Bovine spongiform encephalopathy, Denmark

Bovine spongiform encephalopathy, Denmark

Information received on 20/11/2009 from Dr Jan Mousing, Chief Veterinary Officer, Danish Veterinary and Food Administration, Ministry of Food, Agriculture and Fisheries, Soborg, Denmark

Summary

Report type Immediate notification
Start date 17/11/2009
Date of first confirmation of the event 19/11/2009
Report date 19/11/2009
Date submitted to OIE 20/11/2009
Reason for notification Reoccurrence of a listed disease
Date of previous occurrence 09/2005
Manifestation of disease Sub-clinical infection
Causal agent Bovine spongiform encephalopathy agent
Nature of diagnosis Laboratory (advanced)
This event pertains to the whole country

New outbreaks Summary of outbreaks Total outbreaks: 1
Location(s) South (Ærøskøbing, Ærø kommune)

Total animals affected Species Susceptible Cases Deaths Destroyed Slaughtered
Cattle 116 1 0 1 0

Outbreak statistics Species Apparent morbidity rate Apparent mortality rate Apparent case fatality rate Proportion susceptible animals lost*
Cattle 0.86% 0.00% 0.00% 0.86%

* Removed from the susceptible population through death, destruction and/or slaughter


Epidemiology Source of the outbreak(s) or origin of infection Unknown or inconclusive

Epidemiological comments The affected animal was born before the tightening of the feed ban in 1997 and 2001. In 1990, feeding ruminant MBM to ruminants was prohibited. In 1997, feeding mammalian MBM to ruminants was prohibited. On 1 January 2001, the Danish Veterinary and Food Administration introduced a total ban on feeding processed animal protein (including meat and bone meal (MBM), fish meal, etc.) to animals that are kept, fattened or bred for the production of food.
Control measures will be conducted in accordance with European Union regulation no. 999/2001.


Control measures Measures applied Quarantine
No vaccination
No treatment of affected animals

Measures to be applied Modified stamping out



Diagnostic test results Laboratory name and type National Veterinary Institute (National laboratory)
Tests and results Species Test Test date Result
Cattle western blotting 19/11/2009 Positive



Future Reporting The event is continuing. Weekly follow-up reports will be submitted.





Encefalopatía espongiforme bovina, Dinamarca

Información recibida el 20/11/2009 desde Dr Jan Mousing, Chief Veterinary Officer, Danish Veterinary and Food Administration, Ministry of Food, Agriculture and Fisheries, Soborg, Dinamarca

Resumen

Tipo de informe Notificación inmediata
Fecha de inicio 17/11/2009
Fecha de la primera confirmación del evento 19/11/2009
Fecha del informe 19/11/2009
Fecha de envio del informe a la OIE 20/11/2009
Motivo de la notificación Reaparición de una enfermedad de la Lista de la OIE
Fecha de la anterior aparición de la enfermedad 09/2005
Manifestación de la enfermedad Infección sub-clínica
Agente causal Agente de la encefalopatía espongiforme bovina
Naturaleza del diagnóstico Pruebas de diagnóstico de laboratorio avanzadas (ej. virología, microscopía electrónica, biología molecular e inmunología)
Este evento concierne todo el país

Nuevos focos Resumen de los focos Número total de focos: 1
Localización South (Ærøskøbing, Ærø kommune)

Número total de animales afectados Especies Susceptibles Casos Muertos Destruidos Sacrificados
Bovinos 116 1 0 1 0

Estadística del foco Especies Tasa de morbilidad aparente Tasa de mortalidad aparente Tasa de fatalidad aparente Proporción de animales susceptibles perdidos*
Bovinos 0.86% 0.00% 0.00% 0.86%

* Descontados de la población susceptible a raíz de su muerte, destrucción o sacrificio


Epidemiología Fuente del o de los focos u origen de la infección Desconocida o no concluyente

Otros detalles epidemiológicos / comentarios El animal afectado nació antes de que se endureciera en 1997 y 2001 la prohibición relativa a la alimentación animal. En 1990, se prohibió alimentar a los rumiantes con harinas de carne y hueso de rumiante. En 1997, se prohibió alimentar a los rumiantes con harinas de carne y hueso de mamífero. El 1 de enero de 2001, la Administración danesa de veterinaria y de alimentos introdujo una prohibición total de alimentar los animales criados o engordados para la producción de alimentos con proteínas animales transformadas (incluyendo harinas de carne y hueso, harinas de pescado, etc.).
Las medidas de control se aplicarán de acuerdo con el reglamento n° 999/2001 de la Unión Europea.


Medidas de Control Medidas implementadas Cuarentena
Vacunación: no
Ningún tratamiento de los animales afectados

Medidas para implementar Sacrificio sanitario parcial



Resultados de las pruebas diagnósticas Nombre y tipo de laboratorio Instituto veterinario nacional (Laboratorio nacional)
Pruebas y resultados Especies Prueba Fecha de la prueba Resultados
Bovinos prueba de inmunodetección 19/11/2009 Positivo



Informes futuros El episodio continúa. Informes de seguimiento semanales serán enviados





Encéphalopathie spongiforme bovine, Danemark

Information reçue le 20/11/2009 de Dr Jan Mousing, Chief Veterinary Officer, Danish Veterinary and Food Administration, Ministry of Food, Agriculture and Fisheries, Soborg, Danemark

Résumé

Type de rapport Notification immédiate
Date de début 17/11/2009
Date de première confirmation de l´événement 19/11/2009
Date du rapport 19/11/2009
Date d'envoi à l'OIE 20/11/2009
Raison de notification Réapparition d’une maladie appartenant à la liste de l'OIE
Date de la précédente apparition de la maladie 09/2005
Manifestation de la maladie Infection sub-clinique
Agent causal Agent de l'encéphalopathie spongiforme bovine
Nature du diagnostic Tests approfondis en laboratoire (i.e. virologie, microscopie électronique, biologie moléculaire, immunologie)
Cet événement se rapporte à tout le pays

Nouveaux foyers Récapitulatif des foyers Nombre total de foyers : 1
Localisation(s) South (Ærøskøbing, Ærø kommune)

Nombre total d'animaux atteints Espèce(s) Sensibles Cas Morts Détruits Abattus
Bovins 116 1 0 1 0

Statistiques sur le foyer Espèce(s) Taux de morbidité apparent Taux de mortalité apparent Taux de fatalité apparent Proportion d'animaux sensibles perdus*
Bovins 0.86% 0.00% 0.00% 0.86%

* Soustraits de la population sensible suite à la mort, à l´abattage et/ou à la destruction


Epidémiologie Source du/des foyer(s) ou origine de l´infection Inconnue ou incertaine

Autres renseignements épidémiologiques / Commentaires L'animal atteint est né avant le durcissement ayant eu lieu en 1997 et 2001 de l'interdiction relative aux aliments pour animaux. En 1990, les farines de viande et d'os provenant de ruminants ont été interdites dans l’alimentation pour ruminants. En 1997, les farines de viande et d'os provenant de mammifères ont été interdites dans l’alimentation pour ruminants. Le 1er janvier 2001, l’Administration vétérinaire et alimentaire danoise a introduit une interdiction totale d'alimenter les animaux engraissés ou élevés pour la production de denrées alimentaires avec des protéines animales transformées (y compris les farines de viande et d'os, la farine de poisson, etc.).
Les mesures de lutte seront appliquées conformément au règlement de l'Union européenne n° 999/2001.


Mesures de lutte Mesure de lutte appliquées Quarantaine
Pas de vaccination
Aucun traitement des animaux atteints

Mesures à appliquer Abattage sanitaire partiel



Résultats des tests de diagnostics Nom du laboratoire et type Institut vétérinaire national (Laboratoire national)
Tests et résultats Espèce(s) Test Date du test Résultat
Bovins western blot 19/11/2009 Positif



Rapports futurs Cet événement se poursuit. Des rapports de suivi hebdomadaires devront être envoyés.





https://www.oie.int/wahis/reports/en_imm_0000008664_20091120_135911.pdf




Tuesday, November 17, 2009

SEAC NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS (IBNC) FROM THE VETERINARY LABORATORIES AGENCY (VLA) SEAC 103/1


http://bse-atypical.blogspot.com/2009/11/seac-new-results-on-idiopathic.html






TSS

CANADA, USA, specified risk materials (SRMs), Environment, Fertilizer, AND Politics, just more BSe

CANADA, USA, specified risk materials (SRMs), Environment, Fertilizer, AND Politics, just more BSe


October 27, 2009

Honourable Minister Gerry Ritz

Minister of Agriculture and Agri-Food Canada 930 Carling Ave Ottawa, ON K1A 0C5

Dear Minister Ritz,

We, as representatives of beef and dairy cattle and beef processing industry organizations, have appreciated the opportunity to speak with you several times with respect to the cost disadvantage of slaughtering cattle in Canada. The primary cause of this disadvantage is the cost of removing and disposing of specified risk materials (SRMs). A survey of Canadian slaughter facilities conducted this summer indicates that the average cost of complying with the 2007 federal SRM removal and disposal regulation is $31.70 per animal over 30 months old (OTM).

The Beef Value Chain Roundtable reviewed this matter at its September 15 meeting and made the following recommendation: “The Beef Value Chain Roundtable supports the findings of the Canadian Meat Council with regard to the costs associated in complying with the enhanced feed ban. The Roundtable asks Governments to promptly implement a plan to offset the costs associated with meeting the requirements of the enhanced feed ban. This recommendation would serve to be a transition measure only until a remedy is found to restore competitiveness.”

The undersigned organizations request that the Government of Canada immediately create an OTM Cattle SRM Disposal Compensation Program. Specifically, we request a payment of $31.70/head be made to abattoirs for every OTM animal slaughtered in Canada. Both federally and provincially inspected facilities should be eligible for this payment. With an estimated annual OTM slaughter of 750,000 head, the program would cost approximately $24 million per year.

The primary objective of any assistance must be to maintain OTM slaughter capacity in Canada. If we fail to achieve this objective, we will lose thousands of jobs throughout the nation, and Canadian beef and dairy cattle producers will be at the mercy of any disruptive US trade rules that may be introduced in the future. All the excellent work you are doing to re-establish market access for Canadian beef will be wasted if we lose the capacity to slaughter our own cattle in Canada. We are already seeing that with reduced OTM slaughter in Canada, beef imports have increased dramatically in 2009. Neither beef nor dairy cattle producers want to return to the pre-BSE practice where large numbers of Canadian OTM cattle went to the US for processing while large quantities of non-NAFTA beef were imported to satisfy Canada’s beef demand.

We request that this OTM Cattle SRM Disposal Compensation Program remain in effect until the SRM removal and disposal policies of Canada and the United States can be harmonized. As an industry, we are committed to work closely with your officials to reduce the volumes and costs of SRM removal. There are several critical actions, that when achieved, can have a significant impact on improving our competitive position with our American counterparts. But it is also widely recognized that any of these beneficial measures will take time to implement, and that immediate need for cash remains in the short term. We recommend that a review process be formalized to ensure these improvements are implemented and the OTM Cattle SRM Disposal Compensation Program can be adjusted when necessary.

In closing, we thank you for your recognition of this serious matter and we urge you to respond quickly. As we are now entering the peak OTM slaughter season, our request requires urgent attention to ensure that Canadian facilities can compete for their fair share of this business.

Sincerely,

Brad Wildeman, President Canadian Cattlemen’s Association Jacques Laforge, President Dairy Farmers of Canada Laurent Pellerin, President Canadian Federation of Agriculture Brian Read, Chair - Beef Committee Canadian Meat Council Kevin Golding, President Canadian Renderers Association Michel Dessureault, President La Fédération des producteurs de bovins du Québec Serge Michel, Chairman of the board Levinoff-Colbex SEC Brian Nilsson, President XL Foods Shane Murphy, President Atlantic Beef Producers Dennis Laycraft, Industry Co-Chair Beef Value Chain Roundtable Scott Entz, Vice President and General Manager Cargill Beef

http://www.cattle.ca/pdf/srm-letter.pdf


Other Priority Issues and Required Actions Competitiveness The top challenge facing the Canadian cattle industry today is that several factors are contributing to a lack of competitiveness in the cattle feeding and beef processing sectors. Left unchecked, greater numbers of cattle will be fed and slaughtered in the US and increasing quantities of beef will be imported into Canada. A high Canadian dollar exacerbates these problems necessitating swift action.

Required Actions

Promptly implement a plan to offset the cost of disposal of Specified Risk Materials (SRMs) as required by the enhanced feed ban. This would be a transitional measure until remedies are implemented to restore industry competitiveness. See coalition letter requesting a creation of an OTM Compensation Program .

Remove the prohibition on using SRM meat and bone meal as fertilizer as a way to restore value for the SRMs Traceability should not impede commerce. Pilot projects currently underway testing scanning equipment in auction marts need to be completed prior to proceeding. Regulating additional costs to producers will put industry at greater disadvantage. Implement 2008 Federal Election commitment to cut diesel excise tax from 4 cents to 2 cents per litre, Ensure Canada’s approval process for products (veterinary/pharmaceutical, pesticides, biologics, new forage and grain varieties, etc) are as or more efficient than our international competitors such as the United States and Australia. Ensure enforcement by regulators is commensurate with consequences of non-compliance (eg: fines for lost CCIA tags; high value meat removal around spinal cord). ...SNIP...END

FULL TEXT ;

http://www.cattle.ca/other-priority-issues-and-required-actions/


CANADA


> Remove the prohibition on using SRM meat and bone meal as fertilizer as a way to restore value for the SRMs<


USA


13. Q: Can CMPAF be rendered for use as fertilizer?


A: This rule does not place any restrictions on the use of CMPAF as fertilizer.



http://www.fda.gov/AnimalVeterinary/GuidanceComplianceEnforcement/ComplianceEnforcement/BovineSpongiformEncephalopathy/ucm114453.htm






SEAC 103/3

MAMMALIAN MEAT AND BONE-MEAL AS FERTILISER ON AGRICULTURAL LAND

ISSUE

1. The Department for Environment, Food and Rural Affairs (Defra) has asked SEAC to consider a risk assessment (Annex A) entitled “Risk assessment of TSE related risks associated with the use of rendered Category 3 animal by-products (ABP) as fertiliser on non-pasture land” produced by the Veterinary Laboratories Agency.

BACKGROUND

2. In 2005, at its 87th meeting, SEAC considered (Annex B) a ‘release assessment’ which evaluated the amount of potential infectivity available in the soil of non-pasture land following the application of Category 3-derived1 fertiliser. In summary, the committee concluded:

• It was content with the approach used and assumptions made in the risk assessment.

• The assessment predicted that TSE infectivity levels on land as a result of the application of fertiliser would be extremely low. However, because of the likely heterogeneous nature of infectivity in fertiliser and the uneven spread of fertiliser, TSE infectivity levels might be higher in some geographical locations than predicted.

• Controls to ensure that Category 3 ABP are processed separately from Category 1 and Category 2 ABP2 be audited.

1 Category 3 is low risk material, most of which is fit for human consumption, but not intended for human consumption.

2 Categories 1 & 2 are the highest risk materials, animals with a suspected or confirmed TSE, Specified Risk Material, condemned meat, diseased animals etc. • A watching brief be kept on CWD and BARB cases to assess the possible persistence of the agent in the environment.

3. Domestic TSE legislation was then amended in 2006 to lift the ban on the application of Category 3-derived mammalian meat and bone meal (MMBM) as organic fertiliser and soil improvers (OFSI) on agricultural land. Also in 2006 EU Animal By-Products legislation was amended3 to permit application of OFSI to land in accordance with certain conditions. This change in EU legislation was underpinned by an EFSA Opinion of 3 March 2004 (Annex C).

4. The EU Animal By-Products Regulation (1774/2002) requires that the category 3-derived MMBM must have been submitted to “Method 1” rendering. Method 1 is the most stringent of the seven rendering methods permitted by the Regulation. The animal by-products must be reduced to a particle size of no greater than 50mm, heated to a core temperature of more than 133°C at 3 bar pressure (absolute) for at least 20 minutes without interruption. The EU ABP Regulation is now being renegotiated and Defra are considering whether it is appropriate to seek a relaxation of the requirement for Method 1 rendering. To this end Defra need an understanding of the difference in the risk of transmitting a TSE, as between the use of Method 1 and Method 7, which is potentially the least stringent method. This is because Method 7 does not prescribe any particle size, time, temperature or pressure standards on the processing of animal by-products but requires the processed product to comply with a microbiological standard set out in the Regulation. It can only be used for Category 3 animal by-products.

5. If there is a difference in risk in this context Defra would then consider whether it would be feasible to manage any increased risk resulting from the use of Method 7, for example the better labelling of the fertiliser or by reducing its palatability to animals.

6. In order to inform this consideration, Defra commissioned a full risk assessment to evaluate the danger to cattle and sheep of becoming infected with BSE and/or scrapie as a result of the change to the domestic TSE legislation in the use of rendered Category 3 ABP with regard to MMBM being converted into fertiliser and applied to nonpasture land. This new risk assessment, which SEAC is now invited to consider, represents a significant overhaul of the original assessment and includes additional analyses.

3 Regulation (EC) 181/2006 amended the ABP Regulation 1774/2002 as regards the use of organic fertilisers and soil improvers (except manure).

7. The main changes compared to the previous release assessment

are:

• the values assigned to parameters within the release assessment have been amended to take account of an increase in scientific knowledge, legislative changes and the decline in disease incidence over time.

• account is taken of a case study investigating the palatability to ruminants of fertilisers applied to land.

• a new exposure assessment and a new dose response model are included.

NEW RESULTS

8. The effects of each of the seven processing methods on TSE infectivity are not known, with the exception of limited experimental data regarding Method 1 as set out in the risk assessment. Due to the absence of such information, the risk assessment makes a number of assumptions in order to compare two scenarios based on the use of the processing methods at opposite ends of the range permitted in legislation: Method 1 and Method 7.

9. The main conclusions from the risk assessment are that the number of animals infected with a TSE disease annually, due to exposure to fertilizer produced from Category 3 ABP according to Method 1 is low (i.e. below one). Indeed, there is 90% certainty that the maximum number would be one new infection. The assessment concludes that when considering fertiliser produced by Method 7 the estimated mean number of new BSE new infections in cattle is 1.1, the number of new infections of scrapie is 47 and the number of new infections of sheep BSE is 0.04.

FUTURE RESEARCH

10. The risk assessment also considers what further investigations might help to reduce the uncertainty in the risk assessment and concludes that the following information would be helpful:

• The proportion of processed materials destined for fertiliser production.

• The average yearly livestock stocking density on grassland.

• The average depth of penetration of the fertiliser within the top soil upon application.

• The reduction rate in TSE infectivity due to processing into fertiliser.

• The proportion of scrapie that is masking sheep BSE disease.

• The probability that a scrapie infected sheep is slaughtered for human consumption in GB.

ADVICE SOUGHT

11. SEAC is asked to:

• consider the scientific validity of the methodology used, and the assumptions made, in the new risk assessment and to comment on its findings; and

• whether any other information, other than that suggested above, would be likely to improve the uncertainties associated with the assumptions made in the risk assessment.

