tim.kauffman@afge.org
RACHEL MADDOW
Trump set to decimate USDA research, fire hundreds of scientists
Rachel Maddow reports on the approaching midnight deadline set for USDA researchers to respond to a short notice reassignment or be fired, with most scientist expected to be fired, gutting one of the premiere U.S. taxpayer-funded scientific institutions.
July 15, 2019
This is concerning for many reasons, and i will try and refrain from political turmoil, but why really is this happening $$$
what about science???
let's just look at some science, shall we.
show me the transmission studies...tss
FOOD FOR THOUGHT
Scientists Desert USDA As Agency Relocates To Kansas City Area
July 17, 20196:35 AM ET
Merrit Kennedy 2018 square
MERRIT KENNEDY
Secretary of Agriculture Sonny Perdue, shown here on Capitol Hill in April, announced last month that most staff from two USDA research agencies were being relocated to the Kansas City region. J. Scott Applewhite/AP Two vital research agencies at the U.S. Department of Agriculture are hemorrhaging staff as less than two-thirds of the researchers asked to relocate from Washington to the Kansas City area have agreed to do so.
When U.S. Secretary of Agriculture Sonny Perdue announced the planned new location of the research agencies last month, he said it "will be placing important USDA resources closer to many stakeholders" and "increasing the probability of attracting highly-qualified staff with training and interests in agriculture."
But groups such as the Union of Concerned Scientists call it a "blatant attack on science" that will "especially hurt farmers, ranchers and eaters at a particularly vulnerable time."
The American Federation of Government Employees, the union representing the USDA's Economic Research Service and the National Institute of Food and Agriculture, said the relocation "has resulted in catastrophic attrition at USDA's top research agencies."
"Evidence suggests that the relocation of these agencies is an attempt to hollow out and dismantle USDA science that helps farmers and protects our food supply," the union added.
The USDA gave employees until just before midnight on Monday to notify their employers whether they planned to accept the relocation.
On Tuesday, a USDA spokesperson told NPR that at ERS, 72 employees accepted relocation and 99 declined or did not respond. At NIFA, the spokesperson said 73 accepted and 151 declined or did not respond. That means the total number that accepted is about 36% of those reported.
The USDA spokesperson said that these numbers may fluctuate until Sept. 30, the date employees are expected to report to the area, and employees can change their statuses until then.
They added that the USDA is working "to ensure separating employees have the resources they need as well as efforts to implement an aggressive hiring strategy to maintain the continuity of ERS and NIFA's work."
Last month, the USDA said that of the 644 jobs in the two agencies, 544 would be relocated and 100 would remain in the D.C. area. The numbers reported on Tuesday by the USDA do not appear to account for some 150 positions that the USDA initially announced would be relocated.
The department did not immediately respond to explain the difference, though the employees' union has reported high rates of "retirements, employees securing new jobs, and employees choosing to be terminated." A statement last month from three Democratic senators said that ERS had a vacancy rate of 20% and NIFA had a vacancy rate of 26.4%.
NIFA provides grants for research on agriculture-related science, and the ERS conducts research and analysis on topics such as outlooks on major crops and livestock, how much food is going to cost and whether U.S. households will be food secure.
It's not yet clear whether the research agencies will be located in Kansas or Missouri, according to The Kansas City Star.
Lawmakers from both states, including Kansas Sen. Jerry Moran, have supported the move. "My first thought was Kansas City would be the perfect place," the Republican said, as NPR's Frank Morris reported.
An ex-employee of ERS recently told Morris that "efforts by the secretary ... have just destroyed morale." He said the way the agency is run has become increasingly partisan, and he resigned after the surprise announcement about relocations.
"I think it's had its intended effect. People have left, morale is low. The agency will take a long time to recover from the damage that's been inflicted," the former employee told Morris.
Some of ERS' recent studies, as Morris noted, may be politically uncomfortable for the Trump administration:
"ERS studies, for instance, concluded that the 2017 tax cuts championed by the administration would most benefit the richest farmers, and that the Supplemental Nutrition Assistance Program, which Trump wants to cut, is good for the economy."
Perdue said last month that the move would save the USDA some $300 million. That number has been met with skepticism by some analysts. The Agricultural & Applied Economics Association estimated the relocation would actually cost taxpayers between $83 million and $182 million, partially due to the lost value of the research from staffers who decide not to move.
USDA workers sound alarm about agency relocation
JULY 15, 201903:40
July 15, 2019, 12:21 PM CDT
By Aaron Franco
Today is the last day for hundreds of federal workers at the U.S. Department of Agriculture to make a difficult decision.
Their choice: Agree to leave Washington and report to work in Kansas City on Sept. 30 or be fired with a limited chance to appeal.
The move is part of a “directed reassignment” plan announced by Agriculture Secretary Sonny Perdue on June 13 that would relocate 547 employees from two agencies — the Economic Research Service and the National Institute of Food and Agriculture — to an office building in Kansas City.
The Trump administration has framed the move as an effort to save taxpayers money and bring researchers closer to the farmers they serve.
But employees within the two agencies are now speaking out, calling the move an effort to “eviscerate” the agency and “silence” researchers doing work that runs counter to the administration’s goals.
Economist Laura Dodson, who agreed to speak to NBC News as a union steward for AFGE Local 3403, says the decision has left her agency in disarray.
“Come Sept. 30, I don't know who my boss is going to be. I don't know if I'm going to have a division director. I don't even know who the administrator of my agency will be,” Dodson said. “I don't know what the status of my projects will be. I don't know if the survey we run every year is going to be able to keep going. I am not even sure where I'll be commuting to.”
Union officials estimate as many as 70 percent of NIFA employees and 60 percent of ERS employees will refuse to relocate and look for work elsewhere, based on data from an informal survey.
In a press release, Perdue described the move as an effort to save taxpayers money and bring researchers closer to stakeholders.
“We did not undertake these relocations lightly, and we are doing it to enhance long-term sustainability and success of these agencies,” he said.
But three current ERS employees have expressed concerns that the administration has a different motive.
“I don't think anybody believes that their justification is anything more than a fig leaf over the true motives, which are to eviscerate this agency,” one research economist told NBC News.
He and two other USDA employees spoke on the condition of anonymity, saying they feared that sharing their thoughts publicly would be detrimental as they search for another federal job. All three are declining to move to Kansas City.
“I think that a lot of the work that our agency does is profoundly inconvenient to the agenda of the current administration. To be clear, we've been inconvenient to past administrations. But I think that this administration doesn't want to hear nonpartisan facts and analysis that cut counter to their plans and their narrative,” the researcher said. “If they thought that moving us to Kansas City was in the best interests of us fulfilling our congressionally mandated mission, they would do this over the course of years. But they're doing it over the course of months because they know that people are going to quit and that's what they want. They want to silence the work that we do.”
All three employees pointed to work on the 2017 tax law's impact on family farms, a report on agricultural exports in the wake of the trade war with China and a study that found net economic benefits to food assistance as possible reasons for the relocation, although none could provide proof of a direct connection between their publication and the USDA’s actions.
“Nobody's been called into a room and told they can't publish this,” another ERS economist said.
The same employee pointed to the president’s proposed 2020 budget, which calls for a staffing cut at ERS from 329 to 160, a reduction of close to 50 percent.
NBC News has reached out to Perdue for comment but has not heard back.
The employees who choose to relocate are required to report to work at the Kansas City location on Sept. 30. Union representatives have petitioned agency leadership to extend the deadline to decide on whether to move, but the administration has not granted those requests.
Scientists flee USDA as research agencies move to Kansas City area
BY REBECCA BEITSCH - 07/15/19 07:19 PM EDT
A Trump administration decision to move researchers from the U.S. Department of Agriculture (USDA) to the Kansas City area is threatening to spark the flight of more than half of the staff selected to move, gutting the agency of its top scientific voices.
Staff have until midnight Monday to decide whether to uproot and join the department as it moves its research branches from Washington, D.C., lured by $26 million in promised incentives from state and local officials.
Critics see the move, set to be completed by Sept. 30, as yet another example of the Trump administration looking to sideline scientists and researchers, keeping them away from the corridors of power. Administration officials deny that, calling it a cost-saving move intended to have researchers closer to farmers.
The decision comes as other agencies are also planning to relocate parts of their teams amid suspicions about the move. For example, the Interior Department is expected to announce new headquarters for the Bureau of Land Management on Tuesday.
“Moving these researchers out of Washington puts them out of earshot from policymakers. A lot of the research that scientists and economists do at [the USDA] has policy implications, and members of Congress need this information and need to have face-to-face meetings with these researchers,” Rebecca Boehm, with the Union of Concerned Scientists, told The Hill.
“It keeps science out of the policymaking process. And we’ve seen many times that this administration doesn’t like facts or research that isn’t convenient or [is] an impediment to their agenda, so I think moving them away helps accomplish that,” she added.
The move affects two wings of the USDA. Economic Research Service (ERS) employees analyze the agricultural market, but their research is much broader, including looking at food stamps, rural poverty and conservation.
National Institute of Food and Agriculture (NIFA) employees work with universities to fund research and coordinate the process that issues research grants on agriculture-related subjects, including climate change adaptation.
The two agencies voted to unionize in response to the move, as Democrats in both chambers and a number of groups that regularly work with the two agencies lobby to keep them in Washington.
Estimates tallied by employees show 70 percent of ERS employees designated for the Kansas City office will not be moving. For NIFA, 45 percent of those surveyed said they will not move. Overall, the move was expected to impact 547 staff between the two agencies.
But the numbers of staff refusing to move may grow. Some employees said staff at both agencies are trying not to tip their hands, saying they will move only if they do not find another job in the D.C. area.
So far, just 27 ERS staff out of 250 have committed to moving to the Kansas City area, according to the employee tallies.
The UDSA argues the move will save $300 million over 15 years, but critics have said their cost-benefit analysis was shoddy and did not follow guidelines.
A different cost-benefit analysis from the Agricultural and Applied Economics Association found the move would cost taxpayers between $83 million and $182 million.
Democrats have blocked USDA funding from supporting the move and asked the agency to turn over information about its decisionmaking process, and they have sponsored legislation to keep the two agencies in Washington.
“I am appalled with the Trump administration’s decision to force hundreds of Washington-based USDA research staffers to uproot their lives to Kansas City in order to keep their livelihoods,” Rep. Chellie Pingree (D-Maine), who sponsored the legislation, said in a statement when the move was announced.
“Many of these staffers believe their relocation is an effort to silence their research into topics that do not align with the Trump administration’s political agenda, including the study of climate change and benefits of low-income food assistance,” she added.
Employees had a list of complaints about a move they have likened to Amazon’s search for a second headquarters, as the USDA examined bids from 139 cities.
