spontaneous TSE of any species has never been proven. THERE is NO evidence of a 'spontaneous' TSE anywhere that is infectious and shows the pathology of any natural TSE. what prusiner and soto produced looked like no nature TSE. are we expected to believe that the tooth fairy and or santa claus brought this disease to us? i think not. we have mad cows in Alabama, we have mad cow feed in Alabama, we have mad cows in Texas, we have mad cow feed in Texas.

My Photo
Location: BACLIFF, Texas, United States

My mother was murdered by what I call corporate and political homicide i.e. FOR PROFIT! she died from a rare phenotype of CJD i.e. the Heidenhain Variant of Creutzfeldt Jakob Disease i.e. sporadic, simply meaning from unknown route and source. I have simply been trying to validate her death DOD 12/14/97 with the truth. There is a route, and there is a source. There are many here in the USA. WE must make CJD and all human TSE, of all age groups 'reportable' Nationally and Internationally, with a written CJD questionnaire asking real questions pertaining to route and source of this agent. Friendly fire has the potential to play a huge role in the continued transmission of this agent via the medical, dental, and surgical arena. We must not flounder any longer. ...TSS

Wednesday, January 28, 2009

TAFS1 Position Paper on Specified Risk Materials (January, 2009)


(January 2009)

TAFS1 Position Paper on Specified Risk Materials

Specified Risk Materials, or SRM, are tissues that have been designated for removal from the carcases of cattle, and excluded from human food. They have been shown, or assumed, to contain significant amounts of BSE infectivity in infected animals. By prohibiting their consumption it is considered to provide a substantial reduction in risk to consumers in countries where BSE has been shown to exist and in countries having a likely BSE-risk. SRM are also designated in sheep and goats. This was stipulated as a precautionary measure assuming that sheep and goats may have become infected with BSE. The finding of BSE in one goat has confirmed this assumption. SRM are also usually removed from animal feed as well, and this strengthens more general feed bans that are intended to prevent infection of cattle and small ruminants with BSE and lead to the elimination of BSE in each country. This document essentially concentrates on SRM in the context of human health, except in explaining the evolution of definitions and protective measures. Considerable confusion surrounds the term “specified risk materials” or SRM. This confusion ranges from the reasons for designation of such tissues or organs for destruction rather than consumption, and the extent to which it is necessary to ensure full compliance with regulations that require their removal from the food chain. This note briefly summarises the reasons for the designation of SRM, and concludes by listing current rules in the Europe. This table will be modified as rules change. Although the table includes a list of sheep and goat tissues that are defined as SRM, the note primarily addresses the background to bovine SRM.

Why are tissues designated as SRM?

? This note does not propose to describe the full chronology of SRM definition, but will give an explanation for the designation of each current SRM below.

? In 1989, in the early stages of the BSE eradication programme in the United Kingdom, it was recognised that for every cow that was identified with clinical

1 TAFS is an international platform created by a group of scientists, food industry experts, animal health regulators, epidemiologists, diagnosticians, food producers, and consumers. Its purpose is to establish and maintain lines of communication for the dissemination of reliable information to the public that can maintain confidence in the safety of food with regard to Transmissible Animal Diseases (TAD).



BSE there must have been others that were infected, but apparently healthy, that were being slaughtered for human consumption. These could not be detected while alive and prevented from being slaughtered for consumption. It was therefore felt that reliance on the slaughter and destruction of clinically affected cattle was insufficient to protect public health, and that additional measures were required.

? As a result, consideration was given to whether the entire carcase represented a risk to consumer, or whether it was possible to identify specific tissues that could be removed and excluded from the food chain. In other words, in the absence of evidence that BSE did actually represent a risk to humans, what acceptable and proportionate additional safety measures could be put in place? Was it a ban on the consumption of any bovine tissues, or was it possible to avoid taking any action at all?

? By 1989 research had not progressed to the point of being able to identify which bovine tissues were infectious, other than brain(3,16). The authorities therefore resorted to an analysis of known data from the similar disease of sheep, scrapie(20). Some limited research had been done that indicated the range of tissues that might be infectious, and the extent to which they might be infectious. In other words it was clear that some tissues contained higher levels of infectivity than others, and logically could be considered to represent a greater risk to consumers. This conservative approach aimed to minimise risk of human exposure through food.