SEAC SECRETARIAT

NOVEMBER 2009

ANNEX A

A copy of “Risk assessment of TSE related risks associated with the use of rendered Category 3 animal by-products as fertiliser on non-pasture land”.

ANNEX B

Paper from SEAC

http://www.seac.gov.uk/papers/103-3.pdf




Prions Adhere to Soil Minerals and Remain Infectious

Christopher J. Johnson1,2, Kristen E. Phillips3, Peter T. Schramm3, Debbie McKenzie2, Judd M. Aiken1,2, Joel A. Pedersen3,4*

1 Program in Cellular and Molecular Biology, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 2 Department of Animal Health and Biomedical Sciences, School of Veterinary Medicine, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 3 Molecular and Environmental Toxicology Center, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 4 Department of Soil Science, University of Wisconsin Madison, Madison, Wisconsin, United States of America

Abstract Top An unidentified environmental reservoir of infectivity contributes to the natural transmission of prion diseases (transmissible spongiform encephalopathies [TSEs]) in sheep, deer, and elk. Prion infectivity may enter soil environments via shedding from diseased animals and decomposition of infected carcasses. Burial of TSE-infected cattle, sheep, and deer as a means of disposal has resulted in unintentional introduction of prions into subsurface environments. We examined the potential for soil to serve as a TSE reservoir by studying the interaction of the disease-associated prion protein (PrPSc) with common soil minerals. In this study, we demonstrated substantial PrPSc adsorption to two clay minerals, quartz, and four whole soil samples. We quantified the PrPSc-binding capacities of each mineral. Furthermore, we observed that PrPSc desorbed from montmorillonite clay was cleaved at an N-terminal site and the interaction between PrPSc and Mte was strong, making desorption of the protein difficult. Despite cleavage and avid binding, PrPSc bound to Mte remained infectious. Results from our study suggest that PrPSc released into soil environments may be preserved in a bioavailable form, perpetuating prion disease epizootics and exposing other species to the infectious agent.

http://www.plospathogens.org/article/info:doi%2F10.1371%2Fjournal.ppat.0020032


Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles

Christopher J. Johnson1,2, Joel A. Pedersen3, Rick J. Chappell4, Debbie McKenzie2, Judd M. Aiken1,2*

1 Program in Cellular and Molecular Biology, University of Wisconsin-Madison, Madison, Wisconsin, United States of America, 2 Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, Wisconsin, United States of America, 3 Department of Soil Science and Molecular and Environmental Toxicology Center, University of Wisconsin-Madison, Madison, Wisconsin, United States of America, 4 Biostatistics and Medical Informatics, University of Wisconsin Medical School, Madison, Wisconsin, United States of America

Soil may serve as an environmental reservoir for prion infectivity and contribute to the horizontal transmission of prion diseases (transmissible spongiform encephalopathies [TSEs]) of sheep, deer, and elk. TSE infectivity can persist in soil for years, and we previously demonstrated that the disease-associated form of the prion protein binds to soil particles and prions adsorbed to the common soil mineral montmorillonite (Mte) retain infectivity following intracerebral inoculation. Here, we assess the oral infectivity of Mte- and soil-bound prions. We establish that prions bound to Mte are orally bioavailable, and that, unexpectedly, binding to Mte significantly enhances disease penetrance and reduces the incubation period relative to unbound agent. Cox proportional hazards modeling revealed that across the doses of TSE agent tested, Mte increased the effective infectious titer by a factor of 680 relative to unbound agent. Oral exposure to Mte-associated prions led to TSE development in experimental animals even at doses too low to produce clinical symptoms in the absence of the mineral. We tested the oral infectivity of prions bound to three whole soils differing in texture, mineralogy, and organic carbon content and found soil- bound prions to be orally infectious. Two of the three soils increased oral transmission of disease, and the infectivity of agent bound to the third organic carbon-rich soil was equivalent to that of unbound agent. Enhanced transmissibility of soil-bound prions may explain the environmental spread of some TSEs despite the presumably low levels shed into the environment. Association of prions with inorganic microparticles represents a novel means by which their oral transmission is enhanced relative to unbound agent.

snip...

Discussion These experiments address the critical question of whether soil particle­bound prions are infectious by an environmentally relevant exposure route, namely, oral ingestion. Oral infectivity of soil particle­bound prions is a conditio sine qua non for soil to serve as an environmental reservoir for TSE agent. The maintenance of infectivity and enhanced transmissibility when TSE agent is bound to the common soil mineral Mte is remarkable given the avidity of the PrPTSE­Mte interaction [22]. One might expect the avid interaction of PrPTSE with Mte to result in the mineral serving as a sink, rather than a reservoir, for TSE infectivity. Our results demonstrate this may not be the case. Furthermore, sorption of prions to complex whole soils did not diminish bioavailability, and in two of three cases promoted disease transmission by the oral route of exposure. While extrapolation of these results to environmental conditions must be made with care, prion sorption to soil particles clearly has the potential to increase disease transmission via the oral route and contribute to the maintenance of TSE epizootics.

Two of three tested soils potentiated oral prion disease transmission. The reason for increased oral transmissibility associated with some, but not all, of the soils remains to be elucidated. One possibility is that components responsible for enhancing oral transmissibility were present at higher levels in the Elliot and Bluestem soils than in the Dodge soil. The major difference between the Dodge soil and the other two soils was the extremely high natural organic matter content of the former (34%, [22]). The Dodge and Elliot soils contained similar levels of mixed-layer illite/smectite, although the contribution of smectite layers was higher in the Dodge soil (14%­16%, [22]). The organic matter present in the Dodge soil may have obstructed access of PrPTSE to sorption sites on smectite (or other mineral) surfaces.

The mechanism by which Mte or other soil components enhances the oral transmissibility of particle-bound prions remains to be clarified. Aluminosilicate minerals such as Mte do not provoke inflammation of the intestinal lining [39]. Although such an effect is conceivable for whole soils, soil ingestion is common in ruminants and other mammals [25]. Prion binding to Mte or other soil components may partially protect PrPTSE from denaturation or proteolysis in the digestive tract [22,40] allowing more disease agent to be taken up from the gut than would otherwise be the case. Adsorption of PrPTSE to soil or soil minerals may alter the aggregation state of the protein, shifting the size distribution toward more infectious prion protein particles, thereby increasing the specific titer (i.e., infectious units per mass of protein) [41]. In the intestine, PrPTSE complexed with soil particles may be more readily sampled, endocytosed (e.g., at Peyer's patches), or persorbed than unbound prions. Aluminosilicate (as well as titanium dioxide, starch, and silica) microparticles, similar in size to the Mte used in our experiments, readily undergo endocytotic and persorptive uptake in the small intestine [42­44]. Enhanced translocation of the infectious agent from the gut lumen into the body may be responsible for the observed increase in transmission efficiency.

Survival analysis indicated that when bound to Mte, prions from both BH and purified PrPTSE preparations were more orally infectious than unbound agent. Mte addition influenced the effective titer of infected BH to a lesser extent than purified PrPTSE. Several nonmutually exclusive factors may explain this result: (1) other macromolecules present in BH (e.g., lipids, nucleic acids, other proteins) compete with PrPTSE for Mte binding sites; (2) prion protein is more aggregated in the purified PrPTSE preparation than in BH [45], and sorption to Mte reduces PrPTSE aggregate size, increasing specific titer [41]; and (3) sorption of macromolecules present in BH to Mte influences mineral particle uptake in the gut by altering surface charge or size, whereas the approximately 1,000-fold lower total protein concentration in purified PrPTSE preparations did not produce this effect.

We previously showed that other inorganic microparticles (kaolinite and silicon dioxide) also bind PrPTSE [22]. All three types of microparticles are widely used food additives and are typically listed as bentonite (Mte), kaolin (kaolinite), and silica (silicon dioxide). Microparticles are increasingly included in Western diets. Dietary microparticles are typically inert and considered safe for consumption by themselves, do not cause inflammatory responses or other pathologies, even with chronic consumption, and are often sampled in the gut and transferred from the intestinal lumen to lymphoid tissue [39,46,47]. Our data suggest that the binding of PrPTSE to dietary microparticles has the potential to enhance oral prion disease transmission and warrants further investigation.

In conclusion, our results provide compelling support for the hypothesis that soil serves as a biologically relevant reservoir of TSE infectivity. Our data are intriguing in light of reports that naïve animals can contract TSEs following exposure to presumably low doses of agent in the environment [5,7­9]. We find that Mte enhances the likelihood of TSE manifestation in cases that would otherwise remain subclinical (Figure 3B and 3C), and that prions bound to soil are orally infectious (Figure 5). Our results demonstrate that adsorption of TSE agent to inorganic microparticles and certain soils alter transmission efficiency via the oral route of exposure.

snip...full text is here:

http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.ppat.0030093


http://pathogens.plosjournals.org/perlserv/?request=get-pdf&file=10.1371_journal.ppat.0030093-L.pdf


http://pathogens.plosjournals.org/perlserv/?request=get-pdf&file=10.1371_journal.ppat.0030093-S.pdf


PLoS ONE. 2008; 3(8): e2969. Published online 2008 August 13. doi: 10.1371/journal.pone.0002969. PMCID: PMC2493038

Copyright This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.


Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production


Cathrin E. Bruederle,1* Robert M. Hnasko,1 Thomas Kraemer,2 Rafael A. Garcia,3 Michael J. Haas,3 William N. Marmer,3 and John Mark Carter1 1USDA-ARS WRRC, Foodborne Contaminants Research Unit, Albany, California, United States of America 2Forensic Toxicology, Institute of Legal Medicine, Saarland University, Homburg/Saar, Germany 3USDA-ARS ERRC, Fats, Oils and Animal Coproducts Research Unit, Wyndmoor, Pennsylvania, United States of America Neil Mabbott, EditorUniversity of Edinburgh, United Kingdom * E-mail: cathrin.bruederle@gmail.comConceived and designed the experiments: CEB RMH WNM JMC. Performed the experiments: CEB RMH TK. Analyzed the data: CEB TK JMC. Contributed reagents/materials/analysis tools: CEB RMH TK RAG MJH JMC. Wrote the paper: CEB. Received April 21, 2008; Accepted July 24, 2008. Other Sections? AbstractIntroductionResultsDiscussionMaterials and MethodsSupporting InformationReferencesAbstract The epidemic of bovine spongiform encephalopathy (BSE) has led to a world-wide drop in the market for beef by-products, such as Meat-and-Bone Meal (MBM), a fat-containing but mainly proteinaceaous product traditionally used as an animal feed supplement. While normal rendering is insufficient, the production of biodiesel from MBM has been suggested to destroy infectivity from transmissible spongiform encephalopathies (TSEs). In addition to producing fuel, this method simultaneously generates a nutritious solid residue. In our study we produced biodiesel from MBM under defined conditions using a modified form of alkaline methanolysis. We evaluated the presence of prion in the three resulting phases of the biodiesel reaction (Biodiesel, Glycerol and Solid Residue) in vitro and in vivo. Analysis of the reaction products from 263K scrapie infected MBM led to no detectable immunoreactivity by Western Blot. Importantly, and in contrast to the biochemical results the solid MBM residue from the reaction retained infectivity when tested in an animal bioassay. Histochemical analysis of hamster brains inoculated with the solid residue showed typical spongiform degeneration and vacuolation. Re-inoculation of these brains into a new cohort of hamsters led to onset of clinical scrapie symptoms within 75 days, suggesting that the specific infectivity of the prion protein was not changed during the biodiesel process. The biodiesel reaction cannot be considered a viable prion decontamination method for MBM, although we observed increased survival time of hamsters and reduced infectivity greater than 6 log orders in the solid MBM residue. Furthermore, results from our study compare for the first time prion detection by Western Blot versus an infectivity bioassay for analysis of biodiesel reaction products. We could show that biochemical analysis alone is insufficient for detection of prion infectivity after a biodiesel process.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/



Sunday, April 12, 2009

CWD UPDATE Infection Studies in Two Species of Non-Human Primates and one Environmental reservoir infectivity study and evidence of two strains

http://chronic-wasting-disease.blogspot.com/2009/04/cwd-update-infection-studies-in-two.html


DEPENDS ALSO what were calling srm's now?

WITH the atypical BSE's, ARS said they were going to update and possibly enhance SRM regulations as the transmission studies were due out in 2009 i.e. (h-BSE, and l-BSE) ??

Animal fats/oils certified with maximum insoluble impurities of less than 0.15% in weight (bovine origin animal fats imported for animal consumption must also come from animals that passed FSIS inspection, and must not be derived from the head, distal ileum, spinal cord, or vertebral column of cattle of any age);

http://www.aphis.usda.gov/newsroom/hot_issues/bse/background/bse_trade_ban_status.shtml...


http://www.aphis.usda.gov/newsroom/hot_issues/bse/background/bse_trade_ban_status.shtml...



2. Annex XI, Part A is amended as follows:

(a) point 1(a)(i) is replaced by the following:

"(i) the skull excluding the mandible and including the brain and eyes, and the spinal cord of bovine animals aged over 12 months, the vertebral column excluding the vertebrae of the tail, the spinous and transverse processes of the cervical, thoracic and lumbar vertebrae and the median sacral crest and wings of the sacrum, but including the dorsal root ganglia of bovine animals aged over 24 months, and the tonsils, the intestines from the duodenum to the rectum and the mesentery of bovine animals of all ages;"

http://eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=OJ:L:2005:317:0004:01:EN:HTML



HOWEVER, as with other non-effective BSE regulations put forth by the O.I.E., SRM regulations are being watered down now by AGE. ...

The sensitivity of PrPTSE detection is still lower than certain bioassays: failure to detect PrPTSE does not guarantee absence of infectivity in a tissue. Opinion on the likelihood of the infectivity in SRM derived from cattle at different age groups estimated by back calculation modelling...

http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/biohaz_op_ej476_srm_en.pdf?ssbinary=true



Tuesday, November 10, 2009

Surveillance On the Bovine Spongiform Encephalopathy and rabies in Taiwan and USA

http://usdavskorea.blogspot.com/2009/11/surveillance-on-bovine-spongiform.html



Monday, October 19, 2009

Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009

http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html



2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006

http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html



Monday, October 26, 2009

MAD COW DISEASE, AND U.S. BEEF TRADE

MAD COW DISEASE, CJD, TSE, SOUND SCIENCE, COMMERCE, AND SELLING YOUR SOUL TO THE DEVIL

http://usdameatexport.blogspot.com/2009/10/mad-cow-disease-and-us-beef-trade.html



IN A NUT SHELL ;

(Adopted by the International Committee of the OIE on 23 May 2006)

11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,

http://www.oie.int/eng/Session2007/RF2006.pdf



Docket APHIS-2006-0026 Docket Title Bovine Spongiform Encephalopathy; Animal Identification and Importation of Commodities Docket Type Rulemaking Document APHIS-2006-0026-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions, Identification of Ruminants and Processing and Importation of Commodities Public Submission APHIS-2006-0026-0012 Public Submission Title Comment from Terry S Singletary

http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801e47e1



Docket APHIS-2006-0041 Docket Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities Docket Type Rulemaking Document APHIS-2006-0041-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived From Bovines Public Submission APHIS-2006-0041-0028 Public Submission Title Comment from Terry S Singletary

Comment 2006-2007 USA AND OIE POISONING GLOBE WITH BSE MRR POLICY

THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted products from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone. These are the facts as I have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species.

MY personal belief, since you ask, is that not only the Canadian border, but the USA border, and the Mexican border should be sealed up tighter than a drum for exporting there TSE tainted products, until a validated, 100% sensitive test is available, and all animals for human and animal consumption are tested. all we are doing is the exact same thing the UK did with there mad cow poisoning when they exported it all over the globe, all the while knowing what they were doing. this BSE MRR policy is nothing more than a legal tool to do just exactly what the UK did, thanks to the OIE and GW, it's legal now. and they executed Saddam for poisoning ???

go figure. ...

http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f8151



Docket APHIS-2006-0041 Docket Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities Docket Type Rulemaking Document APHIS-2006-0041-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived From Bovines Public Submission APHIS-2006-0041-0028.1 Public Submission Title Attachment to Singletary comment

January 28, 2007

Greetings APHIS,

I would kindly like to submit the following to ;

BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01

http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f8152&disposition=attachment&contentType=msw8



Thursday, November 12, 2009

BSE FEED RECALL Misbranding of product by partial label removal to hide original source of materials 2009

http://madcowfeed.blogspot.com/2009/11/bse-feed-recall-misbranding-of-product.html



http://madcowtesting.blogspot.com/



HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory

http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648027c28e&disposition=attachment&contentType=pdf



TSS

Transcriptional changes in the brain of cattle orally infected with BSE precede detection of infectivity

J. Virol. doi:10.1128/JVI.00352-09 Copyright (c) 2009, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Transcriptional changes in the brain of cattle orally infected with BSE precede detection of infectivity

Yue Tang, Wei Xiang, Steve A.C. Hawkins, Hans A. Kretzschmar, and Otto Windl* Department of Molecular Pathogenesis and Genetics and Department of Pathology, Veterinary Laboratories Agency, Woodham Lane, New Haw, Surrey KT15 3NB, UK; Institute of Neuropathology, Ludwig-Maximilians-University Munich, Munich, Germany

* To whom correspondence should be addressed. Email: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000173/!x-usc:mailto:o.windl@vla.defra.gsi.gov.uk.

Abstract

Bovine spongiform encephalopathy (BSE) is a fatal, transmissible, neurodegenerative disease of cattle. BSE can be transmitted experimentally between cattle through the oral route and in this study brain tissue samples from animals at different time points post inoculation were analysed for changes in gene expression. The aims of this study were to identify differentially regulated genes during the progression of BSE using microarray based gene expression profiling and to understand the effect of prion pathogenesis on gene expression. A total of 114 genes were found to be differentially regulated over the time course of the infection and many of these 114 genes encode proteins involved in immune response, apoptosis, cell adhesion, stress response and transcription. This study also revealed a broad correlation between gene expression profiles and the progression of BSE in cattle. At 21 months post inoculation, the largest number of differentially regulated genes was detected, suggesting that there are many pathogenic processes in the animal brain even prior to the detection of infectivity in the CNS of these orally dosed cattle. Moreover, evidence is presented to suggest that it is possible to predict the infectious status of animals using the expression profiles from this study.



http://jvi.asm.org/cgi/content/abstract/JVI.00352-09v1?etoc



Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie. Emerg Infect Dis. 2009 Aug; [Epub ahead of print]



http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html



Monday, June 01, 2009

Biochemical typing of pathological prion protein in aging cattle with BSE



http://bse-atypical.blogspot.com/2009/06/biochemical-typing-of-pathological.html



Sunday, June 07, 2009

L-TYPE-BSE, H-TYPE-BSE, C-TYPE-BSE, IBNC-TYPE-BSE, TME, CWD, SCRAPIE, CJD, NORTH AMERICA



http://bse-atypical.blogspot.com/2009/06/l-type-bse-h-type-bse-c-type-bse-ibnc.html



Sunday, May 10, 2009

Identification and characterization of bovine spongiform encephalopathy cases diagnosed and NOT diagnosed in the United States



http://bse-atypical.blogspot.com/2009/05/identification-and-characterization-of.html



Sunday, December 28, 2008

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



http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.html



Saturday, February 28, 2009

NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS "All of the 15 cattle tested showed that the brains had abnormally accumulated PrP" 2009 SEAC 102/2



http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html



Saturday, June 13, 2009

BSE FEED VIOLATIONS USA UPDATE From 01/01/2009 To 06/10/2009



http://madcowfeed.blogspot.com/2009/06/bse-feed-violations-usa-update-from.html



Thursday, March 19, 2009

MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA



http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html



WHO WILL FOLLOW THE CHILDREN FOR CJD SYMPTOMS ???

