27 0 2 1 0 0 30
2002 31 0 2 2 0 1 36
2003 27 1 1 0 0 0 29
2004 42 0 1 1 0 0 44
2005 42 0 1 1 0 0 44
2006 39 0 1 3 1 0 44
2007 35 0 0 4 0 0 39
2008 48 0 1 0 0 0 49
2009 48 0 3 2 0 0 53
2010 35 0 3 0 0 0 38
2011 46 0 3 1 0 1 51
2012 62 0 1 0 0 0 63
2013 50 0 0 0 1 0 51
2014 49 0 4 0 1 0 54
2015 23 0 1 0 0 0 24
Total 719 4 27 22 3 2 777

CJD Cases by Province/Territory October 31, 2015

Incidence of CJD Deaths Reported by CJDSS in Canada
As of October 31, 2015
 
Year of Death Total CJD Cases Population of Canada Incidence Rate
Cases with definite & probable diagnosis to date.2014 Population SourceExternal Link
1999 32 30,492,106 1.05
2000 35 30,783,969 1.14
2001 30 31,130,030 0.96
2002 36 31,450,443 1.14
2003 29 31,734,851 0.91
2004 44 32,037,434 1.37
2005 44 32,352,233 1.36
2006 44 32,678,986 1.35
2007 39 33,001,076 1.18
2008 49 33,371,810 1.47
2009 53 33,756,714 1.57
2010 38 34,131,451 1.11
2011 51 34,472,304 1.48
2012 63 34,880,248 1.81
2013 51 35,289,003 1.45
2014 54 35,675,834 1.51
2015 24 35,702,707 0.81

http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/stats-eng.php
 
 
Saturday, March 21, 2015
 
*** Canada and United States Creutzfeldt Jakob TSE Prion Disease Incidence Rates Increasing
 
 
Saturday, March 21, 2015
 
***Canada and United States Creutzfeldt Jakob TSE Prion Disease Incidence Rates Increasing ***
 
 
CANADA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic CJD’s). ...tss
 
PLEASE NOTE, type determination pending Creutzfeldt Jakob Disease (tdpCJD) in Canada is also on a steady increase.
 
please see ;
 
> 3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.
 
CJD Deaths Reported by CJDSS1, 1994-20122
 
As of May 31, 2012
 
Deaths of Definite and Probable CJD
 
Year Sporadic Iatrogenic Familial GSS FFI vCJD Total
 
1994 2 0 0 1 0 0 3
 
1995 3 0 0 0 0 0 3
 
1996 13 0 0 0 0 0 13
 
1997 16 0 1 1 0 0 18
 
1998 22 1 0 1 0 0 24
 
1999 26 2 2 1 0 0 31
 
2000 32 0 0 3 0 0 35
 
2001 27 0 2 1 0 0 30
 
2002 31 0 2 2 0 1 36
 
2003 27 1 1 0 0 0 29
 
2004 42 0 1 0 0 0 43
 
2005 42 0 0 2 0 0 44
 
2006 39 0 1 3 1 0 44
 
2007 35 0 0 4 0 0 39
 
2008 48 0 1 0 0 0 49
 
2009 48 0 3 2 0 0 53
 
2010 34 0 3 0 0 0 37
 
2011 37 0 2 1 0 1 41
 
2012 1 0 0 0 0 0 1
 
Total 525 4 19 22 1 2 573
 
1. CJDSS began in 1998
 
2. Data before 1998 are retrospective and partial, data from 1998 to 2008 are complete, and data for 2009 - 2012 are provisional
 
3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.
 
CJD Deaths Reported by CJDSS1, 1994-20122
 
As of May 31, 2012
 
 
SEE DECEMBER 2012 CANADA
 
 
Saturday, June 15, 2013
 
Canada Fraser Health Statement on Creutzfeldt-Jakob Disease outbreak
 
 
 
P.179: Sporadic Creutzfeldt-Jakob disease in Canada
 
Zheng Wang,1 Gerard Jansen,1,2 Stacy Sabourin,1 Rolande D’Amour,1 Tim Connolly,1 Jennifer Kruse,1 David J Knox,3 Neil R Cashman,4 and Michael B Coulthart1 1The Canadian Creutzfeldt-Jakob Disease Surveillance System; Public Health Agency of Canada; Ottawa, ON Canada; 2Department of Pathology; Ottawa Hospital; Ottawa, ON Canada; 3National Microbiology Laboratory; Public Health Agency of Canada; Winnipeg, MB Canada; 4Brain Research Centre; University of British Columbia; Vancouver, BC Canada
 
Background. Sporadic Creutzfeldt-Jakob Disease (sCJD) is a fatal, transmissible neurodegenerative disease. Systematic surveillance has repeatedly shown annual mortality in the range 1 to 2 per million population, has elucidated key characteristics of sCJD, and led to recognition of a new form of CJD, variant CJD (vCJD), which is associated with BSE. In 1998, Canada launched comprehensive national CJD surveillance to assess the characteristics of CJD in Canada, identify any acquired cases of CJD (such as vCJD, of which 2 imported cases have been identified in Canada to date), and mitigate public health risks. This study describes the epidemiology of sCJD in Canada from 1998 to 2012.
 
Methods. Case ascertainment was based on internationally accepted criteria. Demographic and medical information were collected by standardized questionnaire and medical chart review. Poisson regression and descriptive analysis were employed.
 
Results. A total of 563 sCJD deaths (definite: 462, probable: 101) in Canadian residents were registered from 1998 to 2012. Average annual sCJD mortality was 1.2 per million population, increasing gradually from 0.9 in 1999 to 1.7 in 2012 (P = 0.0004). All provinces saw average annual mortalities ranging from 1.0 to 1.6 (P = 0.25), except three territories where population is small (~25,000 to ~45,000) and no cases were identified. sCJD occurred at similar rates in males (1.1) and females (1.2) (P = 0.21). sCJD was rare under 50 years of age with only 11 cases identified (2.7%). Mortality increased after 50 and peaked at 7.4 per million in the 70–74 age group. Median age at death was 69 and median duration of illness was 4 months. Genotype at codon 129 (N = 358) revealed that the MM subgroup accounted for 223 (62%, median age at death: 69, duration: 4), the MV subgroup was 82 (23%, median age at death: 68, duration: 9), and the VV subgroup was 53 (23%, median age at death: 66, duration: 5). Results of molecular typing (Parchi Scheme) for 256 cases are; MM1: 140, MM2: 11, MV1: 28, MV2: 18, VV1: 5, VV2: 25, Mixture: 29.
 
