-------- Original Message --------
Subject: Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)
Date: Sun, 11 Jul 2004 21:34:22 -0500
From: "Terry S. Singeltary Sr."
To: fdadockets@oc.fda.gov CC: regulations@aphis.usda.gov, burt.pritchett@fda.gov
Docket
No. 04-047-l
No. 04-021ANPR
No. 2004N-0264
NEW BSE SAFEGUARDS
Federal Measures to Mitigate BSE Risks: Considerations for Further Action
http://www.fda.gov/cvm/index/updates/bseanprm.htm
Greetings FDA, USDA and APHIS et al,
I would kindly like to comment on the continued delay of the regulations that have been proposed for years to reduce the risk of BSE/TSE in the USA. Each day that is wasted debating this issue allows this agent to spread, and many many more humans and animals become needlessly exposed to this agent via a multitude of potential routes and sources right here in the USA. TO continue to ignore the new findings from several scientists about the fact that BSE is not the only strain of TSE in cattle, the fact that new atypical strains of TSE are showing up in not only cattle, but sheep and the fact that the new strain of TSE in cattle seems to be more similar to sporadic CJD as opposed to the nv/v CJD, to continue to ignore these findings will only further spread this agent.
CWD and Scrapie have been running rampant in the USA for decades. BOTH of which have been rendered and fed back to animals for human/animal consumption for decades. All of which transmits to primates by the natural and non-forced oral consumption of TSE scrapie, CJD, Kuru agent (and CWD by inoculation).
Strong Scientific evidence discovered back in the 80s support the fact that a TSE has been prevalent in the USA bovine for decades, either undetected or ignored. IF you consider the recent stumbling and staggering TEXAS cow that was showing all signs of a CNS/TSE disorder that was ordered to be rendered without BSE/TSE test, brains, spinal cord, head and all (as to no possible evidence left of TSE), I would think the 'ignored' or 'covered up' to be the better terminology. Then you have the Downer in Washington state that was actually a good walker and then all the banned Canadian products that some how found it's way across the border into the USA, considering all this, it is very difficult for me to believe that the FDA/USDA/APHIS et al are doing everything possible to protect the 'consumer'. Hardly the case;
Congressman Henry Waxmans Letter to the Honorable Ann Veneman
http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_may_13_let.pdf
-------- Original Message --------
Subject: Re: Congressman Henry Waxmans Letter to the Honorable Ann Veneman on failure by USDA/APHIS TO TEST TEXAS MAD COW
Date: Wed, 9 Jun 2004 16:48:31 -0500
From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de References: <40a8cd52.1070308@wt.net>
######## Bovine Spongiform Encephalopathy #########
USA BSE RED BOOK
October 1998
BSE Red Book 2.1-36
7.2.1.7 Laboratory Coordination--The Laboratory Coordination Officer will advise the READE(3 Director concerning laboratory capabilities and appropriate laboratory examinations to be conducted to provide needed results as rapidly as possible. This individual will assist with interpretation of results.
seems that if the 'enhanced BSE/TSE testing program' is to test some 400,000+ animals in 1 1/2 years, they better hurry up, times a wasting.
BSE Red Book 2.1-39
7.6 Depopulation Procedures
Under no circumstances may BSE suspects be sent fo slaughhter or rendering.
snip...
BSE Red Book 2.1-40
7.7 Disposal Under no circumstances may BSE suspects be sent to slaughter or rendering. Notify FDA, CVM if you suspect that the carcass of a BSE-confirmed animal has moved to rendering or animal feed manufacturing. Field personel should arrange for the carcass to be transported to and examined by a qualified veterinary pathologist or field veterinary medical officer. After the pathologic examination has been completed and the necessary diagnostic specimens have been obtained, field personnel should arrange for disposal of the carcass. Before a method of disposal is selected, there are many factors that must be considered, and often other State and Federal agencies must be consulted. The environmental and legal impacts of the operation must be considered. Upon recommendation of the State or Federal agencies, VS may consider other disposal methods.
snip...
7.7.3 Rendering Because BSE is spread by rendered animal protein, BSE-suspect and confirmed carcasses must not be rendered, unless the rendered material is incinerated. Notify FDA, CVM if you suspect that dead BSE animals or carcasses have moved to rendering or animal feed manufacturing.
snip...
7.10.11 Prevention--Suspects and animals confirmed to have BSE must not be rendered. Producers, feed mills, and rendering establishments should adhere to U.S. State and local rendering policies and FDA regulations concerning the feeding of rendered animal protein to ruminants.
TSS
Terry S. Singeltary Sr. wrote:
######## Bovine Spongiform Encephalopathy #########
ONE HUNDRED EIGHTH CONGRESS CONGRESS OF THE UNITED STATES HOUSE OF REPRESENTATIVES COMMITTEE ON GOVERNMENT REFORM 2157 RAYBURN HOUSE OFFICE BUILDING WASHINGTON, DC 20515-6143
www.house.gov/reform
May 13, 2004
The Honorable Ann M. Veneman Secretary of Agriculture Department of Agriculture 1400 Independence Avenue, SW Washington, DC 20250
Dear Madam Secretary:
1 am writing to express concern that the recent failure of the U.S. Department of Agriculture (USDA) to test a Texas cow with neurological symptoms for bovine spongiform encephalopathy (BSE) may reflect wider problems in the surveillance program. USDA apparently does not keep track of how many cows condemned for central nervous system symptoms are tested for BSE nor does it require that suspect carcasses be held pending testing. Effective surveillance and control of BSE in the United States require a reliable system for ensuring that potentially infected cows are tested and that no infected materials enter the animal or human food supply.
Under USDA regulations, any cow that exhibits signs of central nervous system (CNS) problems must be condemned by Food Safety Inspection Service (FSIS) personnel at the plant.1 According to a 1997 Animal and Plant Health Inspection Service (APHIS) Memorandum, brain samples all of such animals should be sent for BSE testing.2 The memorandum notes that "[i]t is essential that brain specimens be collected from adult cattle condemned for CNS signs as part of our national surveillance of BSE."3
The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel
1 9 CFR 309.4.
2 USDA APHIS, Veterinary Services Memorandum No. 580.16. Procedures/or Investigation of Adult Cattle With Clinical Signs of Central Nervous System (CNS) Disease and Procedures for Surveillance of Downer Cows for Bovine Spongiform Encephalopathy (BSE) (June 11,1997).
3 Id.
4 U.S. Confirms a Failure to Use Mad Cow Test, Wall Street Journal (May 4, 2004).
The Honorable Ann M. Veneman May 13,2004 Page 2
at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5
This sequence of events is troubling, and it raises the question of whether this is an isolated incident. In 1997, USDA noted a major gap between the number of cattle condemned for CNS symptoms and the number of these cows actually tested for mad cow disease. The Department found:
Based on information provided by the Food Safety and Inspection Service (FSIS), the number of adult cattle (2 years of age or greater) condemned at slaughter due to CNS signs is much greater than the number whose brains have been collected for testing.6
Despite recognizing the problem more than six years ago, however, USDA apparently did not adopt procedures to ensure that these samples would be collected. In March 2004, the Government Reform Committee asked USDA to provide, for each of the last five years, the number of BSE tests performed on cattle condemned by FSIS inspectors on the basis of CNS symptoms.7 In response, USDA provided information on the numbers of cattle condemned for CNS symptoms by FSIS, but replied that "[i]t is not possible to determine, from the data we currently collect, how many of these cattle were tested by APHIS for BSE."8 It thus appears that not only does USDA not routinely track the gap between the number of condemned and tested cattle, but that USDA could not even calculate this gap when requested to do so by Congress.
There also appears to be a lack of clarity regarding the disposition of cattle with CNS symptoms while BSE tests are pending. In the past, companies could send cattle awaiting BSE testing results for rendering, which would allow their remains to be used in feed for animals other than ruminants, such as pigs and chickens. After this incident, both FDA and USDA policy appear to have changed in different ways.
USDA policy has apparently shifted to requesting that companies not send cattle to rendering while awaiting test results. A May 5, 2004 memo from APHIS states, "it is requested though not required that [the cattle] not go to inedible rendering until the sample comes
USDA's San Angelo Vets and Techs Ordered Not to Test Suspect Cow, Meating Place (May 5, 2004).
6 USDA APHIS, supra note 2.
7 Letter from Rep. Tom Davis and Rep. Henry A- Waxman to Secretary of Agriculture Ann M. Veneman (Mar. 8, 2004).
8 Letter from Ronald F. Hicks, Assistant Administrator, Office of Program Evaluation, Enforcement, and Review- FSIS. to Reo. Henrv A. Waxman- Attachment 1 (Mar. 22- 2004).
The Honorable Ann M. Veneman May 13,2004 Page 3
back negative."9 There is no explanation of why this course of action is requested, but not required.
FDA policy also appears to have shifted towards prohibiting the use of carcasses of cattle with CNS symptoms and indeterminate BSE status in certain types of animal feed. On April 30, FDA requested that the rendering company holding the remains of the Texas cow either destroy them or use them exclusively in swine feed. m the case that the remains are included in swine feed, FDA "will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs."10
Any confusion over what to do with cattle condemned for CNS symptoms awaiting testing for BSE seems unnecessary. The obvious approach is to require companies either to destroy the carcasses or hold them until test results become available. Such a policy would avoid any need for complicated traceback procedures after the discovery of a positive result. According to the information provided to the Committee by USDA, the FSIS has condemned only 200 to 250 cows per year because of signs of central nervous system damage." Mandating the destruction or holding of their carcasses would have minimal economic impact.
The experience with the BSE-infected cow in Washington State illustrates the prudence of waiting for the results of BSE tests. Prior to December 2003, USDA permitted cattle that were sampled as part of the BSE surveillance program to enter commerce even while BSE tests were pending. As a result, when the BSE-infected cow was discovered, it had already entered the food supply. This led to a complicated and partially successful traceback procedure in which hundreds of thousands of pounds of beef had to be destroyed. Because of this debacle, USDA quickly developed a new policy to require holding all carcasses from the human food chain during BSE testing.
