Monday, August 3, 2020

National List of Reportable Animal Diseases (NLRAD) proposed rule CWD, Scrapie, BSE, TSE, Prion Disease Singeltary Submission Docket APHIS-2017-0002

National List of Reportable Animal Diseases (NLRAD) proposed rule CWD, Scrapie, BSE, TSE, Prion Disease Singeltary Submission Docket APHIS-2017-0002

Regulatory Analysis and Development Policy and Program Development Division Animal and Plant Health Inspection Service Station 3A-03.8, 4700 River Road Unit 118 Riverdale, MD 20737-1238

Submitted electronically to docket APHIS-2017-0002 at http://www.regulations.gov

July 29, 2020

To Whom It May Concern:

We would like to thank the United States Department of Agriculture (USDA) Animal and Plant Health Inspection Service (APHIS) for the opportunity to comment on the National List of Reportable Animal Diseases (NLRAD) proposed rule. The National Pork Producers Council (NPPC) is the global voice for the US pork industry and consists of 42 affiliated state organizations representing America’s 60,000 pork producers. The American Association of Swine Veterinarians (AASV) is a professional association of veterinarians specializing in swine health, welfare, and production. Over 1,500 AASV members represent all facets of the veterinary profession including practice, research, allied industry, public health, government, academia, and education. The Swine Health Information Center (SHIC) has a mission to protect and enhance the health of the United States swine herd through coordinated global disease monitoring, targeted research investments that minimize the impact of future disease threats, and analysis of swine health data. SHIC works directly with the pork industry and public and private industry partners and organizations to facilitate effective and coordinated response to emerging swine diseases.

NPPC, AASV and SHIC support APHIS in its efforts to ensure that the United States is compliant with its reporting obligations as a member of the World Animal Health Organization (OIE) and has a rational, consistent procedure for collecting and responding to information concerning animal diseases of concern. The adoption of the NLRAD will satisfy this need. However, we do have some concerns with the NLRAD proposal that we encourage APHIS to address. The NLRAD has a discrete purpose: to collect and collate information concerning the diagnoses of specific named animal diseases and conditions. The pork industry also recognizes that APHIS has a legitimate need to solicit information about unusual animal health events from a wide range of stakeholders. However, we have significant concerns about conflating these two needs under one NLRAD reporting mechanism. We suggest that APHIS develop a second portal under the National Animal Health Monitoring System (NAHMS) umbrella to collect voluntary reports of suspicious animal health events. For clarity, we will address “suspicious animal health events,” “notifiable diseases and conditions,” and “monitored diseases” requirements separately.

Suspicious Animal Health Events

NPPC, AASV and SHIC concur with APHIS that under-reporting of notifiable animal diseases within the United States can have significant domestic and international ramifications. However, it must be acknowledged that false or premature reports can similarly have damaging consequences. For these reasons, animal health professionals, or indeed any individuals other than veterinarians, should not be obligated to report under the NLRAD when they are not credentialled to make a diagnosis of a specific animal disease. We also have significant concern with requiring veterinarians to report information concerning animal health events that do not meet the case definition of a disease or condition named on the NLRAD, especially since there is no defined response plan for such reports.

The pork industry appreciates APHIS’ rationale in wanting to collect information that falls under the “emerging disease” criteria in the proposed NLRAD rule. However, the proposed criteria are highly subjective—too subjective to mandate reporting. Requiring the reporting of an epidemiological change of a known (but not notifiable) animal disease, for example, creates a significant burden on veterinarians, other animal health professionals, APHIS, and state animal health agencies. For veterinarians and other animal health professionals, it removes discretion in determining the significance of clinical, diagnostic, and/or field observations. For APHIS and state animal health agencies, it will result in a significant increase of reports with no clear methodology or identified resources for analysis and response.

We strongly suggest that APHIS develop an additional portal to receive voluntary reports of suspicious animal health events. This portal could be utilized by veterinarians to report information that falls under the “emerging” classification in the proposed NLRAD rule when, in their professional judgement, they encounter an animal health event that is not classified under the NLRAD but that merits the attention of animal health officials.

Crucially, this system could also be used by other individuals—animal health professionals, producers, or other members of the public with specialized knowledge—to report suspicious animal health events.

Such a portal would have a logical home under the Center for Epidemiology and Animal Health’s Risk Identification Unit. It would provide APHIS with needed information without compromising the intent or utility of the proposed NLRAD system. APHIS must also ensure that information provided is secured, and that confidential information is fully protected. At the same time, validated reports of suspicious animal health events should be shared in summary form with animal industries and other animal health stakeholders.

Notifiable Diseases and Conditions

It is critical that APHIS implement a NLRAD system that has clear, carefully delineated reporting requirements, prevents duplicity of reporting, and that is fully resourced. As indicated above, the pork industry does not feel that this can be accomplished by folding in broader surveillance needs. These needs can be addressed by breaking down the NLRAD proposal into three components: what is to be reported, who is to report it, and how it is to be reported. What is to be reported: Reporting should only be mandated for specific diseases or conditions explicitly listed on the NLRAD. APHIS has indicated that it will publish case definitions for each listed disease and has proposed a process to amend the list itself when new diseases or conditions need to be added. These are appropriate and needed enhancements. It is critical that there be a clear case definition for every disease or condition listed on the NLRAD. What is missing is clarity around response to the report. A veterinary diagnostic laboratory or veterinarian making report of a notifiable animal disease or condition should be provided information concerning the likely response to said report.

A response plan must be published for each and every disease or condition. The case definition document should be extended to contain this information, or a companion document created specific to each response. For diseases or conditions with extensive response plans published elsewhere, these can be referenced and succinctly summarized. If the mandated response is a foreign animal disease investigation, this should be stated. If the report is only required to satisfy national reporting requirements to the OIE, this should be clearly indicated.

In other words, the likely response (realizing that not all mitigating circumstances can be addressed) to a report should be clearly stated for everything listed on the NLRAD. The response document should also clearly state the recommended and/or required actions for the reporter to take or convey as appropriate to the attending veterinarian or owner of the affected animals.

The pork industry does not support formal sub-classification of notifiable disease and conditions into “Emergency,” “Emerging,” and “Regulated” categories. While we appreciate the intent of this proposal, it unnecessarily blends response and surveillance activities with reporting requirements. As we have stated, the “emerging” category should be dealt with outside the NLRAD framework. An “emergency” categorization is irrelevant as all notifiable diseases and conditions must be immediately reported; the “regulated” category is also moot in the context of reporting requirements.

