>Our Investigator reported a telephone discussion with Mr. Barry G.
>Companies, Inc. During this discussion Mr. Harrison, reportedly, claimed
>requirement. This claimed exemption is based on the fact the products
>pets. We cannot accept this claimed exemption because while some horses
>containing prohibited materials.
Perhaps you should pester FDA about this "loophole". Apparently, "pet food" does not have to bear the warning labels specified for food animals.
I can't see any serious objection to expanding the label requirement to ALL animal food, not just food animals.
Also, horses are "ruminants", so it's disturbing that they might escape the feed ban by being classified as "pets". Another good reason to extend the warning labels and regulation to all animal foods.
Perhaps you could submit a request for ruling to the FDA on this issue to propose amending the regulation to include all animal foods, including pet foods.
Robert A. LaBudde, PhD, PAS, Dpl. ACAFS e-mail: ral@lcfltd.com Least Cost Formulations, Ltd. URL: http://lcfltd.com/ 824 Timberlake Drive Tel: 757-467-0954 Virginia Beach, VA 23464-3239 Fax: 757-467-2947
From: "Todd M. Gerber"
> Reply-To: Bovine Spongiform Encephalopathy
Date: Fri, 17 Aug 2001 08:57:21 -0400 Content-Type: text/plain Parts/Attachments: Parts/Attachments text/plain (136 lines)
Reply Reply ######## Bovine Spongiform Encephalopathy #########
I have a neighbor who is a dairy farmer. He tells me that he knows of several farmers who feed their cattle expired dog food. These farmers are unaware of any dangers posed to their cattle from the pet food contents. For these farmers, the pet food is just another source of protein.
Todd Gerber
"Cook, Nancy" @UNI-KARLSRUHE.DE> on 08/16/2001 01:52:58 PM
Please respond to Bovine Spongiform Encephalopathy
Sent by: Bovine Spongiform Encephalopathy
To: BSE-L@UNI-KARLSRUHE.DE cc: Subject: Re: [BSE-L] MAD COW/HORSE FEED BAN VIOLATIONS WARNING LETTER July 20, 200 1
######## Bovine Spongiform Encephalopathy #########
Robert, just wanted to comment on your request that the "Do not feed to Cattle or other Ruminants" statement be placed on all animal feeds. In 1997, we undertook a broad, five city survey to determine what effect that statement might have in the marketplace if it occurred on pet food labels.
Overwhelmingly, and in all locations, an immediate and severe effect was projected, not only into pet food, but into the Meat Counter as well, as people struggled with the idea that "if it's not good for ruminants (whatever they are?), why should I feed it to my pets, and oh, by the way, why should I eat beef at all if it's a problem?"
The Office of Management and Budget agreed with our findings and advised FDA that the labeling was not needed on pet food for retail sale or for laboratory animal feed. However, salvage products are required to bear the statement, since those products are often used for swine feed.
In most states, pets are classified as dogs and cats. Specialty pets are other caged and "aquariumed" critters. Horses and rabbits are classified as livestock.
Hope this is helpful.
Nancy K. Cook Pet Food Institute 2025 M Street, Suite 800 Washington, DC 20036 202-367-1120 202-367-2120 (fax)
-----Original Message-----
From: Robert A. LaBudde [mailto:ral@LCFLTD.COM]
Sent: Tuesday, August 14, 2001 11:43 PM
To: BSE-L@UNI-KARLSRUHE.DE Subject:
Re: MAD COW/HORSE FEED BAN VIOLATIONS WARNING LETTER July 20, 2001
######## Bovine Spongiform Encephalopathy #########
At 01:41 PM 8/14/01 -0700, Terry wrote:
>DEPARTMENT OF HEALTH AND HUMAN SERVICE
> >July 20, 2001 >
>Our Investigator reported a telephone discussion with Mr. Barry G.
>Harrison who identified himself as the Corporate Counsel of the Farnam
>Companies, Inc. During this discussion Mr. Harrison, reportedly, claimed >the products in question are exempt from the cautionary statement
>requirement. This claimed exemption is based on the fact the products >are intended only for the equine market and your firm defines horses as
>pets. We cannot accept this claimed exemption because while some horses
>may be held as pets, horses are also working animals and in some parts
>of North America, food animals.
> >Based on our knowledge of working ranches, horse feed is often stored in
>the same general area as ruminant feed making a conspicuous cautionary
>statenmit vital on feeds and supplements,
>containing prohibited materials.
Terry:
Perhaps you should pester FDA about this "loophole". Apparently, "pet food" does not have to bear the warning labels specified for food animals.
I can't see any serious objection to expanding the label requirement to ALL animal food, not just food animals.
Also, horses are "ruminants", so it's disturbing that they might escape the feed ban by being classified as "pets". Another good reason to extend the warning labels and regulation to all animal foods.
Perhaps you could submit a request for ruling to the FDA on this issue to propose amending the regulation to include all animal foods, including pet foods.