That process was put on pause during the government shutdown, but on June 16 employees were told they had a month to decide whether they’d like to move to the Kansas City area or leave the agency.
Employees would then have two months to move to Kansas City — they must be there by the end of the fiscal year — but school in the area is slated to start Aug. 12, putting added pressure on those with families to quickly make a move.
Employees say they are getting conflicting information about how much of their moving costs will be covered by the government. Other key details about the move are also unknown so far, according to the employees.
The USDA said it was working to make the move as smooth as possible but did not respond to several specific questions about the move from The Hill.
“USDA has determinedly worked to ensure employees have the resources they need to make informed decisions about their employment and to ensure the transition is as smooth as possible,” the agency said in a statement.
Employees say morale is at an all-time low and they worry about the future of an agency that is already hemorrhaging staff and having trouble completing its work.
“Honestly, I’m not sure how we’re going to bounce back or if we will,” said Laura Dodson, an agricultural economist with ERS who is now a union steward. “This agency is the product of like 50 years of institutional knowledge and gathering up researchers who are very specialized in their fields.”
Employees also say there are contradictions between what the USDA says it hopes to achieve with the move and how it would actually impact the department.
“It was sort of get fired or go,” said Ariela Zycherman, a national program leader with NIFA who is still weighing a move to Kansas City.
“People keep saying, ‘Those East Coasters don’t want to come to Kansas or Missouri.’ The fact of matter is that’s not really the issue,” she said. “Many of us would move to Kansas City, but there are questions about future of agency and its effectiveness and questions about the way this was hastily rolled out and whether it will have long-term effects on our families’ well-being.”
The USDA has argued the move will allow employees to be closer to farmers — something employees say shows a fundamental misunderstanding of what they do.
“I think the biggest misconception around this is, we don’t serve individual farmers,” Dodson said. “Our stakeholders are primarily Congress and program leads and agencies and nonprofits in D.C. or people that come to meet with multiple entities in D.C."
“I think our presence will be very much diminished. I think we’ll be quite literally out of sight and out of mind,” Dodson added.
The bipartisan Kansas and Missouri delegation pushed hard to bring the offices to the Kansas City area, calling it a hub for research and a talented workforce and touting the lower cost compared to Washington, D.C.
But employees say the hectic way the move has been handled has soured many about the USDA.
“I’ve never experienced morale like this in any job,” said Wesley Dean, a national program leader in sociology for NIFA. “My colleagues are deeply committed to the mission of the agency and see their positions as an opportunity to both shape the future of their scientific disciplines and to serve the American people.
“These highly motivated civil servants feel as if their expertise and dedication to the agency and the public has been undermined and dismissed by the department,” Dean added.
TAGS CHELLIE PINGREE USDA U.S. DEPARTMENT OF AGRICULTURE ECONOMIC RESEARCH SERVICE
FOR IMMEDIATE RELEASE June 26, 2019 Contact: Tim Kauffman 202-639-6405/202-374-6491 tim.kauffman@afge.org
USDA Economic Research Service Faces Mission Catastrophic Attrition with September Move 21 Categories: USDA
4 out of 5 employees likely to decline reassignment, union data suggest WASHINGTON – The U.S. Department of Agriculture’s Economic Research Service (ERS) is projected to experience catastrophic employee attrition as a result of the short-notice move of three-quarters of all ERS employees out of the National Capital Region, according to attrition data obtained and compiled by American Federal Government Employees Local 3403 as part of a summary of all employees.
ERS could expect more than 4 out of 5 of the more than 200 employees being reassigned to temporary offices in Kansas City to decline relocation. Given the aggressive timeline to move all positions before the end of the current fiscal year, AFGE Local 3403 estimates that 2 out of 3 employees are certain they will decline relocation. Attrition data is listed by research divisions below. The Information Services Division may experience nearly 100% attrition or no one relocating. The Resource & Rural Economics Division may experience more than 90% attrition, with the Food Economics Division experiencing 89% attrition. The Market and Trade Economics Division and Office of Administrator could anticipate 3 out of 4 employees to decline to relocate.
Including the 76 ERS employees identified to remain in Washington, D.C., the attrition across ERS is projected to be 50-60%. However, many of those remaining in D.C. also say they are seeking new employment because they are scheduled to be reassigned to a yet-to-be identified new facility within the National Capital Region.
Agriculture Secretary Sonny Perdue announced June 13 that 250 ERS employees are among the more than 550 USDA research employees scheduled to move to Kansas City on or before Sept. 30.
“The current and projected attrition will curtail research data products that encompass commodity estimates, agricultural sector forecasts, food and farm economic and statistical indicators for U.S. agriculture, conservation, and food policy and markets,” Local 3403 Acting Vice President Kevin Hunt said.
For example, ERS commodity outlook program delivers timely, independent, and objective information about agricultural markets and provides projections of U.S. and world agricultural commodity production, consumption, and trade. These outlook reports are highly anticipated for U.S. and global markets. Other ERS data products include forecasts of farm business and household income, commodity cost of production, outlook reports covering major crops and livestock products, annual 10-year projections for the farm sector, forecasts of the Consumer Price Index (CPI) for food, estimates of U.S. and international agricultural productivity, rural county typologies, state fact sheets, annual reports on food security of U.S. households, the Food Access Research Atlas, the Food Environment Atlas, and Cost Estimates of Foodborne Illnesses.
These attrition findings include retirements, employees securing new jobs, and employees choosing to be terminated. In addition, many employees who may relocate to Kansas City tell AFGE Local 3403 that they may only relocate short term until they find employment in their preferred localities.
AFGE ANALYSIS OF ERS PROPOSED RELOCATIONS
Topline: The relocation crisis created by Secretary Perdue has resulted in catastrophic attrition at USDA’s top research agencies. This threatens congressionally mandated scientific research related to agriculture and food systems and ERS’s standing as a Federal Principal Statistical Agency is put at serious risk. Evidence suggests that the relocation of these agencies is an attempt to hollow out and dismantle USDA science that helps farmers and protects our food supply.
Congress needs to provide oversight on the relocation immediately to ensure critical agriculture research is not irreparably damaged. Rehiring and retraining new employees could take years to achieve and even longer to reach current capacity. The low number of employees relocating to Kansas City highlights that relocation has been poorly incentivize for remaining in civil service.
Table 1: Estimated attrition rates at ERS from the announcement of the relocation through October 1, 2019.
Mission Program Areas
Attrition rate
Reassigned Employees
Total Employees
Not moving
Not moving and Maybe not moving
Not moving
Not moving and Maybe not moving
Markets and Trade Economics (MTED)
72%
78%
53%
57%
Food Economics (FED)
81%
92%
62%
71%
Rural and Resource Economics (RRED)
53%
89%
40%
67%
Information Services (ISD)
85%
100%
43%
50%
Office of Administrator (OA)
45%
79%
36%
64%
ERS
69%
87%
48%
61%
Table 2: Estimated number of reassigned ERS employees relocating to Kansas City through October 1, 2019.
Mission Program Areas
Number of employees moving to Kansas City
Moving
Moving and maybe moving
Markets and Trade Economics (MTED)
12
15
Food Economics (FED)
4
10
Rural and Resource Economics (RRED)
5
21
Information Services (ISD)
0
5
Office of Administrator (OA)
6
16
ERS
27
67
Notes: Relocation first announced August 9, 2018. The reassigned employees are ERS employees that were reassigned or would have been reassigned had they remained at ERS. Total employees includes reassigned employees and the employees staying in the National Capital Region.
Source: AFGE Local 3403 summary of ERS employees. For examples of ERS research, see: https://www.ers.usda.gov/ or https://www.ers.usda.gov/amber-waves/
###
The American Federation of Government Employees (AFGE) is the largest federal employee union, representing 700,000 workers in the federal government and the government of the District of Columbia.
Secretary Perdue Announces Kansas City Region as Location for ERS and NIFA Move puts ERS, NIFA closer to customers, expected to save nearly $300 million nominally
Release & Contact Info Press Release Release No. 0091.19 Contact: USDA Press Email: press@oc.usda.gov
(Washington, D.C., June 13, 2019) – U.S. Secretary of Agriculture Sonny Perdue today announced the U.S. Department of Agriculture (USDA) will relocate the Economic Research Service (ERS) and National Institute of Food and Agriculture (NIFA) to the Kansas City Region.
“Following a rigorous site selection process, the Kansas City Region provides a win win – maximizing our mission function by putting taxpayer savings into programmatic outputs and providing affordability, easy commutes, and extraordinary living for our employees,” said Secretary Perdue. “The Kansas City Region has proven itself to be hub for all things agriculture and is a booming city in America’s heartland. There is already a significant presence of USDA and federal government employees in the region, including the Kansas City ‘Ag Bank’ Federal Reserve. This agriculture talent pool, in addition to multiple land-grant and research universities within driving distance, provides access to a stable labor force for the future. The Kansas City Region will allow ERS and NIFA to increase efficiencies and effectiveness and bring important resources and manpower closer to all of our customers.”
USDA conducted a Cost Benefit Analysis and conservative estimates show a savings of nearly $300 million nominally over a 15-year lease term on employment costs and rent or about $20 million per year, which will allow more funding for research of critical needs like rural prosperity and agricultural competitiveness, and for programs and employees to be retained in the long run, even in the face of tightening budgets. On top of that, state and local governments offered generous relocation incentives packages totaling more than $26 million. Finally, this relocation will give USDA the opportunity to attract a diverse staff with training and interest in agriculture. To learn more about USDA's Cost Benefit Analysis, you may view the USDA Cost Benefit Analysis document (PDF, 331 KB).
“We did not undertake these relocations lightly, and we are doing it to enhance long-term sustainability and success of these agencies. The considerable taxpayer savings will allow us to be more efficient and improve our ability to retain more employees in the long run. We will be placing important USDA resources closer to many stakeholders, most of whom live and work far from Washington, D.C. In addition, we are increasing the probability of attracting highly-qualified staff with training and interests in agriculture, many of whom come from land-grant universities. We look forward to this new chapter as we seek to fulfill our motto at USDA, which is to ‘do right and feed everyone,’” added Secretary Perdue.
Secretary Perdue sent this letter (PDF, 39.1 KB) to all USDA employees this morning and will be holding an all hands meeting with ERS and NIFA employees today to discuss the decision, the process, and next steps.
In addition, USDA announced in August the realignment of ERS under the Office of the Chief Economist. While we believe there is considerable synergies and benefits to a realignment, after hearing feedback from stakeholders and Members of Congress, USDA will not move forward with the realignment plans. The agency of ERS will remain under the Research, Education, and Economics mission area.