Should it be necessary, APHIS has already established under this proposal a mechanism to mandate reporting to the NLRAD for new or emerging syndromes. It can name the syndrome as a condition, establish a clear case definition, and publish it to the NLRAD. This can be accomplished rapidly and with appropriate consultation with industry and other animal health stakeholders. It will also allow for concurrent development of a response plan, and allocation of resources if needed. Again, the disease or condition should not be added to the NLRAD if a response plan has not been developed. Satisfaction of international reporting obligations is itself a response plan for endemic disease, in some cases, and this should be clearly stated if no other response is intended.

We also strongly suggest that APHIS not exclude “wildlife” from the NLRAD reporting requirements. Any disease or condition listed on the NLRAD should be reportable for any subject species, any population within that species be it wild, feral, captive or farmed.

In summary, reporting should only be mandated for specific, named diseases and conditions. Each named disease or condition should have a clear case definition. All relevant state and federal animal health authorities, as well as industry, should have common understanding of the response, if any, to the report of the disease or condition.

Who is to report it: Given the potential ramifications of a report of a notifiable disease, official reporting should be limited to both public and private veterinary diagnostic laboratories, which are credentialled to confirm the diagnosis of notifiable diseases. Veterinarians who diagnose a notifiable disease or condition without utilizing a veterinary diagnostic laboratory should also have a duty to report.

We have already suggested a mechanism by which other animal health professionals, and indeed any other individuals, can notify state and/or federal animal health officials of unusual animal health observations or events if they are not in a position to bring their concerns to the attention of a veterinarian with whom they have a relationship. This notification pathway again would be independent of that used by veterinarians to report confirmed or suspected diagnoses of discrete notifiable animal disease or conditions. Ultimately any observation of a suspicious animal health event will require the intervention of a veterinarian and/or veterinary diagnostic laboratory if substantiated. It is the laboratory or veterinarian who should officially notify if the ultimate diagnosis is reportable.

In summary, mandated reporting under the NLRAD should be limited to veterinary diagnostic laboratories that have confirmed the diagnosis of a reportable disease or condition. Veterinarians who have arrived at a confirmed or presumed diagnosis that falls under an established case definition without utilizing a veterinary diagnostic laboratory should also have a duty to report. Alternative mechanisms, distinct from NLRAD, should be developed and/or promoted for laypersons to notify animal health officials of suspicious events.

How it is to be reported: NPPC appreciates that APHIS explored a single portal for reporting, and that not all states have equally robust animal health agencies. We support that APHIS require all veterinary diagnostic laboratories, or veterinarians operating independent of such, report notifiable animal diseases and conditions to the NLRAD electronic portal as proposed upon diagnosis.

It is not clear, however, why APHIS is mandating that report also be made to the state in which the animal is located. APHIS should be in position to ensure that the state is immediately and automatically notified of a report to the NLRAD portal.

We understand, and support that many states do in fact have a reporting requirement for certain animal diseases or conditions. These should stand. Many veterinarians will prefer to notify their state animal health officials of their diagnosis as well as report to the NLRAD. This should also remain a viable option. The federal regulation should dictate federal reporting requirements; state regulations and accepted practice should dictate state reporting requirements.

As with the proposed portal for reporting suspicious animal health events, APHIS should ensure that the reporting system is secure and that confidential and identifying information is protected from public release. Reports should be summarized and provided to the animal industries and other animal health stakeholders promptly— especially if they concern non-endemic diseases or conditions.

In summary, the NLRAD should only mandate reporting to the proposed federal NLRAD portal. APHIS should ensure that the appropriate state agency is immediately notified upon receipt of a report. APHIS should let states determine their own direct reporting requirements for diagnostic laboratories, veterinarians and other animal health professionals under their jurisdiction, as is current practice.

NPPC, AASV and SHIC support the establishment of a NLRAD for notifiable animal diseases and conditions. The NLRAD should consist of a discrete list of named animal diseases and conditions, each with a published case definition and response plan. Reporting requirements should be limited to veterinarians who have a confirmed or presumed diagnosis of a disease or condition named on the NLRAD. The report should be made to the federal NLRAD portal as proposed, with states reserving the right to establish their own reporting requirements. The NLRAD should inform but not replace robust animal health monitoring and surveillance programs.

Monitored Animal Diseases

NPPC, AASV and SHIC can only support mandating state reporting of monitored animal diseases if both APHIS and states have the necessary resources to compile and transmit this information electronically, and if APHIS has the resources to analyze and contextualize this information when making it publicly available or reporting it to the OIE. In proposing the NLRAD, APHIS indicates that it expects up to a tenfold increase in reported data. While this does support the assertation that it will provide a clearer picture of the status of monitored diseases, it will be more resource intensive to manage this amount of data. APHIS should ensure that it can accomplish this without compromising other animal health programs. It also suggests that many, if not most, states are not currently voluntarily providing this information. It is even more critical that states not have to divert resources from other animal health programs to fulfill this reporting requirement. If APHIS is not in position to provide states with funding and other needed resources required to fulfill this mandate, it should not be enacted at this time. In summary, NPPC, AASV and SHIC support the establishment of a NLRAD that consists of named animal diseases and conditions with established case definitions. Reporting requirements for notifiable animal diseases and conditions should be limited to veterinary diagnostic laboratories and veterinarians, and such reports under the federal rule should be made exclusively to the proposed NLRAD portal. Mandated reporting of monitored animal diseases by states should only be enacted if states can be provided the resources needed to facilitate such reporting. APHIS should develop a voluntary portal separate and distinct from the NLRAD for receiving reports of suspicious animal health events.

Thank you for the opportunity to comment on this important topic.

Sincerely,

Harry Snelson, DVM Executive Director American Association of Swine Veterinarians

Liz Wagstrom, DVM, MS, DACVPM Chief Veterinarian National Pork Producers Council

Paul Sundberg, DVM, PhD, DACVPM Executive Director, Swine Health Information Center


U.S. National List of Reportable Animal Diseases (NLRAD) System Standards - Proposed



In summary, NPPC, AASV and SHIC support the establishment of a NLRAD that consists of named animal diseases and conditions with established case definitions. Reporting requirements for notifiable animal diseases and conditions should be limited to veterinary diagnostic laboratories and veterinarians, and such reports under the federal rule should be made exclusively to the proposed NLRAD portal. Mandated reporting of monitored animal diseases by states should only be enacted if states can be provided the resources needed to facilitate such reporting. APHIS should develop a voluntary portal separate and distinct from the NLRAD for receiving reports of suspicious animal health events...end

MY question is, who is to monitor the real threat of chronic wasting disease and or scrapie TSE Prion in Pigs, if it has not happened already and in the food supply chain for human and animals, and who is to debate what that might look like? 

