USDA Scientists Have Been Put On Lockdown Under Trump
“Starting immediately and until further notice” the department’s main research division “will not release any public-facing documents,” according to an internal memo. UPDATE: The order was rescinded by the department on Tuesday.
Originally posted on Jan. 24, 2017, at 4:25 a.m. Updated on Jan. 24, 2017, at 1:00 p.m.
The US Department of Agriculture has banned scientists and other employees in its main research division from publicly sharing everything from the summaries of scientific papers to USDA-branded tweets as it starts to adjust to life under the Trump administration, BuzzFeed News has learned.
The ban was rescinded on Tuesday.
According to an email sent Monday morning and obtained by BuzzFeed News, the department told staff — including some 2,000 scientists — at the agency’s main in-house research arm, the Agricultural Research Service (ARS), to stop communicating with the public about taxpayer-funded work.
“Starting immediately and until further notice, ARS will not release any public-facing documents,” Sharon Drumm, chief of staff for ARS, wrote in a department-wide email shared with BuzzFeed News.
“This includes, but is not limited to, news releases, photos, fact sheets, news feeds, and social media content,” she added. Indeed, the last tweet from ARS’s official account was sent the day before Trump’s inauguration on Jan. 20.
Though the terse internal note did not explicitly mention the new presidential administration, department scientists around the country interpreted it as a message from Trump that changes were coming to the department. The memo was also met with some confusion. When asked if the notice constituted a halt on the publication of academic articles, one regional director told scientists that research papers could be published in academic journals and presented at conferences, but that all media interviews must be approved by the office of communications in Washington.
In a statement on Tuesday to BuzzFeed News, the department acknowledged sending an internal email that halted the release of “informational products like news releases and social media content” on Monday. “Scientific publications, released through peer reviewed professional journals are not included,” he added.
“As the U.S. Department of Agriculture’s chief scientific in-house research agency, ARS values and is committed to maintaining the free flow of information between our scientists and the American public as we strive to find solutions to agricultural problems affecting America,” Christopher Bentley, a spokesperson for ARS, said in the statement.
Though some Agricultural Research Service work touches on sensitive subjects like pesticides and genetically modified food, its research is generally less politically charged than that conducted by other agencies, especially those focused on understanding climate change, such as the Environmental Protection Agency. But under the Obama administration, the Agriculture Department funneled research money into finding ways of cutting down the release of methane, a potent greenhouse gas, from cows.
The nomination of former Gov. Sonny Perdue of Georgia as agriculture secretary puts the fate of that and other department research touching on climate change into question. Like President Trump himself, Perdue has in the past bucked the overwhelming consensus among climate scientists that Earth’s atmosphere and oceans are warming due to human activity.
“It’s become a running joke among the public,” Perdue wrote in the National Review in 2014, “and liberals have lost all credibility when it comes to climate science because their arguments have become so ridiculous and so obviously disconnected from reality.”
Other agencies are under lockdown as well since Trump moved into the White House. Employees at the National Park Service were told to stop tweeting from official park accounts. The Trump administration has also imposed a freeze on grants and contracts from the EPA, the Huffington Post and ProPublica reported on Monday. The EPA, too, is no longer issuing press releases or posting on social media, according to the reports.
USDA scrambles to ease concerns after researchers were ordered to stop publishing news releases
By Jose A. DelReal January 24 at 6:42 PM
Employees of the scientific research arm at the Agriculture Department were ordered Monday to cease publication of “outward facing” documents and news releases, raising concerns that the Trump administration was seeking to influence distribution of their findings.
Department officials scrambled to clarify the memo Tuesday afternoon, after intense public scrutiny and media requests, stating that the Agricultural Research Service (ARS) had not “blacked out public information” and adding that scientific articles published through professional peer-reviewed journals have not been banned. Such a decree would have conflicted with established scientific integrity standards and previous media guidance “encouraging, but not requiring, USDA scientists to communicate with the media about their scientific findings.”
The memo's shortness and terse language seems to have exacerbated the confusion: “Starting immediately and until further notice, ARS will not release any public-facing documents. This includes, but is not limited to, news releases, photos, fact sheets, news feeds, and social media content,” wrote ARS chief Sharon Drumm in an email to employees.
The ARS guidance was not issued in coordination with other offices at the USDA, department officials said, and partially contradicted a department-wide memo that went out on the same day. The USDA-wide memo, issued by the department's acting deputy administrator, Michael Young, was intended to offer guidance on “interim procedures” until a new secretary takes over USDA.
Young stressed during a phone call with reporters Tuesday evening that his guidance does not place a gag order on publication to scientific journals, does not place a blanket freeze on press releases, or prohibit food safety announcements.
“The ARS guidance was not reviewed by me. I would not have put that kind of guidance out. My guidance has to do with policy-related announcement and that sort of thing,” Young said during a phone call with reporters early Tuesday evening. “I had my memo drafted before the ARS memo, I was not a part of it.”
Young’s memo, a copy of which was given to The Washington Post, emphasizes that press releases and policy statements must be routed through the office of the secretary for approval: “In order for the Department to deliver unified, consistent messages, it's important for the Office of the Secretary to be consulted on media inquiries and proposed response to questions related to legislation, budgets, policy issues, and regulations,” said the memo. “Policy-related statements should not be made to the press without notifying and consulting the Office of the Secretary. That includes press releases and on and off the record conversations.”
Young stressed that he is a “career official,” not a partisan appointee, and said that the memo he issued closely mirrored one sent at the beginning of the Obama administration. He also said he shared the memo with Trump transition official Sam Clovis before issuing it.
“This is really just formalizing again what is fairly standard practice within the department. I just felt like, yeah, I want to be cautious because I don’t want any surprises on my watch. I was trying to avoid any surprises,” he said.
The Agricultural Research Service employs thousands of in-house scientists, maintains scores of research locations around the country and boasts a $1 billion budget. It is tasked with conducting research to “develop and transfer solutions to agricultural problems of high national priority,” according to the USDA. That research focuses on topics such as food safety, nutrition, animal and crop production, and agricultural sustainability.
