REPORT OF THE MEETING OF THE OIE SCIENTIFIC COMMISSION FOR ANIMAL DISEASES Paris, 9–13 September 2019 BSE, TSE, PRION
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REPORT OF THE MEETING OF THE OIE SCIENTIFIC COMMISSION FOR ANIMAL DISEASES Paris, 9–13 September 2019
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A meeting of the OIE Scientific Commission for Animal Diseases (the Commission) was held at OIE Headquarters in Paris, France, from 9 to 13 September 2019.
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Annex 7 (contd) AHG on BSE risk assessment and surveillance/March 2019
34 Scientific Commission/September 2019
3. Atypical BSE
The Group discussed and endorsed with minor revisions an overview of relevant literature on the risk of atypical BSE being recycled in a cattle population and its zoonotic potential that had been prepared ahead of the meeting by one expert from the Group. This overview is provided as Appendix IV and its main conclusions are outlined below. With regard to the risk of recycling of atypical BSE, recently published research confirmed that the L-type BSE prion (a type of atypical BSE prion) may be orally transmitted to calves1 . In light of this evidence, and the likelihood that atypical BSE could arise as a spontaneous disease in any country, albeit at a very low incidence, the Group was of the opinion that it would be reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle were to be exposed to contaminated feed. Therefore, the recycling of atypical strains in cattle and broader ruminant populations should be avoided.
The Group acknowledged the challenges in demonstrating the zoonotic transmission of atypical strains of BSE in natural exposure scenarios. Overall, the Group was of the opinion that, at this stage, it would be premature to reach a conclusion other than that atypical BSE poses a potential zoonotic risk that may be different between atypical strains.
4. Definitions of meat-and-bone meal (MBM) and greaves
The Group discussed and endorsed a document prepared ahead of the meeting by two experts of the Group on the definitions of meat-and-bone meal (MBM) and greaves.
According to the Glossary of the Terrestrial Animal Health Code (hereafter the Terrestrial Code), MBM currently “means the solid protein products obtained when animal tissues are rendered, and includes any intermediate protein product other than peptides of a molecular weight less than 10,000 daltons and aminoacids” and greaves “means the protein-containing residue obtained after the partial separation of fat and water during the process of rendering”. The Group considered that the rationale to differentiate MBM and greaves was unclear. The Group also emphasised a lack of common understanding in different countries of what greaves are as well as a variety of practices as to how greaves are used.
The Group pointed out that, based on this definition, it was unclear whether greaves could be considered intermediate protein products. If so, it would be relevant to include greaves and MBM in a single definition. The Group proposed a definition of “protein meal” encompassing both MBM and greaves as follows: “protein meal means any final or intermediate solid protein-containing product, obtained when animal tissues are rendered, excluding blood and blood products, peptides of a molecular weight less than 10,000 daltons and amino-acids”.
The Group noted that MBM (and greaves) were relevant not only for BSE but also for other OIE listed diseases (i.e., Chapter 8.1. on anthrax; Chapter 8.4. on infection with Brucella abortus, B. melitensis and B. suis; Chapter 8.11. on infection with Mycobacterium tuberculosis complex; Chapter 14.8. on scrapie; and Chapter 15.3 on infection with porcine reproductive and respiratory syndrome virus).
The Group recommended the proposed definition of “protein meal” should apply, at this stage, for the purpose of Chapters 11.4. and 1.8. of the Terrestrial Code. Whether this definition would also be relevant for the other disease-specific Chapters listed above should be further assessed by the OIE. If considered relevant for other diseases, the proposed definition could ultimately replace the definitions of MBM and greaves in the Glossary of the Terrestrial Code.
AHG on BSE risk assessment and surveillance/March 2019 Annex 7 (contd)
Scientific Commission/September 2019 35
5. Revision of Chapter 11.4. of the Terrestrial Code
5.1. Draft Article 11.4.1. General provisions
The Group revised draft Article 11.4.1. to ensure better alignment with the recommended structure of disease-specific Chapters of the Terrestrial Code. To improve clarity, the Group agreed to add definitions of terms applicable to this Chapter, including a case definition.
To address a question raised by the Scientific Commission at its February 2019 meeting, and consistent with the rationale of the ad hoc Group on BSE risk assessment at its November 2018 meeting, the Group concluded that the occurrence of a case of atypical BSE, regardless of the origin (imported or indigenous), would not impact a country’s BSE risk status by itself (see section 5.4. of this report). Nevertheless, based on the consideration of recent findings for L-type BSE presented above and provided in Appendix IV, the Group emphasised that the potential recycling of all BSE agents, not only of classical BSE, was important to be considered in the exposure assessment. For this, atypical BSE is not completely disregarded in the recognition of a country’s BSE risk status as the existing Article 11.4.1. implies. To avoid misleading statements, the phrase “For the purposes of official BSE risk status recognition, BSE excludes 'atypical BSE' as a condition believed to occur spontaneously in all cattle populations at a very low rate” was proposed to be removed from Article 11.4.1. The Group consequently amended draft Articles 11.4.1. and 11.4.2. point 1.b. to indicate the potential for atypical BSE to be recycled in a cattle population if cattle were to be exposed to contaminated feed, and draft Article 11.4.3. points 3.a. and 4. to clarify the impact and the way to address atypical BSE cases (section 5.4. of this report).
5.2. Draft Article 11.4.1.bis. Safe commodities
With regard to safe commodities, the Group took note of the definition provided in the Glossary of the Terrestrial Code (i.e., “means a commodity that can be traded without the need for risk mitigation measures specifically directed against a particular listed disease, infection or infestation and regardless of the status of the country or zone of origin for that disease, infection or infestation”) as well as the provisions of the recent Chapter 2.2. of the Terrestrial Code (Criteria applied by the OIE for assessing the safety of commodities, first adopted in May 2017).
The Group noted that for the commodities listed under current Article 11.4.1. points 1.g. and 1.h., measures specifically directed against BSE to mitigate the risk of cross contamination by the BSE agent were explicitly stated. Point 1.g.: “deboned skeletal muscle meat (excluding mechanically separated meat) from cattle which passed ante- and post-mortem inspections; which were not subjected to a stunning process with a device injecting compressed air or gas into the cranial cavity, or to a pithing process, prior to slaughter; and which has been prepared in a manner to avoid contamination with tissues listed in Article 11.4.14.” ; and point 1.h.: “blood and blood by-products from cattle which were not subjected to a stunning process with a device injecting compressed air or gas into the cranial cavity, or to a pithing process, prior to slaughter”). Considering that inclusion of these commodities in an Article specifically listing safe commodities is no longer consistent with either the Glossary or Chapter 2.2., the Group sought advice from the Code Commission and agreed with their recommendation that these commodities should not be listed as safe commodities and would need to be addressed in separate articles of Chapter 11.4. (i.e., Draft Articles 11.4.9. to 11.4.11. and 11.4.13.)
The Group noted that “semen and in vivo derived cattle embryos” were listed as safe commodities in current Article 11.4.1. point 1.b. and discussed whether in vitro derived cattle embryos could also be considered safe commodities. Considering that scientific evidence was only published on in vivo derived cattle embryos2
the Group could not recommend in vitro derived cattle embryos be specifically listed as safe commodities.
The Group pointed out that “semen and in vivo derived cattle embryos” should not necessarily only be “collected and handled in accordance with the recommendations of the International Embryo Transfer Society” as recommended in current Article 11.4.1. point 1.b., but rather in accordance with relevant Chapters of the Terrestrial Code.
To address a request received by the OIE from the European Serum Products association, the Group discussed whether animal serum used in culture media could be considered a safe commodity. The Group pointed out that under current Article 11.4.1. point 1.h., the provisions for BSE pertaining to “blood and blood by-products” applied to “animal serum used in culture media”, meaning risks are effectively managed as long as this blood by-product originates from cattle which were not subjected to a stunning process with a device injecting compressed air or gas into the cranial cavity, or to a pithing process, prior to slaughter. These requirements are included in draft Article 11.4.13.
5.3. Draft Article 11.4.2. The BSE risk of the cattle population of a country, zone or compartment The Group clarified that the BSE risk status of a cattle population should be determined based on: (i) a comprehensive risk assessment, (ii) the continuous implementation of a passive surveillance programme to detect the emergence or re-emergence of classical BSE, and (iii) the history of occurrence and management of cases of classical or atypical BSE.
The Group reviewed the listed steps of a risk assessment for the purpose of BSE. The Group complemented the provisions on the last step of the assessment (i.e., risk estimation) to better capture the expected outcome of the risk estimation (i.e., “provide an overall measure of the risk that BSE agents have been recycled in the cattle population through the feeding of ruminant-derived protein meal, with indigenous cases arising as a consequence”).
The Group agreed that consistent with the provisions of current Article 11.4.2., Members should review their BSE risk assessment annually.
5.4. Draft Article 11.4.3. Negligible BSE risk
The Group reviewed draft Article 11.4.3. and addressed unresolved issues from an earlier meeting of the ad hoc Group on BSE risk assessment, as well as the questions raised by the Scientific Commission at its February 2019 meeting.
a) Demonstration of the implementation of a ruminant-to-ruminant feed ban
At its November 2018 meeting, the ad hoc Group on BSE risk assessment did not decide whether demonstrating that protein meal derived from ruminants have not been fed to ruminants:
- could be considered to be implicitly encompassed in draft Article 11.4.3. point 1.a. as drafted in November 2018 (i.e., “a risk assessment should demonstrate that the likelihood of cattle population being exposed to BSE agent has been negligible for at least 8 years”); or
- should be made explicit for the sake of clarity, common understanding by Members, and therefore harmonised implementation of Article 11.4.3.
The Group agreed to complement draft Article 11.4.3. points 1.a. and 1.b. to clearly emphasise that protein meal derived from ruminants should not have been fed to ruminants regardless of the pathway for achieving a negligible BSE risk status (i.e., husbandry practices or effective and continuous mitigation of each identified risk).
b) Impact of the occurrence of case(s) of BSE
Consistent with the approach proposed in section 5.1. of this report, the Group further amended draft Article 11.4.3. point 3.a. to clearly state that the Member could be granted a negligible BSE risk status provided that if there has been a case, this case was either imported or diagnosed as atypical BSE. At its November 2018 meeting, the ad hoc Group on BSE risk assessment noted that draft Article 11.4.3. needed to be further revised to clearly state that if there has been an indigenous case of classical BSE in an animal born 8 or less years ago in a country or zone already recognised as posing a negligible BSE risk, the Member could regain its negligible BSE risk status provided that a subsequent investigation confirmed that the likelihood of the BSE agent being recycled within the cattle population remained negligible. The Group accordingly amended draft Article 11.4.3. point 3.b.ii.
c) Complete destruction or disposal of any cases of BSE
At its February 2019 meeting, the Scientific Commission requested clarifications on whether the last provision of draft Article 11.4.3. (which requested that any cases of BSE have been completely destroyed) also applied to atypical BSE. In accordance with the overview on “Atypical BSE: the risk of being recycled in a cattle population and its zoonotic potential” (section 3 of this report and Appendix IV), the Group re-affirmed its previous position and, to improve clarity, amended draft Article 11.4.3. point 4., indicating that any cases of BSE either classical or atypical that have been detected should be completely destroyed or disposed of in such a way that ensures they do not enter the animal feed chain to prevent the recycling of BSE agents.
5.5. Draft Article 11.4.4. Controlled BSE risk
The Group refined draft Article 11.4.4. to ensure consistency of wording and numbering with draft Article 11.4.3.
5.6. Current Article 11.4.6. Recommendations for importation of bovine commodities from a country, zone or compartment posing a negligible BSE risk
The Group agreed with the opinion of the ad hoc Group on BSE which met in August 2016 which emphasised that provisions of current Article 11.4.6. were not applicable to commodities listed as safe commodities (current Article 11.4.1.) or to commodities for which recommendations were prescribed in other articles of Chapter 11.4. (i.e., current Articles 11.4.7., 11.4.10., and from 11.4.13. to 11.4.18.). The Group reviewed the list of commodities addressed in the other relevant articles of Chapter 11.4. and could not identify any remaining commodities which were not covered. The Group therefore recommended Article 11.4.6. be removed.
5.7. Draft Article 11.4.6. Recommendations for importation of cattle from a country, zone or compartment posing a negligible BSE risk
The Group noted that current Article 11.4.7. provided recommendations for the importation of cattle from a country, zone or compartment posing a negligible BSE risk but where there has been an indigenous case. The Group considered that in light of the provisions of draft Article 11.4.3., which clearly define the conditions related to the occurrence of an indigenous case, it was no longer relevant to provide such recommendations. The same recommendations would apply for the importation of live cattle from any country, zone or compartment posing a negligible BSE risk. The title of the draft article was amended accordingly.
The Group noted that current Article 11.4.7. point 1. on the permanent identification of cattle required measures to be taken on same feed cohort or birth cohort animals when an indigenous case of classical BSE was identified. Consistent with the recommendations of the ad hoc Group on BSE risk assessment at its July 2018 meeting, the Group agreed that the measures for cohort animals would not provide a significant gain in risk reduction as long as the likelihood of BSE being recycled within the cattle population continues to be negligible. As a result, the Group concluded that current Article 11.4.7. point 1. was no longer necessary.
Regarding the requirement of current Article 11.4.7. point 2. that cattle were born “after the date from which the ban on the feeding of ruminants with meat-and-bone meal and greaves derived from ruminants had been effectively enforced”, the Group advised that rather the cattle were born in the country, zone or compartment “during the period when the likelihood of the BSE agent being recycled in the cattle population has been demonstrated to be negligible”, consistent with Draft Article 11.4.3. point 1.
The Group discussed the provisions for trade that should apply to cattle older than the period for which the likelihood of the BSE agent being recycled in the cattle population has been assessed to be negligible. The Group noted that a country or zone applying for the official recognition of a negligible BSE risk status may be able to demonstrate that the likelihood of the BSE agent being recycled in the cattle population has been negligible for more than 8 years. In that case, this should be acknowledged in the report of the ad hoc Group on BSE Risk Status Evaluation of Members. This would allow countries or zones newly recognised as having a BSE negligible risk status to export cattle older than 8 years based on the provisions of draft Article 11.4.6. The Group emphasised that it should be possible for an applicant Member to document the BSE risk assessment for a period of more than eight years and that it would be necessary to make it explicit in the relevant sections of the BSE questionnaire.
5.8. Draft Article 11.4.7. Recommendations for importation of cattle from a country, zone or compartment posing a controlled BSE risk
Consistent with the approach proposed in draft Article 11.4.6., the Group advised that the provisions on the permanent identification of cattle were no longer necessary and that the cattle selected for export should be born in the country, zone or compartment during the period when the likelihood of the BSE agent being recycled in the cattle population has been demonstrated to be negligible. Consequently, this period should be acknowledged in the report of the ad hoc Group on BSE Risk Status Evaluation of Members. 5.9. Draft Article 11.4.8. Recommendations for importation of cattle from a country, zone or compartment posing an undetermined BSE risk
The Group reviewed the recommendations listed in current Article 11.4.9. (Recommendations for the importation of cattle from a country, zone or compartment posing an undetermined BSE risk) and pointed out that compliance with the provisions listed in points 1 (“the feeding of ruminants with meat-and-bone meal and greaves derived from ruminants has been banned and the ban has been effectively enforced”) and 3.b. (cattle selected for export “were born at least two years after the date from which the ban on the feeding of ruminants with meat-and-bone meal and greaves derived from ruminants was effectively enforced”) would be difficult to institute and assess considering that a feed ban may not have been implemented in countries, zones or compartments posing an undetermined BSE risk.
The Group therefore recommended that draft Article 11.4.8. should focus on the demonstration that an individual animal has never been fed with feed containing ruminant-derived protein meal (see section 4 of this report). The Group acknowledged that this would be difficult to certify and that a permanent individual identification, recording and traceability system from birth and throughout the lifetime of the animal prior to export would be a pre-requisite to allow such a demonstration to be made. This option would, however, allow for bilateral negotiations of such trade.