Conclusion. Characteristics of sCJD in Canada are consistent with those observed in other countries. The increase in sCJD mortality can be partly attributed to increased awareness of CJD among Canadian clinicians. These findings support the conclusion that Canadian CJD surveillance system is sufficiently sensitive to accurately characterize the epidemiology of sCJD in Canada, and to detect potential additional cases of acquired CJD such as vCJD or human chronic wasting disease.
 
Conclusion. Characteristics of sCJD in Canada are consistent with those observed in other countries. The increase in sCJD mortality can be partly attributed to increased awareness of CJD among Canadian clinicians. These findings support the conclusion that Canadian CJD surveillance system is sufficiently sensitive to accurately characterize the epidemiology of sCJD in Canada, and to detect potential additional cases of acquired CJD such as vCJD or human chronic wasting disease.
 
 
HD.18: Creutzfeldt-Jakob disease reporting in Canada
 
Zheng Wang,1 Gerard H. Jansen,1, 2 Elina Olsen,1 Rolande D’Amour,1 Stacy Sabourin,1 Tim Connolly,1 Jennifer Kruse,1 Neil Cashman3 and Michael Coulthart1 1Public Health Agency of Canada; Ottawa, ON CA; 2Department of Pathology; Ottawa Hospital; Ottawa, ON CA; 3Brain Research Centre; University of British Columbia; Vancouver, BC CA
 
Background. To deal with risks of infectious transmission of Creutzfeldt-Jakob disease (CJD), in 1998 the Government of Canada launched a prospective national CJD surveillance system (CJDSS). In 2000, CJD became nationally notifiable in Canada, and since then all Canadian Provinces and Territories (P/Ts) have made CJD reportable. It has been recognized that the CJDSS registers more cases of CJD than are reported to P/T Ministries of Health (PTMH). Because the CJDSS may not legally share personal information with PTMH, in 2008 the CJDSS began to systematically discuss the issue of CJD reporting with referring health care professionals (HCP). The present study was undertaken to estimate any changes in P/T CJD reporting from 2008, and to identify possible areas for further improvement.
 
Materials and Methods. P/T CJD data were retrieved from the Public Health Agency of Canada’s National Notifiable Disease System (NNDS) database, and compared with CJDSS data. CJDSS intake sheets were examined, to determine if the case had been reported to the PTMH at the time of notification.
 
Results. From 2005 to 2010, NNDS received complete data on CJD from 5 P/Ts. During the same period, 134 cases of CJD (probable or neuropathologically confirmed) were reported by the 5 P/Ts while 210 CJD deaths (probable or definite) were recorded in the CJDSS from the same 5 P/Ts. Between 2008 and 2010 there was an increase of ~48% in P/T CJD reports compared with the period 2005–2007. In contrast, the CJDSS registered only ~12% more CJD deaths between 2008 and 2010 compared with 2005–2007, supporting an interpretation of improved P/T reporting. Examination of intake sheets from 172 notifications that were made to the CJDSS from the same 5 P/Ts between 2008 and 2010 revealed that 30 were known to have been reported to PTMH at the time of referring (24 were CJD, 5 were non-CJD, and 1 was unclassifiable). 142 were not reported or had unknown reporting status. Reasons cited by HCPs for not reporting included (1) uncertainty of the CJD diagnosis; (2) uncertainty regarding responsibility for reporting; (3) lack of awareness that CJD is reportable; and (4) uncertainty regarding when or how to report.
 
Conclusion. The considerable increase of CJD reports in P/Ts since 2008 occurred concurrently with efforts of the CJDSS to engage HCPs on the issue of CJD reporting requirements. P/T CJD reports may include non-CJD cases. Inter-jurisdiction collaboration is underway to further improve CJD reporting.
 
 
Risk.49: Creutzfeldt-Jakob Disease in Canada, 1998–2009
 
Zheng Wang,1,† Gerard Jansen,1, 2 Elina Olsen,1 Stacy Sabourin,1 Rolande D’Amour,1 Tim Connolly,1 Jennifer Kruse,1 Neil Cashman3 and Michael Coulthart1
 
1The Canadian Creutzfeldt-Jakob Disease Surveillance System; Public Health Agency of Canada; Ottawa, ON Canada; 2Department of Pathology; Ottawa Hospital; Ottawa, ON Canada; 3Brain Research Centre; University of British Columbia; Vancouver, BC Canada†Presenting author; Email: zheng.wang@phac-aspc.gc.ca
 
Background. Creutzfeldt-Jakob Disease (CJD) is a fatal, transmissible neurodegenerative disease with sporadic, genetic and acquired forms. In 1998, Canada launched comprehensive national CJD surveillance to assess the characteristics of CJD in Canada and its risks to the health of Canadians. This study describes the broad characteristics of CJD in Canada from 1998–2009.
 
Methods. Case ascertainment was based on internationally accepted criteria. Demographic information and risk-factor data were collected by standardized questionnaire and medical chart review. Poisson regression, descriptive analysis, and case investigation were employed.
 