Saturday, May 2, 2009

U.S. GOVERNMENT SUES WESTLAND/HALLMARK MEAT OVER USDA CERTIFIED DEADSTOCK DOWNER COW SCHOOL LUNCH PROGRAM



http://downercattle.blogspot.com/2009/05/us-government-sues-westlandhallmark.html



Sunday, April 12, 2009 BSE MAD COW TESTING USA 2009 FIGURES Month Number of Tests

Feb 2009 -- 1,891

Jan 2009 -- 4,620



http://www.aphis.usda.gov/newsroom/hot_issues/bse/surveillance/ongoing_surv_results.shtml



SEE FULL TEXT ;



http://madcowtesting.blogspot.com/2009/04/bse-mad-cow-testing-usa-2009-figures.html



Monday, May 4, 2009

Back to the Past With New TSE Testing Agricultural Research/May-June 2009



http://madcowtesting.blogspot.com/2009/05/back-to-past-with-new-tse-testing.html



Saturday, June 13, 2009

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009

snip...



http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html




Terry S. Singeltary Sr.

P.O. Box 42

Bacliff, Texas USA 77518

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

TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation

(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).

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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

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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

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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

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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).

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? 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).

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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

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References

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.


http://ec.europa.eu/food/food/biosafety/bse/roadmap_en.pdf



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.


http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/opinion_biohaz_06_en1.pdf?ssbinary=true




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.


http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/biohaz_opinion_ej220_srmremove_en1.pdf?ssbinary=true




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.


http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/biohaz_opinion_ej227_bse_goat_v2_en1.pdf?ssbinary=true




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-

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assessment of the BSE related risk of bovine intestines after processing into natural sausage casings. The EFSA Journal. 464: 1-14.


http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/biohaz_op_ej464_bovine_casings_en,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.


http://www.efsa.europa.eu/cs/BlobServer/Scientific_Opinion/biohaz_op_ej700_bovine_tongue_rev2_en,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;


http://ec.europa.eu/food/food/biosafety/bse/chronology_en.htm




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: Rev.Sci.et 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

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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.


http://europa.eu.int/comm/food/fs/sc/ssc/out234_en.pdf



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).


http://europa.eu.int/comm/food/fs/sc/ssc/out241_en.pdf




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


http://europa.eu.int/comm/food/fs/sc/ssc/out257_en.pdf




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).


http://europa.eu.int/comm/food/fs/sc/ssc/out281_en.pdf




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


http://ec.europa.eu/food/fs/sc/ssc/out296_en.pdf




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


http://tafsforum.org/position_papers/TAFS_POSITION_PAPER_ON_TESTING_OF_CATTLE_FOR_BSE_070516.pdf



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


http://www.tafsforum.org/position_papers/TAFS%20POSITION%20STATEMENT%20ON%20BSE%20IN%20SMALL%20RUMINANTS_2009.pdf




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:

40-41.

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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.


http://www.who.int/bloodproducts/tse/WHO%20TSE%20Guidelines%20FINAL-22%20JuneupdatedNL.pdf







http://www.tafsforum.org/position_papers/TAFS_POSITION_PAPER_SPECIFIED%20RISK%20MATERIALS_2009.pdf






UPDATED:TAFS POSITION PAPER ON SPECIFIED RISK MATERIALS (January, 2009)



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




http://bse-atypical.blogspot.com/2009/01/bovine-spongiform-encephalopathy-h-bse.html





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.




http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=411017&fy=2008




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.




http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490





CHAPTER 3 Animal Disease Eradication Programs and Control and Certification Programs

snip...

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.

snip...




http://www.aphis.usda.gov/publications/animal_health/content/printable_version/AHR_Web_PDF_07/D_Chapter_3.pdf





NOR-98 Scrapie FY 2008 to date 1




http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps





ATYPICAL TSEs in USA CATTLE AND SHEEP ?




http://www.bseinquiry.gov.uk/files/sc/seac17/tab03.pdf





Monday, December 1, 2008

When Atypical Scrapie cross species barriers




http://nor-98.blogspot.com/2008/12/when-atypical-scrapie-cross-species.html






Tuesday, January 06, 2009

CWD Update 93 December 29, 2008




http://chronic-wasting-disease.blogspot.com/2009/01/cwd-update-93-december-29-2008.html





Sunday, December 28, 2008

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




http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.html





[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:

snip...




http://edocket.access.gpo.gov/2008/pdf/E8-28189.pdf






Greetings,

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 ;


snip...




http://madcowfeed.blogspot.com/2008/12/docket-no-fda2008d0597-draft-guidance.html





November 25, 2008


Update On Feed Enforcement Activities To Limit The Spread Of BSE





http://madcowfeed.blogspot.com/2008/11/november-2008-update-on-feed.html




http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html




http://madcowspontaneousnot.blogspot.com/





TSS

In vivo prion protein intestinal uptake in fish

1: APMIS. 2008 Mar;116(3):173-80.

In vivo prion protein intestinal uptake in fish.

Dalla Valle AZ, Iriti M, Faoro F, Berti C, Ciappellano S.
Department of Food Science and Microbiology (DISTAM), Section of Human Nutrition, University of Milan, Milan, Italy.

Intestinal uptake of abnormal prion protein (PrP(Sc)), the pathological agent involved in transmissible spongiform encephalopathies (TSEs), has been investigated in rainbow trout (Oncorhynchus mykiss). Experimental procedures were conducted in vivo by immunohistological PrP(Sc) localization in intestine and pyloric caeca after forced feeding of infected material. Results indicate that PrP(Sc) was absorbed by the intestinal mucosa and that it persisted in the fish gastrointestinal tract for up to 3 days in pyloric caeca and for up to 7 days in the distal intestine. It did not remain longer than 15 days in the fish intestine; furthermore, it did not cross the intestinal barrier.

PMID: 18377582 [PubMed - in process]


http://www.ncbi.nlm.nih.gov/pubmed/18377582?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum



> Results indicate that PrP(Sc) was absorbed by the intestinal mucosa and that it persisted

> in the fish gastrointestinal tract for up to 3 days in pyloric caeca and for up to 7 days in the

> distal intestine.

> It did not remain longer than 15 days in the fish intestine;


WOULD this not be a potential risk factor for transmission of the PrPSc agent to cattle and other species via fish by-products and or fish feed ???



vCJD in the USA * BSE in U.S.

15 November 1999

snip...


Our feeding and rendering practices have mirrored that of the U.K. for years, some say it was worse. Everything from the downer cattle, to those scrapie infected sheep, to any roadkill, including the city police horse and the circus elephant went to the renders for feed and other products for consumption. Then they only implemented a partial feed ban on Aug. 4, 1997, but pigs, chickens, dogs, and cats, and humans were exempt from that ban. So they can still feed pigs and chickens those potentially TSE tainted by-products, and then they can still feed those by-products back to the cows.

***I believe it was Dr. Joe Gibbs, that said, the prion protein, can survive the digestinal track. So you have stopped nothing.

It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses. Speaking of autopsies, I have a stack of them, from CJD victims. You would be surprised of the number of them, who ate cow brains, elk brains, deer brains, or hog brains.


snip...


full text ;


http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406



Subject: CANADA BSE FACT SHEET FOR FISH BY-PRODUCT RENDERERS UPDATE
Date: June 5, 2007 at 1:16 pm PST

FACT SHEET FOR FISH BY-PRODUCT RENDERERS
Overview
On July 12, 2007, a series of amendments to the Feeds Regulations, 1983, and the Health of Animals Regulations will come into effect, to further protect animal health and accelerate the eradication of bovine spongiform encephalopathy (BSE) in Canada. Since BSE was first reported in Canada in 2003, Canada’s trading partners have demanded additional assurances and certification of animal products, by-products, and feeds containing these ingredients. In addition to banning the use of certain cattle tissues in animal feed, pet food and fertilizers, the regulatory amendments will also introduce new controls on animal product renderers. It is noteworthy that many of our trading partners consider fish by-products to be an animal product.

For the purposes of this fact sheet, fish by-product renderers are defined as those who receive inedible offal, fish or fish by-products from fish processing plants or other sources and render it to produce fish meal or fish oil products.

New requirements for fish by-product renderers
As a result of the regulatory amendments described above, the following requirements will apply to all fish by-product rendering facilities as of July 12, 2007:

All rendering facilities (including those processing fish by-products) must obtain and operate under a permit issued by the Canadian Food Inspection Agency (CFIA), and be subject to routine inspection by the CFIA;
Rendering facilities that import fish by-products will be required to obtain a Health of Animals import permit;
Rendering facilities that export fish by-products (including fish meal and fish oil) will be required to obtain a CFIA export certification; and
Fish by-product renderers are required to keep production and distribution records for 10 years.
One of the benefits of these amendments will be enhanced traceability of fish meal and fish oil from both domestic and import sources through the feed system. Fish meal and fish oil have a broad range of applications in animal feeds and fertilizers. Identifying the locations and origin of primary ingredients, such as fish meal and fish oil, allows the CFIA to more effectively direct its resources to monitoring and sampling activities related to the safety of these products. Sampling and testing these ingredients directly, rather than the finished feed products, provides a more accurate picture of the safety of the ingredients.

CFIA fish by-product rendering survey
To prepare for the new regulatory requirements, the CFIA is undertaking a survey of fish by-product renderers across Canada. At some time in the next few months, if you are a fish by-product renderer, you will be contacted by someone from the CFIA, who will make arrangements to inspect your facility. The primary purpose of the survey is to collect information on how many fish rendering facilities operate separately from other renderers, and the types and quantities of products they produce. The CFIA needs this information to plan for inspections and the preparation and issuance of fish rendering permits. It is important to note that all information collected will be considered confidential.

Conducting the survey will allow CFIA Feed Program inspectors to inform renderers about the inspection process and answer questions. Inspectors will also take the opportunity to discuss the additional requirements for importing and exporting fish meal and fish oil that will apply when the regulatory amendments come into effect.

If you are a fish by-product renderer, you are encouraged to discuss the requirements of the rendering permit program with the CFIA inspector performing the survey, and arrange to undergo a preliminary inspection. At the time of the survey, the inspector will leave a copy of the application for a Rendering Plant permit with the facility manager and answer any questions.

Rendering Plant Operating Permits
Rendering permits are issued for a period of one year, normally beginning on April 1st and ending on March 31st. There are no fees for a permit. Permit issuance is subject to an inspection of the rendering facility showing that it is in full compliance with the regulations. Once a fish by-product renderer has been identified, and a preliminary inspection completed, a temporary rendering permit will be issued to them. Any necessary modifications must be completed, and the facilities must be in full compliance with regulatory requirements, when the amended regulations enter into force on July 12, 2007.

BY JULY 12, 2007, ALL FISH BY-PRODUCT RENDERERS MUST HAVE A CFIA RENDERING PERMIT TO CONTINUE OPERATING.

For more information, please contact a CFIA Feed Program Specialist in your area at the appropriate telephone number:

Atlantic Area: 902-426-1410
Québec Area: 514-283-3815 (ext. 377)
Ontario Area: 519-826-2910
Western Area: 204-983-7441


http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/enhren/fispoie.shtml


Feed Ban Enhancement
Questions and Answers


http://www.inspection.gc.ca/english/anima/feebet/rumin/enhqueste.shtml



SEE EXAMPLE OF TONNAGE OF FEED FOR FISH AT ONE MILL


Mr. Dwayne Holifield, B.S., manager of the research farm led the tour of the Delta Western Feed Mill in Indianola, MS. Delta Western Research Center has several tenth-acre ponds. The ponds are used for research projects involving nutrition and field trials of therapeutic products. The research center also has a second mill used to produce smaller lots of experimental catfish feeds. The research unit works extensively with NWAC. The main mill produces about 230,000 tons of catfish feed annually representing thirty percent of the 825,000 tons of catfish sold annually. Railroad lines bring grain products used in the feed directly to the mill. Three large warehouses store ground corn, wheat middlings and soybean meal that are pumped directly into the mill as needed. The mill has doubled its finished-feed storage capacity over the last two years to a capacity of 5,000 tons. The mill operates two 8 - 10 hour shifts depending on the time of year. The storage area is filled completely by the end of the second shift and emptied by mid-morning the next day. The feed is delivered to farms in large tanker type trucks. Each truck has a capacity of 20 tons and can be completely filled in 2 1/2 minutes.


http://www.fda.gov/cvm/Sep_Oct01.htm#2378


What we know about the herd of origin What we know about the herd of origin
􀁘􀁘 Owner was former catfish farmer who moved Owner was former catfish farmer who moved
to Alberta in 2001 to Alberta in 2001
􀁘􀁘 Owner inexperienced in cattle production Owner inexperienced in cattle production
􀁘􀁘 Cow was part of 80 cow herd assembled Cow was part of 80 cow herd assembled
from multiple sources from multiple sources
􀁘􀁘 No identification saved from index case No identification saved from index case
􀁘􀁘 Source of index case not recorded



http://www.vet.ohio-state.edu/assets/courses/vm510/EpidemiologyOfBSE.pdf


The rancher, Marwyn Peaster, a former Mississippi catfish farmer who had married an area woman and started farming in the area, had taken off. He was upset that the TV crew had shown up his land.

http://www.sportsshooter.com/news/950


Dr. Detwiler: Canada based that question because the herd that that animal came from was in Saskatchewan, in an area with CWD. That was one of the questions they faced right off the bat: is this BSE or is this some kind of transmission from CWD-infected elk in the area? Not only the histological lesions were classic BSE lesions, but clinically it's very difficult because if you miss the other behavioral changes, which this owner did. It was someone who had been a catfish farmer. He missed the early signs. The animal presented to slaughter as a down animal, non-responsive. Clinically it looked like just a down cow, but they did send that on to the United Kingdom and they did do some comparison glycoform patterns. Those haven’t been validated, but at least on preliminary work, it looked like classical BSE.

http://bse-atypical.blogspot.com/



QUESTION - was this farmer feeding catfish feed to his cattle ???


Feeding Farmed Fish

snip...


Farming animals has suffered from the recent crises of Mad Cow Disease as well as the disastrous consequences of the accidental or fraudulent contamination of feeds with dioxins and other undesirable products. These events have accentuated the general suspicion of consumers and brought the necessary application of new and more complex laws, being more restrictive and therefore imposing more costs for the producers.

Aquaculture does and must carry the image of food security in respect of the consumer. But it must continue constantly to battle against hearsay and unfounded criticism.

Since aquaculture started in Europe, aquaculture feeds contain neither antibiotics (except in the case of authorized therapeutic treatment), nor hormones, nor growth enhancers or additives that could have existed in other areas of animal production. The traceability of the products used at all stages of the production process up to the consumer's purchase is, without doubt, the best answer to give confidence.

The European Union imports products from third countries that do not always respect the same sanitary restrictions, a position which leads to food production costs that are considerably lower than in the Member States (without referring to social costs and ecological considerations). One can assert that the fish feeds produced in the EU are 10% more expensive, at an equivalent nutritive content, than elsewhere, in particular since the withdrawal of protein-rich terrestrial animal by-products (from abattoirs).

We must therefore pay attention to this discrepancy which exists and is growing in Europe and well as with other regions of the world. The trade of seafood and aquaculture products is international and the identification [labelling] of products at the level of the consumer's purchase is another point which has not been completely resolved, in spite of the wishes of all of the professionals of the feed and aquaculture production sectors of the EU as well as the new rules for labelling and identification that have been law since the 1st January 2002.

The new European legislation that is being elaborated for the use of animal by-products must follow the Directive 90/667/CEE that establishes «the veterinary rules for the disposal and processing of animal waste, for its placing on the market and for the prevention of pathogens in feedstuffs of animal or fish origin» . This new legislation classes animal by-products as a function of their potential risks and defines their conditions of destruction or use, where only products that are qualified as being of 'low risk' can be used for animal feeds by those establishments that have been approved for such an activity.

Unfortunately, the fish meals and oils that are derived from the fisheries dedicated to this activity have been assimilated with the by-products of terrestrial animals and are thus considered as being waste materials at the same level as the waste products obtained from abattoirs or kitchen waste. In addition to the fact that these fisheries are managed by quotas and are wholly natural products of very high food quality, this simplified and negative classification is a source of very serious confusion.

In particular, the rather negative image that has been given to these natural products will complicate any information and communication action of the international aquaculture community. This question merits all of our attention when we look to increase the importance of the products of fisheries and aquaculture.


snip...see full text ;

http://www.feap.info/production/feeds/sabautcipa_en.asp


Fish farming under threat?

The possibility of a disease crossing the species barrier hangs like a Damocles sword over a number of farming sectors, including fish farming. ‘All farmed fish are fed feed with a 40% to 55% protein content. This can include animal protein and, hence, potentially pathogenic prion proteins,’ explains Theodoros Sklaviadis of the University of Thessaloniki (GR).

In 1997, Carla Bolis, a researcher at the University of Milan (IT), discovered a normal prion protein, previously believed to exist only in mammals, in the brain of salmon. This means it is important to determine the risk of TSE in fish, as the programme coordinated by Sklaviadis is seeking to do. This work focuses on two areas. The first is a systematic search in the genomes of trout, sea bass and bream for the coding sequences of the prion protein in order to analyse homologies with mammal genes. The second involves feeding these fish food containing BSE and scrapie prions, to see whether it is possible to start an infection. ‘Given the incubation period of the disease, the results will not be available for several years,’ Sklaviadis warns. Patience is called for if we want to ensure that Europe’s fish farmers never experience a “mad fish” crisis.


http://ec.europa.eu/research/rtdinfo/39/01/article_302_en.html



see where USA still feeds fish banned mad cow feed. ...tss


Archive Number 20060809.2235
Published Date 09-AUG-2006
Subject PRO/AH/EDR> BSE, bovine - USA (02): feed recall



BSE, BOVINE - USA (02): FEED RECALL
*********************************************
A ProMED-mail post

ProMED-mail is a program of the
International Society for Infectious Diseases


[1]
Date: Wed, 9 Aug 2006 22:26:49 +0100
From: "Mary Marshall"
Source: Cattle Network 8 Aug 2006 [edited]



Huge Feed Recall Due To Mammalian Protein
---------------------------------------------
The Food and Drug Administration announced 2 recalls, one for 27 million
pounds of feed produced in Michigan and the other an unknown amount of feed
produced in Kentucky. Both were suspected of being adulterated with ruminant
or mammalian protein, including ruminant meat and bone meal in the 2nd
recall.