Research publicized on the USDA's website this month includes papers such as “Helping Arizona Wheat Growers Maximize Resources” and “Test Uses Novel Antibodies to Detect Shiga Toxins.”
The “public-facing documents” memo Monday, which was first reported by BuzzFeed, raised fears that the new Trump administration was attempting to filter articles about ongoing scientific research being conducted by ARS.
The ARS sought to ease those concerns Tuesday afternoon. Young also said Tuesday evening that he had spoken with ARS and suggested he might support clarifying or rescinding the research agency’s confusing guidance.
“As the U.S. Department of Agriculture’s chief scientific in-house research agency, ARS values and is committed to maintaining the free flow of information between our scientists and the American public as we strive to find solutions to agricultural problems affecting America,” ARS said in a statement to The Post Tuesday afternoon, seeking to clarify the scope of the memo.
USDA and ARS have issued media guidance in the past. Under the Obama administration, guidance published in 2013 stipulated that USDA employees should clear any “media inquiries on topics that are sensitive” with public affairs staffers. That media guidance, which appeared to have been last updated in 2016, also urges them to communicate with supervisors about “any instances where they feel public affairs or communications staff is stifling their ability to communicate about their work.”
The USDA does not yet have a permanent department head. Former Georgia governor Sonny Perdue was nominated by President Trump to head the USDA last week but has not yet begun the confirmation process. The congressional committee overseeing his hearing has not given guidance on when his hearing will take place, pending his submission of necessary paperwork.
Tue Jan 24, 2017 | 6:30pm EST USDA disavows gag-order emailed to scientific research unit The U.S. Department of Agriculture said on Tuesday that an internal email sent to staff at its Agricultural Research Service unit this week calling for a suspension of “public-facing documents,” including news releases and photos, was flawed and that new guidance has been sent out to replace it.
The ARS focuses on scientific research into the main issues facing agriculture, including long-term climate change. President Donald Trump has cast doubt on whether man-made climate change is real and has railed against ex-President Barack Obama's efforts to combat it.
"This internal email was released without Departmental direction, and prior to Departmental guidance being issued," USDA said in a statement. "ARS will be providing updated direction to its staff."
It said peer-reviewed scientific papers from the unit should not be blocked. "ARS values and is committed to maintaining the free flow of information between our scientists and the American public."
The original email, sent Jan. 23, said: "Starting immediately and until further notice, ARS will not release any public-facing documents. This includes, but is not limited to, news releases, photos, fact sheets, news feeds, and social media content."
USDA officials said that after the email was sent, acting USDA Deputy Secretary Michael L. Young sent out a three-page memo to USDA agency department heads and other key agency officials outlining the interim procedures staff should follow.
A copy of the interim procedures memo, dated Jan. 23 and seen by Reuters, shows many of the steps reflect either the same or similar measures taken by the previous administration. Reuters also saw a memo, dated Jan. 22, 2009, that was sent to agency officials by former Agriculture Secretary Tom Vilsack.
The 2017 memo, however, differs in two main areas.
It centralizes the agency’s media inquiries and social media presence through the Office of the Secretary. As part of that, the memo asks USDA agencies to “review their websites, blog posts and other social media and, consistent with direction you will receive from the Office of Communication, remove references to policy priorities and initiatives of the previous Administration.”
It also rescinds the ability of USDA agencies to close an office or notify local delegations of office closures.
(Reporting by P.J. Huffstutter; Writing by Richard Valdmanis; Editing by Leslie Adler)
Disturbing to say the least, very disturbing. please let me explain...
Nature 485, 279–280 (17 May 2012) doi:10.1038/485279b
Published online 16 May 2012
2012-05-16 05:31 AM Terry S. Singeltary Sr. said: I kindly wish to submit the following please ;
ONE need not look any further than the USDA et al, when it comes to ?undue influence?.
I have followed the mad cow USDA debacle ever since the first mad cow was covered up in Texas, let alone the second one that finally took and act of congress and the Honorable Phyllis Fong of the OIG. if not for that, that second mad cow in Texas would have never been confirmed either. then you can move on to the Alabama, and Washington mad cow, and not much has changed since. Still the same old USDA et al. just look at the atypical L-type BASE BSE case in California recently, and the false and misleading statements there from by the USDA et al. NOTHING has changed, except their stories, time and time again. They claim of all those firewalls in place, BSE surviellance, BSE testing, BSE feed ban, all three of those firewalls have failed terribly in the USA, but yet to hear the USDA et al tell it, everything is O.K., no problem, feed ban in place since August 4, 1997, BUT YET, the USDA et al fail to tell you, this mad cow firewall was nothing than ink on paper, it was a PARTIAL AND VOLUNTARY feed ban to begin with, that up until 2006, the amounts of banned suspect mad cow protein that was going into commerce, was measured in TONNAGE, 2007, the measurements were measured in POUNDS, where in 2007, 10 years, one decade, post partial, and voluntary BSE feed ban, there were 10,000,000 MILLION POUNDS, of banned, suspect mad cow protein, mixed with blood, that went out into commerce. AFTER that mad cow warning letter, the warning letters ceased to exist. they never published anymore that I could find. They claim the BSE testing was doing it?s job, until they found out that not only their testing techniques were wrong, but they were TESTING HEALTHY CATTLE, THEY NEW DID NOT HAVE BSE. all this again proven by the OIE and the GAO. They claim the BSE surveillance program worked, again, a lie. Just look at the GAO and OIE reports about that ENHANCED BSE SURVEILLANCE PROGRAM to test only healthy cows, OR, the OBEX ONLY DIAGNOSTIC criteria that was used. They claim NO link to sporadic CJD, and this is false as well. IN my opinion, until we get corporate industry out of policy decision making for the USDA, APHIS, FSIS, FDA et al, until that is changed, you will never have any sound science policy making for consumer safety. they call it GREED $$$ SOURCE REFERENCES MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...
***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model
***Infectivity in skeletal muscle of BASE-infected cattle
***feedstuffs- It also suggests a similar cause or source for atypical BSE in these countries.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans.
