Notice: Animal Disease Traceability (ADT) Summary of Feedback on the ADT Program
USDA Animal and Plant Health Inspection Service sent this bulletin at 09/18/2017 06:06 PM EDT
The United States Department of Agriculture’s (USDA) Animal Plant and Health Inspection Service (APHIS) has released a report titled Animal Disease Traceability (ADT) Summary of Feedback on the ADT Program. Since the publication of the Code of Federal Regulations (CFR) Title 9 Part 86 – Traceability for Livestock Moving Interstate in January 2013, APHIS has sought feedback on the ADT framework from industry and State, Tribal, and Federal animal health officials with the goal of enhancing our tracing capabilities for emergency response, disease control, and eradication programs. This report provides a summary of the most recent stakeholder feedback that USDA APHIS received through a public comment period and during a series of nine public meetings held across the country in April through July of this year. The purpose of the comment period and these public meetings was to hear from industry and other stakeholders regarding their experiences with ADT by asking: (1) What areas are working well? (2) What aspects are challenging, confusing, or problematic? (3) How can these obstacles be rectified? (4) What level of traceability should be considered if we are to move beyond the basic traceability framework?
This summary of feedback will also be included as part of the Animal Disease Traceability (ADT) Summary of Program Reviews and Preliminary Next Step Recommendations document that will be presented by USDA APHIS at the Traceability Forum—co-hosted by the National Institute for Animal Agriculture (NIAA) and the United States Animal Health Association (USAHA) in Denver, Colorado, on September 26 – 27, 2017.
Click here to view Animal Disease Traceability (ADT) Summary of Feedback on the ADT Program. You may also obtain a copy by written request to the ADT staff at email@example.com.
For further information, contact:
Dr. Sunny Geiser-Novotny Cattle Health Staff/ADT Veterinarian Surveillance, Preparedness, and Response Services APHIS Veterinary Services 2150 Centre Avenue, Building B, Mailstop 3E13, Room 3E97 Fort Collins, CO 80526 (970) 494-7372.
Animal Disease Traceability
Summary of Feedback on the ADT Program
Since the publication of the Code of Federal Regulations (CFR) Title 9 Part 86, “Traceability for Livestock Moving Interstate” in January 2013, the Animal and Plant Health Inspection Service (APHIS) has sought feedback on the ADT framework from industry and State, Tribal and Federal animal health officials with the goal of enhancing our tracing capabilities for emergency response, disease control and eradication programs. This report summarizes the most recent stakeholder feedback that APHIS received during a series of nine public meetings held across the country in April thru July of this year and through a Federal Registry notice requesting comment on the program. The purpose of these public meetings and comment period was to hear from industry and other stakeholders regarding their experiences with ADT: What areas are working well? What aspects are challenging, confusing or problematic? How can these obstacles be rectified? And what level of traceability should be considered if we are to move beyond the basic traceability framework?
Participants in attendance at the ADT public meetings expressed appreciation for the opportunity to discuss the ADT framework and collaborate on future traceability options with APHIS. Both meeting attendees and written comments acknowledged that the general framework has been successful in improving the official identification of covered livestock and the documentation of interstate movement; and the availability of those records. The information below summarizes the general concerns with the original framework and those for consideration of future traceability opportunities.
Confidentiality and Security of Information Systems: The issue of confidentiality continues to be an issue of concern among producers as is the overall security of the information technology systems (IT). The producers indicated support for changes made when ADT was implemented that placed more responsibility for holding their information at the State-level.
Liability: Producer liability remains an area of concern. While earlier discussions on animal identification (ID) primarily focused on tracing diseased animals to an individual’s premises that may not have been responsible for the animal when it was infected, more current discussions also express concern on liability related to injury of animals or personnel when working cattle for tagging, manually reading tags, etc.
Cost: Meeting attendees and commenters expressed that the cost of traceability must be distributed across all sectors of the industry. In particular, if electronic ID (EID) technology is implemented as the only method of official ID, the cow/calf industry should not cover the cost when the entire industry benefits. Commenters noted that other sectors would contribute significantly to the cost of the infrastructure for EID, and as a result, the cost to implement EID would not be borne by the
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cow/calf sector alone.
Small Producers: APHIS should consider issues associated with requiring small producers to comply with an enhanced traceability regulation, including costs that are proportionally higher for this segment of the industry due to economy of scale and management limitations (for example, the ability to tag their own cattle). This sector includes a significant number of producers and cattle, thus their viability can impact markets and other service providers. Producers that sell their beef products direct to consumers provided many written comments that expressed their concerns about the cost and burden associated with animal ID, in particular electronic methods. Individuals from this sector also noted that their animals are already traceable from custom slaughter facilities back to their premises.
Common Issues Regarding the Current ADT Framework
Focus of ADT: APHIS should administer ADT for animal disease control and leave marketing opportunities to Agricultural Marketing Service (AMS) programs and the private sector. However, feedback also acknowledged the need for the United States to have a national traceability program to meet international trading partners’ requirements for animal disease control and felt the two topics are linked to one another.