? The outcome was a list of tissues that could be removed without destroying the economic basis of the industry, and could still be defended as proportionate should the measures be challenged in court. It was recognized that other tissues, which are not on the list, might be infectious, but at such low levels that detection was difficult.

? The initial listing in the UK excluded these tissues, then called Specified Bovine Offals (SBO), from the human food chain(20). In September 1990 they were also excluded from all animal food, and this reinforced the feed ban that was the major measure introduced to eradicate BSE. The term SBO was later changed to SRM and also adopted in EU and other legislation.

? The development in recent years of rapid (post mortem) diagnostic tests has not eliminated the need to remove SRM. Although extremely effective, the tests are still only effective in the later stages of incubation, so they cannot detect all infected animals(27).

Has BSE infectivity been detected in all SRM listed later in this position paper?

? Yes. Research on bovine tissues, from naturally and experimentally infected cattle, has now progressed to the point where there is a clearer picture of which tissues are infectious, and those where no infectivity has been found(1, 2, 5, 13, 17, 18, 19, 21, 23, 26, 28-35) .

? In naturally infected cattle the brain, spinal cord and retina (eye) have been shown to be infectious(5,16, 35). In addition, positivity or infectivity was detected in some peripheral nerves that would not normally be removed as SRM(5,17,18,19). The amount of infectivity present is low, and considered be up to 1000-fold lower than the brain.

? In experimentally infected cattle, brain and spinal cord were again been confirmed to be infectious, but in addition the distal ileum (lower small intestine) also contained significant amounts of infectivity(31, 32). Two key ganglia, which are key intermediate points linking the central and peripheral nervous systems, namely



the trigeminal and dorsal root ganglia (DRG), were also clearly infectious(32, 33). This is not surprising given their close association with central nervous tissue. Peripheral nerves have also been demonstrated to become positive after the brain and spinal cord(1, 19). Completion of bioassay studies has also enabled a better understanding of the sequence of events, and rate of accumulation of infectivity, especially in relation to ileum, brain and spinal cord(1,2), and have confirmed the basic assumptions upon risk management policy were based.

? In addition, in experimentally infected cattle, a single positive result has indicated the possible presence of infectivity in bone marrow at about the time of clinical onset(33). Further attempts to resolve this anomaly, by inoculation of cattle with bone marrow collected at different time points, were unsuccessful(21), and concluded that the presence of infectivity was either a rare event, or was more consistently present at levels below the limits of detection. As discussed by EFSA in the context of risk from lingual tonsil(11), this was considered to represent a negligible consumer risk when considered alongside the low prevalence of BSE in the EU at that time.

? In addition, a low amount of infectivity was detected in tonsil early in the incubation and maintained during the time course(13,32, 34).

? A single calf inoculated with pooled third eyelid tissue from naturally infected cows has succumbed to BSE, indicating the presence of infectivity in the pooled tissue. None of the remaining four inoculated cattle became infected, so this result remains uninterpretable(35).

Why are other tissues/organs not expected to be infectious included in the list for exclusion from consumption?

? Some SRM have not been inherently shown to be infected, but with experience it is clear that their close association with other SRM, especially the central nervous system, represents a real risk of cross contamination(26). Again, a precautionary approach has been adopted.

? For example, the skull has not been demonstrated to be inherently infectious, but it is impossible to remove the brain from the skull without leaving traces of brain tissue behind(26). Similarly the eye is also infected. Therefore, the definition of skull as SRM acknowledges the remaining risk due to the retained brain tissue, or contamination with brain as a result of the slaughtering process. The designation of skull means that the practicalities of compliance and enforcement are easier to handle, and there is less exposure of abattoir operators to brain tissue while it remains encased within the skull. ? The vertebral column is also designated because of its close association with dorsal root ganglia (DRG) and due to contamination with spinal cord tissue. DRG sit just on the outside of the spine where the spinal nerves pass through from the spinal cord(26). If the vertebral column (spine) was left attached to meat, for example in a T-bone steak, there is therefore a danger that the DRG would be consumed. The spinal cord contamination arises as a result of the splitting process as the saw that cuts the carcase in half passes through the cord and contaminates the cut surface of the spine. ? In both situations described above the use of vertebral column for the production of mechanically recovered meat, or mechanically separated meat, would strip off the DRG and contamination, transferring infectivity into the MRM/MSM which is used in manufactured meat products. Indeed, European legislation has gone further