Background: USDA announced in August it would undertake the relocations for three main reasons:
To improve USDA’s ability to attract and retain highly qualified staff with training and interests in agriculture, many of whom come from land-grant universities. USDA has experienced significant turnover in these positions, and it has been difficult to recruit employees to the Washington, D.C. area, particularly given the high cost of living and long commutes. To place these important USDA resources closer to many of our stakeholders, most of whom live and work far from the Washington, D.C. area. To benefit the American taxpayers. There will be significant savings on employment costs and rent, which will allow more employees to be retained in the long run, even in the face of tightening budgets. As part of the rigorous site selection process, USDA narrowed the 136 Expressions of Interest received using a set of established criteria defined by USDA, NIFA, and ERS leadership. The criteria included:
Quality of Life: Subcategory examples include Diversity Index, Residential Housing Costs, Access to Healthcare, and Home and Community Safety Ranking. Costs (Capital and Operating): Subcategory examples include Commercial Real Estate Costs, CPI Index, and Wage Costs. Workforce: Subcategory examples include Labor Force Growth Rate, Unemployment Rate, and the Labor Force Population. Logistics / IT Infrastructure: Subcategory examples include Lodging Availability, Proximity to Customers, and Airport Accessibility. The top Expressions of Interest were reviewed in detail, and USDA selected a short list of locations offering existing buildings with sufficient space to meet ERS and NIFA requirements.
While 90% of USDA employees are located outside of the D.C. area, ERS and NIFA are the only USDA agencies that don’t have representation outside of the national Capital Region (NCR). Upon the relocation announcement, USDA proposed that sufficient staff levels would remain in the NCR to complete mission critical activities that require physical presence in or near Washington, D.C. at the recommendation of customers and stakeholders. In both the cases of ERS and NIFA, leadership reviewed the critical functions and staffing needs within and outside the NCR. Senior ERS and NIFA staff, with input from partner agencies and stakeholders, recommended to Secretary Perdue the critical functions to be retained within the NCR.
Out of NIFA’s 315 positions, 294 will relocate while 21 will stay in the NCR. Of the 329 ERS positions, 253 will relocate while 76 will stay in the Washington, D.C. area.
As a result of this move, no ERS or NIFA employees will be involuntarily separated. Every employee who wants to continue working will have an opportunity to do so, although that will mean moving to a new location for most. Employees will be offered relocation assistance and will receive the same base pay as before, and the locality pay for the new location.
USDA will be working with the General Services Administration to secure a permanent lease space through a competitive process in the Kansas City Region. USDA will continue to keep ERS and NIFA employees apprised as updates occur.
#
USDA is an equal opportunity provider, employer and lender.
Sent: Mon, Jul 22, 2019 1:02 pm
Subject: APHIS Administrator Announces Several Senior Leadership Changes
Dear Stakeholders:
I want to share with you several changes taking place in important APHIS leadership positions.
Dr. Mark Davidson will be an Associate Administrator, filling the position previously held by Mike Gregoire, who retired earlier this year. Most recently, Dr. Davidson has been serving as Deputy Administrator for Marketing and Regulatory Programs Business Services (MRPBS) after many years in Veterinary Services (VS). In this position, he will oversee the work of VS, Animal Care (AC), and MRPBS.
Ms. Bernadette Juarez will be the Deputy Administrator for Biotechnology Regulatory Services, succeeding Dr. Mike Firko, who is retiring at the end of the month. Ms. Juarez has been serving as the Deputy Administrator for AC since early 2016, after earlier service as the Director of APHIS Investigative and Enforcement Services and before that as an attorney with USDA’s Office of the General Counsel. While we recruit for a permanent successor, Dr. Betty Goldentyer, currently AC’s Associate Deputy Administrator, will serve as Acting Deputy Administrator. Dr. Jerry Rushin will act as AC’s Associate Deputy Administrator.
Dr. Jack Shere will also become an Associate Administrator, filling the position previously held by Dr. Mary Bohman, who left the Agency earlier this year. Dr. Shere has been serving as Deputy Administrator for VS and Chief Veterinary Officer (CVO) since early 2016 after many years in VS field leadership positions. In his new role, Dr. Shere will concentrate on emergency preparedness and planning, as well as homeland and national security issues. Among his duties will be a special focus on the emerging African swine fever threat throughout the world.
Dr. Burke Healey, currently the VS Associate Deputy Administrator, will succeed Dr. Shere as the VS Deputy Administrator and CVO. Prior to serving in this position, Dr. Healey held several VS field leadership positions and served as the State Veterinarian for Oklahoma.
Dr. Rosemary Sifford, currently the VS Associate Deputy Administrator for Strategy and Policy (S&P), will succeed Dr. Healey as the VS Associate Administrator. Prior to serving in this position, Dr. Sifford served in VS field leadership positions and was also an Agricultural Quarantine Inspection veterinarian for our Plant Protection and Quarantine program.
Dr. Sarah Tomlinson, currently the VS Executive Director for S&P, will succeed Dr. Sifford as VS Associate Deputy Administrator for S&P. Prior to serving in this position, Dr. Tomlinson served VS as the Coordinator for the National Animal Health Laboratory Network as well as a veterinary epidemiologist. We will recruit for a permanent successor to Dr. Tomlinson.
Dr. Thomas McKenna, currently Director for District One of VS Field Operations (FiOps), will be a new FiOps Executive Director. He will also serve as the FiOps Acting Associate Deputy Administrator while we recruit for a permanent successor to Dr. Brian McCluskey, who recently left the Agency.
All these changes will be effective on August 4, 2019.
I want to express my appreciation for everything these leaders have done in their current and previous positions. They have all contributed to our noble missions of feeding and clothing the world and protecting vulnerable animals. Please join me in wishing them all the best as they embark on their new adventures. Shea Signature Kevin Shea Administrator
FRIDAY, FEBRUARY 20, 2015
APHIS Freedom of Information Act (FOIA) Appeal Mouse Bio-Assays 2007-00030-A Sheep Imported From Belgium and the Presence of TSE Prion Disease Kevin Shea to Singeltary 2015
http://transmissiblespongiformencephalopathy.blogspot.com/2015/02/aphis-freedom-of-information-act-foia.html
http://transmissiblespongiformencephalopathy.blogspot.com/2015/02/aphis-freedom-of-information-act-foia.html
WEDNESDAY, FEBRUARY 13, 2019
cwd, bse, scrapie, cjd, tse prion, we need to build a wall to protect the world from mad cow type disease in Texas
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date: Tue, 9 Jan 2001 16:49:00 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
snip...
[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.
[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]
[host Richard] could you repeat the question?
[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[not sure whom ask this] what group are you with?
[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.
[not sure who is speaking] could you please disconnect Mr. Singeltary
[TSS] you are not going to answer my question?
[not sure whom speaking] NO
snip...see full archive and more of this;
===============end...tss
2001
Scientific Advisors and Consultants Staff 2001 Advisory Committee TSE PRION Singeltary Submission
Freas
Monday, January 08,2001 3:03 PM FDA Singeltary submission 2001
Greetings again Dr. Freas and Committee Members,
I wish to submit the following information to the Scientific Advisors and Consultants Staff 2001 Advisory Committee (short version). I understand the reason of having to shorten my submission, but only hope that you add it to a copy of the long version, for members to take and read at their pleasure, (if cost is problem, bill me, address below). So when they realize some time in the near future of the 'real' risks i speak of from human/animal TSEs and blood/surgical products. I cannot explain the 'real' risk of this in 5 or 10 minutes at some meeting, or on 2 or 3 pages, but will attempt here:
fda link is dead in the water;
snip...see full text
2019
49. The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L
E. D. Cassmanna,b, S. J. Moorea,b, R. D. Kokemullera, A. Balkema-Buschmannc, M. H. Groschupcand J. J. Greenleea
aVirus and Prion Research Unit, National Animal Disease Center, ARS, United States Department of Agriculture, Ames, IA, USA (EDC, SJM, RDK, JJG); bOak Ridge Institute for Science and Education (ORISE) through an interagency agreement between the U.S. Department of Energy (DOE) and the U.S. Department of Agriculture (USDA). ORISE is managed by ORAU under DOE contract number DE-SC0014664. (EDC, SJM), Department of Veterinary Pathology, Iowa State University, Ames, IA, USA (JDS); cInstitute of Novel and Emerging Infectious Diseases, Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health, Greifswald – Isle of Riems, Germany (ABB, MHG)
CONTACT E. D. Cassmann eric.cassmann@usda.gov
ABSTRACT
Introduction: Transmissible mink encephalopathy (TME) is a fatal neurologic prion disease of farmed mink. Epidemiologic and experimental evidence following a Wisconsin outbreak in 1985 has linked TME to low-type bovine spongiform encephalopathy (BSE-L). Evidence suggests that farmed mink were likely exposed through feeding of BSE-L infected downer cattle. The interspecies transmission of TME to cattle has been documented. Recently, we demonstrated the susceptibility of sheep to cattle passaged TME by intracranial inoculation. The aim of the present study was to compare ovine passaged cattle TME to other prion diseases of food-producing animals. Using a bovine transgenic mouse model, we compared the disease phenotype of sheep TME to BSE-C and BSE-L.
Materials and Methods: Separate inoculants of sheep passaged TME were derived from animals with the VRQ/VRQ (VV136) and ARQ/VRQ (AV136) prion protein genotype. Transgenic bovinized mice (TgBovXV) were intracranially inoculated with 20 µl of 1% w/v brain homogenate. The disease phenotypes were characterized by comparing the attack rates, incubation periods, and vacuolation profiles in TgBovXV mice.
Results: The attack rate for BSE-C (13/13), BSE-L (18/18), and TMEVV (21/21) was 100%; whereas, the TMEAV group (15/19) had an incomplete attack rate. The average incubation periods were 299, 280, 310, and 541 days, respectively. The vacuolation profiles of BSE-L and TMEVV were most similar with mild differences observed in the thalamus and medulla. Vacuolation profiles from the BSE-C and TMEAV experimental groups were different than TMEVVand BSE-L.
Conclusion: Overall the phenotype of disease in TME inoculated transgenic mice was dependent on the sheep donor genotype (VV vs AV). The results of the present study indicate that TME isolated from VRQ/VRQ sheep is similar to BSE-L with regards to incubation period, attack rate, and vacuolation profile. Our findings are in agreement with previous research that found phenotypic similarities between BSE-L and cattle passaged TME in an ovine transgenic rodent model. In this study, the similarities between ovine TME and BSE-L are maintained after multiple interspecies passages.
Prion2019 Conference
2007
August 1988
Evidence That Transmissible Mink Encephalopathy Results From Feeding Infected Cattle
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...