Results. A total of 453 CJD deaths in Canadian residents were registered from 1998–2009. Four hundred and fifteen (92%) were sporadic (sCJD), 33 (7%) were genetic and five (1%) were acquired. Average annual sCJD mortality was 1.1 per million population, increasing gradually from 0.9 in 1999 to 1.4 in 2009 (P = 0.27). All provinces saw average annual mortalities ranging from 1.0 to 1.5 (P = 0.85), except three territories where population is small (~25,000 to ~45,000), sCJD occurred equally in both genders at 1.1. sCJD was rare under 50 years of age with only 11 cases identified (2.7%). Mortality increased after 50 and peaked at 8 per million in the 70–74 age group. Median age at death was 69 and median duration of illness was 4 months. Genetic TSE accounted for 33 deaths: 19 were GSS (P102L: 5, D202N: 2, P105T: 2, Q217R:1, A117V: 1, unknown mutation: 8); 13 were familial CJD (E200K: 9, D178N: 2, V203I: 1, V189I:1); one was FFI (D178N). Median age for genetic TSE was 59 and median duration of illness was 27 months. For the five acquired cases of CJD, four were associated with dura mater procedures (3 Lyodura, 1 Tutoplast) and were identified from 1998–2003 in patients aged 14–59. Investigation indicated the infections possibly occurred from 1981–1992 with incubation times from 10–16 years. One biochemically and neuropathologically confirmed variant CJD death occurred in 2002 in a person under 40 years old, likely acquired overseas.
 
Discussion and Conclusion. Characteristics of CJD in Canada are consistent with those observed in other countries. The increase in sCJD mortality can be at least partly attributed to increased awareness of CJD among referring clinicians. The finding of four dura matter associated CJD cases and one imported vCJD case in Canada demonstrate risks to Canadians from acquired CJD exist. Continued surveillance for iatrogenic risks and novel forms of CJD is warranted.
 
 
Monday, August 22, 2016
 
*** CREUTZFELDT JAKOB DISEASE USA 2015 SPORADIC CJD TOTAL FIGURES REACHES HIGHEST ANNUAL COUNT TO DATE AT 239 CONFIRMED CASES ***
 
 
Transmission of scrapie prions to primate after an extended silent incubation period
 
***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.***
 
 
Thursday, August 18, 2016
 
*** PROCEEDINGS ONE HUNDRED AND Nineteenth ANNUAL MEETING of the USAHA BSE, CWD, SCRAPIE, PORCINE TSE PRION October 22 28, 2015 ***
 
 
Tuesday, August 9, 2016
 
*** Concurrence with OIE Risk Designations for Bovine Spongiform Encephalopathy [Docket No. APHIS-2015-0055]
 
 
Saturday, July 23, 2016
 
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
 
 
Tuesday, July 26, 2016
 
*** Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016
 
 
Saturday, July 16, 2016
 
*** Importation of Sheep, Goats, and Certain Other Ruminants [Docket No. APHIS-2009-0095]RIN 0579-AD10
 
WITH great disgust and concern, I report to you that the OIE, USDA, APHIS, are working to further legalize the trading of Transmissible Spongiform Encephalopathy TSE Pion disease around the globe.
 
THIS is absolutely insane. it’s USDA INC.
 
 
Thursday, October 22, 2015
 
*** Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened those mad cows in Texas ***
 
 
Monday, June 20, 2016
 
*** Specified Risk Materials SRMs BSE TSE Prion Program ***
 
 
Thursday, April 14, 2016
 
Arizona 22 year old diagnosed with Creutzfeldt Jakob Disease CJD
 
 
Thursday, January 15, 2015
 
41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease CJD TSE Prion: Case Report
 
 
Saturday, January 17, 2015
 
*** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease
 
 
Saturday, December 12, 2015
 
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
 
 
Sunday, August 21, 2016
 
Kay Ellen Roedl Schwister Deceased August 7, 2016 at the age of 53 with Creutzfeldt-Jakob disease CJD TSE Prion spontaneous sporadic, zoonosis, or iatrogenic?
 
 
Monday, August 22, 2016
 
*** CREUTZFELDT JAKOB DISEASE USA 2015 SPORADIC CJD TOTAL FIGURES REACHES HIGHEST ANNUAL COUNT TO DATE AT 239 CONFIRMED CASES ***
 
 
*** Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle ***
 
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
 
snip...
 
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
 
 
 
 
In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
 
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...
 
 
”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” ...page 26.
 
 
*** Calling Canadian beef unsafe is like calling your twin sister ugly," Dopp said.
 
Thursday, August 25, 2016
 
*** FSIS Green Bay Dressed Beef Recalls Beef Products Due To Possible Specified Risk Materials Contamination the most high risk materials for BSE TSE PRION AKA MAD COW TYPE DISEASE ***
 
 
IN my opinion, the BSE MRR policy, which overtook the BSE GBR risk assessments for each country, and then made BSE confirmed countries legal to trade mad cow disease, which was all brought forth AFTER that fateful day December 23, 2003, when the USA lost it’s gold card i.e. BSE FREE status, that’s the day it all started. once the BSE MRR policy was shoved down every countries throat by USDA inc and the OIE, then the legal trading of Scrapie was validated to be a legal trading commodity, also shoved through by the USDA inc and the OIE, the world then lost 30 years of attempted eradication of the BSE TSE prion disease typical and atypical strains, and the BSE TSE Prion aka mad cow type disease was thus made a legal trading commodity, like it or not. it’s all about money now folks, trade, to hell with human health with a slow incubating disease, that is 100% fatal once clinical, and forget the fact of exposure, sub-clinical infection, and friendly fire there from i.e. iatrogenic TSE prion disease, the pass it forward mode of the TSE PRION aka mad cow type disease. it’s all going to be sporadic CJD or sporadic ffi, or sporadic gss, or now the infamous VPSPr. ...problem solved $$$
 
 
 
Terry S. Singeltary Sr.
 
 
 

Thursday, August 4, 2016

Secretary's Advisory Committee on Animal Health [Docket No. APHIS-2016-0046] TSE PRION DISEASE ?

 [Federal Register Volume 81, Number 149 (Wednesday, August 3, 2[Notices][Pages 51176-51177] From the Federal Register Online via the Government Publishing Office [www.gpo.gov] [FR Doc No: 2016-18341]
 
-----------------------------------------------------------------------
 
DEPARTMENT OF AGRICULTURE
 
Animal and Plant Health Inspection Service
 
[Docket No. APHIS-2016-0046]
 
Secretary's Advisory Committee on Animal Health; Intent To Renew
 
AGENCY: Animal and Plant Health Inspection Service, USDA.
 
ACTION: Notice of intent.
 