than just designating vertebral column as an SRM. The use of ruminant bones for production of mechanically recovered meat (MRM) is prohibited. Have all tissues been tested for the presence of infectivity?

? No. There are limits to the number of tissues that can be tested. Decisions on which tissues to test have historically been driven by several factors such as:-

? which represent a risk to consumers because they are eaten,

? which are key tissues in understanding the biology of BSE in cattle, and

? which represent a risk to humans through the manufacture of other products such as pharmaceuticals and medical devices.

? Nevertheless, based upon evidence from other species (sheep scrapie) and the results of assays of bovine tissues, and audits of the use of bovine tissues, it is considered that all key tissues have been assayed. Will the list be dynamic?

? Yes(14). Research is still ongoing, and it is still possible that infectivity will be detected in tissues that have been negative so far. The use of cattle for infectivity assays, or technological breakthroughs to produce alternative assay systems (see above) mean that the analytical sensitivity of current assays is greater than those used in earlier studies. It is therefore not possible to exclude the possibility that new positive results will arise. Their significance, in terms of quantifying the amount of infectivity present, will be critical to risk assessments that will determine whether authorities define them as SRM.

? Nevertheless, current evidence suggests that this is a theoretical rather than real scenario. Authorities and expert committees cannot however remain oblivious to new findings, and may need to take into account consumer confidence as well as risk assessments in determining whether or not to add new tissues to the SRM list.

? Also it has to be taken into account that new findings of positive tissues may come at a time when the prevalence of BSE is very low and decreasing and the vast majority of cattle consumed have to be considered uninfected. In this situation authorities may conclude that the addition of further tissues to the list may be disproportionate to the risk. This has indeed been the case in relation to peripheral nerves, which have not been designated at SRM.

? In the TSE roadmap of the EU, published in July 2005(6), next steps in the BSE policy on different points are evaluated. Concerning SRM it is accepted that the list of SRM could be modified in the medium term, based on new and evolving scientific knowledge and the results of the surveillance programs, and subject to appropriate evaluation and consultation.

Designated bovine SRM in Europe

? Brain – expected to be infectious by extrapolation from sheep scrapie, and subsequently confirmed for BSE. Experimental evidence suggests that the brain becomes infectious in the later stages of incubation.

? Spinal cord – expected to be infectious by extrapolation from sheep scrapie, and subsequently confirmed for BSE. Experimental evidence suggests that the spinal cord becomes infectious in the later stages of incubation(1).

? Tonsil – expected to be infectious by extrapolation from sheep scrapie, but not subsequently confirmed for BSE from naturally infected cattle, even by bioassay



in cattle. Result from experimentally infected cattle, suggests that the palatine tonsil becomes infectious in the early stage of the incubation and the very low infectivity is maintained during the time course(7,13,34). Tongue itself is not considered as SRM. However, according to EU-legislation, “tongue should be harvested by a transverse cut rostral to the lingual process of the basihyoid bone”, due to possible contamination of tonsil tissue. Further consideration of the residual risk associated with lymphoid tissue that remains within the tongue after adopting this removal procedure did not result in recommendations for more extensive trimming of the tongue(11). In part this was due to the low prevalence of BSE in the EU by that time.