Beef Feeders: The inclusion of beef feeders in the official ID requirement was the primary topic of discussion at public meetings. While a large number of stakeholders acknowledged that beef feeders need to be included in the official ID requirements at some point, the consensus was to address the gaps in the current framework, which covers beef breeding cattle over 18 months of age and all dairy, before expanding the official ID requirements to beef feeder cattle. Additional points of consensus regarding the official ID for beef feeders included:
• The expansion of regulations for the official ID of beef feeders under18 months of age must conform to normal rule making procedures.
• Beef feeders could be included after an expanded framework is fully functional for breeding animals, including the requirement for official ID with EID and the supporting infrastructure.
• The U.S. Department of Agriculture should conduct a study to determine the level of traceability warranted for beef feeder cattle.
• Other individuals suggested that requirements for beef feeders be implemented incrementally, with the initial objective to obtain birth premises ID and tag retirement, and then phase in the collection of movement data as infrastructure is established over time.
• While beef feeder cattle official ID requirements should be delayed, discussion on processes to include in this sector should continue in order to ensure an implementation plan is prepared.
• A cost benefit analysis should be conducted on official ID/traceability of beef feeder cattle to support future discussions/decisions on this topic.
• Livestock markets, while supportive of tagging sites for the population currently covered, explained that the burden of tagging beef feeders at their auctions is not feasible and solutions to tag at the farm/ranch or before arriving at the auctions are essential.
• Alternative solutions to tagging beef feeder cattle at the markets should be explored. One suggestion was to apply the official tag for these cattle at the first receiving premises, when these cattle are worked for management purposes, with records of tags applied that provide
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contact of the person responsible for the cattle when sold at the markets.
• Some individuals expressed concern that the official ID of all beef feeders would diminish market advantages and premiums of added-value programs.
ID to Birth Premises: To achieve better traceability, most individuals supported the need to apply official ID at the birth premises for animals that are covered by the official ID regulation. If that is not practical, they supported tagging at change of ownership or first point of commingling, versus at the time of first interstate movement, provided the animals are traceable to the birth premises. Since beef cattle under 18 months of age would remain exempt until determined otherwise, adult beef animals would be officially identified when first shipped after 18 months of age for ownership change or commingling.
Flexibility and Exemptions: Feedback from the meetings clearly indicated that industry feels the current framework is too flexible and that there are too many exemptions, which causes confusion regarding the regulations. While recalling the reasons they were established and their intent, there was strong consensus that the exemptions create too many traceability gaps in the classes of cattle and bison covered under the current rule. Additionally, the exemptions make enforcement of the existing regulation more challenging, as it is difficult to determine if an animal at subsequent locations required official ID earlier in life.
State Differences: There was strong consensus that there needs to be more standardization and uniformity of State import requirements. Preparing interstate certificates of veterinary inspection (ICVIs) has become very complicated. Individuals referenced the requirement by some States to record official ID numbers of dairy steers on ICVIs as one example of how State regulations differ from the Federal regulation and from one State to another.
Uniform Enforcement: The livestock markets voiced concerns that enforcement of the current regulation is inconsistent and unfairly targets markets, while private treaty sales and online auctions are not monitored or held to the same degree of accountability. They identified the lack of enforcement for other industry sectors as a gap that must be rectified. There was a strong sentiment that more stringent enforcement actions at the markets will drive sales back into the country. However, most individuals agreed that compliance would automatically improve if all cattle (less beef feeders) required ID on first movement from the birth premises.
EID Technology: Industry participants and animal health officials agreed that EID is necessary to achieve cost-effective traceability. Producers, market managers, accredited veterinarians, and others expressed concerns about cattle handling challenges and economic losses created by the need to restrain cattle to manually read and record the official ID number on small visual-only eartags. While the National Uniform Eartagging System (NUES) tags, traditionally known as the metal clip “brite” tags, are inexpensive to purchase, individuals from across the industry indicated there is significant expense throughout the production chain associated with their use. Feedback also indicated that many support the phase out of free NUES tags and that APHIS needs to eliminate them as an official method of ID. However, multiple issues need to be addressed before the transition to EID can occur, including:
• If radio frequency ID (RFID) is to be utilized, the establishment of standards, including one technology (low-frequency (LF) vs ultra-high frequency (UHF)) is critical. Most stakeholders were supportive of a dual technology tag as an interim measure.
• The infrastructure must be in place to support the transition to EID.
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• Cost remains the primary concern of producers and representatives from other sectors of the industry regarding EID, and both the reader infrastructure and tags need to be addressed. However, the use of EID would provide substantial savings due to the increased efficiency associated with the technology.
• State and Federal animal health officials noted that EID would likely increase the use of electronic forms, in particular electronic ICVIs. Obtaining records electronically would decrease cost and improve the completeness and accuracy of the data. Additionally, retiring animal numbers at slaughter would be feasible, where it has been cost-prohibitive with visual-only tags.
• Individuals suggested a cost analysis on metal NUES tags to show the full cost of tags when working cattle to manually record ID numbers (labor, stress and shrink, injury, etc.), as well as their limitations relative to traceability, e.g., tag retirement. This analysis will likely help support the justification for EID technology.