Vita Plus Corp., Gagetown, Michigan, has recalled 27 694 240 pounds of dairy
feed produced between February of 2005 and 16 Jun 2006, because it is
believed it was contaminated with mammalian protein. The feed was
distributed in Michigan and the recall is complete.

Burkmann Feeds LLC, Glasgow, Kentucky, has recalled an unknown amount of custom
feed because it contains an ingredient called Pro-Lak, which may contain
ruminant-derived meat and bone meal. The Burkmann feed was distributed in
Kentucky.

[By Pete Hisey on Tuesday, August 08, 2006 ]

--
Mary Marshall


*****
[2]
Date: 7 Aug 2006
From: Terry Singeltary
Source: FDA [weekly] Enforcement Report, 2 Aug 2006 [edited]



(1) PRODUCT: Animal and fish feeds Recall # V-112-6

CODE: Product manufactured from 1 Feb 2005 to 6 Jun 2006

RECALLING FIRM/MANUFACTURER: Alabama Farmers Cooperative, Inc.,
Decatur, Alabama, by telephone, fax, email and visit on 9 Jun 2006.
FDA initiated recall is complete.

REASON: Animal and fish feeds which were possibly contaminated with
ruminant-based protein not labeled as "Do not feed to ruminants."

VOLUME OF PRODUCT IN COMMERCE: 125 tons

DISTRIBUTION: Alabama and Florida

(2) PRODUCT: Bulk custom dairy feeds manufactured from concentrates,
Recall # V-113-6

CODE: All dairy feeds produced between 1 Feb 2005 and 16 Jun 2006 and
containing H. J. Baker recalled feed products.

RECALLING FIRM/MANUFACTURER: Vita Plus Corp., Gagetown, Michigan, by
visit beginning on 21 Jun 2006. Firm initiated recall is complete.

REASON: The feed was manufactured from materials that may have been
contaminated with mammalian protein.

VOLUME OF PRODUCT IN COMMERCE: 27 694 240 lbs

DISTRIBUTION: Michigan

(3) PRODUCT: Bulk custom made dairy feed, Recall # V-114-6

CODE: None

RECALLING FIRM/MANUFACTURER: Burkmann Feeds LLC, Glasgow, Kentucky,
by letter on 14 Jul 2006. Firm initiated recall is ongoing.

REASON: Custom made feeds contain ingredient called Pro-Lak, which
may contain ruminant derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE: Unknown

DISTRIBUTION: Kentucky

--
Terry Singeltary


[A codified rule indicates that no mammalian material is to be
included in feed for ruminants. When it is found that such a
situation has occurred, then a recall is issued. Several years ago, a
similar situation happened in Gonzales, Texas, and the herd was
depopulated. The difference must be that the regulatory authorities
do not know where all the herds are that have consumed the feed. - Mod.TG]

[see also:
BSE, bovine - USA: feed recall 20060621.1718]
..................................................tg/msp/jw


************************************************************


Subject: MAD COW FDA FEED WARNING LETTER NO. 2007-NOL-01 October 26, 2006 H.J. Baker & Bro., Inc.
Date: November 7, 2006 at 9:08 am PST

Food and Drug Administration

New Orleans District

404 BNA Drive, Building 200, Suite 500

Nashville, TN 37217

Telephone: 615-366-7801

Facsimile: 615-366-7802

October 26, 2006

WARNING LETTER NO. 2007-NOL-01

FEDERAL EXPRESS

OVERNIGHT DELIVERY

Mr. Christopher V. B. Smith

Corporate President, CEO

H. J. Baker & Bro., Inc.

228 Saugatuck Avenue

Westport, Connecticut 06880

Dear Mr. Smith:

On June 6, 8, 12-15, and 23, 2006, a U.S . Food and Drug Administration (FDA) investigator inspected your animal feed protein supplement manufacturing facility, located at 603 Railroad Avenue, Albertville, Alabama. The inspection revealed significant deviations from the requirements set forth in Title 21, Code ofFederal Regulations, Part 589.2000 (21 CFR 589.2000), Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation, resulting in products being manufactured and distributed by your facility because they are adulterated within the meaning of Section 402(a)(4) [21 USC 342(a)(4)] of the Federal Food, Drug, and Cosmetic Act (the Act) and misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)(1)] of the Act.

Our investigation determined adulteration resulted from the failure of your firm to establish and implement measures sufficient to prevent commingling or cross-contamination . The adulterated feed was subsequently misbranded because it was not properly labeled. Specifically, we found :

" Your firm failed to establish and use cleanout procedures or other means to prevent carry-over of products which contain or may contain protein derived from mammalian tissues into animal protein or feeds which may be used for ruminants, as required by 21 CFR 589.2000(e)(1)(iii)(B) .

Specifically, you failed to establish and use such measures for a screw auger installed in February 2005 . This auger is used to convey both prohibited and non-prohibited material to bulk storage bins.

In addition, you failed to follow the cleanout procedure your firm had developed for the receiving systems. Your feed is, therefore, adulterated under Section 402(a)(4) [21 USC 342(a)(4)] of the Act.

" You failed to label all products which contained or may have contained prohibited materials with the BSE cautionary statement, "Do not feed to cattle or other ruminants," as required by 21 CFR 589.2000(e)(1)(i) . Such products are misbranded under Section 403(3) [21 USC 343(a)(1)] of the Act. These misbranded products include the three Pro-Pak products mentioned below, as well as Page 2 - H. J . Baker & Bro., Inc., Albertville, Alabama Warning Letter No. 2007-NOL-O 1 those bulk loads of individual feed ingredients processed through this common screw auger and distributed between the time it was installed in February 2005, and June 9, 2006 .

This letter is not intended to serve as an all-inclusive list of violations at your facility. As a
manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct these violations, and you should establish a system whereby violations do not recur. Failure to promptly correct these violations may result in regulatory action, such as seizure and/or injunction,

without further notice.

We acknowledge your June 16, 2006, voluntary recall of three products you manufactured from February 2005 to June 2006. The three products recalled were: Pro-Lak Protein Concentrate for

Lactating Dairy Animals;

Pro-Amino II for PreFresh and Lactating Cows;


***and, Pro-Pak Marine & Animal Protein Concentrate for Use in Animal Feed. Recall effectiveness checks and other measures


will determine the merit of this recall . We recognize you now label all products with the required BSE cautionary statement and we also acknowledge your intent, given verbally to New Orleans District management of the FDA, to discontinue the production of supplements which do not contain prohibited

materials. In your written response to this letter, please confirm in writing you have taken these steps.

snip...


http://www.fda.gov/foi/warning_letters/g6104d.pdf



Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA,
MS, AL, GA, AND TN 11,000+ TONS
Date: August 16, 2006 at 9:19 am PST

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II
______________________________

snip...
______________________________

PRODUCT

*** a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet,
50 lb. bags, Recall # V-121-6;


b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet,
50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower,
50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD
Medicated, 50 lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags,
Recall # V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags,
Recall # V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher,
50 lb bags, Recall # V-127-6
CODE
All products manufactured from 02/01/2005 until 06/20/2006
RECALLING FIRM/MANUFACTURER
Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit
on June 20, 2006, and by letter on June 23, 2006.
Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated
recall is ongoing.
REASON
Poultry and fish feeds which were possibly contaminated with ruminant based
protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
7,541-50 lb bags
DISTRIBUTION
AL, GA, MS, and TN

END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006

###


http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html


Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125
TONS Products manufactured from 02/01/2005 until 06/06/2006

Date: August 6, 2006 at 6:16 pm PST

PRODUCT

*** a) CO-OP 32% Sinking Catfish, Recall # V-100-6;

b) Performance Sheep Pell W/Decox/A/N, medicated,
net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;

*** d) CO-OP 32% Sinking Catfish Food Medicated,
Recall # V-103-6;

e) "Big Jim's" BBB Deer Ration, Big Buck Blend,
Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted,
Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020,
Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete
Feed for Chickens from Hatch to 20 Weeks, Medicated,
Bacitracin Methylene Disalicylate, 25 and 50 Lbs,
Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying
Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED,
net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs,
Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs,
Recall # V-112-6
CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER
Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and
visit on June 9, 2006. FDA initiated recall is complete.
REASON
Animal and fish feeds which were possibly contaminated with ruminant based
protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
125 tons
DISTRIBUTION
AL and FL


END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###


http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html


MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE
Sun Jul 16, 2006 09:22
71.248.128.67


RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals,
Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg),
Recall # V-080-6;

*** c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL
FEED, Recall # V-081-6;

d) Feather Meal, Recall # V-082-6
CODE
a) Bulk
b) None
c) Bulk
d) Bulk
RECALLING FIRM/MANUFACTURER
H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and
by press release on June 16, 2006. Firm initiated recall is ongoing.
REASON
Possible contamination of animal feeds with ruminent derived meat and bone
meal.
VOLUME OF PRODUCT IN COMMERCE
10,878.06 tons
DISTRIBUTION
Nationwide

END OF ENFORCEMENT REPORT FOR July 12, 2006

###


http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html


Mr. Sturm was found to hold animals on his farm under conditions that are so inadequate that diseased animals and/or medicated animals bearing potentially harmful drug residues are likely to enter the food supply. In addition, he failed to use the drug, Albon, containing sulfadimethoxine, in conformance with the labeling.

A warning letter was issued to the following firms for violations related to 21 CFR Part 589.2000—Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE).

*** • Scott Nelson, Owner, Integra Fish Foods, Inc., Grand Junction, CO

• Bruce A. Burgett, General Manager, The Carrollton Farmers Exchange, Carrollton, OH

Violations included failure to label feeds that contain, or may contain, prohibited materials with the required cautionary statement "Do Not Feed to Cattle or Other Ruminants," insufficient customer records to track the distribution of products, and lack of written procedures for cleaning or flushing equipment after mixing feeds containing prohibited material.


http://www.fda.gov/cvm/Sep_Oct01.htm



look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;

Risk of oral infection with bovine spongiform encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys

Summary

The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.

snip...

BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. icip= intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula

Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa

It is clear that the designing scientists must also have shared Mr Bradley's surprise

at the results because all the dose levels right down to 1 gram triggered infection.

http://www.bseinquiry.gov.uk/files/ws/s145d.pdf

6. It also appears to me that Mr Bradley's answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight; particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the "attack rate"

experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that the designing scientists must have also shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.

http://www.bseinquiry.gov.uk/files/ws/s147f.pdf

PDF] Guidance for Industry 69File Format: PDF/Adobe Acrobat - View as HTML The Food and Drug Administration (FDA) has prepared this guide in accordance ... If a feed intended for ruminants contains animal protein, the protein can ... www.fda.gov/cvm/Guidance/guidance69.pdf - Similar pages - Note this

http://www.fda.gov/cvm/Guidance/guidance69.pdf

[PDF] Guidance for Industry 70File Format: PDF/Adobe Acrobat - View as HTML If a feed is intended for ruminants contains animal protein, the protein can ... with On-Farm Feed Mixing Operations,” FDA Guidance for Industry 69. ... www.fda.gov/cvm/Guidance/guidance70.pdf - Similar pages - Note this

WHAT IS THE PURPOSE AND SCOPE OF THIS REGULATION?

This regulation is designed to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE), sometimes referred to as “Mad Cow Disease,” through animal feed. The regulation prohibits the use of certain proteins derived from mammalian tissue in feeding ruminant animals. An example is meat and bone meal derived from cattle. However, certain products are exempt from this regulation.

# The following protein products derived from mammals are exempt.:

Blood and blood products P Gelatin Milk products (milk and milk proteins) Pure porcine (pork) or pure equine (horse) protein products Inspected meat products, such as plate waste, which have been cooked and offered for human food and further heat processed for animal feed

# The following nonmammalian protein products are exempt:

Poultry

***Marine (fish) ***

Vegetable

# The following products are also exempt because they are not protein or tissue:

Grease Fat Amino acids

Tallow Oil

Dicalcium phosphate

We refer to the exempted products throughout this guide as “nonprohibited material.” We refer to all mammalian protein that is not exempted as “prohibited material.”

Prohibited material and/or feeds containing prohibited material cannot be fed to ruminant animals. “Ruminant animals” are any animals with a four-chambered stomach including cattle, sheep, goats, buffalo, elk, and deer.

http://www.fda.gov/cvm/Guidance/guidance70.pdf

[PPT] Detection of Ruminant MBM Prohibited ProteinFile Format: Microsoft Powerpoint - View as HTML Detection of Ruminant MBM Prohibited Protein. Development of an assay to address the needs of the feed industry. Ensure consumer confidence in FDA ... aafco.org/Portals/0/public/Frank_Klein.ppt - Similar pages - Note this

http://aafco.org/Portals/0/public/Frank_Klein.ppt

[PDF] M A M M A L I A N P R O T E I N F E E D I N G B A N Feeders of ...File Format: PDF/Adobe Acrobat - View as HTML ruminant and non-ruminant feeds. If this isn't possible,. you must properly and thoroughly clean .... prohibited animal protein products:. www.fda.gov/cvm ... aafco.org/Portals/0/Public/BSE_aafco_brochure.pdf - Similar pages - Note this

Protein products derived from non-mammalian sources are exempt:

•Poultry; marine (fish); vegetable

The following products are also exempt because they are not protein or tissue:

•Fats and oils, including grease and tallow; amino acids; dicalcium phosphate Exempted animal protein products Mammalian protein products that are exempt from the feed ban are non-prohibited proteins.

•Blood and blood products; milk products (milk and milk proteins); pure porcine (pork) or pure equine (horse) protein products; inspected meat products (such as plate waste) which have been cooked and offered for human consump - tion and further heat processed for animal feed; gelatin.

http://aafco.org/Portals/0/Public/BSE_aafco_brochure.pdf

AND THE CIRCLE OF GREED IS COMPLETE $$$

Using Byproducts to Feed Dairy Cattle Donna M. Amaral-Phillips and R.W. Hemken

Various byproducts from feed processing industries are available for dairy farmers to incorporate into diets fed to dairy cows and replacement heifers. Using these feeds offers at least two benefits:

• may decrease the feed costs depending on prices of byproducts and grains.

• helps dispose of these byproducts in an ecologically sound manner.

Table 1. Nutrient composition of selected byproducts and cereal grains on a dry matter basis.

Dry Matter (%) Dry Matter Basis Crude Protein (%)

Blood meal, ring dried 92 95.5 1.06 0.30 0.30

snip...

Fish meal, anchovy 92 71.2 1.01 4.06 2.69

Fish meal, menhaden 92 68.5 1.06 5.34 3.05

snip...

Feather meal 93 92 0.98 0.33 0.50

Non-ruminant Meat meal 94 57.6 1.01 8.86 4.20 Non-Ruminant Meat and Bone Meal 92 54 0.74 10.60 4.73

snip...

Tallow 99 ------ 2.06 ------ ------

snip...

Blood Meal

1. Byproduct of the rendering industry.

2. Made from clean, fresh animal blood exclusive of the urine, hair, stomach contents, etc.

3. Flash drying process produces a more uniform product with a higher lysine content.

4. Due to potential palatability problems, best used in total mixed rations (TMR). Needs to be added slowly over a two-week period. Palatability problems may be encountered if added to grain mixes fed in the parlor or through a computer feeder.

5. Limit intake to 0.5-1.0 lbs/cow/day in total mixed rations.

Fish Meal

1. Made from clean, dried, ground, and undecomposed fish.

2. Rich in essential amino acids. The amino acid profile may be similar to that required for the synthesis of milk protein.

3. Due to potential palatability problems, best used in total mixed rations. Needs to be added slowly over a two-week period. Problems may be encountered if added to grain mixes fed in the parlor or through a computer feeder.

Hydrolyzed Feather Meal

1. Byproduct from the pressure treatment of clean, undecomposed feathers from slaughtered poultry.

2. Low in lysine and methionine which are believed to control milk production. However, this product is high in cysteine which may substitute for methionine in milk production.

3. Due to potential palatability problems, best used in total mixed rations. Needs to be added slowly over a two-week period. Problems may be encountered if added to grain mixes fed in the parlor or through a computer feeder.

4. Limit intake to 0.3 lbs/cow/day in total mixed rations.

Non-Ruminant Meat Meal

1. A rendered product from the carcasses of swine or poultry excluding blood, hair, hoof, hide trimmings, feces, and stomach. Similar to meat and bone meal except no minimum phosphorus concentration required.

2. Due to potential palatability problems, best used in total mixed rations. Needs to be added slowly over a two-week period. Problems may be encountered if added to grain mixes fed in the parlor or through a computer feeder.

3. Limit intake to 1.5-2.5 lbs/cow/day in total mixed rations.

4. Do not feed ruminant derived meat and bone meal back to ruminants.

Non-Ruminant Meat and Bone Meal

1. A rendered product from the carcass of swine or poultry excluding blood, hair, hoof, hide trimmings, feces, and stomach. It contains a minimum of 4% phosphorus with a calcium content that does not exceed 2.2 times the phosphorus concentration.

2. Due to potential palatability problems, best used in total mixed rations. Needs to be added slowly over a two-week period. Palatability problems may be encountered if added to grain mixes fed in the parlor or through a computer feeder.

3. Limit intake to 1.5-2.5 lbs/cow/day in total mixed rations.

4. Do not feed ruminant derived meat and bone meal back to ruminants.

Tallow

1. Derived primarily from rendered beef fat but may include other animal fats.

2. Requires special handling equipment because at room temperature it is a solid or semi-solid. To be mixed within feed, it must be heated so that it can be melted.

3. Nine different grades of tallow are sold. Good quality (fancy bleachable) tallow should be used for the most consistent animal response.

4. Limit to 1 lb/1200 lb cow/day.

http://www.uky.edu/Ag/AnimalSciences/dairy/extension/nut00158.pdf

STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995

snip...

To minimise the risk of farmers' claims for compensation from feed compounders.

To minimise the potential damage to compound feed markets through adverse publicity.

To maximise freedom of action for feed compounders, notably by maintaining the availability of meat and bone meal as a raw material in animal feeds, and ensuring time is available to make any changes which may be required.

snip...

THE FUTURE

4..........

MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.

5. Tests _may_ show that ruminant feeds have been sold which contain illegal traces of ruminant protein. More likely, a few positive test results will turn up but proof that a particular feed mill knowingly supplied it to a particular farm will be difficult if not impossible.

6. The threat remains real and it will be some years before feed compounders are free of it. The longer we can avoid any direct linkage between feed milling _practices_ and actual BSE cases, the more likely it is that serious damage can be avoided. ...