Friday, May 11, 2012
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits
***In addition, the present data will support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE.
please see my full full source reference list here ;
Wednesday, May 16, 2012
Independent experts should be kept from undue suspicion as well as undue influence
IN REPLY TO ;
Nature 485, 279–280 (17 May 2012) doi:10.1038/485279b
Published online 16 May 2012
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)
where would we be today with sound science, from where we were 30 years ago, if not for the cloak of secrecy and save the industry at all cost mentality?
when you have a peer review system for science, from which a government constantly circumvents, then you have a problem with science, and humans die.
Professor Collinge et al, and others, have had troubles in the past with the Government meddling in scientific findings, that might in some way involve industry, never mind human and or animal health.
FOR any government to continue to circumvent science for monetary gain, fear factor, or any reason, shame, shame on you.
snip...see full Singeltary Nature comment here;
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
>>> The only tenable public line will be that "more research is required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
ARS RESEARCH TSE PRION AKA MAD COW TYPE DISEASE
Friday, August 14, 2015
Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation
ARS VIRUS AND PRION RESEARCH / Research / Publication #277212
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation
item Greenlee, Justin item Nicholson, Eric item Smith, Jodi item Kunkle, Robert item Hamir, Amirali
Submitted to: Journal of Veterinary Diagnostic Investigation Publication
Type: Peer Reviewed Journal Publication Acceptance
Date: July 12, 2012
Publication Date: November 1, 2012
Citation: Greenlee, J.J., Nicholson, E.M., Smith, J.D., Kunkle, R.A., Hamir, A.N. 2012.
Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation.
Journal of Veterinary Diagnostic Investigation. 24(6):1087-1093.
Interpretive Summary: Chronic Wasting Disease (CWD), a fatal neurodegenerative disease that occurs in farmed and wild cervids (deer and elk) of North America, is a transmissible spongiform encephalopathy (TSE). TSEs are caused by infectious proteins called prions that are resistant to various methods of decontamination and environmental degradation. Cattle could be exposed to chronic wasting disease (CWD) by contact with infected farmed or free-ranging cervids. The purpose of this study was to assess the potential transmission of CWD from elk to cattle after intracranial inoculation, the most direct route to test the potential of a host to replicate an isolate of the prion agent. This study reports that only 2 of 14 calves inoculated with CWD from elk had clinical signs or evidence of abnormal prion protein accumulation. These results suggest that cattle are unlikely to be susceptible to CWD if inoculated by a more natural route. This information could have an impact on regulatory officials developing plans to reduce or eliminate TSEs and farmers with concerns about ranging cattle on areas where CWD may be present.
***Cattle could be exposed to the agent of chronic wasting disease (CWD) through contact with infected farmed or free-ranging cervids or exposure to contaminated premises. The purpose of this study was to assess the potential for CWD derived from elk to transmit to cattle after intracranial inoculation. Calves (n=14) were inoculated with brain homogenate derived from elk with CWD to determine the potential for transmission and define the clinicopathologic features of disease.
Cattle were necropsied if clinical signs occurred or at the termination of experiment (49 months post-inoculation (MPI)).
Clinical signs of poor appetite, weight loss, circling, and bruxism occurred in two cattle (14%) at 16 and 17 MPI, respectively.
Accumulation of abnormal prion protein (PrP**Sc) in these cattle was confined to the central nervous system with the most prominent immunoreactivity in midbrain, brainstem, and hippocampus with lesser immunoreactivity in the cervical spinal cord.
*** The rate of transmission was lower than in cattle inoculated with CWD derived from mule deer (38%) or white-tailed deer (86%).
Additional studies are required to fully assess the potential for cattle to develop CWD through a more natural route of exposure, but a low rate of transmission after intracranial inoculation suggests that risk of transmission through other routes is low.
***A critical finding here is that if CWD did transmit to exposed cattle, currently used diagnostic techniques would detect and differentiate it from other prion diseases in cattle based on absence of spongiform change, distinct pattern of PrP**Sc deposition, and unique molecular profile.
Monday, April 04, 2016
*** Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle ***
Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies Location: Virus and Prion Diseases of Livestock
Title: TRANSMISSION OF CHRONIC WASTING DISEASE AGENT OF MULE DEER (CWD**MD) TO SUFFOLK SHEEP BY INTRACEREBRAL ROUTE
Authors Hamir, Amirali Kunkle, Robert Cutlip, Randall - ARS RETIRED Miller, Janice - ARS RETIRED Williams, Elizabeth - UNIVERSITY OF WYOMING Richt, Juergen Submitted to: European Society of Veterinary Pathology
Publication Type: Abstract Publication Acceptance Date: June 5, 2006 Publication Date: August 31, 2006
Citation: Hamir, A., Kunkle, R., Cutlip, R., Miller, J., Williams, E., Richt, J. 2006.
Transmission of chronic wasting disease agent of mule deer (CWD**md) to Suffolk sheep by intracerebral route [abstract]. European Society of Veterinary Pathology 24th Annual Meeting. Paper No. P63. p. 171-172.
Technical Abstract: Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) that has been identified in captive and free-ranging cervids in the U.S. since 1967. To determine the transmissibility of CWD to sheep, 8 Suffolk lambs [4 QQ and 4 QR at codon 171 of prion protein (PRNP) gene] were inoculated intracerebrally with a pooled brain suspension from 28 mule deer naturally affected with CWD (CWD**md). Two other lambs (1 QQ and 1 QR at codon 171 of the PRNP gene) were kept as non-inoculated controls. Within 36 months post inoculation (MPI), 2 animals became sick and were euthanized. Only 1 sheep (euthanized at 35 MPI) showed clinical signs that were consistent with those described for scrapie. Microscopic lesions of spongiform encephalopathy (SE) were only seen in the sheep with the clinical signs of TSE and its tissues were positive for the abnormal prion protein (PrP**res) by immunohistochemistry and Western blot. Between 36 and 60 MPI, 3 other sheep were euthanized because of conditions unrelated to TSE. The remaining 3 sheep remained non-clinical at the termination of the study (72 MPI) and were euthanized at that time. One of the 3 animals revealed SE and its tissues were positive for PrP**res. Both sheep positive for PrP**res were homozygous QQ at codon 171. Retrospective examination of the PRNP genotype of the 2 TSE-positive animals revealed that the sheep with clinical prion disease (euthanized at 35 MPI) was heterozygous (AV) and the sheep with the sub-clinical disease (euthanized at 72 MPI) was homozygous (AA) at codon 136 of the PRNP. These findings demonstrate that transmission of the CWD**md agent to sheep via the intracerebral route is possible. Interestingly, the host genotype may play a significant part in successful transmission and incubation period of CWD**md.