I believe front line inspectors, veterinarians, the ones that see different disease in the field every day SHOULD IMMEDIATELY start to investigate, report, any new livestock animal disease, any delay in reporting would only help spread the disease. there is enough bureaucracy and red tape now, a fine example is separating TSE Prion disease into different disease entities i.e. cwd, scrapie, bse, cpd (CAMEL PRION DISEASE). To bring another disease reporting entity into play would only delay action imo.   

Also, state by state regulations on surveillance, tracing efforts, testing, of livestock disease, there must a a scientific standard for all to follow. you cannot have one state doing one thing, and another state doing something else, just does not work...terry

***> cattle, pigs, sheep, cwd, tse, prion, oh my!

***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). 

Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.



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 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" 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. 




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.....


the feds just released this statement and you should read this very carefully about the mad cow feed ban that never was, and still isn't, and why this is so important, since USDA APHIS ARS Scientist recent transmitted Chronic Wasting Disease CWD TSE Prion, BY ORAL ROUTES, to PIGS AND SHEEP. this is terrible news, and proves the mad cow feed ban never worked, especially since it really never existed;

ponder this; ***> Adriano Aguzzi...''We even showed that a prion AEROSOL will infect 100% of mice within 10 seconds of exposure''

SUNDAY, SEPTEMBER 1, 2019 

FDA Reports on VFD Compliance

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.


***> Wednesday, January 23, 2019 

***> CFIA SFCR Guidance on Specified risk material (SRM) came into force on January 15, 2019 <***


WEDNESDAY, JUNE 10, 2020 

Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice

Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice

Atypical BSE prions showed a modification in their zoonotic ability after adaptation to sheep-PrP producing agents able to infect TgMet129 and TgVal129, bearing features that make them indistinguishable of sporadic Creutzfeldt-Jakob disease prions.

our results clearly indicate that atypical BSE adaptation to an ovine-PrP sequence could modify the prion agent to potentially infect humans, showing strain features indistinguishable from those of classic sCJD prions, even though they might or might not be different agents.

However, the expanding range of TSE agents displaying the capacity to transmit in human-PrP–expressing hosts warrants the continuation of the ban on meat and bone meal recycling and underscores the ongoing need for active surveillance


A REVIEW of facts and science on scrapie zoonosis potential/likelihood and the USA incredible failure of the BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) 

1st up BSE 589.2001 FEED REGULATIONS 


MONDAY, JULY 27, 2020 

Experimental study using multiple strains of prion disease in cattle reveals an inverse relationship between incubation time and misfolded prion accumulation, neuroinflammation and autophagy


THURSDAY, JUNE 25, 2020 

First Report of the Potential Bovine Spongiform Encephalopathy (BSE)-Related Somatic Mutation E211K of the Prion Protein Gene (PRNP) in Cattle


MONDAY, JULY 27, 2020 

APHIS USDA Nor98-like scrapie was confirmed in a sheep sampled at slaughter in May 2020


TUESDAY, JULY 28, 2020 

Geographic variation in the PRNP gene and its promoter, and their relationship to chronic wasting disease in North American deer


Camel prion disease

Camelus Spongiform Encephalopathy


MONDAY, JULY 6, 2020 

Guidance for reporting 2020 surveillance data on Transmissible Spongiform Encephalopathies (TSE)


MONDAY, JULY 27, 2020 

BSE Inquiry DFA's a review


friendly fire from all of the above

Volume 26, Number 8—August 2020 

Sporadic Creutzfeldt-Jakob Disease among Physicians, Germany, 1993–2018 high proportion of physicians with sCJD were surgeons


THURSDAY, JULY 02, 2020 

Variant Creutzfeldt–Jakob Disease Diagnosed 7.5 Years after Occupational Exposure


SUNDAY, MAY 26, 2019 

Arguments for Alzheimer’s and Parkinson’s diseases caused by prions Stanley B. Prusiner 

''From a large array of bioassays, we conclude that AD, PD, MSA, and the frontotemporal dementias, including PSP and CBD, are all prion diseases''

snip...

P132 Aged cattle brain displays Alzheimer’s-like pathology that can be propagated in a prionlike manner

Ines Moreno-Gonzalez (1), George Edwards III (1), Rodrigo Morales (1), Claudia Duran-Aniotz (1), Mercedes Marquez (2), Marti Pumarola (2), Claudio Soto (1) 

snip...

These results may contribute to uncover a previously unsuspected etiology surrounding some cases of sporadic AD. However, the early and controversial stage of the field of prion-like transmission in non-prion diseases added to the artificial nature of the animal models utilized for these studies, indicate that extrapolation of the results to humans should not be done without further experiments. 

P75 Determining transmissibility and proteome changes associated with abnormal bovine prionopathy 

Dudas S (1,2), Seuberlich T (3), Czub S (1,2) 

In prion diseases, it is believed that altered protein conformation encodes for different pathogenic strains. Currently 3 different strains of bovine spongiform encephalopathy (BSE) are confirmed. Diagnostic tests for BSE are able to identify animals infected with all 3 strains, however, several diagnostic laboratories have reported samples with inconclusive results which are challenging to classify. It was suggested that these may be novel strains of BSE; to determine transmissibility, brain material from index cases were inoculated into cattle. 

In the first passage, cattle were intra-cranially challenged with brain homogenate from 2 Swiss animals with abnormal prionopathy. The challenged cattle incubated for 3 years and were euthanized with no clinical signs of neurologic disease. Animals were negative when tested on validated diagnostic tests but several research methods demonstrated changes in the prion conformation in these cattle, including density gradient centrifugation and immunohistochemistry. Currently, samples from the P1 animals are being tested for changes in protein levels using 2-D Fluorescence Difference Gel Electrophoresis (2D DIGE) and mass spectrometry. It is anticipated that, if a prionopathy is present, this approach should identify pathways and targets to decipher the source of altered protein conformation. In addition, a second set of cattle have been challenged with brain material from the first passage. Ideally, these cattle will be given a sufficient incubation period to provide a definitive answer to the question of transmissibility. 

=====prion 2018===





***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts 

S67 PrPsc was not detected using rapid tests for BSE.