-----------------------------------------------------------------------
 
SUMMARY: We are giving notice that the Secretary of Agriculture intends to renew the charter for the Secretary's Advisory Committee on Animal Health for a 2-year period. The Secretary has determined that the Committee is necessary and in the public interest.
 
FOR FURTHER INFORMATION CONTACT: Dr. Diane L. Sutton, Designated Federal Officer, VS, APHIS, 4700 River Road Unit 43, Riverdale, MD 20737; (301) 851-3509.
 
SUPPLEMENTARY INFORMATION: Pursuant to the Federal Advisory Committee Act (FACA, 5 U.S.C. App.), notice is hereby given that the Secretary of Agriculture intends to renew the Secretary's Advisory Committee on Animal Health (the Committee) for 2 years. The term for the renewed charter will extend from August 8, 2016, to August 7, 2018.
 
 The Committee advises the Secretary on strategies, policies, and programs to prevent, control, or eradicate animal diseases. The Committee considers agricultural initiatives of national scope and significance and advises on matters of public health, conservation of national resources, stability of livestock economies, livestock disease management and traceability strategies, prioritizing animal health imperatives,
 
[[Page 51177]]
 
and other related aspects of agriculture. The Committee Chairperson and Vice Chairperson are elected by the Committee from among its members.
 
 Done in Washington, DC, this 27th day of July 2016. Kevin Shea, Administrator, Animal and Plant Health Inspection Service. [FR Doc. 2016-18341 Filed 8-2-16; 8:45 am] BILLING CODE 3410-34-P
 
 
Sunday, July 17, 2016
 
*** CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL REPORT UPDATE JULY 17 2016
 
 
Saturday, May 28, 2016
 
*** Infection and detection of PrPCWD in soil from CWD infected farm in Korea Prion 2016 Tokyo ***
 
 
Saturday, July 16, 2016
 
Importation of Sheep, Goats, and Certain Other Ruminants [Docket No. APHIS-2009-0095]RIN 0579-AD10
 
WITH great disgust and concern, I report to you that the OIE, USDA, APHIS, are working to further legalize the trading of Transmissible Spongiform Encephalopathy TSE Pion disease around the globe.
 
THIS is absolutely insane. it’s USDA INC.
 
 
Wednesday, May 25, 2016
 
 USDA APHIS National Scrapie TSE Prion Eradication Program April 2016 Monthly Report Prion 2016 Tokyo Update
 
 
 *** 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.
 
 
 Saturday, April 23, 2016
 
 SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 TOKYO
 
 Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
 
 
 Monday, May 02, 2016
 
 *** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
 
 
 Tuesday, June 07, 2016
 
*** Comparison of two US sheep scrapie isolates supports identification as separate strains ***
 
 Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
 
 
 Friday, January 30, 2015
 
*** Scrapie: a particularly persistent pathogen ***
 
 
Thursday, August 04, 2016
 
MEETING ON THE FEASIBILITY OF CARRYING OUT EPIDEMIOLOGICAL STUDIES ON CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN CONFIDENCE CONFIDENTIAL SCJD
 
 
THIS IS most important as well, and you may not be aware of this, if not, you and your colleagues should please take note ‘After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie’, and below this as well, I am now beginning to question the Red Deer Ataxia back in the 70s and 80s, as I did the infamous ‘hound ataxia’.
 
*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie. ***
 
2011
 
*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie. ***
 
 
Primary transmission of CWD versus scrapie prions from small ruminants to ovine and cervid PrP transgenic mice
 
Authors: Sally A. Madsen-Bouterse1, David A. Schneider2, Dongyue Zhuang3, Rohana P. Dassanayake4, Aru Balachandran5, Gordon B. Mitchell6, Katherine I. O'Rourke7  VIEW AFFILIATIONS
 
Published Ahead of Print: 08 July, 2016 Journal of General Virology doi: 10.1099/jgv.0.000539 Published Online: 08/07/2016
 
Development of mice expressing either ovine (Tg338) or cervid (TgElk) prion protein (PrP) have aided in characterization of scrapie and chronic wasting disease (CWD), respectively. Experimental inoculation of sheep with CWD prions has demonstrated the potential for interspecies transmission but, infection with CWD versus classical scrapie prions may be difficult to differentiate using validated diagnostic platforms. In this study, mouse bioassay in Tg338 and TgElk was utilized to evaluate transmission of CWD versus scrapie prions from small ruminants. Mice (>5/homogenate) were inoculated with brain homogenates from clinically affected sheep or goats with naturally-acquired classical scrapie, white-tailed deer with naturally-acquired CWD (WTD-CWD), or sheep with experimentally-acquired CWD derived from elk (sheep-passaged-CWD). Survival time (time to clinical disease) and attack rates (brain accumulation of protease resistant PrP, PrPres) were determined. Inoculation with classical scrapie prions resulted in clinical disease and 100% attack rates in Tg338, but no clinical disease at endpoint (>300 days post inoculation, dpi) and low attack rates (6.8%) in TgElk. Inoculation with WTD-CWD prions yielded no clinical disease or brain PrPres accumulation in Tg338 at endpoint (>500dpi) but rapid onset of clinical disease (~121dpi) and 100% attack rate in TgElk. Sheep-passaged-CWD resulted in transmission to both mouse lines with 100% attack rates at endpoint in Tg338 and an attack rate of ~73% in TgElk with some culled due to clinical disease. These primary transmission observations demonstrate the potential of bioassay in Tg338 and TgElk to help differentiate possible infection with CWD versus classical scrapie prions in sheep and goats.
 
 
P.97: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease and distinct from the scrapie inoculum
 
Justin Greenlee1, S Jo Moore1, Jodi Smith1, M Heather West Greenlee2, and Robert Kunkle1
 
1National Animal Disease Center; Ames, IA USA;
 
2Iowa State University; Ames, IA USA
 
The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n D 5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the 2 inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, 2 distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.
 
 
2012
 
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer
 
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA
 
snip...
 
The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.
 
*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.
 
Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.
 