I appreciate that you have taken steps to enhance the safety of the U.S. food supply since the discovery of BSE in the United States. I urge you to consider the lessons of this latest
9 Memo from John R. Clifford, Acting Deputy Administrator, Veterinary Services, and William Smith, Assistant Administrator, Office of Field Operations, Food Safety and Inspection Service, to VSMT, Regional Directors, Area Veterinarians in Charge, and Veterinary Services, Subject: Policy Statement Regarding BSE Sampling of Condemned Cattle at Slaughter Plants - for Immediate Implementation (May 5, 2004) (online at http://www.aphis.usda.gov/lpa/issues/bse/BSE_APHIS-FSIS.pdf).
10 FDA, Statement on Cow -with Central Nervous System Symptoms (Apr. 20, 2004) (online at http://www.fda.gov/bbs/topics/news/2004/NEW01061.html).
11 The yearly totals of FSIS antemortem CNS condemnation for all adult cattle were 233 (1999), 220 (2000), 201 (2001), 249 (2002), and 247 (2003). The database for 2003 had not yet closed.
The Honorable Ann M. Veneman May 13,2004 Page 4
incident. USDA should develop a process that ensures the tracking of cattle condemned for CNS signs and should institute a policy requiring all carcasses with pending BSE tests to be destroyed or held. If there are any statutory barriers to these steps, please do not hesitate to let me know.
Sincerely,
XXXXX X. XXXXXX
Henry A. Waxman Ranking Minority Member
Congressman Henry Waxmans's Letter to the Honorable Ann Veneman
http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_may_13_let.pdf
TSS
######### http://mailhost-alt.rz.uni-karlsruhe.de/warc/bse-l.html ##########
######### http://mailhost-alt.rz.uni-karlsruhe.de/warc/bse-l.html ##########
NOW, after being told that last year that strict TSE guidelines would be put into place to plug any leaks in the triple TSE fire walls that have been leaking, we see again the same old industry backed rhetoric 'protect the industry at all cost', and again, measures to protect the American consumer from a horrible disease has been set back due to corporate greed. OF course it was said long ago;
It is clear that USDA have little information and _no_ regulatory responsibility for rendering plants in the US...
snip...
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_...
snip...
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin reported that many of his mink were "acting funny", and some had died. At this time, we visited the farm and found that approximately 10% of all adult mink were showing typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of normal habits of cleanliness, deposition of droppings throughout the pen rather than in a single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over their _backs like squirrels. These signs were followed by progressive deterioration of neurologic function beginning with locomoior incoordination, long periods of somnolence in which the affected mink would stand motionless with its head in the corner of the cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. Since previous incidences of TME were associated with common or shared feeding practices, we obtained a careful history of feed ingredients used over the past 12-18 months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed.
http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
DUE to the new 'atypical' TSEs showing up in different species, it is paramount that removing specified risk materials (SRMs) from all animal feed, including pet food, in order to control the risks of cross contamination throughout feed manufacture and distribution and on the farm due to misfeeding is a no brainer. FAILING to do this will only continue to spread this agent.
AGAIN, due to the findings of new 'atypical' TSEs showing up in different species, we must require dedicated equipment or facilities for handling and storing feed and ingredients during manufacturing and transportation, to prevent cross contamination. WE must not let the industry and politics dictate science.
BASE in cattle in Italy of Identification of a second bovine amyloidotic spongiform encephalopathy: Molecular similarities with sporadic Creutzfeldt-Jakob disease
http://www.pnas.org/cgi/content/abstract/0305777101v1
Identification of possible animal origins of prion disease in human beings
snip...
A further comparison6 of BASE with sCJD in people revealed that, at least in terms of PrPSc characteristics, BASE was similar to a particular type of sCJD sCJD(MV2) (figure). These researchers conclude not only that BASE is a new strain of BSE, but also that characteristics of human and animal PrPSc could help to identify potential risk factors for disease in individuals with sCJD of unknown origin.
snip...
THE LANCET " Vol 363 " June 19, 2004 " www.thelancet.com 2013
Characterization of two distinct prion strains derived from bovine spongiform encephalopathy transmissions to inbred mice S. E. Lloyd, J. M. Linehan, M. Desbruslais, S. Joiner, J. Buckell, S. Brandner, J. D. F. Wadsworth and J. Collinge J Gen Virol 2004 85 (8): p. 2471-2478
J Gen Virol -- Future Table of Contents Alert (not yet published...TSS)
Journal of Virological Methods 117 (2004) 2736 Atypical scrapie cases in Germany and France are identified by discrepant reaction patterns in BSE rapid tests A. Buschmanna, A.-G. Biacabe b, U. Ziegler a, A. Bencsik b, J.-Y. Madecb, G. Erhardt c, G. Lühken c, T. Baron b, M.H. Groschup a,? a Federal Research Centre for Virus Diseases of Animals, Institute for Novel and Emerging Infectious Diseases, Boddenblick 5a, 17493 Greifswald-Insel Riems, Germany b AFSSA-Lyon Unité Virologie-ATNC , 31 Avenue Tony Garnier, 69364 Lyon Cedex 07, France c Department of Animal Breeding and Genetics, Justus-Liebig University Giessen, Ludwigstr. 21B, 35390 Giessen, Germany Received 27 August 2003; received in revised form 13 November 2003; accepted 18 November 2003 Abstract The intensified surveillance of scrapie in small ruminants in the European Union (EU) has resulted in a substantial increase of the number of diagnosed cases. Four rapid tests which have passed the EU evaluation for BSE testing of cattle are also recommended currently and used for the testing of small ruminants by the EU authorities. These tests include an indirect ELISA (cELISA), a colorimetric sandwich ELISA (sELISA I), a chemiluminescent sandwich ELISA (sELISA II), and a Western blot (WB). To this point, the majority of samples have been screened by using either sELISA I (predominantly in Germany) or WB (predominantly in France). In this study, it is shown that a number of the German and French scrapie cases show inconsistent results using rapid and confirmatory test methods. Forty-eight German sheep, 209 French sheep and 19 French goat transmissible spongiform encephalopathy (TSE) cases were tested. All cases were recognised by the sELISA I and either one of the confirmatory methods (scrapie-associated fibrils (SAF)-immunoblot or immunohistochemistry). Surprisingly, three rapid tests failed to detect a significant number of scrapie cases (29 in France and 24 in Germany). The possible reasons for these inconsistent reaction patterns of scrapie cases are discussed. Similar discrepancies have not been observed during rapid testing of cattle for BSE, the disease for which all diagnostic methods applied have been evaluated. © 2003 Elsevier B.V. All rights reserved. Keywords: Scrapie; Prion protein; Rapid test; Confirmatory method 1. Introduction
snip...
4. Discussion Since the spring of 2002, rapid tests are being used for active surveillance of scrapie in the national sheep herds of the EU member states. These tests have been approved by the European commission and they include a colorimetric sandwich ELISA, a luminescence sandwich ELISA, an indirect ELISA using chemiluminescence as well as a rapid Western blotting assay. According to EU legislation (EC regulation 999/2001 and amendments), rapid tests are only approved for screening brain samples. In case of a reactive result, the sample has to be examined in the national reference laboratory using one of the OIE approved confirmatory methods which are SAF-immunoblotting and immunohistochemistry. The introduction of this active surveillance programme in the EU using BSE rapid tests demonstrated that scrapie in small ruminants is much more prevalent than had been previously estimated. Moreover, we found that not all scrapie cases are detected equally well by the four applied rapid tests as a significant portion of the samples were found positive with the sELISA I test but were not reactive with the rapid WB and sELISA II. The cELISA could only be used on a rather small number of samples, however, it must be assumed from the available results that it shows a performance similar to that of the rapid WB and sELISA II. Although some of the sELISA I results were weak positive, all cases that were initially detected using this method were confirmed by using OIE-recommended methods. It is therefore concluded that the sELISA I results are true positive, whereas the rapid WB, sELISA II and cELISA results of the same samples must be considered as false negative. This of course presupposes that the currently applied con- firmatory methods do not produce any false positive results. All samples that were first detected by using the rapid WB also gave positive results using the other rapid test methods. This observation supports the hypothesis that the rapid WB fails to detect certain positive sheep. Regrettably, it was not feasible during this study to retest small ruminant field samples that had initially been negative in the rapid WB with the sELISA I test in order to check if any positive samples had been ignored during the first screening. Non-uniform rapid test results were reproducible when selected coded samples were exchanged between the German and French national TSE reference laboratories and the samples were repeatedly positive in the sELISA I. Furthermore, it should be emphasised that the reactivity using this test was generally high (more than four times the cut-off level in most cases), showing that negative results obtained with other methods cannot be explained by threshold levels of protease resistant prion protein in these particular samples alone. Brainstem samples collected in abattoirs and rendering plants do not always fulfill the desired diagnostic quality standards in terms of freshness and in sampling localisation. In the beginning, we therefore could not exclude the possibility that single incongruent test results were due to varying PrPSc concentrations in the brainstems. However, the large number of such samples and the variety of the sample histories argue against such artefacts. However, such effects may explain why a few cases were negative by immunohistochemistry, but positive by SAF-immunoblotting, a diagnostic method where PrPSc is concentrated from larger brain areas. These 53 atypical scrapie cases in France and Germany out of a set of 276 may represent a novel strain of this disease in the field. Similar observations have also been made by the Norwegian National TSE Reference Laboratory, where some sheep scrapie samples were not reactive using the rapid WB (Benestad et al., 2003). However, not all characteristics described for those Nor98 designated cases match the atypical scrapie cases reported