================================================================ Robert A. LaBudde, PhD, PAS, Dpl. ACAFS e-mail: ral@lcfltd.com Least Cost Formulations, Ltd. URL: http://lcfltd.com/ 824 Timberlake Drive Tel: 757-467-0954 Virginia Beach, VA 23464-3239 Fax: 757-467-2947
"Vere scire est per causas scire" ================================================================
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
Subject: Re: MAD COW/HORSE FEED BAN VIOLATIONS WARNING LETTER July 20, 200 1
From: "Cook, Nancy"
Reply-To: Bovine Spongiform Encephalopathy
Date: Thu, 16 Aug 2001 13:52:58 -0400 Content-Type: text/plain Parts/Attachments: Parts/Attachments text/plain (98 lines)
Reply Reply ######## Bovine Spongiform Encephalopathy #########
Robert, just wanted to comment on your request that the "Do not feed to Cattle or other Ruminants" statement be placed on all animal feeds. In 1997, we undertook a broad, five city survey to determine what effect that statement might have in the marketplace if it occurred on pet food labels.
Overwhelmingly, and in all locations, an immediate and severe effect was projected, not only into pet food, but into the Meat Counter as well, as people struggled with the idea that "if it's not good for ruminants (whatever they are?), why should I feed it to my pets, and oh, by the way, why should I eat beef at all if it's a problem?"
The Office of Management and Budget agreed with our findings and advised FDA that the labeling was not needed on pet food for retail sale or for laboratory animal feed. However, salvage products are required to bear the statement, since those products are often used for swine feed.
In most states, pets are classified as dogs and cats. Specialty pets are other caged and "aquariumed" critters. Horses and rabbits are classified as livestock.
Hope this is helpful.
Nancy K. Cook Pet Food Institute 2025 M Street, Suite 800 Washington, DC 20036 202-367-1120 202-367-2120 (fax)
-----Original Message-----
From: Robert A. LaBudde [mailto:ral@LCFLTD.COM]
Sent: Tuesday, August 14, 2001 11:43 PM
To: BSE-L@UNI-KARLSRUHE.DE
Subject: Re: MAD COW/HORSE FEED BAN VIOLATIONS WARNING LETTER July 20, 2001
######## Bovine Spongiform Encephalopathy #########
At 01:41 PM 8/14/01 -0700, Terry wrote: >DEPARTMENT OF HEALTH AND HUMAN SERVICE > >July 20, 2001
>
>Our Investigator reported a telephone discussion with Mr. Barry G.
>Harrison who identified himself as the Corporate Counsel of the Farnam
>Companies, Inc. During this discussion Mr. Harrison, reportedly, claimed
>the products in question are exempt from the cautionary statement
>requirement. This claimed exemption is based on the fact the products
>are intended only for the equine market and your firm defines horses as
>pets. We cannot accept this claimed exemption because while some horses
>may be held as pets, horses are also working animals and in some parts
>of North America, food animals. > >Based on our knowledge of working ranches, horse feed is often stored in >the same general area as ruminant feed making a conspicuous cautionary
>statenmit vital on feeds and supplements, >containing prohibited materials.
Terry:
Perhaps you should pester FDA about this "loophole". Apparently, "pet food" does not have to bear the warning labels specified for food animals.
I can't see any serious objection to expanding the label requirement to ALL animal food, not just food animals.
Also, horses are "ruminants", so it's disturbing that they might escape the feed ban by being classified as "pets". Another good reason to extend the warning labels and regulation to all animal foods.
Perhaps you could submit a request for ruling to the FDA on this issue to propose amending the regulation to include all animal foods, including pet foods.
================================================================
Robert A. LaBudde, PhD, PAS, Dpl. ACAFS e-mail: ral@lcfltd.com Least Cost Formulations, Ltd. URL: http://lcfltd.com/ 824 Timberlake Drive Tel: 757-467-0954 Virginia Beach, VA 23464-3239 Fax: 757-467-2947
"Vere scire est per causas scire" ================================================================
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
Subject: Re: Americans sue FDA and CDC over reporting, blood, pork, CWD lo opholes
From: "Cook, Nancy"
Reply-To: Bovine Spongiform Encephalopathy
Date: Thu, 7 Jan 1999 15:27:58 -0500
Content-Type: text/plain Parts/Attachments: Parts/Attachments text/plain (60 lines) Reply Reply
Once again, it's interesting to note that the press does not (cannot, will not?) understand the difference between nv-CJD and CJD, especially when their sources find it in their best interest to allow confusion to continue and cause more confusion and worry. Nancy K. Cook Pet Food Institute
-----Original Message-----
From: tom [SMTP:tom@cyber-dyne.com]
Sent: Thursday, January 07, 1999 3:06 PM
To: Multiple recipients of list BSE-L Subject: Americans sue FDA and CDC over reporting, blood, pork, CWD loopholes
I posted the full test of both petitions with hot-linked index plus some associated press releases and newstories. They were filed yesterday by several citizens' groups and family members of CJD victims. By some reports it is the front page story on the international edition of USA Today. A summary says:
"The first legal petition demands that the U.S. Centers for Disease Control (CDC) aggressively look for CJD in humans and make CJD a reportable and monitored disease. This petition is also being filed in all fifty states with the appropriate state health officials.