 
Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD)
 
Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National Animal Disease Center, ARS, USDA, Ames, IA provided a presentation on scrapie and CWD in inoculated deer. Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. We inoculated white-tailed deer intracranially (IC) and by a natural route of exposure (concurrent oral and intranasal inoculation) with a US scrapie isolate. All deer inoculated by the intracranial route had evidence of PrPSc accumulation and those necropsied after 20 months post-inoculation (PI) (3/5) had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. A single deer that was necropsied at 15.6 months PI did not have clinical signs, but had widespread distribution of PrPSc. This highlights the facts that 1) prior to the onset of clinical signs PrPSc is widely distributed in the CNS and lymphoid tissues and 2) currently used diagnostic methods are sufficient to detect PrPSc prior to the onset of clinical signs. The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in white-tailed deer after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile consistent with CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like. After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie. Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. While two WB patterns have been detected in brain regions of deer inoculated by the natural route, unlike the IC inoculated deer, the pattern similar to the scrapie inoculum predominates.
 
 
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
 
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS
 
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 this study was 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 were observed daily for clinical signs. Deer were euthanized and necropsied when neurologic disease was evident, and tissues were examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and western blot (WB). One animal was euthanized 15 months post-inoculation (MPI) due to an injury. At that time, examination of obex and lymphoid tissues by IHC was positive, but WB of obex and colliculus were negative. Remaining deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. 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.
 
see full text ;
 
 
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
 
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
 
 
The possibility of any reservoir of infection in wild cervids originating from scrapie in domestic sheep flocks seems remote. Scrapie has been recorded in only three flocks in Wyoming since 1947 and Beth Williams could recall only one previous occurrence in 1966. This had involved a Suffolk flock close to the border with Nebraska. However, there has been one new confirmed and a suspected affected flock this year in Wyoming. In the latter a ewe bought-in from an Illinois flock is incriminated.
 
Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or about that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. Whether they were scrapie infected sheep or not is unclear. There were domestic sheep and goats present in the facility also in the 1960's but there is not evidence that these animals developed scrapie. During the 60's hybridization studies between the Bighorn and domestic sheep were carried
 
PAGE 30
 
out, again, without evidence of scrapie. Domestic goats were also kept at Sybille in the 1960's.
 
Spraker considers that the nasal route is responsible for transmission of CWD through nose to nose contact, which may well occur also between captive and free-living individuals.
 
In domestic cattle of which about 15-20 adults were necropsied per year at the Diagnostic Laboratory, CSU., Spraker had not encountered any lesions suggesting BSE. Polioencephalomalacia (PEM) and Encephalic Listeriosis were the most common morphologic neuropathological diagnoses. No bovine rabies was seen.
 
PAGE 31
 
Appendix I
 
VISIT TO USA - DR A E WRATHALL - INFO ON BSE AND SCRAPIE
 
1. Dr Clark lately of the Scrapie Research Unit, Mission Texas has successfully transmitted ovine and caprine scrapie to cattle. The experimental results have not been published but there are plans to do this. This work was initiated in 1978. A summary of it is:-
 
Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with a 2nd Suffolk scrapie passage:-
 
i/c 1ml i/m, 5ml; s/c 5ml; oral 30ml.
 
1/6 went down after 48 months with a scrapie/BSE-like disease.
 
Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat virus 2/6 went down similarly after 36 months.
 
Expt C Mice inoculated from brains of calves/cattle in expts A & B were resistant, only 1/20 going down with scrapie and this was the reason given for not publishing.
 
Diagnosis in A, B, C was by histopath. No reports on SAF were given.
 
Dr Warren Foote indicated success so far in eliminating scrapie in offspring from experimentally- (and naturally) infected sheep by ET. He had found difficulty in obtaining emhryos from naturally infected sheep (cf SPA).
 
3. Prof. A Robertson gave a brief account of BSE. The US approach was to
 
PAGE 32
 
accord it a very low profile indeed. Dr A Thiermann showed the picture in the "Independent" with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. BSE was not reported in USA.
 
4. Scrapie incidents (ie affected flocks) have shown a dramatic increase since 1978. In 1953 when the National Control Scheme was started there were 10-14 incidents, in 1978 - 1 and in 1988 so far 60.
 
5. Scrapie agent was reported to have been isolated from a solitary fetus.
 
6. A western blotting diagnostic technique (? on PrP} shows some promise.
 
7. Results of a questionnaire sent to 33 states on the subject of the national sheep scrapie programme survey indicated;
 
17/33 wished to drop it 6/33 wished to develop it 8/33 had few sheep and were neutral
 
Information obtained from Dr Wrathall's notes of a meeting of the U.S. Animal Health Association at Little Rock, Arkansas Nov. 1988.
 
kind regards,
 
Terry S. Singeltary Sr., Bacliff, Texas USA -July 29, 2000-
 
please see ;
 
 
 
Their concern deepened as they experimented with ways to sanitize the holding pens in Fort Collins and Sybille. All the deer and elk in the contaminated pens at Sybille were killed, and the pens were left empty for six months to a year. When deer and elk were reintroduced to the pens, they were animals that weren't known to have had direct contact with infected deer and elk. In spite of these efforts, elk in the pens came down with chronic wasting disease within five years after the attempt at sterilizing the facility.
 
In Fort Collins, the effort was even more intense. All the deer and elk in the facility were killed and buried. Then personnel plowed up the soil in the pens in an effort to bury possible disease organisms and sprayed structures and pastures repeatedly with a strong disinfectant. A year later, they took twelve elk calves from the wild and released them in the sanitized holding areas. In the next five years, two of these elk died from chronic wasting disease.
 
 
Sunday, July 10, 2016
 
Primary transmission of CWD versus scrapie prions from small ruminants to ovine and cervid PrP transgenic mice
 
 
Friday, July 29, 2016
 
 IOWA CHRONIC WASTING DISEASE CWD TSE PRION TOTAL TO DATE 304 CASES WILD AND CAPTIVE REPORT UPDATE JULY 2016
 
 
 Wednesday, July 27, 2016
 
 Arkansas CWD 101 positive cases documented to date, Biologists to take additional samples in in southern Pope County, Aug. 1-5
 
 
 Friday, July 01, 2016
 
 TEXAS Thirteen new cases of chronic wasting disease (CWD) were confirmed at a Medina County captive white-tailed deer breeding facility on June 29, 2016
 
 
 *** How Did CWD Get Way Down In Medina County, Texas?
 
 DISCUSSION Observations of natural outbreaks of scrapie indicated that the disease spread from flock to flock by the movement of infected, but apparently normal, sheep which were incubating the disease.
 