***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.

*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***

Posted by Terry S. Singeltary Sr. on 03 Jul 2015 at 16:53 GMT


P.9.21

Molecular characterization of BSE in Canada

Jianmin Yang 1 , Sandor Dudas 2 , Catherine Graham 2 , Markus Czub 3 , Tim McAllister 1 , Stefanie Czub 1 1 Agriculture and Agri-Food Canada Research Centre, Canada; 2 National and OIE BSE Reference Laboratory, Canada; 3 University of Calgary, Canada

Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle. Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres.

Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.

Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal-specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.

Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. It also suggests a similar cause or source for atypical BSE in these countries.

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;




snip...

Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy 

>>> The only tenable public line will be that "more research is required’’ <<< 

>>> possibility on a transmissible prion remains open<<< 

O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ? 

Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy 

Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015) 

snip...see full Singeltary Nature comment here; 

Alzheimer's disease

let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease... 

Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy





Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease 

*** Singeltary comment PLoS *** 

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ? 

Posted by flounder on 05 Nov 2014 at 21:27 GMT 


IN CONFIDENCE

5 NOVEMBER 1992

TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES

[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. 

There are also results to be made available shortly 

(1) concerning a farmer with CJD who had BSE animals, 

(2) on the possible transmissibility of Alzheimer’s and 

(3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]




snip...see full text


Terry S. Singeltary Sr.

Saturday, November 9, 2019

[Docket No. APHIS-2018-0087] Concurrence With OIE Risk Designations for Bovine Spongiform Nicaragua being of negligible risk for BSE

[Federal Register Volume 84, Number 218 (Tuesday, November 12, 2019)] [Notices] [Page 61005] From the Federal Register Online via the Government Publishing Office [www.gpo.gov] [FR Doc No: 2019-24455] 

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Notices Federal Register 

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This section of the FEDERAL REGISTER contains documents other than rules or proposed rules that are applicable to the public. Notices of hearings and investigations, committee meetings, agency decisions and rulings, delegations of authority, filing of petitions and applications and agency statements of organization and functions are examples of documents appearing in this section.

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Federal Register / Vol. 84, No. 218 / Tuesday, November 12, 2019 / Notices

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DEPARTMENT OF AGRICULTURE

Animal and Plant Health Inspection Service

[Docket No. APHIS-2018-0087] 

Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy

AGENCY: Animal and Plant Health Inspection Service, USDA.

ACTION: Notice.

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SUMMARY: We are advising the public of our decision to concur with the World Organization for Animal Health's (OIE) bovine spongiform encephalopathy (BSE) risk designations for Nicaragua. The OIE recognizes this region as being of negligible risk for BSE. We are taking this action based on our review of information supporting the OIE's risk designations for this region.

FOR FURTHER INFORMATION CONTACT: Dr. Kari Coulson, Senior Staff Veterinarian, Strategy and Policy, VS, APHIS, 920 Main Campus Drive, Suite 200, Raleigh, NC 27606; (919) 855-7741; email: kari.f.coulson@usda.gov.

SUPPLEMENTARY INFORMATION: The regulations in 9 CFR part 92 subpart B, ``Importation of Animals and Animal Products; Procedures for Requesting BSE Risk Status Classification With Regard To Bovines'' (referred to below as the regulations), set forth the process by which the Animal and Plant Health Inspection Service (APHIS) classifies regions for bovine spongiform encephalopathy (BSE) risk. Section 92.5 of the regulations provides that all countries of the world are considered by APHIS to be in one of three BSE risk categories: Negligible risk, controlled risk, or undetermined risk. These risk categories are defined in Sec. 92.1. Any region that is not classified by APHIS as presenting either negligible risk or controlled risk for BSE is considered to present an undetermined risk. The list of those regions classified by APHIS as having either negligible risk or controlled risk can be accessed on the APHIS website at https://www.aphis.usda.gov/aphis/ourfocus/animalhealth/animal-and-animal-product-import-information/animal-health-status-of-regions. The list can also be obtained by writing to APHIS at Regionalization Evaluation Services, 4700 River Road Unit 38, Riverdale, MD 20737. Under the regulations, APHIS may classify a region for BSE in one of two ways. One way is for regions that have not received a risk classification from the World Organization for Animal Health (OIE) to request classification by APHIS. The other way is for APHIS to concur with the classification given to a country or region by the OIE. If the OIE has recognized a country as either BSE negligible risk or BSE controlled risk, APHIS will seek information to support our concurrence with the OIE classification. This information may be publicly available information, or APHIS may request that countries supply the same information given to the OIE. APHIS will announce in the Federal Register, subject to public comment, its intent to concur with an OIE classification. In accordance with that process, we published a notice\1\ in the Federal Register on June 17, 2019 (84 FR 28001, Docket No. APHIS-2018- 0087), in which we announced our intent to concur with the OIE recognition of Nicaragua as being a region of negligible risk for BSE. We solicited comments on the notice for 60 days ending on August 16, 2019. We received one comment by that date, from a private citizen. 

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 \1\ To view the comment we received, go to https://www.regulations.gov/docket?D=APHIS-2018-0087. 

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 The commenter voiced doubts about the efficacy of the BSE minimal risk region policy, concerns about other prion diseases such as chronic wasting disease circulating in the United States and the world, and skepticism that the ruminant-to-ruminant feed ban has been effectively enforced. The commenter did not, however, address our preliminary concurrence with the OIE's risk designation for Nicaragua or the documentation made available to support that action. Therefore, in accordance with the regulations in Sec. 92.5, we are announcing our decision to concur with the OIE risk classification of Nicaragua as a region of negligible risk for BSE.

 Authority: 7 U.S.C. 1622 and 8301-8317; 21 U.S.C. 136 and 136a; 31 U.S.C. 9701; 7 CFR 2.22, 2.80, and 371.4.

 Done in Washington, DC, this 4th day of November 2019. Kevin Shea, Administrator, Animal and Plant Health Inspection Service. [FR Doc. 2019-24455 Filed 11-8-19; 8:45 am] BILLING CODE 3410-34-P 



***> The potential impact on imports from Nicaragua and Costa Rica, which APHIS is classifying as regions of undetermined risk for BSE

GBR II: Botswana (I), Brazil (I), Colombia, Costa Rica (II), El Salvador (I), Unlikely but not excluded India, Kenya, Mauritius, Namibia (I), Nicaragua (I), Nigeria, Norway (I), Pakistan, Sweden (II). Swaziland (I)


Bovine product imports from other countries that are not currently subject to BSE-related restrictions are not expected to be significantly affected. Over the 5 years 2007-2011, annual imports from such countries as a group averaged 8 to 9 percent of all U.S. bovine product imports by volume (10 to 11 percent by value), with over 95 percent of these products coming from Mexico, Nicaragua, and Costa Rica. Imports from Mexico already meet the requirements of a region of controlled risk for BSE largely by way of FSIS requirements. 