The second legal petition demands that the Food and Drug Administration (FDA) close serious loopholes in U.S. animal feed regulations which currently allow types of cannibalistic feeding practices known to cause and spread 'mad cow' type diseases in animals and humans. For instance, current U.S. regulations allow calves to be fed milk replacer containing cattle blood protein, and pigs to be fed back to pigs and cattle. U.S. sheep infected with scrapie, a 'mad cow' type disease, can be used for pet and pig feed in the U.S.
Commenting on today's legal actions Bradley Miller, National Director of the Humane Farming Association stated, "TSEs represent a potentially devastating threat to both human and animal health. Our government's response to date has been shamefully inadequate. These legal actions provide a blueprint by which federal and state agencies can act decisively to prevent a TSE epidemic in this country."
Dr. Michael Hansen, Research Associate of Consumer's Union commented, "The current increase of TSEs in wildlife and humans shows that the time for effective prevention may be running out. The federal agencies must immediately take action to avert what could become a very significant public health problem."
Andrew Kimbrell, public interest attorney and Director of the Center for Food Safety stated, "Given what we know now, it is unconscionable that the CDC is not strictly monitoring this disease, and that the FDA is still allowing the feeding of blood and other animal by-products to animals. The federal agencies are obviously putting the interests of agribusiness companies ahead of their duty to protect the public from this terrible and fatal group of diseases. We will go to court if necessary to ensure that the agencies do their job in protecting human health and animal welfare."
tom
IN CONFIDENCE
SUSPECT BSE IN A HORSE
You will wish to be aware that on Thursday afternoon 25 June the T/DVO Powys received a phone call from a veterinary Surgeon reporting his suspicion that a horse had contracted BSE after having been fed cattle cake. The clinical symptoms described were similar to those shown by cattle there being a similar case some months ago on the same premises.
*** DEFRA TO SINGELTARY ON HOUND STUDY AND BSE 2001 ***
DEFRA Department for Environment, Food & Rural Affairs
Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904 6287 E-mail: h.mcdonagh.defra.gsi.gov.uk
GTN: FAX:
Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518
21 November 2001
Dear Mr Singeltary
TSE IN HOUNDS
Thank you for e-mail regarding the hounds survey. I am sorry for the long delay in responding.
As you note, the hound survey remains unpublished. However the Spongiform Encephalopathy Advisory Committee (SEAC), the UK Government's independent Advisory Committee on all aspects related to BSE-like disease, gave the hound study detailed consideration at their meeting in January 1994. As a summary of this meeting published in the BSE inquiry noted, the Committee were clearly concerned about the work that had been carried out, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.
Later, at their meeting in June 95, The Committee re-evaluated the hound study to see if any useful results could be gained from it. The Chairman concluded that there were varying opinions within the Committee on further work. It did not suggest any further transmission studies and thought that the lack of clinical data was a major weakness.
Overall, it is clear that SEAC had major concerns about the survey as conducted. As a result it is likely that the authors felt that it would not stand up to r~eer review and hence it was never published. As noted above, and in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether additional work should be performed to examine dogs for evidence of TSE infection. Although the Committee had mixed views about the merits of conducting further work, the Chairman noted that when the Southwood Committee made their recommendation to complete an assessment of possible spongiform disease in dogs, no TSEs had been identified in other species and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less
As this study remains unpublished, my understanding is that the ownership of the data essentially remains with the original researchers. Thus unfortunately, I am unable to help with your request to supply information on the hound survey directly. My only suggestion is that you contact one of the researchers originally involved in the project, such as Gerald Wells. He can be contacted at the following address.
Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, KT 15 3NB, UK
You may also wish to be aware that since November 1994 all suspected cases of spongiform encephalopathy in animals and poultry were made notifiable. Hence since that date there has been a requirement for vets to report any suspect SE in dogs for further investigation. To date there has never been positive identification of a TSE in a dog.
I hope this is helpful
Yours sincerely 4
HUGH MCDONAGH BSE CORRESPONDENCE SECTION
======================================
HOUND SURVEY
I am sorry, but I really could have been a co-signatory of Gerald's minute.
I do NOT think that we can justify devoting any resources to this study, especially as larger and more important projects such as the pathogenesis study will be quite demanding.
If there is a POLITICAL need to continue with the examination of hound brains then it should be passed entirely to the VI Service.
J W WILESMITH Epidemiology Unit 18 October 1991
Mr. R Bradley
cc: Mr. G A H Wells
3.3. Mr R J Higgins in conjunction with Mr G A Wells and Mr A C Scott would by the end of the year, indentify the three brains that were from the ''POSITIVE'' end of the lesion spectrum.