• Smaller producers that sell their products direct to consumers are not supportive of EID technology and noted that their animals are already highly traceable.
• There was support at one meeting for establishing a nationally standardized alternative movement document to ICVIs with an electronic version.
• There was support to increase the value and volume of owner shipper statements (OSS) by implementing an efficient process to collect and store OSS information by offering an electronic version.
• One State animal health official suggested that APHIS develop a national ICVI form.
• ADT should define a movement document, including the necessary data elements as the minimum standard, and the importing States should determine any additional requirements for animal health certificates, ICVIs, permits, etc.
Collection of ID at Slaughter: As reported in the ADT assessment, APHIS noted some inconsistencies with tag collection and their accurate correlation to the carcass. APHIS is working with their field personnel and Food Safety Inspection Service to correct this issue. State animal health officials and industry recognize this shortfall and also identify it as a high-priority gap in the current framework that needs to be rectified.
Official ID Tags
• Consideration should be given to one basic official eartag to increase the awareness of which tag is official. Doing so would lessen its accidental removal and improve compliance.
• There are differing views on using the same eartag for both official ID and management. Some producers prefer the same tag for both purposes, as it makes the tagging process more efficient and the official tag works well with herd management practices. Other producers commented that when they purchase cattle with official IDs with existing management numbers on the same tag, it creates conflict with their management numbering systems and, subsequently, they prefer not to have such tags used for ADT.
• ID devices that are approved for AMS’ Process Verified Program and those designated as official by APHIS ADT should be compatible.
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Brand certificates and inspection: Individuals commented on the long-term value of brands and brand inspection. Commenters stated that official ID tags should not be represented as an alternative or promoted to replace brands. Animal health officials in brand States noted the value of brands and brand inspection for proof of ownership and that they can provide information when conducting traceback investigations, but admitted that brands alone do not provide the level of traceability needed for disease control.
Outreach: Many commenters indicated that APHIS and States will need to ensure enhanced outreach efforts to reach producers regarding traceability requirements.
Recording Official ID Numbers: The issue of recording individual ID numbers on ICVIs was raised, with the suggestion to consider listing ranges of numbers to avoid having to rework cattle after a sale to obtain the specific IDs going to each premises. Individuals also suggested that a premises ID number tag could suffice for traceability to avoid the current challenge of recording individual IDs.
Cattle Imported to the United States: Some industry participants expressed concern regarding mandating traceability in the domestic herd for ADT while allowing importation of animals and/or products from countries affected with foot-and-mouth disease (FMD) and tuberculosis (TB), such as Brazil and Mexico, respectively. In addition, attendees brought up the quality of diagnostic tests/vaccination options related to TB and brucellosis and the lack of available funding to improve those and the FMD vaccine bank.
Data Systems: Many State animal health officials expressed concern that APHIS’ data systems are not efficient and indicated that even enhanced traceability will fail without efforts to increase electronic submission of data and data sharing capabilities.
''Data Systems: Many State animal health officials expressed concern that APHIS’ data systems are not efficient and indicated that even enhanced traceability will fail without efforts to increase electronic submission of data and data sharing capabilities.''
well, since APHIS/USDA et al could not say a word about Mad Cow Disease i.e. Bovine Spongiform Encephalopathy BSE TSE Prion, and the failed attempt at trying at trying to eradicate that, instead, simply to not speak about it. all the while science has now linked sporadic Creutzfeldt Jakob Disease sCJD to typical and atypical BSE, typical and atypical Scrapie, and to Chronic Wasting Disease CWD in cervid, and while still excluding the facts of an incredibly failed BSE Surveillance, BSE Testing, and BSE feed ban policies. not speaking of the fact now that Chronic Wasting Disease CWD TSE Prion in cervid have been transmitted to the Macaque and to the Pig, ORALLY, and that the feed ban does not stop these feeding practices. i thought i should bring this attention to the world...Terry S. Singeltary Sr.
FRIDAY, AUGUST 20, 2010 USDA: Animal Disease Traceability August 2010 USDA: Animal Disease Traceability August 2010
as a consumer, my opinion (if that matters), you need some sort of traceability for your livestock. I don't want to know anything about your family, your income, your kids, your sex life, nothing but to be able to trace that animal from farm to fork. I want to know whether or not if that animal has been fed animal protein, antibiotics, and if myself or my family do get sick, we should be able to trace that product. I don't see the problem. you can trace every part on your car, I can find out anything I want about you on the internet. why can't I do that with a cow?
let's review a few things about the NAIS, why we need it past and present. let's review first the few mad cows that were accidently found, birth cohorts, herd cohorts etc., and how efficient or NOT the traceability of those 4 animals were....oops, that's right, the first stumbling and staggering mad cow in Texas was sent straight to the render, did not pass GO(inspection), did not get $200.(prion rapid test), and of course, was never confirmed. THEN the second mad cow, the one that would never have been confirmed if not for an act of Congress and the Honorable Fong of the OIG, and scientist from the EU and the USA asking questions, meanwhile the BSE MRR was being finalized. Then after 7 months of sitting on the shelf, after a secret test had already turned up positive, but yet still 7 months no confirmation on a BSE positive test that by the BSE Red Books, it should have been a 48 hour turnaround on that test. Finally, the 2nd Texas mad cow was confirmed positive BSE. later termed atypical h-BSE. Then you had the Alabama mad cow, now termed g-h-BSEalabama, and then of course the mad cow old Luther capped in Washington state, the white one, that changed colors, and then was said to be a Canadian traitor c-BSE mad cow. IT's all Canada's fault ;-(NOT)
Be sure to see the latest data on the typical and atypical cases of BSE and Scrapie and any human CJD TSE there from. This is down toward the bottom of the posting.