The potential impact on imports from Nicaragua and Costa Rica, which APHIS is classifying as regions of undetermined risk for BSE, should be minimal at most. Almost all imports from those two countries are of boneless beef that already satisfy the rule's requirements, again, largely by way of FSIS requirements.


FINAL REPORT OF A MISSION CARRIED OUT IN NICARAGUA FROM 13 to 24 JANUARY 2003

IN ORDER TO EVALUATE THE CONTROLS ON THE PRODUCTION AND EXPORT OF BOVINE FRESH MEAT AND TO EVALUATE THE GENERAL ANIMAL HEALTH SITUATION

The number of BSE examinations carried out is shown in the table below.

Year CNS symptoms Normal slaughter Total

1999 

0 0 0

2000 

5 8 13

2001 

17 124 141

2002 

51 148 199

Samples are checked using histo-pathology and immuno-histo-chemistry.

All samples have so far been negative for BSE.

It was noted that:

• The knowledge among farmers of BSE was very limited. In one case, it was admitted that animals with CNS symptoms were sometimes without contacting a veterinarian.

• The sampling of normal slaughtered animals in the monitoring programme is not fully in accordance with the OIE international Animal Health Code.

• Considerable delays were seen in the delivery of the results from the international reference laboratory of the University of San Carlos, in Guatemala.

4.7.3. Specified Risk Materials

There are no rules on SRM disposal and it is normally used for human consumption. According to the CA, in the case of EU exports, SRM would be removed.

4.7.4. Rendering

Since 2001, there are legal requirements in place concerning the minimum treatment parameters to be met (133ºC, 3 bar, 20 min). It was further explained that the treatments actually used were 150-160ºC, 6,2 bar for 20 minutes. During visits to the rendering plants attached to the slaughterhouses it was noted that:

15

• The measurements were made on the steam used to provide energy for the process and not inside the process chamber. It was not possible to verify that the process parameters had been met for the processed MBM (a validation of the process has not been made by the CCA).

• The raw material was not reduced to a particle size less than 50 mm before processing.

4.7.5. Feed ban

Since 2001 there is a partial bovine feed ban in place. This prohibits the feeding of bone meal, meat meal and meat and bone meal to bovine animals. During a visit to a single-line feed mill it was noted that:

• No evidence could be shown regarding official controls of the feed ban.

No samples had been taken to detect the presence of PAP in ruminant feeds, either by the company or the official services.

snip...

6.4. BSE controls

Nicaragua has a favourable GBR status (GBR I). Nonetheless, there was a lack of awareness among farmers, and the comparatively high number of normal slaughtered animals included in the BSE monitoring programme may hamper the detection of BSE.

The weaknesses identified in the feed ban and animal waste treatment raise doubts as to the effectiveness of the BSE protection system. If the BSE agent were present in Nicaragua, its recycling could not be prevented by the current control measures.


Table 3. Results of the GBR assessments through 2005

GBR I: Highly unlikely

Argentina (I), Australia (I), Iceland, New Caledonia, New Zealand (I), Panama (I), Paraguay (I), Singapore, Uruguay (I), Vanuatu

GBR II: Unlikely but not excluded

Botswana (I), Brazil (I), Colombia, Costa Rica (II), El Salvador (I), India, Kenya, Mauritius, Namibia (I), Nicaragua (I), Nigeria, Norway (I), Pakistan, Sweden (II). Swaziland (I)

GBR III: Likely but not confirmed or confirmed at a lower level A

lbania, Andorra, Austria, Belarus, Belgium, Bulgaria, Chile (I), Croatia, Denmark, Canada (II), Cyprus, Czech Republic, Estonia, Finland, Former Yugoslav Republic of Macedonia, France, Germany, Greece, Hungary, Ireland, Israel, Italy, Latvia, Lithuania, Luxembourg, Malta, Mexico, Poland, The Netherlands, Romania, San Marino, Slovak Republic, Slovenia, South Africa, Spain, Switzerland, Turkey, USA (II)

GBR IV: Confirmed at a higher level

Portugal, United Kingdom 


Table 3. Results of the GBR assessments through 2005

GBR I: Argentina (I), Australia (I), Iceland, New Caledonia, New Zealand (I), Highly unlikely Panama (I), Paraguay (I), Singapore, Uruguay (I), Vanuatu

GBR II: Botswana (I), Brazil (I), Colombia, Costa Rica (II), El Salvador (I), Unlikely but not excluded India, Kenya, Mauritius, Namibia (I), Nicaragua (I), Nigeria, Norway (I), Pakistan, Sweden (II). Swaziland (I)

GBR III: Albania, Andorra, Austria, Belarus, Belgium, Bulgaria, Chile (I), Likely but not confirmed or Croatia, Denmark, Canada (II), Cyprus, Czech Republic, Estonia, confirmed at a lower level Finland, Former Yugoslav Republic of Macedonia, France, Germany, Greece, Hungary, Ireland, Israel, Italy, Latvia, Lithuania, Luxembourg, Malta, Mexico, Poland, The Netherlands, Romania, San Marino, Slovak Republic, Slovenia, South Africa, Spain, Switzerland, Turkey, USA (II)

GBR IV: Portugal, United Kingdom Confirmed at a higher level


Dromedary Camels Algeria Prion (Mad Camel Disease) TSE BSE MRR Import Export Risk Factors Excluding Grains and Plants

*** please see files of U.K. exports of M.B.M. AND OTHER MEAT PRODUCTS (metric tonnes), and to the countries (including Germany), they went to; 

UK EXPORTS OF MBM TO WORLD




OTHERS

BEEF AND VEAL




LIVE CATTLE


FATS 


EMBRYOS


GELATIN ETC


SEMEN


MEAT



***> Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;




***> Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products


A Proposed Rule by the Animal and Plant Health Inspection Service on 03/16/2012 

We are proposing to establish a system for classifying regions as to BSE risk that is consistent with the system employed by the World Organization for Animal Health (OIE), the international standard-setting organization for guidelines related to animal health. The conditions we are proposing for the importation of specified commodities are based on internationally accepted scientific literature and, except in a few instances, are consistent with guidelines set out in the OIE’s Terrestrial Animal Health Code. We are also proposing to classify certain specified countries as to BSE risk and are proposing to remove BSE restrictions on the importation of cervids and camelids and products derived from such animals. 