TSE in dogs have not been documented simply because OF THE ONLY STUDY, those brain tissue samples were screwed up too. see my investigation of this here, and to follow, later follow up, a letter from defra, AND SEE SUSPICIOUS BRAIN TISSUE SAF's. ...TSS
TSE & HOUNDS
GAH WELLS (very important statement here...TSS)
HOUND STUDY
AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.
snip...
76 pages on hound study;
snip...
The spongiform changes were not pathognomonic (ie. conclusive proof) for prion disease, as they were atypical, being largely present in white matter rather than grey matter in the brain and spinal cord. However, Tony Scott, then head of electron microscopy work on TSEs, had no doubt that these SAFs were genuine and that these hounds therefore must have had a scrapie-like disease. I reviewed all the sections myself (original notes appended) and although the pathology was not typical, I could not exclude the possibility that this was a scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian degeneration was also present in the white matter of the hounds, another feature of scrapie.
38.I reviewed the literature on hound neuropathology, and discovered that micrographs and descriptive neuropathology from papers on 'hound ataxia' mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had done much of this work, and I obtained original sections from hound ataxia cases from him. This enabled me provisionally to conclude that Robert Higgins had in all probability detected hound ataxia, but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination of single restricted microscopic fields that there was no distinction between the white matter vacuolation present in BSE and scrapie cases, and that occurring in hound ataxia and the hound survey cases.
39.Hound ataxia had reportedly been occurring since the 1930's, and a known risk factor for its development was the feeding to hounds of downer cows, and particularly bovine offal. Circumstantial evidence suggests that bovine offal may also be causal in FSE, and TME in mink. Despite the inconclusive nature of the neuropathology, it was clearly evident that this putative canine spongiform encephalopathy merited further investigation.
40.The inconclusive results in hounds were never confirmed, nor was the link with hound ataxia pursued. I telephoned Robert Higgins six years after he first sent the slides to CVL. I was informed that despite his submitting a yearly report to the CVO including the suggestion that the hound work be continued, no further work had been done since 1991. This was surprising, to say the very least.
41.The hound work could have provided valuable evidence that a scrapie-like agent may have been present in cattle offal long before the BSE epidemic was recognised. The MAFF hound survey remains unpublished.
Histopathological support to various other published MAFF experiments
42.These included neuropathological examination of material from experiments studying the attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice (RVC 1994).
It was thought likely that at least some, and probably all, of the cases in zoo animals were caused by the BSE agent. Strong support for this hypothesis came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and scrapie to mice: strain variation and species barrier. Philosophical Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation period and lesion profile in six strains of mice inoculated with brain homogenates from an affected kudu and the nyala, was similar to that seen when this panel of mouse strains was inoculated with brain from cattle with BSE. The affected zoo bovids were all from herds that were exposed to feeds that were likely to have contained contaminated ruminant-derived protein and the zoo felids had been exposed, if only occasionally in some cases, to tissues from cattle unfit for human consumption.
snip...
NEW URL ;
OR-09: Canine spongiform encephalopathy—A new form of animal prion disease
Monique David, Mourad Tayebi UT Health; Houston, TX USA
It was also hypothesized that BSE might have originated from an unrecognized sporadic or genetic case of bovine prion disease incorporated into cattle feed or even cattle feed contaminated with prion-infected human remains.1 However, strong support for a genetic origin of BSE has recently been demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2 Furthermore, a specific prion protein strain causing BSE in cattle is believed to be the etiological agent responsible for the novel human prion disease, variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in a number countries, including France, Italy, Ireland, the Netherlands, Canada, Japan, US and the UK with the largest number of cases. Naturally occurring feline spongiform encephalopathy of domestic cats4 and spongiform encephalopathies of a number of zoo animals so-called exotic ungulate encephalopathies5,6 are also recognized as animal prion diseases, and are thought to have resulted from the same BSE-contaminated food given to cattle and humans, although and at least in some of these cases, a sporadic and/or genetic etiology cannot be ruled out. The canine species seems to display resistance to prion disease and no single case has so far been reported.7,8 Here, we describe a case of a 9 week old male Rottweiler puppy presenting neurological deficits; and histological examination revealed spongiform vacuolation characteristic of those associated with prion diseases.9 Initial biochemical studies using anti-PrP antibodies revealed the presence of partially proteinase K-resistant fragment by western blotting. Furthermore, immunohistochemistry revealed spongiform degeneration consistent with those found in prion disease and displayed staining for PrPSc in the cortex.
Of major importance, PrPSc isolated from the Rottweiler was able to cross the species barrier transmitted to hamster in vitro with PMCA and in vivo (one hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100% attack rate (n = 4) and animals displayed untypical lesional profile and shorter incubation period.
In this study, we show that the canine species might be sensitive to prion disease and that PrPSc isolated from a dog can be transmitted to dogs and hamsters in vitro using PMCA and in vivo to hamsters.
If our preliminary results are confirmed, the proposal will have a major impact on animal and public health and would certainly lead to implementing new control measures for ‘canine spongiform encephalopathy’ (CSE).