SEE full text ;

http://www.bseinquiry.gov.uk/files/yb/1995/08/24002001.pdf

like i said, and endless cycle of greed, i.e. FOR PROFIT ONLY $$$

USDA CERTIFIED DEAD STOCK DOWNER COW SCHOOL LUNCH PROGRAM LIST OF SCHOOLS AFFECTED STATE BY STATE (dead stock downers i.e. non-ambulatory, the most high risk for mad cow disease)

http://downercattle.blogspot.com/

TSS

specified risk materials (SRM)

re-mad cow downers and kids


>>>But let's not forget that all specified risk materials, i.e. brain and
spinal tissue, are removed from the food supply on all cattle, whether they
can walk or not. The bottom line is that, even if my girls ate ground beef
from a cow that tested positive to BSE, their risk of being abused is
greater than their risk of acquiring BSE. And, no, I don't believe in or
practice child abuse.<<<

http://www.hpj.com/archives/2008/feb08/feb18/Cowsorkids.cfm


i had to laugh when i read that, as sad and disgusting as it is. i wanted to post this as a comment, but the data i have is much to long to post. facts usually are. if you think that feed ban of 8/4/97 held, please think again. it was only ink on paper. also, please read the latest science on the last two mad cows in in the USA i.e. Alabama and Texas. the BASE mad cow, whether it be h or l BASE, its much more virulent to humans than the UK BSE. this is fact. i am not anti meat eater. i am anti stupid, anti corporate homicide, i,e. for profit. how could anyone feel safe by beef in the usa via USDA certified is beyond me. we must stop the big ag factory farming policy of 'don't look, dont find'. and the incubation period. these kids will not know if they will die from cjd for years and even decades to come. and if you think that is the only slaughterhouse that allow downers to still go into the human food chain, think again. i know of one right here in texas. nope, big ag has such a strangle hold on USDA, it will take much more than a democrat or republican to clean it up, there to worried about baseball and those over paid brats and steroids. ................ oh well, i have probably said too much///


Washington January 31, 2008 snip...


http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2008/02/0028.xml


> TRANSCRIPT: USDA Officials Hold Technical Briefing Regarding Inhumane

> Handling Allegations



THE title is very misleading. A better title in my opinion would have read ;


HIGHLY SUSPECT BSE, H-BASE, MAD COW BEEF DISTRIBUTED NATIONALLY (35 states
to date), to CHILDREN AND THE ELDERLY


USDA CERTIFIED H-BASE MAD COW SCHOOL LUNCH PROGRAM


http://cjdmadcowbaseoct2007.blogspot.com/2008/02/usda-certified-h-base-mad-cow-school.html




Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518





Certain Aspects related to the Feeding of Animal Proteins to Farm
Animals[1] - Scientific Opinion of the Panel on Biological Hazards
Question number: EFSA-Q-2007-084



Adopted date: 17/10/2007 Summary

Opinion

Summary

The European Food Safety Authority (EFSA) was requested by the European Parliament (EP) to assess, with respect to Bovine Spongiform Encephalopathy (BSE), the safety for human health of the utilisation of non-ruminant Meat and Bone Meal (MBM). More specifically, EFSA was requested (i) to evaluate the risk from using non-ruminant MBM in pig and poultry feed, once it is possible to distinguish protein origin up to different species and (ii) the introduction of certain tolerance levels with regard to small quantities of MBM in animal feed and the parameters which could be utilized to define these tolerance levels and quantities.

The EFSA opinion takes account of the general control measures in place in the European Union (EU) and assumes the effectiveness of these controls in avoiding cross-contamination, both deliberate and accidental. This opinion considers all available scientific data and information related to the risk of transmission of the BSE agent through feed and, by this means, addresses the risk of causing BSE related exposure to humans, as well as risks related to some other TSE agents. In replying to the above mentioned questions, this assessment only considers the use of pig Processed Animal Proteins[2] (PAPs) in poultry feed and the use of poultry PAPs in pig feed. With respect to the introduction of certain tolerance levels with regards to small quantities of MBM in animal feed, this assessment considers such a tolerance for animal proteins of any species in animal feed.

To date, no Transmissible Spongiform Encephalopathies (TSEs) have been identified as occurring in pigs or poultry under natural conditions. Taking account of the epidemiological situation of BSE in cattle in the EU, which indicates a decreasing trend, together with the current control measures in place to avoid exposure of pigs and poultry to BSE contaminated material, the EFSA Scientific Panel on Biological Hazards (BIOHAZ) concluded that the risk of transmitting BSE to pigs utilizing poultry PAPs and vice versa is negligible. Consequently in this scenario any increase in the exposure risk of BSE to humans would be negligible. If TSE in birds or pigs is identified in the future as occurring under natural conditions, the assessment presented here will no longer be valid.

The BIOHAZ Panel further concluded that the risk of transmitting BSE through small quantities of animal proteins in feed to ruminants can not be excluded, but considering the current protective measures in place in the EU[3], the few infected animals that could arise from this contamination would probably not be able to sustain the BSE epidemic but would increase the human exposure risk to BSE. The risk of transmitting BSE to non-ruminants is considered to be lower than to ruminants, as long as intra-species recycling is avoided. Consequently in this scenario the increase in the exposure risk of BSE to humans is negligible.

In the event that a tolerance level was required to be set up in order to quantify animal proteins in animal feed, the BIOHAZ Panel considered the Limit of Quantification (LOQ) of the method used to set such tolerance level as the parameter required. However the BIOHAZ Panel concluded that it is currently not possible to set a LOQ because of insufficient data on the performance of relevant detection methods for quantification. It is therefore recommended that studies be conducted to define the LOQ for different types of animal proteins in feed. In a hypothetical situation in which pigs are allowed to be fed with poultry PAPs and vice versa or, in general, inter-species recycling is allowed, currently it is not possible to quantify the level of contamination with non authorized products containing animal proteins in feed. Accordingly it is technically not possible at present to determine whether the contamination is below or above a defined tolerance level.

The BIOHAZ Panel further concluded that compared to the current measures in place in EU, the introduction of a tolerance level, which has to be defined at a certain level above the LOQ, will lead to an increase in the risk of transmission of BSE or other TSEs, depending on the species. This increased risk can not be quantified. ___________________________ [1] For citation purposes: Opinion of the Scientific Panel on Biological Hazards on a request from the European Parliament on Certain Aspects related to the Feeding of Animal Proteins to Farm Animals, The EFSA Journal (2007) Journal number 576, 1-41 [2] In Commission Regulation (EC) No 829/2007 of 28 June 2007 is defined as: “animal protein derived entirely from Category 3 material, which have been treated in accordance with Chapter II of Annex VII so as to render them suitable for direct use as feed material or for any other use in feedingstuffs, including petfood, or for use in organic fertilisers or soil improvers; however, it does not include blood products, milk, milk-based products, colostrum, gelatine, hydrolysed proteins and dicalcium phosphate, eggs and egg-products, tricalcium phosphate and collagen”. [3] Regulation (EC) 999/2001 as amended and Regulation (EC) 1774/2002 as amended.

Publication date: 15/11/2007

http://www.efsa.europa.eu/EFSA/Scientific_Opinion/biohaz_op_ej576_animal_proteins_summary_en.pdf

http://www.efsa.europa.eu/EFSA/Scientific_Opinion/biohaz_op_ej576_animal_proteins_en.pdf


If only a proportion of infected cattle can be detected, does testing provide significant consumer protection?

The extent to which testing increases consumer protection is still open to question, especially if other protective measures are in place (see below).

It is conceivable that tissues not previously recognised as infected may still be found as research continues. Infectivity levels are expected to be extremely low, and undetectable with the tools used so far. If these tissues were otherwise consumed then the destruction of the carcase would afford the consumer a greater degree of protection. If the tissues are not sufficiently infectious to pose a health risk, and/or are not consumed, then the additional protection provided may be nil.

Recent results from Japan and Germany confirm this point(2,11,12,14), with positivity or infectivity being detected in some peripheral nerves that would not normally be removed as SRM. The amount of infectivity present is low, and considered be up to 1000-fold lower than the brain. Unpublished evidence suggests that these become positive only after the brain and spinal cord. This therefore confirms that testing and removal of positive animals does provide some additional, as yet unquantifiable, protection to consumers over and above that provided by removal of SRM. Given that detection of positivity or infectivity in some peripheral nerves coincides with the onset of clinical signs, it is probable that such animals would be detected before slaughter, and therefore excluded from the food chain.

http://www.tafsforum.org/position_papers/TAFS_POSITION_PAPER_ON_TESTING_OF_CATTLE_FOR_BSE_070516.pdf


10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007

Date: March 21, 2007 at 2:27 pm PST RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II ___________________________________

PRODUCT

Bulk cattle feed made with recalled Darling’s 85% Blood Meal, Flash Dried, Recall # V-024-2007

CODE

Cattle feed delivered between 01/12/2007 and 01/26/2007

RECALLING FIRM/MANUFACTURER

Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.

Firm initiated recall is ongoing.

REASON

Blood meal used to make cattle feed was recalled because it was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

42,090 lbs.

DISTRIBUTION

WI

___________________________________

PRODUCT

Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI – 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J – PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A-BYPASS ML W/SMARTA, Recall # V-025-2007

CODE

The firm does not utilize a code - only shipping documentation with commodity and weights identified.

RECALLING FIRM/MANUFACTURER

Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.

REASON

Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

9,997,976 lbs.

DISTRIBUTION

ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html


Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV

Date: September 6, 2006 at 7:58 am PST

PRODUCT

a) EVSRC Custom dairy feed, Recall # V-130-6; b) Performance Chick Starter, Recall # V-131-6; c) Performance Quail Grower, Recall # V-132-6; d) Performance Pheasant Finisher, Recall # V-133-6.

CODE None

RECALLING FIRM/MANUFACTURER

Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.

REASON

Dairy and poultry feeds were possibly contaminated with ruminant based protein.

VOLUME OF PRODUCT IN COMMERCE

477.72 tons

DISTRIBUTION

AL ______________________________

PRODUCT

a) Dairy feed, custom, Recall # V-134-6; b) Custom Dairy Feed with Monensin, Recall # V-135-6. CODE None. Bulk product

RECALLING FIRM/MANUFACTURER

Recalling Firm: Burkmann Feed, Greeneville, TN, by Telephone beginning on June 28, 2006.

Manufacturer: H. J. Baker & Bro., Inc., Albertville, AL. Firm initiated recall is complete.

REASON

Possible contamination of dairy feeds with ruminant derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE

1,484 tons

DISTRIBUTION

TN and WV

http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html


Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA, MS, AL, GA, AND TN 11,000+ TONS

Date: August 16, 2006 at 9:19 am PST

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II ______________________________

PRODUCT

Bulk custom made dairy feed, Recall # V-115-6

CODE None

RECALLING FIRM/MANUFACTURER

Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or about July 14, 2006. FDA initiated recall is ongoing.

REASON

Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE

Approximately 2,223 tons

DISTRIBUTION

KY

______________________________

PRODUCT

Bulk custom made dairy feed, Recall # V-116-6

CODE None

RECALLING FIRM/MANUFACTURER

Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006. FDA initiated recall is ongoing.

REASON

Custom made feeds contain ingredient called Pro-Lak which may contain ruminant derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE

1,220 tons

DISTRIBUTION

KY

______________________________

PRODUCT

Bulk custom made dairy feed, Recall # V-117-6

CODE None

RECALLING FIRM/MANUFACTURER

Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated recall is completed.

REASON

Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE

40 tons

DISTRIBUTION

LA and MS

______________________________

PRODUCT

Bulk Dairy Feed, Recall V-118-6

CODE None

RECALLING FIRM/MANUFACTURER

Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA initiated recall is complete.

REASON

Possible contamination of animal feed ingredients, including ingredients that are used in feed for dairy animals, with ruminant derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE

7,150 tons

DISTRIBUTION

MS

______________________________

PRODUCT

Bulk custom dairy pre-mixes, Recall # V-119-6

CODE None

RECALLING FIRM/MANUFACTURER

Walthall County Co-op, Tylertown, MS, by telephone on June 26, 2006. Firm initiated recall is complete.

REASON

Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE

87 tons

DISTRIBUTION

MS

______________________________

PRODUCT

Bulk custom dairy pre-mixes, Recall # V-120-6

CODE None

RECALLING FIRM/MANUFACTURER

Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete.

REASON

Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE

350 tons

DISTRIBUTION

AL and MS

______________________________

PRODUCT

a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6; b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6; c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6; d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6; e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6; f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6; g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6

CODE

All products manufactured from 02/01/2005 until 06/20/2006

RECALLING FIRM/MANUFACTURER

Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.

REASON

Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".

VOLUME OF PRODUCT IN COMMERCE

7,541-50 lb bags

DISTRIBUTION

AL, GA, MS, and TN

END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006

###

http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html


Subject: MAD COW FEED RECALL MI MAMMALIAN PROTEIN VOLUME OF PRODUCT IN COMMERCE 27,694,240 lbs

Date: August 6, 2006 at 6:14 pm PST

PRODUCT

Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6

CODE

All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products.

RECALLING FIRM/MANUFACTURER

Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm initiated recall is complete.

REASON

The feed was manufactured from materials that may have been contaminated with mammalian protein.

VOLUME OF PRODUCT IN COMMERCE

27,694,240 lbs

DISTRIBUTION

MI

END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html


Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006

Date: August 6, 2006 at 6:16 pm PST

PRODUCT

a) CO-OP 32% Sinking Catfish, Recall # V-100-6; b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6; c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6; d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6; e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6; f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6; g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6; h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6; i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6; j) CO-OP LAYING CRUMBLES, Recall # V-109-6; k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6; l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6; m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6

CODE

Product manufactured from 02/01/2005 until 06/06/2006

RECALLING FIRM/MANUFACTURER

Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.

REASON

Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".

VOLUME OF PRODUCT IN COMMERCE

125 tons

DISTRIBUTION

AL and FL

END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html


Subject: MAD COW FEED RECALL KY VOLUME OF PRODUCT IN COMMERCE ????? Date: August 6, 2006 at 6:19 pm PST

PRODUCT

Bulk custom made dairy feed, Recall # V-114-6

CODE None

RECALLING FIRM/MANUFACTURER

Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated recall is ongoing.

REASON

Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE

?????

DISTRIBUTION

KY

END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html


CJD WATCH MESSAGE BOARD TSS

MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE

Sun Jul 16, 2006 09:22

71.248.128.67

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II

______________________________

PRODUCT

a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6; b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6; c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6; d) Feather Meal, Recall # V-082-6 CODE a) Bulk b) None c) Bulk d) Bulk

RECALLING FIRM/MANUFACTURER

H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.

REASON

Possible contamination of animal feeds with ruminent derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE

10,878.06 tons

DISTRIBUTION

Nationwide

END OF ENFORCEMENT REPORT FOR July 12, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html


Subject: MAD COW FEED BAN WARNING LETTER ISSUED MAY 17, 2006

Date: June 27, 2006 at 7:42 am PST

Public Health Service

Food and Drug Administration

New Orleans District 297 Plus Park Blvd. Nashville, TN 37217

Telephone: 615-781-5380 Fax: 615-781-5391

May 17, 2006

WARNING LETTER NO. 2006-NOL-06

FEDERAL EXPRESS OVERNIGHT DELIVERY

Mr. William Shirley, Jr., Owner Louisiana.DBA Riegel By-Products 2621 State Street Dallas, Texas 75204

Dear Mr. Shirley:

On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration (FDA) investigator inspected your rendering plant, located at 509 Fortson Street, Shreveport, Louisiana. The inspection revealed significant deviations from the requirements set forth in Title 21, Code of Federal Regulations, Part 589.2000 [21 CFR 589.2000], Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation; products being manufactured and distributed by your facility are misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)(1)] of the Federal Food, Drug, and Cosmetic Act (the Act).

Our investigation found you failed to provide measures, including sufficient written procedures, to prevent commingling or cross-contamination and to maintain sufficient written procedures [21 CFR 589.2000(e)] because:

You failed to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues into animal protein or feeds which may be used for ruminants. For example, your facility uses the same equipment to process mammalian and poultry tissues. However, you use only hot water to clean the cookers between processing tissues from each species. You do not clean the auger, hammer mill, grinder, and spouts after processing mammalian tissues.

You failed to maintain written procedures specifying the clean-out procedures or other means to prevent carryover of protein derived from mammalian tissues into feeds which may be used for ruminants.

As a result . the poultry meal you manufacture may contain protein derived from mammalian tissues prohibited in ruminant feed. Pursuant to 21 CFR 589.2000(e)(1)(i), any products containing or may contain protein derived from mammalian tissues must be labeled, "Do not feed to cattle or other ruminants." Since you failed to label a product which may contain protein derived from mammalian tissues with the required cautionary statement. the poultry meal is misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the Act.

This letter is not intended as an all-inclusive list of violations at your facility. As a manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct these violations, and you should establish a system whereby violations do not recur. Failure to promptly correct these violations may result in regulatory action, such as seizure and/or injunction, without further notice.

You should notify this office in writing within 15 working days of receiving this letter, outlining the specific steps you have taken to bring your firm into compliance with the law. Your response should include an explanation of each step taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within 15 working days, state the reason for the delay and the date by which the corrections will be completed. Include copies of any available documentation demonstrating corrections have been made.

Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S. Food and Drug Administration, 2424 Edenborn Avenue, Suite 410, Metairie, Louisiana 70001. If you have questions regarding any issue in this letter, please contact Mr. Rivero at (504) 219-8818, extension 103.

Sincerely,

/S

Carol S. Sanchez Acting District Director New Orleans District

http://www.fda.gov/foi/warning_letters/g5883d.htm


SINCE THE LAST TIME I REPORTED :

Subject: USDA FSIS QUARTERLY ENFORCEMENT REPORT (BSE) July 1, 2005 through September 30, 2005

Date: March 20, 2006 at 12:58 pm PST

YOU can see that report at the bottom of this update.

UPDATEs AS FOLLOWS ;

UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT July 1, 2006 through September 30, 2006

snip...

Table 5. Administrative Actions: Large HACCP Plants (7/01/06 to 9/30/06)

Administrative Actions Pending or Taken at Large HACCP Plants [includes actions initiated in prior quarters]

CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS

On 6/15/06, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

snip...

EXCEL CORP 00086R M FORT MORGAN, CO

On 8/11/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8. On 12/22/04, plant appealed the withholding action. Appeal was denied on 1/25/05.

snip...

TYSON FRESH MEATS INC. 09268 M PASCO, WA X On 7/28/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

TYSON FRESH MEATS INC. 00245D M EMPORIA, KS X On 12/23/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

TYSON FRESH MEATS INC. 00245L M LEXINGTON, NE X On 3/10/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

snip...

