Why is USDA "only" testing 25,000 samples a year?
SIMPLE MATH, IF YOU DON'T TEST IN SUFFICIENT NUMBERS, YOU DON'T FIND, PROBLEM SOLVED!
Why is USDA "only" testing 25,000 samples a year?
USDA's surveillance strategy is to focus on the targeted populations where we are most likely to find disease if it is present. This is the most effective way to meet both OIE and our domestic surveillance standards. After completing our enhanced surveillance in 2006 and confirming that our BSE prevalence was very low, an evaluation of the program showed that reducing the number of samples collected to 40,000 samples per year from these targeted, high risk populations would allow us to continue to exceed these standards. In fact, the sampling was ten times greater than OIE standards. A subsequent evaluation of the program in 2016 using data collected over the past 10 years showed that the surveillance standards could still be met with a further reduction in the number of samples collected by renderers and 3D/4D establishments which have a very low OIE point value because the medical history of these animals is usually unknown. Therefore, in 2016, the number of samples to be tested was reduced to 25,000 where it remains today.
How can USDA find every case of BSE in the United States when you are only testing 25,000 animals? The goal of our BSE surveillance program, even under the enhanced program, has never been to detect every case of BSE. Our goal is determine whether the disease exists at very low levels in the U.S. cattle population, and we do this by testing those animals most likely to have BSE. It is the longstanding system of interlocking safeguards, including the removal of specified risk materials - or the parts of an animal that would contain BSE - at slaughter and the FDA's ruminant-to- ruminant feed ban that protect public and animal health from BSE.
Why didn’t USDA continue to test animals at the enhanced surveillance level? USDA's 2004-2006 enhanced surveillance program was initiated in response to the first detection of BSE in the United States and was designed to detect the overall prevalence of the disease in this country. This required a very intensive effort and it allowed us to estimate extremely low prevalence levels of disease. Once that prevalence level was determined, USDA modified its testing levels to monitor any changes in the level of disease. Our current testing of approximately 25,000 targeted animals a year allows USDA to detect BSE at the very low level of less than 1 case per million adult cattle, assess any change in the BSE status of U.S. cattle, and identify any rise in BSE prevalence in this country.
FOOD AND DRUG ADMINISTRATION DEPARTMENT OF HEALTH AND HUMAN SERVICES
This transcripts has not been edited or corrected, but appears as received from the commercial transcribing service. Accordingly, the food and Drug Administration makes no representation as to its accuracy.
Meeting of: TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES ADVISORY COMMITTEE September 18, 2006
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Let's move to North America and a brief update here on BSE in Canada. As a reminder, Canada has been doing active surveillance, targeted surveillance, in the population where they are most likely to find disease since 1991.
As everybody knows, in 2003, they identified their first native case, in May of 2003. After that period, they significantly increased their surveillance.
So, these are just their numbers, in 2003, about 5,700 samples, two positives. One was the one that we found here in the United States in Washington State in December of 2003. So, increasing their surveillance again, with no cases in 2004, two in 2005, and five to date in 2006.
They did provide a very detailed epidemiological summary that was made public in January of this year. They are continuing that work and hopefully will have some more updates out fairly soon.
What this summary shows, it really talks about their geographic cluster theory, and the idea that the links between rendering, feed production, livestock production, tend to occur in clusters, in a fairly well defined geographic area. It is only logical, then, that that would be where the disease could cycle, would be in that type of a cluster.
What this report shows, which went through the first five cases, I believe, it does define links between most of these cases and links in this cluster.
There are also linkages in the more recent cases, again, to that same cluster and, as I mentioned earlier, hopefully they will be putting out some more updates with as good epi work in the near future.
To focus a bit on Japan, BSE was first identified in Japan in late 2001. Actually, it was September 2001. They imposed a feed ban, than, after that first diagnosis. So, the feed ban has only been in place since 2001.
Here is the number of cases. It stays about the same here until the past two years, where it has jumped up a bit.
One note about Japan. A lot of their surveillance and the testing numbers that you see have been primarily in clinically normal animals, or animals presented at slaughter.
It has only been since about 2004 that they have really increased their focus on the targeted animals or the risk population, as we would define it.
Now, let's move to the United States. As everybody knows, we have been doing active surveillance in the United States since 1990, and we are targeting the population where the disease is most likely to be diagnosed. That is the most efficient way for us to conduct a surveillance system.
The assumption is that if we can't find disease in that population, then it is even more unlikely for us to find it in the non-targeted population.
So, we can use the data that we get from that targeted sampling to extrapolate information to the broader cattle population.
Our targeted population has always been, and continues to be, those animals that have some type of a clinical abnormality that could even remotely be considered consistent with BSE.
So, these would be non-ambulatory animals, dead stock, which are animals that die for some unexplained reason, central nervous system cases, either called to our field people or on farms.
We work with veterinary diagnostic labs, public health labs, for rabies negative animals, and then we also work with our colleagues in FSIS, for those animals that are condemned on ante-mortem inspections when presented to slaughter.
Everybody knows we ran an enhanced BSE surveillance program that began in June 2004. Our initial intention was to run that for 12 to 18 months, with the goal of getting as many samples from the targeted population as we could.
We actually ran on a bit longer than the 18 months and ran through August of 2006, greater than 785,000 tests during that whole enhanced program. During that time frame, there were two positives identified during that effort.
Just to show on a monthly basis what we did in our enhanced program, as you can see, there is a little bit of a cycle.
With the population that we are sampling -- these are animals that are clinically abnormal in some way, and with the facilities where we were collecting, these are animal disposal facilities, rendering facilities, 3D, 4D, salvage slaughter plants.
Animals tend to get sicker, die, be culled in the winter. So, we always had a little peak in the winter. I just wanted to show folks, most folks don't quite understand exactly where we were sampling and why that might occur.
Let me explain a bit about OIE standards. These are the international animal health standards for BSE surveillance.
This reflects changes to those standards in May 2005. This is what we are using as our guidance for how we do surveillance from here on out.
It is a weighted point system. Previously it was a simple table that said if you had cattle population X, you need to get Y number of samples.
Now it is an interesting system where it recognizes that you are more likely to find the disease in certain subpopulations.
So, you get more points for that population where you are most likely to find the disease. We have four surveillance streams.
They are clinical suspect, which would be those animals with really pretty classic clinical signs of BSE, causality slaughter -- these would be those animals -- these are European terms, sometimes they fit with North American terms, sometimes they don't.
Casualty slaughter are those animals that are clinically abnormal. They would be condemned on antemortem inspections.
So, these are those non-ambulatory animals, could be the very weak, emaciated, thin, just some type of a subtle abnormality.
Fallen stock are dead stock, essentially, those animals that die for unknown reasons. Then, healthy slaughter is pretty self explanatory.
I don't know if you can actually read this. Hopefully you can. This shows the point system where it recognizes that you are most likely to find disease here in a clinical suspect.
So, you get 750 points for a clinical suspect between four and seven years old. That subpopulation is where you are really most likely to find disease if it is present.
You get essentially limited points for sampling in routine slaughter. So, what countries can do to use this table, you can access whatever population you like to meet the standards, and then the table says you need to get X number of points for a certain design prevalence, 300,000 points over a seven year period at a design prevalence of one in 100,000.
So, a country can then use this table and figure out what type of samples in what population they want to sample to reach those numbers of points.
So, you could sample a pretty small number of clinical suspects and reach that point value, or design prevalence, or you can sample a much higher number of routine slaughters. It recognizes that you can access both of those populations. It is just how many samples you want to get.
We did a summary of not only our enhanced surveillance program, but also what we have done for surveillance for the past seven years. That was made public in April of this year.
Just to give you kind of a graphic example of how to do this point system, these are the points that we obtained in our surveillance for the past seven years.
So, close to three million OIE points over the past seven years in the different surveillance streams. For those who ask about this healthy slaughter one, knowing that we really are not sampling healthy slaughter animals, this is a function of our data base.
Especially in some of these earlier years, our data might be somewhat limited. If we could not pull out of the data base a specific clinical sign, to assign this to one of the other surveillance streams, by default it would go into the healthy slaughter for this calculation.
So, with that summary of data, not only did we put out there just a raw data summary, we also did an estimate of BSE prevalence in the United States.
We used two methods to do this. One is the BsurvE model, which is a model developed by the Europeans with some input from our colleagues down under in New Zealand.
It looks at what we know from the epidemiology of the disease in Europe and factors in population data when animals are most likely to leave the population.
It can be used to help a country set up a surveillance system, can also be used to estimate prevalence.
We then also tweaked this model a bit and came up with what we call the Baysian birth cohort model, which incorporates what we would expect to see the effects of a feed ban, which the Bsurv doesn't show, and it also sets up some linkages between birth cohorts.
We also did several sensitivity analyses in this report, just to make sure that our assumptions weren't way off base.
The overall conclusion was that the BSE prevalence in the United States is very low, less than one infected animal per one million adult cattle.
If you are interested in most likely values, with the Bsurv model the most likely value was seven infected animals, with the BBC model the most likely value was four.
With the sensitivity analyses, those values ranged from one up to about 40, which all of those then led us to this conclusion, pretty solid, that the prevalence is less than one infected animal per one million cattle.
So, what are we doing now and where are we going from there? We have used these same methods and have moved forward into what we call ongoing surveillance.
We have been transitioning here since the end of August. What we figure is about 40,000 samples per year, again, still from this targeted population.
This will allow us to continue to monitor the status of U.S. cattle and will allow us to detect prevalence if it starts to increase.
We did this calculation, again, based on our analysis of the enhanced surveillance data and using the Bsurv model.
We first of all looked at OIE recommendations, which are at a design prevalence of one in 100,000. We wanted to make that a bit more sensitive. We wanted to stick with one per one million. So, we used the Bsurv model to estimate sample numbers and points.
Again, think of that basic premise that I described for the OIE, with a different number of points for different subpopulations.
With this, we need to get three million analytical points over a seven year time frame. When we look at what we did in enhanced, we averaged about 9.5 points per sample. So, we just divided and that gets you to about 40,000 samples per year, assuming we will get the same average points over a seven year time frame.
That is a very quick run through of both an update of what is going on in the world, what the international standards are, and where we are headed in the future. I think I have time for questions.
DR. TELLING: Yes, you do. Thank you, Dr. Ferguson. Are there any questions?