 There was no evidence that the disease spread to adjacent flocks in the absent of such movements or that vectors or other host species were involved in the spread of scrapie to sheep or goats; however, these possibilities should be kept open...
 
 
 
 
 Monday, July 18, 2016
 
 Texas Parks Wildlife Dept TPWD HIDING TSE (CWD) in Deer Herds, Farmers Sampling Own Herds, Rapid Testing, False Negatives, a Recipe for Disaster
 
 
 Tuesday, August 02, 2016
 
Chronic wasting disease of deer – is the battle to keep Europe free already lost?
 
From: Terry S. Singeltary Sr.
 
Sent: Tuesday, August 02, 2016 1:38 PM
 
To: editorial@bva-edit.co.uk
 
Cc: delete
 
 
***moving on, I am beginning to question this Red Deer Ataxia, kind of reminds me of the infamous hound ataxia and the hound study for BSE. but that’s another very long drawn out debacle. I can share some links below for those that might still be interested in this old stuff, but they are questioning now the mad dog disease i.e. or what I call CSE canine spongiform encephalopathy...
 
Red Deer Ataxia or Chronic Wasting Disease CWD TSE PRION?
 
could this have been cwd in the UK back in 1970’S ???
 
 
 
 
 
Monday, February 14, 2011
 
THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER
 
NO, NO, NOT NO, BUT HELL NO !
 
Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011
 
 
OR-09: Canine spongiform encephalopathy—A new form of animal prion disease
 
Monique David, Mourad Tayebi UT Health; Houston, TX USA
 
It was also hypothesized that BSE might have originated from an unrecognized sporadic or genetic case of bovine prion disease incorporated into cattle feed or even cattle feed contaminated with prion-infected human remains.1 However, strong support for a genetic origin of BSE has recently been demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2 Furthermore, a specific prion protein strain causing BSE in cattle is believed to be the etiological agent responsible for the novel human prion disease, variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in a number countries, including France, Italy, Ireland, the Netherlands, Canada, Japan, US and the UK with the largest number of cases. Naturally occurring feline spongiform encephalopathy of domestic cats4 and spongiform encephalopathies of a number of zoo animals so-called exotic ungulate encephalopathies5,6 are also recognized as animal prion diseases, and are thought to have resulted from the same BSE-contaminated food given to cattle and humans, although and at least in some of these cases, a sporadic and/or genetic etiology cannot be ruled out. The canine species seems to display resistance to prion disease and no single case has so far been reported.7,8 Here, we describe a case of a 9 week old male Rottweiler puppy presenting neurological deficits; and histological examination revealed spongiform vacuolation characteristic of those associated with prion diseases.9 Initial biochemical studies using anti-PrP antibodies revealed the presence of partially proteinase K-resistant fragment by western blotting. Furthermore, immunohistochemistry revealed spongiform degeneration consistent with those found in prion disease and displayed staining for PrPSc in the cortex.
 
Of major importance, PrPSc isolated from the Rottweiler was able to cross the species barrier transmitted to hamster in vitro with PMCA and in vivo (one hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100% attack rate (n = 4) and animals displayed untypical lesional profile and shorter incubation period.
 
In this study, we show that the canine species might be sensitive to prion disease and that PrPSc isolated from a dog can be transmitted to dogs and hamsters in vitro using PMCA and in vivo to hamsters.
 
If our preliminary results are confirmed, the proposal will have a major impact on animal and public health and would certainly lead to implementing new control measures for ‘canine spongiform encephalopathy’ (CSE).
 
References 1. Colchester AC, Colchester NT. The origin of bovine spongiform encephalopathy: the human prion disease hypothesis. Lancet 2005; 366:856-61; PMID:16139661; http:// dx.doi.org/10.1016/S0140-6736(05)67218-2.
 
2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation. PLoS Pathog 2008; 4:e1000156; PMID:18787697; http://dx.doi.org/10.1371/journal. ppat.1000156.
 
3. Collinge J. Human prion diseases and bovine spongiform encephalopathy (BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662; http://dx.doi.org/10.1093/ hmg/6.10.1699.
 
4. Wyatt JM, Pearson GR, Smerdon TN, Gruffydd-Jones TJ, Wells GA, Wilesmith JW. Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Vet Rec 1991; 129:233-6; PMID:1957458; http://dx.doi.org/10.1136/vr.129.11.233.
 
5. Jeffrey M, Wells GA. Spongiform encephalopathy in a nyala (Tragelaphus angasi). Vet Pathol 1988; 25:398-9; PMID:3232315; http://dx.doi.org/10.1177/030098588802500514.
 
6. Kirkwood JK, Wells GA, Wilesmith JW, Cunningham AA, Jackson SI. Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu (Tragelaphus strepsiceros). Vet Rec 1990; 127:418-20; PMID:2264242.
 
7. Bartz JC, McKenzie DI, Bessen RA, Marsh RF, Aiken JM. Transmissible mink encephalopathy species barrier effect between ferret and mink: PrP gene and protein analysis. J Gen Virol 1994; 75:2947-53; PMID:7964604; http://dx.doi.org/10.1099/0022-1317- 75-11-2947.
 
8. Lysek DA, Schorn C, Nivon LG, Esteve-Moya V, Christen B, Calzolai L, et al. Prion protein NMR structures of cats, dogs, pigs, and sheep. Proc Natl Acad Sci U S A 2005; 102:640-5; PMID:15647367; http://dx.doi.org/10.1073/pnas.0408937102.
 
9. Budka H. Neuropathology of prion diseases. Br Med Bull 2003; 66:121-30; PMID:14522854; http://dx.doi.org/10.1093/bmb/66.1.121.
 