here. In particular, all Nor98 cases display a strong signal at 12 kDa that seems to be absent in a number of the German and French cases. We therefore postulate that at least three different scrapie phenotypes A. Buschmann et al. / Journal of Virological Methods 117 (2004) 2736 35 (typical scrapie and two atypical strains) exist within the European sheep flock. To determine critical factors affecting the rapid WB detection of PrPSc, we undertook a series of exchange experiments. The detection of atypical cases was improved after replacing the rapid WB homogenisation buffer supplied within the testkit of which the composition is undisclosed by an in-house homogenisation buffer containing desoxycholate and NP40 as detergents. Attempts were also made to replace the proteinase K solution, the detection antibody (by mab L42 that is directed to the same epitope as mab 6H4), and the conjugate antibody. Although no single critical step was revealed that alone enabled the detection of samples, these modifications altogether led to positive results for almost all atypical samples. It became also evident that minor changes in the sample treatment may have major effects when the modified SAF-immunoblotting technique was applied: while some of the atypical samples were negative with this method in which the first ultracentrifugation step is omitted and PK digestion is performed prior to SAF preparation, the same samples became clearly positive when the other SAF preparation protocol was applied. However, the physiochemical characteristics of ovine PrPSc derived from different scrapie isolates that are the basis for the observed effects still need further research efforts. PrP molecules derived from animals affected with different TSE strains vary in their cleavage sites for proteinase K digestion and therefore display different molecular weights when analysed in immunoblot (Hill et al., 1998; Baron et al., 2000; Stack et al., 2002). For example, the N-terminus of PrP derived from BSE-affected sheep is digested further by proteinase K than PrP derived from scrapie-affected sheep and therefore leads to a residual PrP of a lower molecular mass. This effect has been proposed as a possible diagnostic marker to differentiate between BSE and scrapie infections in sheep. Our experiments showed that this variation in the PK cleavage site between scrapie and BSE in sheep has no impact on the performance of the rapid tests on ovine BSE PrPSc since all commercial rapid tests detect PrPSc derived from experimentally BSE infected sheep of the PrPARQ/ARQ genotype (data not shown). Moreover, WB and sELISA II use the same monoclonal antibody (mab 6H4; Korth et al., 1997) which binds to an epitope far away from the PK cleavage site (aa 144148) and would therefore not be expected to react differently with scrapie- and BSE-derived PrPSc. The same is the case with the French immunoblot test that uses mab SAF 84 (Demart et al., 1999), binding to an epitope in the same region of the protein (aa 125163). No information is available on the PrP epitopes that are targeted in the sELISA I and cELISA. TSE infectivity can only be confined reliably, to date, by transmission experiments to an appropriate host. As it cannot be ruled out completely at this stage that non-infectious PrPC may also form intracellular aggregates with increased protease resistance and hydrophobicity that may lead to false positive results in diagnostic tests, the level of infectivity of such atypical cases is currently being examined by inoculation into RIII, C57B1 and VM95 mice. In case of a transmission to these mouse strains, the lesion profile scores will be determined and PrPSc will be analysed concerning its glycotype and PK resistance. The use of rapid tests for small ruminants was introduced by the EU Commission on the basis of their successful evaluation for BSE testing in cattle (Moynagh and Schimmel, 1999) in order to achieve an overview of the scrapie prevalence in the EU. Unfortunately, no independent evaluation has been performed in the EU to date to reveal the individual rapid tests performance on small ruminant scrapie cases. Therefore, their specificity and sensitivity for this use can only be estimated by the results of samples selected randomly that have been tested individually by the manufacturers. Inconsistencies in the ability of rapid tests to identify positive cases would question the current efforts to intensify and standardise the scrapie surveillance in the EU member states. Our data show that the actual numbers of scrapie cases and the prevalence of scrapie may be seriously underestimated in countries where rapid tests that may produce false-negative results are used. In the German epidemiosurveillance scheme for scrapie, the sELISA I is applied for testing of more than 80% of the samples, while in France 60% of the samples are tested with the rapid WB. Therefore, it must be accepted that the current EU-wide epidemiosurveillance programme can only give a general impression of the scrapie situation but may miss on average up to 12% of the true number of German scrapie cases and up to 16% of the French cases (estimated numbers take into account the applied test methods and the numbers of atypical cases since 2002). This must be kept in mind when scrapie prevalence data obtained by BSE rapid testing are interpreted. Acknowledgements We wish to acknowledge Matthias Kramer and Sandra Göbel (FRCVDA-Wusterhausen, Germany) and Didier Calavas (AFSSA-Lyon, France) for epidemiological data, Bertrand Bedhom (LABOGENA, France) for genotype analysis of French scrapie cases and J. Grassi (C.E.A.-Saclay, France) for supply of SAF 70 and SAF 84 antibody. This work was partly funded by the German Ministry of Consumer Protection, Nutrition and Agriculture (BMVEL). References
snip...END
Vet Pathol -- Ersdal et al. 40 (2): 164
... up PrP rapidly at a young age, as Heggebø et al. ... Ersdal, MJ Ulvund) and 133449/111 (SL Benestad) from the ... Vet Rec 147:439-441, 2000[ISI][Medline]; Bendheim PE ...
http://www.vetpathology.org/cgi/content/full/40/2/164 -
[PDF] Accumulation of Pathogenic Prion Protein (PrP ) in Nervous and ...
File Format: PDF/Adobe Acrobat ... 166 Vet Pathol 40:2, 2003 Ersdal, Ulvund, Benestad, and Tranulis ... RPLN Ileum Lambs RPLN DJLN Ileum Spleen F89/160.1.5 L42 R521 R505 ORourke et al. ... http://www.vetpathology.org/cgi/reprint/40/2/164.pdf -
[PDF] SCIENTIFIC PAPERS File Format: PDF/Adobe Acrobat ... 2003 Mar- 2003 Mar 31; 34(2):185-92. SEAC/SCI/79/17 Ersdal C, Ulvund MJ, Benestad SL, Tranulis MA. ... Vet Rec. ... SEAC/SCI/79/25 He L, Lu XY, Jolly AF et al. ... http://www.seac.gov.uk/papers/SEAC-SCI-79.pdf -
SCRAPIE - NORWAY: NEW PHENOTYPE ***************************************** A ProMED-mail post
ProMED-mail, a program of the International Society for Infectious Diseases
Date: 16 Nov 2003 From: Terry Singletary Source: The Veterinary Record, 16 Aug 2003 [edited]
[With new information, it appears there is potentially a new phenotype of atypical' BSE/TSE in animals in Japan and France. The article below indicates a new strain of Scrapie, the 'Nor98', which also has negative IHC and histology. Although this article does not suggest a link to the atypical forms seen in cattle, it does seem more than coincidence that there are also appearing different strains, or perhaps atypical strains of scrapie as well. It has been believed for years that there is a link between BSE and scrapie; perhaps this is another bit of research that should be carefully examined. Mod.TG]
Cases of scrapie with unusual features in Norway and designation of a new type, Nor98. The Veterinary Record, 16 August 2003, vol. 153, no. 7, pp. 202-208(7) Benestad S.L.; Sarradin P.; Thu B.; Schonheit J.; Tranulis M.A.; Bratberg B.
Abstract: 5 cases of scrapie with unusual features have been diagnosed in Norway since 1998. The affected sheep showed neurological signs dominated by ataxia, and had the PrP genotypes homozygous A136 H154 Q171/ A136H154Q171 or heterozygous A136H154Q171/A136R154Q171, which are rarely associated with scrapie. Brain histopathology revealed neuropil vacuolisation essentially in the cerebellar and cerebral cortices; vacuolation was less prominent in the brainstem, and no lesions were observed at the level of the obex. The deposits of PrPSc were mainly in the cortex of the cerebellum and cerebrum, and no PrPSc was detectable by immunohistochemistry or ELISA in the lymphoid tissues investigated.
Western blot analysis showed that the glycotype was different from other known scrapie strains and from the BSE strain. From a diagnostic point of view, these features indicate that this type of scrapie, designated Nor98, could have been overlooked and may be of significance for sampling in scrapie surveillance programmes.
Document Type: Research article ISSN: 0042-4900
DOI (article): NO_DOI SICI (online): 0042-4900(20030816)153:7L.202;1- Publisher: BVA Publications
-- ProMED-mail
NOT to forget the 'atypical' VERMONT USA' sheep scrapie/BSE/TSE? back in 2000 with the testing conveniently ignored and put off once again with animal TSEs. Why I ask?
SCRAPIE ''ATYPICAL'' TSE IN SHEEP VERMONT UPDATE 2004
Greetings,
IN the year 2000, some sheep in Vermont were confiscated due to what the USDA/APHIS said was an 'atypical TSE'.
WE were told there would be additional testing to confirm exactly what TSE we were dealing with;
Release No. 0141.02
Ed Curlett (301) 734-3256 Jerry Redding (202) 720-6959
TESTING TO CONTINUE ON IMPORTED SHEEP CONFISCATED LAST YEAR
WASHINGTON, April 11, 2002 -- The U.S. Department of Agriculture today announced that tests conducted on a flock of sheep confiscated last year from a farm in Vermont confirm that two of the 125 sheep tested positive for an atypical undifferentiated transmissible spongiform encephalopathy (TSE) of foreign origin. The flock of 125 sheep was confiscated in March 2001 after four animals from an associated flock tested positive for TSE in July 2000. USDA will continue to conduct additional tests to determine the type of TSE in these sheep.
"These results confirm our previous conclusions were correct and that we took the appropriate preventative actions in confiscating these animals," said Bobby Acord, administrator of USDAs Animal and Plant Health Inspection Service. "USDAs actions to confiscate, sample and destroy these sheep were on target. As a result of our vigilance, none of these confiscated animals entered the animal or human food supply."
The sheep, imported from Belgium and the Netherlands in 1996, were placed under certain federal restrictions when they entered the country as part of USDA's scrapie control efforts. In 1998, USDA learned that it was likely that sheep from Europe were exposed to feed contaminated with bovine spongiform encephalopathy. At that time, the state of Vermont, at the request of USDA, imposed a quarantine on these flocks, which prohibited slaughter or sale for breeding purposes.
On July 10, 2000, several sheep from the flock tested positive for a TSE, a class of degenerative neurological diseases that is characterized by a very long incubation period and a 100 percent mortality rate in infected sheep. Two of the better known varieties of TSE are scrapie in sheep and BSE in cattle. There is no evidence that scrapie poses a risk to human health.