DR. GESCHWIND: Dr. Ferguson, when you were talking about the Japanese cases, could you comment about the ages of the animals?
Before 2004, I believe they were testing every cattle within a certain age range, and that they did find BSE cattle among those that would not be identified with the current methods in the United States. Can you comment on that?
DR. FERGUSON: I am not quite sure what you expect me to comment on. I think as we all know Japan, in 2001, by their regulations, required that every animal slaughtered, regardless of age, be tested for BSE.
They have recently changed that reg slightly, and it is only animals 20 months of age and older be tested at slaughter.
They did find two animals, a 21 month old and a 23 month old -- unless my memory escapes me at this point in time -- young animals, apparently normal at slaughter.
They were positive on the screening tests, negative on IHC, and then positive again with the way Japan has done the western blot.
They have put those into mice to see if there is transmission. To the best of my knowledge, those results aren't out there yet, but there is no indication that they have gotten any signs of disease in those mice.
snip...see full report;
https://www.fda.gov/animal-veterinary/bovine-spongiform-encephalopathy/ruminant-feed-inspections
October 6th-12th, 126th Meeting 2022 Resolutions
RESOLUTION NUMBER: 33 Approved
SOURCE: COMMITTEE ON CATTLE AND BISON
SUBJECT MATTER: Cattle Contact Tracing System
BACKGROUND INFORMATION:
Animal health officials across the United States (US) are tasked with protecting the cattle industry. Animal disease traceability (ADT) is a critical component to mitigating potentially economic significant diseases that could be detrimental to normal business operations. Traces are routinely conducted by animal health officials on cattle to mitigate potential disease spread. Traditional components of ADT have limited animal health officials to effectively perform a quick traceback and subsequent response time. Current ADT tools that are available for animal health officials allow for a limited trace on a current animal forward and backward (bookend tracing). Additional contacts during a trace can be determined throughout the process. However, with the current information flow, these close contacts may take additional time that could hinder a response which could be economically detrimental to the industry in the case of a potential foreign animal disease such as foot and mouth disease.
In early 2018, Kansas cattle producers led an effort that resulted in the CattleTrace pilot project which began work to develop a purpose-built infrastructure to track cattle movement through the supply chain (contact tracing) to collect the minimal data necessary for contact tracing. The data points include an individual animal identification (ID) number, a GPS location, and date and time of the read to track animals in the event of a disease outbreak. Tag readers were located at producers’ operations, livestock markets, feed yards and beef processors. The pilot project was a collaborative partnership between the state of Kansas, United States Department of Agriculture (USDA), and producer stakeholders.
The goal for the pilot project was to:
Develop a purpose-built infrastructure for a contact traceability system,
Evaluate the infrastructure,
Determine the value proposition of the system at each production segment and across the industry.
Simultaneously, multiple other states including Florida, Texas, and Kentucky conducted pilot projects with collaborative funding from USDA, Animal and Plant Health Inspection Service. Project objectives ranged from testing effectiveness of both forms of radio
USAHA 2022 Resolution 33 / page 2
frequency identification (RFID) along with different forms of RFID identification, such as ultra-high frequency backtags.
In January 2020, these efforts from major beef producing regions announced a partnership to form US CattleTrace, a stand-alone, non-profit organization solely focused on animal disease contact traceability. Today, the goal is to develop a national infrastructure for disease contact traceability used by state and federal animal health officials fed by private industry’s use of the infrastructure for individualized management practices. The organization aims to continue pursuing a voluntary, hands-free, speed of commerce contact tracing system. The organization will utilize the most current forms of ID that allow for the animal disease traceability system to operate at the speed of commerce within multiple segments of the cattle industry.
State and federal animal health officials’ continued support of RFID tags and collaboration with industry directed at utilization of a contact tracing infrastructure would directly enhance animal disease traceability efforts of cattle on a national level for a quick, accurate and timely response.
Additionally, sharing of existing contact trace data (ID, time, date, location) by individual state and federal animal health officials with contact tracing systems such as US CattleTrace would serve to expand the database size and geography enhancing the effectiveness and accuracy of contact traces.
RESOLUTION:
The United States Animal Health Association urges state animal health officials and the United States Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services to work with industry to enhance cattle contact tracing efforts for economically significant diseases through collaboration and sharing of current cattle contact traceability data. This data should utilize and grow the cattle contact trace infrastructure in which readers can collect and share the critical datapoints (ID, Time, Date & GPS Location).
SE1796 Atypical Prion Proteins in cattle - SE1796
***>Assuming no other factors influenced the levels of correct diagnosis and that the numbers estimated for 1997 to 1999 were a true representation of the potential under-diagnosis of the entire epidemic up until 1999, then the total number of missed cases positive for BSE could have been in the region of 5,500.
***>As a result, using more sensitive diagnostic assays, we were able to diagnose BSE positive cattle from the years 1997-1999 inclusive that were originally negative by vacuolation. From these data we have estimated that approximately 3% of the total suspect cases submitted up until the year 1999 were mis-diagnosed.
YOU know, Confucius is confused again LOL, i seem to have remembered something in line with this here in the USA...
USDA did not test possible mad cows
By Steve Mitchell
United Press International
Published 6/8/2004 9:30 PM
WASHINGTON, June 8 (UPI) -- The U.S. Department of Agriculture claims ittested 500 cows with signs of a brain disorder for mad cow disease last year, but agency documents obtained by United Press International show the agency tested only half that number.
"These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."
THIS WAS DONE FOR A REASON!
THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine, and these were probably from the most high risk cattle pool, the ones the USDA et al, SHOULD have been testing. ...TSS
TEXAS 2ND MAD COW THAT WAS COVERED UP, AFTER AN ACT OF CONGRESS, AND CALLS FROM TSE PRION SCIENTIST AROUND THE GLOBE, THIS 2ND MAD COW IN TEXAS WAS CONFIRMED
THE USDA MAD COW FOLLIES POSITIVE TEST COVER UP
JOHANNS SECRET POSTIVE MAD COW TEST THAT WERE IGNORED
OIG AND THE HONORABLE FONG CONFIRMS TEXAS MAD AFTER AN ACT OF CONGRESS 7 MONTHS LATER
TEXAS MAD COW
THEY DID FINALLY TEST AFTER SITTING 7+ MONTHS ON A SHELF WHILE GW BORE THE BSE MRR POLICY, i.e. legal trading of all strains of TSE. now understand, i confirmed this case 7 months earlier to the TAHC, and then, only after i contacted the Honorable Phyllis Fong and after an act of Congress, this animal was finally confirmed ;
During the course of the investigation, USDA removed and tested a total of 67 animals of interest from the farm where the index animal's herd originated. All of these animals tested negative for BSE. 200 adult animals of interest were determined to have left the index farm. Of these 200, APHIS officials determined that 143 had gone to slaughter, two were found alive (one was determined not to be of interest because of its age and the other tested negative), 34 are presumed dead, one is known dead and 20 have been classified as untraceable. In addition to the adult animals, APHIS was looking for two calves born to the index animal. Due to record keeping and identification issues, APHIS had to trace 213 calves. Of these 213 calves, 208 entered feeding and slaughter channels, four are presumed to have entered feeding and slaughter channels and one calf was untraceable.
Executive Summary In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample from November 2004, that had originally been classified as negative on the immunohistochemistry test, was confirmed positive on SAF immunoblot (Western blot). The U.S. Department of Agriculture (USDA) identified the herd of origin for the index cow in Texas; that identification was confirmed by DNA analysis. USDA, in close cooperation with the Texas Animal Health Commission (TAHC), established an incident command post (ICP) and began response activities according to USDA’s BSE Response Plan of September 2004. Response personnel removed at-risk cattle and cattle of interest (COI) from the index herd, euthanized them, and tested them for BSE; all were negative. USDA and the State extensively traced all at-risk cattle and COI that left the index herd. The majority of these animals entered rendering and/or slaughter channels well before the investigation began. USDA’s response to the Texas finding was thorough and effective.
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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.
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.
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4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
Audit Report Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy (BSE) Surveillance Program – Phase II and Food Safety and Inspection Service Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III
UNITED STATES DEPARTMENT OF AGRICULTURE OFFICE OF INSPECTOR GENERAL Washington, D.C. 20250 January 25, 2006 REPLY TO ATTN OF: 50601-10-KC TO: W. Ron DeHaven Administrator Animal and Plant Health Inspection Service Barbara Masters Administrator Food Safety and Inspection Service ATTN: William J. Hudnall Deputy Administrator Marketing Regulatory Program Business Services William C. Smith Assistant Administrator Office of Program Evaluation, Enforcement, and Review FROM: Robert W. Young /s/ Assistant Inspector General for Audit SUBJECT: Animal and Plant Health Inspection Service - Bovine Spongiform Encephalopathy (BSE) Surveillance Program - Phase II and Food Safety and Inspection Service - Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III This report presents the results of our audit of the enhanced BSE surveillance program and controls over specified risk materials and advanced meat recovery products. Your written response to the official draft report, dated January 20, 2006, is included as exhibit G with excerpts of the response and the Office of Inspector General’s (OIG) position incorporated into the Findings and Recommendations section of the report, where applicable. We accept the management decisions for all recommendations. Please follow your agency’s internal procedures in forwarding documentation for final action to the Office of the Chief Financial Officer (OCFO). We are providing a separate memorandum to the agencies and OCFO that provides specific information on the actions to be completed to achieve final action. We appreciate your timely response and the cooperation and assistance provided to our staff during the audit USDA/OIG-A/50601-10-KC/ Page i
Executive Summary
Animal and Plant Health Inspection Service - Bovine Spongiform Encephalopathy (BSE) Surveillance Program - Phase II and Food Safety and Inspection Service - Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III
Results in Brief This report evaluates elements of the interlocking safeguards in place to protect United States (U.S.) beef from Bovine Spongiform Encephalopathy, widely known as BSE or "mad cow disease." Since 1990, the U.S. Department of Agriculture (USDA), Animal and Plant Health Inspection Service (APHIS), has led a multi-agency effort to monitor and prevent BSE from entering the food supply. After discovering a BSE-positive cow in December 2003, APHIS expanded its BSE surveillance program. To further protect the food supply, USDA banned materials identified as being at risk of carrying BSE (specified risk materials (SRM)), such as central nervous system tissue. As part of this effort, USDA’s Food Safety and Inspection Service (FSIS) required beef slaughter and processing facilities to incorporate controls for handling such materials into their operational plans. Onsite FSIS inspectors also inspect cattle for clinical signs in order to prevent diseased animals from being slaughtered for human consumption. To evaluate the effectiveness of the safeguards, we assessed APHIS’ implementation of the expanded surveillance program, as well as FSIS’ controls to prevent banned SRMs from entering the food supply.