BSE, USDA, NAIS, AND TRACEABILITY
Let's look at how the USDA et al trace BSE aka mad cow cases, birth, and index herd cattle in the past (or rather how they could not trace them).
TEXAS MAD COW (h-BSE), that was finally tested and documented 7+ months after an act of Congress, and Scientist from all over the Globe questioning the testing methods and negative findings of this Texas mad cow. ...
TEXAS h-BSE MAD COW CASE THAT WAS FINALLY DOCUMENTED
Birth Cohort The owner of Farm A kept very few herd records; this made finding documentation on this cow’s birth cohort difficult. The birth cohort, by definition, included all cattle born on the positive animal’s birth premises within 1 year, before or after, the positive animal’s date of birth. The index cow was approximately 12 years of age in November 2004, but there was no exact birth date in the herd records. A potential age range of 11 to 13 years was used to sufficiently cover the animal’s most likely age. Using this range, all cattle born on the index premises between 1990 and 1995 were considered part of the birth cohort. In lieu of the owner’s records, herd records from Veterinary Services’ Generic Database (GDB) were used to compile a list of brucellosis calfhood vaccination (CV) tag numbers from the index herd that corresponded to animals to be included in the birth cohort. There were 121 animals identified through GDB as having been calfhood vaccinated on the index farm between 1991 and 1994. The owner of Farm A did not calfhood vaccinate after 1994. Moreover, calfhood vaccinates include only heifers. Therefore, the list of 121 animals was not a complete list of all birth cohorts. However the tracing that response personnel conducted on other COI was designed to account for the remainder of the birth cohorts.
Feed Cohort ...
Tracing of Progeny
The 2003/2004 progeny of the index cow was known to have left the farm through a specific livestock market sometime between February and October 2004. The 2002/2003 progeny of the index cow left the farm through the same market sometime between January
and December 2003. Response personnel learned early in the investigation that animals from the index farm were sold not only under the index farm owner’s name and that of his wife, but also by other members of the owner’s immediate family. Additionally, there were no herd records to indicate the gender of the two at-risk progeny. Therefore, market records for February through October 2004 and January through December 2003 were obtained for all calves sold both by Farm A’s owner and by members of his immediate family; response personnel traced all such calves to determine their disposition. With the index herd being composed of mixed breed beef cattle, the calves that left the farm were genetically unsuitable for use as replacement animals or for sale as breeding stock, a fact that was confirmed by the trace work and the documentation of the final disposition of the calves of interest.
Response personnel ultimately identified 213 calves of interest to be traced. Of these, 208 were confirmed to have entered known rendering/slaughter channels, 4 were presumed to have entered rendering/slaughter channels, and 1 was purchased in cash through a livestock market with no buyer name or contact information (this animal was classified as untraceable. See Appendix 1). A calf was categorized as presumed to have entered rendering/slaughter channels if it passed through at least one livestock market subsequent to its original sale and could not be individually traced due to unknown resale date and new backtag, but all calves resold matching that description during an appropriate date range were purchased by known rendering/slaughter order buyers.
It was not possible to DNA test the calves that entered known rendering and slaughter channels – most were of an age in which they were likely to have been slaughtered prior to the time of the investigation. There were no calves traced to farms outside of rendering and slaughter channels.
Tracing of Birth Cohorts
Since there were essentially no records maintained on the index farm, it was necessary to compile the list of known birth cohorts using brucellosis CV tag numbers for this herd from the period 1991 to 1994. The calves vaccinated during that time period were part of the index cow’s birth cohort and tracing activities centered on finding those animals. There were 121 animals whose CV tag number and/or tattoo included them as part of the birth cohort. Of those 121 animals, 67 animals were definitively accounted for (42 were found in the index herd, removed, and tested BSE negative; 25 were identified as having left Farm A through the market system and were traced, 11 of those were reported slaughtered, 13 were classified as presumed dead, and 1 was found alive, euthanized, and tested BSE negative). Of the remaining 54 animals from the birth cohort, there may have been several that died within the index herd, but the majority likely left the herd without identification and would have been either re-tagged at the livestock market or consigned directly to slaughter without identification. To account for these remaining birth cohorts, all adult cattle that left the index farm since 1990 were traced as COI.