On July 14, 2000, USDA issued a declaration of extraordinary emergency to acquire the sheep. This action was contested by the flock owners. A federal district court judge ruled in favor of USDA based on the merits of the case. The flock owners appealed to the Second Circuit Court requesting a stay, which was denied. The sheep were confiscated by USDA in March 2001 and transported to USDA's National Veterinary Services Laboratories in Ames, Iowa, where they were humanely euthanized. Tissue samples were collected from the sheep for diagnostic testing and USDA will continue with additional tests which could take up to 2 - 3 years to complete. In all, USDA has acquired 380 sheep from a total of three flocks. All of the animals were humanely euthanized, sampled and disposed and did not enter the animal or human food supply.
Our goal continues to be to prevent, detect and eradicate foreign animal diseases to protect American agriculture, natural resources and consumers," said Acord. "We will continue to utilize the scientific results of these and other tests conducted during the last several years to strengthen our extensive surveillance, monitoring and prevention efforts."
For more information about USDAs ongoing surveillance, monitoring and prevention efforts as it relates to this situation, please visit www.aphis.usda.gov/oa/tse/index.html
#
NOW, June 2004 those same test that we were told would start in 2002, have yet to be started. THE TSE those VERMONT sheep was supposedly to have had, has yet to be confirmed.
WHY?
IGNORING the fact Scrapie does transmit to primates by their non forced consumption of known infectious scrapie tissues.
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
IGNORING the fact Scrapie transmission studies have never been done on man.
IGNORING the fact surveillance for TSE in man in the USA and other places around the globe is terribly under funded and lacking in guidance. to date some 25 states make it reportable, with some states having an age bracket only documenting the younger victims. leaving the door open to spread the agent through the medical and surgical arena.
With the recent announcement of the UK contingency plan for the emergence of naturally occurring BSE in sheep June 2004, and the terrible implications for human health this would cause, full text some 31 pages;
http://www.defra.gov.uk/corporate/consult/bseinsheep/bseinsheep.pdf
you would have thought that this would have been at the top of someone's priority list. However, it does not look that way.
I ask again, WHY?
I wish to submit the following;
-------- Original Message -------- Subject: Re: AW: [BSE-L] USDA did not test possible mad cows - Dr. Detwiler, what about those sheep? Date: Sun, 13 Jun 2004 11:27:24 -0500 From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de References: <13.2d20eaae.2df84fb9@aol.com> <40c8c7a0.1080107@wt.net>
######## Bovine Spongiform Encephalopathy #########
Greetings list members,
Thought I should let the list know that Dr. Detwiler kindly replied to my question about the delayed 'atypical' TSE testing in the Vermont sheep and tried to explain what caused the delay. If I interpreted it correctly, seems it was the fault of the U.K. ;
-------- Original Message -------- Subject: Sheep Date: Sat, 12 Jun 2004 14:26:04 EDT From: LAVET22@aol.com To: flounder@wt.net
Mr. Singeltary.
I hope this finds you well. As you are aware I left the USDA last year. I can only update you on the sheep before that time. Contact was established with the UK on doing the bioassay studies. They agreed. However, we were prioritized after their own needs, hence the delay. I am aware that there are now additional labs in Europe running the mouse bioassay strain typing. You will have to contact USDA for further word.
Linda Detwiler =========
My reply to Dr. Detwiler;
-------- Original Message -------- Subject: Re: Sheep Date: Sat, 12 Jun 2004 13:53:57 -0500 From: "Terry S. Singeltary Sr." To: LAVET22@aol.com References: <54.2bd2ac1e.2dfca4bc@aol.com>
hello Dr. Detwiler,
thanks for your kind reply.
However, we were prioritized after their own needs, hence the delay.
not sure i understand that?
You will have to contact USDA for further word.
already done that, and there answer was;
5/20/04
Dear Mr. Singeltary,
The Western blot tests on these animals were completed in April of this year. That means that we can begin the mouse inoculations. To get the results of the Western blot tests, you will need to submit a Freedom of Information Act request through our FOIA office. The FAX number there is 301-734-5941.
Have a nice day,
Jim Rogers APHIS LPA
and with my previous attempts for information via the FOIA through this administration (as you are probably very well aware of) they have all been ignored/refused. so any further attempts would be fruitless i am sure.
thanks anyway...
kindest regards, Terry
LAVET22@aol.com wrote:
Mr. Singeltary.
snip...
TSS
Terry S. Singeltary Sr. wrote:
######## Bovine Spongiform Encephalopathy #########
Greetings Dr. Detwiler,
glad to see you are still with us, you had become very silent lately. hope you are enjoying semi retirement.
recently, i inquired through the BSE-L and via USDA official about those Vermont sheep via belgium which there was an Extraordinary Declaration of Emergency declared here in the USA due to atypical scrapie. The thread is;
Confiscation of Sheep in Vermont and testing results ? Thu, 20 May 2004 12:10:03 -0500 "Terry S. Singeltary Sr." Bovine Spongiform Encephalopathy BSE-L
Imported Belgium/Netherlands Sheep Test Results Background Factsheet Veterinary Services April 2002 APHIS
snip...
Additional tests will be conducted to determine exactly what TSE the animals haveBSE or scrapie. These tests involve the use of bioassays that consist of injecting mice with tissue from the infected animals and waiting for them to develop disease. This testing may take at least 2 to 3 years to complete.
http://www.aphis.usda.gov/lpa/pubs/fsheet_faq_notice/fs_ahvtsheeptr.pdf
DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E. (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES
http://frwebgate.access.gpo.gov/cgi-bin/getdoc.cgi?dbname=2000_register&docid=fr20jy00-32
DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES [2]
http://frwebgate.access.gpo.gov/cgi-bin/getdoc.cgi?dbname=2000_register&docid=fr20jy00-31
or if those old urls dont work, go here;
DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES - Terry S. Singeltary Sr. 7/20/00 (0)
[Federal Register: July 20, 2000 (Volume 65, Number 140)] [Notices] [Page 45018] >From the Federal Register Online via GPO Access [wais.access.gpo.gov] [DOCID:fr20jy00-32]
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DEPARTMENT OF AGRICULTURE
Office of the Secretary
[Docket No. 00-072-1]
Declaration of Extraordinary Emergency Because of an Atypical Transmissible Spongiform Encephalopathy (Prion Disease) of Foreign Origin
A transmissible spongiform encephalopathy (TSE) (prion disease) of foreign origin has been detected in the United States. It is different from TSE's previously diagnosed in the United States. The TSE was detected in the progeny of imported sheep. The imported sheep and their progeny are under quarantine in Vermont. Transmissible spongiform encephalopathies are degenerative fatal diseases that can affect livestock. TSE's are caused by similar, as yet uncharacterized, agents that usually produce spongiform changes in the brain. Post-mortem analysis has indicated positive results for an atypical TSE of foreign origin in four sheep in Vermont. Because of the potentially serious consequences of allowing the disease to spread to other livestock in the United States, it is necessary to seize and dispose of those flocks of sheep in Vermont that are affected with or exposed to the disease, and their germ plasm. The existence of the atypical TSE of foreign origin represents a threat to U.S. livestock. It constitutes a real danger to the national economy and a potential serious burden on interstate and foreign commerce. The Department has reviewed the measures being taken by Vermont to quarantine and regulate the flocks in question and has consulted with appropriate officials in the State of Vermont. Based on such review and consultation, the Department has determined that Vermont does not have the funds to compensate flock owners for the seizure and disposal of flocks affected with or exposed to the disease, and their germ plasm. Without such funds, it will be unlikely to achieve expeditious disposal of the flocks and germ plasm. Therefore, the Department has determined that an extraordinary emergency exists because of the existence of the atypical TSE in Vermont. This declaration of extraordinary emergency authorizes the Secretary to seize, quarantine, and dispose of, in such manner as he deems necessary, any animals that he finds are affected with or exposed to the disease in question, and their germ plasm, and otherwise to carry out the provisions and purposes of the Act of July 2, 1962 (21 U.S.C. 134-134h). The State of Vermont has been informed of these facts.
Dated: This declaration of extraordinary emergency shall become effective July 14, 2000. Dan Glickman, Secretary of Agriculture. [FR Doc. 00-18367 Filed 7-19-00; 8:45 am] BILLING CODE 3410-34-P
http://frwebgate.access.gpo.gov/cgi-bin/getdoc.cgi?dbname= 2000_register&docid=fr20jy00-32 ================================ [Federal Register: July 20, 2000 (Volume 65, Number 140)] [Notices] [Page 45018] >From the Federal Register Online via GPO Access [wais.access.gpo.gov] [DOCID:fr20jy00-31]
======================================================================== Notices Federal Register ________________________________________________________________________
This section of the FEDERAL REGISTER contains documents other than rules or proposed rules that are applicable to the public. Notices of hearings and investigations, committee meetings, agency decisions and rulings, delegations of authority, filing of petitions and applications and agency statements of organization and functions are examples of documents appearing in this section.
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DEPARTMENT OF AGRICULTURE
Office of the Secretary
[Docket No. 00-072-2]
Declaration of Emergency Because of an Atypical Transmissible Spongiform Encephalopathy (Prion Disease) of Foreign Origin
A transmissible spongiform encephalopathy (TSE) (prion disease) of foreign origin has been detected in the United States. It is different from TSE's previously diagnosed in the United States. The TSE was detected in the progeny of imported sheep. The imported sheep and their progeny are under quarantine in Vermont. Transmissible spongiform encephalopathies are degenerative fatal diseases that can affect livestock. TSE's are caused by similar, as yet uncharacterized, agents that usually produce spongiform changes in the brain. Post-mortem analysis has indicated positive results for an atypical TSE of foreign origin in four sheep in Vermont. Because of the potentially serious consequences of allowing the disease to spread to other livestock in the United States, it is necessary to seize and dispose of those flocks of sheep in Vermont that are affected with or exposed to the disease, and their germ plasm. The existence of the atypical TSE of foreign origin represents a threat to U.S. livestock. It constitutes a real danger to the national economy and a potential serious burden on interstate and foreign commerce. APHIS has insufficient funds to carry out the seizure and disposal of animals and germ plasm necessary to eliminate this disease risk. These funds would be used to compensate the owners of the animals and germ plasm for their seizure and disposal in accordance with 21 U.S.C. 134a. Therefore, in accordance with the provisions of the Act of September 25, 1981, as amended (7 U.S.C. 147b), I declare that there is an emergency that threatens the livestock industry of this country and hereby authorize the transfer and use of such funds as may be necessary from appropriations or other funds available to agencies or corporations of the United States Department of Agriculture to seize and dispose of animals that are affected with or exposed to this TSE, and their germplasm, in accordance with 21 U.S.C. 134a.