We are proposing to make these amendments after conducting a thorough review of relevant scientific literature and a comprehensive evaluation of the issues and concluding that the proposed changes to the regulations would continue to guard against the introduction of BSE into the United States, while allowing the importation of additional animals and animal products into this country. In this document we are also affirming the position we took in removing the delay of applicability of certain provisions of the rule entitled “Bovine Spongiform Encephalopathy; Minimal-Risk Regions and Importation of Commodities,” published in the Federal Register on January 4, 2005 (70 FR 460-553). The delay of applicability was removed in a final rule entitled “Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines,” published in the Federal Register on September 18, 2007 (72 FR 53314- 53379).

DATES: We will consider all comments that we receive on or before...snip...end...LOL!

snip...

We are proposing to establish a system for classifying regions as to BSE risk that is consistent with the system employed by the World Organization for Animal Health (OIE), the international standard-setting organization for guidelines related to animal health. The conditions we are proposing for the importation of specified commodities are based on internationally accepted scientific literature and, except in a few instances, are consistent with guidelines set out in the OIE’s Terrestrial Animal Health Code. We are also proposing to classify certain specified countries as to BSE risk and are proposing to remove BSE restrictions on the importation of cervids and camelids and products derived from such animals. We are 

2 proposing to make these amendments after conducting a thorough review of relevant scientific literature and a comprehensive evaluation of the issues and concluding that the proposed changes to the regulations would continue to guard against the introduction of BSE into the United States, while allowing the importation of additional animals and animal products into this country. In this document we are also affirming the position we took in removing the delay of applicability of certain provisions of the rule entitled “Bovine Spongiform Encephalopathy; Minimal-Risk Regions and Importation of Commodities,” published in the Federal Register on January 4, 2005 (70 FR 460-553). The delay of applicability was removed in a final rule entitled “Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines,” published in the Federal Register on September 18, 2007 (72 FR 53314- 53379).

DATES: We will consider all comments that we receive on or before...

snip... 

Cervids and Camelids

 In prohibiting the importation of all ruminants from regions listed in § 94.18(a)(1) and (a)(2), the current regulations prohibit the importation from such regions of cervids and camelids, and products derived from such animals, from such regions. However, live cervids and camelids and products derived from cervids and camelids are eligible for importation from BSE minimal-risk regions without restriction regarding BSE.

 In this document, we are proposing to remove all restrictions with regard to BSE from the importation of live cervids and camelids and their products from any region of the world. Although BSE has been shown to be naturally and experimentally transmitted to a wide range of ruminants, natural transmission of BSE has not been reported in cervids or camelids. One ongoing study shows that red deer (cervus elaphus) developed clinical signs similar to chronic wasting disease upon intracerebral inoculation of BSE-infected brain (Martin, et al., 2007); however red deer challenged intra-gastrically with BSE-infected brain developed neither clinical signs of disease nor presence of PrPsc at post-mortem examination. In addition, surveillance in the United Kingdom and European cervid population did not show any evidence of any TSEs



99

Therefore, APHIS considers the BSE risk from removing import restrictions on cervids and camelids and their products to be very low. The OIE Code with respect to BSE does not address trade in cervids or camelids. Ovines and Caprines In this proposal, we continue to apply the current import prohibitions and restrictions regarding ovines and caprines (e.g., sheep and goats) and their products. We are in the process of developing a proposal to amend the BSE regulations as they affect the importation of ovines and caprines and products derived from such animals. Upon completion of such a proposal, we will publish it in the Federal Register for public comment. Because this proposed rule contains no subs



PLEASE, NOTE TO THE WORLD, THE USA BSE MRR i.e. BSE, Surveillance, Testing, Feed Ban, was a TOTAL FAILURE!

America BSE 589.2001 FEED REGULATIONS, BSE SURVEILLANCE, BSE TESTING, and CJD TSE Prion

so far, we have been lucky. to date, with the science at hand, no cwd transmitted to cattle, that has been documented, TO DATE, WITH THE SCIENCE AT HAND, it's not to say it has not already happened, just like with zoonosis of cwd i.e. molecular transmission studies have 
shown that cwd transmission to humans would look like sporadic cjd, NOT nvCJD or what they call now vCJD. the other thing is virulence and or horizontal transmission. this is very concerning with the recent fact of what seems to be a large outbreak of a new tse prion disease in camels in Africa. there is much concern now with hay, straw, grains, and such, with the cwd tse prion endemic countries USA, Canada. what is of greatest concern is the different strains of cwd, and the virulence there from? this thing (cwd) keeps mutating to different strains, and to different species, the bigger the chance of one of these strains that WILL TRANSMIT TO CATTLE OR HUMANS, and that it is documented (i believe both has already occured imo with scienct to date). with that said, a few things to ponder, and i am still very concerned with, the animal feed. we now know from transmission studies that cwd and scrapie will transmit to pigs by oral routes. the atypical bse strains will transmit by oral routes. i don't mean to keep kicking a mad cow, just look at the science; 

***> cattle, pigs, sheep, cwd, tse, prion, oh my! 

***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). 

Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable. 



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 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" 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. 




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 *** 


FRIDAY, OCTOBER 25, 2019 

Experts testify United States is underprepared for bioterrorism threats Transmissible Spongiform Encephalopathy TSE Prion disease 


FRIDAY, OCTOBER 25, 2019 

Presidential Executive Order 13895 of October 22, 2019 President's Council of Advisors on Science and Technology Dumbing Down Sound Science BSE TSE Prion Stacking the deck$$$ 


THURSDAY, SEPTEMBER 26, 2019 

USDA Scientific Integrity Policy Departmental Regulation 1074-001 Breached 


MONDAY, OCTOBER 21, 2019 

Departmental Freedom of Information Act Regulations FOIA Dumbing Down of America Under the Trump Regime 


TUESDAY, MARCH 26, 2019 

Joint Statement from President Donald J. Trump USA and President Jair Bolsonaro Brazil FOREIGN POLICY BSE TSE Prion aka mad cow disease


SATURDAY, JUNE 01, 2019 

Brazil reports another cases of mad cow disease atypical BSE TSE Prion

PLEASE BE ADVISED THERE IS NO SCIENTIFIC PROOF THAT ANY ATYPICAL BSE TSE PRION IS OF A SPONTANEOUS OLD AGE DISEASE, NOT CAUSED BY FEED, THIS IS FALSE AND UNPROVEN, IN FACT, ATYPICAL BSE OF THE L AND H TYPE ARE TRANSMISSIBLE BY ORAL ROUTE. THIS STATEMENT THAT ATYPICAL BSE IS A SPONTANEOUS EVENT CAUSED BY OLD AGE, CAUSED BY NOTHING, IS ABSOLUTELY A LIE, AND THE GOVERNMENT OF BRAZIL, AND OTHER GOVERNMENTS THAT PRODUCE SUCH STATEMENTS, KNOWS THIS IS AN UNPROVEN STATEMENT...TERRY SINGELTARY SR.