5.10.Draft Article 11.4.9. Recommendations for importation of fresh meat and meat products from a country, zone or compartment posing a negligible BSE risk
The Group reviewed the recommendations listed in current Article 11.4.10., and, consistent with the proposed approach in draft Article 11.4.6., the Group recommended that meat and meat products imported from a country, zone or compartment posing a negligible BSE risk should be derived from cattle that passed ante-mortem inspection and were born during the period when the likelihood of the BSE agent being recycled in the cattle population has been assessed to be negligible. The Group proposed alternative provisions for meat and meat products derived from cattle that were not born during this period.
The Group reviewed the recommendation made by the ad hoc Group on BSE which met in August 2016 proposing that the fresh meat and meat products imported from a country, zone or compartment posing a negligible BSE risk should be produced and handled in a manner which ensures that such products do not contain and are not contaminated with skull, brain, eyes and spinal cord and mechanically separated meat from the skull from cattle over 60 or 72 months of age. Considering that, based on the provisions of draft Article 11.4.3., the likelihood of the BSE agents (atypical and classical) being recycled in the cattle population would have been demonstrated to be negligible, and acknowledging that atypical BSE would remain at a very low level and with a potential uniform presentation in any cattle population, the Group considered that specific recommendations targeting atypical BSE for international trade from a country, zone or compartment posing a negligible BSE risk would be disproportionate to the likely level of risk. As a result, the Group did not fully endorse the proposal made by the 2016 ad hoc Group on BSE.
The Group emphasised that post-mortem inspection is not considered relevant for BSE and recommended any reference to post-mortem inspection to be removed throughout draft Chapter 11.4.
5.11.Draft Article 11.4.10. Recommendations for importation of fresh meat and meat products from a country, zone or compartment posing a controlled BSE risk
The Group reviewed the recommendations listed in current Article 11.4.11. and only made editorial changes for the sake of clarity and harmonisation with draft Article 11.4.11.
5.12.Draft Article 11.4.11. Recommendations for importation of fresh meat and meat products from a country, zone or compartment posing an undetermined BSE risk
The Group reviewed the recommendations listed in current Article 11.4.12. and agreed with the opinion of the ad hoc Group on BSE which met in August 2016 that point 2.b. of current Article 11.4.12., should be removed. Point 2.b. currently recommends that fresh meat and meat products should be produced and handled to ensure that such products do not contain and are not contaminated with nervous and lymphatic tissues exposed during the deboning process. The Group agreed that these measures would have been implemented out of an abundance of caution based on a comparison with scrapie. Indeed, pathogenesis studies have subsequently confirmed that BSE in cattle amplifies almost exclusively in the CNS and the ileal Peyer’s patches, with later limited centrifugal spread of infectivity along nerve fibres into the periphery in the clinical stages of the disease3, 4 . As a result, the Group concluded that the removal of these tissues is not relevant to mitigate the BSE risk.
The Group noted that current Article 11.4.12. point 2.c. required that fresh meat and meat products should be produced and handled in a manner which ensures that such products do not contain and are not contaminated with mechanically separated meat from the skull and from the vertebral column from cattle over 12 months of age. The Group discussed the age limit of 12 months and agreed that it was originally implemented out of an abundance of caution in the early 2000s when there was significant uncertainty. However, experiences gained since then have confirmed that the occurrence of clinical cases in cattle less than three years of age is a rare event. For example, even in Great Britain, the country with the highest levels of exposure to BSE, only 0.15% of almost 137,000 BSE cases, for which there was reliable age data, were less than 36 months of age over the course of the entire epidemic 5 . In addition, experimental oral challenge studies in cattle with a one-gram dose of highly infectious brain material indicate that the detection of infectivity in central nervous system (CNS) in the majority of animals likely occurs only after 42 months-post-exposure (Arnold et al., 2007). The one-gram dose used in this study is likely to represent a reasonable worst-case exposure scenario for naturally infected cattle. Considering that the average
3 Espinosa JC, Morales M, Castilla J, Rogers M, Torres JM. Progression of prion infectivity in asymptomatic cattle after oral bovine spongiform encephalopathy challenge. Journal of General Virology. 2007; 88, 1379-1383.
4 Balkema-Buschmann A, Fast C, Kaatz M, Eiden M, Ziegler U, McIntyre L, Keller M, Hills B, Groschup MH. Pathogenisis of classical and atypical BSE in cattle. Preventive Veterinary Medicine. 2011; 102 (2):112-117.
5 Animal and Plant Health Agency (March 2019). (1) Age related statistics, available from:
https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/795724/pub-tse-statage.pdf, and (2) General statistics on
BSE cases in Great Britain, available from:
https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/795723/pub-tse-statgen.pdf
incubation period of cattle infected in the field is in the range of 5.0 to 5.5 years, these authors considered that their findings “offer considerable scope for modulation of current regulations”. The Group concluded that maintaining an age limit of 12 months would be disproportionate to the level of risk and recommended it be aligned with the age limit suggested for the importation of meat and meat products from a country, zone or compartment posing a controlled BSE risk (i.e., 30 months).
5.13.Draft Article 11.4.12. Recommendations for importation of cattle-derived protein meal from a country, zone or compartment posing a negligible BSE risk
Current Article 11.4.13. was revised consistent with the change in definition presented in section 4 of this report (i.e., from “meat-and-bone meal or greaves” to “protein meal”).
The Group recommended revising the scope from “ruminant-derived meat-and-bone meal or greaves” to “cattle-derived protein meal” as cattle (Bos taurus and B. indicus) are the species of relevance for BSE as defined in draft Article 11.4.1. Furthermore, as stated in draft Article 11.4.1., the recommendations in this chapter are intended to mitigate the human and animal health risks associated with the presence of the BSE agents in cattle only. As a result, the recommendations in draft Articles 11.4.6. to 11.4.18. are all about mitigating the BSE risks associated with the trade of commodities derived from cattle. Including “ruminants” more broadly in draft Article 11.4.14. would be beyond the scope of the BSE Chapter. It’s worth noting that Article 14.8.11., concerning scrapie, recommends to not trade MBM containing any sheep or goat protein from countries not considered free from scrapie, and does not impose restrictions for trade of ruminant-derived MBM.
Consistent with the revision proposed in draft Article 11.4.6., the Group recommended revising current Article 11.4.13. point 1. which provides recommendations for importation from negligible BSE risk countries where there has been an indigenous case of BSE. Indeed, provisions regarding the occurrence of an indigenous case of BSE, in a country, zone or compartment posing a negligible BSE risk were no longer considered relevant in light of the provisions of draft Article 11.4.3. The Group emphasised that the age of the cattle should be taken into consideration to ensure that they were born during the period when the likelihood of the BSE agent being recycled in the cattle population was assessed to be negligible. The Group discussed whether recommendations could be developed for the importation of cattle-derived protein meal from countries, zones or compartments posing a controlled or undetermined BSE risk provided these protein meals are free from those commodities listed in draft Article 11.4.14. that are associated with the vast majority of BSE infectivity. However, the Group determined that the proper implementation of this requirement would be difficult to verify and stressed that the BSE risk associated with any improper implementation of this requirement would be significant considering the importance of protein meal in the recycling of BSE. The Group therefore concluded that it was not appropriate to develop recommendations for the importation of cattle-derived protein meal from countries, zones or compartments posing a controlled or undetermined BSE risk.
5.14.Draft Article 11.4.13. (New Article). Recommendations for importation of blood and blood products Considering that the Group recommended that blood and blood products should no longer be listed as safe commodities (see section 5.2. of this report and draft Article 11.4.1.bis.) to comply with the recently adopted Chapter 2.2. of the Terrestrial Code, the Group drafted a new article to provide recommendations for the importation of blood and blood products.
The Group clarified that the provisions in this Article relate to blood and to blood products rather than to blood by-products. A blood by-product refers to one that is not intended to be produced but that results from processing of blood when a different final product is intended (which would be a blood product). Blood product refers to derived product from blood, which, together with blood are the scope of this Article.
The recommendations provided for blood and blood products derived from ruminants which were not born in a country, zone or compartment posing a negligible BSE risk during the period when the likelihood of the BSE agent being recycled in the cattle population has been demonstrated to be negligible ensure that cross contamination with nervous tissue is avoided.
5.15.Draft Article 11.4.14. Recommendations regarding commodities associated with the vast majority of BSE infectivity
The Group considered the recommendation made by the ad hoc Group on BSE which met in August 2016 proposing that the restriction applicable to tonsils be removed and reviewed the scientific evidence6 supporting this proposal. The Group concurred with the ad hoc Group that the restriction applicable to tonsils should be removed.
As emphasised in section 5.12. of this report, the Group agreed that current scientific evidence does not support an age limit of 12 months. The Group therefore recommended removing point 3. of current Article 11.4.14.
Consistent with current Article 11.4.13. point 2., and with the rationale presented in section 5.13. of this report, the Group emphasised that cattle-derived protein meal, or any commodities containing such products, which originate from a country, zone or compartment posing a controlled or undetermined BSE risk should not be traded. Therefore, the Group proposed to move this recommendation to draft Article 11.4.14. point 3.
The Group reviewed the recommendation made by the ad hoc Group on BSE which met in August 2016 proposing that the commodities “from cattle that were at the time of slaughter over 60 or 72 months of age originating from a country, zone or compartment defined in Article 11.4.3., the following commodities, and any commodity contaminated by them, should not be traded for the preparation of food, feed, fertilisers, cosmetics, pharmaceuticals including biologicals, or medical devices: brains, eyes, spinal cord and skull. Protein products, food, feed, fertilisers, cosmetics, pharmaceuticals or medical devices prepared using these commodities (unless covered by other Articles in this chapter) should also not be traded.” This provision and age limit were proposed to mitigate the risk associated with atypical BSE. Consistent with the rationale presented in section 5.10. of this report, the Group determined that the proposal made by the ad hoc Group in 2016 was disproportionate to the level of risk and did not endorse it.
5.16.Draft Article 11.4.15. Recommendations for importation of gelatine and collagen prepared from bones and intended for food or feed, cosmetics, pharmaceuticals including biologicals, or medical devices
The Group reviewed the steps that bones should be subjected to for the preparation of gelatine and collagen as described in current Article 11.4.15. point 2.b. The Group considered a report from EFSA7 and agreed that the steps listed in point 2.b. were sufficient to ensure that “the relative human exposures due to gelatine produced from bones including the skull and vertebral column sourced from cattle of any age are very low (< 10-5 ) and do not support the continuation of the restriction prohibiting the inclusion of skull and vertebral column”. The Group therefore determined that the provision of exclusion in current Article 11.4.15. point 2.a. (i.e., “vertebral columns from cattle over 30 months of age at the time of slaughter and skulls have been excluded”) could not be justified.
6 EFSA Panel on Biological Hazards. Scientific Opinion on the revision of the quantitative risk assessment (QRA) of the BSE risk posed by processed animal proteins. The EFSA Journal. 2011; 9(1):1947 doi:10.2903/j.efsa.2011.1947. The infectivity of tonsils is estimated to be <0.01% of the total amount of infectivity represented by the different tissues of a clinical case. The EFSA report cites the level of infectivity in tonsils to be 10-6.5 CoID50/g, which is in the same order of magnitude as that for the peripheral nervous system (PNS). Such levels of infectivity are extremely low, so low that it would be in fact biologically implausible to ingest a sufficient amount of tissue from an infected animal to pose a credible risk. This has been widely accepted for the PNS and it is not classified as a high risk tissue. As a result, it is reasonable to conclude that the risk posed by tonsillar tissue is insignificant.
7 EFSA Panel on Biological Hazards. Opinion of the Scientific Panel on biological hazards (BIOHAZ) on the “Quantitative assessment of the human BSE risk posed by gelatine with respect to residual BSE [1]”. The EFSA Journal. 2006; 4(1):312, 1–29 doi:10.2903/j.efsa.2006.312
Furthermore, the Group considered that the steps of the process described in point 2.b. were common industrial practices and were not specifically directed against BSE. Therefore, the Group contemplated whether, in light of the definition of safe commodities provided in the Glossary of the Terrestrial Code and of the provisions of Chapter 2.2. of the Terrestrial Code, gelatine and collagen prepared from bones and intended for food or feed, cosmetics, pharmaceuticals including biologicals, or medical devices could be considered safe commodities provided they are subjected to the processes currently described in point 2.b. of Article 11.4.15. After seeking advice from the Code Commission, the Group remained uncertain whether or not this would be fully consistent with Chapter 2.2. As a result, the Group proposed to maintain this provision in draft Article 11.4.15. at this stage and to refer the proposal to include it in the list of safe commodities to the Code Commission for further deliberation.
The Group reviewed the recommendation made by the ad hoc Group on BSE which met in August 2016 proposing that the commodities should come from a country, zone or compartment posing a negligible BSE risk and should be derived from cattle which have passed ante- and post-mortem inspections and the skull from cattle over 60 or 72 months of age at the time of slaughter should be excluded. Consistent with the rationale presented in section 5.10. of this report, the Group determined that this proposal was disproportionate to the level of risk and did not endorse it.
5.17.Draft Article 11.4.16. Recommendations for importation of tallow (other than as defined in Article 11.4.1.bis) intended for food, feed, fertilisers, cosmetics, pharmaceuticals including biologicals, or medical devices
The Group considered the opinion of the ad hoc Group on BSE that met in August 2016 which recommended that tallow coming from a country, zone or compartment posing a negligible BSE risk should not have been prepared using tissues listed in current Article 11.4.14. Consistent with the rationale presented in section 5.10. of this report, the Group determined that this proposal was disproportionate to the level of risk and did not endorse it.
The Group reviewed a recent study undertaken by Fast et al.8 where BSE infectivity was detected in tallow produced by standard rendering methods (20 minutes at 95° C) using mesentery with embedded nervous tissue from the celiac and mesenteric ganglion complex from a clinical case of classical BSE that had been experimentally infected by the oral route. While this provides proof of principle that prion infectivity in adipose tissue is associated with the nervous tissue attached to the mesentery, it is important to note that the level of infectivity (tested by transgenic mouse bioassay) was extremely low with positive findings in only 1 out of 6 mice. This indicates that the levels of infectivity would likely have been less than that detected in semitendinosus muscle where 9 out of 13 transgenic mice were positive (Kaatz et al., 20129 ).
In the latter study, the level of infectivity was estimated to be at least 6 logs less than the brain. In light of these findings, the Group was of the opinion that the level of infectivity in tallow derived from mesenteric fat would be negligible.
The Group agreed that, based on the evidence available to date, the exclusion of those materials listed in point 1. of draft Article 11.4.14. in the preparation of tallow, ensures the effective mitigation of potential BSE risks regardless of whether the country, zone or compartment of origin has controlled or undetermined BSE risk status. As a result, the Group proposed to remove the specific reference to controlled BSE risk in point 2 of current Article 11.4.16. With this change, tallow would be eligible for trade from a country, zone or compartment posing a controlled or undetermined BSE risk as long as it derived from cattle that passed ante-mortem inspection and had not been prepared using the commodities listed in point 1 of draft Article 11.4.14.
5.18.Draft Article 11.4.17. Recommendations for importation of dicalcium phosphate (other than as defined in Article 11.4.1.bis) intended for food, feed, fertilisers, cosmetics, pharmaceuticals including biologicals, or medical devices
As dicalcium phosphate can be considered a co-product of bone gelatine, the Group concurred with the opinion of the ad hoc Group on BSE which met in August 2016 which recommended that dicalcium phosphate should originate from products compliant with the requirements of the relevant article within Chapter 11.4. (i.e., draft Article 11.4.15.). However, the Group emphasised that this provision should only apply to countries, zones, or compartments posing a controlled or undetermined BSE risk.
Furthermore, the Group clarified that dicalcium phosphate is rather a co-product than a by-product of bone gelatine as it is produced along with gelatine when the material of origin is bone. Both gelatine and dicalcium phosphate share the initial production steps (i.e., decreasing and demineralization) and are both intended outputs of the process.
5.19.Draft Article 11.4.18. Recommendations for importation of tallow derivatives (other than those made from tallow as defined in Article 11.4.1.bis) intended for food, feed, fertilisers, cosmetics, pharmaceuticals including biologicals, or medical devices
The Group considered the provisions of current Article 11.4.18. point 3. which recommend that tallow derivatives should have been produced by hydrolysis, saponification or transesterification using high temperature and pressure. The Group considered that these measures were common industrial practices and were not specifically directed against BSE. Therefore, the Group contemplated if in light of the definition of safe commodities provided in the Glossary of the Terrestrial Code and of the provisions of Chapter 2.2. of the Terrestrial Code, tallow derivatives could be considered safe commodities provided they are subjected to the process described in current Article 11.4.18. point 3. However, after receiving preliminary advice from the Code Commission, the Group proposed to maintain the corresponding provision in draft article 11.4.15. at this stage, and to refer the proposal to include it in the list of safe commodities to the Code Commission for further consideration.