In June 2004, APHIS implemented its expanded surveillance program; participation by industry in this surveillance program is voluntary. As of May 2005, over 350,000 animals were sampled and tested for BSE. To date, two animals tested positive for BSE; one tested positive after implementation of the expanded surveillance program.
USDA made significant efforts to implement the expanded BSE surveillance program. Much needed to be done in a short period of time to establish the necessary processes, controls, infrastructure, and networks to assist in this effort. In addition, extensive outreach and coordination was undertaken with other Federal, State, and local entities, private industry, and laboratory and veterinary networks. This report provides an assessment as to the progress USDA made in expanding its surveillance effort and the effectiveness of its controls and processes. This report also discusses the limitations of its program and data in assessing the prevalence of BSE in the U.S. herd.
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40 ELISA test procedures require two additional (duplicate) tests if the initial test is reactive, before final interpretation. If either of the duplicate tests is reactive, the test is deemed inconclusive.
41 Protocol for BSE Contract Laboratories to Receive and Test Bovine Brain Samples and Report Results for BSE Surveillance Standard Operating Procedure (SOP), dated October 26, 2004.
42 The NVSL conducted an ELISA test on the original material tested at the contract laboratory and on two new cuts from the sample tissue.
43 A visual examination of brain tissue by a microscope.
44 A localized pathological change in a bodily organ or tissue.
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PLEASE SEE FLAMING EVIDENCE THAT THE USDA ET AL COVERED UP MAD COW DISEASE IN TEXAS ;
PAGE 43;
Section 2. Testing Protocols and Quality Assurance Controls
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FULL TEXT 130 PAGES
Comments on technical aspects of the risk assessment were then submitted to FSIS.
Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary.
This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:
Owens, Julie From: Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent: Monday, July 24, 2006 1:09 PM To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98 8/3/2006
Greetings FSIS, I would kindly like to comment on the following ;
Suppressed peer review of Harvard study October 31, 2002.
October 31, 2002 Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States Conducted by the Harvard Center for Risk Analysis, Harvard School of Public Health and Center for Computational Epidemiology, College of Veterinary Medicine, Tuskegee University Final Report Prepared for U.S. Department of Agriculture Food Safety and Inspection Service Office of Public Health and Science Prepared by RTI Health, Social, and Economics Research Research Triangle Park, NC 27709 RTI Project Number 07182.024
Thursday, April 9, 2009
Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed Thursday, April 09, 2009
Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed
FULL TEXT OF GOA REPORT BELOW (takes a while to load)
2. Mad Cow Disease: Improvements in the Animal Feed Ban and Other Regulatory Areas Would Strengthen U.S. Prevention Efforts. GAO-02-183, January 25.
8 hr BSE confirmation turnaround took 7+ months to confirm this case, so the BSE MRR policy could be put into place. ...TSS
-------- Original Message --------
Subject: re-USDA's surveillance plan for BSE aka mad cow disease
Date: Mon, 02 May 2005 16:59:07 -0500
From: "Terry S. Singeltary Sr."
Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at OIG, ...............
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There will be several more emails of my research to follow. I respectfully request a full inquiry into the cover-up of TSEs in the United States of America over the past 30 years. I would be happy to testify...
Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box , Bacliff, Texas USA 77518 xxx xxx xxxx
Date: June 14, 2005 at 1:46 pm PST
In Reply to:
Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding further analysis of BSE Inconclusive Test Results
posted by TSS on June 13, 2005 at 7:33 pm:
Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary for Marketing and Regulatory Programs resigns. Three days later same mad cow found in November turns out to be positive. Both resignation are unexpected. just pondering... TSS
Sunday, January 10, 2021
APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission June 17, 2019
APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission
Greetings APHIS et al,
I would kindly like to comment on APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], and my comments are as follows, with the latest peer review and transmission studies as references of evidence.
THE OIE/USDA BSE Minimal Risk Region MRR is nothing more than free pass to import and export the Transmissible Spongiform Encephalopathy TSE Prion disease. December 2003, when the USDA et al lost it's supposedly 'GOLD CARD' ie BSE FREE STATUS (that was based on nothing more than not looking and not finding BSE), once the USA lost it's gold card BSE Free status, the USDA OIE et al worked hard and fast to change the BSE Geographical Risk Statuses i.e. the BSE GBR's, and replaced it with the BSE MRR policy, the legal tool to trade mad cow type disease TSE Prion Globally. The USA is doing just what the UK did, when they shipped mad cow disease around the world, except with the BSE MRR policy, it's now legal.
Also, the whole concept of the BSE MRR policy is based on a false pretense, that atypical BSE is not transmissible, and that only typical c-BSE is transmissible via feed. This notion that atypical BSE TSE Prion is an old age cow disease that is not infectious is absolutely false, there is NO science to show this, and on the contrary, we now know that atypical BSE will transmit by ORAL ROUTES, but even much more concerning now, recent science has shown that Chronic Wasting Disease CWD TSE Prion in deer and elk which is rampant with no stopping is sight in the USA, and Scrapie TSE Prion in sheep and goat, will transmit to PIGS by oral routes, this is our worst nightmare, showing even more risk factors for the USA FDA PART 589 TSE PRION FEED ban.
The FDA PART 589 TSE PRION FEED ban has failed terribly bad, and is still failing, since August 1997. there is tonnage and tonnage of banned potential mad cow feed that went into commerce, and still is, with one decade, 10 YEARS, post August 1997 FDA PART 589 TSE PRION FEED ban, 2007, with 10,000,000 POUNDS, with REASON, Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. you can see all these feed ban warning letters and tonnage of mad cow feed in commerce, year after year, that is not accessible on the internet anymore like it use to be, you can see history of the FDA failure August 1997 FDA PART 589 TSE PRION FEED ban here, but remember this, we have a new outbreak of TSE Prion disease in a new livestock species, the camel, and this too is very worrisome.
WITH the OIE and the USDA et al weakening the global TSE prion surveillance, by not classifying the atypical Scrapie as TSE Prion disease, and the notion that they want to do the same thing with typical scrapie and atypical BSE, it's just not scientific.
WE MUST abolish the BSE MRR policy, go back to the BSE GBR risk assessments by country, and enhance them to include all strains of TSE Prion disease in all species. With Chronic Wasting CWD TSE Prion disease spreading in Europe, now including, Norway, Finland, Sweden, also in Korea, Canada and the USA, and the TSE Prion in Camels, the fact the the USA is feeding potentially CWD, Scrapie, BSE, typical and atypical, to other animals, and shipping both this feed and or live animals or even grains around the globe, potentially exposed or infected with the TSE Prion. this APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], under it's present definition, does NOT show the true risk of the TSE Prion in any country. as i said, it's nothing more than a legal tool to trade the TSE Prion around the globe, nothing but ink on paper.
AS long as the BSE MRR policy stays in effect, TSE Prion disease will continued to be bought and sold as food for both humans and animals around the globe, and the future ramifications from friendly fire there from, i.e. iatrogenic exposure and transmission there from from all of the above, should not be underestimated. ...
SUNDAY, OCTOBER 16, 2022
USDA Transmissible Spongiform Encephalopathy TSE Prion Action Plan National Program 103 Animal Health 2022-2027
APHIS Indemnity Regulations [Docket No. APHIS-2021-0010] RIN 0579-AE65 Singeltary Comment Submission
Comment from Singeltary Sr., Terry
Posted by the Animal and Plant Health Inspection Service on Sep 8, 2022
https://www.regulations.gov/comment/APHIS-2021-0010-0003
https://downloads.regulations.gov/APHIS-2021-0010-0003/attachment_1.pdf
August 2007
HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory
TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2007. With all the science to date refuting it, to continue to validate this myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, surgical, blood, medical, cosmetics etc. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
This would further have to be broken down to strain of species and then the route of transmission would further have to be broken down. Accumulation and Transmission are key to the threshold from sub-clinical to clinical disease, and key to all this, is to stop the amplification and transmission of this agent, the spreading of, no matter what strain. In my opinion, to continue with this myth that the U.K. strain of BSE (one strain TSE in cows), and the nv/v CJD (one strain TSE humans) and that all the rest of human TSE are just one single strain i.e. sporadic CJD (when to date there are 6 different phenotypes of sCJD, and growing per Gambetti et al), and that no other animal TSE transmits to humans, to continue with this masquerade will only continue to spread, expose, and kill, who knows how many more in the years and decades to come. ONE was enough for me, My Mom, hvCJD i.e. Heidenhain Variant CJD, DOD 12/14/97 confirmed, which is nothing more than another mans name added to CJD, like CJD itself, Jakob and Creutzfeldt, or Gerstmann-Straussler-Scheinker syndrome, just another CJD or human TSE, named after another human.