 
*** DEFRA TO SINGELTARY ON HOUND STUDY AND BSE 2001 ***
 
DEFRA Department for Environment, Food & Rural Affairs
 
Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904 6287 E-mail: h.mcdonagh.defra.gsi.gov.uk
 
GTN: FAX:
 
Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518
 
21 November 2001
 
Dear Mr Singeltary
 
TSE IN HOUNDS
 
Thank you for e-mail regarding the hounds survey. I am sorry for the long delay in responding.
 
As you note, the hound survey remains unpublished. However the Spongiform Encephalopathy Advisory Committee (SEAC), the UK Government's independent Advisory Committee on all aspects related to BSE-like disease, gave the hound study detailed consideration at their meeting in January 1994. As a summary of this meeting published in the BSE inquiry noted, the Committee were clearly concerned about the work that had been carried out, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.
 
Later, at their meeting in June 95, The Committee re-evaluated the hound study to see if any useful results could be gained from it. The Chairman concluded that there were varying opinions within the Committee on further work. It did not suggest any further transmission studies and thought that the lack of clinical data was a major weakness.
 
Overall, it is clear that SEAC had major concerns about the survey as conducted. As a result it is likely that the authors felt that it would not stand up to r~eer review and hence it was never published. As noted above, and in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether additional work should be performed to examine dogs for evidence of TSE infection. Although the Committee had mixed views about the merits of conducting further work, the Chairman noted that when the Southwood Committee made their recommendation to complete an assessment of possible spongiform disease in dogs, no TSEs had been identified in other species and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less
 
critical. For more details see- http://www.bseinquiry, gov.uk/files/yb/1995/06/21005001 .pdf
 
As this study remains unpublished, my understanding is that the ownership of the data essentially remains with the original researchers. Thus unfortunately, I am unable to help with your request to supply information on the hound survey directly. My only suggestion is that you contact one of the researchers originally involved in the project, such as Gerald Wells. He can be contacted at the following address.
 
Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, KT 15 3NB, UK
 
You may also wish to be aware that since November 1994 all suspected cases of spongiform encephalopathy in animals and poultry were made notifiable. Hence since that date there has been a requirement for vets to report any suspect SE in dogs for further investigation. To date there has never been positive identification of a TSE in a dog.
 
I hope this is helpful
 
Yours sincerely 4
 
HUGH MCDONAGH BSE CORRESPONDENCE SECTION
 
======================================
 
HOUND SURVEY
 
I am sorry, but I really could have been a co-signatory of Gerald's minute.
 
I do NOT think that we can justify devoting any resources to this study, especially as larger and more important projects such as the pathogenesis study will be quite demanding.
 
If there is a POLITICAL need to continue with the examination of hound brains then it should be passed entirely to the VI Service.
 
J W WILESMITH Epidemiology Unit 18 October 1991
 
Mr. R Bradley
 
cc: Mr. G A H Wells
 
 
3.3. Mr R J Higgins in conjunction with Mr G A Wells and Mr A C Scott would by the end of the year, indentify the three brains that were from the ''POSITIVE'' end of the lesion spectrum.
 
 
TSE in dogs have not been documented simply because OF THE ONLY STUDY, those brain tissue samples were screwed up too. see my investigation of this here, and to follow, later follow up, a letter from defra, AND SEE SUSPICIOUS BRAIN TISSUE SAF's. ...TSS
 
 
TSE & HOUNDS
 
GAH WELLS (very important statement here...TSS)
 
HOUND STUDY
 
AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.
 
snip...
 
 
76 pages on hound study;
 
snip...
 
 
The spongiform changes were not pathognomonic (ie. conclusive proof) for prion disease, as they were atypical, being largely present in white matter rather than grey matter in the brain and spinal cord. However, Tony Scott, then head of electron microscopy work on TSEs, had no doubt that these SAFs were genuine and that these hounds therefore must have had a scrapie-like disease. I reviewed all the sections myself (original notes appended) and although the pathology was not typical, I could not exclude the possibility that this was a scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian degeneration was also present in the white matter of the hounds, another feature of scrapie.
 
38.I reviewed the literature on hound neuropathology, and discovered that micrographs and descriptive neuropathology from papers on 'hound ataxia' mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had done much of this work, and I obtained original sections from hound ataxia cases from him. This enabled me provisionally to conclude that Robert Higgins had in all probability detected hound ataxia, but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination of single restricted microscopic fields that there was no distinction between the white matter vacuolation present in BSE and scrapie cases, and that occurring in hound ataxia and the hound survey cases.
 
39.Hound ataxia had reportedly been occurring since the 1930's, and a known risk factor for its development was the feeding to hounds of downer cows, and particularly bovine offal. Circumstantial evidence suggests that bovine offal may also be causal in FSE, and TME in mink. Despite the inconclusive nature of the neuropathology, it was clearly evident that this putative canine spongiform encephalopathy merited further investigation.
 
40.The inconclusive results in hounds were never confirmed, nor was the link with hound ataxia pursued. I telephoned Robert Higgins six years after he first sent the slides to CVL. I was informed that despite his submitting a yearly report to the CVO including the suggestion that the hound work be continued, no further work had been done since 1991. This was surprising, to say the very least.
 
41.The hound work could have provided valuable evidence that a scrapie-like agent may have been present in cattle offal long before the BSE epidemic was recognised. The MAFF hound survey remains unpublished.
 
Histopathological support to various other published MAFF experiments
 
42.These included neuropathological examination of material from experiments studying the attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice (RVC 1994).
 
 
It was thought likely that at least some, and probably all, of the cases in zoo animals were caused by the BSE agent. Strong support for this hypothesis came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and scrapie to mice: strain variation and species barrier. Philosophical Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation period and lesion profile in six strains of mice inoculated with brain homogenates from an affected kudu and the nyala, was similar to that seen when this panel of mouse strains was inoculated with brain from cattle with BSE. The affected zoo bovids were all from herds that were exposed to feeds that were likely to have contained contaminated ruminant-derived protein and the zoo felids had been exposed, if only occasionally in some cases, to tissues from cattle unfit for human consumption.
 
snip...
 