5.20.Draft Article 11.4.19. Procedures for the reduction of BSE infectivity in protein meal The Group did not propose any revision to the procedures for the reduction of BSE infectivity in protein meal.
5.21.Draft Article 11.4.20. Passive surveillance
The Group reviewed and endorsed the revised Article on BSE surveillance drafted by the ad hoc Group on BSE surveillance in October 2018 and made only minor editorial changes.
6. Revision of Chapter 1.8. of the Terrestrial Code
The Group reviewed and edited draft Chapter 1.8. (the BSE “questionnaire”) which was only initially drafted by the ad hoc Group on BSE risk assessment at its November 2018 meeting and completed electronically by the experts ahead of this meeting. Major edits in the structure of the BSE questionnaire were done to ensure full consistency between this document and revised Chapter 11.4.
6.1. General considerations
At its November 2018 meeting, the ad hoc Group on BSE risk assessment did not reach a consensus regarding whether or not applicant Members should undertake and document a BSE risk assessment, or alternatively, if the BSE “questionnaire” should facilitate the compilation of sufficient data to enable the ad hoc Group on BSE Risk Status Evaluation of Members to undertake the BSE risk assessment. The Group discussed these options and agreed that applicant Members should document the necessary body of evidence and undertake the risk assessment. In addition, the Group recommended that likelihood estimates for each step of the risk assessment process as well as the final risk estimate should be consistent with and based on the guidance provided in the OIE Handbook on Import Risk Analysis for Animals and Animal Products.
The Group acknowledged that “questionnaires” for the official recognition of status for other diseases (i.e., Chapters 1.7. and 1.9. to 1.12.) do not justify why certain information is necessary nor offer detailed guidelines on how it should be provided. However, the Group was of the opinion that applicant Members for the official recognition of a BSE risk status would benefit from detailed guidance to assist them in undertaking a comprehensive risk assessment. Furthermore, the Group was of the opinion that Chapter 1.8. should, as much as possible, be designed to be a “user friendly”, standalone document without extensive cross-references to other Chapters of the Terrestrial Code.
Consistent with the recommendations for trade applicable to various commodities, applicant Members would have the option of providing evidence for a different period of time (more than eight years if applying for negligible risk status, or for the time they have it if applying for a controlled risk status) in support of a determination, by the ad hoc Group on BSE Risk Status Evaluation of Members, of the actual period when the likelihood of the BSE agent being recycled in the cattle population has been assessed to be negligible. See sections 5.7. and 5.8. of this report.
6.2. Draft Article 1.8.5. point 1. Entry assessment
Based on the experience of the OIE ad hoc Group on BSE Risk Status Evaluation of Members, applicant Members tend to provide extensive amounts of data, information, tables, and figures in their applications which do not necessarily inform the risk assessment. The Group re-affirmed its previous position that detailed quantitative information (e.g., volume, statistics, etc.) on imported commodities was not informative for the entry assessment as long as either the commodities were imported under conditions consistent with the recommendations laid out in Chapter 11.4. or it can be demonstrated that an equivalent level of assurance was provided. The emphasis should be on documenting the measures applied to imported commodities depending on the BSE risk status of the country or zone of origin together with how the Competent Authority verifies compliance through supporting legislation, certification, and regulations.
6.3. Draft Article 1.8.5. point 2. Exposure assessment
The Group discussed how an applicant Member should determine which pathway (i.e., either livestock industry practices or effective and continuous mitigation of each identified risk) to follow during the application for official recognition of its BSE risk status. The Group indicated that it would be based on the conclusions arising from livestock industry practices and the associated likelihood that the cattle population has been exposed to either classical or atypical BSE agents. If the applicant Member concluded that the likelihood has been non-negligible, an evaluation of BSE specific mitigation measures should be performed. The Group agreed that the applicant should provide information on livestock industry practices regardless of the pathway chosen as this provides indispensable background information.
If an applicant Member concluded that the likelihood that the cattle population has been exposed to either classical or atypical BSE agents has been negligible as a result of its livestock industry practices, but the ad hoc Group on BSE Risk Status Evaluation of Members reached a different conclusion, the application for a BSE risk status would be rejected. The applicant Member would then be invited to apply for the recognition of its BSE risk status based on the effective and continuous mitigation of each identified risk. Current Article 11.4.2. point 1.b. recommends that “if the entry assessment identifies a risk factor, an exposure assessment should be conducted”. Consistent with the provisions of draft Article 11.4.2., the Group stressed that in the revised framework for BSE, an exposure assessment should be undertaken regardless of the outcome of the entry assessment. Indeed, in accordance with the findings of the overview on “Atypical BSE: the risk of being recycled in a cattle population and its zoonotic potential” (section 3 of this report and Appendix IV), the potential recycling of atypical BSE in any cattle population should be considered and, if necessary, mitigated.
6.4. Draft Article 1.8.5. point 3. Consequence assessment
The Group explained the circumstances that could lead to the recycling of BSE agents in a cattle population. In particular, the Group outlined the series of events that could initiate a cycle of BSE infectivity within a cattle population and made clear that recycling would arise when this cycle is repeated one or more times.
The Group emphasised that any level of recycling within a given period was sufficient to conclude that the consequences of exposure to contaminated feed for that period within the cattle population was nonnegligible. 6.5. Draft Article 1.8.5. point 4. Risk estimation
The risk estimation is the final step of the BSE risk assessment, and should provide an overall measure of the risk that the BSE agents have been recycled in the cattle population through the feeding of cattle with ruminant-derived protein meal, with indigenous cases arising as a consequence.
6.6. Draft Article 1.8.6. BSE surveillance
Current Article 1.8.4. on BSE surveillance was revised to reflect the new provisions for BSE surveillance defined in draft Article 11.4.20.
6.7. Draft Article 1.8.7. Recovery of a BSE risk status
The Group provided some guidance for Members applying for the recovery of a previously recognised negligible BSE risk status suspended following non-compliance with any of the 4 provisions of Article 11.4.3, including the occurrence of an indigenous case of classical BSE in an animal born within the preceding 8 years.
7. Potential impact of the revision of the BSE standards on the official BSE risk status currently recognised
Based on the provisions of draft Chapter 11.4. an exposure assessment should be undertaken regardless of the outcome of the entry assessment. However, in accordance with the provisions of current Chapter 11.4. (Article 11.4.2. point 1.b.), some Members have had an official BSE risk status recognised by the OIE based on a negligible likelihood of entry despite a non-negligible likelihood of exposure at the time of the assessment. The OIE Secretariat pre-identified 18 Members which may be impacted by the revision of the BSE standards, if a negligible likelihood of exposure cannot be demonstrated.
The Group agreed that updated information should be gathered on the likelihood of exposure to the BSE agents, including through the 2019 annual reconfirmation campaign as necessary. The Group recommended that based on the updated information collected, the likelihood of exposure to the BSE agents should be (re)assessed under the responsibility of the Scientific Commission with the support of the ad hoc Group on BSE Risk Status Evaluation of Members if necessary.
If based on the updated assessment, the likelihood of exposure is assessed to be non-negligible for some Members, the Scientific Commission would have to determine how the recognised status would be impacted. The Group emphasised that the BSE risk posed by a Member’s cattle population has not changed as a result of the proposed changes to the Chapter and a pragmatic approach would be required to ensure against any disproportionate impact on individual Members.
8. Retention on the list of negligible or controlled BSE risk status
The Group discussed the level of evidence that should be provided by Members annually to confirm compliance with the relevant provisions of draft Articles 11.4.3. and 11.4.4. to be retained on the list of countries or zones with negligible or controlled BSE risk status.
The Group advised that Members should annually:
- confirm that the risk assessment for BSE has been reviewed indicating whether or not the conclusion has changed and when it has, provide the updated risk assessment to the OIE;
- provide documented evidence that passive surveillance for BSE has been implemented in accordance with the provisions of draft Article 11.4.20;
- confirm that there have not been any cases of classical BSE in indigenous cattle born less than 8 years ago;
- confirm, in addition to the information provided through notifications made in accordance with the requirements of Chapter 1.1. of the Terrestrial Code, that any BSE cases detected have been completely destroyed or disposed of.
The Group agreed that based on these provisions, an annual reconfirmation form would be drafted by the OIE Secretariat and circulated to the Group for its review.
In addition, to increase confidence in the annual review of the BSE risk assessment and its conclusions, the Group suggested that Members could be requested to provide an updated risk assessment either at a given frequency (e.g., every 10 years), or when selected for comprehensive review by the Scientific Commission (i.e., 10% of the official BSE risk status each year). The Group recommended this proposal be referred to the Scientific Commission for its consideration.
9. Recommendations for the consideration of the OIE
The Group recommended the overview on “Atypical BSE: the risk of being recycled in a cattle population and its zoonotic potential” (Appendix IV) be referred to the Biological Standards Commission in support of the update of Chapter 3.4.5. of the Terrestrial Manual (section 5.1. of this report). The Group also recommended that consistency should be ensured between the list of behavioural or clinical signs related to BSE defined in draft Article 11.4.20. and those listed in Chapter 3.4.5. of the Terrestrial Manual.
The Group recommended that when assessing applications for the recognition of a BSE risk status, the ad hoc Group on BSE Risk Status Evaluation of Members should specify the date from which likelihood of the BSE agent being recycled in the cattle population is assessed to be negligible. This period could be longer than 8 years for Members applying for a negligible risk status, or for the time there is sufficient evidence for Members applying for a controlled risk status (sections 5.7. and 5.8. of this report).
The Group noted that whether the definition of “protein meal” proposed for the purpose of Chapters 11.4. and 1.8. is relevant for other disease-specific Chapters (i.e., Chapter 8.1. on anthrax; Chapter 8.4. on infection with Brucella abortus, B. melitensis and B. suis; Chapter 8.11. on infection with Mycobacterium tuberculosis complex; Chapter 14.8. on scrapie; and Chapter 15.3. on infection with porcine reproductive and respiratory syndrome virus) should be further assessed by the OIE. See Section 4 of this report.
The Group recommended that the following commodities be further considered by the Code Commission for inclusion as safe commodities:
- gelatine and collagen prepared from bones subjected to the process described in draft Article 11.4.15. point 2. and intended for food or feed, cosmetics, pharmaceuticals including biologicals, or medical devices (section 5.16. of this report); and
- tallow derivatives produced by hydrolysis, saponification or transesterification using high temperature and pressure (section 5.19. of this report).
The Group recommended that the potential impact of revisions of the BSE standards on the currently recognised BSE risk status should be further assessed by the Scientific Commission with the support of the ad hoc Group on BSE Risk Status Evaluation of Members as necessary. See section 7 of this report.
The Group emphasised that training by the OIE on the procedures and requirements for the official recognition of the BSE risk status of a country or zone would be beneficial for Members upon the adoption of the revised provisions.
The Group noted that due to the nature of BSE, OIE standards are likely to need to be reassessed in the future in light of emerging scientific evidence and the evolution of the global situation for BSE.
10. Finalisation and adoption of the report
The Group reviewed and amended the draft report. The Group agreed that the report reflected the discussions.
snip...
Annex 7 (contd) AHG on BSE risk assessment and surveillance/March 2019 52 Scientific Commission/September 2019
Annex IV
Atypical bovine spongiform encephalopathy (BSE) – transmissibility among cattle and its zoonotic potential
OIE ad hoc Group on BSE risk assessment and surveillance – March 2019
This overview of relevant literature was prepared by Dr N. Murray on behalf of the OIE ad hoc Group on BSE risk assessment and surveillance, and was edited and endorsed by this ad hoc Group. It aims to gather current scientific literature to support the assessment of the risk of recycling of atypical BSE in a cattle population and its zoonotic potential to support an informed risk-based revision of the provisions for atypical BSE outlined in Articles 11.4.2. and 11.4.3. of the Terrestrial Animal Health Code.
I. Implications for the cattle population of a country (risk of recycling)
Atypical BSE is a neurological disease of cattle caused by misfolded prion proteins with different conformations than those of the classical BSE (C-BSE). Two phenotypes of atypical BSE have been recognised, designated Htype or L-type based on Western Blot characteristics of the unglycosylated PrP following proteinase-K (PK) digestion (Casalone et al., 2004, Biacabe et al., 2004), both are transmissible to cattle following intracerebral inoculation (Lombardi et al., 2008; Fukuda et al., 2009; Konold et al., 2012; Balkema-Buschmann et al., 2011; Okada et al., 2011).
As discussed in a previous report from an OIE ad hoc Group on BSE (August 2016), epidemiological data from Europe as well as from Brazil, Canada, Israel, Japan and the United States of America (USA) all support the contention that atypical BSE is likely to arise spontaneously in all cattle populations at a very low rate.
Simmons et al. (2017) highlighted the fact that in experimental inoculation models in cattle, the incubation periods of H- and L-BSE were similar to or shorter than those observed with C-BSE (Balkema-Buschmann, Ziegler, et al., 2011; Fukuda et al., 2009; Konold et al., 2012; Lombardi et al., 2008). Based on pooled data for 110 atypical cases for which the age is known from the European Union (EU) and the OIE for countries outside the EU from 2001 to 2019, most cases (>91.7%) have been detected in animals 8 years or older10 (European Commission, 2016; EFSA 2016, 2017, 2018). The youngest case reported to date was almost 67 months old (5.6 years) (World Organisation for Animal Health, 2019).
In recently published research work, Okada and colleagues, 2017, confirmed that the L-type BSE prion can be orally transmitted. Of 16 calves challenged with various amounts of infectious brain material, only 1 animal, which was given a high dose (50 grams), developed clinical signs after a lengthy incubation period of 88 months (7.3 years). The rest of the calves (1 that received the same dose, and 15 that received lower doses) did not show clinical signs and results were negative by Western blot and immunohistochemistry analyses after 51-94 months post inoculation. Although this study is limited, its results suggest a low likelihood of oral transmission of L-BSE agent among calves. Moreover, based on the dose-response curve estimated by Wells et al. (2007), for a comparable amount of infectivity for C-BSE, the corresponding incubation period would be approximately 55 months, indicating that C-BSE would be more infectious.
In contrast, there have not been any substantiated reports of the successful oral transmission of H-BSE in cattle. Initial reports from Dudas et al., 2014 based on RT-QuIC pointed to the possibility of oral transmission following a very high dose (100 grams of brain material), although the individual did not display clinical signs and the findings from standard molecular or immunohistochemical assays were all negative. Investigations are ongoing in an attempt to clarify these findings.
Although significant uncertainty remains regarding the origin of C-BSE, several studies involving the serial passage of H-BSE and L-BSE in transgenic and wild-type mice have revealed their potential to lead to the emergence of a C-BSE-like phenotype (Baron et al., 2011; Torres et al., 2011; Bencsik et al., 2013) or other novel strains (Masujin et al., 2016). Whether or not one or both of these atypical strains led to the emergence of C-BSE remains speculative; however, the similarities between transmissible mink encephalopathy (TME), first reported in the USA in 1947 (Hartsough and Burger, 1965), and L-BSE indicate that TME may have been a surrogate indicator for the presence of L-BSE in cattle populations in those countries such as the USA, Canada, Germany, Finland and Russia where outbreaks of TME had been reported decades before C-BSE was first recognised in the 10 Pulled data from 110 atypical cases: 49 H-BSE, 58 L-BSE and 3 of unknown atypical type. The mean age at diagnosis was 11.6 years (from 5.5 to 18 years). 78.2% were between 10 and 15 years old.
AHG on BSE risk assessment and surveillance/March 2019 Annex 7 (contd) Scientific Commission/September 2019 53
United Kingdom in 1986 (Hadlow and Karstad, 1968; Marsh et al., 1991; McKenzie et al., 1996; Baron et al., 2007; Comoy et al., 2013). Although TME was originally thought to have occurred as a result of feeding mink with scrapie infected sheep carcases, oral challenge studies did not confirm this (Marsh et al., 1991). Importantly, in an outbreak reported in the USA in 1985, mink had never been fed sheep products; instead they had been fed on products derived from dead and sick dairy cattle (March et al., 1991). Similarly, from an outbreak in Canada in 1963, mink had reportedly been fed with products derived from cattle but not sheep (Hadlow and Karstad, 1968).