WE are only kidding ourselves with the current diagnostic criteria for human and animal TSE, especially differentiating between the nvCJD vs the sporadic CJD strains and then the GSS strains and also the FFI fatal familial insomnia strains or the ones that mimics one or the other of those TSE? Tissue infectivity and strain typing of the many variants
Manuscript
of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
Terry S. Singeltary Sr. P.O. Box Bacliff, Texas USA 77518 flounder9@verizon.net
[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle
9/13/2005
PDF]Freas, William TSS SUBMISSION File Format: PDF/Adobe Acrobat - Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ... http://web.archive.org/web/20170301223601/https://www.fda.gov/OHRMS/DOCKETS/AC/01/slides/3681s2_09.pdf
Subject: SV: McDonald's Corp. seven scientists and experts and a pharmaceutical supplier Seriologicals Corp. U.S. NOT PROTECTED AGAINST MAD COW DISEASEFrom: Karin Irgens <Karin.Irgens@MATTILSYNET.NO>Reply To: Bovine Spongiform Encephalopathy <BSE-L@LISTS.AEGEE.ORG>Date: Thu, 12 Jan 2006 16:54:12 +0100 Content-Type: text/plain Parts/Attachments: text/plain (8651 lines)##################### Bovine Spongiform Encephalopathy #####################Hello TerryDo you have the link for this text from 7 scientists ?Best regards, Karin-----Opprinnelig melding-----Fra: Bovine Spongiform Encephalopathy [mailto:BSE-L@aegee.org] På vegne av Terry S. Singeltary Sr.Sendt: 11. januar 2006 19:31Til: BSE-L@aegee.orgEmne: Re: McDonald's Corp. seven scientists and experts and a pharmaceutical supplier Seriologicals Corp. U.S. NOT PROTECTED AGAINST MAD COW DISEASE##################### Bovine Spongiform Encephalopathy #####################Subject: Re: McDonald's Corp. seven scientists and experts and a pharmaceutical supplier Seriologicals Corp. U.S. NOT PROTECTED AGAINST MAD COW DISEASEDate: January 11, 2006 at 9:27 am PSTDecember 19, 2005Division of Dockets Management (HFA-305)Food and Drug Administration5630 Fishers LaneRoom 1061 Rockville, MD 20852Re: Docket No: 2002N-0273 (formerly Docket No. 02N-0273)Substances Prohibited From Use in Animal Food and FeedDear Sir or Madame:The McDonalds Corporation buys more beef than any other restaurant in the United States. It is essential for our customers and our company that the beef has the highest level of safety. Concerning BSE, the most effective way to insure this is to create a system that processes cattle that are not exposed to the disease. As a company we take numerous precautions via our strict specifications to help and assure this, however we feel that the force of federal regulation is important to ensure that the risk of exposure in the entire production system is reduced to as close to zero as possible. The exemptions in the current ban as well as in the newly proposed rule make this difficult if not impossible, as there are still legal avenues for ruminants to consume potentially contaminated ruminant protein. In addition, the USDA still has not implemented a system of identification and traceability. It is our opinion that the government can take further action to reduce this risk and appreciate the opportunity to submit comments to this very important proposed rule.After the identification of bovine spongiform encephalopathy (BSE) in indigenous North American cattle, the U.S. Department of Agriculture (USDA) responded rapidly to implement measures to protect public health in regard to food. Our company recognizes and supports the importance of the current feed ban which went into effect in August 1997. However, given what is known about the epidemiology and characteristically long incubation period of BSE, we urge the FDA to act without further delay and implement additional measures which will reduce the risk of BSE recycling in the US cattle herd. We caution against using the 18 month enhanced surveillance as a justification to relax or impede further actions. While this surveillance indicates an epidemic is not underway, it does not clear the US cattle herd from infection. The positive cases indicate probable exposure prior to the 1997 feed ban, a time when BSE appears to have been circulating in animal feed. BSE cases are most likely clustered in time and location, so while enhanced surveillance provides an 18 month snapshot, it does not negate the fact that US and Canadian cattle were exposed to BSE and that the current feed controls contain “leaks”.We feel that for the FDA to provide a more comprehensive and protective feed ban, specified risk materials (SRMs) and deadstock must be removed from all animal feed and that legal exemptions which allow ruminant protein to be fed back to ruminants (with the exception of milk) should be discontinued.SRMs, as defined by the USDA, are tissues which, in a BSE infected animal, are known to either harbor BSE infectivity or to be closely associated with infectivity. If SRMs are not removed, they may introduce BSE infectivity and continue to provide a source of animal feed contamination. Rendering will reduce infectivity but it will not totally eliminate it. This is significant, as research in the United Kingdom has shown that a calf may be infected with BSE by the ingestion of as little as .001 gram of untreated brain.The current proposed rule falls short of this and would still leave a potential source of infectivity in the system. In fact by the FDA’s own statement the exempted tissues which are known to have infectivity (such as distal ileum, DRGs, etc) would cumulatively amount to approximately 10% of the infectivity in an infected animal. Leaving approximately 10% of the infectious tissues in the system is not good enough. The proposed rule still allows the possibility for cattle to be exposed to BSE through:Feeding of materials currently subject to legal exemptions from the ban (e.g., poultry litter, plate waste) Cross feeding (the feeding of non-ruminant rations to ruminants) on farms; and Cross contamination of ruminant and non-ruminant feedWe are most concerned that the FDA has chosen to include a provision that would allow tissues from deadstock into the feed chain. We do not support the provision to allow the removal of brain and spinal cord from down and deadstock over 30 months of age for several reasons. These are the animals with the highest level of infectivity in tissues which include more than brain and spinal cord. Firstly, there are two issues regarding the complex logistics of this option. We do not feel that it is possible to have adequate removal especially during the warmer months. In addition, we do not feel that there are adequate means to enforce complete removal. Unlike slaughterhouses, there are no government inspectors at rendering plants or deadstock collection points.Most importantly, there is emerging information that at end stage disease (a natural BSE case); infectivity may also be included in additional tissues such as peripheral nerves (Buschmann and Groschup, 2005 – see attached). This published work supports publicly reported studies in Japan where by western blot testing, prions have been found in the peripheral nerves of a naturally infected 94-month-old cow. If this is the case, the amount of infectivity left in the system from an infected bovine would surpass 10% and the full extent is still unknown.McDonalds has convened it own International Scientific Advisory Committee (ISAC) as well as co-sponsored a symposium of TSE scientists on the issue of tissue distribution. The consensus of both groups was that the pathogenesis of BSE might not be entirely different from TSEs in other species at the point where the animal is showing signs of the disease. These scientists feel that the studies as reported above have merit. The current studies not only re-enforce the risk of down and deadstock but also appear to provide additional information that these animals may be a potential source of greater levels of infectivity into the feed system. Hence, we suggest that the FDA consult with TSE scientists as well.Leaving the tissues from the highest risk category of cattle in the animal feed chain will effectively nullify the intent of this regulation. This point is illustrated by the 2001 Harvard risk assessment model that demonstrated that eliminating dead and downer, 4D cattle, from the feed stream was a disproportionately effective means of reducing the risk of re-infection.“The disposition of cattle that die on the farm would also have a substantial influence on the spread of BSE if the disease were introduced.” The base case scenario showed that the mean total number of ID50s (i.e., dosage sufficient to infect 50 percent of exposed cattle) from healthy animals at slaughter presented to the food/feed system was 1500. The mean total number of ID50s from adult cattle deadstock presented to the feed system was 37,000. This illustrates the risk of “4D cattle” (i.e., deadstock).From the Harvard Risk Assessment, 2001, Appendix 3A Base Case and Harvard Risk Assessment, 2001 Executive SummaryMcDonalds also urges agencies of the US government to work with academia and industry on research in the following areas:· Methods to inactivate TSEs agents which then may allow a product to be used and even fed to animals without risk· Alternative uses for animal byproducts which would maintain some valueIn July 2004, McDonalds in cooperation with others sponsored a meeting at Penn State. The purpose of the meeting was to review work conducted by Dr. Bruce Miller looking at the feasibility of using carcasses and animal byproducts as renewable alternatives to fossil fuels in large energy generating boilers. A number of government representatives were also invited to this meeting. We are aware that Dr. Miller continues this work which shows great promise. We suggest that the FDA explore the possibility of this alternative use that may also have a positive impact on the environment.The McDonalds Corporation will continue to work with the FDA and other government agencies to implement a strong BSE risk control program. We would like to reiterate our opinion that for the FDA to provide a more comprehensive and protective feed ban, specified risk materials (SRMs) and deadstock must be removed from all animal feed and that legal exemptions which allow ruminant protein to be fed back to ruminants (with the exception of milk) should be discontinued. Thank you for the opportunity to submit these comments to the public record.Respectfully,Dick CrawfordCorporate Vice President, Government Relationsxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx===========================================================================December 20, 2005Division of Dockets Management (HFA-305)Food and Drug Administration5630 Fishers LaneRoom 1061Rockville, MD 20852Re: Docket No: 2002N-0273 (formerly Docket No. 02N-0273)Substances Prohibited From Use in Animal Food and FeedDear Sir or Madame:As scientists and recognized experts who have worked in the field of TSEs for decades, we are deeply concerned by the recent discoveries of indigenous BSE infected cattle in North America and appreciate the opportunity to submit comments to this very important proposed rule We strongly supported the measures that USDA and FDA implemented to protect public health after the discovery of the case of bovine spongiform encephalopathy (BSE) found in Washington State in 2003. We know of no event or discovery since then that could justify relaxing the existing specified risk material (SRM) and non-ambulatory bans and surveillance that were implemented at that time. Further, we strongly supported the codification of those changes, as well as additional measures to strengthen the entire feed and food system. The discovery of additional cases of indigenous BSE in North America since that time has validated our position and strengthened our convictions.We caution against using the 18 month enhanced surveillance as a justification to relax or impede further actions. While this surveillance has not uncovered an epidemic, it does not clear the US cattle herd from infection. While it is highly likely that US and Canadian cattle were exposed to BSE prior