Dated: This declaration of emergency shall become effective July 14, 2000. Dan Glickman, Secretary of Agriculture. [FR Doc. 00-18368 Filed 7-19-00; 8:45 am] BILLING CODE 3410-34-P
I was told that ;
-------- Original Message -------- Subject: Re: hello Dr. Sutton...question please...scrapie...TSS Date: Thu, 20 May 2004 14:36:09 -0400 From: Jim.D.Rogers@aphis.usda.gov To: flounder@wt.net
Dear Mr. Singeltary,
The Western blot tests on these animals were completed in April of this year. That means that we can begin the mouse inoculations. To get the results of the Western blot tests, you will need to submit a Freedom of Information Act request through our FOIA office. The FAX number there is 301-734-5941.
Have a nice day,
Jim Rogers APHIS LPA =========
Dr. Detwiler, my question is, why have these very important test been delayed for so long when we were told they were to have been started some 2+ years ago?
who made this call to delay these very important test and why ?
thank you, with kindest regards,
Terry
Linda Detwiler wrote:
######## Bovine Spongiform Encephalopathy #########
snip...
######### http://mailhost-alt.rz.uni-karlsruhe.de/warc/bse-l.html ##########
WHAT ABOUT THE POTENTIAL FOR BSE IN SHEEP AND GOATS OR ANY OF THE OTHER NEW ''ATYPICAL'' TSEs SHOWING UP?
02-Jun-04, 10:45 BSE IN SHEEP CONTINGENCY PLAN - CONSULTATION LAUNCH
Defra and the other UK Agriculture and Rural Affairs Departments today launched a consultation on the UK contingency plan on possible actions if BSE were confirmed in sheep.
http://www.wired-gov.net/WGLaunch.aspx?ARTCL=24789
The total prevalence of scrapie in the USA is really unknown.
USA SCRAPIE Infected and Source Flocks;
As of September 30, 2003, there were 50 scrapie infected and source flocks (figure 3 ). There were 73 newly infected flocks reported in FY 2003 (figure 4 ). In addition, 351 scrapie cases were also confirmed and reported by the National Veterinary Services Laboratories (NVSL) (figures 5
and 6 ). No case of scrapie in goats was reported in FY 2003. The last case was confirmed in August 2002. New infected and source flock numbers and the number of these flocks released in FY 2003 are depicted in chart 4 . Sixty flocks, which is equivalent to 82 percent of the new scrapie infected and source flocks identified in FY 2003, were released or put on clean-up plans in FY 2003.
http://www.aphis.usda.gov/vs/nahps/scrapie/yearly_report/yearly-report.html
CWD USA
Current Distribution of CWD among Captive Cervid Herds Map Image
Click on the Picture above to See a Larger Image
Bullet Represents captive elk herds that are currently CWD-positive. Bullet Represents captive deer herds that are currently CWD-positive.
Depopulated Captive Cervid Herds Map Image
Click on the Picture above to See a Larger Image Bullet Represents CWD-positive captive elk herds that were depopulated due to CWD. Bullet Represents CWD-positive captive deer herds that were depopulated due to CWD.
Current Distribution of Chronic Wasting Disease in Free-Ranging Cervids Map Image Click on the Picture above to See a Larger Image
Bullet Represents counties in which CWD has been identified in free-ranging cervids. Note that large counties in the western states make the CWD area appear larger than actual extent. Refer to state wildlife agencies (links on the State Information page) for more detailed information on wildlife occurrances.
http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html
DUE to the new 'atypical' TSEs showing up, prohibiting the use of all mammalian and poultry protein in ruminant feed, to prevent cross contamination, is the only way to assure that CWD, Scrapie, BSE and all new 'atypical' TSEs will not cross-contaminate.
CATTLE have gone clinical with TSE as young as 20 months, to only be concerned and to set regulations only for the 30 month and older cattle is not sufficient to prevent the spread of this agent. The age limit should be 12 months;
DEAD STOCK DOWNERS are of major concern for TSEs. DUE not ignore the sub clinical TSE population. TO change regulations and to only focus on the CNS (stumbling, staggering and twitching cow), will further help spread this agent by ignoring the younger documented cows that have been documented (as young as 20 month, see documentation of these young cattle with BSE/TSE);
Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA [takes a few minutes to load]
https://web01.aphis.usda.gov/BSEcom.nsf/BSEFrameset?OpenFrameSet&Frame=BottomFrame&Src=_25t156hb3dtmisrjjconjcc9n6ph6ccr66oqjgdpo74qm6e1l68qjcp9hc4o30dhgckq34phfc8rjgoj16orjep9ic8o66c9i64s3achl6pi68cpg60r38eb675i3ujrgcln48rr3elmmarjk4p0nat3f8pp62rb5cg0_
THE BSE/TSE SUB CLINICAL COW
Broken bones and such may be the first signs of a sub clinical BSE/TSE cow;
SUB CLINICAL PRION INFECTION
MRC-43-00 Issued: Monday, 28 August 2000
NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH FINDINGS RELEVANT TO CJD AND BSE
A team of researchers led by Professor John Collinge at the Medical Research Council Prion Unit1 report today in the Proceedings of the National Academy of Sciences, on new evidence for the existence of a ?sub-clinical? form of BSE in mice which was unknown until now.
The scientists took a closer look at what is known as the ?species barrier? - the main protective factor which limits the ability of prions2 to jump from one species to infect another. They found the mice had a ?sub-clinical? form of disease where they carried high levels of infectivity but did not develop the clinical disease during their normal lifespan. The idea that individuals can carry a disease and show no clinical symptoms is not new. It is commonly seen in conventional infectious diseases.
Researchers tried to infect laboratory mice with hamster prions3 called Sc237 and found that the mice showed no apparent signs of disease. However, on closer inspection they found that the mice had high levels of mouse prions in their brains. This was surprising because it has always been assumed that hamster prions could not cause the disease in mice, even when injected directly into the brain.
In addition the researchers showed that this new sub-clinical infection could be easily passed on when injected into healthy mice and hamsters.
The height of the species barrier varies widely between different combinations of animals and also varies with the type or strain of prions. While some barriers are quite small (for instance BSE easily infects mice), other combinations of strain and species show a seemingly impenetrable barrier. Traditionally, the particular barrier studied here was assumed to be robust.
Professor John Collinge said: "These results have a number of important implications. They suggest that we should re-think how we measure species barriers in the laboratory, and that we should not assume that just because one species appears resistant to a strain of prions they have been exposed to, that they do not silently carry the infection. This research raises the possibility, which has been mentioned before, that apparently healthy cattle could harbour, but never show signs of, BSE.
"This is a timely and unexpected result, increasing what we know about prion disease. These new findings have important implications for those researching prion disease, those responsible for preventing infected material getting into the food chain and for those considering how best to safeguard health and reduce the risk that theoretically, prion disease could be contracted through medical and surgical procedures."
ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS SET BY THE JOURNAL.
FOR FURTHER INFORMATION CONTACT THE MRC PRESS OFFICE ON 020 7637 6011 (OFFICE HOURS) OR 07818 428297 OR 0385 774357 (OUT-OF-OFFICE-HOURS) OR PROFESSOR JOHN COLLINGE ON 020 7594 3760. PLEASE NOTE THAT OWING TO TRAVEL COMMITMENTS PROFESSOR COLLINGE WILL ONLY BE AVAILABLE UNTIL 16.30 ON FRIDAY 25 AUGUST AND CONTACTABLE AGAIN ON MONDAY 28 AUGUST VIA THE MRC PRESS OFFICE. DR ANDREW HILL (A CO-AUTHOR ON THE PAPER) FROM THE DEPARTMENT OF PATHOLOGY AT THE UNIVERSITY OF MELBOURNE WILL BE AVAILABLE ON 00 61 3 8344 3995 (DURING OFFICE HOURS) OR 00 61 3 9443 0009 (OUT-OF-OFFICE HOURS). PLEASE NOTE THAT AUSTRALIA IS TEN HOURS AHEAD OF UK TIME.
NOTES FOR EDITORS
Professor Collinge is a consultant neurologist and Director of the newly formed MRC Prion Unit based at The Imperial College School of Medicine at St Mary?s Hospital. He is also a member of the UK Government?s Spongiform Encephalopathy Advisory Committee (SEAC). The MRC prion unit is was set up in 1999, and its work includes molecular genetic studies of human prion disease and transgenic modelling of human prion diseases.
Prions are unique infectious agents that cause fatal brain diseases such as Creutzfeldt-Jakob disease (CJD) in humans and scrapie and BSE (mad cow disease) in animals. In some circumstances prions from one species of animals can infect another and it is clear that BSE has done this to cause the disease variant CJD in the UK and France. It remains unclear how large an epidemic of variant CJD will occur over the years ahead.
The strain of prion used here to infect the mice is the Sc237 strain (also known as 263K) which infects hamsters, and until now was assumed not to infect mice.
This research was funded by the Medical Research Council and Wellcome Trust.
The Medical Research Council (MRC) is a national organisation funded by the UK tax-payer. Its business is medical research aimed at improving human health; everyone stands to benefit from the outputs. The research it supports and the scientists it trains meet the needs of the health services, the pharmaceutical and other health-related industries and the academic world. MRC has funded work which has led to some of the most significant discoveries and achievements in medicine in the UK. About half of the MRC?s expenditure of £345 million is invested in over 50 of its Institutes and Units, where it employs its own research staff. The remaining half goes in the form of grant support and training awards to individuals and teams in universities and medical schools.