? Intestine – the distal ileum was expected to be infectious by extrapolation from sheep scrapie, and this was subsequently confirmed for BSE in experimentally infected cattle especially in the early stages of incubation. Logic suggests that it must also be infectious in naturally infected cattle in the early stages of incubation. This infectivity was particularly associated with Peyer’s patches(29), collections of lymphoid tissue that form a first line of defence against infection through the intestinal wall. This result has not been replicated in naturally infected cattle, although immunostaining methods have shown the presence of abnormal prion protein in the nervous plexuses of the intestine. This discrepancy is considered to be most probably due to the fact that the Peyer’s patches regress as cattle reach maturity, and consequently reduce the likelihood of finding any infectivity that may remain. The majority of infected cows die of clinical BSE at five to seven years of age, after the Peyer’s patches have regressed. Nevertheless, the positive immunostaining of the nervous plexuses, which extend throughout the intestine, does justify continued listing of intestine as SRM while there is a danger that cattle will have been exposed to BSE(10,25).

? Skull – designated because of association with brain and eye, with resultant contamination through the slaughtering process or because of residual brain tissue following removal of the brain.

? Vertebral column – designated because of a combination of close association with DRG, and the superficial contamination of the cut surface of the spine with spinal cord during the carcase splitting process.

? Age restrictions(8, 26) – all of the above tissues will not necessarily be designated for all ages of cattle consumed. This is because experimental evidence has suggested that they only represent a risk at particular stages of the incubation. If a tissue is infectious early in the incubation then it is normal to designate the tissue for all ages. If infectivity is detected late in the incubation then it is possible to designate the tissue in older animals only, especially where the designation is a result of contamination (eg. vertebral column).

Designated ovine SRM

? SRM designated in sheep are based primarily on evidence from the study of sheep scrapie, but the outcome is consistent with our understanding of the behaviour of BSE in sheep that are susceptible to infection with BSE(4,9,15). ? The designation adopts a cautious balance between significantly reducing the risk to consumers should BSE be present in the sheep and goat population and the introduction of extensive SRM removal which would significantly damage sheep and meat industries in affected countries(9,22,24).



? There is no doubt that the confirmation that BSE is present in the sheep population will result in an immediate revision of this list, or possibly even a prohibition of the consumption of certain categories of sheep meat. The confirmation of BSE in a goat(12) did not however have this effect on the definition of SRM. The list of SRMs in small ruminants was not modified as a result of this finding (see position paper on BSE in small ruminants).



A summary of designated SRM in Europe as at January 2009 European Union and Switzerland Cattle Skull (including brain and eyes) 12 months Tonsils All ages Spinal cord 12 months Vertebral column (including dorsal root ganglia - DRG – but excluding vertebrae of the tail and the transverse processes of lumbar and thoracic vertebrae) 30 months Intestines and mesentery All ages Sheep and goats Skull (including brain and eyes) 12 month Spinal cord 12 months Tonsils 12 months Ileum All ages Spleen All ages




1. Arnold, M, A., Ryan, J.B.M., Konold, T., Simmons, M.M., Spencer, Y.I., Wear, A., Chaplin, M., Stack, M., Czub, S., Mueller, R., Webb, P.R., Davis, A., Spiropoulos, J., Holdaway, J., Hawkins, S.A.C., Austin, A.R. & Wells, G.A.H. (2007). Estimating the temporal relationship between PrPSc detection and incubation period in experimental bovine spongiform encelphalopathy of cattle. J. Gen. Virol. 88:3198-3208.

2. Arnold, M.A., Hawkins, S.A.C., Green, R., Dexter, I. & Wells, G.A.H. (2009). Pathogenesis of experimental bovine spongiform encephalopathy (BSE): estimation of tissue infectivity according to incubation period. Vet. Res. 40:08

3. Barlow R.M., & Middleton D J (1990). Dietary transmission of bovine spongiform encephalopathy to mice. Vet. Rec, 126:111-112.

4. Bellworthy, S.J., Hawkins, S.A.C., Green, R.B., Blamire, I., Dexter, G., Dexter, I., Lockey, R., Jeffrey, M., Ryder, S., Berthelin-Baker, C. & Simmons, M.M. (2005) Tissue distribution of bovine spongiform encephalopathy infectivity in sheep following oral challenge – preliminary results. Vet. Rec. 156:197-202.

5. Buschmann A., Groschup MH. (2005). Highly BSE-sensitive transgenic mice confirm the essential restriction of infectivity to the nervous system in clinically diseased cattle. J Infect Dis. 192:934-42.