Table 6. Administrative Actions: Small HACCP Plants (7/01/06 to 9/30/06)

Administrative Actions Pending or Taken at Small HACCP Plants [includes actions initiated in prior quarters]

SSOP HACCP SPS INH INT Other LOI LOW

BOOKER PACKING COMPANY 07162 M BOOKER, TX 6/2/06 6/5/06 X 9/19/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

SSOP HACCP SPS INH INT Other LOI LOW

GULF PACKING COMPANY 00696 M00696 P SAN BENITO, TX 2/25/06 2/26/06 X 8/31/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

HI COUNTRY BEEF JERKY 01248 M01248 P LINCOLN, MT 3/24/06 4/14/06 X 8/31/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

WEST MISSOURI BEEF 05821 M ROCKVILLE, MO 3/2/06 3/16/06 4/13/06 4/17/06 X 8/15/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]

GIBSON PACKING COMPANY 05843 M05843 P SEYMOUR, MO 9/21/06 X Plant failed to meet regulatory requirements for Escherichia coli Biotype 1 (E. coli). The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

SSOP HACCP SPS INH INT Other LOI LOW

HORMANN MEAT COMPANY 05544 M05544 P FAIR GROVE, MO 6/15/06 6/22/06 X 9/26/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

ROCK CREEK SLAUGHTER CO. 09150 M09150 P LOOKOUT MOUNTAIN, GA 3/16/06 4/14/06 6/30/06 7/5/06 X 8/11/06 On 3/16/06, an enforcement action concerning failure to meet regulatory requirements for Escherichia coli Biotype 1 (E.coli) was issued. The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

THEURER'S QUALITY MEATS, INC. 31647 M31647 P LEWISTON, UT 7/25/05 7/29/05 X 7/25/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

http://www.fsis.usda.gov/PDF/QER_Q4_FY2006.pdf


UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT April 1, 2006 through June 30, 2006

Table 5. Administrative Actions: Large HACCP Plants (4/01/06 to 6/30/06)

CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS X On 6/15/06, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

snip...

EXCEL CORP 00086R M FORT MORGAN, CO 2/22/05 X On 8/11/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8. On

12/22/04, plant appealed the withholding action. Appeal was denied on 1/25/05.

snip...

TYSON FRESH MEATS INC 00245L M LEXINGTON, NE X On 3/10/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

snip...

SSOP HACCP SPS INH INT Other LOI LOW

TYSON FRESH MEATS INC. 09268 M PASCO, WA X On 7/28/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

TYSON FRESH MEATS INC. 00245D M EMPORIA, KS X On 12/23/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

snip...

Administrative Actions Pending or Taken at Small HACCP Plants [includes actions initiated in prior quarters]

BOOKER PACKING COMPANY 07162 M BOOKER, TX 4/13/06 4/19/06 X Plant failed to meet regulatory requirements for Escherichia coli Biotype 1 (E. coli).

6/2/06 6/5/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

GULF PACKING COMPANY 00696 M00696 P SAN BENITO, TX 2/25/06 2/26/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

???

3/24/06 4/14/06

X

The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

WEST MISSOURI BEEF 05821 M ROCKVILLE, MO 3/2/06 3/16/06 4/13/06 4/17/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

C & C MEAT SALES, INC., 18494 M18494 P, DURHAM, NC ... FAILURE TO COMPLY CONCERNING SRM MATERIAL.

snip...

FRESH FARMS BEEF 18579 M RUTLAND, VT 12/16/05 12/28/05 X 4/13/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

FRONTIER FOODS & COLD STORAGE, INC 20741 M20741 P EL PASO, TX 5/31/06 X On 6/8/06, DM closed case by firm’s requested voluntary withdrawal. The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

HORMANN MEAT COMPANY 05544 M05544 P FAIR GROVE, MO 6/15/06 6/22/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 7/1/05 7/28/05 10/12/05 10/24/05 X 5/19/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

ROCK CREEK SLAUGHTER CO. 09150 M09150 P LOOKOUT MOUNTAIN, GA 3/16/06 4/14/06 6/30/06 X On 3/16/06, an enforcement action concerning failure to meet regulatory requirements for Escherichia coli Biotype 1 (E.coli) was issued. The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

SAVORY CONNECTION, INC., 31764 M31764 P, SELINGSGROVE, PA. ... FAILURE TO COMPLY CONCERNING SRM MATERIAL.

snip...

STEAK MASTER, 21159 M21159 P, ELWOOD, NE. ... FAILURE TO COMPLY CONCERNING SRM MATERIAL.

snip...

THE MEAT SHOP 31561 M BENSON, VT 8/18/05 9/6/05 9/9/05 X 4/4/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

THEURER'S QUALITY MEATS, INC. 31647 M31647 P LEWISTON, UT 7/25/05 7/29/05 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

WALNUT VALLEY PACKING L.L.C. 32007 M32007 P EL DORADO, KS 12/15/05 12/30/05 X 5/4/06 The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

http://www.fsis.usda.gov/PDF/QER_Q3_FY2006.pdf


UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT January 1, 2006 through March 31, 2006

Table 5. Administrative Actions: Large HACCP Plants (1/01/06 to 3/31/06)

CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS X 3/13/06 On 10/11/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

snip...

EXCEL CORP. 00086R M FORT MORGAN, CO 8/11/04 2/22/05 X On 8/11/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

On 12/22/04, plant appealed the withholding action. Appeal was denied on 1/25/05.

snip...

TYSON FRESH MEATS INC. 00245L M 3/12/04 3/18/04 X

LEXINGTON, NE

X On 3/10/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

snip...

TYSON FRESH MEATS INC. 09268 M PASCO, WA X On 7/28/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

TYSON FRESH MEATS INC. 00245D M EMPORIA, KS X On 12/23/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

snip...

Administrative Actions Pending or Taken at Small HACCP Plants [includes actions initiated in prior quarters]

GULF PACKING COMPANY, 00696 M00696 P, SAN BENITO, TX, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

snip...

HI COUNTRY BEEF JERKY, 01248 M01248 P, LINCOLN, MT, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

snip...

HITCHIN POST STEAK COMPANY, 20773 M20773 P, KANSAS CITY, KS, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

snip...

NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

ROCK CREEK SLAUGHTER CO., 09150 M09150 P, FAIRBURY, NE, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

snip...

WEST MISSOURI BEEF 05821 M ROCKVILLE, MO 3/2/06 3/16/06 X The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

Table 7. Administrative Actions: Very Small HACCP Plants (1/01/06 to 3/31/06)

A.J. CEKAK'S MEAT MARKET 21562 M ORD. NE, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

snip...

ALTA VISTA LOCKER 31931 M ALTA VISTA, KS, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

snip...

C&C MEAT SALES, INC. 18494 M18494 P UPPER MARLBORO, MD 2/27/06 3/16/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

FRESH FARMS BEEF 18579 M RUTLAND, VT 12/16/05 12/28/05 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

H AND P MEATS 21352 M SOUTH PITTSBURG, TN 7/28/05 8/8/05 8/17/05 8/19/05 X 3/6/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

PARADISE LOCKER MEATS 31865 M31865 P TRIMBLE, MO 9/21/05 10/7/05 X 1/13/06 The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

PARAGON SPRAY DRYING, L.L.C. 31762 M31762 P WAUKON, IA 9/6/05 9/12/05 X 2/9/06 The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 7/1/05 7/28/05 10/12/05 10/24/05 X The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

SAVORY CONNECTION, INC. 31764 M31764 P SELINGSGROVE, PA 3/14/06 3/31/06 X The enforcement action included, as basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

STEAK MASTER, 21159 M21159 P, ELWOOD, NW, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

snip...

TEARS MARKET, 04535 M04535 P, PENN YAN, NY, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

snip...

THE MEAT SHOP, 31561 M BENSON, VT, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

snip...

THEURER'S QUALITY MEATS, INC. 31647 M31647 P, LEWISTON, UT, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

snip...

TOOELE VALLEY MEATS 20594 M20594 P, GRANTSVILLE, UT, ... FAILURE TO COMPLY CONCERNING SRM MATERIAL

snip...

WALNUT VALLEY PACKING L.L.C. 32007 M32007 P EL DORADO, KS 12/15/05 12/30/05 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

WILLIAM. G. MEST PACKING CO. 04431 M STRYKERSVILLE, NY 2/2/06 2/23/06 X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material. On 3/21/06, NOIE was modified and reissued. On 6/29/06, NOIE was rescinded.

YODER BROTHERS MEAT PROCESSING 17301 M PARIS, TN 10/3/05 10/12/05 X 2/23/06 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

snip...

http://www.fsis.usda.gov/PDF/QER_Q1_FY2006.pdf


UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT October 1, 2005 through December 31, 2005

SRM REMOVAL USA

UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT October 1, 2005 through December 31, 2005

snip....

CARGILL MEAT SOLUTIONS 00086K M DODGE CITY, KS X X On 10/11/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

EXCEL CORP 00086R M FORT MORGAN, CO 2/22/05 X X On 8/11/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8. On 12/22/04, plant appealed the withholding action. Appeal was denied on 1/25/05.

00245L M LEXINGTON, NE 3/12/04 3/18/04 X 5/4/05 X X On 3/10/05, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

9/16/05 9/29/05 X X TYSON FRESH MEATS INC. 09268 M PASCO, WA X X On 7/28/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

TYSON FRESH MEATS INC. X X 00245D M EMPORIA, KS On 12/23/04, a withholding action concerning labels for Advanced Meat Recovery System product was taken in accordance with 9 CFR Part 500.8.

DESERET MEAT 04852 M SPANISH FORK, UT 7/20/05 8/1/05 X X 12/29/05 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

NORTHERN PACKING COMPANY INC. 00571 M BRIAR HILL, NY 12/9/05 12/23/05 X X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

A.J. CEKAK'S MEAT MARKET 9/1/05 9/20/05 X X X On 9/1/05, an enforcement action 21562 M concerning failure to meet regulatory ORD, NE requirements for Escherichia coli Biotype 1 (E. coli) was taken. The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

ALTA VISTA LOCKER 10/5/05 10/26/05 X X The enforcement action included, as a 31931 M basis, failure of the establishment toALTA VISTA, KS comply with Agency requirements concerning specified risk material.

BROWN'S PROCESSING 13100 M13100 P ELSBERRY, MO 8/8/05 8/16/05 X X X 11/16/05 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

CHAMPLAIN BEEF INC 2/28/05 3/4/05 3/8/05 X X X 08547 M WHITEHALL, NY 10/17/05 X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

FIVE STAR PACK INC. 9/1/05 9/9/05 X X 12/29/05 On 9/1/05, an enforcement action 08725 M08725 P concerning failure to meet regulatory GOLDEN CITY, MO requirements for Escherichia coli Biotype 1 (E. coli) was taken. The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material. FRESH FARMS BEEF 12/16/05 12/28/05 X X X The enforcement action included, as a 18579 M basis, failure of the establishment toRUTLAND, VT comply with Agency requirements concerning specified risk material.

GOETZ AND SONS WESTERN 11/15/05 11/23/05 12/1/05 X X MEATS INC 06245 M06245 P EVERETT, WA 12/17/05 12/28/05 X X X On 12/17/05, firm violated a regulatory control action by selling U.S.D.A retained product.

H AND P MEATS 21352 M SOUTH PITTSBURG, TN 7/28/05 8/8/05 8/17/05 8/19/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

HOPKINS PACKING COMPANY 11069 M BLACKFOOT, ID 7/28/05 8/1/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

NORTHWEST PREMIUM MEATS LLC 11032 M11032 P NAMPA, ID 7/26/05 7/29/05 X X 11/15/05 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

PARADISE LOCKER MEATS 31865 M31865 P TRIMBLE, MO 9/21/05 10/7/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material. PARAGON SPRAY DRYING, LLC 31762 M31762 P WAUKON, IA 9/6/05 9/12/05 X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 7/1/05 7/28/05 10/12/05 10/24/05 X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

S & S MEAT COMPANY 01046 M01046 P KANSAS CITY, MO 8/4/05 8/19/05 X X 11/16/05 The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

STEAK MASTER 21159 M21159 P ELWOOD, NE 11/4/05 11/17/05 X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

THE MEAT SHOP 31561 M BENSON, VT 8/18/05 9/6/05 9/9/05 X X X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

THEURER'S QUALITY MEATS, INC 31647 M31647 P LEWISTON, UT 7/27/05 7/29/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

TOOELE VALLEY MEATS 20594 M20594 P GRANTSVILLE, UT 7/25/05 8/1/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

WALNUT VALLEY PACKING LLC 32007 M32007 P EL DORADO, KS 12/15/05 12/30/05 X X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

YODER BROTHERS MEAT PROCESSING 17301 M PARIS, TN 10/3/05 10/12/05 X X The enforcement action included, as a basis, failure of the establishment to comply with Agency requirements concerning specified risk material.

full text 54 pages ;

http://www.fsis.usda.gov/PDF/QER_Q1_FY2006.pdf


Subject: USDA FSIS QUARTERLY ENFORCEMENT REPORT (BSE) July 1, 2005 through September 30, 2005 Date: March 20, 2006 at 12:58 pm PST

UNITED STATES DEPARTMENT OF AGRICULTURE FOOD SAFETY AND INSPECTION SERVICE QUARTERLY ENFORCEMENT REPORT July 1, 2005 through September 30, 2005

snip...

Administrative Actions Pending or Taken at Small HACCP Plants [includes actions initiated in prior quarters]

snip...

DESERET MEAT 04852 M SPANISH FORK, UT 07/27/05 08/01/05 X On 7/27/05, a suspension action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3.

snip...

Administrative Actions Pending or Taken at Small HACCP Plants [includes actions initiated in prior quarters]

snip...

MONTEBELLO MEAT PROCESSING, INC 19075 M19075 P MANATI, PR 08/01/05 08/18/05 X 09/26/05 On 8/1/05, an enforcement action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.

snip...

Table 7. Administrative Actions: Very Small HACCP Plants (7/01/05 to 9/30/05)

snip...

A.J. CEKAK'S MEAT MARKET 09/01/05 09/20/05 On 9/1/05, an enforcement action

21562 M

concerning failure to meet regulatory ORD, NE requirements for Escherichia coli X X X Biotype 1 (E. coli) and Bovine Spongiform Encephalopathy/Specified Risk Material was taken in accordance with 9 CFR Part 500.4.

snip...

Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]

snip...

BROWN'S PROCESSING 13100 M13100 P ELSBERRY, MO 08/08/05 08/16/05 X On 8/8/05, an enforcement action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.

snip...

Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]

snip...

FIVE STAR PACK INC. 08725 M08725 P GOLDEN CITY, MO 09/01/05 09/09/05 X X On 9/1/05, an enforcement action concerning failure to meet regulatory requirements for Escherichia coli Biotype 1 (E. coli) and Bovine Spongiform Encephalopathy/Specified Risk Material was taken in accordance with 9 CFR Part 500.4.

snip...

Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]

snip...

H AND P MEATS 21352 M SOUTH PITTSBURG, TN 07/28/05 08/08/05 08/17/05 08/19/05 X X On 8/17/05, a suspension action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3.

snip...

HOPKINS PACKING COMPANY 11069 M BLACKFOOT, ID 07/28/05 08/01/05 X On 7/28/05, a suspension action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3.

snip...

Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]

snip...

NORTHWEST PREMIUM MEATS LLC 11032 M11032 P NAMPA, ID 07/26/05 07/29/05 X X On 7/26/05, a suspension action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3.

snip...

PARADISE LOCKER MEATS 31865 M31865 P TRIMBLE, MO 09/21/05 X On 9/21/05, an enforcement action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.

PARAGON SPRAY DRYING, LLC 31792 M31792 P WAUKON, IA 09/06/05 09/12/05 X On 9/6/05, an enforcement action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.

snip...

Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]

snip...

RANDALL MEAT COMPANY 10669 M HOT SPRINGS, AR 07/01/05 07/28/05 X On 7/1/05, an enforcement action concerning Bovine Spongiform Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.

snip...

Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]

snip...

08/04/05

08/19/05

On 8/4/05,

an enforcement action 01046 M01046 P concerning Bovine SpongiformKANSAS CITY, MO X X Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.4.

Administrative Actions Pending or Taken at Very Small HACCP Plants [includes actions initiated in prior quarters]

snip...

THE MEAT SHOP 08/18/05 09/06/05

09/09/05

On 9/6/05, a suspension action 31561 M concerning Bovine SpongiformBENSON, VT Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3. XX X X X

THEURER'S QUALITY MEATS, 07/27/05 07/29/05

On 7/27/05, a suspension action INC concerning Bovine Spongiform31647 M31647 P Encephalopathy and Specified Risk X X

LEWISTON, UT Material was taken in accordance with 9 CFR Part 500.3.

TOOELE VALLEY MEATS 07/25/05 08/01/05

On 7/25/05, a suspension action 20594 M20594 Pconcerning Bovine Spongiform

GRANTSVILLE, UT X X Encephalopathy and Specified Risk Material was taken in accordance with 9 CFR Part 500.3.

snip...

52 pages

http://www.fsis.usda.gov/PDF/QER_Q4_FY2005.pdf


PREVIOUS

http://www.fsis.usda.gov/PDF/QER_Q3_FY2005.pdf


http://www.fsis.usda.gov/PDF/QER_Q2_FY2005.pdf


http://www.fsis.usda.gov/PDF/QER_Q1_FY2005.pdf


P04.27

Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route

Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany

Background:

In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.

Aims:

The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.

Methods:

Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).

Results:

In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.

Conclusions:

Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian v CJD as fast as intracerebrally inoculated animals.

The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf


What Do We Feed to Food-Production Animals? A Review of Animal FeedIngredients and Their Potential Impacts on Human Health

Amy R. Sapkota,1,2 Lisa Y. Lefferts,1,3 Shawn McKenzie,1 and Polly Walker11Johns Hopkins Center for a Livable Future, Bloomberg School of PublicHealth, Baltimore, Maryland, USA; 2Maryland Institute forApplied Environmental Health, College of Health and Human Performance,University of Maryland, College Park, Maryland, USA;3Lisa Y. Lefferts Consulting, Nellysford, Virginia, USA

snip...

Table 1. Animal feed ingredients that are legally used in U.S. animal feeds

Animal

Rendered animal protein from Meat meal, meat meal tankage, meat and bonemeal, poultry meal, animal the slaughter of food by-product meal, dried animal blood, blood meal, feather meal, egg-shell production animals andother meal, hydrolyzed whole poultry, hydrolyzed hair, bone marrow, andanimal animals digest from dead, dying, diseased, or disabled animals including deer and elk Animal waste Dried ruminant waste, dried swine waste, dried poultry litter, and undried processed animal waste products

snip...