Tracing of Cattle of Interest
The investigation revealed that many animals left Farm A, arrived at markets without any identification tags, and were subsequently re-tagged at the market. Due to lack of farm records, it is unknown which of these re-tagged animals may have belonged to the birth cohort. As a result, all animals that may have left Farm A since 1990 were traced as COI. Additionally, animals from the index farm were sold not only under the index farm owner’s name and that of his wife, but also by other members of the owner’s immediate family; therefore, cattle sold from the index farm by all pertinent family members were traced. There were some older animals that left the index farm but were able to be excluded from further trace work because they were known not to have been part of the birth cohort or feed cohort of the index cow despite their being of the appropriate age. The index farm owner’s late father had maintained a herd of cattle separate from the index farm but which was added to the index farm in 1997. Complete herd test data and CV data from the GDB was obtained for the father’s herd and those animals were excluded from the tracing activities.
There were a total of 200 COI traced: 143 were reported to have been slaughtered (131 of those were confirmed as having been slaughtered), 1 is known to have died previously and was buried, 2 were found alive (1 was a known birth cohort that tested negative, 1 was determined not to be one of the cattle of interest due to her young age), 34 were classified as presumed dead, 20 were classified as untraceable. (See Appendix 1). Animals were confirmed at slaughter using GDB slaughter testing data or the hard copies of slaughter testing Form 4-54.
An animal was classified as presumed dead if records that could be used to advance the tracing of the animal were exhausted or did not exist, and the age of the animal at the time of the investigation was estimated to be at least 11 years old or older. Since the index herd was not a purebred or seedstock operation, and animals leaving the herd were unlikely to be purchased as replacement cattle, standard industry practices indicated that most adult animals that had left the herd would have been culled and slaughtered by the time they were in this age group. Additionally, this age cutoff was arrived at through review of market records and the specific years in which Farm A sold cattle through the market. An animal was classified as untraceable if all records to advance the tracing of the animal were exhausted or did not exist, and the age of the animal at the time of the investigation was estimated to be less than 11 years of age (the animal, therefore, could not be presumed dead).
Trace Herd 1
The owner of Trace Herd 1 was identified as having received one of the adult COI from the index herd. Trace Herd 1 contained 909 head of cattle in multiple pastures and was placed under hold order on 7/21/05. Upon completion of herd inventory, the animal of interest was not found within the herd. A GDB search of all recorded herd tests conducted on Trace Herd 1 and all market sales by the owner failed to locate the identification tag of the animal of interest and she was subsequently classified as untraceable. The hold order on Trace Herd 1 was released on 8/8/05.
Trace Herd 2
Trace Herd 2 was identified as having received one of the adult COI from the index herd. Trace Herd 2 contained 19 head of cattle on one pasture and was placed under hold order on 7/25/05. The owner of Trace Herd 2 identified the animal of interest by her eartag while he was feeding his cattle out of a bucket and individually penned her for inspection by field personnel. While the cow was identified as one of the animals that had left the index farm, her age by dentition was estimated to be only 5 years old, which was too young to have placed her as part of the birth or feed cohort of the index animal. She was classified as found alive but determined not to be one of the COI; the hold order on Trace Herd 2 was released on 7/26/05.
Trace Herd 3
The owner of Trace Herd 3 was identified as possibly having received an animal of interest. The herd was placed under hold order on 7/27/05. The herd inventory was conducted on 7/28/05. The animal of interest was not present within the herd, and the hold order was released on 7/28/05. The person who thought he sold the animal to the owner of Trace Herd 3 had no records and could not remember who else he might have sold the cow to. Additionally, a search of GDB for all cattle sold through the markets by that individual did not result in a match to the animal of interest. The animal of interest traced to this herd was classified as untraceable because all leads were exhausted.
Trace Herd 4
The owner of Trace Herd 4 was identified as having received one of the COI through an order buyer. Trace Herd 4 was placed under hold order on 7/29/05. A complete herd inventory was conducted on 8/22/05 and 8/23/05. There were 233 head of cattle that were examined individually by both State and Federal personnel for all man-made identification and brands. The animal of interest was not present within the herd. Several animals were reported to have died in the herd sometime after they arrived on the premises in April 2005. A final search of GDB records yielded no further results on the eartag of interest at either subsequent market sale or slaughter. With all leads having been exhausted, this animal of interest has been classified as untraceable. The hold order on Trace Herd 4 was released on 8/23/05.
Trace Herd 5
The owner of Trace Herd 5 was identified as having received two COI and was placed under hold order on 8/1/05. Trace Herd 5 is made up of 67 head of cattle in multiple pastures. During the course of the herd inventory, the owner located records that indicated that one of the COI, a known birth cohort, had been sold to Trace Herd 8 where she was subsequently found alive. Upon completion of the herd inventory, the other animal of interest was not found within the herd. A GDB search of all recorded herd tests conducted on Trace Herd 5 and all market sales by the owner failed to locate the identification tag of the animal of interest and she was subsequently classified as untraceable due to all leads having been exhausted. The hold order on Trace Herd 5 was released on 8/8/05.