6. EC (2005) – European Commission – The TSE Roadmap. Com(2005) 322 Final.

7. EFSA (2004). - Opinion of the Scientific Panel on Biological Hazards of the European Food Safety Authority on BSE risk from bovine tonsil and consumption of bovine tongue. The EFSA Journal 41: 1-4.

8. EFSA (2005). - Opinion of the Scientific Panel on Biological Hazards on the assessment of the age limit in cattle for the removal of certain specified risk materials (SRM). The EFSA Journal. 220: 1-7.

9. EFSA (2005). - Opinion of the Scientific Panel on Biological Hazards on a quantitative assessment of risk posed to humans by tissues of small ruminants in case BSE is present in these animal populations” The EFSA Journal. 227: 1-11.

10. EFSA (2007). - Opinion of the Scientific Panel on Biological Hazards on a request from the European Commission on quantitative histological studies and the re-



assessment of the BSE related risk of bovine intestines after processing into natural sausage casings. The EFSA Journal. 464: 1-14.,4.pdf?ssbinary=true

11. EFSA (2008). Scientific Opinion of the Scientific Panel on Biological Hazards on a request from the European Commission on consumption of beef tongue: human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings. EFSA Journal. 700: 1-24.,1.pdf?ssbinary=true

12. Eloit M, Adjou K, Coulpier M, Fontaine JJ, Hamel R, Lilin T, Messiaen S, Andreoletti O, Baron T, Bencsik A, Biacabe AG, Beringue V, Laude H, Le Dur A, Vilotte JL, Comoy E, Deslys JP, Grassi J, Simon S, Lantier F, Sarradin P.(2005). BSE agent signatures in a goat. Vet Rec. 156:523-4.

13. Espinosa, J-C., Morales, ,M., Castilla, J., Rogers, M. and Torres, J.M. (2007). Progression of prion infectivity in asymptomatic cattle after oral bovine spongiform encephalopathy challenge. J. Gen. Virol. 88. 1379-1383

14. European Commission (2007). BSE legislation - Chronological list;

15. Foster, J. D., Hope, J. & Fraser, H. (1993). Transmission of bovine spongiform encephalopathy to sheep and goats. The Veterinary Record. 133: 339-341.

16. Fraser H, McConnell I, Wells G A H & Dawson M (1988) – Transmission of bovine spongifrom encephalopathy to mice. Vet Rec. 123:472.

17. Hoffmann, C., Ziegler, U., Buschmann, A., Weber, A., Kupfer, L., Oelschlegel, A., Hammerschmidt, B. and Groschup, M.J. (2007). Prions spread via the autonomic nervous system in cattle incubating bovine spongiform encephalopathy. J. Gen. Virol. 88: 1048-1055.

18. Iwata, N., Sato, Y. Higuchi, Y. Nohtomi, K. Nagata, N. Hasegawa, H. Tobiume, M. Nakamura, Y., Hagiwara, K., Furuoka, H, Horiuchi, M. Yamakawa, Y & Sata.T (2006). Distribution of PrP(Sc) in Cattle with Bovine Spongiform Encephalopathy Slaughtered at Abattoirs in Japan. Jpn J Infect Dis. 59:100-7.

19. Masujin, K., Matthews, D., Wells, G.A.H., Mohri, S. & Yokoyama, T. (2007) Prions in the peripheral nerves of bovine spongiform encephalopathy-affected cattle. J. Gen. Virol. 88:1850-1858.

20. Prince M. J., Bailey J. A., Barrowman, P. R., Bishop, K. J., Campbell, G. R., Wood J. M. (2003). Bovine spongiform encephalopathy, In: Tech. Office international des Epizooties. 22 (1):37-60.

21. Sohn, H.J., Lee, Y.H., Green, R.B., Spencer, Y.I., Hawkins, S.A.C., Stack, M.J., Konold, T., Wells, G.A.H., Matthews, D., Cho.I.S. & Joo.Y.S. (2009). Bone marrow



infectivity in cattle exposed to the bovine spongiform encephalopathy agent. Vet. Rec. (in press).