MONDAY, MAY 20, 2019
Tracking and clarifying differential traits of classical- and atypical L-type bovine spongiform encephalopathy prions after transmission from cattle to cynomolgus monkeys
SUNDAY, APRIL 14, 2019
Estimation of prion infectivity in tissues of cattle infected with atypical BSE by real time-quaking induced conversion assay
WEDNESDAY, APRIL 24, 2019
USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019
TUESDAY, MARCH 26, 2019
Joint Statement from President Donald J. Trump USA and President Jair Bolsonaro Brazil FOREIGN POLICY BSE TSE Prion aka mad cow disease
SATURDAY, JUNE 01, 2019
Brazil reports another cases of mad cow disease atypical BSE TSE Prion
PLEASE BE ADVISED THERE IS NO SCIENTIFIC PROOF THAT ANY ATYPICAL BSE TSE PRION IS OF A SPONTANEOUS OLD AGE DISEASE, NOT CAUSED BY FEED, THIS IS FALSE AND UNPROVEN, IN FACT, ATYPICAL BSE OF THE L AND H TYPE ARE TRANSMISSIBLE BY ORAL ROUTE. THIS STATEMENT THAT ATYPICAL BSE IS A SPONTANEOUS EVENT CAUSED BY OLD AGE, CAUSED BY NOTHING, IS ABSOLUTELY A LIE, AND THE GOVERNMENT OF BRAZIL, AND OTHER GOVERNMENTS THAT PRODUCE SUCH STATEMENTS, KNOWS THIS IS AN UNPROVEN STATEMENT...TERRY SINGELTARY SR.
TUESDAY, JULY 16, 2019
Spain Bovine Spongiform Encephalopathy BSE TSE Prion July 5 2019
WEDNESDAY, AUGUST 15, 2018
The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
WEDNESDAY, APRIL 24, 2019
USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019
SUNDAY, APRIL 14, 2019
Estimation of prion infectivity in tissues of cattle infected with atypical BSE by real time-quaking induced conversion assay
WEDNESDAY, APRIL 17, 2019
Estimating the impact on food and edible materials of changing scrapie control measures: The scrapie control model
TUESDAY, MARCH 26, 2019 USDA ARS 2018
USAHA RESOLUTIONS TWO PRONGED APPROACH NEEDED FOR ADVANCING CATTLE TRACEABILITY
THURSDAY, MARCH 14, 2019
USDA APHIS CDC FDA BSE TSE PRION UPDATE 2019
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
MONDAY, JUNE 24, 2019
APHIS, FSIS, USDA, FDA, Transmissible Spongiform Encephalopathy TSE, BSE, CWD, Scrapie, Camel TSE Prion Disease, CJD Humans
WEDNESDAY, JUNE 26, 2019
''CWD has also been diagnosed in several free-ranging white-tailed deer harvested on ranches in close proximity to the remaining CWD positive breeding facilities within Medina County in central Texas. Genetic tests performed on those hunter-harvested deer found that the genetic composition of the subject animals were more closely related to deer in nearby captive facilities, as opposed to those in the surrounding free-range population.''
HOUSE COMMITTEE ON NATURAL RESOURCES SUBCOMMITTEE ON OVERSIGHT AND INVESTIGATIONS TESTIMONY TEXAS TPWD
WEDNESDAY, JUNE 26, 2019
Subcommittee Hearing: Chronic Wasting Disease: The Threats to Wildlife, Public Lands, Hunting, and Health
video
CHRONIC WASTING DISEASE CONGRESS Serial No. 107-117 May 16, 2002
CHRONIC WASTING DISEASE
JOINT OVERSIGHT HEARING BEFORE THE SUBCOMMITTEE ON FORESTS AND FOREST HEALTH JOINT WITH THE SUBCOMMITTEE ON FISHERIES CONSERVATION, WILDLIFE AND OCEANS OF THE COMMITTEE ON RESOURCES U.S. HOUSE OF REPRESENTATIVES ONE HUNDRED SEVENTH CONGRESS SECOND SESSION
May 16, 2002
Serial No. 107-117
snip...
Mr. MCINNIS. Today, this joint Subcommittee hearing will explore an issue of immeasurable importance to the growing number of communities in wide-ranging parts of this country, the growing incidence of Chronic Wasting Disease in North America’s wild and captive deer and elk populations. In a matter of just a few months, this once parochial concern has grown into something much larger and much more insidious than anyone could have imagined or predicted.
As each day passes, this problem grows in its size, scope, and consequence. One thing becomes clear. Chronic Wasting Disease is not a Colorado problem. It is a Wisconsin problem or a Nebraska or Wyoming problem. It is a national problem and anything short of a fully integrated, systematic national assault on this simply will not do, which is precisely why we brought our group together here today.
snip...
So this is a disease that is spreading throughout the continent and it is going to require a national response as well as the efforts that are currently taking place in States like Wisconsin, Colorado, Nebraska, Wyoming, the interest they now have down in Texas and some of the neighboring States that have large white-tailed deer population and also elk.
This is a huge issue for us, Mr. Chairman, in the State of Wisconsin. I want to commend Governor McCallum and your staff and the various agencies for the rapid response that you have shown, given the early detection of CWD after the last deer hunting season. The problem that we have, though, is just a lack of information, good science in regards to what is the best response, how dangerous is this disease. We cannot close the door, quite frankly, with the paucity of scientific research that is out there right now in regards to how the disease spreads, the exposure of other livestock herds—given the importance of our dairy industry in the State, that is a big issue—and also the human health effects.
WEDNESDAY, JUNE 19, 2019
Experts urge immediate action to contain the epidemic Chronic Wasting Disease CWD TSE Prion
2019
friendly fire, pass it forward, they call it iatrogenic cjd, or what i call 'tse prion poker', are you all in $$$
SATURDAY, MARCH 16, 2019
Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices) Guidance for Industry and Food and Drug Administration Staff Document issued on March 15, 2019 Singeltary Submission
TUESDAY, APRIL 09, 2019
Horizon Health Network Moncton Hospital notified more than 700 patients after two cases of CJD were diagnosed both patients had undergone cataracts surgery before being diagnosed
THURSDAY, AUGUST 17, 2017
*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017
Singeltary et al
FRIDAY, JUNE 21, 2019
CJD TSE Prion cases update USA, Texas, Canada, and UK
MONDAY, FEBRUARY 25, 2019
MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019
There is NO proof that the atypical TSE are spontaneous.please show me these transmission studies ?on the other hand, we now know that the L-type atypical BSE is much more virulent than the typical C-BSE, and we now know that theH-type atypical BSE will transmit to humans.WHY can it not be that these atypical cases are simply from feed that had different strains of TSE ? WHY is it that no one will comment on the studies that was suppose to show infectivity of tissues from atypical BSE ?WHY is it I had to file a FOIA on that issue?L-type atypical BSE (BASE) is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice.BSE-H is also transmissible in our humanized Tg mice.SEE Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 et al 2009 ;Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009snip...I ask Professor Kong ;Thursday, December 04, 2008 3:37 PMSubject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk AssessmentIS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....Professor Kong reply ;.....snipAs to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.Best regards,Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USAP.4.23 Transmission of atypical BSE in humanized mouse modelsLiuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USABackground: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were argely undefined.Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice.Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time. The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice. BSE-H is also transmissible in our humanized Tg mice. The possibility of more than two atypical BSE strains will be discussed.Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.see full text ;snip...full test Singeltary et al PLOSTHURSDAY, JULY 20, 2017USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200LET'S take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.This new prionopathy in humans?the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow,WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ???there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$ALABAMA MAD COW g-h-BSEalabamaIn this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America.This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD.This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene.We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.Saturday, August 14, 2010BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY (see mad cow feed in COMMERCE IN ALABAMA...TSS)her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008). This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine-human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks. Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail:maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA NATURE|Vol 457|26 February 2009Thursday, July 24, 2014*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigationsThursday, July 24, 2014*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigationsTHURSDAY, FEBRUARY 14, 2013Unique Properties of the Classical Bovine Spongiform Encephalopathy Strain and Its Emergence From H-Type Bovine Spongiform Encephalopathy Substantiated by VM Transmission StudiesSaturday, August 14, 2010BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY(see mad cow feed in COMMERCE IN ALABAMA...TSS)2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006P02.35Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSEBiacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, SwedenWestern blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK-resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.57 The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK.