Trace Herd 6
The owner of Trace Herd 6 was identified as possibly having received an animal of interest and was placed under hold order on 8/1/05. This herd is made up of 58 head of cattle on two pastures. A herd inventory was conducted and the animal of interest was not present within the herd. The owner of Trace Herd 6 had very limited records and was unable to provide further information on where the cow might have gone after he purchased her from the livestock market. A search of GDB for all cattle sold through the markets by that individual did not result in a match to the animal of interest. Additionally, many of the animals presented for sale by the owner of the herd had been re-tagged at the market effectually losing the traceability of the history of that animal prior to re-tagging. The animal of interest traced to this herd was classified as untraceable due to all leads having been exhausted. The hold order on Trace Herd 6 was released on 8/3/05.
Trace Herd 7
The owner of Trace Herd 7 was identified as having received an animal of interest and was placed under hold order on 8/1/05. Trace Herd 7 contains 487 head of cattle on multiple pastures in multiple parts of the State, including a unit kept on an island. The island location is a particularly rough place to keep cattle and the owner claimed to have lost 22 head on the island in 2004 due to liver flukes. Upon completion of the herd inventory, the animal of interest was not found present within Trace Herd 7. A GDB search of all recorded herd tests conducted on Trace Herd 7 and all market sales by the owner failed to locate the identification tag of the animal of interest. The cow was subsequently classified as untraceable. It is quite possible though that she may have died within the herd, especially if she belonged to the island unit. The hold order on Trace Herd 7 was released on 8/8/05.
Trace Herd 8
Trace Herd 8 received an animal of interest, which happened to be a known birth cohort of the index cow, from Trace Herd 5. Trace Herd 8 consists of 146 head of cattle that were placed under hold order on 8/4/05. A herd inventory was conducted, the birth cohort was found alive in the herd, and she was purchased and euthanized. The hold order on Trace Herd 8 was released on 8/4/05. The cow was sampled on 8/5/05 and BSE tested by ELISA at NVSL. Results were negative (as reported on 8/6/05); carcass disposal was completed by alkaline digestion.
Analysis of Data on Presumed Dead and Untraceable Animals
CEAH performed an analysis of the minimum estimated ages of those COI that were classified as either presumed dead or untraceable to determine the likely disposition of those animals based on their ages. Moreover, CEAH performed an analysis of the likely disposition of the one calf that was classified as untraceable during the investigation.
OF course, the birth and herd cohorts of this highly suspect, stumbling and staggering mad cow in Texas, will never be known ;
FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).
FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.
To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.
Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.
FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.
BSE UPDATE ALABAMA March 17, 2006
BSE Update From Alabama
News Date March 27, 2006
Alabama Agriculture Commissioner Ron Sparks and Alabama State Veterinarian Dr. Tony Frazier with the Alabama Department of Agriculture and Industries (ADAI) and USDA have provided an update on their ongoing joint investigation of the cow that died from bovine spongiform encephalopathy (BSE) in Alabama.
Since the investigation began, the ADAI and the USDA have followed multiple leads in the traceback process. At this time, 13 locations and 32 movements of cattle have been examined with 27 of those being substantially completed. Additional investigations of locations and herds will continue. In addition, state and federal officials have confirmed that a black bull calf was born in 2005 to the index animal (the red cow). The calf was taken by the owner to a local stockyard in July 2005 where the calf died. The calf was disposed of in a local landfill and did not enter the human or animal food chain.
Without a premises or animal ID program in place, the traceback process to find the herd of origin of the index cow is time-consuming and difficult. It includes conducting interviews, reviewing of records and documents, and testing of cattle DNA. State and federal officials have discovered several herds of interest and they are planning to use DNA testing to determine DNA linkage between the index cow and the herds. Through the DNA testing of these herds, investigators will attempt to find a genetic path that could lead to the herd of origin. Sparks stressed that the DNA testing being conducted on the herds is for genetic markers and is not a test for the disease BSE.
As part of the thorough investigative process, a large number of cattle may be tested in this phase and the number of herds included will continue to grow as the traceback progresses. Leads will be followed by state and federal officials until they are exhausted. Even when an index animal is traced to its birth herd, often cohorts of that animal are no longer in that herd. In addition, even if an animal's cohort has been exposed to the same infective material in feed, the other animals will not necessarily contract BSE.
BSE is not a contagious disease that spreads animal to animal, or animal to human. BSE spreads in cattle through the consumption of feed containing specified risk material (brain and spinal cord) derived from BSE infected cattle. The United States banned the use of such protein supplements in cattle feed since 1997. Sparks says that beef consumption in this country is safe and there are measures in place to see that it continues to be safe. For example, downer animals are not allowed to enter commerce for human consumption and there is a ban on feeding ruminant derived protein to cattle. (Contact: Bob Ehart)
News Contact: Bob Ehart; 202-296-9680
SNIP...see full text ;
FRIDAY, AUGUST 20, 2010
USDA: Animal Disease Traceability August 2010
Saturday, August 16, 2008
Qualitative Analysis of BSE Risk Factors in the United States February 13, 2000 at 3:37 pm PST (BSE red book)
48 hour traceback for BSE mad cow disease in the USA ???
NOT in your lifetime !