TUESDAY, OCTOBER 29, 2019 

USDA Abruptly Halts Animal ID Plan As Experts Testify USA Underprepared For Bioterrorism Threats Such As BSE TSE Prion aka Mad Cow Disease 


FRIDAY, OCTOBER 11, 2019 

CattleTrace to Host First-Ever Industry Symposium


TUESDAY, MARCH 26, 2019 

USDA ARS 2018 USAHA RESOLUTIONS TWO PRONGED APPROACH NEEDED FOR ADVANCING CATTLE TRACEABILITY

RESOLUTION NUMBER: 34 APPROVED

SOURCE: COMMITTEE ON CATTLE AND BISON


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


*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** 




FRIDAY, JULY 26, 2019 

Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species


atypical and typical BSE and Scrapie Zoonosis
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations 

Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France 

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). 

Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. 

*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, 

***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), 

***is the third potentially zoonotic PD (with BSE and L-type BSE), 

***thus questioning the origin of human sporadic cases. 

We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. 

=============== 

***thus questioning the origin of human sporadic cases*** 

=============== 

***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. 

============== 


***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. 

***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 

***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. 

 
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

Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,

Natalia Fernandez-Borges a. and Alba Marin-Moreno a

"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France

Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion... Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.

To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.

These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.

Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. 

Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 

These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. 

 
***> why do we not want to do TSE transmission studies on chimpanzees $

5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. 

***> I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. 

***> Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

snip...

R. BRADLEY



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. 


***> 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. <***

Transmission of scrapie prions to primate after an extended silent incubation period 

Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation

Abstract 

Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.

SNIP...

Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. 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.

The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.

We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.

Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.

The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.

Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.

Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.

Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.

Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.

In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free... Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.



ZOONOSIS OF CWD, BSE, SCRAPIE, TSE PRION


CWD TSE Prion Zoonosis

i was very surprised that no mention of the study out of Canada with oral transmission of CWD to Macaque. 

i have spoken with Stefanie Czub and Professor Aguzzi, whom toured her lab afterwards, about these studies. the transmission studies were valid. plus, we know that cwd zoonosis would NOT look like nvCJD, but would look like sporadic CJD of some type. see;

> However, to date, no CWD infections have been reported in people.
key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
Chronic Wasting Disease CWD TSE Prion aka mad deer disease zoonosis
We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;
(3) Reliable essays can be established to detect CWD infection in humans; and
(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
Prion 2017 Conference
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen 
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. 
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. 
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. 
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS 
PRION 2018 CONFERENCE
Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).
To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years.
After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.
Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate.
The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.
Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.
The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD..
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;
P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States
Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA..
SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD
states.
AND ANOTHER STUDY;
P172 Peripheral Neuropathy in Patients with Prion Disease
Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio..
IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017,
AND
included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%),
AND
THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.
snip…
see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below…terry
PRION 2019 ABSTRACTS 

1. Interspecies transmission of the chronic wasting disease agent

Justin Greenlee

Virus and Prion Research Unit, National Animal Disease Center, USDA Agriculture Research Service

ABSTRACT

The presentation will summarize the results of various studies conducted at our research center that assess the transmissibility of the chronic wasting disease (CWD) agent to cattle, pigs, raccoons, goats, and sheep. This will include specifics of the relative attack rates, clinical signs, and microscopic lesions with emphasis on how to differentiate cross-species transmission of the CWD agent from the prion diseases that naturally occur in hosts such as cattle or sheep. Briefly, the relative difficulty of transmitting the CWD agent to sheep and goats will be contrasted with the relative ease of transmitting the scrapie agent to white-tailed deer.

53. Evaluation of the inter-species transmission potential of different CWD isolates

Rodrigo Moralesa, Carlos Kramma,b, Paulina Sotoa, Adam Lyona, Sandra Pritzkowa, Claudio Sotoa

aMitchell Center for Alzheimer’s disease and Related Brain Disorders, Dept. of Neurology, McGovern School of Medicine University of Texas Health Science Center at Houston, TX, USA; bFacultad de Medicina, Universidad de los Andes, Santiago, Chile

ABSTRACT

Chronic Wasting Disease (CWD) has reached epidemic proportions in North America and has been identified in South Korea and Northern Europe. CWD-susceptible cervid species are known to share habitats with humans and other animals entering the human food chain. At present, the potential of CWD to infect humans and other animal species is not completely clear. The exploration of this issue acquires further complexity considering the differences in the prion protein sequence due to species-specific variations and polymorphic changes within species. While several species of cervids are naturally affected by CWD, white-tailed deer (WTD) is perhaps the most relevant due to its extensive use in hunting and as a source of food. Evaluation of inter-species prion infections using animals or mouse models is costly and time consuming. We and others have shown that the Protein Misfolding Cyclic Amplification (PMCA) technology reproduces, in an accelerated and inexpensive manner, the inter-species transmission of prions while preserving the strain features of the input PrPSc. In this work, we tested the potential of different WTD-derived CWD isolates to transmit to humans and other animal species relevant for human consumption using PMCA. For these experiments, CWD isolates homozygous for the most common WTD-PrP polymorphic changes (G96S) were used (96SS variant obtained from a pre-symptomatic prion infected WTD). Briefly, 96GG and 96SS CWD prions were adapted in homologous or heterologous substrate by PMCA through several (15) rounds. End products, as well as intermediates across the process, were tested for their inter-species transmission potentials. A similar process was followed to assess seed-templated misfolding of ovine, porcine, and bovine PrPC. Our results show differences on the inter-species transmission potentials of the four adapted materials generated (PrPC/PrPSc polymorphic combinations), being the homologous combinations of seed/substrate the ones with the greater apparent zoonotic potential. Surprisingly, 96SS prions adapted in homologous substrate were the ones showing the easiest potential to template PrPC misfolding from other animal species. In summary, our results show that a plethora of different CWD isolates, each comprising different potentials for inter-species transmission, may exist in the environment. These experiments may help to clarify an uncertain and potentially worrisome public health issue. Additional research in this area may be useful to advise on the design of regulations intended to stop the spread of CWD and predict unwanted zoonotic events.