2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation. PLoS Pathog 2008; 4:e1000156; PMID:18787697;
http://dx.doi.org/10.1371/journal. ppat.1000156.
3. Collinge J. Human prion diseases and bovine spongiform encephalopathy (BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662;
http://dx.doi.org/10.1093/ hmg/6.10.1699.
4. Wyatt JM, Pearson GR, Smerdon TN, Gruffydd-Jones TJ, Wells GA, Wilesmith JW. Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Vet Rec 1991; 129:233-6; PMID:1957458;
http://dx.doi.org/10.1136/vr.129.11.233.
6. Kirkwood JK, Wells GA, Wilesmith JW, Cunningham AA, Jackson SI. Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu (Tragelaphus strepsiceros). Vet Rec 1990; 127:418-20; PMID:2264242.
7. Bartz JC, McKenzie DI, Bessen RA, Marsh RF, Aiken JM. Transmissible mink encephalopathy species barrier effect between ferret and mink: PrP gene and protein analysis. J Gen Virol 1994; 75:2947-53; PMID:7964604;
http://dx.doi.org/10.1099/0022-1317- 75-11-2947.
8. Lysek DA, Schorn C, Nivon LG, Esteve-Moya V, Christen B, Calzolai L, et al. Prion protein NMR structures of cats, dogs, pigs, and sheep. Proc Natl Acad Sci U S A 2005; 102:640-5; PMID:15647367;
http://dx.doi.org/10.1073/pnas.0408937102.
=======================================
2013
Strain characteristics of the in vitro-adapted rabbit and dog BSE agent remained invariable with respect to the original cattle BSE prion, suggesting that the naturally low susceptibility of rabbits and dogs to prion infections should not alter their zoonotic potential if these animals became infected with BSE.
=======================================
Neurobiology of Disease
Bovine Spongiform Encephalopathy Induces Misfolding of Alleged Prion-Resistant Species Cellular Prion Protein without Altering Its Pathobiological Features
Enric Vidal3, Natalia Fernández-Borges1, Belén Pintado4, Montserrat Ordóñez3, Mercedes Márquez6, Dolors Fondevila5,6, Juan María Torres7, Martí Pumarola5,6, and Joaquín Castilla1,2 + Author Affiliations
1CIC bioGUNE, 48160 Derio, Bizkaia, Spain,
2IKERBASQUE, Basque Foundation for Science, 48011 Bilbao, Bizkaia, Spain,
3Centre de Recerca en Sanitat Animal, Campus de la Universitat Autònoma de Barcelona (UAB)-IRTA, 08193 Bellaterra, Barcelona, Spain,
4Centro Nacional de Biotecnología, Campus de Cantoblanco, 28049 Cantoblanco, Madrid, Spain,
5Department of Animal Medicine and Surgery, Veterinary Faculty, UAB, 08193 Bellaterra (Cerdanyola del Vallès), Barcelona, Spain,
6Murine Pathology Unit, Centre de Biotecnologia Animal i Teràpia Gènica, UAB, 08193 Bellaterra (Cerdanyola del Vallès), Barcelona, Spain, and
7Centro de Investigación en Sanidad Animal-Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, 28130 Valdeolmos, Madrid, Spain
Author contributions: E.V., N.F.-B., and J.C. designed research; E.V., N.F.-B., B.P., M.O., M.M., D.F., and J.C. performed research; E.V., N.F.-B., B.P., and J.C. contributed unpublished reagents/analytic tools; E.V., N.F.-B., B.P., M.O., M.M., D.F., J.M.T., M.P., and J.C. analyzed data; E.V. and J.C. wrote the paper.
Abstract
Bovine spongiform encephalopathy (BSE) prions were responsible for an unforeseen epizootic in cattle which had a vast social, economic, and public health impact. This was primarily because BSE prions were found to be transmissible to humans. Other species were also susceptible to BSE either by natural infection (e.g., felids, caprids) or in experimental settings (e.g., sheep, mice). However, certain species closely related to humans, such as canids and leporids, were apparently resistant to BSE. In vitro prion amplification techniques (saPMCA) were used to successfully misfold the cellular prion protein (PrPc) of these allegedly resistant species into a BSE-type prion protein. The biochemical and biological properties of the new prions generated in vitro after seeding rabbit and dog brain homogenates with classical BSE were studied. Pathobiological features of the resultant prion strains were determined after their inoculation into transgenic mice expressing bovine and human PrPC. Strain characteristics of the in vitro-adapted rabbit and dog BSE agent remained invariable with respect to the original cattle BSE prion, suggesting that the naturally low susceptibility of rabbits and dogs to prion infections should not alter their zoonotic potential if these animals became infected with BSE. This study provides a sound basis for risk assessment regarding prion diseases in purportedly resistant species.