Although, as discussed above, the passage of H-BSE or L-BSE has been proposed as a possible explanation for the origin of C-BSE, transformation of L-BSE or H-BSE to C-BSE has not been observed so far in transmission studies in cattle. That being said, it is likely that, compared to various rodent models, an insufficient number of passages have been undertaken.
It is worth noting that sheep and goats are susceptible to L-BSE following intracerebral inoculation without lymphoid involvement in most individuals (Simmons et al., 2016; Gielbert et al., 2018; Vallino-Costassa et al., 2018). As discussed by Houston and Andreoletti (2018), C-BSE appears to increase in virulence for humans if it is first passaged in sheep. Whether or not this is the same for atypical strains remains to be determined.
Conclusions on transmissibility of atypical BSE among cattle
Given that cattle have been successfully infected by the oral route, at least for L-BSE, it is reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle are exposed to contaminated feed. In addition, based on reports of atypical BSE from several countries that have not had C-BSE, it appears likely that atypical BSE would arise as a spontaneous disease in any country, albeit at a very low incidence in old cattle. In the presence of livestock industry practices that would allow it to be recycled in the cattle feed chain, it is likely that some level of exposure and transmission may occur. As a result, since atypical BSE can be reasonably considered to pose a potential background level of risk for any country with cattle, the recycling of both classical and atypical strains in the cattle and broader ruminant populations should be avoided.
II. Zoonotic potential
Experimental studies
There are tremendous challenges in demonstrating the zoonotic transmission of atypical strains of BSE in natural exposure scenarios based on experimental studies involving:
• In vivo models including non-human primates (macaques and lemurs) (Comoy et al., 2008; Ono et al., 2011; Mestre-Frances et al., 2012), humanised transgenic mice that either overexpress human PrP or express it at normal physiological levels (Béringue et al., 2007; Béringue et al., 2008; Kong et al., 2008; Wilson et al., 2012)
o artificial routes of challenge such as intracerebral inoculation;
o large doses of infectious material whether administered parenterally or orally.
• In vitro models including PMCA (protein misfolding cyclic amplification) reactions where brain homogenates from humans or transgenic mice containing PrPc are used as a substrate (Barria et al., 2014a; Barria et al., 2014b);
Annex 7 (contd) AHG on BSE risk assessment and surveillance/March 2019
54 Scientific Commission/September 2019
In addition, not all studies are in agreement, for example:
• PMCA results suggest that atypical BSE poses a lower zoonotic risk than C-BSE since neither L-BSE nor HBSE produced detectable human PrPres when brain homogenates from humans or transgenic mice representative of human prion protein genotypes (codon 129 MM and VV) were used as substrates. In contrast, both C-BSE and variant Creutzfeldt-Jacob disease (vCJD) successfully converted human PrPc to PrPres in a codon 129 (M allele) dependent manner (Barria et al., 2014a; Barria et al., 2014b).
• Using humanized transgenic mice (tg650) overexpressing human PrP, H-BSE failed to transmit indicating the existence of a robust transmission barrier whereas the potential zoonotic risk from L-BSE appeared to be higher than C-BSE with attack rates on first passage of 100% and 30%, respectively. An attack rate of 100% for C-BSE was only achieved on third passage (Béringue et al., 2008).
• Initial findings using transgenic mice expressing physiological levels of the human PrP representative of the three genotypes correlating with human susceptibility to TSEs (codon 129 MM, MV, VV) were suggestive of a significant transmission barrier between both L-BSE and H-BSE and humans (Wilson et al., 2012). However, on subsequent passage into bovinized transgenic mice (Bov6), some of the mice originally challenged with LBSE were found to harbour low levels of infectivity in their brains (Wilson et al., 2013). Interestingly, in an earlier study, C-BSE was not transmitted to the same lines of humanized transgenic mice (Bishop et al., 2006), whereas vCJD was successfully transmitted to all three lines. This is likely to be indicative of a significant cattle to human barrier for C-BSE, but a substantially reduced barrier for human-to-human transmission once that barrier is overcome. It is worth noting that an important limitation of these studies is the lifespan of mice that is much shorter than the incubation period of humans having only a single copy of the allele.
• Studies involving the intracerebral challenge of non-human primates (cynomolgus macaques) indicate that LBSE is more virulent than C-BSE with shorter incubation periods (~20 months vs 38 months) (Comoy et al., 2008; Ono et al., 2011). While a similarly short incubation period was observed in mouse lemurs challenged through the oral route with L-BSE (Mestre-Frances et al., 2012), transmission of C-BSE was only observed after initially being passaged in macaques (Bons et al., 2002). This finding would also support the contention that L-BSE is more virulent than C-BSE. L-BSE has reportedly been transmitted to macaques by the oral route although a direct comparison with C-BSE does not appear to have been made (Comoy 2010; BIOHAZ, 2011). The results of this work have yet to be formally published (Comoy E, pers comm, 2019).
Tissue distribution of atypical BSE in cattle
The uncertainty associated with the actual route of acquiring the disease, if any, limits the implementation of appropriate studies investigating the pathogenesis of atypical BSE and the accumulation, progression and detection of PrPSc and infectivity in different tissues. Nevertheless, a limited number of studies have been undertaken (Appendix A of EFSA, 2014). PrPres has been detected in the peripheral nervous system (PNS) of cattle intracerebrally inoculated with L-BSE (Iwamaru et al., 2010) and H-BSE (Okada et al., 2013) as calves. As with C-BSE, PrPres from animals challenged with L-BSE was found to accumulate in both central and peripheral nerve tissues in a time-dependent manner suggesting that propagation was initially in the central nervous system (CNS) followed by spread into the PNS (Iwamaru et al., 2010). The levels of infectivity in the PNS were approximately 1,000 times lower than those in the CNS. PrPres was not detected in lymphoid tissues. Infectivity was detected in the skeletal muscle from a 14-year-old natural case of L-BSE as well as from an experimentally infected cow that had been inoculated intracerebrally as a calf (Suardi et al., 2012). In this study, infectivity was not found in the spleen, cervical lymph nodes or kidneys of either the natural or experimentally infected cows.
Potential link between atypical BSE and sporadic Creutzfeldt-Jacob disease (sCJD)
It has been reported that the biochemical signature of L-BSE in an intracerebrally inoculated macaque was similar to that of the MM2 cortical subtype of human sCJD (Comoy et al., 2013) raising the possibility that if L-BSE crossed the species barrier into humans it could present as sCJD. In a study involving humanized transgenic mice, Kong et al., 2008, also reported that similarities between L-BSE and sCJD where the electrophoretic pattern of L-BSE and that of Type 2 PrPres from sCJD patients were indistinguishable. The possibility that the two diseases are causally linked was subsequently investigated by Jaumain et al., 2016, who compared the phenotypic traits of
AHG on BSE risk assessment and surveillance/March 2019 Annex 7 (contd)
Scientific Commission/September 2019 55
L-BSE isolates with those from representative human sCJD cases. Although evidence of an aetiological link was not found, they nevertheless cautioned that an unrecognised form of CJD may emerge from the accidental transfer of L-BSE to humans.
Conclusions on the zoonotic potential of atypical BSE
Given the findings to date, the associated uncertainties and challenges in drawing inferences from studies involving surrogate models such as non-human primates, transgenic mice and molecular techniques, some tentative conclusions can nevertheless be drawn that inform potential zoonotic risks:
• While L-BSE poses a potentially greater zoonotic risk than C-BSE, the risk associated with H-BSE is likely to be less.
• Consistent with C-BSE, both H and L-BSE are likely to be essentially restricted to the CNS with involvement of the PNS at substantially lower levels arising later in the disease process.
• It is highly unlikely that lymphoid and other tissues outside the CNS and PNS are involved in the pathogenesis of H and L-BSE.
• It would be reasonable to assume based on the limited evidence available to date that the distribution of atypical BSE is similar to C-BSE with the exception of the distal ileum and tonsils.
• Potential human exposure to atypical BSE would be by the oral route that is unlikely to be repeated at an individual level considering that atypical BSE is a rare disease that is likely to arise spontaneously in old cattle.
• If atypical BSE were to break the species barrier, a form of CJD may emerge with the potential for a substantially reduced barrier for subsequent human-to-human transmission.
• Although the likelihood of human exposure to atypical BSE with the species barrier being breached may be considered to be extremely low, the consequences as experienced with C-BSE would be high if exposure results in infection.
At this stage it would be premature to reach a conclusion other than that atypical BSE poses a potential zoonotic risk that although may be different between atypical strains, nevertheless justifies a consideration of measures to prevent recycling in the cattle population to protect both the human food supply and the ruminant feed chain.
Annex 2
MEETING OF THE OIE SCIENTIFIC COMMISSION FOR ANIMAL DISEASES
Paris, 9–13 September 2019
_______
List of Participants
MEMBERS
Dr Cristóbal Zepeda (President)
APHIS Attaché, Brazil
7500 Brasilia Place
Dulles, VA 20189-7500
UNITED STATES OF AMERICA
Tel: +55 61 3312 7725
Cristobal.zepeda@usda.gov
Dr Kris De Clercq (Vice-President)
Centre d’Etudes et de Recherches
Vétérinaires et Agrochimiques
Department of Virology
Section Epizootic Diseases
CODA-CERVA-VAR
Groeselenberg 99
B-1180 Ukkel
BELGIUM
Tel.: +32 2 379 0400
kris.declercq@sciensano.be
Dr Baptiste Dungu (2nd VicePresident)
CEO – Onderstepoort Biological
Products
SOUTH AFRICA
Tel.: +27 12 522 1607
Baty@obpvaccines.co.za
Dr Silvia Bellini (Member)
Istituto Zooprofilattico Sperimentale
della Lombardia e dell’Emilia
Romagna ‘Bruno Ubertini’
Via Bianchi 9
25124 Brescia
ITALY
Tel: +39 366 588 8774
Silvia.bellini@izsler.it
Dr Misheck Mulumba (Member)
Agricultural Research Council
Private Bag X05
Onderstepoort 01110
Pretoria
SOUTH AFRICA
Tel: +27 12 529 9338
mumulbam@arc.agric.za
Dr Zengren Zheng (Member)
Chief Scientist & Deputy
Director of China Animal Health
and Epidemiology Center (CAHEC)
No. 369 Nan Jing Road
Qingdao
PEOPLE’S REPUBLIC OF CHINA
Zhengzr62@126.com
OIE HEADQUARTERS
Dr Gregorio Torres
Head of Science Department
g.torres@oie.int
Dr Stefano Messori
Chargé de mission
Science Department
s.messori@oie.int
Dr Jee Yong Park
Chargé de mission
Science Department
j.y.park@oie.int
Dr Neo Mapitse
Head of Status Department
n.mapitse@oie.int
Dr Min Kyung Park
Deputy Head of Status Department
m.park@oie.int
Dr Anna-Maria Baka
Chargée de mission
Status Department
am.baka@oie.int
REFERENCES
SNIP...END SEE FULL TEXT;
PLEASE SEE MY correspondence with OIE over the decades (at the bottom of this report see that history) about the BSE GBR vs MRR and CWD zoonosis and reporting on CWD for the past 2 plus decades, and still nothing about CWD TSE Prion in the above report, so sad...tss
sporadic creutzfeldt jakob disease sCJD as a zoonotic, zoonosis disease, what if?
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
PLEASE NOTE;
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).
In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.
https://www.nature.com/articles/srep11573
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160
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.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
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
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
FRIDAY, OCTOBER 23, 2020
Scrapie TSE Prion Zoonosis Zoonotic, what if?
MONDAY, DECEMBER 16, 2019
Chronic Wasting Disease CWD TSE Prion aka mad cow type disease in cervid Zoonosis Update
***> ''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***
10. ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD DEER ELK DISEASE IN HUMANS, has it already happened, that should be the question...
''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II)
EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ... See all authors
First published: 17 January 2018 https://doi.org/10.2903/j.efsa.2018.5132 ;
also, see;
8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data.
***> In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison.
The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers.. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.
snip...
The tissue distribution of infectivity in CWD‐infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure.
CJD FOUNDATION VIRTUAL CONFERENCE CJD Foundation Research Grant Recipient Reports Panel 2 Nov 3, 2020
zoonotic potential of PMCA-adapted CWD PrP 96SS inoculum
4 different CWD strains, and these 4 strains have different potential to induce any folding of the human prion protein.
***> PIGS, WILD BOAR, CWD <***
***> POPULATIONS OF WILD BOARS IN THE UNITED STATES INCREASING SUPSTANTUALLY AND IN MANY AREAS WE CAN SEE A HIGH DENSITY OF WILD BOARS AND HIGH INCIDENT OF CHRONIC WASTING DISEASE
HYPOTHOSIS AND SPECIFIC AIMS
HYPOTHOSIS
BSE, SCRAPIE, AND CWD, EXPOSED DOMESTIC PIGS ACCUMULATE DIFFERENT QUANTITIES AND STRAINS OF PRIONS IN PERIPHERAL TISSUES, EACH ONE OF THEM WITH PARTICULAR ZOONOTIC POTENTIALS
Final Report – CJD Foundation Grant Program A.
Project Title: Systematic evaluation of the zoonotic potential of different CWD isolates. Principal Investigator: Rodrigo Morales, PhD.
Systematic evaluation of the zoonotic potential of different CWD isolates. Rodrigo Morales, PhD Assistant Professor Protein Misfolding Disorders lab Mitchell Center for Alzheimer’s disease and Related Brain Disorders Department of Neurology University of Texas Health Science Center at Houston Washington DC. July 14th, 2018
Conclusions and Future Directions • We have developed a highly sensitive and specific CWD-PMCA platform to be used as a diagnostic tool. • Current PMCA set up allow us to mimic relevant prion inter-species transmission events. • Polymorphic changes at position 96 of the prion protein apparently alter strain properties and, consequently, the zoonotic potential of CWD isolates. • Inter-species and inter-polymorphic PrPC → PrPSc conversions further increase the spectrum of CWD isolates possibly present in nature. • CWD prions generated in 96SS PrPC substrate apparently have greater inter-species transmission potentials. • Future experiments will explore the zoonotic potential of CWD prions along different adaptation scenarios, including inter-species and inter-polymorphic.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Author item MOORE, SARAH - Orise Fellow item Kunkle, Robert item KONDRU, NAVEEN - Iowa State University item MANNE, SIREESHA - Iowa State University item SMITH, JODI - Iowa State University item KANTHASAMY, ANUMANTHA - Iowa State University item WEST GREENLEE, M - Iowa State University item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:
Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.
Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 month challenge groups). The remaining pigs (>6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.
Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP
Author item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018 Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44.