It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE. 32The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture. 33The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive.The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995.Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre. 34The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE...32 Clark, W., Hourrigan, J. and Hadlow, W. (1995) Encephalopathy in Cattle Experimentally Infected with the Scrapie Agent, American Journal of Veterinary Research, 56, 606-1233 YB88/10.00/1.1Technical Abstract:Prion strains may vary in their ability to transmit to humans and animals. Few experimental studies have been done to provide evidence of differences between U.S. strains of scrapie, which can be distinguished by incubation times in inbred mice, microscopic lesions, immunoreactivity to various antibodies, or molecular profile (electrophoretic mobility and glycoform ratio). Recent work on two U.S. isolates of sheep scrapie supports that at least two distinct strains exist based on differences in incubation time and genotype of sheep affected. One isolate (No. 13-7) inoculated intracerebrally caused scrapie in sheep AA at codon 136 (AA136) and QQ at codon 171 (QQ171) of the prion protein in an average of 19 months post-inoculation (PI) whereas a second isolate (No. x124) caused disease in less than 12 months after oral inoculation in AV136/QQ171 sheep. Striking differences were evident when further strain analysis was done in R111, VM, C57Bl6, and C57Bl6xVM (F1) mice. No. 13-7 did not induce disease in any mouse strain at any time post-inoculation (PI) nor were brain tissues positive by western blot (WB). Positive WB results were obtained from mice inoculated with isolate No. x124 starting at day 380 PI. Incubation times averaged 508, 559, 601, and 633 days PI for RIII, C57Bl6, VM, and F1 mice, respectively. Further passage will be required to characterize these scrapie strains in mice.***>This work provides evidence that multiple scrapie strains exist in U.S. sheep.One of these isolates (TR316211) behaved like the CH1641 isolate, with PrPres features in mice similar to those in the sheep brain. From two other isolates (O100 and O104), two distinct PrPres phenotypes were identified in mouse brains, with either high (h-type) or low (l-type) apparent molecular masses of unglycosylated PrPres, the latter being similar to that observed with CH1641, TR316211, or BSE. Both phenotypes could be found in variable proportions in the brains of the individual mice. In contrast with BSE, l-type PrPres from "CH1641-like" isolates showed lower levels of diglycosylated PrPres. From one of these cases (O104), a second passage in mice was performed for two mice with distinct PrPres profiles. This showed a partial selection of the l-type phenotype in mice infected with a mouse brain with predominant l-type PrPres, and it was accompanied by a significant increase in the proportions of the diglycosylated band. These results are discussed in relation to the diversity of scrapie and BSE strains.In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.- 59-P-088 Transmission of experimental CH1641-like scrapie to bovine PrP overexpression miceKohtaro Miyazawa1, Kentaro Masujin1, Hiroyuki Okada1, Yuichi Matsuura1, Takashi Yokoyama21Influenza and Prion Disease Research Center, National Institute of Animal Health, NARO, Japan; 2Department of Planning and General Administration, National Institute of Animal Health, NAROIntroduction: Scrapie is a prion disease in sheep and goats. CH1641-lke scrapie is characterized by a lower molecular mass of the unglycosylated form of abnormal prion protein (PrpSc) compared to that of classical scrapie. It is worthy of attention because of the biochemical similarities of the Prpsc from CH1641-like and BSE affected sheep. We have reported that experimental CH1641-like scrapie is transmissible to bovine PrP overexpression (TgBoPrP) mice (Yokoyama et al. 2010). We report here the further details of this transmission study and compare the biological and biochemical properties to those of classical scrapie affected TgBoPrP mice.Methods: The details of sheep brain homogenates used in this study are described in our previous report (Yokoyama et al. 2010). TgBoPrP mice were intracerebrally inoculated with a 10% brain homogenate of each scrapie strain. The brains of mice were subjected to histopathological and biochemical analyses.Results: Prpsc banding pattern of CH1641-like scrapie affected TgBoPrP mice was similar to that of classical scrapie affected mice. Mean survival period of CH1641-like scrapie affected TgBoPrP mice was 170 days at the 3rd passage and it was significantly shorter than that of classical scrapie affected mice (439 days). Lesion profiles and Prpsc distributions in the brains also differed between CH1641-like and classical scrapie affected mice.Conclusion: We succeeded in stable transmission of CH1641-like scrapie to TgBoPrP mice. Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIESTitle: Comparison of two US sheep scrapie isolates supports identification as separate strainsAuthorsitem Moore, Sarah - item Smith, Jodi item West Greenlee, Mary - item Nicholson, Eric item Richt, Juergen item Greenlee, JustinSubmitted to: Veterinary Pathology Publication Type: Peer Reviewed Journal Publication Acceptance Date: December 22, 2015 Publication Date: N/AInterpretive Summary: Scrapie is a fatal disease of sheep and goats that causes damaging changes in the brain. The infectious agent is an abnormal protein called a prion that has misfolded from its normal state. Whether or not a sheep will get scrapie is determined primarily by their genetics. Furthermore, different scrapie strains exist that may result in a different expression of disease such as shorter incubation periods, unusual clinical signs, or unique patterns of lesions within the brain. This study evaluated two U.S. scrapie isolates in groups of sheep with varying susceptibilities to scrapie. Our data indicates that there are differences in incubation periods, sheep genotype susceptibilities, and lesion profiles that support designating these scrapie isolates as unique strains. The identification of a new scrapie strain in the United States means that control measures, methods of decontamination, and the potential for transmission to other species may need to be reevaluated. This information is useful to sheep farmers and breeders that are selectively breeding animals with genotypes resistant to the most prevalent strain of scrapie and could impact future regulations for the control of scrapie in the United States. Technical Abstract: Scrapie is a naturally occurring transmissible spongiform encephalopathy (TSE) of sheep and goats. There are different strains of sheep scrapie that are associated with unique molecular, transmission, and phenotype characteristics, but very little is known about the potential presence of scrapie strains within sheep in the US. Scrapie strain and PRNP genotype could both affect susceptibility, potential for transmission, incubation period, and control measures required for eliminating scrapie from a flock. Here we evaluate two US scrapie isolates, No. 13-7 and x124, after intranasal inoculation to compare clinical signs, incubation periods (IP), spongiform lesions, and patterns of PrPSc deposition in sheep with scrapie-susceptible PRNP genotypes (QQ171). After inoculation with x124, susceptibility and IP were associated with valine at codon 136 (V136) of the prion protein: VV136 had short IPs (6.9 months), AV136 sheep were 11.9 months, and AA136 sheep did not develop scrapie. All No.13-7 inoculated sheep developed scrapie with IP’s of 20.1 months for AA136 sheep, 22.8 months for AV136 sheep, and 26.7 months for VV136 sheep. Patterns of immunoreactivity in the brain were influenced by challenge isolate and host genotype. Differences in PrPSc profiles versus isolate were most striking when examining brains from sheep with the VV136 genotype. In summary, intranasal inoculation with isolates x124 and No. 13-7 resulted in differences in IP, sheep genotype susceptibility, and PrPSc profile that support designation as separate strains.Last Modified: 6/6/201631Appendix I VISIT TO USA - OR A E WRATHALL — INFO ON BSE AND SCRAPIEDr Clark lately of the scrapie Research Unit, Mission Texas hassuccessfully transmitted ovine and caprine scrapie to cattle. Theexperimental results have not been published but there are plans to dothis. 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 witha 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 Goatvirus 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 embryos from naturally infected sheep (cf SPA).Prof. A Robertson gave a brief accout of BSE. The us approach was to32accord 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 indicated17/33 wished to drop it6/33 wished to develop it8/33 had few sheep and were neutralInformation obtained from Dr Wrathall‘s notes of a meeting of the u.s.Animal Health Association at Little Rock, Arkansas Nov. 1988.33In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells3. 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. ...also see hand written notes ;Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected CattleOver 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...EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSUREThis is provided by the statistically significant increase in the incidence of sheep scrape from 1985, as determined from analyses of the submissions made to VI Centres, and from individual case and flock incident studies. ........REPORT OF THE WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY 1989snip...4.2.9 ...Also, if it resulted from a localised chance transmission of the scrapie strain from sheep to cattle giving rise to a mutant, a different pattern of disease would have been expected: its range would have increased with time. Thus the evidence from Britain is against the disease being due to a new strain of the agent, but we note that in the United States from 1984 to 1988 outbreaks of scrapie in sheep flocks are reported to have Increased markedly, now being nearly 3 times as high as during any previous period (18).Monday, September 13, 2010atypical BSE strains and sporadic CJD strains, is there a connection and why shouldn't there be $snip...see full text;INDEED, thanks to the O...I.E., and the U.S.D.A. SSS policy, and the fact they are using science dated back to 1985 still in some cases. THE infamous June 2004 enhanced bse surveillance program was set up to fail from the beginning, and fail they did, not only with the surveillance for TSE, but also the partial and voluntary feed ban of August 4, 1997 was nothing but ink on paper. What i predicted a decade ago, has in fact come to pass, the TSE agent has mutated in every species from CWD now at two documented strains, BSE with 4 strains documented to date (c-BSE, h-BSE [typical h-BSE or the one and only documented g-h-BSEalabama strain?], l-BSE, and the IBNC BSE), and the different Scrapie strains are too many to count, not included the atypical Nor-98 and or BSE in sheep. with the 3 strains of BSE documented in North America to date, the two strains of CWD, TME, and all the strains of Scrapie, with 5 cases of the Nor-98 atypical scrapie cases already documented in 2010 here in the USA, all of which of the past two decades have been rendered and fed to food producing animals for animals and humans, and any human TSE there from ??? please note that the sporadic CJD case here in the USA has had a steady increase since 1997. it's not rocket science. what the USDA, FDA et al have used is junk science, bought and paid for by your local cattle dealer i.e. INDUSTRY. the BSE MRR policy was nothing more than a legal tool to do the same thing when the U.K. poisoned the globe with BSE, except now it's legal $$$these are the facts as i have come to know them. just my take. ...Let's take a look at the facts shall we $BOVINE SPONGIFORM ENCEPHALOPATHY, SCRAPIE, CWD, CJD, NORTH AMERICA TYPICAL AND ATYPICALExperimental Transmission of H-type Bovine Spongiform Encephalopathy to Bovinized Transgenic Micesnip...see full text;IBNC BSE TSE Prion mad cow disease***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***Posted by Terry S. Singeltary Sr. on 03 Jul 2015 at 16:53 GMT***> NEW TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE (MAD CAMEL DISEASE) IN A NEW SPECIES <***NEW OUTBREAK OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE IN A NEW SPECIESSubject: Prion Disease in Dromedary Camels, AlgeriaOur identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.Wednesday, May 30, 2018Dromedary camels in northern Africa have a neurodegenerative prion disease that may have originated decades ago***> IMPORTS AND EXPORTS <***
SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BANWEDNESDAY, JULY 11, 2018CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS FDA EMERGENCY REQUEST FOR RULE CHANGE USA Section 21 C.F.R. 589.2000TUESDAY, JULY 10, 2018CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS*** ''but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs.''CONFIDENTIAL SPONGIFORM ENCEPHALOPATHY OF PIGS
APHIS, FSIS, USDA, FDA, Transmissible Spongiform Encephalopathy TSE, BSE, CWD, Scrapie, Camel TSE Prion Disease, CJD Humans Singeltary Submissions
APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission
Comment from Terry Singeltary
The is a Comment on the Animal and Plant Health Inspection Service (APHIS) Notice: Concurrence with the World Organization for Animal Health's Risk Designation for Bovine Spongiform Encephalopathy
For related information, Open Docket Folder Comment APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission
Greetings APHIS et al,
I would kindly like to comment on APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], and my comments are as follows, with the latest peer review and transmission studies as references of evidence.
THE OIE/USDA BSE Minimal Risk Region MRR is nothing more than free pass to import and export the Transmissible Spongiform Encephalopathy TSE Prion disease. December 2003, when the USDA et al lost it's supposedly 'GOLD CARD' ie BSE FREE STATUS (that was based on nothing more than not looking and not finding BSE), once the USA lost it's gold card BSE Free status, the USDA OIE et al worked hard and fast to change the BSE Geographical Risk Statuses i.e. the BSE GBR's, and replaced it with the BSE MRR policy, the legal tool to trade mad cow type disease TSE Prion Globally. The USA is doing just what the UK did, when they shipped mad cow disease around the world, except with the BSE MRR policy, it's now legal.
Also, the whole concept of the BSE MRR policy is based on a false pretense, that atypical BSE is not transmissible, and that only typical c-BSE is transmissible via feed. This notion that atypical BSE TSE Prion is an old age cow disease that is not infectious is absolutely false, there is NO science to show this, and on the contrary, we now know that atypical BSE will transmit by ORAL ROUTES, but even much more concerning now, recent science has shown that Chronic Wasting Disease CWD TSE Prion in deer and elk which is rampant with no stopping is sight in the USA, and Scrapie TSE Prion in sheep and goat, will transmit to PIGS by oral routes, this is our worst nightmare, showing even more risk factors for the USA FDA PART 589 TSE PRION FEED ban.