Received January 18, 2013. Revision received March 7, 2013. Accepted March 23, 2013. Copyright © 2013 the authors 0270-6474/13/337778-09$15.00/0
Friday, March 8, 2013
Dogs may have been used to make Petfood and animal feed
Monday, March 26, 2012
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE
Monday, February 14, 2011
THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER
NO, NO, NOT NO, BUT HELL NO !
Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011
Monday, March 8, 2010
Canine Spongiform Encephalopathy aka MAD DOG DISEASE
Greetings again FDA, OIG et al,
I am trying to find out more information on another recall, that contains possible mad cow protein? but we do not know for sure, the way the recall warning letters are being wrote up now.
I had to file FOIA last week for the same thing. see ;
Saturday, August 29, 2009
FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009
MONDAY, MARCH 8, 2010 Canine Spongiform Encephalopathy aka MAD DOG DISEASE Greetings,
Another Big Myth about Transmissible Spongiform Encephalopathy, is that TSE will not transmit to dogs. This is simply NOT TRUE. IT is perfectly legal to feed dogs and cats here in the USA bovine meat and bone meal. Canine dementia is real. how many dogs and cats here in the USA are tested for mad cow disease ? I just received this F.O.I.A. request, and thought I would post it here with a follow up on MAD DOG DISEASE. This is a follow up with additional data I just received on a FOIA request in 2009 ;
DEPARTMENT OF HEALTH & HUMAN SERVICES Public Health Service Food and Drug Administration Rockville MD 20857
Terry Singeltary P.O. box 42. Bacliff, TX USA 77518
Dear Requestor
In reply refer to: F2009-7430
This is in response to your Freedom of Information Act (FOIA) request received by the Food and Drug Administration (FDA) on September 10,2009 which you ask for Recall V-258-2009. I apologize for the delay in our response to you. Enclosed you will find the records you requested. The following charges will be included in a monthly invoice:
Reproduction Search Review Total 5 Pages hour $.50 $ $.50
The above charges may not reflect final charges for this request. Please DO NOT send any payment until you receive an invoice from the Agency's Freedom of Information Staff (HFI-35).
Sincerely yours,
Sandy McGeehan Paralegal Specialist Communications Staff Center for Veterinary Medicine
Memorandum
Date August 26, 2009
From CVM Animal Health Hazard Evaluation Committee
Subject Problem:
Fargam Land & Grain recalled 429,128 pounds of ground corn because it may have been contaminated with prohibited material (material prohibited for use in ruminant feed by the 1997 BSE feed regulation) and was not labeled with the cautionary statement.
The feed mill received two semi trailer loads of barley that had been recalled by Mars Petcare US because it had been contaminated by dog food, some of which is formulated to contain bovine origin meat and bone meal.
The auger used to receive the barley was used to receive two truck loads of corn before the feed mill became aware of the problem with the barley. This potentially allowed some of the dog food in the barley to be carried over into the corn.
Recall Event IDIRES #: 52103
DAF/Surveillance #: 09234
CVM Recall and Emergency Coordinator (Kathy Hemming-Thompson), HFV -234
Field/RES Report Data:
Recalling firm: Fargam Land & Grain 505 Burlington Rd Saginaw, TX 76179
Manufacturer: Mars Petcare US 1 Doane Rd Clinton, OK 73601
Product & Code: Bulk ground corn; 70AY -02
Quantity Manufactured: 429,128 pounds
Quantity Distributed: 429,128 pounds
Recall Contact: Phil Farr, Owner, Fargam Land & Grain, Saginaw, TX
FDA District: Dallas
Field Recommended Classification: Class III
Effectiveness Check Level: Direct Accounts
Page 2 of 4 - DAF 09234 - Health Hazard Evaluation
Background: The firm is a feed mill that stores and manufactures products intended for use in animal feed. Its business is commingled with Saginaw Flakes, a feed mill which is under the same ownership, and located across the street from Fargam Land & Grain. A limited inspection was conducted to determine compliance with CP 7371.009 after the firm notified the Office of the Texas State Chemist that it had received four semi trailer loads of barley that may have contained dog food.
ReView:
SNIP...
HISTORY F.O.I.A.
Saturday, August 29, 2009
FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009
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
Tuesday, November 3, 2009
re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited material Recall # V-258-2009 and Recall # V-256-2009
From: Terry S. Singeltary Sr.
To: CVMHomeP@cvm.fda.gov
Cc: FOIASTAFF@oig.usda.gov ; paffairs@oig.hhs.gov ; HHSTips@oig.hhs.gov ; phyllis.fong@oig.usda.gov
FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
September 4, 2009
TO:
Food and Drug Administration
Division of Freedom of Information (HFI-35)
Office of Shared Services
Office of Public Information and Library Services
5600 Fishers Lane
Rockville, MD 20857
Or requests may be sent via fax to: fax number 301-443-1726 or 301-443-1719. If experience difficulty sending a fax, please call (301) 443-2414.
FROM:
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
Greetings FDA FOIE, and the Honorable Phyllis Fong et al @ OIG FOIA,
ANOTHER FOIA REQUEST PLEASE !