Interpretive Summary:
Technical Abstract: We have previously shown that the chronic wasting disease (CWD) agent from white-tailed deer can be transmitted to domestic pigs via intracranial or oral inoculation although with low attack rates and restricted PrPSc accumulation. The objective of this study was to assess the potential for cross-species transmission of pig-passaged CWD using bioassay in transgenic mice. Transgenic mice expressing human (Tg40), bovine (TgBovXV) or porcine (Tg002) PRNP were inoculated intracranially with 1% brain homogenate from a pig that had been intracranially inoculated with a pool of CWD from white-tailed deer. This pig developed neurological clinical signs, was euthanized at 64 months post-inoculation, and PrPSc was detected in the brain. Mice were monitored daily for clinical signs of disease until the end of the study. Mice were considered positive if PrPSc was detected in the brain using an enzyme immunoassay (EIA). In transgenic mice expressing porcine prion protein the average incubation period was 167 days post-inoculation (dpi) and 3/27 mice were EIA positive (attack rate = 11%). All 3 mice were found dead and clinical signs were not noted prior to death. One transgenic mouse expressing bovine prion protein was euthanized due to excessive scratching at 617 dpi and 2 mice culled at the end of the study at 700 dpi were EIA positive resulting in an overall attack rate of 3/16 (19%). None of the transgenic mice expressing human prion protein that died or were euthanized up to 769 dpi were EIA positive and at study end point at 800 dpi 2 mice had positive EIA results (overall attack rate = 2/20 = 10%). The EIA optical density (OD) readings for all positive mice were at the lower end of the reference range (positive mice range, OD = 0.266-0.438; test positive reference range, OD = 0.250-4.000). To the authors’ knowledge, cervid-derived CWD isolates have not been successfully transmitted to transgenic mice expressing human prion protein. The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.
cwd scrapie pigs oral routes
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation
S. Jo Moore1,2, M. Heather West Greenlee3, Naveen Kondru3, Sireesha Manne3, Jodi D. Smith1, Robert A. Kunkle1, Anumantha Kanthasamy3 and Justin J. Greenlee1* + Author Affiliations
1Virus and Prion Research Unit, National Animal Disease Center, USDA, Agricultural Research Service, Ames, Iowa, United States of America 2Oak Ridge Institute for Science and Education, Oak Ridge, Tennessee, United States of America 3Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, Iowa, United States of America
ABSTRACT
Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of chronic wasting disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Crossbred piglets were assigned to one of three groups: intracranially inoculated (n=20), orally inoculated (n=19), or non-inoculated (n=9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled (‘market weight’ groups). The remaining pigs (‘aged’ groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by western blotting (WB), antigen-capture immunoassay (EIA), immunohistochemistry (IHC) and in vitro real-time quaking induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC and/or WB. Using RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from one or more pigs in each inoculated group. Bioassay was positive in 4 out of 5 pigs assayed. This study demonstrates that pigs can support low-level amplification of CWD prions, although the species barrier to CWD infection is relatively high. However, detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.
IMPORTANCE We challenged domestic swine with the chronic wasting disease agent by inoculation directly into the brain (intracranially) or by oral gavage (orally). Disease-associated prion protein (PrPSc) was detected in brain and lymphoid tissues from intracranially and orally inoculated pigs as early as 8 months of age (6 months post-inoculation). Only one pig developed clinical neurologic signs suggestive of prion disease. The amount of PrPSc in the brains and lymphoid tissues of positive pigs was small, especially in orally inoculated pigs. Regardless, positive results in orally inoculated pigs suggest that it may be possible for swine to serve as a reservoir for prion disease under natural conditions.
FOOTNOTES
↵*Corresponding author: Email: justin.greenlee@ars.usda.gov This is a work of the U.S. Government and is not subject to copyright protection in the United States. Foreign copyrights may apply.
----Original Message-----
From: Terry Singeltary
To: Tracy.A.Nichols
Sent: Fri, Mar 30, 2018 12:51 pm
Subject: Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018
Greetings APHIS, USDA, Dr. Tracy Nichols, et al,
I wish to kindly submit my comments on the Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards please. i have submitted online and sent a hard copy to Dr. Nichols via email. i know that my concern may not be the same concern as others, but ramifications from cwd tse prion can be long lasting, and science is still emerging. however, the science today warrants immediate and further actions be taken. my comments, with reference materials, are as follows, and will be formatted in such a way, i will address issues by numbers 1-10, and under each one of my comments by each number, i will reference my comments with science to back up what i am stating/asking...thank you kindly, terry
snip...see full text;
WEDNESDAY, NOVEMBER 4, 2020
CWD TSE PRION, SCRAPIE, BSE, AND PORCINE, PIGS, WILD BOAR, ZOONOTIC ZOONOSIS RISK FACTORS AND POTENTIALS
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. snip... The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip.....
In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
snip.....
36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip.....
In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip..... In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.
snip.....
Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.
snip.....
***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are;
BSE TESTING (failed terribly and proven to be a sham)
BSE SURVEILLANCE (failed terribly and proven to be a sham)
BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham)
these are facts folks. trump et al just admitted it with the feed ban.
see;
FDA Reports on VFD Compliance
John Maday
August 30, 2019 09:46 AM VFD-Form 007 (640x427)
Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.
SUNDAY, SEPTEMBER 1, 2019
***> FDA Reports on VFD Compliance
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
TUESDAY, NOVEMBER 17, 2020
The European Union summary report on surveillance for the presence of transmissible spongiform encephalopathies (TSE) in 2019 First published 17 November 2020
WEDNESDAY, OCTOBER 28, 2020
EFSA Annual report of the Scientific Network on BSE-TSE 2020 Singeltary Submission
WEDNESDAY, JULY 31, 2019
The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L
THURSDAY, SEPTEMBER 24, 2020
The emergence of classical BSE from atypical/ Nor98 scrapie
THURSDAY, AUGUST 20, 2020
Why is USDA "only" BSE TSE Prion testing 25,000 samples a year?
MONDAY, NOVEMBER 23, 2020
Transmissible Spongiform Encephalopathy TSE Prion Cervid Global Report November 2020
MONDAY, MAY 20, 2019
Tracking and clarifying differential traits of classical- and atypical L-type bovine spongiform encephalopathy prions after transmission from cattle to cynomolgus monkeys
SUNDAY, APRIL 14, 2019
Estimation of prion infectivity in tissues of cattle infected with atypical BSE by real time-quaking induced conversion assay
WEDNESDAY, APRIL 24, 2019
USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019
WEDNESDAY, JULY 31, 2019
The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L
WEDNESDAY, MAY 29, 2019
Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures USDA HERE'S YOUR SIGN!
WEDNESDAY, OCTOBER 28, 2020
EFSA Annual report of the Scientific Network on BSE-TSE 2020 Singeltary Submission
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).
In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.
SUNDAY, OCTOBER 11, 2020
Bovine adapted transmissible mink encephalopathy is similar to L-BSE after passage through sheep with the VRQ/VRQ genotype but not VRQ/ARQ
SUNDAY, OCTOBER 4, 2020
Cattle Meat and Offal Imported from the United States of America, Canada and Ireland to Japan (Prions) Food Safety Commission of Japan
TUESDAY, SEPTEMBER 29, 2020
ISO's Updated 22442 Animal Tissue Standards — What Changed? TSE Prion!
''Why is USDA "only" testing 25,000 samples a year?
USDA's surveillance strategy is to focus on the targeted populations where we are most likely to find disease if it is present. This is the most effective way to meet both OIE and our domestic surveillance standards. After completing our enhanced surveillance in 2006 and confirming that our BSE prevalence was very low, an evaluation of the program showed that reducing the number of samples collected to 40,000 samples per year from these targeted, high risk populations would allow us to continue to exceed these standards. In fact, the sampling was ten times greater than OIE standards. A subsequent evaluation of the program in 2016 using data collected over the past 10 years showed that the surveillance standards could still be met with a further reduction in the number of samples collected by renderers and 3D/4D establishments which have a very low OIE point value because the medical history of these animals is usually unknown. Therefore, in 2016, the number of samples to be tested was reduced to 25,000 where it remains today.''
Introduction
USDA conducts surveillance for Bovine spongiform encephalopathy (BSE), referred to as "mad cow disease", in cattle to determine if, and at what level, the disease is present in the U.S. cattle population. Our surveillance program allows us to assess any change in the BSE disease status of U.S. cattle, and identify any rise in BSE prevalence in this country. Identifying any changes in the prevalence of disease allows us to match our preventive measures - feed ban for animal health, and specified risk material removal for public health - to the level of disease in U.S. cattle.
It is the longstanding system of interlocking safeguards, including the removal of specified risk materials - or the parts of an animal that would contain BSE - at slaughter and the FDA's ruminant-to-ruminant feed ban that protect public and animal health from BSE.
It is the longstanding system of interlocking safeguards, including the removal of specified risk materials - or the parts of an animal that would contain BSE - at slaughter and the FDA's ruminant-to-ruminant feed ban that protect public and animal health from BSE.
Why did USDA decrease the number of samples per year in 2006?
After the first confirmation of BSE in an animal in Washington State in December 2003, USDA evaluated its BSE surveillance efforts in light of that finding. We determined that we needed to immediately conduct a major surveillance effort to help determine the prevalence of BSE in the United States. Our goal over a 12-18 month period was to obtain as many samples as possible from the segments of the cattle population where we were most likely to find BSE if it was present. This population of cattle was exhibiting some signs of disease. We conducted this enhanced surveillance effort from June 2004 - August 2006. In that time, we collected a total of 787,711 samples and estimated the prevalence of BSE in the United States to be between 4-7 infected animals in a population of 42 million adult cattle. We consequently modified our surveillance efforts based on this prevalence estimate to a level we can monitor for any potential changes, should they occur. Our statistical analysis indicated that collecting approximately 40,000 samples per year from the targeted cattle population would enable us to conduct this monitoring.
Why is USDA "only" testing 25,000 samples a year?
USDA's surveillance strategy is to focus on the targeted populations where we are most likely to find disease if it is present. This is the most effective way to meet both OIE and our domestic surveillance standards. After completing our enhanced surveillance in 2006 and confirming that our BSE prevalence was very low, an evaluation of the program showed that reducing the number of samples collected to 40,000 samples per year from these targeted, high risk populations would allow us to continue to exceed these standards. In fact, the sampling was ten times greater than OIE standards. A subsequent evaluation of the program in 2016 using data collected over the past 10 years showed that the surveillance standards could still be met with a further reduction in the number of samples collected by renderers and 3D/4D establishments which have a very low OIE point value because the medical history of these animals is usually unknown. Therefore, in 2016, the number of samples to be tested was reduced to 25,000 where it remains today.
How can USDA find every case of BSE in the United States when you are only testing 25,000 animals?
The goal of our BSE surveillance program, even under the enhanced program, has never been to detect every case of BSE. Our goal is determine whether the disease exists at very low levels in the U.S. cattle population, and we do this by testing those animals most likely to have BSE. It is the longstanding system of interlocking safeguards, including the removal of specified risk materials - or the parts of an animal that would contain BSE - at slaughter and the FDA's ruminant-to- ruminant feed ban that protect public and animal health from BSE.
Why didn’t USDA continue to test animals at the enhanced surveillance level?
USDA's 2004-2006 enhanced surveillance program was initiated in response to the first detection of BSE in the United States and was designed to detect the overall prevalence of the disease in this country. This required a very intensive effort and it allowed us to estimate extremely low prevalence levels of disease. Once that prevalence level was determined, USDA modified its testing levels to monitor any changes in the level of disease. Our current testing of approximately 25,000 targeted animals a year allows USDA to detect BSE at the very low level of less than 1 case per million adult cattle, assess any change in the BSE status of U.S. cattle, and identify any rise in BSE prevalence in this country.
Is USDA's surveillance program a food safety or public health measure?
The primary, and most effective, food safety or public health measure is the removal of specified risk materials (SRMs) - or the parts of an animal that would contain BSE - from every animal at slaughter. USDA's BSE surveillance program is not a food safety measure; it is an animal health monitoring measure. However, it does support existing public health and food safety measures. By allowing us to monitor the level of disease in the US cattle population, we can help determine the appropriate level of public health and animal health measures required, and whether they should be increased or decreased.
Why doesn't USDA test every animal at slaughter?
There is currently no test to detect the disease in a live animal. BSE is confirmed by taking samples from the brain of an animal and testing to see if the infectious agent - the abnormal form of the prion protein - is present. The earliest point at which current tests can accurately detect BSE is 2 to 3 months before the animal begins to show symptoms, and the time between initial infection and the appearance of symptoms is about 5 years. Therefore, there is a long period of time during which current tests would not be able to detect the disease in an infected animal.
Since most cattle are slaughtered in the United States at a young age, they are in that period where tests would not be able to detect the disease if present. Testing all slaughter cattle for BSE could produce an exceedingly high rate of false negative test results and offer misleading assurances of the presence or absence of disease.
Simply put, the most effective way to detect BSE is not to test all animals, which could lead to false security, but to test those animals most likely to have the disease, which is the basis of USDA's current program.
Since most cattle are slaughtered in the United States at a young age, they are in that period where tests would not be able to detect the disease if present. Testing all slaughter cattle for BSE could produce an exceedingly high rate of false negative test results and offer misleading assurances of the presence or absence of disease.
Simply put, the most effective way to detect BSE is not to test all animals, which could lead to false security, but to test those animals most likely to have the disease, which is the basis of USDA's current program.
What animals are USDA testing in the surveillance program? These are random samples at slaughter, aren't they?
No. USDA's BSE surveillance program is specifically targeted to the population most likely to have the disease, if it is present. This population is NOT clinically healthy animals that would be presented for slaughter. Rather, it includes animals that have some type of abnormality, such as central nervous system signs; non-ambulatory, or a "downer"; emaciated; or died for unknown reasons. Because these animals would not pass the required ante-mortem inspection requirements at slaughter for human consumption, we collect the majority of our samples at facilities other than slaughter facilities - at rendering or salvage facilities, on-farm, at veterinary clinics or veterinary diagnostic laboratories. With this targeted approach, we can monitor the presence of disease in the US cattle population in a much more efficient and meaningful way. The key to surveillance is to look where the disease is going to occur.
Key Points: BSE Ongoing Surveillance Plan
Note: This Fact Sheet is based on the USDA Animal and Plant Health Inspection Service (APHIS) Bovine Spongiform Encephalopathy (BSE) Ongoing Surveillance Plan, July 20, 2006. To learn more, read the complete BSE Ongoing Surveillance Plan (PDF, 187 KB).
KEY POINTS
In addition to a stringent feed ban imposed by the Food and Drug Administration in 1997 as well as the removal of all specified risk material which could harbor BSE, USDA has a strong surveillance program in place to detect signs of BSE in cattle in the United States. In fact, we test for BSE at levels greater than World Animal Health Organization standards. The program samples approximately 25,000 animals each year and targets cattle populations where the disease is most likely to be found. The targeted population for ongoing surveillance focuses on cattle exhibiting signs of central nervous disorders or any other signs that may be associated with BSE, including emaciation or injury, and dead cattle, as well as non-ambulatory animals. Samples from the targeted population are taken at farms, veterinary diagnostic laboratories, public health laboratories, slaughter facilities, veterinary clinics, and livestock markets.
USDA's National Veterinary Services Laboratories (NVSL) in Ames, IA, along with contracted veterinary diagnostic laboratories, use rapid screening tests as the initial screening method on all samples. Any inconclusive samples undergo further testing and analysis at NVSL.
NOT A FOOD SAFETY TEST
BSE tests are not conducted on cuts of meat, but involve taking samples from the brain of a dead animal to see if the infectious agent is present. We know that the earliest point at which current tests can accurately detect BSE is 2-to-3 months before the animal begins to show symptoms. The time between initial infection and the appearance of symptoms is about 5 years. Since most cattle that go to slaughter in the United States are both young and clinically normal, testing all slaughter cattle for BSE might offer misleading assurances of safety to the public.
The BSE surveillance program is not for the purposes of determining food safety. Rather, it is an animal health surveillance program. USDA's BSE surveillance program allows USDA to detect the disease if it exists at very low levels in the U.S. cattle population and provides assurances to consumers and our international trading partners that the interlocking system of safeguards in place to prevent BSE are working..
The safety of the U.S. food supply from BSE is assured by the removal of specified risk materials - those tissues known to be infective in an affected animal - from all human food. These requirements have been in place since 2004.
The BSE surveillance program is not for the purposes of determining food safety. Rather, it is an animal health surveillance program. USDA's BSE surveillance program allows USDA to detect the disease if it exists at very low levels in the U.S. cattle population and provides assurances to consumers and our international trading partners that the interlocking system of safeguards in place to prevent BSE are working..
The safety of the U.S. food supply from BSE is assured by the removal of specified risk materials - those tissues known to be infective in an affected animal - from all human food. These requirements have been in place since 2004.
ONGOING BSE SURVEILLANCE PROGRAM SUMMARY
USDA's BSE surveillance program samples approximately 25,000 animals each year and targets cattle populations where the disease is most likely to be found. The statistically valid surveillance level of 25,000 is consistent with science-based internationally accepted standards. This level allows USDA to detect BSE at the very low level of less than 1 case per million adult cattle, assess any change in the BSE status of U.S. cattle, and identify any rise in BSE prevalence in this country.
The targeted population for ongoing surveillance focuses on cattle exhibiting signs of central nervous disorders or any other signs that may be associated with BSE, including emaciation or injury, and dead cattle, as well as nonambulatory animals. Samples from the targeted population are taken at farms, veterinary diagnostic laboratories, public health laboratories, slaughter facilities, veterinary clinics, and livestock markets.