The Wellcome Trust is the world's largest medical research charity with a spend of some £600 million in the current financial year 1999/2000. The Wellcome Trust supports more than 5,000 researchers, at 400 locations, in 42 different countries to promote and foster research with the aim of improving human and animal health. As well as funding major initiatives in the public understanding of science, the Wellcome Trust is the country's leading supporter of research into the history of medicine.
http://www.mrc.ac.uk/index/public_interest/public-press_office/public-press_releases_2000/public-mrc-43-00.htm
USDA/APHIS ET AL MUST GET BSE/TSE TESTING DONE CORRECTLY
THE recent findings of positive 'inconclusives' that turned up negative was not only a nightmare to the consumer, but also to the farmers and industry as well. Using Prionics or Bio-Rad or whatever rapid TSE test will never eliminate the potential for human error. IF we look at the recent discovery of the BSE in Switzerland in the Zoo Zebu, the testing they perform would have eliminated this mix-up;
Diagnosis:
A. Laboratory where diagnosis was made: Institute of Animal Neurology, University of Bern (OIE Reference Laboratory for bovine spongiform encephalopathy).
B. Diagnostic tests used:
- histology;
- immunohistochemistry;
- ELISA (two different kits);
- western blot.
All tests gave positive results.
http://www.oie.int/eng/info/hebdo/AIS_38.HTM#Sec9
ALSO, if we look at the USA BSE EMERGENCY RESPONSE PLAN, where it states;
Subject: U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary Date: Tue, 4 May 1999 18:25:12 -0500 From: "Terry S. Singeltary Sr." Reply-To: BSEL To: BSEL snip... If additional tests do suggest a presumptive diagnosis of BSE, an NVSL pathologist will hand carry the sample to the United Kingdom for confirmation. It is at this critical point, when NVSL suggests a diagnosis of BSE and is preparing to send the sample to the United Kingdom, that this BSE Response Plan is initiated. The Plan begins the preliminary notification from NVSL to APHIS. Preliminary Notification The director of NVSL is responsible for immediately notifying the APHIS, Veterinary Services (VS) deputy administrator when tests suggest a presumptive diagnosis of BSE. Once NVSL has made a presumptive diagnosis of BSE, APHIS and FSIS field activities will also be initiated. APHIS will receive notification (either confirming or not confirming NVSL's diagnosis) from the United Kingdom anywhere between 24 and 96 hours. (The international animal health community has recognized the United Kingdom's Central Veterinary Laboratory {CVL} as the world's reference laboratory for diagnosing BSE. Other countries, including Belgium, France, Ireland, Luxembourg, the Netherlands, Portugal, and Switzerland, have all sent samples to this lab to confirm their first case of BSE). snip...end...TSS
WHY is the UK not going to verify the findings of BSE/TSE in tissue samples as the original BSE emergency response plan told them too?
I think that having several different rapid TSE test kits (Prionics, Bio-Rad etc.) along with the IHC and finally the OIE reference laboratory for confirmation is the best possible answer. Prusiner et al have a test that is some 1,000 times more sensitive and I only ponder why we are not using it? My fear is that once testing becomes more sensitive, more tissue/organ will become known to hold infectivity of some titre of the TSE agent. THEN we must ponder if _accumulation_ may play a role? With the threat from new atypical TSEs in many species and the real threat from iatrogenic CJD, the fact that we do not yet know how these new 'atypical' phenotpyes will transmit and how infectious there tissues may be, we must act now, we cannot flounder any longer.
Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA [takes a few minutes to load]
https://web01.aphis.usda.gov/BSEcom.nsf/BSEFrameset?OpenFrameSet&Frame=BottomFrame&Src=_25t156hb3dtmisrjjconjcc9n6ph6ccr66oqjgdpo74qm6e1l68qjcp9hc4o30dhgckq34phfc8rjgoj16orjep9ic8o66c9i64s3achl6pi68cpg60r38eb675i3ujrgcln48rr3elmmarjk4p0nat3f8pp62rb5cg0_
Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]
http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt
Docket Management Docket: 02N-0273 - Substances Prohibited From Use in
Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed
Comment Number: EC -10
Accepted - Volume 2
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html
PART 2
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html
PDF]Freas, William TSS SUBMISSION
File Format: PDF/Adobe Acrobat -
Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary
Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf
Asante/Collinge et al, that BSE transmission to the 129-methionine
genotype can lead to an alternate phenotype that is indistinguishable
from type 2 PrPSc, the commonest _sporadic_ CJD;
http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm
Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice in Manufacturing, Packing, or Holding Dietary Ingredients a Comment Number: EC -2 Accepted - Volume 7
http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm
[PDF] Appendices to PL107-9 Inter-agency Working Group Final Report 1-1 File Format: PDF/Adobe Acrobat - View as HTML Agent, Weapons of Mass Destruction Operations Unit Federal Bureau of those who provided comments in response to Docket No. ... Meager 8/18/01 Terry S. Singeltary Sr ...
www.aphis.usda.gov/lpa/pubs/pubs/PL107-9_Appen.pdf
Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION TO DOCKET 2003N-0312]
http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt
# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of 2002; [TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] - TSS 1/27/03 (0)
Docket Management
Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305 Comment Number: EC-254 [TSS SUBMISSION]
http://www.fda.gov/ohrms/dockets/dockets/02n0276/02N-0276-EC-254.htm
Dockets Entered On October 2, 2003 Table of Contents, Docket #, Title, 1978N-0301,
OTC External Analgesic Drug Products, ... EMC 7, Terry S. Singeltary Sr. Vol #: 1, ...
www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm
Daily Dockets Entered on 02/05/03
DOCKETS ENTERED on 2/5/03. ... EMC 4 Terry S. Singeltary Sr. Vol#: 2. ... Vol#: 1.
03N-0009 Federal Preemption of State & Local Medical Device Requireme. ...
www.fda.gov/ohrms/dockets/dailys/03/Feb03/020503/020503.htm
Docket Management
Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater
Comment Number: EC -1
Accepted - Volume 1
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be11.html
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfe.html
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfc.html
Daily Dockets - 04/10/03
... 00D-1662 Use of Xenotransplantation Products in Humans. EMC 98 Terry S. Singeltary Sr. Vol#: 3. 01F ... www.fda.gov/ohrms/dockets/dailys/03/Apr03/041003/041003.htm - 05-20-2003 - Cached
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed
EMC 1 Terry S. Singeltary Sr. Vol #: 1
-------- Original Message --------
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material >From Deer and Elk in Animal Feed; Availability Date: Fri, 16 May 2003 11:47:37 -0500 From: "Terry S. Singeltary Sr." To: fdadockets@oc.fda.gov
Greetings FDA,
i would kindly like to comment on;
Docket 03D-0186
FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Several factors on this apparent voluntary proposal disturbs me greatly, please allow me to point them out;
1. MY first point is the failure of the partial ruminant-to-ruminant feed ban of 8/4/97. this partial and voluntary feed ban of some ruminant materials being fed back to cattle is terribly flawed. without the _total_ and _mandatory_ ban of all ruminant materials being fed back to ruminants including cattle, sheep, goat, deer, elk and mink, chickens, fish (all farmed animals for human/animal consumption), this half ass measure will fail terribly, as in the past decades...
2. WHAT about sub-clinical TSE in deer and elk? with the recent findings of deer fawns being infected with CWD, how many could possibly be sub-clinically infected. until we have a rapid TSE test to assure us that all deer/elk are free of disease (clinical and sub-clinical), we must ban not only documented CWD infected deer/elk, but healthy ones as well. it this is not done, they system will fail...
3. WE must ban not only CNS (SRMs specified risk materials), but ALL tissues. recent new and old findings support infectivity in the rump or ass muscle. wether it be low or high, accumulation will play a crucial role in TSEs.
4. THERE are and have been for some time many TSEs in the USA. TME in mink, Scrapie in Sheep and Goats, and unidentified TSE in USA cattle. all this has been proven, but the TSE in USA cattle has been totally ignored for decades. i will document this data below in my references.
5. UNTIL we ban all ruminant by-products from being fed back to ALL ruminants, until we rapid TSE test (not only deer/elk) but cattle in sufficient numbers to find (1 million rapid TSE test in USA cattle annually for 5 years), any partial measures such as the ones proposed while ignoring sub-clinical TSEs and not rapid TSE testing cattle, not closing down feed mills that continue to violate the FDA's BSE feed regulation (21 CFR 589.2000) and not making freely available those violations, will only continue to spread these TSE mad cow agents in the USA. I am curious what we will call a phenotype in a species that is mixed with who knows how many strains of scrapie, who knows what strain or how many strains of TSE in USA cattle, and the CWD in deer and elk (no telling how many strains there), but all of this has been rendered for animal feeds in the USA for decades. it will get interesting once someone starts looking in all species, including humans here in the USA, but this has yet to happen...
6. IT is paramount that CJD be made reportable in every state (especially ''sporadic'' cjd), and that a CJD Questionnaire must be issued to every family of a victim of TSE. only checking death certificates will not be sufficient. this has been proven as well (see below HISTORY OF CJD -- CJD QUESTIONNAIRE)
7. WE must learn from our past mistakes, not continue to make the same mistakes...
REFERENCES
Six white-tailed deer fawns test positive for CWD
MADISON -- Six fawns in the area of south central Wisconsin where chronic wasting disease has been found in white-tailed deer have tested positive for the disease, according to Department of Natural Resources wildlife health officials. These are the youngest wild white-tailed deer detected with chronic wasting disease (CWD) to date.
Approximately 4,200 fawns, defined as deer under 1 year of age, were sampled from the eradication zone over the last year. The majority of fawns sampled were between the ages of 5 to 9 months, though some were as young as 1 month. Two of the six fawns with CWD detected were 5 to 6 months old. All six of the positive fawns were taken from the core area of the CWD eradication zone where the highest numbers of positive deer have been identified.
snip...
http://www.dnr.state.wi.us/org/caer/ce/news/on/2003/on20030513.htm#art4
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Issued: Monday, 28 August 2000 NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH FINDINGS RELEVANT TO CJD AND BSE
A team of researchers led by Professor John Collinge at the Medical Research Council Prion Unit1 report today in the Proceedings of the National Academy of Sciences, on new evidence for the existence of a 'sub-clinical' form of BSE in mice which was unknown until now.
The scientists took a closer look at what is known as the 'species barrier' - the main protective factor which limits the ability of prions2 to jump from one species to infect another. They found the mice had a 'sub-clinical' form of disease where they carried high levels of infectivity but did not develop the clinical disease during their normal lifespan. The idea that individuals can carry a disease and show no clinical symptoms is not new. It is commonly seen in conventional infectious diseases.