Conclusions

Food-animal production in the United States has changed markedly in the past century, and these changes have paralleled major changes in animal feed formulations. While this industrialized system of food-animal production may result in increased production efficiencies, some of the changes in animal feeding practices may result in unintended adverse health consequences for consumers of animal-based food products. Currently, the use of animal feed ingredients, including rendered animal products, animal waste, antibiotics, metals, and fats, could result in higher levels of bacteria, antibiotic resistant bacteria, prions, arsenic, and dioxin like compounds in animals and resulting animal-based food products intended for human consumption. Subsequent human health effects among consumers could include increases in bacterial infections (antibiotic resistant and nonresistant) and increases in the risk of developing chronic (often fatal) diseases such as vCJD. Nevertheless, in spite of the wide range of potential human health impacts that could result from animal feeding practices, there are little data collected at the federal or state level concerning the amounts of specific ingredients that are intentionally included in U.S. animal feed. In addition, almost no biological or chemical testing is conducted on complete U.S. animal feeds; insufficient testing is performed on retail meat products; and human health effects data are not appropriately linked to this information. These surveillance inadequacies make it difficult to conduct rigorous epidemiologic studies and risk assessments that could identify the extent to which specific human health risks are ultimately associated with animal feeding practices. For example, as noted above, there are insufficient data to determine whether other human foodborne bacterial illnesses besides those caused by S. enterica serotype Agona are associated with animal feeding practices. Likewise, there are insufficient data to determine the percentage of antibiotic-resistant human bacterial infections that are attributed to the nontherapeutic use of antibiotics in animal feed. Moreover, little research has been conducted to determine whether the use of organoarsenicals in animal feed, which can lead to elevated levels of arsenic in meat products (Lasky et al. 2004), contributes to increases in cancer risk. In order to address these research gaps, the following principal actions are necessary within the United States: a) implementation of a nationwide reporting system of the specific amounts and types of feed ingredients of concern to public health that are incorporated into animal feed, including antibiotics, arsenicals, rendered animal products, fats, and animal waste; b) funding and development of robust surveillance systems that monitor biological, chemical, and other etiologic agents throughout the animal-based food-production chain “from farm to fork” to human health outcomes; and c) increased communication and collaboration among feed professionals, food-animal producers, and veterinary and public health officials.

REFERENCES...snip...end

Sapkota et al.668 VOLUME 115 NUMBER 5 May 2007 • Environmental Health Perspectives

http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1867957&blobtype=pdf


Calves were challenged by mouth with homogenised brain from confirmed cases of BSE. Some received 300g (3 doses of 100g), some 100g, 10g or 1g. They were then left to develop BSE, but were not subjected to the normal stresses that they might have encountered in a dairy herd. Animals in all four groups developed BSE. There has been a considerable spread of incubation period in some of the groups, but it appears as if those in the 1 and 10g challenge groups most closely fit the picture of incubation periods seen in the epidemic. Experiments in progress indicate that oral infection can occur in some animals with doses as low as 0.01g and 0.001g. ......... http://www.defra.gov.uk/animalh/bse/science-research/pathog.html#dose


look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused7% (1 of 14) of the cows to come down with BSE;

Risk of oral infection with bovine spongiform encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, NathalieLescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-PhilippeDeslysSummary The uncertain extent of human exposure to bovine spongiformencephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease(vCJD)--is compounded by incomplete knowledge about the efficiency of oralinfection and the magnitude of any bovine-to-human biological barrier totransmission. We therefore investigated oral transmission of BSE tonon-human primates. We gave two macaques a 5 g oral dose of brain homogenatefrom a BSE-infected cow. One macaque developed vCJD-like neurologicaldisease 60 months after exposure, whereas the other remained free of diseaseat 76 months. On the basis of these findings and data from other studies, wemade a preliminary estimate of the food exposure risk for man, whichprovides additional assurance that existing public health measures canprevent transmission of BSE to man.

snip...

BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%)1/15 (7%)

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculumused in our study with primates against a bovine brain inoculum with asimilar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. icip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infectedorally with similar BSE brain inocula

Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa


It is clear that the designing scientists must

also have shared Mr Bradley's surprise at the results because all the dose

levels right down to 1 gram triggered infection.

http://www.bseinquiry.gov.uk/files/ws/s145d.pdf


The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that thedesigning scientists must have also shared Mr Bradley's surprise at the resultsbecause all the dose levels right down to 1 gram triggered infection.

http://www.bseinquiry.gov.uk/files/ws/s147f.pdf


2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)

http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml


IS THERE A SCRAPIE-LIKE DISEASE IN CATTLE ?

In April of 1985, a mink rancher in Wisconsin reported a debilitating neurologic disease in his herd which we diagnosed as TME by histopathologic findings confirmed by experimental transmission to mink and squirrel monkeys. The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle and a few horses. She had never been fed.

We believe that these findings may indicate the presence of a previously unrecognized scrapie-like disease in cattle and wish to alert dairy practitioners to this possibility.

snip...

PROCEEDINGS OF THE SEVENTH ANNUAL WESTERN CONFERENCE FOR FOOD ANIMAL VETERINARY MEDICINE, University of Arizona, March 17-19, 1986

http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf


OBSERVATIONS AND RESULTS

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.

Experimental Transmission. The clinical diagnosis of TME was confirmed by histopaihologic examination and by experimental transmission to mink after incubation periods of four months. To investigate the possible involvement of cattle in this disease cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally with a brain suspension from affected mink. Each developed a fatal spongiform encephalopathy after incubation periods of 18 and 19 months.

DISCUSSION

These findings suggest that TME may result from feeding mink infected cattle and we have alerted bovine practitioners that there may exist an as yet unrecognized scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new bovine spongiform encephalopathy has recently been reported in England (Wells et al., 1987), and investigators are presently studying its transmissibility and possible relationship to scrapie. Because this new bovine disease in England is characterized by behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be confused with rabies in the United Stales and not be diagnosed. Presently, brains from cattle in the United States which are suspected of rabies infection are only tested with anti-rabies virus antibody and are not examined histopathologically for lesions of spongiform encephalopathy.

We are presently pursuing additional studies to further examine the possible involvement of cattle in the epidemiology of TME. One of these is the backpassage of our experimental bovine encephalopathy to mink. Because (here are as yet no agent- specific proteins or nucleic acids identified for these transmissible neuropathogens, one means of distinguishing them is by animal passage and selection of the biotype which grows best in a particular host. This procedure has been used to separate hamster-adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral backpassage of the experimental bovine agent resulted in incubations of only four months indicating no de-adaptation of the Stetsonville agent for mink after bovine passage. Mink fed infected bovine brain remain normal after six months. It will be essential to demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic association is to be confirmed.

ACKNOWLEDGEMENTS

These studies were supported by the College of Agricultural and Life Sciences, University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United States Department of Agriculture. The authors also wish to acknowledge the help and encouragement of Robert Hanson who died during the course of these investigations.

REFERENCES

Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and natural transmission. J. Infec. Dis. 115:393-399. Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson, D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861. Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and clinical observations. 3. Infec. Dis. 115:387-392. Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the transmissible mink encephalopathy agent. 3. ViroL 3:176-180. Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460. Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle? Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary Medicine. University of Arizona, pp 20. Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M., Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy in cattle. Vet. Rec. 121:419-420.

MARSH

http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf


Saturday, December 01, 2007

Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model

Volume 13, Number 12–December 2007 Research

Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle andL-type Bovine Spongiform Encephalopathy in a Mouse Model

Thierry Baron,* Anna Bencsik,* Anne-Gaëlle Biacabe,* Eric Morignat,* andRichard A. Bessen†*Agence Française de Sécurité Sanitaire des Aliments–Lyon, Lyon, France; and†Montana State University, Bozeman, Montana, USA

Abstract

Transmissible mink encepholapathy (TME) is a foodborne transmissible spongiform encephalopathy (TSE) of ranch-raised mink; infection with a ruminant TSE has been proposed as the cause, but the precise origin of TME is unknown. To compare the phenotypes of each TSE, bovine-passaged TME isolate and 3 distinct natural bovine spongiform encephalopathy (BSE) agents (typical BSE, H-type BSE, and L-type BSE) were inoculated into an ovine transgenic mouse line (TgOvPrP4). Transgenic mice were susceptible to infection with bovine-passaged TME, typical BSE, and L-type BSE but not to H-type BSE. Based on survival periods, brain lesions profiles, disease-associated prion protein brain distribution, and biochemical properties of protease-resistant prion protein, typical BSE had a distint phenotype in ovine transgenic mice compared to L-type BSE and bovine TME.The similar phenotypic properties of L-type BSE and bovine TME in TgOvPrP4mice suggest that L-type BSE is a much more likely candidate for the origin of TME than is typical BSE.

snip...

Conclusion

These studies provide experimental evidence that the Stetsonville TME agentis distinct from typical BSE but has phenotypic similarities to L-type BSE in TgOvPrP4 mice. Our conclusion is that L-type BSE is a more likely candidate for a bovine source of TME infection than typical BSE. In the scenario that a ruminant TSE is the source for TME infection in mink, this would be a second example of transmission of a TSE from ruminants to non-ruminants under natural conditions or farming practices in addition to transmission of typical BSE to humans, domestic cats, and exotic zoo animals(37). The potential importance of this finding is relevant to L-type BSE, which based on experimental transmission into humanized PrP transgenic mice and macaques, suggests that L-type BSE is more pathogenic for humans than typical BSE (24,38).

http://www.cdc.gov/eid/content/13/12/1887.htm?s_cid=eid1887_e


Transmissible Mink Encephalopathy TME

http://transmissible-mink-encephalopathy.blogspot.com/


USA MAD COW CASES IN ALABAMA AND TEXAS

***PLEASE NOTE***

USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it today), please note that both the ALABAMA COW, AND THE TEXAS COW, both were ''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007 11:52 PM. ...TSS

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=19779


P02.35

Molecular Features of the Protease-resistant Prion Protein (PrPres) in H- type BSE

Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden

Western blot analyses of PrPres accumulating in the brain of BSE- infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H- type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK–resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C- terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) *** reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.

FC5.5.2

Transmission of Italian BSE and BASE Isolates in Cattle Results into a Typical BSE Phenotype and a Muscle Wasting Disease

Zanusso, G1; Lombardi, G2; Casalone, C3; D’Angelo, A4; Gelmetti, D2; Torcoli, G2; Barbieri, I2; Corona, C3; Fasoli, E1; Farinazzo, A1; Fiorini, M1; Gelati, M1; Iulini, B3; Tagliavini, F5; Ferrari, S1; Monaco, S1; Caramelli, M3; Capucci, L2 1University of Verona, Neurological and Visual Sciences, Italy; 2IZSLER, Italy; 3IZSPLVA, Italy; 4University of Turin, Animal Pathology, Italy; 5Isituto Carlo Besta, Italy

The clinical phenotype of bovine spongiform encephalopathy has been extensively reported in early accounts of the disorder. Following the introduction of statutory active surveillance, almost all BSE cases have been diagnosed on a pathological/molecular basis, in a pre-symptomatic clinical stage. In recent years, the active surveillance system has uncovered atypical BSE cases, which are characterized by distinct conformers of the PrPSc, named high-type (BSE-H) and low-type (BSE-L), whose clinicopathological phenotypes remain unknown. We recently reported two Italian atypical cases with a PrPSc type similar to BSE-L, pathologically characterized by PrP amyloid plaques. Experimental transmission to TgBov mice has recently disclosed that BASE is caused by a distinct prion strain which is extremely virulent. A major limitation of transmission studies to mice is the lack of reliable information on clinical phenotype of BASE in its natural host. In the present study, we experimentally infected Fresian/Holstein and Alpine/Brown cattle with Italian BSE and BASE isolates by i.c. route. BASE infected cattle showed survival times significantly shorter than BSE, a finding more readily evident in Fresian/Holstein, and in keeping with previous observations in TgBov mice. Clinically, BSE-infected cattle developed a disease phenotype highly comparable with that described in field BSE cases and in experimentally challenged cattle. On the contrary, BASE-inoculated cattle developed an amyotrophic disorder accompanied by mental dullness. The molecular and neuropathological profiles, including PrP deposition pattern, closely matched those observed in the original cases. This study further confirms that BASE is caused by a distinct prion isolate and discloses a novel disease phenotype in cattle, closely resembling the phenotype previous reported in scrapie-inoculated cattle *** and in some subtypes of inherited and sporadic Creutzfeldt-Jakob disease. Oral Abstracts 14

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf


Subject: In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells

Gerald Wells: Report of the Visit to USA, April-May 1989

snip...

The general opinion of those present was that BSE, as an overt disease phenomenon, _could exist in the USA, but if it did, it was very rare. The need for improved and specific surveillance methods to detect it as recognised...

snip...

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...please read this old full text document !

http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf


In this context, a word is in order about the US testing program. After the discovery of the first (imported) cow in 2003, the magnitude of testing was much increased, reaching a level of >400,000 tests in 2005 (Figure 4). Neither of the 2 more recently indigenously infected older animals with nonspecific clinical features would have been detected without such testing, and neither would have been identified as atypical without confirmatory Western blots. Despite these facts, surveillance has now been decimated to 40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and invites the accusation that the United States will never know the true status of its involvement with BSE.

In short, a great deal of further work will need to be done before the phenotypic features and prevalence of atypical BSE are understood. More than a single strain may have been present from the beginning of the epidemic, but this possibility has been overlooked by virtue of the absence of widespread Western blot confirmatory testing of positive screening test results; or these new phenotypes may be found, at least in part, to result from infections at an older age by a typical BSE agent, rather than neonatal infections with new "strains" of BSE. Neither alternative has yet been investigated.

http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm


CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006

The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.

The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.

These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.

"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."

Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.

USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.

"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end

http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r

CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...

http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm

PAUL BROWN COMMENT TO ME ON THIS ISSUE

Tuesday, September 12, 2006 11:10 AM

"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency."

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=8125


Volume 12, Number 12–December 2006

PERSPECTIVE

On the Question of Sporadic

or Atypical Bovine SpongiformEncephalopathy and

Creutzfeldt-Jakob Disease

Paul Brown,* Lisa M. McShane,† Gianluigi Zanusso,‡ and Linda Detwiler§

A link between BSE and

sporadic CJD has been suggested on the basis of laboratory

studies but is unsupported by epidemiologic observation.

Such a link might yet be established by the discovery

of a specific molecular marker or of particular combinations

of trends over time of typical and atypical BSE and various

subtypes of sporadic CJD, as their numbers are influenced

by a continuation of current public health measures that

exclude high-risk bovine tissues from the animal and

human food chains.

SNIP...

Sporadic CJD

The possibility that at least some cases of apparently sporadic CJD might be due to infection by sporadic cases of BSE cannot be dismissed outright. Screening programs needed to identify sporadic BSE have yet to be implemented, and we know from already extant testing programs that at least a proportion of infected animals have no symptoms and thus would never be identified in the absence of systematic testing. Thus, sporadic BSE (or for that matter, sporadic disease in any mammalian species) might be occurring on a regular basis at perhaps the same annual frequency as sporadic CJD in humans, that is, in the range of 1 case per million animals.

Whether humans might be more susceptible to atypical forms of BSE cannot be answered at this time. Experimentally transmitted BASE shows shorter incubation periods than BSE in at least 1 breed of cattle, bovinized transgenic mice, and Cynomolgus monkeys (12,13). In humanized transgenic mice, BASE transmitted, whereas typical BSE did not transmit (13). Paradoxically, the other major phenotype (H) showed an unusually long incubation period in bovinized transgenic mice (12).

The limited experimental evidence bearing on a possible relationship between BSE and sporadic CJD is difficult to interpret. The original atypical BASE strain of BSE had a molecular protein signature very similar to that of 1 subtype (type 2 M/V) of sporadic CJD in humans (5). In another study, a strain of typical BSE injected into humanized mice encoding valine at codon 129 showed a glycopattern indistinguishable from the same subtype of sporadic CJD (15). In a third study, the glycopatterns of both the H and L strains of atypical BSE evidently did not resemble any of the known sporadic CJD subtypes (12).

To these molecular biology observations can be added the epidemiologic data accumulated during the past 30 years. The hypothesis that at least some cases of apparently sporadic CJD are due to unrecognized BSE infections cannot be formally refuted, but if correct, we might expect by now to have some epidemiologic evidence linking BSE to at least 1 cluster of apparently sporadic cases of CJD. Although only a few clusters have been found (and still fewer published), every proposed cluster that has been investigated has failed to show any common exposure to bovines. For that matter, no common exposure has been shown to any environmental vehicles of infection, including the consumption of foodstuffs from bovine, ovine, and porcine sources, the 3 livestock species known to be susceptible to transmissible spongiform encephalopathies. Additional negative evidence comes from several large case-control studies in which no statistically significant dietary differences were observed between patients with sporadic CJD and controls (16,17).

On the other hand, the difficulty of establishing a link between BSE and CJD may be compounded by our ignorance of the infectious parameters of a sporadic form of BSE (e.g., host range, tissue distribution of infectivity, route of transmission, minimum infectious dose for humans, whether single or multiple). Presumably, these parameters would resemble those of variant CJD; that is, high infectivity central nervous system and lymphoreticular tissues of an infected cow find their way into products consumed by humans. Transmissions that might have occurred in the past would be difficult to detect because meat products are generally not distributed in a way that results in detectable geographic clusters.

Barring the discovery of a specific molecular signature (as in variant CJD), the most convincing clue to an association will come from the observation of trends over time of the incidence of typical and atypical BSE and of sporadic and variant CJD. With 4 diseases, each of which could have increasing, unchanging, or decreasing trends, there could be 81 (34) possible different combinations. However, it is highly likely that the trends for typical BSE and variant CJD will both decrease in parallel as feed bans continue to interrupt recycled contamination. The remaining combinations are thus reduced to 9 (32), and some of them could be highly informative.

For example, if the incidence of atypical BSE declines in parallel with that of typical BSE, its candidacy as a sporadic form of disease would be eliminated (because sporadic disease would not be influenced by current measures to prevent oral infection). If, on the other hand, atypical BSE continues to occur as typical BSE disappears, this would be a strong indication that it is indeed sporadic, and if in addition at least 1 form of what is presently considered as sporadic CJD (such as the type 2 M/V subtype shown to have a Western blot signature like BASE) were to increase, this would suggest (although not prove) a causal relationship (Figure 5).

Recognition of the different forms of BSE and CJD depends upon continuing systematic testing for both bovines and humans, but bovine testing will be vulnerable to heavy pressure from industry to dismantle the program as the commercial impact of declining BSE cases ceases to be an issue. Industry should be aware, however, of the implications of sporadic BSE. Its occurrence would necessitate the indefinite retention of all of the public health measures that exclude high-risk bovine tissues from the animal and human food chains, whereas its nonoccurrence would permit tissues that are now destroyed to be used as before, once orally acquired BSE has disappeared.

SNIP...

PLEASE READ FULL TEXT ;

http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm?s_cid=eid06_0965_e


THE SEVEN SCIENTIST REPORT ***

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf


full text ;

http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html


Thursday, January 31, 2008

Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform Encephalopathy Prion Strain

J. Virol. doi:10.1128/JVI.02561-07 Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Thursday, January 31, 2008

Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform Encephalopathy Prion Strain

J. Virol. doi:10.1128/JVI.02561-07 Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform Encephalopathy Prion Strain

Qingzhong Kong*, Mengjie Zheng, Cristina Casalone, Liuting Qing, Shenghai Huang, Bikram Chakraborty, Ping Wang, Fusong Chen, Ignazio Cali, Cristiano Corona, Francesca Martucci, Barbara Iulini, Pierluigi Acutis, Lan Wang, Jingjing Liang, Meiling Wang, Xinyi Li, Salvatore Monaco, Gianluigi Zanusso, Wen-Quan Zou, Maria Caramelli, and Pierluigi Gambetti* Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; CEA, Istituto Zooprofilattico Sperimentale, 10154 Torino, Italy; Department of Neurological and Visual Sciences, University of Verona, 37134 Verona, Italy

* To whom correspondence should be addressed. Email: qxk2@case.edu. pxg13@case.edu.