Transmission of chronic wasting disease of mule deer to Suffolk sheep following intracerebral inoculation
Amir N. Hamir,1 Robert A. Kunkle, Randall C. Cutlip, Janice M. Miller, Elizabeth S. Williams, Juergen A. Richt
Abstract. To determine the transmissibility of chronic wasting disease (CWD) to sheep, 8 Suffolk lambs of various prion protein genotypes (4 ARQ/ARR, 3 ARQ/ARQ, 1 ARQ/VRQ at codons 136, 154, and 171, respectively) were inoculated intracerebrally with brain suspension from mule deer with CWD (CWDmd). Two other lambs were kept as noninoculated controls. Within 36 months postinoculation (MPI), 2 inoculated animals became sick and were euthanized. Only 1 sheep (euthanized at 35 MPI) showed clinical signs that were consistent with those described for scrapie. Microscopic lesions of spongiform encephalopathy (SE) were only seen in this sheep, and its tissues were determined to be positive for the abnormal prion protein (PrPres) by immunohistochemistry and Western blot. Three other inoculated sheep were euthanized (36 to 60 MPI) because of conditions unrelated to TSE. The 3 remaining inoculated sheep and the 2 control sheep did not have clinical signs of disease at the termination of the study (72 MPI) and were euthanized. Of the 3 remaining inoculated sheep, 1 was found to have SE, and its tissues were positive for PrPres. The sheep with clinical prion disease (euthanized at 35 MPI) was of the heterozygous genotype (ARQ/VRQ), and the sheep with subclinical disease (euthanized at 72 MPH) was of the homozygous ARQ/ARQ genotype. These findings demonstrate that transmission of the CWDmd agent to sheep via the intracerebral route is possible. Interestingly, the host genotype may play a notable part in successful transmission and incubation period of CWDmd. snip...
Thus far, among domestic animals, CWDmd has been transmitted by the intracerebral route to a goat18 and cattle.5–7 The present findings demonstrate that it is also possible to transmit CWDmd agent to sheep via the intracerebral route. However, the only sheep to develop clinical TSE within 35 MPI was genotypically AV at PRNP codon 136, suggesting that host genotype may play a notable part in successful transmission of the disease in this species. Although in Suffolk sheep the AV variant at codon 136 is very rare,17 selective breeding of Suffolk sheep with this codon has begun in the hope of testing this differential susceptibility hypothesis in a future study of CWDmd transmission to sheep. Key words: Chronic wasting disease; immunohistochemistry; intracerebral transmission; prion protein; sheep; spongiform encephalopathy.
Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies Location: Virus and Prion Diseases of Livestock
Title: EXPERIMENTAL SECOND PASSAGE OF CHRONIC WASTING DISEASE (CWD(MULE DEER)) AGENT TO CATTLE
Authors Hamir, Amirali Kunkle, Robert Miller, Janice - ARS RETIRED Greenlee, Justin Richt, Juergen Submitted to: Journal of Comparative Pathology Publication Type: Peer Reviewed Journal Publication Acceptance Date: July 25, 2005 Publication Date: January 1, 2006 Citation: Hamir, A.N., Kunkle, R.A., Miller, J.M., Greenlee, J.J., Richt, J.A. 2006.
Experimental second passage of chronic wasting disease (CWD(mule deer)) agent to cattle. Journal of Comparative Pathology. 134(1):63-69. Interpretive Summary: To compare the findings of experimental first and second passage of chronic wasting disease (CWD) in cattle, 6 calves were inoculated into the brain with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but the CWD agent was detected in their CNS tissues by 2 laboratory techniques (IHC and WB). These findings demonstrate that inoculated cattle amplify CWD agent but also develop clinical CNS signs without manifestation of microscopic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, namely, sheep scrapie. The current study confirms previous work that indicates that the diagnostic tests currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of microscopic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB.
Technical Abstract: To compare clinicopathological findings of first and second passage of chronic wasting disease (CWD) in cattle, a group of calves (n=6) were intracerebrally inoculated with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and lost weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but PrPres was detected in their CNS tissues by immunohistochemistry (IHC) and Western blot (WB) techniques. These findings demonstrate that intracerebrally inoculated cattle not only amplify CWD PrPres but also develop clinical CNS signs without manifestation of morphologic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, scrapie. The current study confirms previous work that indicates the diagnostic techniques currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of neuropathologic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB.
***These findings demonstrate that inoculated cattle amplify CWD agent but also develop clinical CNS signs without manifestation of microscopic lesions of SE.
*** Wednesday, September 21, 2011
Evidence for distinct CWD strains in experimental CWD in ferrets
Wednesday, October 12, 2011
White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation
Wednesday, July 06, 2011
Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation
Scrapie in swine: A diagnostic challenge
Justin J Greenlee1, Robert A Kunkle1, Jodi D Smith1, Heather W. Greenlee2
1National Animal Disease Center, US Dept. of Agriculture, Agricultural Research Service, United States; 2Iowa State University College of Veterinary Medicine A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested. Since swine can be fed rations containing ruminant derived components in the United States and many other countries, we conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Scrapie inoculum was a pooled 10% (w/v) homogenate derived from the brains of clinically ill sheep from the 4th passage of a serial passage study of the U.S scrapie agent (No. 13-7) through susceptible sheep that were homozygous ARQ at prion protein residues 136, 154, and 171, respectively. Pigs were inoculated intracranially (n=19) with a single 0.75 ml dose or orally (n=24) with 15 ml repeated on 4 consecutive days. Necropsies were done on a subset of animals at approximately six months post inoculation (PI), at the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of TSE until study termination at 80 months PI or when removed due to intercurrent disease (primarily lameness). Brain samples were examined by immunohistochemistry (IHC), western blot (WB), and enzyme-linked immunosorbent assay (ELISA). Brain tissue from a subset of pigs in each inoculation group was used for bioassay in mice expressing porcine PRNP.