to the 1997 feed ban, we do not know how many cattle were infected or how widely the infection was dispersed. BSE cases are most likely clustered in time and location, so while enhanced surveillance provides an 18 month snapshot, it does not negate the fact that US and Canadian cattle were exposed to BSE. We also do not know in any quantitative or controlled way how effective the feed ban has been, especially at the farm level. At this point we cannot even make a thorough assessment of the USDA surveillance as details such as age, risk category and regional distribution have not been released.A number of countries initially attempted to take partial steps in regard to feed controls only to face repeated disappointments in predicted downturns of the epidemic course. We in North America could do this experiment all over again, waiting for each new warning before adding more stringency to our control measures, or we can benefit from the experience of others and take decisive measures now to arrest any further development of underlying cases that is implicit in those already discovered to date.The discovery of 5 indigenous North American cases, including one born after the implementation of the current feed ban, should provide the necessary incentive to implement, monitor and enforce a comprehensive and protective feed ban that is more congruent with the measures that have been proven to be effective throughout the world. In particular, we urge the FDA to act without further delay to strengthen the animal feed regulations by implementing the program proposed by the Canadian Food Inspection Agency (CFIA) in the December 11, 2004 Gazette. This includes removing all specified risk materials (SRMs) and deadstock from all animal feed. We also urge that the FDA discontinues the legal exemptions which allow ruminant protein to be fed back to ruminants (with the exception of milk). Many of these exemptions do not exist in other countries.Bovine products and byproducts are used for both food and pharmaceuticals. These human uses require the highest level of safety. Because of the hardy nature of the BSE agent and its high potential for cross contamination, the most effective way to protect bovine products and bovine derived materials from contamination by BSE is to ensure that infected animals or carcasses never enter processing plants. The goal would be to discover and remove infected animals from production as early as possible in the infection and long before they would be sent to slaughter. Until we have diagnostic tools powerful enough to allow us to discover the disease early in its prolonged pre-clinical incubation, we have to rely on the next best strategy which is to prevent any exposure through feed. The exemptions in the current ban as well as in the newly proposed rule make this difficult if not impossible, as they still provide legal avenues for ruminants to consume potentially contaminated ruminant protein.It is our opinion that the proposed rule falls woefully short in effective measures to minimize the potential for further transmissions of the disease. By the FDA’s own analysis, exempted tissues (such as distal ileum, DRGs, etc) contain approximately 10% of the infectivity in affected animals. Thus the proposed rule still allows the possibility for cattle to be exposed to BSE through:1. Feeding of materials currently subject to legal exemptions from the ban (e.g., poultry litter, plate waste)2. Cross feeding (the feeding of non-ruminant rations to ruminants) on farms; and3. Cross contamination of ruminant and non-ruminant feedWe are most concerned that the FDA has chosen to include a provision that would allow tissues from deadstock into the feed chain. We do not believe that down or dead stock should be allowed into the food or feed chain whatever the age of the animal and whether or not the CNS tissues are removed. We do not support the provision to allow removal of brain and spinal cord from deadstock over 30 months for a number of reasons. [RR1] This category of animals contains the highest level of infectivity and that infectivity is in other tissues besides just brain and spinal cord. Recent improvements in the BSE bioassay, have now made it possible to detect BSE infectivity 1000 time more efficiently than before. This assay has revealed the presence of BSE infectivity in some but not all peripheral nerves and in one muscle. (Buschmann and Groschup, 2005) This published and peer reviewed work is consistent with other publicly reported studies in Japan where, by western blot testing, prions were found in the peripheral nerves of a naturally infected 94-month-old cow. We feel that the studies as reported above have merit. The current studies not only re-enforce the risk of down and deadstock but also appear to provide additional information that these animals may be a potential source of greater levels of infectivity into the feed system. We also doubt that brain and spinal cord can be completely removed especially during warmer weather. Given the biological composition of these tissues, they are predisposed to rapid autolysis.As world wide surveillance for BSE increases, several atypical cases of bovine TSE have been discovered. These cases either show no clinical signs, or present as ‘downers’, and have an atypical neuropathology with respect to lesion morphology and distribution, causing problems in both clinical and post-mortem diagnosis. The origin of the cases are unclear but they suggest that even should typical BSE be eliminated, there may be other TSE diseases of cattle that could result by “mutation” and selection. Refeeding of contaminated protein could potentially perpetuate transmission much like typical BSE. An effective feed ban could prevent the expansion of such strains. We also note that there are other species which are susceptible to BSE and the current regulations allow for SRMs to be included in feed for these animals.For BSE to be perpetuated, the animal production system must have a source of agent and a means by which cattle or other susceptible species are exposed to this agent. We feel that in North America, the source and routes of exposure still exist, hence allowing for the continued recycling of BSE. We have detailed the scientific justifications for our position below.Source of the agent: SRMs (Specified Risk Materials)SRMs, as defined by the USDA, are tissues which, in a BSE infected animal, are known to either harbor BSE infectivity or to be closely associated with infectivity. If SRMs are not removed, they may introduce BSE infectivity and continue to provide a source of animal feed contamination. For example, the skull and vertebral column which encase the brain and spinal cord, respectively, can be assumed to have gross contamination. Rendering will reduce infectivity but it will not totally eliminate it. This is significant as research in the United Kingdom has shown that a calf may be infected with BSE by the ingestion of as little as .001 gram of untreated brain.The tissue distribution of infectivity in BSE infected cattle has primarily been determined by 3 studies conducted in the United Kingdom all of which had limitations.In two of the studies, bioassays were done in mice which are at least 1000 fold less sensitive to BSE infection than cattle themselves. Only higher titers of infectivity can be detected by this method. These investigations found infectivity in the brain, spinal cord, retina, trigeminal ganglia, dorsal root ganglia, distal ileum and bone marrow (the bone marrow finding was from one animal). Infectivity was found in distal ileum of experimentally infected calves beginning six months after challenge and continuing at other intervals throughout life. (Wells et. al., 1994; 1998). The bioassay study in calves has produced similar results and in addition infectivity has been found in tonsil. The study is still in progress. Another project has found infectivity in the lymphoid tissue of third eyelid from naturally infected animals. (Dr. Danny Matthews, UK DEFRA, personal communication).While bioassay in cattle is far preferable to mice in terms of sensitivity, cattle nevertheless present their own limitations in terms of the long incubation time and the limited number of animals that can be used for assay compared to rodents. As a consequence the significance of the negative finding for many tissues is questionable. In fact, by the end of 2004 there was increasing evidence in species other than cattle that peripheral nerves and muscle have infectivity. (Bosque et al., 2002; Glatzel et al., 2003;Bartz et al., 2002; Androletti et al., 2004; Mulcahy et al., 2004; Thomzig et al., 2003; Thomzig et al., 2004)In some of these species, studies indicate that the agent migrates to the brain and spinal cord, replicates to high levels in the CNS and then spreads centrifugally from the spinal cord back down through the spinal neurons to the junction of the nerves and muscle into the muscle cells themselves. A recent German study (Buschmann and Groschup, 2005) examined nerves and muscle from a cow naturally infected with BSE and found that infectivity was present in several peripheral nerves and one muscle. The method of detection was bioassay in bovinized transgenic mice that show the same or greater sensitivity to transmission of BSE as cattle. This research concurs with findings by Japanese scientists that BSE infectivity is present in peripheral nerves at least in the clinical stage of disease.It is our opinion that there is increasing evidence that the pathogenesis of BSE might not be entirely different from TSEs in other species at the point of clinical disease in that there is peripheral involvement. We feel that the studies as reported above have merit. The current studies not only re-enforce the risk of down and deadstock but also appear to provide additional information that these animals may be a potential source of greater levels of infectivity into the feed system.In the event that FDA may confer with USDA about the risks associated with peripheral nerves we want to point out one issue. In the recent publication of the final rule on the importation of whole cuts of boneless beef from Japan, 9 CFR Part 94 [Docket No. 05-004-2] RIN 0579-AB93, we disagree with the interpretation provided by USDA, APHIS.APHIS seems to discount the studies conducted by Groschup et al. 2005. on the basis that the transgenic mouse bioassay that they used may be too sensitive. In taking this position they have failed to realize that the point of an assay is to reveal in which tissues the infectivity resides and its relative concentration to brain or spinal cord. For this purpose, no assay can be too sensitive. Of course, the probability of an actual infection will be affected by the efficiency of infection which will be a function of dose, route of exposure and any host barrier effects that are present.We would also like to point out a factual error in the conclusion. APHIS states, “Given these factors, APHIS has determined that the finding of BSE infectivity in facial and sciatic nerves of the transgenic mice is not directly applicable to cattle naturally infected with BSE. Therefore, we do not consider it necessary to make any adjustments to the risk analysis for this rulemaking or to extend the comment period to solicit additional public comment on this issue.” It is incorrect that the infectivity was found in the peripheral nerves of transgenic mice. The peripheral nerves were harvested from a cow naturally infected with BSE. Transgenic mice were used as a bioassay model.From [Docket No. 05-004-2] RIN 0579-AB93[RR2] :“Peripheral NervesIssue: Two commenters stated that the underlying assumption of the proposed rule, that whole cuts of boneless beef from Japan will not contain tissues that may carry the BSE agent, is no longer valid because researchers have found peripheral nervous system tissues, including facial and sciatic nerves, that contain BSE infectivity.