22. SSC – Scientific Steering Committee (2001). Opinon on the safety of small ruminant products should BSE in small ruminants become probable / confirmed, 18-19 October 2001.

23. SSC - Scientific Steering Committee (2001)- Opinion on TSE infectivity distribution in ruminant tissues (state of knowledge, December 2001) (adopted on 10-11 January 2002).

24. SSC - Scientific Steering Committee (2002) Opinion on safe sourcing of small ruminant materials.

25. SSC - Scientific Steering Committee (2002) SSC opinion of 4-5 April 2002 on safe sourcing of small ruminant materials (with special reference to the safety with regard to BSE risks of sheep intestines and casings).

26. SSC - Scientific Steering Committee (2002) Update of the Opinion on TSE Infectivity distribution in ruminant tissues.

27. TAFS (2009). Position paper on the testing of cattle for BSE – purpose and effectiveness.

28. TAFS (2009) – Position paper on BSE in small ruminants.

29. Terry, L.A., Marsh, S., Ryder, S.J., Hawkins, S.A.C., Wells, G.A.H., Spencer, Y.I. (2003). Detection of disease specific PrP in Peyer’s patches of the distal ileum of cattle orally exposed to the BSE agent. Vet. Rec. 152: 387-392.

30. Wells G.A.H., Dawson M ,Hawkins S.A.C., Austin A.R Green R.B., Dexter I., Horigan M.W., &. Simmons M.M. (1996). - Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy. In: Bovine spongiform encephalopathy: The BSE Dilemma, Ed. C.J. Gibbs, Serono Symposia, Norwell, USA Springer-Verlag, New York, Inc. Pp. 28-44.

31. Wells G.A.H., Dawson M ,Hawkins S.A.C., Green R.B., Dexter I., Francis M.E., Simmons M.M., Austin A.R. & Horigan M.W (1994). Infectivity in the ileum of cattle challenged orally with bovine spongiform encephalopathy. Vet. Rec., 135:




32. Wells GA, Hawkins SA, Green RB, Austin AR, Dexter I, Spencer YI, Chaplin MJ, Stack MJ, Dawson M. (1998). Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy (BSE): an update. Vet Rec 142:103-6.

33. Wells GA, Hawkins SA, Green RB, Spencer YI, Dexter I, Dawson M., (1999). Limited detection of sternal bone marrow infectivity in the clinical phase of experimental bovine spongiform encephalopathy (BSE). Vet Rec. 144:292-4

34. Wells GA, Spiropoulos J, Hawkins SA, Ryder SJ. (2005). Pathogenesis of experimental bovine spongiform encephalopathy: preclinical infectivity in tonsil and observations on the distribution of lingual tonsil in slaughtered cattle. Vet Rec. 156:401-7.

35. World Health Organization (2006). WHO Guidelines on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies.


TAFS Position Paper - Specified Risk Materials (148 kB)特定危険部位に関するTAFSポジションペーパー

(Japanese version not updated; status May 2007)

Saturday, January 24, 2009

Bovine Spongiform Encephalopathy h-BSE ATYPICAL USA 2008 Annual Report
Research Project: Study of Atypical BseLocation: Virus and Prion Diseases of Livestock2008 Annual Report

Research Project: Detection of Prp**d in Tissue Samples and Bodily Fluids of Cattle from the German Bse Pathogenesis Study Location: Virus and Prion Diseases of Livestock

2008 Annual Report

1a.Objectives (from AD-416) The overall objective of this cooperative project is to evaluate PrP**D tissue distribution and migration in cattle orally infected with BSE of British origin. To achieve this objective, the following specific approaches will be conducted: (1) the protein misfolding cyclic amplification (PMCA) assay will be used on blinded replicate aliquots of tissue from animals in the BSE study to independently confirm whether PrP**D can be detected in the tissue samples. The Cooperator will function as lead investigator and ARS will confirm test results for the presence or absence of PrP**D in any given sample. (2) The Cooperator will analyze the proteome in tissue samples by two dimensional SDS PAGE. (3) NADC will evaluate microscopic pathology and visual function of the retina of available animals and tissues to assess PrP**D accumulation and visual function effects.