56. Understanding chronic wasting disease spread potential for at-risk species

Catherine I. Cullingham, Anh Dao, Debbie McKenzie and David W. Coltman

Department of Biological Sciences, University of Alberta, Edmonton AB, Canada

CONTACT Catherine I. Cullingham cathy.cullingham@ualberta.ca

ABSTRACT

Genetic variation can be linked to susceptibility or resistance to a disease, and this information can help to better understand spread-risk in a population. Wildlife disease incidence is increasing, and this is resulting in negative impacts on the economy, biodiversity, and in some instances, human health. If we can find genetic variation that helps to inform which individuals are susceptible, then we can use this information on at-risk populations to better manage negative consequences. Chronic wasting disease, a fatal, transmissible spongiform encephalopathy of cervids (both wild and captive), continues to spread geographically, which has resulted in an increasing host-range. The disease agent (PrPCWD) is a misfolded conformer of native cellular protein (PrPC). In Canada, the disease is endemic in Alberta and Saskatchewan, infecting primarily mule deer and white-tail deer, with a smaller impact on elk and moose populations. As the extent of the endemic area continues to expand, additional species will be exposed to this disease, including bison, bighorn sheep, mountain goat, and pronghorn antelope. To better understand the potential spread-risk among these species, we reviewed the current literature on species that have been orally exposed to CWD to identify susceptible and resistant species. We then compared the amino acid polymorphisms of PrPC among these species to determine whether any sites were linked to susceptibility or resistance to CWD infection. We sequenced the entire PrP coding region in 578 individuals across at-risk populations to evaluate their potential susceptibility. Three amino acid sites (97, 170, and 174; human numbering) were significantly associated with susceptibility, but these were not fully discriminating. All but one species among the resistant group shared the same haplotype, and the same for the susceptible species. For the at-risk species, bison had the resistant haplotype, while bighorn sheep and mountain goats were closely associated with the resistant type. Pronghorn antelope and a newly identified haplotype in moose differed from the susceptible haplotype, but were still closely associated with it. These data suggest pronghorn antelope will be susceptible to CWD while bison are likely to be resistant. Based on this data, recommendations can be made regarding species to be monitored for possible CWD infection.

KEYWORDS: Chronic wasting disease; Prnp; wildlife disease; population genetics; ungulates

Thursday, May 23, 2019 

Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts


see full Prion 2019 Conference Abstracts

THURSDAY, OCTOBER 04, 2018
Cervid to human prion transmission 5R01NS088604-04 Update
snip…full text;
SATURDAY, FEBRUARY 09, 2019
Experts: Yes, chronic wasting disease in deer is a public health issue — for people
FRIDAY, JULY 26, 2019 

Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species


Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY 

Date: Fri, 18 Oct 2002 23:12:22 +0100 

From: Steve Dealler 

Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member 

To: BSE-L@ References: <3daf5023 .4080804="" a="" class="yiv5636745079linkified" fg_scanned="1" href="http://wt.net/" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">WT.NET
"">

Dear Terry,

An excellent piece of review as this literature is desparately difficult to get back from Government sites.

What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!

Steve Dealler ===============

SNIP...SEE FULL TEXT AND HISTORY;

MONDAY, FEBRUARY 25, 2019

***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019

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;

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


THURSDAY, AUGUST 08, 2019 

Raccoons accumulate PrPSc after intracranial inoculation with the agents of chronic wasting disease (CWD) or transmissible mink encephalopathy (TME) but not atypical scrapie 


WEDNESDAY, OCTOBER 16, 2019 

Australia Assessment of bulk wheat from Canada Part B: Animal biosecurity risk advice, CWD TSE Prion concerns are mounting 


FRIDAY, NOVEMBER 08, 2019 

EFSA Panel on Biological Hazards (BIOHAZ) Update on chronic wasting disease (CWD) III


FRIDAY, OCTOBER 25, 2019 

27th ANNUAL REPORT 2018 CREUTZFELDT-JAKOB DISEASE SURVEILLANCE


SUNDAY, JANUARY 11, 2015 

Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission


IT is of my opinion, that the OIE and the USDA et al, are the soul reason, and responsible parties, for Transmissible Spongiform Encephalopathy TSE prion diseases, including typical and atypical BSE, typical and atypical Scrapie, and all strains of CWD, and human TSE there from, spreading around the globe. I have lost all confidence of this organization as a regulatory authority on animal disease, and consider it nothing more than a National Trading Brokerage for all strains of animal TSE, just to satisfy there commodity. 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. JUST because of low documented human body count with nvCJD and the long incubation periods, the lack of sound science being replaced by political and corporate science in relations with the fact that science has now linked some sporadic CJD with atypical BSE and atypical scrapie, and the very real threat of CWD being zoonosis, I believed the O.I.E. has failed terribly and again, I call for this organization to be dissolved. ... 

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 


Friday, December 5, 2014 

SPECIAL ALERT The OIE recommends strengthening animal disease surveillance worldwide 


Monday, December 1, 2014 

Germany Bovine Spongiform Encephalopathy BSE CJD TSE Prion disease A Review December 1, 2014 


Friday, November 28, 2014 

BOVINE SPONGIFORM ENCEPHALOPATHY BSE AKA MAD COW DISEASE PORTUGAL CONFIRMED 


Sunday, October 5, 2014 France stops BSE testing for Mad Cow Disease 


Monday, May 5, 2014 

Brazil BSE Mad Cow disease confirmed OIE 02/05/2014 


Sunday, December 28, 2014 

*** Reverse Freedom of Information Act request rFOIA FSIS USDA APHIS TSE PRION aka BSE MAD COW TYPE DISEASE December 2014 *** 


THURSDAY, JULY 20, 2017
USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200

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. 

PRION 2018 CONFERENCE ABSTRACT


WEDNESDAY, AUGUST 15, 2018 

***> The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge


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 ***


*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ; 


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.


***> 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 


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, 


BSE MRR POLICY MUST BE ABOLISHED AND BSE TSE PRION GBR RISK ASSESSMENTS FOR ALL ANIMAL TSE PRION DISEASE BROUGHT FORTH IMMEDIATELY FOR ALL COUNTRIES, OR THE OIE USDA ASSESSMENTS ARE WORTHLESS, imo...

Terry S. Singeltary Sr.