 
NEW URL ;
 
 
Monday, March 26, 2012
 
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE
 
 
Monday, March 8, 2010
 
Canine Spongiform Encephalopathy aka MAD DOG DISEASE
 
 
 
Veterinary Pathology Onlinevet.sagepub.com Published online before print February 27, 2014, doi: 10.1177/0300985814524798 Veterinary Pathology February 27, 2014 0300985814524798
 
Lesion Profiling and Subcellular Prion Localization of Cervid Chronic Wasting Disease in Domestic Cats
 
D. M. Seelig1⇑ A. V. Nalls1 M. Flasik2 V. Frank1 S. Eaton2 C. K. Mathiason1 E. A. Hoover1 1Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO, USA 2Department of Biomedical Sciences, Colorado State University, Fort Collins, CO, USA D. M. Seelig, University of Minnesota, Department of Veterinary Clinical Sciences, Room 339 VetMedCtrS, 6192A (Campus Delivery Code), 1352 Boyd Ave, St Paul, MN 55108, USA. Email address: dseelig@umn.edu
 
Abstract
 
Chronic wasting disease (CWD) is an efficiently transmitted, fatal, and progressive prion disease of cervids with an as yet to be fully clarified host range. While outbred domestic cats (Felis catus) have recently been shown to be susceptible to experimental CWD infection, the neuropathologic features of the infection are lacking. Such information is vital to provide diagnostic power in the event of natural interspecies transmission and insights into host and strain interactions in interspecies prion infection. Using light microscopy and immunohistochemistry, we detail the topographic pattern of neural spongiosis (the “lesion profile”) and the distribution of misfolded prion protein in the primary and secondary passage of feline CWD (FelCWD). We also evaluated cellular and subcellular associations between misfolded prion protein (PrPD) and central nervous system neurons and glial cell populations. From these studies, we (1) describe the novel neuropathologic profile of FelCWD, which is distinct from either cervid CWD or feline spongiform encephalopathy (FSE), and (2) provide evidence of serial passage-associated interspecies prion adaptation. In addition, we demonstrate through confocal analysis the successful co-localization of PrPD with neurons, astrocytes, microglia, lysosomes, and synaptophysin, which, in part, implicates each of these in the neuropathology of FelCWD. In conclusion, this work illustrates the simultaneous role of both host and strain in the development of a unique FelCWD neuropathologic profile and that such a profile can be used to discriminate between FelCWD and FSE.
 
prion chronic wasting disease immunohistochemistry interspecies cat feline spongiform encephalopathy transmissible spongiform encephalopathy adaptation species barrier
 
 
Monday, August 8, 2011 Susceptibility of Domestic Cats to CWD Infection
 
Oral.29: Susceptibility of Domestic Cats to CWD Infection
 
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason†
 
Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu
 
Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness.
 
*** Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.
 
 
 
AD.63:
 
Susceptibility of domestic cats to chronic wasting disease
 
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN USA
 
Domestic and nondomestic cats have been shown to be susceptible to feline spongiform encephalopathy (FSE), almost certainly caused by consumption of bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and free-ranging nondomestic felids scavenge cervid carcasses, including those in areas affected by chronic wasting disease (CWD), we evaluated the susceptibility of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated cats developed signs consistent with prion disease, including a stilted gait, weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from these two cats were pooled and inoculated into cohorts of cats by IC, PO, and intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the symptomatic cats by western blotting and immunohistochemistry and abnormalities were seen in magnetic resonance imaging, including multifocal T2 fluid attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4 IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns consistent with the early stage of feline CWD.
 
*** These results demonstrate that CWD can be transmitted and adapted to the domestic cat, thus raising the issue of potential cervid-to- feline transmission in nature.
 
 
www.landesbioscience.com
 
PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)
 
 
 
FELINE SPONGIFORM ENCEPHALOPATHY FSE
 
 
 
Wednesday, October 17, 2012
 
Prion Remains Infectious after Passage through Digestive System of American Crows (Corvus brachyrhynchos)
 
 
A Quarterly Newsletter from the Southeastern Cooperative Wildlife Disease Study College of Veterinary Medicine The University of Georgia Athens, Georgia 30602
 
Volume 27 January 2012 Number 4
 
Red deer susceptibility to CWD via oral inoculation was demonstrated in a study conducted by collaborators from the U.S. and Canada. Red deer developed clinical signs and had spongiform changes in the brain when euthanatized at 20 MPI. The CWD prion was detectable in neural and lymphoid tissues, endocrine organs, cardiac muscle, nasal mucosa, and other tissues. Although field cases of CWD in red deer have not been reported, results of this study indicate that it could occur, which is not surprising given that elk and red deer are subspecies of Cervus elaphus. The results of this study can be found in the Canadian Veterinary Journal 51: 169-178.
 
In addition, it was reported in May 2011 that natural cases of CWD were found in eight Sika deer (Cervus nippon) and five Sika/red deer crossbreeds during epidemiological investigations of CWD cases in captive elk in Korea.
 
 
Chronic Wasting Disease Susceptibility of Four North American Rodents
 
snip...end...tss
 
Saturday, July 23, 2016
 
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
 
 
Tuesday, July 26, 2016
 
*** Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016
 
 
Monday, August 1, 2016
 
USDA Announces Reopening of Brazilian Market to U.S. Beef Exports and the Potential for Transmissible Spongiform Encephalopathy TSE prion disease Release No. 0175.16
 
 
Tuesday, April 19, 2016
 
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards Singeltary Comment Submission
 
 
 
 
Tuesday, April 19, 2016
 
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards Singeltary Comment Submission
 
 
Monday, June 20, 2016
 
*** Specified Risk Materials SRMs BSE TSE Prion Program
 
 
*** NIH awards $11 million to UTHealth researchers to study deadly CWD prion diseases Claudio Soto, Ph.D. ***
 
 Public Release: 29-Jun-2016
 
 
 Tuesday, July 12, 2016
 
 Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE, TSE, Prion Zoonosis Science History
 
 see history of NIH may destroy human brain collection
 
 
Terry S. Singeltary Sr.