\2\ One of these commenters requested APHIS to explain whether and what additional mitigation measures are needed to reduce the risks that these tissues may be present in Japanese beef. This commenter further requested an additional comment period to obtain public comments to treat this new scientific finding. ---------------------------------------------------------------------------\2\ Bushmann, A., and Groschup, M.; Highly Bovine Spongiform Encephalopathy-Sensitive Transgenic Mice Confirm the Essential Restriction of Infectivity to the Nervous System in Clinically Diseased Cattle. The Journal of Infectious Diseases, 192: 934-42, September 1, 2005. ---------------------------------------------------------------------------Response: APHIS is familiar with the results of the study mentioned by the commenters in which mice, genetically engineered to be highly susceptible to BSE and to overexpress the bovine prion protein, were inoculated with tissues from a BSE-infected cow. This study demonstrated low levels of infectivity in the mouse assay in the facial and sciatic nerves of the peripheral nervous system. APHIS has evaluated these findings in the context of the potential occurrence of infectivity in the peripheral nerves of cattle and the corresponding risks of the presence of infectivity in such tissues resulting in cattle or human exposure to the BSE agent. The results from these experiments in genetically engineered mice should be interpreted with caution, as the findings may be influenced by the overexpression of prion proteins and may not accurately predict the natural distribution of BSE infectivity in cattle. Further, the overexpression of prion proteins in transgenic mice may not accurately mimic the natural disease process because the transgenic overexpressing mice have been shown to develop spontaneous lethal neurological disease involving spongiform changes in the brain and muscle degeneration.\3\ In addition, the route of administration to the mice was both intraperitoneal and intracerebral, which are two very efficient routes of infection as compared to oral consumption. Given these factors, APHIS has determined that the finding of BSE infectivity in facial and sciatic nerves of the transgenic mice is not directly applicable to cattle naturally infected with BSE. Therefore, we do not consider it necessary to make any adjustments to the risk analysis for this rulemaking or to extend the comment period to solicit additional public comment on this issue.”Source of the agent: DeadstockThe total amount of TSE infectivity in a TSE infected animal increases steadily throughout the infection and exponentially once the infectivity reaches the brain. Infected individuals only exhibit recognizable clinical signs once infectivity titers have reached high levels in the brain. Surveillance data collected throughout Europe indicates there is a much greater likelihood for BSE to be detected in dead or down cattle than from healthy normal animals. This has so far also been borne out by the experience in North America. Animals that die of BSE harbor the greatest amount of agent that can be produced by the disease. Leaving the tissues from the highest risk category of cattle in the animal feed chain will effectively nullify the purported intent of this regulation. This point is supported by the 2001 Harvard risk assessment model that demonstrated that eliminating dead and downer, 4D cattle, from the feed stream was a disproportionately effective means of reducing the risk of re-infection.“The disposition of cattle that die on the farm would also have a substantial influence on the spread of BSE if the disease were introduced.” The base case scenario showed that the mean total number of ID50s (i.e., dosage sufficient to infect 50 percent of exposed cattle) from healthy animals at slaughter presented to the food/feed system was 1500. The mean total number of ID50s from adult cattle deadstock presented to the feed system was 37,000. This illustrates the risk of “4D cattle” (i.e., deadstock).From the Harvard Risk Assessment, 2001, Appendix 3A Base Case and Harvard Risk Assessment, 2001 Executive SummaryIt is likely that these numbers would have to be adjusted upwards, if the UK attack rate and Groschup data were considered.Inflammation and TSEsThere have been 3 recent peer reviewed publications which indicate that chronic inflammatory conditions in a host with a TSE may induce prion replication in, or distribution to organs previously thought to be low or no risk. They are as follows:Chronic Lymphocytic Inflammation Specifies the Organ Tropism of Prions (Heikenwalder et. al. 2005 www.sciencexpress.org/20 January 2005/ Page 1/ 10.1126/science.1106460)2. Coincident Scrapie Infection and Nephritis Lead to Urinary Prion Excretion (Seeger et al., Science 14 October 2005:Vol. 310. no. 5746, pp. 324 – 326 DOI: 10.1126/science.1118829)3. PrPsc in mammary glands of sheep affected by scrapie and mastitis (Ligios C., et al. Nature Medicine, 11. 1137 – 1138, 2005)These studies from the Aguzzi laboratory warn that concurrent chronic inflammatory disease could dramatically alter the distribution of BSE infectivity in infected cattle. Down and dead stock are at higher risk for both BSE and other systemic conditions. If the results reported above are also applicable to cattle, the carcasses of dead and down stock affected by BSE might contain even higher levels of infectivity, or contribute infectivity via tissues that are not ordinarily at risk in normal animals.Exposure: Industry Practices or Exemptions which may pose a riskPoultry LitterIn the United States poultry litter can be fed to cattle. There are two potential sources of risk from poultry litter. Poultry litter not only consists of digested feed but also of feed which spills from the cages. As a consequence, the practice of feeding litter back to cattle is by its nature non-compliant with the current feed ban if the poultry themselves are being fed ruminant protein. Given that ruminant protein can no longer be fed to ruminants in the United States and that most, if not all, countries will no longer import North American ruminant MBM, an even larger part of poultry diets is now ruminant MBM. Spillage provides a direct link to back to cattle but feces are also likely to contain infectivity.There is no reason to expect that TSE infectivity would be inactivated by passage through the poultry gut, and only a slim possibility that composting would reduce infectivity at all. Thus poultry feces are another potential route of transmission back to cattle. Evidence for this comes from rodent experiments where infectivity was demonstrated in the feces after being fed: “Laboratory experiments show that mice orally challenged with scrapie have detectable infectivity that passes through the gut. Gut contents and fecal matter may therefore contain infectivity, and it is noted that in experimental oral challenges in cattle conducted in the UK, feces must be treated as medical waste for one month following the challenge. It is concluded that digestive contents and fecal material from livestock or poultry currently being fed with MBM potentially contaminated with BSE should not be used as a feed ingredient for animal feed.” [Proceedings: Joint WHO/FAO/OIE/ Technical Consultation on BSE: public health, animal health and trade. Paris, 10-14 June 2001; and Alan Dickinson, personal communication].It may be possible to remove the risk from poultry litter by sterilization. However, unless or until a method can be developed and validated, poultry litter should be banned from ruminant feed.Ruminant BloodIn contrast with humans, sheep, monkeys, mice and hamsters, including sheep and mice infected with BSE and humans infected with vCJD considered identical to BSE, no infectivity has so far been demonstrated in the blood of BSE infected cattle. However, we consider it unlikely that cattle are the sole outlier to what has been a consistent finding in all other TSE diseases where the measurement has been made with sufficient sensitivity to detect the low levels of infectivity that are present in blood. Rather, this failure is more likely the result of the very small volumes of blood that were used for the inoculations (less than 1 ml), whereas whole transfusions were administered to assay animals in the published sheep scrapie/BSE experiments. If blood is infected then all vascularized tissues can be expected to contain some infectivity in proportion to the content of residual blood.Micro emboli are a possible source of blood-borne agent that could be at much higher titer than blood itself, in slaughtered cattle carrying BSE infection. Stunning can release micro emboli of brain tissue into the circulatory system from where they can be distributed to other tissues in the few moments before the exsanguination and death. (Anil, et al, 2001a & b; Anil et al, 2002; Love, et al, 2000). This source of infection could extend a higher infectivity risk to tissues that would otherwise be at low risk, thereby allowing exposure of cattle through any of the legal exemptions and potentially producing a feed and food risk. Blood-borne contamination may be a special problem where spray-dried blood is being used as a milk replacer for calves, as it is thought that young animals are especially susceptible to infection.Certainly, blood and blood proteins should not be used as feed without conclusive evidence that they are safe.Unfiltered TallowRuminant tallow is exempted from the current feed ban. Tallow contains protein impurities (i.e. MBM) that could be a source of TSE infectivity. There are no impurity level requirements for this tallow. It has been reported that it is standard practice to produce tallow which has an impurity level of .15% or below, but it is not clear that this is fully adequate to remove the risk of transmission and there is no requirement to meet even this standard. We urge that protein contaminants be excluded from tallow and that SRMs also be removed.Plate WastePlate waste is not limited to meat (muscle tissue). For example, cuts that include a portion of the spinal cord or that are contaminated by cord or ganglia during preparation could contain high levels of infectivity if derived from a TSE infected animal late in the preclinical stage of infection. At best this material would only be exposed to normal cooking temperatures. USDA, APHIS experience with the Swine Health Protection Act has revealed that plate waste also includes uncooked trimmings and bones. Although the current FDA regulation requires the plate waste be treated again, there are no specifications which would render a TSE agent inactive. Of greatest risk would be any bovine source of infectivity but also sheep scrapie, although not known to be a risk for human consumption, is one of the possible origins of BSE. The sheep scrapie agent is known to be widely dispersed including relatively high titers in lymphoid as well as nervous tissue. We support the USDA’s opposition to the exemption of “plate waste” as stated in written comments since 1997.Exposure: Cross Feeding and Cross ContaminationThe UK epidemiology has clearly shown that BSE contaminated feed is the primary if not sole vehicle for the transmission of BSE between cattle. Moreover, results from the United Kingdom’s attack rate study indicate that it does not take much exposure to transmit BSE to cattle. Recent results from the attack rate study which is still in progress have found that .1 g of brain transmitted BSE by the oral route to 3 cows out of 15 thus far, and .01 and .001gr of brain have transmitted BSE (1 cow out of 15). (Danny Matthews, DEFRA presentation at TAFS meeting, Washington, DC April 2004).Rendering may reduce infectivity but it does not eliminate it. (Taylor et al, 1995; Taylor et al, 1997; Schreuder et al, 1998). Given that BSE can be transmitted to cattle via an oral route with just .001 gram of infected tissue, it may not take much infectivity to contaminate feed and keep the disease recycling. This is especially true in countries like the US and Canada which do not have dedicated lines and equipment to manufacture and process feed for ruminants and non-ruminants.In addition, epidemiological investigations in European countries have shown that cross feeding and cross contamination on