Abstract

Bovine spongiform encephalopathy (BSE), the prion disease in cattle, was widely believed to have only one strain (BSE-C). BSE-C causes the fatal prion disease named new variant Creutzfeldt-Jacob disease in humans. Two atypical BSE strains, BASE (or BSE-L) and BSE-H, have been discovered in several countries since 2004; their transmissibility and phenotypes in humans are unknown. We investigated the infectivity and human phenotype of BASE by inoculating transgenic (Tg) mice expressing the human prion protein with brain homogenates from two BASE-affected cattle. Sixty percent of the inoculated Tg mice became infected after 20-22 months incubation, a transmission rate higher than those reported for BSE-C. A quarter of BASE-infected Tg mice, but none of the Tg mice infected with a sporadic human prion disease, showed presence of pathogenic prion protein isoforms in the spleen, indicating that the BASE prion is intrinsically lymphotropic. The pathological prion protein isoforms in BASE-infected humanized Tg mouse brains are different from those of the original cattle BASE or sporadic human prion disease. Minimal brain spongiosis and long incubation time are observed in the BASE-infected Tg mice. These results suggest that, in humans, BASE is a more virulent BSE strain and likely lymphotropic.

http://jvi.asm.org/cgi/content/abstract/JVI.02561-07v1?papetoc


for those interested, further into this study, it gets very interesting ;

http://cjdmadcowbaseoct2007.blogspot.com/2008/02/evaluation-of-human-transmission-risk.html


Subject: Aspects of the Cerebellar Neuropathology in Nor98

Date: September 26, 2007 at 4:06 pm PST

P03.141

Aspects of the Cerebellar Neuropathology in Nor98

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute, Norway

Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. *** The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf


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


12/10/76 AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON SCRAPIE Office Note CHAIRMAN: PROFESSOR PETER WILDY

snip...

A The Present Position with respect to Scrapie A] The Problem

Scrapie is a natural disease of sheep and goats. It is a slow and inexorably progressive degenerative disorder of the nervous system and it ia fatal. It is enzootic in the United Kingdom but not in all countries.

The field problem has been reviewed by a MAFF working group (ARC 35/77). It is difficult to assess the incidence in Britain for a variety of reasons but the disease causes serious financial loss; it is estimated that it cost Swaledale breeders alone $l.7 M during the five years 1971-1975. A further inestimable loss arises from the closure of certain export markets, in particular those of the United States, to British sheep.

It is clear that scrapie in sheep is important commercially and for that reason alone effective measures to control it should be devised as quickly as possible.

Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"

Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.

snip...

76/10.12/4.6

http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf


Epidemiology of Scrapie in the United States 1977

http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf


SCRAPIE PROGRAM FY REPORT 2007

Prepared by National Center for Animal Health Programs Ruminant Health Programs Team November 15, 2007

snip...

Infected and Source Flocks

During FY 2007, there were a total of 76 new infected or source flocks identified. Of those new flocks identified, 30 were infected flocks and 46 were source flocks (Figure 2). As of September 30, 2007, there were 38 scrapie infected and source flocks with open statuses (Figure 3). ...

snip...

In FY 2007, 331 scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL), including 59* Regulatory Scrapie Slaughter Surveillance (RSSS) cases (Figure 5 and Slide 16). In FY 2007, two field cases, one validation case, and two RSSS cases were consistent with Nor-98 scrapie. The Nor98-like cases originated from flocks in California, Minnesota, Colorado, Wyoming and Indiana respectively. Nineteen cases of scrapie in goats have been reported since 1990 (Figure 6). The last goat case was reported in September 2007.

snip...

see full report here ;

http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/yearly_report.pps


Friday, February 15, 2008

SCRAPIE and TSE to human UPDATE 2008 (ambiguous terms of transition and reality set in)

http://nor-98.blogspot.com/2008/02/scrapie-and-tse-to-human-update-2008.html


TSS

January 2008 Update on Feed Enforcement Activities to Limit the Spread of BSE

January 24, 2008

January 2008 Update on Feed Enforcement Activities to Limit the Spread of BSE

To help prevent the establishment and amplification of Bovine Spongiform Encephalophathy (BSE) through feed in the United States, the Food and Drug Administration (FDA) implemented a final rule that prohibits the use of most mammalian protein in feeds for ruminant animals. This rule, Title 21 Part 589.2000 of the Code of Federal Regulations, here called the Ruminant Feed Ban, became effective on August 4, 1997.

The following is an update on FDA enforcement activities regarding the ruminant feed ban. FDA's Center for Veterinary Medicine (CVM) has assembled data from the inspections that have been conducted AND whose final inspection report has been recorded in the FDA's inspection database as of January 12, 2008. As of January 12, 2008, FDA had received over 59,000 inspection reports. The majority of these inspections (approximately 70%) were conducted by State feed safety officials, with the remainder conducted by FDA officials.

Inspections conducted by FDA or State investigators are classified to reflect the compliance status at the time of the inspection based upon the objectionable conditions documented. These inspection conclusions are reported as Official Action Indicated (OAI), Voluntary Action Indicated (VAI), or No Action Indicated (NAI).

An OAI inspection classification occurs when significant objectionable conditions or practices were found and regulatory sanctions are warranted in order to address the establishment's lack of compliance with the regulation. An example of an OAI inspection classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspections classified with OAI violations will be promptly re-inspected following the regulatory sanctions to determine whether adequate corrective actions have been implemented.

A VAI inspection classification occurs when objectionable conditions or practices were found that do not meet the threshold of regulatory significance, but do warrant advisory actions to inform the establishment of findings that should be voluntarily corrected. Inspections classified with VAI violations are more technical violations of the Ruminant Feed Ban. These include provisions such as minor recordkeeping lapses and conditions involving non-ruminant feeds.

An NAI inspection classification occurs when no objectionable conditions or practices were found during the inspection or the significance of the documented objectionable conditions found does not justify further actions.

The results to date are reported here both by “segment of industry” and “in total”. NOTE – A single firm can operate as more than one firm type. As a result, the categories of the different industry segments are not mutually exclusive.

RENDERERS

These firms are the first to handle and process (i.e., render) animal proteins and to send these processed materials to feed mills and/or protein blenders for use as a feed ingredient.

Number of active firms whose initial inspection has been reported to FDA – 267

Number of active firms handling materials prohibited from use in ruminant feed – 165 (62 % of those active firms inspected)

Of the 165 active firms handling prohibited materials, their most recent inspection revealed that:

0 firms (0%) were classified as OAI

5 firms (3.0 %) were classified as VAI

LICENSED FEED MILLS

FDA licenses these feed mills to produce medicated feed products. The license is required to manufacture and distribute feed using certain potent drug products, usually those requiring some pre-slaughter withdrawal time. This licensing has nothing to do with handling prohibited materials under the feed ban regulation. A medicated feed license from FDA is not required to handle materials prohibited under the Ruminant Feed Ban.

Number of active firms whose initial inspection has been reported to FDA – 1,077

Number of active firms handling materials prohibited from use in ruminant feed – 473 (44 % of those active firms inspected)

Of the 473 active firms handling prohibited materials, their most recent inspection revealed that:

0 firms (0%) were classified as OAI

8 firms (1.7 %) were classified as VAI

FEED MILLS NOT LICENSED BY FDA

These feed mills are not licensed by the FDA to produce medicated feeds.

Number of active firms whose initial inspection has been reported to FDA – 5,207

Number of active firms handling materials prohibited from use in ruminant feed – 2,544 (49 % of those active firms inspected)

Of the 2,544 active firms handling prohibited materials, their most recent inspection revealed that:

0 firms (0%) were classified as OAI

43 firms (1.7 %) were classified as VAI

PROTEIN BLENDERS

These firms blend rendered animal protein for the purpose of producing quality feed ingredients that will be used by feed mills.

Number of active firms whose initial inspection has been reported to FDA – 398

Number of active firms handling materials prohibited from use in ruminant feed – 191 (48 % of those active firms inspected)

Of the 191 active firms handling prohibited materials, their most recent inspection revealed that:

0 firm (0%) was classified as OAI

3 firms (1.6 %) were classified as VAI

RENDERERS, FEED MILLS, AND PROTEIN BLENDERS MANUFACTURING WITH PROHIBITED MATERIAL

This category includes only those firms that actually use prohibited material to manufacture, process, or blend animal feed or feed ingredients.

Total number of active renderers, feed mills, and protein blenders whose initial inspection has been reported to FDA – 6,628

Number of active renderers, feed mills, and protein blenders processing with prohibited materials – 505 (7.6 %)

Of the 505 active renderers, feed mills, and protein blenders processing with prohibited materials, their most recent inspection revealed that:

0 firms (0%) were classified as OAI

22 firms (4.4 %) were classified as VAI

OTHER FIRMS INSPECTED

Examples of such firms include ruminant feeders, on-farm mixers, pet food manufacturers, animal feed salvagers, distributors, retailers, and animal feed transporters.

Number of active firms whose initial inspection has been reported to FDA – 19,481

Number of active firms handling materials prohibited from use in ruminant feed – 6,275 (32 % of those active firms inspected)

Of the 6,275 active firms handling prohibited materials, their most recent inspection revealed that:


0 firms (0%) were classified as OAI

155 firms (2.5 %) were classified as VAI

TOTAL FIRMS

Note that a single firm can be reported under more than one firm category; therefore, the summation of the individual OAI/VAI firm categories will be more than the actual total number of OAI/VAI firms, as presented below.

Number of active firms whose initial inspection has been reported to FDA – 21,630

Number of active firms handling materials prohibited from use in ruminant feed – 6,927 (32 % of those active firms inspected)

Of the 6,927 active firms handling prohibited materials, their most recent inspection revealed that:

0 firms (0%) were classified as OAI

162 firms (2.3 %) were classified as VAI


http://www.fda.gov/cvm/BSE0108.htm



Greetings,

VAI violations can consist of many breaches, that in the end, could cause tainted product to be distributed.

im just goint to pick out one from last year, and i just ponder how they would have classified this ;


10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA
2007


Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling’s 85% Blood Meal, Flash Dried,
Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was
cross-contaminated with prohibited bovine meat and bone meal that had been
manufactured on common equipment and labeling did not bear cautionary BSE
statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI

___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL
Prot-Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal,
TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY
Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST
POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI – 8# SPECIAL
DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J – PROTEIN/LACTATION, ROCK
CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC
MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY,
A-BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with
commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm
initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross
contaminated with prohibited meat and bone meal and the labeling did not
bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007


http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html



FC5.5.1

BASE Transmitted to Primates and MV2 sCJD Subtype Share PrP27-30 and PrPSc

C-terminal Truncated Fragments Zanusso, G1; Commoy, E2; Fasoli, E3; Fiorini, M3; Lescoutra, N4; Ruchoux, MM4; Casalone, C5; Caramelli, M5; Ferrari, S3; Lasmezas, C6; Deslys, J-P4; Monaco, S31University of Verona, of Neurological and Visual Sciences, Italy; 2CEA, IMETI/SEPIA,France; 3University of Verona, Neurological and Visual Sciences, Italy; 4IMETI/SEPIA,France; 5IZSPLVA, Italy; 6The Scripps Research Insitute, USA

The etiology of sporadic Creutzfeldt-Jakob disease (sCJD), the most frequent humanprion disease, remains still unknown. The marked disease phenotype heterogeneity observed in sCJD is thought to be influenced by the type of proteinase K-resistantprion protein, or PrPSc (type 1 or type 2 according to the electrophoretic mobility ofthe unglycosylated backbone), and by the host polymorphic Methionine/Valine (M/V)codon 129 of the PRNP. By using a two-dimensional gel electrophoresis (2D-PAGE)and imunoblotting we previously showed that in sCJD, in addition to the PrPSc type, distinct PrPSc C-terminal truncated fragments (CTFs) correlated with different sCJD subtypes. Based on the combination of CTFs and PrPSc type, we distinguished three PrPSc patterns: (i) the first was observed in sCJD with PrPSc type 1 of all genotypes,;(ii) the second was found in M/M-2 (cortical form); (iii) the third in amyloidogenic M/V-2 and V/V-2 subtypes (Zanusso et al., JBC 2004) . Recently, we showed that sCJD subtype M/V-2 shared molecular and pathological features with an atypical form of BSE, named BASE, thus suggesting a potential link between the two conditions. This connection was further confirmed after 2D-PAGE analysis, which showed an identical PrPSc signature, including the biochemical pattern of CTFs. To pursue this issue, we obtained brain homogenates from Cynomolgus macaques intracerebrally inoculatedwith brain homogenates from BASE. Samples were separated by using a two dimensional electrophoresis (2D-PAGE) followed by immunoblotting. We here show that the PrPSc pattern obtained in infected primates is identical to BASE and sCJDMV-2 subtype. These data strongly support the link, or at least a common ancestry, between a sCJD subtype and BASE.

This work was supported by Neuroprion (FOOD-CT-2004-506579)



FC5.5.2

Transmission of Italian BSE and BASE Isolates in Cattle Results into a Typical BSE Phenotype and a Muscle Wasting Disease

Zanusso, G1; Lombardi, G2; Casalone, C3; D’Angelo, A4; Gelmetti, D2;Torcoli, G2; Barbieri, I2; Corona, C3; Fasoli, E1; Farinazzo, A1; Fiorini, M1; Gelati,M1; Iulini, B3; Tagliavini, F5; Ferrari, S1; Monaco, S1; Caramelli, M3; Capucci, L21University of Verona, Neurological and Visual Sciences, Italy; 2IZSLER, Italy; 3IZSPLVA,Italy; 4University of Turin, Animal Pathology, Italy; 5Isituto Carlo Besta, Italy

The clinical phenotype of bovine spongiform encephalopathy has been extensively reported in early accounts of the disorder. Following the introduction of statutory active surveillance, almost all BSE cases have been diagnosed on a pathological/molecularbasis, in a pre-symptomatic clinical stage. In recent years, the active surveillance system has uncovered atypical BSE cases, which are characterized by distinctconformers of the PrPSc, named high-type (BSE-H) and low-type (BSE-L), whose clinicopathological phenotypes remain unknown. We recently reported twoItalian atypical cases with a PrPSc type similar to BSE-L, pathologically characterized by PrP amyloid plaques. Experimental transmission to TgBov mice has recently disclosed that BASE is caused by a distinct prion strain which is extremely virulent. Amajor limitation of transmission studies to mice is the lack of reliable information onclinical phenotype of BASE in its natural host. In the present study, we experimentally infected Fresian/Holstein and Alpine/Brown cattle with Italian BSE and BASE isolatesby i.c. route. BASE infected cattle showed survival times significantly shorter than BSE, a finding more readily evident in Fresian/Holstein, and in keeping with previous observations in TgBov mice. Clinically, BSE-infected cattle developed a disease phenotype highly comparable with that described in field BSE cases and inexperimentally challenged cattle. On the contrary, BASE-inoculated cattle developed an amyotrophic disorder accompanied by mental dullness. The molecular and neuropathological profiles, including PrP deposition pattern, closely matched those observed in the original cases. This study further confirms that BASE is caused by a distinct prion isolate and discloses a novel disease phenotype in cattle, closely resembling the phenotype previous reported in scrapie-inoculated cattle and insome subtypes of inherited and sporadic Creutzfeldt-Jakob disease.



P04.27

Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route

Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3;Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J11Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France;3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Diseasecontrol, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany

Background:

In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.

Aims:

The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.

Methods:

Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).

Results:

In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.

Conclusions:

Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.

The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf



ALSO, look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;

Risk of oral infection with bovine spongiform encephalopathy agent inprimates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, NathalieLescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-PhilippeDeslys

Summary

The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease(vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of diseaseat 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.

snip...


BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%)1/15 (7%)

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculumused in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was
inoculated into mice and cattle.8 *Data are number of animalspositive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of
bioassays is generally judged to be about plus or minus 1 log. icip=intracerebral and intraperitoneal.


Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula

Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa



It is clear that the designing scientists must

also have shared Mr Bradley’s surprise at the results because all the dose

levels right down to 1 gram triggered infection.

http://www.bseinquiry.gov.uk/files/ws/s145d.pdf



6. It also appears to me that Mr Bradley’s answer (that it would take lessthan say 100 grams) was probably given with the benefit of hindsight; particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the "attackrate" experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection. The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams. It is clear that the designing scientists must have also shared Mr Bradley’s surprise at the results because all the dose levels right down to 1 gram triggered infection.

http://www.bseinquiry.gov.uk/files/ws/s147f.pdf



APHIS-2006-0041-0006 TSE advisory committee for the meeting December 15, 2006

http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8



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



Attachment to Singletary comment

January 28, 2007


Greetings APHIS,


I would kindly like to submit the following to ;


BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES
[Docket No. APHIS-2006-0041] RIN 0579-AC01


[Federal Register: January 9, 2007 (Volume 72, Number 5)]
[Proposed Rules]
[Page 1101-1129]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr09ja07-21]

http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f8152



BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS
DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01
Date: January 9, 2007 at 9:08 am PST


http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f3412



[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)



http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf



[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle

03-025IFA
03-025IFA-2
Terry S. Singeltary


Page 1 of 17



http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf



Thursday, January 3, 2008

ANIMAL HEALTH REPORT 2006 (BSE h-BASE EVENT IN ALABAMA, Scrapie, and CWD)

http://animalhealthreport2006.blogspot.com/2008/01/animal-health-report-2006-bse-h-base.html



BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA

http://madcowtesting.blogspot.com/



CREUTZFELDT JAKOB DISEASE MAD COW BASE UPDATE USA

http://cjdmadcowbaseoct2007.blogspot.com/



Archive Number 20071105.3602
Published Date 05-NOV-2007
Subject PRO/AH/EDR> Prion disease update 2007 (07)

PRION DISEASE UPDATE 2007 (07)

snip...

[In submitting these data, Terry S. Singeltary Sr. draws attention to the
steady increase in the "type unknown" category, which, according to their
definition, comprises cases in which vCJD could be excluded. The total of 26
cases for the current year (2007) is disturbing, possibly symptomatic of the
circulation of novel agents. Characterization of these agents should be
given a high priority. - Mod.CP]

http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963


There is a growing number of human CJD cases, and they were presented last
week in San Francisco by Luigi Gambatti(?) from his CJD surveillance
collection.

He estimates that it may be up to 14 or 15 persons which display selectively
SPRPSC and practically no detected RPRPSC proteins.


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm



http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf




full text ;

Friday, January 11, 2008
CJD HUMAN TSE REPORT UK, USA, CANADA, and Mexico JANUARY 2008

http://cjdmadcowbaseoct2007.blogspot.com/2008/01/cjd-human-tse-report-uk-usa-canada-and.html




Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518