At six-months PI, no evidence of scrapie infection was noted by any diagnostic method. However, at 51 months of incubation or greater, 5 animals were positive by one or more methods: IHC (n=4), WB (n=3), or ELISA (n=5). Interestingly, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study).
Swine inoculated with the agent of scrapie by the intracranial and oral routes do not accumulate abnormal prion protein (PrPSc) to a level detectable by IHC or WB by the time they reach typical market age and weight. However, strong support for the fact that swine are potential hosts for the agent of scrapie comes from positive bioassay from both intracranially and orally inoculated pigs and multiple diagnostic methods demonstrating abnormal prion protein in intracranially inoculated pigs with long incubation times.
Dr. Greenlee is Research Veterinary Medical Officer in the Virus and Prion Research Unit at the National Animal Disease Center, US Department of Agriculture, Agricultural Research Service. He applies his specialty in veterinary anatomic pathology to focused research on the intra- and interspecies transmission of prion diseases in livestock and the development of antemortem diagnostic assays for prion diseases. In addition, knockout and transgenic mouse models are used to complement ongoing experiments in livestock species. Dr. Greenlee has publications in a number of topic areas including prion agent decontamination, effects of PRNP genotype on susceptibility to the agent of sheep scrapie, characterization of US scrapie strains, transmission of chronic wasting disease to cervids and cattle, features of H-BSE associated with the E211 K polymorphism, and the development of retinal assessment for antemortem screening for prion diseases in sheep and cattle. Dr. Greenlee obtained his DVM degree and completed the PhD/residency program in Veterinary Pathology at Iowa State University. He is a Diplomate of the American College of Veterinary Pathologists.
***In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research, however, suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD is affecting wild and farmed cervid populations in endemic areas with some deer populations decreasing as a result.
Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle
Authors: Nicholas Haley1, Christopher Siepker2, Justin Greenlee3, Jürgen Richt4
VIEW AFFILIATIONS Affiliations: 1 1Midwestern Univerisity 2 2Kansas State University 3 3USDA, Agricultural Research Service 4 4Kansas State University
Published Ahead of Print: 31 March, 2016 Journal of General Virology doi: 10.1099/jgv.0.000438 Published Online: 31/03/2016
Chronic wasting disease (CWD) is a fatal neurodegenerative disease, classified as a prion disease or transmissible spongiform encephalopathy (TSE) similar to bovine spongiform encephalopathy (BSE). Cervids affected by CWD accumulate an abnormal protease resistant prion protein throughout the central nervous system (CNS), as well as in both lymphatic and excretory tissues - an aspect of prion disease pathogenesis not observed in cattle with BSE. Using seeded amplification through real time quaking induced conversion (RT-QuIC), we investigated whether the bovine host or prion agent was responsible for this aspect of TSE pathogenesis. We blindly examined numerous central and peripheral tissues from cattle inoculated with CWD for prion seeding activity. Seeded amplification was readily detected in the CNS, though rarely observed in peripheral tissues, with a limited distribution similar to that of BSE prions in cattle. This seems to indicate that prion peripheralization in cattle is a host-driven characteristic of TSE infection.
Sunday, January 22, 2012
Chronic Wasting Disease CWD cervids interspecies transmission
SATURDAY, JANUARY 14, 2017
CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL UPDATE JANUARY 14, 2017
Wednesday, December 21, 2016
TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2016 ANNUAL REPORT ARS RESEARCH
Monday, January 09, 2017
Oral Transmission of L-Type Bovine Spongiform Encephalopathy Agent among Cattle CDC Volume 23, Number 2—February 2017
SATURDAY, JUNE 12, 2010
PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical
Thursday, April 24, 2008
RE-FOIA OF DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E. OF FOREIGN ORIGIN IN THE UNITED STATES [Docket No. 00-072-1]
SATURDAY, FEBRUARY 27, 2010
FINAL REPORT OF THE TESTING OF THE BELGIAN (VERMONT) SHEEP February 27, 2010
Veterinary Laboratories Agency - Weybridge
New Haw, Addlestone, Surrey KT15 3NB United Kingdom
Telephone +44 (0)1932 341111 Facsimile +44 (0)1932 347046 '
Web site http://www.vla.gov.uk
Veterinary Laboratories Agency
Your ref: MPL-6197-7-37
Our ref: FT1294
This is the FINAL report for contract MPL-6197-7-37 The testing of the Belgian (Vermont) sheep.
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
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
Greetings BSE-L Members et al,
you can’t believe what I got in the US Postal mail today. the wife would not pick it up yesterday, because there was a $6.00 charge for a certified letter from USDA Kevin Shea for about 5 pages. I went to the PO today, told the girls in the back that if it’s an affidavit, a warrant, summons, I don’t want it, send it back. but it was certified. scared me. but the curiosity got to me, so i coughed up 6 bucks, and took a chance. low and behold, after my last appeal to this decade plus old quest was turned down, even though I already had the answer from another source, APHIS et al finally stumbled across those old mouse bio-assays. they had them all along.
what the industry sent me first was better, because it had some of the good stuff i.e. redacted.
this all started way back around the year 2,000, when in my opinion, the USDA et al let these sheep in the USA from Belgium, when they should not have because of atypical BSE in Belgium. I started asking for the these mouse bio-assays back in or around 2003 or before, then I had to get official with FOIA, because no one would answer my questions.
well, it’s February 20, 2015, over a decade later, and I don’t know how many denials, here’s what was in the mail yesterday, February 19, 2015 ;
United States Department of Agriculture
Animal and Plant Health Inspection Service Marketing and Regulatory Programs Animal and Plant Health Inspection Service Legislative and Public Affairs Freedom of Information 4700 River Road Unit 50 Riverdale, MD. 20737-1232
FEB 10 2015
Terry S. Singletary Sr. P.O. Box 42 Bacliff, Texas 77518
Re: FOIA Appeal # 2007-00030-A
Dear Mr. Singletary:
This letter is in response to the Freedom of Information Act (FOIA) appeal that you submitted regarding FOIA request 07-566. Your appeal challenged the APHIS FOIA Office's search for the "Mouse Bio-Assays" on the sheep imported from Belgium. We apologize for the delayed response.