farm can be a significant vehicle for continued BSE transmission even after feed bans are well established. Cross feeding is the practice of feeding meal for poultry or pigs or pet food (which can legally contain ruminant MBM) to cattle on the same farm. This is usually due to simple human error or negligence. (Hoinville, 1994; Hoinville et al, 1995; Doherr et al, 2002a; Stevenson et al, 2000)FDA, CVM reports that compliance with the existing feed ban is high. For the most part this does not include the compliance level on the farm. There are hundreds of thousands of farms in the US. Many of these have multiple species. That is, they raise cattle, pigs, chickens etc., on the same premises. The sheer numbers of farms make it very difficult to assure compliance on farm and to adequately cover all farms by inspection. Even if the rendering industry and feed industry can maintain 100% compliance at their facilities, if a producer inadvertently feeds chicken feed containing bovine MBM to their cattle, they negate a perfect compliance rate higher in the chain. Recent data from the Harvard BSE risk assessment suggest that the level of misfeeding on farms plays a significant role in the ability of the agent to recycle. In fact George Gray, principal investigator for the study, stated that if, in the United States, misfeeding were to occur at a level of 15%, the R0 would be over 1, indicating that the BSE level would not be declining. (George Gray presentation at the Meeting on BSE Prevention in North America: An Analysis of the Science and Risk; January 27, 2005, Washington, DC.)The May 2003 Canadian BSE case illustrates the difficulty of on farm enforcement and its serious ramifications. The BSE positive cow was rendered and the MBM distributed to various locations. Two of these locations were poultry farms which mixed their own feed. The farms also had cattle. The subsequent investigation could not eliminate the possibility that the cattle had been fed the same feed as the poultry. The cattle on these farms were completely depopulated.Human error is extremely difficult to prevent, and managing the risk through enforcement is problematical when confronted with the extreme logistical challenges of on farm monitoring. By eliminating the highest risk materials (SRMs and deadstock) which could introduce infectivity into the feed stream, the MBM resulting from processing becomes inherently safer. If mistakes are then made on farm, they no longer contribute to the recycling of BSE.Exposure: Susceptibility of other SpeciesFelinesA transmissible spongiform encephalopathy has been diagnosed in eight species of captive wild ruminants as well as exotic felines (cheetahs, pumas, a tiger and an ocelot) and domestic cats (Wyatt 1991). There have been over 80 domestic cat cases of Feline Spongiform Encephalopathy (FSE) in Great Britain, and cats in Norway, Northern Ireland, Lichtenstein and Switzerland. The agent isolated from several of these cases is indistinguishable from BSE in cattle using strain typing in mice, suggesting that FSE is actually BSE in exotic and domestic cats. Epidemiological evidence suggests BSE contaminated feed to be the probable source of infection in these species. (MAFF Progress Report, June 1997), thus providing additional supporting evidence for the dangers of BSE contaminated feed and reinforcing the necessity of removing all sources of potential contamination from the feed stream.Other speciesStudies conducted at the National Institutes of Health Rocky Mountain Laboratory caution against assuming that animals which do not become clinically ill are not infected. It is unknown if certain animals may become carriers, i.e., become infected, shed agent but do not progress to clinical disease. Infection of certain rodent species with different TSE strains suggests the possibility of a carrier state (Race and Chesebro, 1998; Race et. al, 2001, Race et al., 2002). In the more recent studies, mice were inoculated with 263K hamster scrapie. There was a prolonged period (approximately one year) where there was no evidence of replication of infectivity. Furthermore, there was no evidence of PrPres during this phase of inactive persistence, which was followed by a period of active replication of infectivity and agent adaptation. In most cases, PrPres was not detected in the active phase as well. It is important to determine if this persistence and adaptation occurs in other species exposed to TSEs as it may have significance in feeding programs which continually expose other species to BSE infectivity. For example, if BSE infected brain and spinal cord are continually fed to certain species, it may be possible for the agent to persist and adapt in these new species. Over time, the ‘resistant’ species may become a source of agent. The results of Race and colleagues, warns that an inactive persistent phase might not produce detectable PrPres, yet there would be infectivity (Race et. al., 2001).Pigs displayed evidence of TSE infection after exposure to BSE by 3 distinct parenteral routes. Evidence of infectivity was found in the CNS, stomach, intestine and pancreas (Dawson et. al., 1990). Oral transmission has also been attempted in swine, but after an observation period of 84 months there was neither clinical nor pathological evidence of infection (Dawson et. al., 1990). Parenteral and oral transmission has also been attempted in chickens with no evidence of disease. Tissues from the BSE-challenged pigs and chickens were inoculated into susceptible mice to look for residual infectivity, but to date none has been found. In both instances the detection sensitivity was limited by the use of mice for bioassay instead of same species transmissions into cattle (or pigs and chickens).If any of these scenarios played out and inapparent infections became established in commercial species, those species could become reservoirs for reinfection of cattle and perpetuation or reintroduction of the epidemic. We also do not know if atypical cases of BSE are more pathogenic for other species and if chronic inflammation may influence the susceptibility of other species. We offer these possibilities to reinforce the need to eliminate all possible sources of infectivity from the feed stream.In January 2005, the European Union announced that BSE had been confirmed in a goat in France illustrating that the disease can be naturally transmitted to one of the small ruminants. The potential ramifications of this and the logistical challenges associated with controlling BSE in sheep or goats also provides a justification for removing SRMs from all animal feed. Although these species are covered under the current regulations the cross contamination and cross feeding aspects stated for cattle are applicable.The need to remove high risk material from all animal feed is also supported by other bodies with expertise in the field of TSEs:Recommendations of the World Health Organization (WHO)The World Health Organization (WHO) has issued the following recommendations for countries with BSE or those where a known exposure exists:· No part or product of any animal which has shown signs of a TSE should enter any food chain (human or animal). In particular:o All countries must ensure the killing and safe disposal of all parts or products of such animals so that TSE infectivity cannot enter any food chain.o Countries should not permit tissues that are likely to contain the BSE agent to enter any food chain (human or animal).From the report of a WHO Consultation on Public Health Issues related to Human and Animal Transmissible Spongiform Encephalopathies WHO/EMC/DIS 96.147, Geneva, 2-3 April 1996.Office of International Epizooties (OIE)The OIE is recommending that a list of SRMs which include brain, spinal cord, eyes, skull and vertebral column be removed from preparations used for food, feed, fertilizer, etc. If these tissues should not be traded we feel that they should not be used in domestic products either.BSE Code Article 2.3.13.18“From cattle, originating from a country or zone with a minimal BSE risk, that were at the time of slaughter over 30 months of age, the following commodities, and any commodity contaminated by them, should not be traded for the preparation of food, feed, fertilizers, cosmetics, pharmaceuticals including biologicals, or medical devices: brains, eyes and spinal cord, skull, vertebral column and derived protein products. Food, feed, fertilizers, cosmetics, pharmaceuticals or medical devices prepared using these commodities should also not be traded.”ConclusionIn conclusion we urge the FDA to implement, monitor and enforce a comprehensive and protective feed ban that is more congruent with the measures that have been proven to be effective in other countries that have experienced BSE. We do not feel that we can overstate the dangers from the insidious threat from these diseases and the need to control and arrest them to prevent any possibility of spread.We also wish to emphasize that as scientists who have dedicated substantive portions of our careers to defining the risks from TSEs as well as developing strategies for managing those risks, we are confident that technical solutions will be found for many of the challenges posed by these diseases. Thus, we urge the FDA to frame its regulations in terms that allow for the future use of any banned material if it can be proven safe for a given application.Signatories:Paul W. Brown, M.D.Medical Director, USPHS, and Senior Investigator, NIH (retired)Consultant, TSE Risk ManagementxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxEmail: paulwbrown@comcast.netNeil R. Cashman MD Professor, Department of Medicine (Neurology) Diener Chair of Neurodegenerative Diseases Centre for Research in Neurodegenerative Diseases 6 Queen's Park Crescent West Toronto Ontario M5S3H2 xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxe-mail: neil.cashman@utoronto.caLinda A. Detwiler, DVM Consultant, TSE Risk ManagementxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxEmail: LAVet22@aol.comLaura Manuelidis, MDProfessor and Head of Neuropathology, Department of Surgery and Faculty of Neurosciences Yale Medical Schoolxxxxxxxxxxxxxxxxxxxx email: laura.manuelidis@yale.edu xxxxxxxxxxxxxxxxxxxxxxxxJason C. Bartz, Ph.D. Assistant Professor Department of Medical Microbiology and Immunology Creighton University 2500 California Plaza Omaha, NE 68178 xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxRobert B. Petersen, Ph.D.Associate Professor of Pathology and NeuroscienceCase Western Reserve University5-123 Wolstein Building2103 Cornell RoadCleveland, OH 44106-2622xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxEmail rbp@cwru.eduRobert G. Rohwer, Ph.D. Director, Molecular Neurovirology Laboratory Veterans Affairs Medical Center Medical Research Service 151 Assoc. Professor of Neurology School of Medicine University of Maryland at Baltimore 10 N. Greene St. Baltimore, MD 21201 xxxxxxxxxxxxxxxxx xxxxxxxxxxxxxxxemail: rrohwer@umaryland.eduREFERENCESAndreoletti O, Simon S, Lacroux C, Morel N, Tabouret G, Chabert A, Lugan S, Corbiere F, Ferre P, Foucras G, Laude H, Eychenne F, Grassi J, Schelcher F. PrPSc accumulation in myocytes from sheep incubating natural scrapie. Nat Med. 2004 Jun;10(6):591-3. Epub 2004 May 23.Anil,M.H.; Love,S.; Helps,C.R.; McKinstry,J.L.; Brown,S.N.; Philips,A.; Williams,S.; Shand,A.; Bakirel,T.; Harbour,D.A. - Jugular venous emboli of brain tissue induced in sheep by the use of captive bolt guns - Veterinary Record 2001 May 19; 148: 619-20Anil,M.H.; Harbour,D.A. - Current stunning and slaughter methods in cattle and sheep. Potential for carcass contamination with central nervous tissue and microorganisms - Fleischwirtschaft 2001; 11: 123Anil,M.H.; Love,S.; Helps,C.R.; Harbour,D. - Potential for carcass contamination with brain tissue following stunning and slaughter in cattle and sheep - Food Control 2002; 13: 431-6Bartz JC, Kincaid AE, Bessen RA. Retrograde transport of transmissible mink encephalopathy within descending motor tracts. J Virol. 2002 Jun;76(11):5759-68.Bosque PJ, Ryou C, Telling G, Peretz D, Legname G, DeArmond SJ, Prusiner SB. Prions in skeletal muscle. Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3812-7.Bushmann, A., and Groschup, M.; Highly Bovine Spongiform Encephalopathy-Sensitive Transgenic Mice Confirm the Essential Restriction of Infectivity to the Nervous System in Clinically Diseased Cattle. The Journal of Infectious Diseases, 192: 934-42, September 1, 2005.Dawson,M.; Wells,G.A.H.; Parker,B.N.; Scott,A.C. - Primary parenteral transmission of bovine spongiform encephalopathy to the pig - Veterinary Record 1990 Sep 29; 127(13): 338Doherr,M.G.; Hett,A.R.; Rufenacht,J.; Zurbriggen,A.; Heim,D. - Geographical clustering of cases of bovine spongiform encephalopathy (BSE) born in Switzerland after the feed ban - Veterinary Record 2002 Oct 19; 151(16): 467-72Glatzel M, Abela E, Maissen M, Aguzzi A. Extraneural pathologic prion protein in sporadic Creutzfeldt-Jakob disease. N Engl J Med. 2003 Nov 6;349(19):1812-20.Hadlow W. J., Kennedy R. C. & Race R. E. (1982) Natural infection of Suffolk sheep with Scrapie virus. J. Infect. Dis., 146, 657-664Hoinville,L.J. - Decline in the incidence of BSE in cattle born after the introduction of the 'feed ban' - Veterinary Record 1994 Mar 12; 134(11): 274-5Hoinville,L.J.; Wilesmith,J.W.; Richards,M.S. - An investigation of risk factors for cases of bovine spongiform encephalopathy born after the introduction of the 'feed ban' - Veterinary Record 1995 Apr 1; 136(13): 312-8Houston,E.F.; Foster,J.D.; Chong,A.; Hunter,N.; Bostock,C.J. – Transmission of BSE by blood transfusion in sheep – Lancet 2000 Sep 16; 356(9234); 999-1000Hunter,N.; Foster,J; Chong,A.; McCutcheon,S.; Parnham,D.; Eaton,S.; MacKenzie,C.; Houston,E.F. – Transmission of prion diseases by blood transfusion – Journal of General Virology 2002 Nov, 83(Pt 11); 2897-905.Love,S.; Helps,C.R.; Williams,S.; Shand,A.; McKinstry,J.L.; Brown,S.N.; Harbour,D.A.; Anil,M.H. - Methods for detection of haematogenous dissemination of brain tissue after stunning of cattle with captive bolt guns - Journal of Neuroscience Methods 2000 Jun 30; 99(1-2): 53-8Mulcahy ER, Bartz JC, Kincaid AE, Bessen RA. Prion infection of skeletal muscle cells and papillae in the tongue. J Virol. 2004 Jul;78(13):6792-8.Race, R.; Chesebro, B. – Scrapie infectivity found in resistant species. Nature -1998 Apr 23;392(6678):770.Aguzzi,A.; Weissmann,C. - Spongiform encephalopathies. The prion's perplexing persistence. - Nature. 1998 Apr 23;392(6678):763-4Race,R.E.; Raines,A.; Raymond,G.J.; Caughey,B.W.; Chesebro,B. - Long-term subclinical carrier state precedes scrapie replication and adaptation in a resistant species: analogies to bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease in humans. - Journal of Virology 2001 Nov; 75(21): 10106-12Race,R.E.; Meade-White,K.; Raines,A.; Raymond,G.J.; Caughey,B.W.; Chesebro,B. - Subclinical Scrapie Infection in a Resistant Species: Persistence, Replication, and Adaptation of Infectivity during Four Passages. - Journal of Infectious Diseases 2002 Dec 1; 186 Suppl 2: S166-70Schreuder, B.E.C., Geertsma, R.E., van Keulen, L.J.M., van Asten, J.A.A.M., Enthoven, P., Oberthür, R.C., de Koeijer, A.A., Osterhaus, A.D.M.E., 1998. Studies on the efficacy of hyperbaric rendering procedures in inactivating bovine spongiform encephalopathy (BSE) and scrapie agents. Veterinary Record 142, 474-480Stevenson, M. A., Wilesmith, J. W., Ryan, J. B. M., Morris, R.S., Lockhart, J. W., Lin, D. & Jackson, R. (2000) Temporal aspects of bovine spongiform encepalopathy in Great Britain: individual animal-associated risk factors for the disease. Vet. Rec. 147, 349-354.Stevenson, M. A., Wilesmith, J. W., Ryan, J. B. M., Morris, R. S., Lawson, A.B., Pfeiffer, D. U. & Lin, D. (2000) Descriptive spatial analysis of the epidemic of bovine spongiform encephalopathy in Great Britain to June 1997. Vet. Rec. 147, 379-384.Taylor, D.M., Woodgate, S.L., Atkinson, M.J., 1995. Inactivation of the bovine spongiform encephalopathy agent by rendering procedures. Veterinary Record, Vol.137: pp.605-610.Taylor, D.M., Woodgate, S.L., Fleetwood, A.J., Cawthorne, R.J.G., 1997. The effect of rendering procedures on scrapie agent. Veterinary Record, Vol.141, pp 643-649.Thomzig A, Schulz-Schaeffer W, Kratzel C, Mai J, Beekes M. Preclinical deposition of pathological prion protein PrPSc in muscles of hamsters orally exposed to scrapie. J Clin Invest. 2004 May;113(10):1465-72.Thomzig A, Kratzel C, Lenz G, Kruger D, Beekes M. Widespread PrPSc accumulation in muscles of hamsters orally infected with scrapie. EMBO Rep. 2003 May;4(5):530-3.Wilesmith, J.W., Ryan, J. B. M., Hueston, W. D., & Hoinville, L. J. (1992) Bovine spongiform encephalopathy: epidemiological features 1985 to 1990. Vet. Rec., 130, 90-94.Wilesmith, J. W., Wells, G. A. H., Ryan, J. B. M., Gavier-Widen, D., & Simmons, M. M. (1997) A cohort study to examine maternally associated risk factors for bovine spongiform encephalopathy. Vet. Rec., 141, 239-243.Wells G.A.H., Dawson M., Hawkins, S.A.C., Green R. B., Dexter I., Francis M. E., Simmons M. M., Austin A. R., & Horigan M. W. (1994) Infectivity in the ileum of cattle challenged orally with bovine spongiform encephalopathy. Vet. Rec., 135, 40-41.Wells G.A.H., Hawkins, S.A.C., Green R. B., Austin A. R., Dexter I., Spencer, Y. I., Chaplin, M. J., Stack, M. J., & Dawson, M. (1998) Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy (BSE): an update. Vet. Rec., 142, 103-106.Wyatt. J. M. et al. 1991. Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Veterinary Record. 129. 233.---------------------------------------------------------------------------- ----[RR1] I am not sure of the point here. If they are going to use dead stock then certainly they should at a minimum remove the CNS tissue but rather I would think the point should be that we don’t want them using dead stock with or without the CNS included.[RR2]I am not sure that the actual text of the CFR is still required to make the point. However, I am glad I had it to verify the original argument.===========================================================================[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle03-025IFA 03-025IFA-2 Terry S. SingeltaryPage 1 of 17From: Terry S. Singeltary Sr. [flounder9@verizon.net]Sent: Thursday, September 08, 2005 6:17 PMSubject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirementsfor the Disposition of Non-Ambulatory Disabled CattleGreetings FSIS,I would kindly like to submit the following to [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food andRequirements for the Disposition of Non-Ambulatory Disabled CattleTHE BSE/TSE SUB CLINICAL Non-Ambulatory Disabled CattleBroken bones and such may be the first signs of a sub clinical BSE/TSE Non-Ambulatory Disabled Cattle ;snip...FULL TEXT ;let's take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$ALABAMA MAD COW g-h-BSEalabamaIn this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine–human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks.Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USANATURE|Vol 457|26 February 2009> Epidemiological investigations conducted by USDA personnel failed to reveal any evidence of a feed source contaminated with TSE material fed to this animal''This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. Cattle with the EK211 genotype are oronasally susceptible to small doses of the H-BSE agent from either EK211 or EE211 (wild type) donors. Wild-type EE211 cattle remained asymptomatic for the duration of the experiment with this small dose (0.1g) of inoculum. 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.''LMAO!BANNED MAD COW FEED IN COMMERCE IN ALABAMADate: September 6, 2006 at 7:58 am PST PRODUCTa) EVSRC Custom dairy feed, Recall # V-130-6;b) Performance Chick Starter, Recall # V-131-6;c) Performance Quail Grower, Recall # V-132-6;d) Performance Pheasant Finisher, Recall # V-133-6.CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.REASONDairy and poultry feeds were possibly contaminated with ruminant based protein.VOLUME OF PRODUCT IN COMMERCE 477.72 tonsDISTRIBUTION AL______________________________PRODUCT Bulk custom dairy pre-mixes,Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.VOLUME OF PRODUCT IN COMMERCE 350 tonsDISTRIBUTION AL and MS______________________________PRODUCTa) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bagsDISTRIBUTION AL, GA, MS, and TNEND OF ENFORCEMENT REPORT FOR AUGUST 9, 2006###Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006Date: August 6, 2006 at 6:16 pm PST PRODUCTa) CO-OP 32% Sinking Catfish, Recall # V-100-6;b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;j) CO-OP LAYING CRUMBLES, Recall # V-109-6;k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODEProduct manufactured from 02/01/2005 until 06/06/2006RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".VOLUME OF PRODUCT IN COMMERCE 125 tonsDISTRIBUTION AL and FLEND OF ENFORCEMENT REPORT FOR AUGUST 2, 2006###MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II______________________________PRODUCTa) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;d) Feather Meal, Recall # V-082-6 CODEa) Bulkb) Nonec) Bulkd) BulkRECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.REASONPossible contamination of animal feeds with ruminent derived meat and bone meal.VOLUME OF PRODUCT IN COMMERCE 10,878.06 tonsDISTRIBUTION NationwideEND OF ENFORCEMENT REPORT FOR July 12, 2006###10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007Date: March 21, 2007 at 2:27 pm PSTRECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II___________________________________PRODUCTBulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007CODECattle feed delivered between 01/12/2007 and 01/26/2007RECALLING FIRM/MANUFACTURERPfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.Firm initiated recall is ongoing.REASONBlood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.VOLUME OF PRODUCT IN COMMERCE42,090 lbs.DISTRIBUTIONWI___________________________________PRODUCTCustom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007CODEThe firm does not utilize a code - only shipping documentation with commodity and weights identified.RECALLING FIRM/MANUFACTURERRangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.REASONProducts manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.VOLUME OF PRODUCT IN COMMERCE9,997,976 lbs.DISTRIBUTIONID and NVEND OF ENFORCEMENT REPORT FOR MARCH 21, 2007
MONDAY, OCTOBER 10, 2022Docket No: 2002N-0273 (formerly Docket No. 02N-0273) Substances Prohibited From Use in Animal Food and Feed Scientists Comments December 20, 2005SUNDAY, OCTOBER 16, 2022USDA Transmissible Spongiform Encephalopathy TSE Prion Action Plan National Program 103 Animal Health 2022-2027TUESDAY, OCTOBER 18, 2022Assessing the Potential Transmissibility of Bovine and Cervid Prions with a Human Prion Protein-based Model ARS RESEARCH
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.
http://jama.jamanetwork.com/article.aspx?articleid=1031186
TUESDAY, APRIL 05, 2022
2022 American Academy of Neurology Emerging Sciences Abstract Website Incidence of Creutzfeldt-Jakob Disease in the United States 1993-2014
https://creutzfeldt-jakob-disease.blogspot.com/2022/04/incidence-of-creutzfeldt-jakob-disease_5.htmlSUNDAY, MAY 08, 2022
USA National Prion Disease Pathology Surveillance Center Surveillance Update April 11th, 2022
https://creutzfeldt-jakob-disease.blogspot.com/2022/05/usa-national-prion-disease-pathology.htmlSUNDAY, MAY 08, 2022
USA National Prion Disease Pathology Surveillance Center Surveillance Update April 11th, 2022
https://creutzfeldt-jakob-disease.blogspot.com/2022/05/usa-national-prion-disease-pathology.htmlTUESDAY, MAY 24, 2022
Texas Creutzfeldt Jakob Disease CJD TSE Prion Update Singeltary FOIA Request Received May 23, 2022
https://cjdtexas.blogspot.com/2022/05/texas-creutzfeldt-jakob-disease-cjd-tse.html
TUESDAY, MAY 10, 2022 Concordance of CSF RT-QuIC across the European Creutzfeldt-Jakob Disease surveillance network https://creutzfeldt-jakob-disease.blogspot.com/2022/05/concordance-of-csf-rt-quic-across.html
Terry S. Singeltary Sr.
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