I apologize for wasting your time. this could have been handled differently if the FDA et al would just clearly identify these feed recalls with exactly what was in them, and what type recall it is.
I was told that the only way to find any more information on the following recall, i would have to submit a FOIA ? why, i do not know ?
----- Original Message -----
From: Pritchett, Burt To: Terry S. Singeltary Sr. Sent: Thursday, August 27, 2009 3:26 PM Subject: RE: hello Mr. Pritchett Sir !!! mad cow feed question
Terry,
That is the extent of the public information on the recall. If you wish to obtain additional information, you should submit a freedom of information act request through our communications staff. You could send an email request to: CVMHomeP@cvm.fda.gov
Burt
================end...TSS
Greetings again FDA, OIG et al,
SNIP...END
MICHIGAN FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE BREACH APRIL 4, 2017
ONE of these 21 CFR 589.2000 OAI violations of the mad cow feed ban is like one of the old violations when they would report everything to the public, like where i posted previously in 2007, 10 years post mad cow feed ban, where 10 million pounds of mad cow feed was fed out into commerce. i just took a glance for 2017, and in the great state of Michigan, there is already one of the OAI violation of the ruminant feed ban. now you have to request FOIA and wait some 10 years to finally get the answer (like i did with the mad sheep of mad river valley FOIA and the testing there from). ...
11998 DET-DO MI 48846-847 OPR 4/4/2017 OAI
http://www.accessdata.fda.gov/scripts/BSEInspect/bseinspections.csv
THIS April, 4, 2017 violation of the mad cow 21 CFR 589.2000 OAI is very serious for the great state of Michigan, some 20 years post FDA mad cow feed of August 1997. if would most likely take a FOIA request and a decade of wrangling to find out more.
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION
I would kindly like to comment on this FDA BSE/Ruminant Feed Inspections Firms Inventory (excel format)4 format, for reporting these breaches of BSE TSE prion protocols, from the extensive mad cow feed ban warning letters the fda use to put out for each violations. simply put, this excel format sucks, and the FDA et al intentionally made it this difficult to follow the usda fda mad cow follies. this is an intentional format to make it as difficult as possible to follow these breaches of the mad cow TSE prion safety feed protocols. to have absolutely no chronological or numerical order, and to format such violations in a way that they are almost impossible to find, says a lot about just how far the FDA and our fine federal friends will go through to hide these continued violations of the BSE TSE prion mad cow feed ban, and any breaches of protocols there from. once again, the wolf guarding the henhouse $$$
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.
2016
ONE more thing, please remember, the label does not have to say ''deer ration'' for cervid to be pumped up with. you can get the same ''high protein'' from many sources of high protein feed for animals other than cattle, and feed them to cervid...
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling’s 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007. Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI – 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J – PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A-BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
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.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
###
these deer farmers and and 'trophy' LOL! hunters there from will never admit using this BSe cr@p, why should they$$$ but let's see what the UK Government said about it;
What is the risk of chronic wasting disease being introduced into Great Britain? A Qualitative Risk Assessment October 2012
Several different animal feed products are imported into GB from North America. These include processed pet foods and consignments of unfinished feed ingredients for use in animal feed. The amount of imported feed, including pet food, that contains cervid protein is unknown and identified as a significant data gap. As non-ruminant animal feed may be produced with cervid protein (but not from positive CWD animals) in the United States (US), there is a greater than negligible risk that feed with cervid protein is imported from North America into GB. There is, however, uncertainty associated with this estimate.
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...
What is the risk of chronic wasting disease being introduced into Great Britain? A Qualitative Risk Assessment October 2012
Thursday, April 07, 2016
What is the risk of chronic wasting disease being introduced into Great Britain? An updated Qualitative Risk Assessment March 2016
*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***
Sunday, March 20, 2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission
SEE MAD COW FEED VIOLATIONS AFER MAD COW FEED VIOLATIONS ;
Tuesday, April 19, 2016
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards Singeltary Comment Submission
16 years post mad cow feed ban August 1997 2013
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
17 years post mad cow feed ban August 1997
Monday, October 26, 2015
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
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
FRIDAY, OCTOBER 06, 2017
Canada and USA Scrapie BSE TSE Prion Update October 5 2017
WEDNESDAY, OCTOBER 4, 2017
EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of the United States of America (USA) a review 2017
THURSDAY, JULY 20, 2017
USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200
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. ***
P.9.21
Molecular characterization of BSE in Canada
Jianmin Yang 1 , Sandor Dudas 2 , Catherine Graham 2 , Markus Czub 3 , Tim McAllister 1 , Stefanie Czub 1 1 Agriculture and Agri-Food Canada Research Centre, Canada; 2 National and OIE BSE Reference Laboratory, Canada; 3 University of Calgary, Canada
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle. Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres.
Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal-specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.
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;
***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
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?