Researchers tried to infect laboratory mice with hamster prions3 called Sc237 and found that the mice showed no apparent signs of disease. However, on closer inspection they found that the mice had high levels of mouse prions in their brains. This was surprising because it has always been assumed that hamster prions could not cause the disease in mice, even when injected directly into the brain.
In addition the researchers showed that this new sub-clinical infection could be easily passed on when injected into healthy mice and hamsters.
The height of the species barrier varies widely between different combinations of animals and also varies with the type or strain of prions. While some barriers are quite small (for instance BSE easily infects mice), other combinations of strain and species show a seemingly impenetrable barrier. Traditionally, the particular barrier studied here was assumed to be robust.
Professor John Collinge said: "These results have a number of important implications. They suggest that we should re-think how we measure species barriers in the laboratory, and that we should not assume that just because one species appears resistant to a strain of prions they have been exposed to, that they do not silently carry the infection. This research raises the possibility, which has been mentioned before, that apparently healthy cattle could harbour, but never show signs of, BSE.
"This is a timely and unexpected result, increasing what we know about prion disease. These new findings have important implications for those researching prion disease, those responsible for preventing infected material getting into the food chain and for those considering how best to safeguard health and reduce the risk that theoretically, prion disease could be contracted through medical and surgical procedures."
ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS SET BY THE JOURNAL.
FOR FURTHER INFORMATION CONTACT THE MRC PRESS OFFICE ON 020 7637 6011 (OFFICE HOURS) OR 07818 428297 OR 0385 774357 (OUT-OF-OFFICE-HOURS) OR PROFESSOR JOHN COLLINGE ON 020 7594 3760. PLEASE NOTE THAT OWING TO TRAVEL COMMITMENTS PROFESSOR COLLINGE WILL ONLY BE AVAILABLE UNTIL 16.30 ON FRIDAY 25 AUGUST AND CONTACTABLE AGAIN ON MONDAY 28 AUGUST VIA THE MRC PRESS OFFICE. DR ANDREW HILL (A CO-AUTHOR ON THE PAPER) FROM THE DEPARTMENT OF PATHOLOGY AT THE UNIVERSITY OF MELBOURNE WILL BE AVAILABLE ON 00 61 3 8344 3995 (DURING OFFICE HOURS) OR 00 61 3 9443 0009 (OUT-OF-OFFICE HOURS). PLEASE NOTE THAT AUSTRALIA IS TEN HOURS AHEAD OF UK TIME.
NOTES FOR EDITORS
Professor Collinge is a consultant neurologist and Director of the newly formed MRC Prion Unit based at The Imperial College School of Medicine at St Mary's Hospital. He is also a member of the UK Government's Spongiform Encephalopathy Advisory Committee (SEAC). The MRC prion unit is was set up in 1999, and its work includes molecular genetic studies of human prion disease and transgenic modelling of human prion diseases.
Prions are unique infectious agents that cause fatal brain diseases such as Creutzfeldt-Jakob disease (CJD) in humans and scrapie and BSE (mad cow disease) in animals. In some circumstances prions from one species of animals can infect another and it is clear that BSE has done this to cause the disease variant CJD in the UK and France. It remains unclear how large an epidemic of variant CJD will occur over the years ahead.
The strain of prion used here to infect the mice is the Sc237 strain (also known as 263K) which infects hamsters, and until now was assumed not to infect mice.
This research was funded by the Medical Research Council and Wellcome Trust.
The Medical Research Council (MRC) is a national organisation funded by the UK tax-payer. Its business is medical research aimed at improving human health; everyone stands to benefit from the outputs. The research it supports and the scientists it trains meet the needs of the health services, the pharmaceutical and other health-related industries and the academic world. MRC has funded work which has led to some of the most significant discoveries and achievements in medicine in the UK. About half of the MRC's expenditure of £345 million is invested in over 50 of its Institutes and Units, where it employs its own research staff. The remaining half goes in the form of grant support and training awards to individuals and teams in universities and medical schools.
The Wellcome Trust is the world's largest medical research charity with a spend of some £600 million in the current financial year 1999/2000. The Wellcome Trust supports more than 5,000 researchers, at 400 locations, in 42 different countries to promote and foster research with the aim of improving human and animal health. As well as funding major initiatives in the public understanding of science, the Wellcome Trust is the country's leading supporter of research into the history of medicine.
©2002 Medical Research Council Data Protection policy Contact the MRC
http://www.mrc.ac.uk/index/public_interest/public-press_office/public-press_releases_2000/public-mrc-43-00.htm
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Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus ) Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3, Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1
Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1 Department of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, University of Wyoming, Laramie, WY 82070, USA 2 Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, CO 80526-2097, USA3 Colorado State University Veterinary Diagnostic Laboratory, 300 West Drake Road, Fort Collins, CO 80523-1671, USA4 Animal Disease Research Unit, Agricultural Research Service, US Department of Agriculture, 337 Bustad Hall, Washington State University, Pullman, WA 99164-7030, USA5
Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail ehoover@lamar.colostate.edu
Mule deer fawns (Odocoileus hemionus) were inoculated orally with a brain homogenate prepared from mule deer with naturally occurring chronic wasting disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns were necropsied and examined for PrP res, the abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an immunohistochemistry assay modified to enhance sensitivity. PrPres was detected in alimentary-tract-associated lymphoid tissues (one or more of the following: retropharyngeal lymph node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42 days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No PrPres staining was detected in lymphoid tissue of three control fawns receiving a control brain inoculum, nor was PrPres detectable in neural tissue of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue treatment with formic acid, proteinase K and hydrated autoclaving prior to immunohistochemical staining with monoclonal antibody F89/160.1.5. These results indicate that CWD PrP res can be detected in lymphoid tissues draining the alimentary tract within a few weeks after oral exposure to infectious prions and may reflect the initial pathway of CWD infection in deer. The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species.
snip...
These results indicate that mule deer fawns develop detectable PrP res after oral exposure to an inoculum containing CWD prions. In the earliest post-exposure period, CWD PrPres was traced to the lymphoid tissues draining the oral and intestinal mucosa (i.e. the retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and ileocaecal lymph nodes), which probably received the highest initial exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum and spleen in a 10-month-old naturally infected lamb by mouse bioassay. Eight of nine sheep had infectivity in the retropharyngeal lymph node. He concluded that the tissue distribution suggested primary infection via the gastrointestinal tract. The tissue distribution of PrPres in the early stages of infection in the fawns is strikingly similar to that seen in naturally infected sheep with scrapie. These findings support oral exposure as a natural route of CWD infection in deer and support oral inoculation as a reasonable exposure route for experimental studies of CWD.
snip...
http://vir.sgmjournals.org/cgi/content/full/80/10/2757
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now, just what is in that deer feed? _ANIMAL PROTEIN_
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES Date: Sat, 25 May 2002 18:41:46 -0700 From: "Terry S. Singeltary Sr." Reply-To: BSE-L To: BSE-L
8420-20.5% Antler Developer For Deer and Game in the wild Guaranteed Analysis Ingredients / Products Feeding Directions
snip...
_animal protein_
http://www.surefed.com/deer.htm
BODE'S GAME FEED SUPPLEMENT #400 A RATION FOR DEER NET WEIGHT 50 POUNDS 22.6 KG.
snip...
_animal protein_
http://www.bodefeed.com/prod7.htm
Ingredients
Grain Products, Plant Protein Products, Processed Grain By-Products, Forage Products, Roughage Products 15%, Molasses Products, __Animal Protein Products__, Monocalcium Phosphate, Dicalcium Pyosphate, Salt, Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol (source of Vitamin D3), Vitamin E Supplement, Vitamin B12 Supplement, Riboflavin Supplement, Niacin Supplement, Calcium Panothenate, Choline Chloride, Folic Acid, Menadione Soduim Bisulfite Complex, Pyridoxine Hydorchloride, Thiamine Mononitrate, d-Biotin, Manganous Oxide, Zinc Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried Sacchoromyces Berevisiae Fermentation Solubles, Cellulose gum, Artificial Flavors added.
http://www.bodefeed.com/prod6.htm ===================================
MORE ANIMAL PROTEIN PRODUCTS FOR DEER
Bode's #1 Game Pellets A RATION FOR DEER F3153
GUARANTEED ANALYSIS Crude Protein (Min) 16% Crude Fat (Min) 2.0% Crude Fiber (Max) 19% Calcium (Ca) (Min) 1.25% Calcium (Ca) (Max) 1.75% Phosphorus (P) (Min) 1.0% Salt (Min) .30% Salt (Max) .70%
Ingredients
Grain Products, Plant Protein Products, Processed Grain By-Products, Forage Products, Roughage Products, 15% Molasses Products, __Animal Protein Products__, Monocalcium Phosphate, Dicalcium Phosphate, Salt, Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol (source of Vitamin D3) Vitamin E Supplement, Vitamin B12 Supplement, Roboflavin Supplement, Niacin Supplement, Calcium Pantothenate, Choline Chloride, Folic Acid, Menadione Sodium Bisulfite Complex, Pyridoxine Hydrochloride, Thiamine Mononitrate, e - Biotin, Manganous Oxide, Zinc Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried Saccharyomyces Cerevisiae Fermentation Solubles, Cellulose gum, Artificial Flavors added.