The APHIS FOIA Office received your appeal, on July 7, 2007 and assigned it FOIA case number 2007-00030-A.
In response to your appeal, the APHIS FOIA Office performed a second search of records responsive to your initial request. The Agency has since found four (4) pages of responsive records for the "Mouse Bio-Assays" dated October 22,2009. Although these records postdate both your initial request and subsequent appeal by approximately two years; we enclose them in the interest of responsiveness to your request.
We now consider this appeal closed and will take no further action. If you are dissatisfied with this decision, you have the right to judicial review in an appropriate United States District Court in accordance with 5 U.S.C. 552, (2)(4)(B).
Prior to seeking judicial review, you may contact the Office of Government Information Services (OGlS). OGIS was created within the National Archives and Records Administration when the Open Government Act of 2007 amended the FOIA. OGIS provides mediation of FOIA disputes between appellants and federal agencies. Participation in mediation does not affect your right to judicial review. Contact information for OGIS can be found at http:/www.archives.gov/ogis.
Kevin Shea Administrator Enclosure
the next 4 pages is exactly what I received from an industry source way back on Saturday, February 27, 2010. see ;
Saturday, February 27, 2010
FINAL REPORT OF THE TESTING OF THE BELGIAN (VERMONT) SHEEP February 27, 2010
see history below ;
THURSDAY, MARCH 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL
SATURDAY, AUGUST 29, 2009
FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009
Since posting this recall below a few days ago ;
Thursday, August 27, 2009
MAD COW FEED RECALL 2009 Product may have contained prohibited materials (208,820 LBS. THAT COULD CONTAINED PRIONS...TSS) without cautionary statement Subject: 2009 Product may have contained prohibited materials (THAT COULD CONTAIN PRIONS...TSS) without cautionary statement on the label
PRODUCT Bulk Whole Barley, Recall # V-256-2009
CODE No code or lot number.
RECALLING FIRM/MANUFACTURER Mars Petcare US, Clinton, OK, by telephone on May 21, 2009. Firm initiated recall is complete.
REASON Product may have contained prohibited materials without cautionary statement on the label.
VOLUME OF PRODUCT IN COMMERCE 208,820 pounds
DISTRIBUTION TX END OF ENFORCEMENT REPORT FOR AUGUST 26, 2009
I saw this latest mad cow feed warning letter and notice a few changes. thought it looked a little fishy, so looking further i find it seems that now the FDA et al could not say mad cow or BSE, even if they had a mouth full of it, this is exactly what this warning letter recall is about, recalling potential mad cow feed, that might contain prions, that might get fed to cattle or other ruminants. this is the poorest i have seen yet on a warning letter with lack of information. compare it to the feed ban recall warning letter at the bottom. ALSO, This violator violations were so bad, they required an OAI on 05/28/2009, but you would not have noticed this by it's warning letter. SO, you have 208,820 pounds more of suspect mad cow feed IN COMMERCE, feeding to pets, or maybe cattle, who knows, no warning label on it.
NOTHING HAS CHANGED, IT'S ALL STILL VOLUNTARY BSe. ...
I reported this back on Saturday, June 13, 2009 ;
DAL-DO 3007064862 Mars Petcare US #1 Mars Road Clinton OK 73601 OPR PF HP 05/28/2009 OAI Y
An OAI inspection classification occurs when significant objectionable conditions or practices were found and regulatory sanctions are warranted in order to address the establishment's lack of compliance with the regulation. An example of an OAI inspection classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspections classified with OAI violations will be promptly re-inspected following the regulatory sanctions to determine whether adequate corrective actions have been implemented
see full text ;
Since posting this, i thought i might get the FDA to clarify this recall. NO CHANCE, TOP SECRET, MUST REQUEST FOIA ;
Thursday, September 3, 2009
429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
Friday, September 4, 2009
FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
C O N F I R M E D
----- Original Message -----
From: "Terry S. Singeltary Sr."
Sent: Thursday, November 05, 2009 9:25 PM
Subject: [BSE-L] re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited material Recall # V-258-2009 and Recall # V-256-2009
WHAT MAD COW FEED BAN ???
Tuesday, March 2, 2010
Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen Inc 2/11/10 USA
Monday, March 1, 2010
ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010
Terry S. Singeltary Sr. (Submitted question): Monday, April 5, 2010
Update on Feed Enforcement Activities to Limit the Spread of BSE April 5, 2010
*** TUESDAY, JANUARY 17, 2017 ***
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION
Monday, January 2, 2017
Bovine Spongiform Encephalopathy Induces Misfolding of Alleged Prion-Resistant Species Cellular Prion Protein without Altering Its Pathobiological Features
Articles, Neurobiology of Disease
WEDNESDAY, JANUARY 18, 2017
EU-approved rapid tests might underestimate bovine spongiform encephalopathy infection in goats
MONDAY, JANUARY 16, 2017
*** APHIS Bovine Spongiform Encephalopathy (BSE): Ongoing Surveillance Program Last Modified: Jan 5, 2017
SATURDAY, JULY 23, 2016
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
Thursday, December 08, 2016
USDA APHIS National Scrapie Eradication Program October 2016 Monthly Report Fiscal Year 2017 atypical NOR-98 Scrapie
THURSDAY, AUGUST 4, 2016
Secretary's Advisory Committee on Animal Health [Docket No. APHIS-2016-0046] TSE PRION DISEASE
[Federal Register Volume 81, Number 149 (Wednesday, August 3, 2[Notices][Pages 51176-51177] From the Federal Register Online via the Government Publishing Office [www.gpo.gov] [FR Doc No: 2016-18341]
***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.
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama
National Institute of Animal Health; Tsukuba, Japan
To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).
Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.
Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, 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.
P.170: Potential detection of oral transmission of H type atypical BSE in cattle using in vitro conversion
***P.170: Potential detection of oral transmission of H type atypical BSE in cattle using in vitro conversion
Sandor Dudas, John G Gray, Renee Clark, and Stefanie Czub Canadian Food Inspection Agency; Lethbridge, AB Canada
Keywords: Atypical BSE, oral transmission, RT-QuIC
The detection of bovine spongiform encephalopathy (BSE) has had a significant negative impact on the cattle industry worldwide. In response, governments took actions to prevent transmission and additional threats to animal health and food safety. While these measures seem to be effective for controlling classical BSE, the more recently discovered atypical BSE has presented a new challenge. To generate data for risk assessment and control measures, we have challenged cattle orally with atypical BSE to determine transmissibility and mis-folded prion (PrPSc) tissue distribution. Upon presentation of clinical symptoms, animals were euthanized and tested for characteristic histopathological changes as well as PrPSc deposition.
The H-type challenged animal displayed vacuolation exclusively in rostral brain areas but the L-type challenged animal showed no evidence thereof. To our surprise, neither of the animals euthanized, which were displaying clinical signs indicative of BSE, showed conclusive mis-folded prion accumulation in the brain or gut using standard molecular or immunohistochemical assays. To confirm presence or absence of prion infectivity, we employed an optimized real-time quaking induced conversion (RT-QuIC) assay developed at the Rocky Mountain Laboratory, Hamilton, USA.
Detection of PrPSc was unsuccessful for brain samples tests from the orally inoculated L type animal using the RT-QuIC. It is possible that these negative results were related to the tissue sampling locations or that type specific optimization is needed to detect PrPSc in this animal. We were however able to consistently detect the presence of mis-folded prions in the brain of the H-type inoculated animal. Considering the negative and inconclusive results with other PrPSc detection methods, positive results using the optimized RT-QuIC suggests the method is extremely sensitive for H-type BSE detection. This may be evidence of the first successful oral transmission of H type atypical BSE in cattle and additional investigation of samples from these animals are ongoing.
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.
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...
The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite its subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province! ...page 26.
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY
***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.***
Primate Biol., 3, 47–50, 2016 www.primate-biol.net/3/47/2016/ doi:10.5194/pb-3-47-2016 © Author(s) 2016. CC
Attribution 3.0 License.
Walter Bodemer German Primate Center, Kellnerweg 4, 37077 Göttingen, Germany Correspondence to: Walter Bodemer (email@example.com)
Received: 15 June 2016 – Revised: 24 August 2016 – Accepted: 30 August 2016 – Published: 7 September 2016
Most importantly, early signs of an altered circadian rhythm, sleep–wake cycle, and activity and body temperature were recorded in prion-infected animals. This experimental approach would have never been feasible in studies with human CJD cases. After 4–6 years animals developed clinical symptoms highly similar to those typical for CJD. Clinicians conﬁrmed how close the animal model and the human disease matched. Non-neuronal tissue like cardiac muscle and peripheral blood with abnormal, disease-related prion protein were detected in rhesus monkey tissues.
Molecular changes in RNA from repetitive Alu and BC200 DNA elements were identiﬁed and found to be targets of epigenetic editing mechanisms active in prion disease. To conclude, our results with the rhesus monkey model for prion disease proved to be a valid model and increased our knowledge of pathogenic processes that are distinctive to prion disease.
SEE FULL TEXT ;
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
***thus questioning the origin of human sporadic cases***
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
Saturday, April 23, 2016
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with ef?ciency comparable to that of cattle BSE. While the ef?ciency 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.
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Tuesday, July 21, 2009
Transmissible mink encephalopathy - review of the etiology
Saturday, December 01, 2007
Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model
Sunday, December 10, 2006
Transmissible Mink Encephalopathy TME
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
Wednesday, April 25, 2012
4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012
Thursday, October 22, 2015
Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened
Thursday, July 24, 2014
Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan.
*** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.
*** It also suggests a similar cause or source for atypical BSE in these countries. ***
see page 176 of 201 pages...tss
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
Wednesday, July 15, 2015
Additional BSE TSE prion testing detects pathologic lesion in unusual brain location and PrPsc by PMCA only, how many cases have we missed?
***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
censorship is a terrible thing!
Variant Creutzfeldt–Jakob Disease in a Patient with Heterozygosity at PRNP Codon 129
N Engl J Med 2017; 376:292-294January 19, 2017DOI: 10.1056/NEJMc1610003
Share: ArticleMetrics To the Editor:
Prions cause lethal neurodegenerative diseases in mammals and are composed of multichain assemblies of misfolded host-encoded cellular prion protein (PrP). A common polymorphism at codon 129 of the PrP gene (PRNP), where either methionine (M) or valine (V) is encoded, affects the susceptibility to prion disease, as well as the incubation period1 and clinical phenotype of prion disease. Human infection with the epizootic prion disease bovine spongiform encephalopathy resulted in variant Creutzfeldt–Jakob disease, which provoked a public health crisis in the United Kingdom and other regions. All definite cases of variant Creutzfeldt–Jakob disease to date have occurred in patients with the MM genotype at PRNP codon 129.1
A 36-year-old man was referred to the United Kingdom National Prion Clinic in August 2015 with personality change. Over a period of 9 months, he had become uncharacteristically irascible and had progressive episodic memory impairment, gait ataxia, and myoclonus. His score on the Mini–Mental State Examination was 25 (with scores ranging from 0 to 30 and higher scores indicating less impairment); clinical examination revealed extraocular eye-movement abnormalities, pyramidal and cerebellar signs, and multifocal myoclonus. Magnetic resonance imaging of the brain (Figure 1FIGURE 1 MRI of the Brain.) revealed restricted diffusion in the basal ganglia, hypothalami, insular cortexes, and medial thalami but not in the pulvinar nuclei.2 Examination of the cerebrospinal fluid for protein 14-3-3 was negative, as was a real-time quaking-induced conversion assay, although these two tests are known to have low sensitivity for variant Creutzfeldt–Jakob disease.3 His genotype at PRNP codon 129 was MV. During the following 6 months, the patient’s condition declined progressively, and severe dysphagia and agitation occurred shortly before his death in February 2016.