8 YEARS IN REVIEW OF THE MAD COW DEBACLE IN THE USA ;
TUESDAY, AUGUST 22, 2006
BSE ATYPICAL TEXAS AND ALABAMA UPDATE JANUARY 20, 2007
THURSDAY, AUGUST 17, 2017
JAVMA NEWS Atypical BSE found in Alabama cow September 01, 2017
THURSDAY, JULY 20, 2017
USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200
SUNDAY, JULY 23, 2017
atypical L-type BASE Bovine Amyloidotic Spongiform Encephalopathy BSE TSE PRION
SUNDAY, JULY 23, 2017
Experimental Infection of Cattle With a Novel Prion Derived From Atypical H-Type Bovine Spongiform Encephalopathy
WEDNESDAY, JULY 26, 2017
APHIS USDA Emerging Animal Disease Preparedness and Response Plan July 2017
THURSDAY, JULY 13, 2017
EFSA BSE Sixty cases of mad cow disease since 2001 breached feed ban likely the cause
Scientists investigate origin of isolated BSE cases
TUESDAY, AUGUST 8, 2017
Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy [Docket No. APHIS-2016-0092]
BSE YOUNGEST DOCUMENTED TO DATE 20 MONTHS
1992 20 26 15.02 16.02
1.6. YOUNGEST AND OLDEST CASES BY YEAR OF ONSET (FOR PASSIVE SURVEILLANCE CASES) AND ON YEAR OF SLAUGHTER (FOR ACTIVE SURVEILLANCE CASES) AS AT 03/09/2007 NB The last case in an animal aged 30 months or less was in 1996
YR OF ONSET AGE YOUNGEST CASE (mths) AGE 2nd YOUNGEST CASE (mths) AGE 2nd OLDEST (yrs.mths) OLDEST CASE (yrs.mths)
1986 30 33 5.03 5.07
1987 30 31 9.09 10
1988 24 27 10.02 11.01(2)
1989 21 24(4) 12(2) 15.04
1990 24(2) 26 13.03 14
1991 24 26(3) 14.02 17.05
1992 20 26 15.02 16.02
1993 29 30(3) 14.1 18.1
1994 30(2) 31(2) 14.05 16.07
995 24 32 14.09 15.05
1996 29 30 15.07 17.02
1997 37(7) 38(3) 14.09 15.01
1998 34 36 14.07 15.05
1999 39(2) 41 13.07 13.1
2000 40 42 17.08 19.09
2001 45 48 16.01 20.08
2002 47 48(2) 18.04 22.07
2003 46 49 18.07(2) 20.06
2004 49 52 17.04 22.07
2005 36 38 18.01 19.04
2006 48 58 17.05 19.09
2007 81(2) 88 15(02) 17.03
*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***
Sunday, March 20, 2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission
SEE MAD COW FEED VIOLATIONS AFER MAD COW FEED VIOLATIONS ;
Tuesday, April 19, 2016
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards Singeltary Comment Submission
16 years post mad cow feed ban August 1997 2013
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
17 years post mad cow feed ban August 1997
Monday, October 26, 2015
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
TUESDAY, JANUARY 17, 2017
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION
cwd to pig, orally ;
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Location: Virus and Prion Research
Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin
Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:
Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.
Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.6>
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:6>6>
This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.
CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.
Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
snip...see much more here ;
WEDNESDAY, APRIL 05, 2017
Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
MONDAY, AUGUST 14, 2017
Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02). The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
see new link url here ;
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
Chronic Wasting Disease (CWD)
If CWD could spread to people, it would most likely be through eating of infected deer and elk. In a 2006-2007 CDC survey of U.S. residents, nearly 20 percent of those surveyed said they had hunted deer or elk and more than two-thirds said they had eaten venison or elk meat. However, to date, no CWD infections have been reported in people.
Hunters must consider many factors when determining whether to eat meat from deer and elk harvested from areas with CWD, including the level of risk they are willing to accept. Hunters harvesting wild deer and elk from areas with reported CWD should check state wildlife and public health guidance to see whether testing of animals is recommended or required in a given state or region. In areas where CWD is known to be present, CDC recommends that hunters strongly consider having those animals tested before eating the meat.
Tests for CWD are monitoring tools that some state wildlife officials use to look at the rates of CWD in certain animal populations. Testing may not be available in every state, and states may use these tests in different ways. A negative test result does not guarantee that an individual animal is not infected with CWD, but it does make it considerably less likely and may reduce your risk of exposure to CWD.
To be as safe as possible and decrease their potential risk of exposure to CWD, hunters should take the following steps when hunting in areas with CWD:
Do not shoot, handle or eat meat from deer and elk that look sick or are acting strangely or are found dead (road-kill). When field-dressing a deer: Wear latex or rubber gloves when dressing the animal or handling the meat. Minimize how much you handle the organs of the animal, particularly the brain or spinal cord tissues. Do not use household knives or other kitchen utensils for field dressing. Check state wildlife and public health guidance to see whether testing of animals is recommended or required. Recommendations vary by state, but information about testing is available from many state wildlife agencies. Strongly consider having the deer or elk tested for CWD before you eat the meat. If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals. If your animal tests positive for CWD, do not eat meat from that animal. The U.S. Department of Agriculture’s Animal and Plant Health Inspection Service regulates commercially farmed deer and elk. The agency operates a national CWD herd certification program. As part of the voluntary program, states and individual herd owners agree to meet requirements meant to decrease the risk of CWD in their herds. Privately owned herds that do not participate in the herd certification program may be at increased risk for CWD.