The FDA PART 589 TSE PRION FEED ban has failed terribly bad, and is still failing, since August 1997. there is tonnage and tonnage of banned potential mad cow feed that went into commerce, and still is, with one decade, 10 YEARS, post August 1997 FDA PART 589 TSE PRION FEED ban, 2007, with 10,000,000 POUNDS, with REASON, Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. you can see all these feed ban warning letters and tonnage of mad cow feed in commerce, year after year, that is not accessible on the internet anymore like it use to be, you can see history of the FDA failure August 1997 FDA PART 589 TSE PRION FEED ban here, but remember this, we have a new outbreak of TSE Prion disease in a new livestock species, the camel, and this too is very worrisome.
WITH the OIE and the USDA et al weakening the global TSE prion surveillance, by not classifying the atypical Scrapie as TSE Prion disease, and the notion that they want to do the same thing with typical scrapie and atypical BSE, it's just not scientific.
WE MUST abolish the BSE MRR policy, go back to the BSE GBR risk assessments by country, and enhance them to include all strains of TSE Prion disease in all species. With Chronic Wasting CWD TSE Prion disease spreading in Europe, now including, Norway, Finland, Sweden, also in Korea, Canada and the USA, and the TSE Prion in Camels, the fact the the USA is feeding potentially CWD, Scrapie, BSE, typical and atypical, to other animals, and shipping both this feed and or live animals or even grains around the globe, potentially exposed or infected with the TSE Prion. this APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], under it's present definition, does NOT show the true risk of the TSE Prion in any country. as i said, it's nothing more than a legal tool to trade the TSE Prion around the globe, nothing but ink on paper.
AS long as the BSE MRR policy stays in effect, TSE Prion disease will continued to be bought and sold as food for both humans and animals around the globe, and the future ramifications from friendly fire there from, i.e. iatrogenic exposure and transmission there from from all of the above, should not be underestimated. ...
Attachments (1) APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary...
TUESDAY, JUNE 18, 2019
APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018 Singeltary Submission
Comment from Terry Singeltary Sr. The is a Comment on the Animal and Plant Health Inspection Service (APHIS) Notice: Chronic Wasting Disease Herd Certification Program Standards
For related information, Open Docket Folder
Comment Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018
Greetings APHIS, USDA, Dr. Tracy Nichols, et al,
I wish to kindly submit my comments on the Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards please. i have submitted online and sent a hard copy to Dr. Nichols via email. i know that my concern may not be the same concern as others, but ramifications from cwd tse prion can be long lasting, and science is still emerging. however, the science today warrants immediate and further actions be taken, especially about zoonosis potential for cwd tse prion, if it has not happened already. my comments, with reference materials, are as follows, and will be formatted in such a way, i will address issues by numbers 1-10, and under each one of my comments by each number, i will reference my comments with science to back up what i am stating/asking...thank you kindly, terry
1. I believe that immediately, there should be a 'DECLARATION OF EXTRAORDINARY EMERGENCY FOR FOREIGN ANIMAL DISEASE OF THE United States of America USA' due to Chronic Wasting Disease CWD Transmissible Spongiform Encephalopathy TSE Prion disease. All Intercontinental, International, Interstate movements of cervid should be banned immediately from the USA, and documented CWD TSE Prion Countries. ...
snip...
see full text Singeltary Submission for references.
2. Voluntary Chronic Wasting Disease Herd Certification Program should be made MANDATORY immediately, OR NO PERMIT TO FARM DEER OR ELK, PERIOD! you don't want to join, then fine, you don't farm cervid and or any product there from...see full text Singeltary Submission for references.
3. INDEMNITY, NO MORE Federal indemnity program, or what i call, ENTITLEMENT PROGRAM for game farm industry. NO MORE BAIL OUTS FROM TAX PAYERS. if the captive industry can't buy insurance to protect not only themselves, but also their customers, and especially the STATE, from Chronic Wasting Disease CWD TSE Prion or what some call mad deer disease and harm therefrom, IF they can't afford to buy that insurance that will cover all of it, then they DO NOT GET A PERMIT to have a game farm for anything. This CWD TSE Prion can/could/has caused property values to fall from some reports in some places. roll the dice, how much is a state willing to lose?...see full text Singeltary Submission for references.
4. QUARANTINE OF ALL CAPTIVE, BREEDERS, URINE, ANTLER, VELVET, SPERM, OR ANY FACILITY that has been confirmed to have Chronic Wasting Disease CWD TSE Prion, the QUARANTINE should be for 21 years due to science showing what scrapie can do. 5 years is NOT enough. see; Infectious agent of sheep scrapie may persist in the environment for at least 16 years...
snip...see full text Singeltary Submission for references.
PLEASE SEE Singeltary full text file DOWNLOAD ON GOVERNMENT SITE, OR GO TO THIS URL LINK FOR FULL TEXT OF SINGELTARY SUBMISSION TO Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018, PLEASE SEE;
FRIDAY, MARCH 30, 2018
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018
Terry S. Singeltary Sr., Bacliff, Texas USA 77518 flounder9@verizon.net Attachments (1) Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary
MONDAY, MAY 20, 2019
APHIS, USDA, Announces the Finalized Chronic Wasting Disease Herd Certification Program Standards Singeltary Submissions
WEDNESDAY, JUNE 19, 2019
Experts urge immediate action to contain the epidemic Chronic Wasting Disease CWD TSE Prion
WEDNESDAY, MAY 29, 2019
Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures USDA HERE'S YOUR SIGN!
CDC
New Outbreak of TSE Prion in NEW LIVESTOCK SPECIES
Mad Camel Disease
Volume 24, Number 6—June 2018 Research
Prion Disease in Dromedary Camels, Algeria
Abstract
Prions cause fatal and transmissible neurodegenerative diseases, including Creutzfeldt-Jakob disease in humans, scrapie in small ruminants, and bovine spongiform encephalopathy (BSE). After the BSE epidemic, and the associated human infections, began in 1996 in the United Kingdom, general concerns have been raised about animal prions. We detected a prion disease in dromedary camels (Camelus dromedarius) in Algeria. Symptoms suggesting prion disease occurred in 3.1% of dromedaries brought for slaughter to the Ouargla abattoir in 2015–2016. We confirmed diagnosis by detecting pathognomonic neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues from 3 symptomatic animals. Prion detection in lymphoid tissues is suggestive of the infectious nature of the disease. PrPSc biochemical characterization showed differences with BSE and scrapie. Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.
SNIP...
The possibility that dromedaries acquired the disease from eating prion-contaminated waste needs to be considered.
Tracing the origin of prion diseases is challenging. In the case of CPD, the traditional extensive and nomadic herding practices of dromedaries represent a formidable factor for accelerating the spread of the disease at long distances, making the path of its diffusion difficult to determine. Finally, the major import flows of live animals to Algeria from Niger, Mali, and Mauritania (27) should be investigated to trace the possible origin of CPD from other countries.
Camels are a vital animal species for millions of persons globally. The world camel population has a yearly growth rate of 2.1% (28). In 2014, the population was estimated at ≈28 million animals, but this number is probably underestimated.. Approximately 88% of camels are found in Africa, especially eastern Africa, and 12% are found in Asia. Official data reported 350,000 dromedaries in Algeria in 2014 (28).
On the basis of phenotypic traits and sociogeographic criteria, several dromedary populations have been suggested to exist in Algeria (29). However, recent genetic studies in Algeria and Egypt point to a weak differentiation of the dromedary population as a consequence of historical use as a cross-continental beast of burden along trans-Saharan caravan routes, coupled with traditional extensive/nomadic herding practices (30).
Such genetic homogeneity also might be reflected in PRNP. Studies on PRNP variability in camels are therefore warranted to explore the existence of genotypes resistant to CPD, which could represent an important tool for CPD management as it was for breeding programs for scrapie eradication in sheep.
In the past 10 years, the camel farming system has changed rapidly, with increasing setup of periurban dairy farms and dairy plants and diversification of camel products and market penetration (13). This evolution requires improved health standards for infectious diseases and, in light of CPD, for prion diseases.
The emergence of another prion disease in an animal species of crucial importance for millions of persons worldwide makes it necessary to assess the risk for humans and develop evidence-based policies to control and limit the spread of the disease in animals and minimize human exposure. The implementation of a surveillance system for prion diseases would be a first step to enable disease control and minimize human and animal exposure. Finally, the diagnostic capacity of prion diseases needs to be improved in all countries in Africa where dromedaries are part of the domestic livestock.
***> IMPORTS AND EXPORTS <***
***SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN ***
cattle, pigs, sheep, cwd, tse, prion, oh my!
***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006).
Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.
cwd scrapie pigs oral routes
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period.
This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.
Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip.....
In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
snip.....
36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).
The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).
Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.
snip.....
The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip.....
In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.
snip.....
In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.
snip.....
Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.
snip.....
2017 Section 21 C.F.R. 589.2000, Animal Proteins Prohibited in Ruminant Feed
Subject: MICHIGAN FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE BREACH APRIL 4, 2017
MICHIGAN FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE BREACH APRIL 4, 2017
FDA BSE/Ruminant Feed Inspections Firms Inventory
11998 DET-DO MI 48846-847 OPR 4/4/2017 OAI
NAI = NO ACTION INDICATED
OAI = OFFICIAL ACTION INDICATED
VAI = VOLUNTARY ACTION INDICATED
RTS = REFERRED TO STATE
OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions...end...TSS
SEE MASSIVE TONNAGE OF BANNED FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS PRODUCT IN COMMERCE SINCE AUGUST 1997. THE MAD COW FEED BAN WAS AND IS STILL NOTHING BUT INK ON PAPER...TERRY
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
TUESDAY, JANUARY 17, 2017
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION
SATURDAY, JUNE 1, 2019
Traceability of animal protein byproducts in ruminants by multivariate analysis of isotope ratio mass spectrometry to prevent transmission of prion diseases
MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019
BSE INQUIRY EVIDENCE
Why did the appearance of new TSEs in animals matter so much? It has always been known that TSEs will transfer across species boundaries. The reason for this was never known until the genetic nature of the prion gene was fully investigated and found to be involved. The gene is found to have well preserved sites and as such there is a similar gene throughout the animal kingdom...and indeed a similar gene is found in insects! It is NOT clear that the precise close nature of the PrP gene structure is essention for low species barriers. Indeed it is probably easier to infect cats with BSE than it is to infect sheep. As such it is not clear that simply because it is possible to infect BSE from cattle into certain monkeys then other apes will necessarily be infectable with the disease. One factor has stood out, however, and that is that BSE, when inoculated into mice would retain its apparent nature of disease strain, and hence when it was inoculated back into cattle, then the same disease was produced. Similarly if the TSE from kudu was inoculated into mice then a similar distribution of disease in the brain of the mouse is seen as if BSE had been inoculated into the mouse. This phenomenon was not true with scrapie, in which the transmission across a species barrier was known to lose many of the scrapie strain phenomena in terms of incubation period or disease histopathology. This also suggested that BSE was not derived from scrapie originally but we probably will never know.