At autopsy, histologic examination of the brain revealed frequent florid and cluster plaques in cerebral and cerebellar cortexes, microvacuolar degeneration in neuropil, and immunostaining for abnormal PrP in a stellate pericellular and perivascular distribution. Minute amounts of protease-resistant PrP (PrPSc) were seen in lymphoid tissue of the spleen. Immunoblotting of brain homogenate revealed type 4 PrPSc (according to the London classification system), which is pathognomonic of variant Creutzfeldt–Jakob disease.4 (For more details, see the Supplementary Appendix, available with the full text of this letter at NEJM.org.)
This patient’s clinical features differed from those of typical variant Creutzfeldt–Jakob disease, and his neuroimaging features suggested a diagnosis of sporadic Creutzfeldt–Jakob disease. He did not meet the epidemiologic diagnostic criteria for probable or possible variant Creutzfeldt–Jakob disease,5 yet the results of the neuropathological examination and molecular strain typing were consistent with variant Creutzfeldt–Jakob disease. It remains uncertain whether this case marks the start of a second wave of variant Creutzfeldt–Jakob disease in persons with the MV genotype at PRNP codon 129 (the most common genotype in the United Kingdom), mirroring the long incubation periods seen in persons with the MV genotype who have other acquired prion diseases, notably kuru.1 This case emphasizes the importance of performing an autopsy and molecular strain typing in cases of prion disease to ascertain the prevalence of human prion disease related to bovine spongiform encephalopathy.
snip...see full text ;
>>> This patient’s clinical features differed from those of typical variant Creutzfeldt–Jakob disease, and his neuroimaging features suggested a diagnosis of sporadic Creutzfeldt–Jakob disease. He did not meet the epidemiologic diagnostic criteria for probable or possible variant Creutzfeldt–Jakob disease,5 yet the results of the neuropathological examination and molecular strain typing were consistent with variant Creutzfeldt–Jakob disease. <<<
Many more people could still die from mad cow disease in the UK
SHORT SHARP SCIENCE
By Debora MacKenzie
18 January 2017
It’s finally happened. Until now, vCJD – the deadly disease caused by infection with BSE, or “mad cow disease” – has struck only people with a certain genetic makeup. Now, for the first time, researchers have confirmed a case in someone with different genes – a finding that could mean we have been misdiagnosing a new wave of cases.
FRIDAY, JANUARY 20, 2017
Many more people could still die from mad cow disease in the UK
> Many more people could still die from mad cow disease in the UK
and elsewhere in the world...tss
31 March 2001
Like lambs to the slaughter
By Debora MacKenzie
FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer’s, but Singeltary was suspicious. The diagnosis didn’t fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.
Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight to the campaigners’ fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.
“This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie,” says team member Jean-Philippe Deslys of the French Atomic Energy Commission’s medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.
Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD...
Neurobiology Adaptation of the bovine spongiform encephalopathy agent to primates and comparison with Creutzfeldt- Jakob disease: Implications for human health
Corinne Ida Lasmézas*,, Jean-Guy Fournier*, Virginie Nouvel*, Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp, Jean-Jacques Hauw§, James Ironside¶, Moira Bruce, Dominique Dormont*, and Jean-Philippe Deslys* * Commissariat à l'Energie Atomique, Service de Neurovirologie, Direction des Sciences du Vivant/Département de Recherche Medicale, Centre de Recherches du Service de Santé des Armées 60-68, Avenue du Général Leclerc, BP 6, 92 265 Fontenay-aux-Roses Cedex, France; Hôpital Neurologique Pierre Wertheimer, 59, Boulevard Pinel, 69003 Lyon, France; § Laboratoire de Neuropathologie, Hôpital de la Salpêtrière, 83, Boulevard de l'Hôpital, 75013 Paris, France; ¶ Creutzfeldt-Jakob Disease Surveillance Unit, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, United Kingdom; and Institute for Animal Health, Neuropathogenesis Unit, West Mains Road, Edinburgh EH9 3JF, United Kingdom
Edited by D. Carleton Gajdusek, Centre National de la Recherche Scientifique, Gif-sur-Yvette, France, and approved December 7, 2000 (received for review October 16, 2000)
There is substantial scientific evidence to support the notion that bovine spongiform encephalopathy (BSE) has contaminated human beings, causing variant Creutzfeldt-Jakob disease (vCJD). This disease has raised concerns about the possibility of an iatrogenic secondary transmission to humans, because the biological properties of the primate-adapted BSE agent are unknown. We show that (i) BSE can be transmitted from primate to primate by intravenous route in 25 months, and (ii) an iatrogenic transmission of vCJD to humans could be readily recognized pathologically, whether it occurs by the central or peripheral route. Strain typing in mice demonstrates that the BSE agent adapts to macaques in the same way as it does to humans and confirms that the BSE agent is responsible for vCJD not only in the United Kingdom but also in France. The agent responsible for French iatrogenic growth hormone-linked CJD taken as a control is very different from vCJD but is similar to that found in one case of sporadic CJD and one sheep scrapie isolate. These data will be key in identifying the origin of human cases of prion disease, including accidental vCJD transmission, and could provide bases for vCJD risk assessment.
THURSDAY, JANUARY 19, 2017
Variant Creutzfeldt–Jakob Disease in a Patient with Heterozygosity at PRNP Codon 129
Creutzfeldt Jakob Disease CJD
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
Terry S. Singeltary Sr.