USDA's National Veterinary Services Laboratories (NVSL) in Ames, IA, along with contracted veterinary diagnostic laboratories, will continue to use rapid screening tests as the initial screening method on all samples. Any inconclusive samples will be sent to NVSL for further testing and analysis. USDA's surveillance program uses OIE's weighted surveillance points system, which was adopted in May 2005 and reflects international scientific consensus that the best BSE surveillance programs focus on obtaining quality samples from targeted subpopulations rather than looking at the entire adult cattle population.
The number of points a sample receives correlates directly to an animal's clinical presentation at the time of sampling. The highest point values are assigned to those samples from animals with classic clinical signs of the disease. The lowest point values correspond to clinically normal animals tested at routine slaughter.
The goal of this weighted approach is to ensure that countries sample those cattle populations where the disease is most likely to be found. This system is not different from USDA's previous BSE surveillance approach, it is simply a different method for evaluating surveillance programs. Both approaches target those cattle populations where BSE is most likely to be found. The OIE is simply assigning point values to different categories of animals.
USDA has been targeting these subpopulations since BSE surveillance was initiated in 1990, and will continue to do so under the OIE weighted approach. Under the OIE guidelines, points compiled over a period of 7 consecutive years are used as evidence of adequate surveillance. At the current ongoing level of surveillance, the United States will far exceed OIE guidelines under the point system.
The targeted population for ongoing surveillance focuses on cattle exhibiting signs of central nervous disorders or any other signs that may be associated with BSE, including emaciation or injury, and dead cattle, as well as nonambulatory animals. Samples from the targeted population are taken at farms, veterinary diagnostic laboratories, public health laboratories, slaughter facilities, veterinary clinics, and livestock markets.
USDA's National Veterinary Services Laboratories (NVSL) in Ames, IA, along with contracted veterinary diagnostic laboratories, will continue to use rapid screening tests as the initial screening method on all samples. Any inconclusive samples will be sent to NVSL for further testing and analysis. USDA's surveillance program uses OIE's weighted surveillance points system, which was adopted in May 2005 and reflects international scientific consensus that the best BSE surveillance programs focus on obtaining quality samples from targeted subpopulations rather than looking at the entire adult cattle population.
The number of points a sample receives correlates directly to an animal's clinical presentation at the time of sampling. The highest point values are assigned to those samples from animals with classic clinical signs of the disease. The lowest point values correspond to clinically normal animals tested at routine slaughter.
The goal of this weighted approach is to ensure that countries sample those cattle populations where the disease is most likely to be found. This system is not different from USDA's previous BSE surveillance approach, it is simply a different method for evaluating surveillance programs. Both approaches target those cattle populations where BSE is most likely to be found. The OIE is simply assigning point values to different categories of animals.
USDA has been targeting these subpopulations since BSE surveillance was initiated in 1990, and will continue to do so under the OIE weighted approach. Under the OIE guidelines, points compiled over a period of 7 consecutive years are used as evidence of adequate surveillance. At the current ongoing level of surveillance, the United States will far exceed OIE guidelines under the point system.
Current Monthly Test Results
APHIS reports ongoing surveillance test totals monthly.
Collection Month | FY2020 | Number of Valid Samples | OIE Points |
|---|---|---|---|
| October | 2019 | 1,152 | 23,238 |
| November | 2019 | 1,569 | 36,255 |
| December | 2019 | 1,531 | 19,100 |
| January | 2020 | 2,340 | 29,204 |
| February | 2020 | 3,293 | 47,333 |
| March | 2020 | 3,115 | 27,953 |
| April | 2020 | 2,194 | 13,334 |
| May | 2020 | 1,660 | 21,163 |
| June | 2020 | 1,294 | 25,063 |
| July | 2020 | 128 | 5,966 |
Total as of July 1, 2020 | 18,276 | 248,609 | |
Beginning in Fiscal Year 2016, the BSE ongoing surveillance program will sample approximately 25,000 animals each year. Under the program, USDA will continue to collect samples from a variety of sites and from the cattle populations where the disease is most likely to be detected.
***> P.108: Successful oral challenge of adult cattle with classical BSE
Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge; Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology Laboratory; Truro, Nova Scotia, Canada
Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and food-borne fatal neurological disease which can be orally transmitted to cattle and humans. Due to the presence of contaminated milk replacer, it is generally assumed that cattle become infected early in life as calves and then succumb to disease as adults. Here we challenged three 14 months old cattle per-orally with 100 grams of C-type BSE brain to investigate age-related susceptibility or resistance. During incubation, the animals were sampled monthly for blood and feces and subjected to standardized testing to identify changes related to neurological disease. At 53 months post exposure, progressive signs of central nervous system disease were observed in these 3 animals, and they were euthanized. Two of the C-BSE animals tested strongly positive using standard BSE rapid tests, however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.. Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.
***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE.
We are further examining explanations for the unusual disease presentation in the third challenged animal.
P98 The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
Greenlee JJ (1), Moore SJ (1), and West Greenlee MH (2) (1) United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Virus and Prion Research Unit, Ames, IA, United States (2) Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, United States.
In 2006, a case of H-type bovine spongiform encephalopathy (BSE) was reported in a cow with a previously unreported prion protein polymorphism (E211K).
The E211K polymorphism is heritable and homologous to the E200K mutation in humans that is the most frequent PRNP mutation associated with familial Creutzfeldt-Jakob disease.
Although the prevalence of the E211K polymorphism is low, cattle carrying the K211 allele develop H-type BSE with a rapid onset after experimental inoculation by the intracranial route.
The purpose of this study was to investigate whether the agents of H-type BSE or H-type BSE associated with the E211K polymorphism transmit to wild type cattle or cattle with the K211 allele after oronasal exposure.
Wild type (EE211) or heterozygous (EK211) cattle were oronasally inoculated with either H-type BSE from the 2004 US Htype BSE case (n=3) or from the 2006 US H-type case associated with the E211K polymorphism (n=4) using 10% w/v brain homogenates.
Cattle were observed daily throughout the course of the experiment for the development of clinical signs.
At approximately 50 months post-inoculation, one steer (EK211 inoculated with E211K associated H-BSE) developed clinical signs including inattentiveness, loss of body condition, weakness, ataxia, and muscle fasciculations and was euthanized.
Enzyme immunoassay confirmed that abundant misfolded protein was present in the brainstem, and immunohistochemistry demonstrated PrPSc throughout the brain.
Western blot analysis of brain tissue from the clinically affected steer was consistent with the E211K H-type BSE inoculum.
With the experiment currently at 55 months post-inoculation, no other cattle in this study have developed clinical signs suggestive of prion disease. This study demonstrates that the H-type BSE agent is transmissible by the oronasal route.
These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
WEDNESDAY, AUGUST 15, 2018
***> The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
MONDAY, JANUARY 09, 2017
Oral Transmission of L-Type Bovine Spongiform Encephalopathy Agent among Cattle
CDC Volume 23, Number 2—February 2017
*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
Detection of PrPBSE and prion infectivity in the ileal Peyer’s patch of young calves as early as 2 months after oral challenge with classical bovine spongiform encephalopathy
Ivett Ackermann1 , Anne Balkema‑Buschmann1 , Reiner Ulrich2 , Kerstin Tauscher2 , James C. Shawulu1 , Markus Keller1 , Olanrewaju I. Fatola1 , Paul Brown3 and Martin H. Groschup1*
Abstract
In classical bovine spongiform encephalopathy (C-BSE), an orally acquired prion disease of cattle, the ileal Peyer’s patch (IPP) represents the main entry port for the BSE agent. In earlier C-BSE pathogenesis studies, cattle at 4–6 months of age were orally challenged, while there are strong indications that the risk of infection is highest in young animals. In the present study, unweaned calves aged 4–6 weeks were orally challenged to determine the earli‑ est time point at which newly formed PrPBSE and BSE infectivity are detectable in the IPP. For this purpose, calves were culled 1 week as well as 2, 4, 6 and 8 months post-infection (mpi) and IPPs were examined for BSE infectivity using a bovine PrP transgenic mouse bioassay, and for PrPBSE by immunohistochemistry (IHC) and protein misfolding cyclic amplifcation (PMCA) assays. For the frst time, BSE prions were detected in the IPP as early as 2 mpi by transgenic mouse bioassay and PMCA and 4 mpi by IHC in the follicular dendritic cells (FDCs) of the IPP follicles. These data indi‑ cate that BSE prions propagate in the IPP of unweaned calves within 2 months of oral uptake of the agent.
In summary, our study demonstrates for the frst time PrPBSE (by PMCA) and prion infectivity (by mouse bioassay) in the ileal Peyer’s patch (IPP) of young calves as early as 2 months after infection. From 4 mpi nearly all calves showed PrPBSE positive IPP follicles (by IHC), even with PrPBSE accumulation detectable in FDCs in some animals. Finally, our results confrm the IPP as the early port of entry for the BSE agent and a site of initial propagation of PrPBSE and infectivity during the early pathogenesis of the disease. Terefore, our study supports the recommendation to remove the last four metres of the small intestine (distal ileum) at slaughter, as designated by current legal requirements for countries with a controlled BSE risk status, as an essential measure for consumer and public health protection.
PLOS ONE Journal
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT
***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.
***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.
*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***
http://www.plosone.org/annotation/listThread.action?root=86610
***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.
*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***
http://www.plosone.org/annotation/listThread.action?root=86610
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
snip...
14th ICID International Scientific Exchange Brochure - Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary Bacliff, TX, USA
Background: An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods: 12 years independent research of available data
Results: I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion: I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary Bacliff, TX, USA
Background: An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods: 12 years independent research of available data
Results: I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion: I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
snip...see full text;
P98 The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
Greenlee JJ (1), Moore SJ (1), and West Greenlee MH (2) (1) United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Virus and Prion Research Unit, Ames, IA, United States (2) Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, United States.
reading up on this study from Prion 2018 Conference, very important findings ;
***> This study demonstrates that the H-type BSE agent is transmissible by the oronasal route.
***> These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
PRION 2018 CONFERENCE ABSTRACT
WEDNESDAY, OCTOBER 24, 2018
Experimental Infection of Cattle With a Novel Prion Derived From Atypical H-Type Bovine Spongiform Encephalopathy
let's take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.
This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$
ALABAMA MAD COW g-h-BSEalabama
In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.
her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).
This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine–human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks.
Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA
NATURE|Vol 457|26 February 2009
> Epidemiological investigations conducted by USDA personnel failed to reveal any evidence of a feed source contaminated with TSE material fed to this animal
LMAO!
BANNED MAD COW FEED IN COMMERCE IN ALABAMA
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 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
###
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
###
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
###
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED 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
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
***> Wednesday, January 23, 2019
***> CFIA SFCR Guidance on Specified risk material (SRM) came into force on January 15, 2019 <***
In the USA, USDA et al sometimes serves SRM’s up as appetizers or horderves.
Thursday, November 28, 2013
Department of Justice Former Suppliers of Beef to National School Lunch Program Settle Allegations of Improper Practices and Mistreating Cows
seems USDA NSLP et al thought that it would be alright, to feed our children all across the USA, via the NSLP, DEAD STOCK DOWNER COWS, the most high risk cattle for mad cow type disease, and other dangerous pathogens, and they did this for 4 years, that was documented, then hid what they did by having a recall, one of the largest recalls ever, and they made this recall and masked the reason for the recall due to animal abuse (I do not condone animal abuse), not for the reason of the potential for these animals to have mad cow BSE type disease (or other dangerous and deadly pathogens). these TSE prion disease can lay dormant for 5, 10, 20 years, or longer, WHO WILL WATCH OUR CHILDREN FOR THE NEXT 5 DECADES FOR CJD ???
Saturday, September 21, 2013
Westland/Hallmark: 2008 Beef Recall A Case Study by The Food Industry Center January 2010 THE FLIM-FLAM REPORT
DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ???
this recall was not for the welfare of the animals. ...tss you can check and see here ; (link now dead, does not work...tss)
try this link ;
Sunday, November 13, 2011
*** California BSE mad cow beef recall, QFC, CJD, and dead stock downer livestock
Wednesday, March 2, 2016
RANCHO He did not know that they were placing healthy cow heads next to suspect carcasses BSE TSE Prion
Sunday, June 14, 2015
Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain Specified Risk Materials BSE TSE Prion
Thursday, June 12, 2014
Missouri Firm Recalls Ribeye and Carcass Products That May Contain Specified Risk Materials 4,012 pounds of fresh beef products because the dorsal root ganglia may not have been completely removed
Saturday, November 10, 2012
Wisconsin Firm Recalls Beef Tongues That May Contain Specified Risk Materials Nov 9, 2012 WI Firm Recalls Beef Tongues
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
Sunday, October 18, 2009
Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, October 17, 2009
Thursday, October 15, 2009
Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, Oct 15, 2009
Thursday, June 26, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials
Tuesday, July 1, 2008
Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs
Friday, August 8, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs 941,271 pounds with tonsils not completely removed
Saturday, April 5, 2008
SRM MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS KANSAS
Wednesday, April 30, 2008
Consumption of beef tongue: Human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings
Wednesday, April 30, 2008
Consumption of beef tongue: Human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings
Friday, October 15, 2010
BSE infectivity in the absence of detectable PrPSc accumulation in the tongue and nasal mucosa of terminally diseased cattle
SPECIFIED RISK MATERIALS SRMs
USDA BSE TSE PRION SURVEILLANCE, FEED, TESTING, SRM FIREWALLS...LMAO!
THE USDA FDA TRIPLE MAD COW DISEASE FIREWALL, WERE NOTHING MORE THAN INK ON PAPER !
infamous august 4, 1997 BSE TSE prion mad cow feed ban, part of usda fda et al TRIPLE MAD COW FIREWALL, 10 YEARS AFTER ;
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED 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
16 years post mad cow feed ban August 1997
2013
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
17 years post mad cow feed ban August 1997
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
*** Monday, October 26, 2015 ***
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015 ***
Thursday, July 24, 2014
*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations
SEE MORE;
Tuesday, September 10, 2019
THURSDAY, JULY 20, 2017
USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200
WEDNESDAY, APRIL 24, 2019
***> USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019 <***
MONDAY, JANUARY 09, 2017
Oral Transmission of L-Type Bovine Spongiform Encephalopathy Agent among Cattle
CDC Volume 23, Number 2—February 2017
*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
TUESDAY, AUGUST 28, 2018
USDA finds BSE infection in Florida cow 08/28/18 6:43 PM
http://animalhealthreportpriontse..blogspot.com/2018/08/usda-finds-bse-infection-in-florida-cow.html
WEDNESDAY, AUGUST 29, 2018
USDA Announces Atypical Bovine Spongiform Encephalopathy Detection USDA 08/29/2018 10:00 AM EDT
WEDNESDAY, AUGUST 29, 2018
Transmissible Spongiform Encephalopathy TSE Prion Atypical BSE Confirmed Florida Update USA August 28, 2018
H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism:
clinical and pathologic features in wild-type and E211K cattle following intracranial inoculation
H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism: clinical and pathologic features in wild-type and E211K cattle following intracranial inoculation
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism: clinical and pathologic features in wild-type and E211K cattle following intracranial inoculation
Authors
item Moore, Sarah - item West Greenlee, Mary - item Smith, Jodi item Nicholson, Eric item Vrentas, Catherine item Greenlee, Justin
Submitted to: Prion
Publication Type: Abstract Only
Publication Acceptance Date: August 12, 2015
Publication Date: May 25, 2015
Citation: Moore, S.J., West Greenlee, M.H., Smith, J., Nicholson, E., Vrentas, C., Greenlee, J. 2015. H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism: clinical and pathologic features in wild-type and E211K cattle following intracranial inoculation. Prion 2015. p. S5.