------------------------------------------------------------------------
TSE in wild UK deer? The first case of BSE (as we now realise) was in a nyala in London zoo and the further zoo cases in ungulates were simply thought of as being interesting transmissions of scrapie initially. The big problem started to appear with animals in 1993-5 when it became clear that there was an increase in the CJD cases in people that had eaten deer although the statistics involved must have been questionable. The reason for this was that the CJD Surveillance was well funded to look into the diet of people dying of CJD. This effect is not clear with vCJD...if only because the numbers involved are much smaller and hence it is difficult to gain enough statistics. They found that many other foods did not appear to have much association at all but that deer certainly did and as years went by the association actually became clearer. The appearance of vCJD in 1996 made all this much more difficult in that it was suddenly clearer that the cases of sporadic CJD that they had been checking up until then probably had nothing to do with beef...and the study decreased. During the period there was an increasing worry that deer were involved with CJD..
see references:
DEER BRAIN SURVEY
i have not updated my blogspot url with all this data archived, but i will work on it...but until then, i have updated this on the above links with live urls to the actual BSE Inquiry documents...
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Fri, 18 Oct 2002 23:12:22 +0100
From: Steve Dealler
Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ References: <3daf5023 .4080804="" a="" href="http://wt.net/" nbsp="" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">wt.net
Dear Terry,
An excellent piece of review as this literature is desparately difficult to get back from Government sites.
What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!
Steve Dealler ===============
BSE Inquiry Steve Dealler
Management In Confidence
BSE: Private Submission of Bovine Brain Dealler
reports of sheep and calf carcasses dumped...
re-scrapie to cattle GAH Wells BSE Inquiry
https://web.archive.org/web/20090506043931/http://www.bseinquiry.gov.uk/files/yb/1993/12/09001001.pdf
https://web.archive.org/web/20090506065716/http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf
Dr. Dealler goes rogue to confirm BSE
Confirmation BSE Dealler's mad cow
BSE vertical transmission
1993 cjd report finds relationship with eat venison and cjd increases 9 fold, let the cover up begin...tss
FINDINGS
*** 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). ***
*** 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). ***
*** 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 ;
GAME FARM INDUSTRY WANTS TO COVER UP FINDINGS OF INCREASE RISK TO CJD FROM CERVID
BSE INQUIRY
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.
The BSE Inquiry / Statement No 324
Dr James Kirkwood (not scheduled to give oral evidence)
Statement to the BSE Inquiry
James K Kirkwood BVSc PhD FIBiol MRCVS
[This witness has not been asked to give oral evidence in Phase 1 of the Inquiry]
1. I became involved in the field of TSEs through my work as Head of the Veterinary Science Group at the Zoological Society of London’s Institute of Zoology. I held this post from November 1984 until June 1996, when I took up my present post at UFAW. During this time, concurrent with the BSE epidemic, cases of scrapie-like spongiform encephalopathies occurred in animals at the Zoological Society of London’s collections at Regent’s Park and Whipsnade and in other zoos. It was appropriate to investigate the epidemiology of these cases in order to try to determine the possible impact on zoo animals and breeding programmes, and to consider how the disease in zoo animals might be controlled.
2. Throughout the period from 1985 to March 1996, I worked at the Institute of Zoology (IoZ). I was Head of the Veterinary Science Group of the IoZ and Senior Veterinary Officer of the Zoological Society of London (ZSL). I was responsible for the provision of the veterinary service for the ZSL collections.
3. During the period from 1985 to March 1996, scrapie-like spongiform encephalopathies were diagnosed in the following animals which died, or were euthanased, at London Zoo and Whipsnade:
Animal Sex Date of Death Age (mos)
Arabian Oryx Oryx leucoryx F 24.3.89 38
Greater kudu Tragelaphus strepsiceros (Linda) F 18.8.89 30
Greater kudu (Karla) F 13.11.90 19 Greater kudu (Kaz) M 6.6.91 37
Greater kudu (Bambi) M 24.10.91 36
Greater kudu (346/90) M 26.2.92 18
Greater kudu (324/90) F 22.11.92 38
Cheetah Acinonyx jubatus (Michelle) F 22.12.93 91
All these cases were described in papers published in the scientific literature (as cited below).
EYES, RETINA, SHOULD NOT BE USED IN SCHOOLS, BAB, SOB, MRM,
BSE, PET FOOD, CRUSHED HEADS
IN PARTICULAR CRUSHED HEADS
YOU explained that imported crushed heads were extensively used in the petfood industry...
In particular I do not believe one can say that the levels of the scrapie agent in pet food are so low that domestic animals are not exposed.
BSE IN PETFOOD
1. The Secretary asked on 19 April whether I was content with the advice in para 3 of the record of the meeting on 17 March with the Parliamentary Secretary (Mr Thompson). The simple answer is ''not entirely''.
2. On occasions, material obtained from slaughterhouses will be derived from sheep affected with scrapie or cattle that may be incubating BSE for use in petfood manufacture. Some of this material must be classified as high risk since it contains brain, spinal cord, spleen or lymphatic glands.
Meldrum's notes on pet foods and materials used
IN CONFIDENCE CJD TO CATS...
It should be noted that under experimental conditions cats succumb to an encephalopathy after intracerebral inoculation of material derived from patients affected with Creutzfeldt-Jakob Disease.
Confidential BSE and __________________
3. I have thought very hard about whether the Branch should carry out a similar exercise with meat and meat products for human foods. On balance I do NOT think we should undertake it, but a final decision has not been taken and you may wish to discuss this further. ...
1st case natural FSE
NATURAL SPONGIFORM ENCEPHALOPATHY IN A DOMESTIC CAT
1. We have heard from MAFF that a domestic Siamese cat from the Bristol area has had spongiform encephalopathy confirmed. Although there are previous instances of experimental infection in cats, there have been no previous natural infections reported. The assumption must be the cat became infected by scrapie/BSE agent in it's food. ...
FSE and pharmaceuticals
1. An analysis by MCA Professional staff of the results to the questionnaire sent out to industry to obtain additional data about the use of animal materials of any origin in the manufacture of pharmaceutical products for human use, reveals that material of feline or canine origin is used in only two licensed products. In both instances the material is sourced from outside the U.K. and from areas currently believed to be free from B.S.E.
CONFIDENTIAL
Confidential cats/dogs and unsatisfactory posture MAFFs failure to assure key research
3. First, I am very uneasy about the relative lack of urgency and interest that MAFF appear to hold for getting the necessary research programme on BSE and related encephalopathies started, and getting it going fast. FOR EXAMPLE, MR BRADLEY of CVL said that there were difficulties in organizing transmission experiments from the brain of the cat which died of an encephalopathy in Bristol. There were arguments going on about who should pay for this work. Should it be MAFF, the Bristol Veterinary School or someone else? Dr. Tyrrell was clearly exasperated.
snip...
11. The Committee were even LESS FORTHCOMING on what their reaction might be if an encephalopathy is found in another species, perhaps in DOGS. Their first reaction was that, as with the cats, the first step could be to investigate whether this was really a new disease, or simply one that had not previously been recognized and to see whether it has any links to BSE, scrapie or other transmissible encephalopathies. Indeed, some members of the Committee seem to regard the whole question of another species as a hypothetical question to be addressed only when it happened. A rather UNSATISFACTORY POSTURE.
12. In advance of your meeting with Dr Tyrrell on Monday morning, I have not voiced my ANXIETIES about the support the Committee is receiving from MAFF to anyone OTHER THAN DR PICKLES. ...
SPONGIFORM ENCEPHALOPATHY IN A CAPTIVE PUMA
an article in yesterday's Times (attached) which suggested that the puma concerned had never ''eaten any part of a cow or sheep which, in the opinion of Government Scientists, could transmit the species to a different species''.
3. You explained to me that this was INCORRECT. The position was as set out in the briefing for Prime Minister's questions attached to Mr Taylor's note. The puma had probably been fed low quality beef meat in the form of split carcasses. ...
Subject: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY Date: Thu, 17 Oct 2002 17:04:51 -0700 From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To: BSE-L
Greetings BSE-L,
is there any other CWD surveys/testing in the UK on their deer? what sort of testing has been done to date on UK/EU deer? any input would be helpful... thank you
DEER SPONGIFORM ENCEPHALOPATHY SURVEY
3. This will be a low key study with no publicity to avoid unnecessary media interest. It will be carried out in two stages ;
(I) A small scale examination of around 30 deer brains to establish the normal histology of the healthy brain; and
(II) A larger scale random examination of 300 or more adult deer brains drawn from both deer farms and parks to establish whether there is any evidence of a cervine spongiform encephalopathy. ...
Ministry of Agriculture Fisheries and Food Veterinary Investigation Centre West House. Station Road. Thirsk Y07 IPZ Telephone: 0845·522065 Fax: 0845·525224
Your reference
Our reference RJH/ASB
Date 4 November 1992
DEER SPONGIFORM ENCEPHALOPATHY SURVEY
Dear Paul
I have now found time to review the 10 deer- brains collected from Mr Walker farm··via Winchester Via Winchester VIC. In answer to your specific question was there sufficient difference in preservation of brain tissue to warrant the extra effort involved in rapid brain removal on the farm, the answer is definitely "Yes." The original five brains (Winchester ref M487/11) showed varying degrees of autolytic vacuolation affecting both white and grey matter throughout the brain. vacuolation and separation of Purkinje cells and marked perivascular spaces. These artifacts made interpretation of subtle, specific pathological vacuolation more difficult. By contrast the second submission (Winchester reference N736/2) showed excellent preservation of white and grey matter. Any vacuolar Change present could be confidently interpreted as pathological albeit of unknown pathogenesis.
I can only reiterate the comments made by Gerald Wells and myself at the preliminary discussion at Weybridge in Autumn 1991. If the survey's purpose is an accurate histopathological interpretation of brain tissue. the material must be collected in a pristine state. This is particularly valid when looking for ar unrecognised and undefined spongiform encephalopathy in a new species. Deer brains are very large structures which take a lot of fixation and therefore must be handled sympathetically from the start. We have already seen the problems encountered in comparatively smaller hound brains where delayed fixation was a major limitation on interpretation of true pathological change.