FEEDING DIRECTIONS Feed as Creep Feed with Normal Diet
http://www.bodefeed.com/prod8.htm
INGREDIENTS
Grain Products, Roughage Products (not more than 35%), Processed Grain By-Products, Plant Protein Products, Forage Products, __Animal Protein Products__, L-Lysine, Calcium Carbonate, Salt, Monocalcium/Dicalcium Phosphate, Yeast Culture, Magnesium Oxide, Cobalt Carbonate, Basic Copper Chloride, Manganese Sulfate, Manganous Oxide, Sodium Selenite, Zinc Sulfate, Zinc Oxide, Sodium Selenite, Potassium Iodide, Ethylenediamine Dihydriodide, Vitamin E Supplement, Vitamin A Supplement, Vitamin D3 Supplement, Mineral Oil, Mold Inhibitor, Calcium Lignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium Bisulfite Complex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid, Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate
DIRECTIONS FOR USE
Deer Builder Pellets is designed to be fed to deer under range conditions or deer that require higher levels of protein. Feed to deer during gestation, fawning, lactation, antler growth and pre-rut, all phases which require a higher level of nutrition. Provide adequate amounts of good quality roughage and fresh water at all times.
http://www.profilenutrition.com/Products/Specialty/deer_builder_pellets.html
===================================================
DEPARTMENT OF HEALTH & HUMAN SERVICES PUBLIC HEALTH SERVICE FOOD AND DRUG ADMINISTRATION
April 9, 2001 WARNING LETTER
01-PHI-12 CERTIFIED MAIL RETURN RECEIPT REQUESTED
Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy Lake, PA 16145 PHILADELPHIA DISTRICT
Tel: 215-597-4390
Dear Mr. Raymond:
Food and Drug Administration Investigator Gregory E. Beichner conducted an inspection of your animal feed manufacturing operation, located in Sandy Lake, Pennsylvania, on March 23, 2001, and determined that your firm manufactures animal feeds including feeds containing prohibited materials. The inspection found significant deviations from the requirements set forth in Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant Feed. The regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE) . Such deviations cause products being manufactured at this facility to be misbranded within the meaning of Section 403(f), of the Federal Food, Drug, and Cosmetic Act (the Act).
Our investigation found failure to label your swine feed with the required cautionary statement "Do Not Feed to cattle or other Ruminants" The FDA suggests that the statement be distinguished by different type-size or color or other means of highlighting the statement so that it is easily noticed by a purchaser.
In addition, we note that you are using approximately 140 pounds of cracked corn to flush your mixer used in the manufacture of animal feeds containing prohibited material. This flushed material is fed to wild game including deer, a ruminant animal. Feed material which may potentially contain prohibited material should not be fed to ruminant animals which may become part of the food chain.
The above is not intended to be an all-inclusive list of deviations from the regulations. As a manufacturer of materials intended for animal feed use, you are responsible for assuring that your overall operation and the products you manufacture and distribute are in compliance with the law. We have enclosed a copy of FDA's Small Entity Compliance Guide to assist you with complying with the regulation... blah, blah, blah...
http://www.fda.gov/foi/warning_letters/g1115d.pdf
==================================
snip...
posted here;
http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed
EMC 7 Terry S. Singeltary Sr. Vol #: 1
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed
EMC 7 Terry S. Singeltary Sr. Vol #: 1
http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm
Chronic Wasting Disease and Potential Transmission to Humans
Ermias D. Belay,*Comments Ryan A. Maddox,* Elizabeth S. Williams, Michael W. Miller,! Pierluigi Gambetti,§ and Lawrence B. Schonberger* *Centers for Disease Control and Prevention, Atlanta, Georgia, USA; University of Wyoming, Laramie, Wyoming, USA; !Colorado Division of Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve University, Cleveland, Ohio, USA
Suggested citation for this article: Belay ED, Maddox RA, Williams ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease and potential transmission to humans. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from: http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm
------------------------------------------------------------------------
Chronic wasting disease (CWD) of deer and elk is endemic in a tri-corner area of Colorado, Wyoming, and Nebraska, and new foci of CWD have been detected in other parts of the United States. Although detection in some areas may be related to increased surveillance, introduction of CWD due to translocation or natural migration of animals may account for some new foci of infection. Increasing spread of CWD has raised concerns about the potential for increasing human exposure to the CWD agent. The foodborne transmission of bovine spongiform encephalopathy to humans indicates that the species barrier may not completely protect humans from animal prion diseases. Conversion of human prion protein by CWD-associated prions has been demonstrated in an in vitro cell-free experiment, but limited investigations have not identified strong evidence for CWD transmission to humans. More epidemiologic and laboratory studies are needed to monitor the possibility of such transmissions.
snip...
Transmission to Other Animals
Concerns have been raised about the possible transmission of the CWD agent to domestic animals, such as cattle and sheep, which may come in contact with infected deer and elk or CWD-contaminated environments. If such transmissions were to occur, they would potentially increase the extent and frequency of human exposure to the CWD agent. In addition, passage of the agent through a secondary host could alter its infectious properties, increasing its potential for becoming more pathogenic to humans. This phenomenon may have occurred with BSE when a strain of scrapie, a possible original source of the BSE outbreak, changed its pathogenic properties for humans after infecting cattle. However, the exact origin of BSE remains unknown.
Although CWD does not appear to occur naturally outside the cervid family, it has been transmitted experimentally by intracerebral injection to a number of animals, including laboratory mice, ferrets, mink, squirrel monkeys, and goats (1 ,26 ). In an experimental study, the CWD agent was transmitted to 3 of 13 intracerebrally injected cattle after an incubation period of 22 to 27 months (27 ). The susceptibility of cattle intracerebrally challenged with the agent of this disease was substantially less than that observed after intracerebral scrapie challenge: nine of nine cattle succumbed to scrapie challenge after intracerebral injection (28 ). In ongoing experimental studies, after >6 years of observation, no prion disease has developed in 11 cattle orally challenged with the CWD agent or 24 cattle living with infected deer herds (E.S. Williams and M.W. Miller, unpub. data) (1 ). In addition, domestic cattle, sheep, and goat residing in research facilities in close contact with infected cervids did not develop a prion disease.
[PLEASE NOTE, THIS HAS BEEN UPDATED TO AN ADDITIONAL 2 COWS AND ONE SHEEP, making the total transmission of CWD to cattle at 5 and one transmission of CWD to one sheep, MILLER ET AL BSE-L...TSS]
Conclusions
The lack of evidence of a link between CWD transmission and unusual cases of CJD, despite several epidemiologic investigations, and the absence of an increase in CJD incidence in Colorado and Wyoming suggest that the risk, if any, of transmission of CWD to humans is low. Although the in vitro studies indicating inefficient conversion of human prion protein by CWD-associated prions raise the possibility of low-level transmission of CWD to humans, no human cases of prion disease with strong evidence of a link with CWD have been identified. However, the transmission of BSE to humans and the resulting vCJD indicate that, provided sufficient exposure, the species barrier may not completely protect humans from animal prion diseases. Because CWD has occurred in a limited geographic area for decades, an adequate number of people may not have been exposed to the CWD agent to result in a clinically recognizable human disease. The level and frequency of human exposure to the CWD agent may increase with the spread of CWD in the United States. Because the number of studies seeking evidence for CWD transmission to humans is limited, more epidemiologic and laboratory studies should be conducted to monitor the possibility of such transmissions. Studies involving transgenic mice expressing human and cervid prion protein are in progress to further assess the potential for the CWD agent to cause human disease. Epidemiologic studies have also been initiated to identify human cases of prion disease among persons with an increased risk for exposure to potentially CWD-infected deer or elk meat (47 ). If such cases are identified, laboratory data showing similarities of the etiologic agent to that of the CWD agent would strengthen the conclusion for a causal link. Surveillance for human prion diseases, particularly in areas where CWD has been detected, remains important to effectively monitor the possible transmission of CWD to humans. Because of the long incubation period associated with prion diseases, convincing negative results from epidemiologic and experimental laboratory studies would likely require years of follow-up. In the meantime, to minimize the risk for exposure to the CWD agent, hunters should consult with their state wildlife agencies to identify areas where CWD occurs and continue to follow advice provided by public health and wildlife agencies. Hunters should avoid eating meat from deer and elk that look sick or test positive for CWD. They should wear gloves when field-dressing carcasses, bone-out the meat from the animal, and minimize handling of brain and spinal cord tissues. As a precaution, hunters should avoid eating deer and elk tissues known to harbor the CWD agent (e.g., brain, spinal cord, eyes, spleen, tonsils, lymph nodes) from areas where CWD has been identified.
snip...
see full text ;
http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734.
http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States
Email Terry S. Singeltary:
flounder@wt.net
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to
comment on the CDC's attempts to monitor the occurrence of emerging
forms of CJD. Asante, Collinge et al [1] have reported that BSE
transmission to the 129-methionine genotype can lead to an alternate
phenotype that is indistinguishable from type 2 PrPSc, the commonest
sporadic CJD. However, CJD and all human TSEs are not reportable
nationally. CJD and all human TSEs must be made reportable in every
state and internationally. I hope that the CDC does not continue to
expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in
the USA in both animal and man. CWD in deer/elk is spreading rapidly and
CWD does transmit to mink, ferret, cattle, and squirrel monkey by
intracerebral inoculation. With the known incubation periods in other
TSEs, oral transmission studies of CWD may take much longer. Every
victim/family of CJD/TSEs should be asked about route and source of this
agent. To prolong this will only spread the agent and needlessly expose
others. In light of the findings of Asante and Collinge et al, there
should be drastic measures to safeguard the medical and surgical arena
from sporadic CJDs and all human TSEs. I only ponder how many sporadic
CJDs in the USA are type 2 PrPSc?
http://www.neurology.org/cgi/eletters/60/2/176#535
BRITISH MEDICAL JOURNAL
http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2
http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1
IN SHORT, we have floundered to long in the regulation of human/animal TSEs. EACH day longer, more and more people will become exposed. YOU can step up to the plate and act now, forget about corporate/political interest, act in the best of public health, with the available science to date (it's all there), or you can pay later. AT what cost you ask, depends which loved one you loose to this agent. THIS goes far beyond the bad hamburger. 85%+ of all CJD (sporadic), did not just happen. sporadic CJD simply means CJD from unknown route and source of agent, and we have many of both right here in the USA. What phenotype is anyone's guess?
ALL SRM must be removed. ALL animals for human/animal consumption must be tested for TSE. ALL human TSEs must be made reportable Nationally and Internationally. with CJD/TSE questionnaire asking real questions as to route and source of agent. THIS must pertain to all ages!
CJD WATCH
http://www.fortunecity.com/healthclub/cpr/349/part1cjd.htm
CJD Watch message board
http://disc.server.com/Indices/167318.html
TERRY S. SINGELTARY SR. P.O. BOX 42 BACLIFF, TEXAS 77518
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