Technical Abstract: In 2006 an H-type bovine spongiform encephalopathy (BSE) case was reported in an animal with an unusual polymorphism (E211K) in the prion protein gene. Although the prevalence of this polymorphism is low, cattle carrying the K211 allele are predisposed to rapid onset of H-type BSE when exposed. The purpose of this study was to investigate the phenotype of this BSE strain in wild-type (E211E) and E211K heterozygous cattle. One calf carrying the wild-type allele and one E211K calf were inoculated intracranially with H-type BSE brain homogenate from the US 2006 case that also carried one K211 allelle. In addition, one wild-type calf and one E211K calf were inoculated intracranially with brain homogenate from a US 2003 classical BSE case. All animals succumbed to clinical disease. Survival times for E211K H-type BSE inoculated catttle (10 and 18 months) were shorter than the classical BSE inoculated cattle (both 26 months). Significant changes in retinal function were observed in H-type BSE challenged cattle only. Animals challenged with the same inoculum showed similar severity and neuroanatomical distribution of vacuolation and disease-associated prion protein deposition in the brain, though differences in neuropathology were observed between E211K H-type BSE and classical BSE inoculated animals. Western blot results for brain tissue from challenged animals were consistent with the inoculum strains. This study demonstrates that the phenotype of E211K H-type BSE remains stable when transmitted to cattle without the E211K polymorphism, and exhibits a number of features that differ from classical BSE in both wild-type and E211K cattle.
*** All animals succumbed to clinical disease. Survival times for E211K H-type BSE inoculated catttle (10 and 18 months) were shorter than the classical BSE inoculated cattle (both 26 months). ***
-------- Original Message --------
Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD
Date: Thu, 28 Nov 2002 10:23:43 -0000
From: "Asante, Emmanuel A" e.asante@ic.ac.uk
To: "'flounder@wt.net'" flounder@wt.net
Dear Terry,
I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention.
Thank you for your interest in the paper.
In respect of your first question, the simple answer is, ***yes. As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc.
I hope reading the paper will enlighten you more on the subject. If I can be of any further assistance please to not hesitate to ask. Best wishes..
Emmanuel Asante
< >
____________________________________
Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac..uk (until 9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now)
_________end...TSS___________________
***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. ***
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan
To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).
Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.
Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
================
Full text Singeltary et al PLOS
THURSDAY, JULY 20, 2017
USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200
LET'S take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.
This new prionopathy in humans?
the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......
wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow,
WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ???
there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$
ALABAMA MAD COW g-h-BSEalabama
In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America.
This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD.
This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene.
We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY (see mad cow feed in COMMERCE IN ALABAMA...TSS)
her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).
This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine-human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks. Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail:maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA NATURE|Vol 457|26 February 2009
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
THURSDAY, SEPTEMBER 26, 2019
Veterinary Biologics Guideline 3.32E: Guideline for minimising the risk of introducing transmissible spongiform encephalopathy prions and other infectious agents through veterinary biologics
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date: Tue, 9 Jan 2001 16:49:00 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
snip...
[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.
[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]
[host Richard] could you repeat the question?
[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[not sure whom ask this] what group are you with?
[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.
[not sure who is speaking] could you please disconnect Mr. Singeltary
[TSS] you are not going to answer my question?
[not sure whom speaking] NO
snip...see full archive and more of this;
P.9.21 Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle. Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres.
Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. * It also suggests a similar cause or source for atypical BSE in these countries.
*** It also suggests a similar cause or source for atypical BSE in these countries. ***
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. *** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. *** It also suggests a similar cause or source for atypical BSE in these countries. ***
see page 176 of 201 pages...tss
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply;
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply;
2020
TUESDAY, SEPTEMBER 29, 2020
ISO's Updated 22442 Animal Tissue Standards — What Changed? TSE Prion!
MONDAY, JULY 6, 2020
Guidance for reporting 2020 surveillance data on Transmissible Spongiform Encephalopathies (TSE)
WEDNESDAY, OCTOBER 28, 2020
EFSA Annual report of the Scientific Network on BSE-TSE 2020 Singeltary Submission
WEDNESDAY, OCTOBER 28, 2020
EFSA Scientific Opinion Potential BSE risk posed by the use of ruminant collagen and gelatine in feed for non‐ruminant farmed animals
WEDNESDAY, OCTOBER 21, 2020
Human Prion Disease Surveillance in Washington State, 2006-2017
MONDAY, OCTOBER 05, 2020
USA, UK, JAPAN, CJD TSE PRION STATISTICS UPDATE OCTOBER 2020
O.I.E. AND CHRONIC WASTING DISEASE CWD TSE PRION IN CERVID ???
PLEASE NOTE, AGAIN, NO MENTION OF CHRONIC WASTING DISEASE CWD TSE PRION, and i have begged the OIE over the decades to address this Transmissible Spongiform Encephalopathy TSE Prion, but sadly, they have failed to act, again...terry
i tried to warn the USDA/OIE inc about CWD starting back around 2001, was laughed at there too. see;
*** URGENT CWD UPDATE Friday, January 17, 2014
FINALLY, 12 years later, the OIE becomes concerned with CWD to humans, not that I did not try and warn them 12 years ago. ...kind regards, terry
Friday, January 17, 2014
Annual report of the Scientific Network on BSE-TSE EFSA, Question No EFSA-Q-2013-01004, approved on 11 December 2013
*** Further, it was addressed that recently discussions have being held at OIE level on Chronic Wasting Disease of cervids.
2002 Singeltary vs O.I.E. on CWD to human risk factor ;
Subject: Re: CWD AMERICA ???
Date: Fri, 12 Jul 2002 19:10:18 +0200
From: "INFORMATION DEPT"
Organization: O.I.E
To: "Terry S. Singeltary Sr."
References: <3D2F0169.3@wt.net> <012901c229b2$ad43bb90$7f00000a@HPKB> 3D2F2358.5010700@wt.net
I agree with you Dr Terry. The OIE, namely the International Animal Health Code Commission is working on making proposals to Member Countries to change the OIE lists so to avoid some the problems mentioned in you e-mail. This will take at least two years before adoption by the International Committee. For BSE, countries asked the OIE to post information on BSE on the OIE web site.
Personally, I am interested in Chronic Wasting Disease and I follow what is distributed through ProMed. Delegates of OIE Member Countries can propose diseases to be added to the list.
Kind regards.
Karim Ben Jebara
----- Original Message -----
From: "Terry S. Singeltary Sr."
To: "INFORMATION DEPT"
Sent: Friday, July 12, 2002 8:43 PM
Subject: Re: CWD AMERICA ???
>>> *** Further, it was addressed that recently discussions have being held at OIE level on Chronic Wasting Disease of cervids. <<<
> hello Dr. Jebara,
>
> many thanks for your swift and kind reply.
>
> if i am not mistaken, it was the same email address.
> it was 3 or 4 weeks ago i wrote, as it is, i don't
> save 'sent' emails anymore, unless very important.
>
> my main concern (besides the fact that a potential TSE
> has been in the USA cattle for some time, but the APHIS
> do not test to find), is that the CWD could very well be
> transmitting to humans, and i just did not see to much
> posted about it on OIE site.
>
> > Coming back to your question, Chronic Wasting Disease is not an OIE
>
> > listed disease. Please see OIE disease lists at
>
> http://www.oie.int/eng/maladies/en_classification.htm#ListeA).
>
> why is this TSE (CWD) not listed and followed as with BSE ?
>
> Article 1.1.3.2.
> 1. Countries shall make available to other countries, through the
> OIE, whatever information is necessary to minimise the spread of
> important animal diseases and to assist in achieving better worldwide
> control of these diseases.
>
> http://www.oie.int/eng/normes/MCode/A_00005.htm
>
> The USA CWD is an important animal disease.
>
> why is it not followed?
>
> > The decision to add or delete a disease from the OIE lists, come
>
> > through proposals made by Member Countries and it has to be adopted by
>
> > the International Committee.
>
> i _urgently_ suggest a proposal to the OIE to follow this disease very
> closely, and to propose _more_ testing in the USA for TSEs in the USA
> cattle...
>
> kindest regards,
> terry
>
> INFORMATION DEPT wrote:
>
> > Dear Sir,
> >
> > This is the first time that I receive your e-mail. To whom have you written
> > in the OIE or to which address?
> >
> > Coming back to your question, Chronic Wasting Disease is not an OIE listed
> > disease. Please see OIE disease lists at
> > http://www.oie.int/eng/maladies/en_classification.htm#ListeA).
> >
> > Countries should report to the OIE any disease even is not listed in the
> > OIE's lists in some conditions (example: an exceptional epidemiological
> > event). Please read Chapter 1.1.3 of the International animal health code to
> > have more information on disease notification and epidemiological
> > information agreed by OIE Member Countries at :
> > http://www.oie.int/eng/normes/MCode/A_00005.htm
> >
> > The decision to add or delete a disease from the OIE lists, come through
> > proposals made by Member Countries and it has to be adopted by the
> > International Committee.
> >
> > Hope that I answered to your question.
> >
> > Best regards.
> >
> > Dr Karim Ben Jebara
> > Head
> > Animal Health Information Department
> > OIE
> >
> >
> >
> > ----- Original Message -----
> > From: "Terry S. Singeltary Sr."
> > To:
> > Sent: Friday, July 12, 2002 6:18 PM
> > Subject: CWD AMERICA ???
> >
> >
> >
> >>I WROTE TO OIE RECENTLY ASKING 'WHY OIE DOES NOT FOLLOW CWD IN
> >>AMERICA' ? with no reply ? i am still seeking an answer ?
> >>
> >>many thanks,
> >>and kind regards,
> >>terry
=====================
MONDAY, MAY 05, 2014
Member Country details for listing OIE CWD 2013 against the criteria of Article 1.2.2., the Code Commission recommends consideration for listing
In response to a Member Country’s detailed justification for listing of chronic wasting disease of cervids (CWD) against the criteria of Article 1.2.2., the Code Commission recommended this disease be reconsidered for listing.
REPORT OF THE MEETING OF THE OIE TERRESTRIAL ANIMAL HEALTH STANDARDS COMMISSION Paris, 17–26 September 2013
Item 5 Criteria for listing diseases (Chapter 1.2.)
Comments were received from Australia, EU, Japan, New Zealand, Switzerland, Thailand and AU-IBAR The Code Commission noted a Member Country’s comment suggesting that greater clarity was needed for the term ‘significant morbidity and mortality’. As noted in the February 2013 report, the Code Commission considered that the structured process of listing diseases, first by an expert group whose conclusions are documented and circulated for Member Countries’ review and comment, then consideration by the World Assembly of Delegates before final adoption, is sufficiently rigorous and transparent.
greetings, what is criteria of Article 1.2.2. ??? curious as to what country detailed justification for listing ???
kind regards, terry
*******UPDATE ON OIE ARTICLE 1.2.2********
OIE Article 1.2.2.
The criteria for the inclusion of a disease, infection or infestation in the OIE list are as follows:
1) International spread of the agent (via live animals or their products, vectors or fomites) has been proven.
AND
2) At least one country has demonstrated freedom or impending freedom from the disease, infection or infestation in populations of susceptible animals, based on the animal health surveillance provisions of the Terrestrial Code, in particular those contained in Chapter 1.4.
AND
3)
a) Natural transmission to humans has been proven, and human infection is associated with severe consequences.
OR
b) The disease has been shown to cause significant morbidity or mortality in domestic animals at the level of a
country or a zone.
OR
c) The disease has been shown to, or scientific evidence indicates that it would, cause significant morbidity or
mortality in wild animal populations.
AND
4) A reliable means of detection and diagnosis exists and a precise case definition is available to clearly identify cases
and allow them to be distinguished from other diseases, infections and infestations.
OR
5) The disease or infection is an emerging disease with evidence of zoonotic properties, rapid spread, or significant morbidity or mortality and a case definition is available to clearly identify cases and allow them to be distinguished from other diseases or infections.
2 2013 © OIE - Terrestrial Animal Health Code Chapter 1.2.- Criteria for the inclusion of diseases, infections and infestations on the OIE list
*** URGENT CWD UPDATE
Friday, January 17, 2014
FINALLY, 12 years later, the OIE becomes concerned with CWD to humans, not that I did not try and warn them 12 years ago. ...
kind regards, terry
Friday, January 17, 2014
Annual report of the Scientific Network on BSE-TSE EFSA, Question No EFSA-Q-2013-01004, approved on 11 December 2013
*** Further, it was addressed that recently discussions have being held at OIE level on Chronic Wasting Disease of cervids.
2002 Singeltary vs O.I.E. on CWD to human risk factor ;
Tuesday, August 9, 2016
Concurrence with OIE Risk Designations for Bovine Spongiform Encephalopathy [Docket No. APHIS-2015-0055]
BILLING CODE: 3410-34-P DEPARTMENT OF AGRICULTURE Animal and Plant Health Inspection Service
snip...see more ;
‘’AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization.’’
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,
snip...see ;
Sunday, October 18, 2015
World Organisation for Animal Health (OIE) and the Institut Pasteur Cooperating on animal disease and zoonosis research
Wednesday, March 11, 2015
OIE and Centers for Disease Control and Prevention Reinforce Collaboration
Thursday, May 30, 2013
World Organization for Animal Health (OIE) has upgraded the United States' risk classification for mad cow disease to "negligible" from "controlled", and risk further exposing the globe to the TSE prion mad cow type disease
U.S. gets top mad-cow rating from international group and risk further exposing the globe to the TSE prion mad cow type disease
The OIE is nothing more than a trading brokerage for the Transmissible Spongiform Encephalopathy TSE prion disease aka mad cow type disease. Frances is still in the midst of a mad cow disease outbreak with atypical BSE cases still growing. mad cow disease is so bad in France, as with the USA, they stopped testing for mad cow disease (France altogether and the USA to figures so low, you would only detect a case of mad cow disease, only by chance).
from the inside looking out ;
Quote: Maybe familirise yourself with the OIE. The primary concern is animal health of the world they are the animal version of the WHO. It is a long way down from that ivory tower but here we go, until pressured by the USA representatives a country could not export animals for 6 years after finding a BSE/BASE positive animal so under the old rules the US would not be able to export anywhere in the world for another 4 1/2 years. Who got the risk levels system put in to allow some trade - your US representatives. You guys want to change rules - OK , but you do not get special rules that only apply to the US. As i have told you before Sand h I market all my own slaughter animals and you know that, so don't do the whole holier than thow act.
With all due respect, it is obvious that you know little about the OIE and how it actually works. Having been to their offices in Paris and talked personally with the Head of the Animal Test Section, you would choke if you knew how many lobby groups attend that office daily. There is a steady stream of paid lobby groups that have one goal in life and that is to sway the Section Heads of each department within the OIE to suit the needs of different jurisdictions around the world, which curiously enough, also includes the USA and Canada. Anyone can go there and chat with them - providing they can provide valid cause to be let in. To say that the only goal of the OIE is animal health is actually only part of their function. They are more than that and my discussions with Dr. Diaz there has showed me that. But to blindly make a statement regarding what they do when you have no idea what they actually do is like eating the skin of the orange and not knowing what is actually under.
Interestingly you state that the US Government applied pressure (to the OIE) I assume and that is a great example of the lobby groups doing their job. So, at the end of the day, one can safely assume that it is the pressure applied by certain influential lobby groups that will determine a likely outcome to an apparent OIE directive. Man alive, isn't it great to live in a democracy wherein the people get to make the choices and not just some "other" interested party or group - say like........Cargill or Tyson for example?
So, one last question, question?
Who wags the tail of that dog?? And for what reason other than one that is purely associated with trade and international agreements and greed?
And you think it is so simply explainable.
end...tss
Subject: UPDATED WHO Guidelines include tissues from Cervidae affected with Chronic Wasting Disease (CWD)
Distribution of infectivity in animal tissue and body fluids
Introduction
A.2.1 The following table (Table A2) presents a guide to the possible presence of TSE infectivity in various tissues and body fluids of cattle (exposed naturally or experimentally and orally to first passage BSE agent), sheep and goats (exposed naturally to scrapie agents and potentially to the BSE agent) irrespective of the stage of incubation. Table A2 has been updated in June 2010 taking account of the updated WHO Guidelines published in 2010 (WHO, 2010).
*** A.2.2 This is the first time that the WHO Guidelines include tissues from Cervidae affected with Chronic Wasting Disease (CWD). CWD has not been reported in Europe despite some surveillance for it and there are no specific regulations in force. Should information on TSE infectivity in CWD be required, for example in regard to Cervidae in zoos or in animals in transit through our ports,*** please see updated 2010 WHO Guidelines.