Page last reviewed: August 17, 2017 Page last updated: August 17, 2017 Content source: Centers for Disease Control and Prevention National Center for Emerging and Zoonotic Infectious Diseases (NCEZID) Division of High-Consequence Pathogens and Pathology (DHCPP)
> 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).***
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
*** WDA 2016 NEW YORK ***
The species barriers and public health threat of CWD and BSE prions
Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University
*** We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions.
*** CWD is unique among prion diseases in its rapid spread in natural populations.
*** BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species.
*** This adaptation has consequences for surveillance of humans exposed to CWD.
Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders
you can see more evidence here ;
2017 PRION 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
Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO
PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS
*** PRION 2017 CONFERENCE VIDEO
SATURDAY, JULY 29, 2017
Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
TUESDAY, JULY 04, 2017
*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD
SUNDAY, JULY 16, 2017
*** Temporal patterns of chronic wasting disease prion excretion in three cervid species ***
TUESDAY, SEPTEMBER 12, 2017
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
TUESDAY, MARCH 28, 2017
*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***
BSE, Scrapie, and CWD, Zoonosis, Zoonotic Disease
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.
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.
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 5, Article number: 11573 (2015) doi:10.1038/srep11573
Download Citation EpidemiologyNeurological manifestationsPrion diseases Received: 16 February 2015 Accepted: 28 May 2015 Published online: 30 June 2015
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.
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.
Saturday, April 23, 2016
Scrapie ZOONOSIS PRION CONFERENCE TOKYO 2016
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 ***
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
Monday, June 20, 2016
Specified Risk Materials SRMs BSE TSE Prion Program
Saturday, April 16, 2016
APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
THURSDAY, JUNE 22, 2017
World Organisation for Animal Health (OIE) to establish liaison office in College Station, Texas
MONDAY, JANUARY 4, 2016
Long live the OIE, or time to close the doors on a failed entity?
WEDNESDAY, MARCH 11, 2015
OIE and Centers for Disease Control and Prevention Reinforce Collaboration
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
OIE STILL FLOUNDERING WITH TSE PRION DISEASE, letting it spread around the globe with the bse mrr policy, and still ignoring cwd, and making atypical scrapie a legal trading commodity.
THURSDAY, MAY 30, 2013
World Organization for Animal Health (OIE) has upgraded the United States' risk classification for mad cow disease to "negligible" from "controlled", and risk further exposing the globe to the TSE prion mad cow type disease
TUESDAY, JULY 17, 2012
O.I.E. BSE, CWD, SCRAPIE, TSE PRION DISEASE Final Report of the 80th General Session, 20 - 25 May 2012
BSE TSE PRION USDA OIE NEEDLESS CONFLICT
2001 FDA CJD TSE Prion Singeltary Submission
*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
THURSDAY, AUGUST 17, 2017
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017
FRIDAY, AUGUST 11, 2017
Infectivity in bone marrow from sporadic CJD patients
Bioassays in transgenic mice expressing the human prion protein revealed the presence of unexpectedly high levels of infectivity in the bone marrow from seven out of eight sCJD cases. These findings may explain the presence of blood-borne infectivity in sCJD patients. They also suggest that the distribution of prion infectivity in peripheral tissues in sCJD patients could be wider than currently believed, with potential implications for the iatrogenic transmission risk of this disease.
THURSDAY, AUGUST 10, 2017
Minimise transmission risk of CJD and vCJD in healthcare settings Updated 10 August 2017
*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery ***
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
National Prion Center could lose all funding just as concern about CWD jumping to humans rises
SATURDAY, JULY 15, 2017
*** National Prion Center could lose all funding just as concern about CWD jumping to humans rises
BSE TSE PRION USDA OIE NEEDLESS CONFLICT
Tracking spongiform encephalopathies in North America
Published: August 2003
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.”
49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD) the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.
Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). "I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source."
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.
To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.
Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.
Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.
"Getting data on TSEs in the USA from the government is like pulling teeth", Singeltary argues. "You get it when they want you to have it, and only what they want you to have."
Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that "current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings"; adding that, "the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure". The USA should develop a system modelled on that established in the UK, he points out.
Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunters "two of whom were friends" who died from pathologically confirmed CJD, says that "at present there are insufficient data to claim transmission of CWD into humans"; adding that "[only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further". Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.
CDC spokesman Ermias Belay says that the CDC "will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat". He notes that although "the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100%" and that "[we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited".
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al  have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
2 January 2000 British Medical Journal U.S.
Scientist should be concerned with a CJD epidemic in the U.S., as well
15 November 1999 British Medical Journal hvCJD in the USA * BSE in U.S.
Terry S. Singeltary Sr.