THURSDAY, AUGUST 17, 2017
JAVMA NEWS Atypical BSE found in Alabama cow September 01, 2017
CWD ZOONOSIS
2017
Subject: ***CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
Chronic Wasting Disease (CWD)
Prevention
If CWD could spread to people, it would most likely be through eating of infected deer and elk. In a 2006-2007 CDC survey of U.S. residents, nearly 20 percent of those surveyed said they had hunted deer or elk and more than two-thirds said they had eaten venison or elk meat. However, to date, no CWD infections have been reported in people.
Hunters must consider many factors when determining whether to eat meat from deer and elk harvested from areas with CWD, including the level of risk they are willing to accept. Hunters harvesting wild deer and elk from areas with reported CWD should check state wildlife and public health guidance to see whether testing of animals is recommended or required in a given state or region. In areas where CWD is known to be present, CDC recommends that hunters strongly consider having those animals tested before eating the meat.
Tests for CWD are monitoring tools that some state wildlife officials use to look at the rates of CWD in certain animal populations. Testing may not be available in every state, and states may use these tests in different ways. A negative test result does not guarantee that an individual animal is not infected with CWD, but it does make it considerably less likely and may reduce your risk of exposure to CWD.
To be as safe as possible and decrease their potential risk of exposure to CWD, hunters should take the following steps when hunting in areas with CWD:
Do not shoot, handle or eat meat from deer and elk that look sick or are acting strangely or are found dead (road-kill). When field-dressing a deer: Wear latex or rubber gloves when dressing the animal or handling the meat. Minimize how much you handle the organs of the animal, particularly the brain or spinal cord tissues. Do not use household knives or other kitchen utensils for field dressing. Check state wildlife and public health guidance to see whether testing of animals is recommended or required. Recommendations vary by state, but information about testing is available from many state wildlife agencies. Strongly consider having the deer or elk tested for CWD before you eat the meat. If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals. If your animal tests positive for CWD, do not eat meat from that animal. The U.S. Department of Agriculture’s Animal and Plant Health Inspection Service regulates commercially farmed deer and elk. The agency operates a national CWD herd certification program. As part of the voluntary program, states and individual herd owners agree to meet requirements meant to decrease the risk of CWD in their herds. Privately owned herds that do not participate in the herd certification program may be at increased risk for CWD.
Page last reviewed: August 17, 2017 Page last updated: August 17, 2017 Content source: Centers for Disease Control and Prevention National Center for Emerging and Zoonotic Infectious Diseases (NCEZID) Division of High-Consequence Pathogens and Pathology (DHCPP)
> However, to date, no CWD infections have been reported in people.
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
TUESDAY, SEPTEMBER 12, 2017
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
Prion 2017 Conference Abstracts CWD
2017 PRION CONFERENCE
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO
PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS
*** PRION 2017 CONFERENCE VIDEO
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
TUESDAY, JULY 04, 2017
*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD
Wednesday, May 24, 2017
PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1
SATURDAY, JULY 29, 2017
Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC
Transmission of scrapie prions to primate after an extended silent incubation period
Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports 5, Article number: 11573 (2015)
doi:10.1038/srep11573
Download Citation
EpidemiologyNeurological manifestationsPrion diseases
Received: 16 February 2015
Accepted: 28 May 2015
Published online: 30 June 2015
Abstract
Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.
snip...
In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free. Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.
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.***
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.
==============
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
Saturday, April 23, 2016
Scrapie ZOONOSIS PRION CONFERENCE TOKYO 2016
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
*** Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
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 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.
*** 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.
IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989
also, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;
''it pains me to no end to even comtemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm...end...tss
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS
This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation. see full text ;
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation
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It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that 1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and 2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate. This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA
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The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.
Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive.
*This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.
Sunday, October 25, 2015
USAHA Detailed Events Schedule – 119th USAHA Annual Meeting CAPTIVE LIVESTOCK CWD SCRAPIE TSE PRION
snip...see more here ;
TUESDAY, MARCH 28, 2017
*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***
MONDAY, OCTOBER 02, 2017
Creutzfeldt Jakob Disease United States of America USA and United Kingdom UK Increasing and Zoonotic Pontential From Different Species
THURSDAY, AUGUST 17, 2017
*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017
Singeltary et al
FRIDAY, AUGUST 11, 2017
Infectivity in bone marrow from sporadic CJD patients
Bioassays in transgenic mice expressing the human prion protein revealed the presence of unexpectedly high levels of infectivity in the bone marrow from seven out of eight sCJD cases. These findings may explain the presence of blood-borne infectivity in sCJD patients. They also suggest that the distribution of prion infectivity in peripheral tissues in sCJD patients could be wider than currently believed, with potential implications for the iatrogenic transmission risk of this disease.
*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery ***
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
THURSDAY, AUGUST 10, 2017
*** Minimise transmission risk of CJD and vCJD in healthcare settings Updated 10 August 2017
National Prion Center could lose all funding just as concern about CWD jumping to humans rises
SATURDAY, JULY 15, 2017
*** National Prion Center could lose all funding just as concern about CWD jumping to humans rises
Terry S. Singeltary Sr.