1b.Approach (from AD-416) The German BSE oral pathogenesis study involves 56 beef cattle orally dosed with BSE containing brain tissue obtained from British cattle. The animal study is managed by the cooperator and various tissues are collected at prescribed times and at necropsy. These tissues will enable the cooperating parties to perform independent confirmation on the presence or absence of PrP**D for verification of PrP**D distribution in tissues. In addition, retinal samples will be analyzed to assess the extent of retinal pathology in infected cattle and visual system function in available remaining live cattle will be tested using electroretinography.

3.Progress Report The overall objective of this cooperative project is to evaluate PrP**d tissue distribution and migration in cattle orally infected with Bovine spongiform encephalopathy (BSE) of British origin. The live-animal phase of this work was completed this year. Samples from this experiment will be brought to the USDA, ARS, National Animal Disease Center for further characterization in the upcoming year. Methods used for monitoring included phone contact, e-mail, and site visits. This project addresses NP 103, component 8.

Research Project: Study of Atypical Bse Location: Virus and Prion Diseases of Livestock

Project Number: 3625-32000-086-05 Project Type: Specific Cooperative Agreement

Start Date: Sep 15, 2004 End Date: Sep 14, 2009

Objective: The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy. The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.

Approach: This project will be done as a Specific Cooperative Agreement with the Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance program to analyze the effectiveness of the U.S diagnostic tools for detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE isolate with atypical BSE isolates will provide further characterization of the U.S. BSE isolate. Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.

CHAPTER 3 Animal Disease Eradication Programs and Control and Certification Programs


In FY 2007, two field cases, one validation study case, and two RSSS cases were consistent with a variant of the disease known as Nor98 scrapie.1 These five cases originated from flocks in California, Minnesota, Colorado, Wyoming, and Indiana, respectively.


NOR-98 Scrapie FY 2008 to date 1


Monday, December 1, 2008

When Atypical Scrapie cross species barriers

Tuesday, January 06, 2009

CWD Update 93 December 29, 2008

Sunday, December 28, 2008

MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy

[Docket No. FDA–2008–D–0597] Draft Guidance for Industry: Small Entities Compliance Guide for Renderers—Substances Prohibited From Use in Animal Food or Feed; Availability AGENCY: Food and Drug Administration, HHS. ACTION:



I kindly wish to submit the following to [Docket No. FDA–2008–D–0597] ;

I would kindly like to once again comment on the failed attempts of the FDA et al to stop the spread of animal TSEs, including BSE, through the legal, and illegal feeding practices, of feeding animal protein to livestock for human and animal consumption. Since the terribly flawed, partial, and voluntary August 4, 1997 ruminant to ruminant feed ban was put into place, literally 100s of thousands of tons of banned animal protein has been fed out into commerce, even as late as 2007, when some 10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. Blood meal used to make cattle feed was recalled because it was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement. NOW, how much of that product that went out into commerce was fed out to cattle, and how much was ever recovered ? AND to think that feeding blood to livestock producing animals is still legal, when scientific study after study shows that TSEs are easily transmitted via blood. IT is absolutely unacceptable that still in 2008, the USA is still feeding highly suspect mad cow feed to USA cattle, and other livestock producing animals. Especially when the last two cases of BSE that were allowed to be tested and reported were of the atypical BSE category, of which we now know the atypical BSE is more virulent than that of the typical BSE, and when ARS research on the atypical BSE said long ago the SRM rules may need to be changed, IF the atypical BSE were to be proven to be more virulent. Why do we continue to flounder? I have submitted to these BSE feed dockets until I am blue in the face, and still to date, they still debate an issue that should have been settled long ago. IT's a fine example of how big ag, big industry, have a stranglehold on sound science and policy making thereof. How many millions of animals and humans have been needlessly exposed to this TSE agent, due to nothing more than ignorance and greed, simply because of a disease that is 100% fatal, but one that has such a long incubation period. For the government and industry as a whole, to continue to flagrantly violate said rules and regulations, in my opinion, should be regarded as criminal, and treated as such. People are dying. ...

Please see references ;


November 25, 2008

Update On Feed Enforcement Activities To Limit The Spread Of BSE


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