The inclusion of infectivity data in CWD in these Tables was considered important for three reasons: 1) CWD is continuing its spread to new regions of North America, 2) infectivity has been convincingly demonstrated in several bodily secretions and excretions of infected deer and 3) CWD is the only form of animal Transmissible Spongiform Encephalopathies (TSE) that exists in the wild and, although not presently considered to be an important concern for human, could pose serious problems of control in the future, especially as a potential source of infection in other animal species.
Monday, May 05, 2014
*** Member Country details for listing OIE CWD 2013 against the criteria of Article 1.2.2., the Code Commission recommends consideration for listing ***
PHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission
Comment from Terry Singeltary
The is a Comment on the Animal and Plant Health Inspection Service (APHIS) Notice: Concurrence with the World Organization for Animal Health's Risk Designation for Bovine Spongiform Encephalopathy
For related information, Open Docket Folder Comment APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission
Greetings APHIS et al,
I would kindly like to comment on APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], and my comments are as follows, with the latest peer review and transmission studies as references of evidence.
THE OIE/USDA BSE Minimal Risk Region MRR is nothing more than free pass to import and export the Transmissible Spongiform Encephalopathy TSE Prion disease. December 2003, when the USDA et al lost it's supposedly 'GOLD CARD' ie BSE FREE STATUS (that was based on nothing more than not looking and not finding BSE), once the USA lost it's gold card BSE Free status, the USDA OIE et al worked hard and fast to change the BSE Geographical Risk Statuses i.e. the BSE GBR's, and replaced it with the BSE MRR policy, the legal tool to trade mad cow type disease TSE Prion Globally. The USA is doing just what the UK did, when they shipped mad cow disease around the world, except with the BSE MRR policy, it's now legal.
Also, the whole concept of the BSE MRR policy is based on a false pretense, that atypical BSE is not transmissible, and that only typical c-BSE is transmissible via feed. This notion that atypical BSE TSE Prion is an old age cow disease that is not infectious is absolutely false, there is NO science to show this, and on the contrary, we now know that atypical BSE will transmit by ORAL ROUTES, but even much more concerning now, recent science has shown that Chronic Wasting Disease CWD TSE Prion in deer and elk which is rampant with no stopping is sight in the USA, and Scrapie TSE Prion in sheep and goat, will transmit to PIGS by oral routes, this is our worst nightmare, showing even more risk factors for the USA FDA PART 589 TSE PRION FEED ban.
The FDA PART 589 TSE PRION FEED ban has failed terribly bad, and is still failing, since August 1997. there is tonnage and tonnage of banned potential mad cow feed that went into commerce, and still is, with one decade, 10 YEARS, post August 1997 FDA PART 589 TSE PRION FEED ban, 2007, with 10,000,000 POUNDS, with 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. you can see all these feed ban warning letters and tonnage of mad cow feed in commerce, year after year, that is not accessible on the internet anymore like it use to be, you can see history of the FDA failure August 1997 FDA PART 589 TSE PRION FEED ban here, but remember this, we have a new outbreak of TSE Prion disease in a new livestock species, the camel, and this too is very worrisome.
WITH the OIE and the USDA et al weakening the global TSE prion surveillance, by not classifying the atypical Scrapie as TSE Prion disease, and the notion that they want to do the same thing with typical scrapie and atypical BSE, it's just not scientific.
WE MUST abolish the BSE MRR policy, go back to the BSE GBR risk assessments by country, and enhance them to include all strains of TSE Prion disease in all species. With Chronic Wasting CWD TSE Prion disease spreading in Europe, now including, Norway, Finland, Sweden, also in Korea, Canada and the USA, and the TSE Prion in Camels, the fact the the USA is feeding potentially CWD, Scrapie, BSE, typical and atypical, to other animals, and shipping both this feed and or live animals or even grains around the globe, potentially exposed or infected with the TSE Prion. this APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], under it's present definition, does NOT show the true risk of the TSE Prion in any country. as i said, it's nothing more than a legal tool to trade the TSE Prion around the globe, nothing but ink on paper.
AS long as the BSE MRR policy stays in effect, TSE Prion disease will continued to be bought and sold as food for both humans and animals around the globe, and the future ramifications from friendly fire there from, i.e. iatrogenic exposure and transmission there from from all of the above, should not be underestimated. ...
Attachments (1) APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary...
TUESDAY, JUNE 18, 2019
APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission
BSE Inquiry DFA's a review
BSE Inquiry
Sunday, May 18, 2008 BSE, CJD, and Baby foods (the great debate 1999 to 2005)
TUESDAY, AUGUST 1, 2017
BSE INQUIRY DFA 17 Medicines and medical devices
Sunday, May 18, 2008 MAD COW DISEASE BSE CJD CHILDREN VACCINES
MONDAY, MAY 19, 2008
SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMS WITH BSE HERD AND ABATTOIRS
THURSDAY, JULY 22, 2010
BSE INQUIRY DFA 18 COSMETICS
Sunday, May 18, 2008
BSE Inquiry DRAFT FACTUAL ACCOUNT DFA
BSE Inquiry DRAFT FACTUAL ACCOUNTS DFA's
DFA 15 Monitoring and Enforcement of the SBO Specified Bovine Offal Regulations
SATURDAY, AUGUST 26, 2017
DFA 14 Consideration of the Risk from Mechanically Recovered Meat (MRM) in 1989-1990
BSE INQUIRY DFA 16 MID 1995 TO THE FINAL DAYS
BSE INQUIRY DFA
Singeltary communication statement to BSE Inquiry 1998
this is all in the world those 300k+ bovine that died with BSE were consuming, a nutritional supplement with srms, i.e. specified risk materials, the most highest risk tissue for the tse prion.
Sender: "Patricia Cantos" <patricia.cantos at bse.org.uk>
To: "Terry S Singeltary Sr. (E-mail)" <flounder at wt.net>
Subject: Your submission to the Inquiry
Date: Fri, 3 Jul 1998 10:10:05 +0100
3 July 1998 Mr Terry S Singeltary Sr. E-Mail: Flounder at wt.net Ref: E2979
Dear Mr Singeltary,
Thank you for your E-mail message of the 30th of June 1998 providing the Inquiry with your further comments. Thank you for offering to provide the Inquiry with any test results on the nutritional supplements your mother was taking before she died.
As requested I am sending you our general Information Pack and a copy of the Chairman's letter. Please contact me if your system cannot read the attachments.
Regarding your question, the Inquiry is looking into many aspects of the scientific evidence on BSE and nvCJD. I would refer you to the transcripts of evidence we have already heard which are found on our internet site at http://www.bse.org.uk. Could you please provide the Inquiry with a copy of the press article you refer to in your e-mail? If not an approximate date for the article so that we can locate it? In the meantime, thank you for you comments. Please do not hesitate to contact me on 0171 261 8332 should you have any queries.
Yours sincerely Patricia Cantos Families Team Leader Attachments TSS
==============
-------- Original Message --------
Subject: re: METABOLIFE AND TSEs GAO-03-494 ''URGENT DATA''
Date: Thu, 01 May 2003 16:04:35 -0400
From: "Marcia G Crosse" <CrosseM at gao.gov>
To: <flounder at wt.net> CC: "Charles W Davenport" <DavenportC at gao.gov>, "Carolyn Feis Korman" <FeisKormanC at gao.gov>, "Martin Gahart" <GahartM at gao.gov>
Mr. Singletary,
We were informed by representatives of Metabolife, Inc. that Metabolife 356 was reformulated to remove bovine complex as an ingredient in the product, approximately September 2001. We did not independently verify the contents of the product.
Sincerely, Marcia Crosse Acting Director Health CarePublic Health and Science Issues U.S. General Accounting Office 441 G Street, N.W. Washington, D.C. 20548
===================
-------- Original Message --------
Subject: Re: METABOLIFE AND TSEs GAO-03-494 ''URGENT DATA''
Date: Thu, 01 May 2003 15:48:52 -0500
From: "Terry S. Singeltary Sr." <flounder at wt.net>
To: Marcia G Crosse <CrosseM at gao.gov>
CC: Charles W Davenport <DavenportC at gao.gov>, Carolyn Feis Korman <FeisKormanC at gao.gov>, Martin Gahart <GahartM at gao.gov> References: <seb14599.014 at GAOGWIA1.GAO.GOV>
THANK YOU!
MIRACLES DO HAPPEN! ;-)
snip...
NOW COMPARE BOVINE INGREDIENTS FROM;
2003 - 2004 Product Catalog
Standard Process Inc.
NATURAL COCOA STANDARDBAR (mad cow candy bar) (i will just list animal organs) bovine adrenal, bovine liver, bovine spleen, ovine spleen, bovine kidney...
NATURAL PEANUT BUTTER STANDARDBAR
bovine adrenal, bovine liver, bovine spleen, ovine spleen, bovine kidney...
USF (MAD COW) OINTMENT (RUB A DUB DUB, KURU ETC) ;
bovine orhic glandular extract
UTROPHIN PMG
bovine uterus PMG
VASCULIN
bovine heart PMG extract, veal bone PMG extract, bovine liever, porcine duodenum, bovine adrenal Cytosol extract, bovine spleen, ovine spleen (some yummy stuff)
IPLEX (neighbors mom died from CJD while taking these pills for years)
bovine eye PMG extract, veal bone PMG, bovine liver, porcine stomach, bovine adrenal, bovine kidney, bovine adrenal Cytosol extract, BOVINE BRAIN, bovine bone, veal bone meal
MYO-PLUS
bovine heart PMG, bovine liver, porcine stomach, bovine orchic extract, bovine spleen, ovine spleen, bovine adrenal Cytosol extract, BOVINE BRAIN
NEUROPLEX
bovine orchic Cytosol extract, bovine spleen, BOVINE BRAIN PMG EXTRACT, BOVINE ANTERIOR PITUITARY, bovine liver, BOVINE PITUITARY PMG EXTRACT, AND MORE BOVINE BRAIN... HOLY MAD COW IN A PILL !!!
NEUROTROPHIN PMG
BOVINE BRAIN PMG
NIACINAMIDE B6 VM
bovine liver, porcine stomach, bovine spleen ovine spleen, BOVINE BRAIN
OCULOTROPHIN PMG BOVINE EYE PMG
ORCHEX
bovine liver, bovine orchic Cytosol extract, porcine stomch, bovine spleen, ovine spleen, BOVINE BRAIN
OSTARPLEX
veal bone PMG extract, veal bone PMG extract, bovine liver, porcine stomach, bovine adrenal, bovine spleen, ovine spleen, BOVINE BRAIN
PARAPLEX
bovine pancreas PMG extract, porcine duodenum, bovine adrenal PMG, BOVINE PITUITARY PMG EXTRACT, bovine thyroid PMG extract
PITUITROPHIN PMG
RUMAPLEX
BOVINE BRAIN, veal bone PMG extract, bovine adrenal, bovine prostate Cytosol extract, veal bone meal, bovine liver PMG extract, bovine spleen, ovine spleen, bovine liver
SENAPLEX
bovine liver PMG extract, bovine adrenal, BOVNE BRAIN, veal bone meal, bovine kidney, bovine orchic extract, bovine spleen, ovine spleen ..........
THESE are just a few of MANY of just this ONE COMPANY...TSS
DEPARTMENT OF HEALTH AND HUMAN SERVICES
FOOD AND DRUG ADMINISTRATION CENTER FOR BIOLOGICS EVALUATION AND RESEARCH
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES ADVISORY COMMITTEE
Friday, January 19, 2001
Holiday Inn Bethesda Versailles I and II 8120 Wisconsin Avenue Bethesda, Maryland
2 PARTICIPANTS Paul W. Brown, M.D., Chairperson William Freas, Ph.D., Executive Secretary
VOTING MEMBERS Ermias D. Belay, M.D. David C. Bolton, Ph.D. Donald S. Burke, M.D. Dean O. Cliver, Ph.D. Bruce M. Ewenstein, M.D., Ph.D. Peter G. Lurie, M.D. Pedro Piccardo, M.D. Stanley B. Prusiner, M.D. Raymond P. Roos, M.D. Elizabeth S. Williams, D.V.M., Ph.D.
VOTING CONSULTANTS Linda A. Detwiler, D.V.M. David Gaylor, Ph.D.
Paul R. McCurdy, M.D. Kenrad E. Nelson, M.D.
NONVOTING CONSULTANT Susan Leitman, M.D.
GUESTS Richard Davey, M.D. Louis Katz, M.D.
snip...
page 501
253
1 DR. BOLTON: I have an additional question about
2 that. What is the assurance that additional locally sourced
3 tracheas are not added into that manufacturing process, thus
4 boosting the yield, if you will, but being returned to the
5 U.S. as being produced from U.S.-sourced raw material?
6 DR. McCURDY: Are there data to indicate how many
7 grams, or whatever, of infected brain are likely to infect
8 an organism, either animal or man, when taken orally?
9 DR. BROWN: If I am not mistaken, and I can be
10 corrected, I think a half a gram is enough in a cow, orally;
11 in other words, one good dietary-supplement pill.
12 DR. McCURDY: What I am driving at is the question
13 we are asked is really not do we wish to regulate these
14 things coming in. I think the statements about difficulties
15 in regulating things in the future or near future for new
16 regulations were probably accurate.
17 But I think that we could exhibit some quite
18 reasonable concern about blood donors who are taking dietary
19 supplements that contain a certain amount of unspecified-
20 origin brain, brain-related, brain and pituitary material.
21 If they have done this for more than a sniff or something
22 like that, then, perhaps, they should be deferred as blood
23 donors.
24 That is probably worse than spending six months in
25 the U.K.
1/19/01
3681t2.rtf(845) page 501
Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice in Manufacturing, Packing, or Holding Dietary Ingredients a Comment Number: EC -2 Accepted - Volume 7
snip...see full text and much more on nutritional supplements and the cjd tse prion;
Abstract
Chronic wasting disease (CWD) is a contagious, fatal prion disease of deer and elk that continues to emerge in new locations. To explore the means by which prions are transmitted with high efficiency among cervids, we examined prion infectivity in the apical skin layer covering the growing antler (antler velvet) by using CWD-susceptible transgenic mice and protein misfolding cyclic amplification. Our finding of prions in antler velvet of CWD-affected elk suggests that this tissue may play a role in disease transmission among cervids. Humans who consume antler velvet as a nutritional supplement are at risk for exposure to prions. The fact that CWD prion incubation times in transgenic mice expressing elk prion protein are consistently more rapid raises the possibility that residue 226, the sole primary structural difference between deer and elk prion protein, may be a major determinant of CWD pathogenesis.
Chronic wasting disease (CWD) of deer, elk, and moose is the only recognized prion disease of wild animals. To date, 15 US states and 2 Canada provinces have reported CWD in wild and/or farm-raised cervids. Outbreaks have also occurred in South Korea as a result of importation of subclinically infected animals (1,2). The unparalleled efficiency of prion transmission in cervids by a largely undefined mechanism, combined with high deer densities in certain areas of North America, complicates strategies for controlling CWD as it continues to emerge in new locations.
Growing antlers of male cervids are covered by a highly innervated and vascularized apical skin layer, referred to as velvet, which is shed after an increase in testosterone and ossification of antlers. Our study objective was to assess whether velvet from CWD-infected elk contains prion infectivity. Our rationale was 2-fold. First, the annual shedding of this material raises the possibility that it may play a role in CWD transmission. Second, although the most likely means of human exposure to CWD prions is consumption of contaminated venison (3), the substantial market for velvet in traditional Asian medicine also warrants concern.
We used CWD-susceptible transgenic (Tg) mice as a sensitive means to detect prions in antler velvet. Bioassays in Tg mice expressing deer prion protein (PrP) (4) and newly created Tg mice expressing elk PrP, demonstrated low levels of CWD prions in antler velvet. We also show that the associated protease-resistant PrP could be amplified in vitro (for detection by Western blot) by protein misfolding cyclic amplification (PMCA). Finally, comparative CWD transmissions in Tg mice indicated that the glutamine (Q) to glutamic acid (E) variation at residue 226, which is the sole primary structural difference between deer and elk PrP, may be a major determinant of CWD pathogenesis in these 2 species.
Thursday, March 19, 2009
Chronic Wasting Disease Prions in Elk Antler Velvet (Nutritional Supplements and CJD)
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor:
In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
Terry S. Singeltary Sr., Bacliff, Texas USA 77518 <flounder9@verizon.net>