The bottom line must be that if a pathologist's expertise is to be used, it is critical to collect artefact free brain material. If the politics or economics do not allow this, then I would suggest that an electron microscopy survey involving detection of scrapie associated fibrils would be much more appropriate.
Best wishes Yours sincerely
R J HIGGINS VIO 92/11.4/2.1
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, identify the three brains that were from the ''POSITIVE'' end of the lesion spectrum.
HOUND SURVEY PATHOLOGICAL REPORT (see positive results) and MAD DOGS AND ENGLISHMAN...
ya'll thought i was making this stuff up didn't ya...i don't make this stuff up!
It is clear that the designing scientists must also have shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.
second supplementary
Why did the appearance of new TSEs in animals matter so much? It has always been known that TSEs will transfer across species boundaries. The reason for this was never known until the genetic nature of the prion gene was fully investigated and found to be involved. The gene is found to have well preserved sites and as such there is a similar gene throughout the animal kingdom...and indeed a similar gene is found in insects! It is NOT clear that the precise close nature of the PrP gene structure is essention for low species barriers. Indeed it is probably easier to infect cats with BSE than it is to infect sheep. As such it is not clear that simply because it is possible to infect BSE from cattle into certain monkeys then other apes will necessarily be infectable with the disease. One factor has stood out, however, and that is that BSE, when inoculated into mice would retain its apparent nature of disease strain, and hence when it was inoculated back into cattle, then the same disease was produced. Similarly if the TSE from kudu was inoculated into mice then a similar distribution of disease in the brain of the mouse is seen as if BSE had been inoculated into the mouse. This phenomenon was not true with scrapie, in which the transmission across a species barrier was known to lose many of the scrapie strain phenomena in terms of incubation period or disease histopathology. This also suggested that BSE was not derived from scrapie originally but we probably will never know.
------------------------------------------------------------------------
TSE in wild UK deer? The first case of BSE (as we now realise) was in a nyala in London zoo and the further zoo cases in ungulates were simply thought of as being interesting transmissions of scrapie initially. The big problem started to appear with animals in 1993-5 when it became clear that there was an increase in the CJD cases in people that had eaten deer although the statistics involved must have been questionable. The reason for this was that the CJD Surveillance was well funded to look into the diet of people dying of CJD. This effect is not clear with vCJD...if only because the numbers involved are much smaller and hence it is difficult to gain enough statistics. They found that many other foods did not appear to have much association at all but that deer certainly did and as years went by the association actually became clearer. The appearance of vCJD in 1996 made all this much more difficult in that it was suddenly clearer that the cases of sporadic CJD that they had been checking up until then probably had nothing to do with beef...and the study decreased. During the period there was an increasing worry that deer were involved with CJD..
see references:
DEER BRAIN SURVEY
1993 cjd report finds relationship with eat venison and cjd increases 9 fold, let the cover up begin...tss
FINDINGS
*** 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 ;
GAME FARM INDUSTRY WANTS TO COVER UP FINDINGS OF INCREASE RISK TO CJD FROM CERVID
BSE INQUIRY
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.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
Management In Confidence
BSE: Private Submission of Bovine Brain Dealler
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Fri, 18 Oct 2002 23:12:22 +0100
From: Steve Dealler
Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ References: <3daf5023 .4080804="" a="" href="http://wt.net/" nbsp="" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">wt.net
Dear Terry,
An excellent piece of review as this literature is desparately difficult to get back from Government sites.
What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!
Steve Dealler
Stephen Dealler is a consultant medical microbiologist deal@airtime.co.uk
===============
https://caninespongiformencephalopathy.blogspot.com/2010/03/canine-spongiform-encephalopathy-aka.html
*** 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 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 peer 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
new url;
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 su
***> 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. <***Transmission of scrapie prions to primate after an extended silent incubation periodEmmanuel 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 Scientific Reports volume 5, Article number: 11573 (2015) | Download CitationAbstractClassical 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...
Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. 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.The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.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.O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populationsEmmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, FrancePrion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),***is the third potentially zoonotic PD (with BSE and L-type BSE),***thus questioning the origin of human sporadic cases.We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.===============***thus questioning the origin of human sporadic cases***===============***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.==============***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.PRION 2016 TOKYOSaturday, April 23, 2016SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X onlineTaylor & FrancisPrion 2016 Animal Prion Disease Workshop AbstractsWS-01: Prion diseases in animals and zoonotic potentialJuan 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. FranceDietary 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. BRADLEYTitle: Transmission of scrapie prions to primate after an extended silent incubation period)*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.WEDNESDAY, JULY 19, 2017USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE and BANNED FEED USDA Detects a Case of Atypical Bovine Spongiform Encephalopathy in AlabamaUSDA Animal and Plant Health Inspection Service sent this bulletin at 07/18/2017 07:05 PM EDTUSDA Detects a Case of Atypical Bovine Spongiform Encephalopathy in AlabamaWashington, D.C., July 18, 2017 – The U.S. Department of Agriculture (USDA) announced an atypical case of Bovine Spongiform Encephalopathy (BSE), a neurologic disease of cattle, in an eleven-year old cow in Alabama. This animal never entered slaughter channels and at no time presented a risk to the food supply, or to human health in the United States.snip...endTUESDAY, AUGUST 7, 2018Unexpected prion phenotypes in experimentally transfused animals: predictive models for humans?
WEDNESDAY, JUNE 19, 2019
Experts urge immediate action to contain the epidemic Chronic Wasting Disease CWD TSE Prion
Content current as of: 03/23/2018
USDA has tested 20,000 animals annually for each of the last 2 years, and approximately 75 percent of these were downers at slaughter. A BSE risk assessment performed by Harvard University's Center for Risk Analysis at the School of Public Health concluded that even if BSE were to occur in the US the measures already taken would largely prevent its spread to animals or humans, and the disease would gradually disappear over a number of years.
seems if you go search the bse mad cow feed excel spread sheet, some of the old OAI violations might have been purged or changed, i don't understand this?
search OAI;
now see from my older records;
2017 Section 21 C.F.R. 589.2000, Animal Proteins Prohibited in Ruminant Feed
Subject: MICHIGAN FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE BREACH APRIL 4, 2017
MICHIGAN FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE BREACH APRIL 4, 2017
FDA BSE/Ruminant Feed Inspections Firms Inventory
11998 DET-DO MI 48846-847 OPR 4/4/2017 OAI
NAI = NO ACTION INDICATED
OAI = OFFICIAL ACTION INDICATED
VAI = VOLUNTARY ACTION INDICATED
RTS = REFERRED TO STATE
OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions...end...TSS
SEE MASSIVE TONNAGE OF BANNED FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS PRODUCT IN COMMERCE SINCE AUGUST 1997. THE MAD COW FEED BAN WAS AND IS STILL NOTHING BUT INK ON PAPER...TERRY
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
TUESDAY, JANUARY 17, 2017
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION
Inspection Information
- Report of Inspection for Compliance with 21 CFR 589.2000 (CVM) (PDF - 1.8MB)
- FDA BSE/Ruminant Feed Inspections Firms Inventory
- FDA BSE/Ruminant Feed Inspections Firms Inventory (excel format)
Comment
APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission
Greetings APHIS et al, I would kindly like to comment on APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], and my comments are as follows, with the latest peer review and transmission studies as references of evidence. THE OIE/USDA BSE Minimal Risk Region MRR is nothing more than free pass to import and export the Transmissible Spongiform Encephalopathy TSE Prion disease. December 2003, when the USDA et al lost it's supposedly 'GOLD CARD' ie BSE FREE STATUS (that was based on nothing more than not looking and not finding BSE), once the USA lost it's gold card BSE Free status, the USDA OIE et al worked hard and fast to change the BSE Geographical Risk Statuses i.e. the BSE GBR's, and replaced it with the BSE MRR policy, the legal tool to trade mad cow type disease TSE Prion Globally. The USA is doing just what the UK did, when they shipped mad cow disease around the world, except with the BSE MRR policy, it's now legal. Also, the whole concept of the BSE MRR policy is based on a false pretense, that atypical BSE is not transmissible, and that only typical c-BSE is transmissible via feed. This notion that atypical BSE TSE Prion is an old age cow disease that is not infectious is absolutely false, there is NO science to show this, and on the contrary, we now know that atypical BSE will transmit by ORAL ROUTES, but even much more concerning now, recent science has shown that Chronic Wasting Disease CWD TSE Prion in deer and elk which is rampant with no stopping is sight in the USA, and Scrapie TSE Prion in sheep and goat, will transmit to PIGS by oral routes, this is our worst nightmare, showing even more risk factors for the USA FDA PART 589 TSE PRION FEED ban. The FDA PART 589 TSE PRION FEED ban has failed terribly bad, and is still failing, since August 1997. there is tonnage and tonnage of banned potential mad cow feed that went into commerce, and still is, with one decade, 10 YEARS, post August 1997 FDA PART 589 TSE PRION FEED ban, 2007, with 10,000,000 POUNDS, with REASON, Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. you can see all these feed ban warning letters and tonnage of mad cow feed in commerce, year after year, that is not accessible on the internet anymore like it use to be, you can see history of the FDA failure August 1997 FDA PART 589 TSE PRION FEED ban here, but remember this, we have a new outbreak of TSE Prion disease in a new livestock species, the camel, and this too is very worrisome. WITH the OIE and the USDA et al weakening the global TSE prion surveillance, by not classifying the atypical Scrapie as TSE Prion disease, and the notion that they want to do the same thing with typical scrapie and atypical BSE, it's just not scientific. WE MUST abolish the BSE MRR policy, go back to the BSE GBR risk assessments by country, and enhance them to include all strains of TSE Prion disease in all species. With Chronic Wasting CWD TSE Prion disease spreading in Europe, now including, Norway, Finland, Sweden, also in Korea, Canada and the USA, and the TSE Prion in Camels, the fact the the USA is feeding potentially CWD, Scrapie, BSE, typical and atypical, to other animals, and shipping both this feed and or live animals or even grains around the globe, potentially exposed or infected with the TSE Prion. this APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], under it's present definition, does NOT show the true risk of the TSE Prion in any country. as i said, it's nothing more than a legal tool to trade the TSE Prion around the globe, nothing but ink on paper. AS long as the BSE MRR policy stays in effect, TSE Prion disease will continued to be bought and sold as food for both humans and animals around the globe, and the future ramifications from friendly fire there from, i.e. iatrogenic exposure and transmission there from from all of the above, should not be underestimated. ... https://bovineprp.blogspot.com/2019/06/aphis-concurrence-with-oie-risk.html Attachments(1)APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary... |
Terry S. Singeltary Sr.
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