Saturday, October 19, 2013

A comparative study of modified confirmatory techniques and additional immuno-based methods for non-conclusive autolytic Bovine spongiform encephalopathy cases

A comparative study of modified confirmatory techniques and additional immuno-based methods for non-conclusive autolytic Bovine spongiform encephalopathy cases


BMC Veterinary Research 2013, 9:212 doi:10.1186/1746-6148-9-212 Rocío Sarasa (rociosar@unizar.es) Dietmar Becher (becher@micromun.de) Juan J Badiola (badiola@unizar.es) Marta Monzón (mmonzon@unizar.es)


ISSN 1746-6148

Article type Research article

Submission date 6 March 2013

Acceptance date 9 October 2013

Publication date 18 October 2013

Article URL http://www.biomedcentral.com/1746-6148/9/212

BMC Veterinary Research

© 2013 Sarasa et al.

This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


A comparative study of modified confirmatory techniques and additional immuno-based methods for non-conclusive autolytic Bovine spongiform encephalopathy cases


Rocío Sarasa1 Email: rociosar@unizar.es Dietmar Becher2 Email: becher@micromun.de Juan J Badiola1 Email: badiola@unizar.es Marta Monzón1* * Corresponding author Email: mmonzon@unizar.es 1 Research Centre for Encephalopathies and Transmissible Emerging Diseases, University of Zaragoza, Zaragoza, Spain 2 Micromun Privates Institut für Mikrobiologische Forschung GmbH, Greifswald,

Germany

Abstract

Background

In the framework of the Bovine Spongiform Encephalopathy (BSE) surveillance programme, samples with non-conclusive results using the OIE confirmatory techniques have been repeatedly found. It is therefore necessary to question the adequacy of the previously established consequences of this non-conclusive result: the danger of failing to detect potentially infected cattle or erroneous information that may affect the decision of culling or not of an entire bovine cohort. Moreover, there is a very real risk that the underreporting of cases may possibly lead to distortion of the BSE epidemiological information for a given country.

In this study, samples from bovine nervous tissue presenting non-conclusive results by conventional OIE techniques (Western blot and immunohistochemistry) were analyzed. Their common characteristic was a very advanced degree of autolysis. All techniques recommended by the OIE for BSE diagnosis were applied on all these samples in order to provide a comparative study.

Specifically, immunohistochemistry, Western blotting, SAF detection by electron microscopy and mouse bioassay were compared. Besides, other non confirmatory techniques, confocal scanning microscopy and colloidal gold labelling of fibrils, were applied on these samples for confirming and improving the results.

snip...

Discussion

All the studied bovine samples were confirmed as BSE positive cases thanks to the results provided by immunocytochemistry, electron microscopy and bioassay. Despite all the applied techniques being standardized for increasing their capability to detect PrPsc, the extremely scarce concentration of PrPsc in the samples is proposed here as the most coherent reason why non-conclusive results (weak signal presenting an unconventional pattern) were provided by Western blotting as well as showing different titers in the bioassay (reflected by the lack of 100% success of transmission in all the mice included in it). Therefore, the positive results provided by immunohistochemistry on murine bioassay ultimately demonstrated that initial samples were infectious and transmitted the disease. This was also concluded by immunocytochemistry and SAF detection by electron microscopy being applied on the initial samples. However, rapid tests and immunoblotting did not result useful for convincingly confirming these results.

Although rapid techniques applied in this study achieved their objective as screening tests by showing a non-conclusive signal in the samples analyzed, they were not able to give definite results, demonstrating a lower sensitivity compared to some of the confirmatory techniques (not all in this occasion, since immunoblotting, despite the combined protocol described, was not able to improve the results provided by rapid tests in terms of sensitivity). Nonconclusive diagnosis obtained by these techniques in the bovine as well as false negative diagnosis in the murine samples have been previously justified on the basis of the low PrPsc concentration and the unsuitable selection of area to be analyzed [29]. Both are unavoidable and intrinsic features for the samples studied here. Overall, these findings might call into question the recent proposal determined by the OIE which dictates that two equal results with two different rapid techniques are enough to give an official BSE confirmation [30]. Furthermore, the results of this study confirm immunocytochemistry as a useful and rapid tool for diagnosis in liquid state samples, solving a relevant problem in BSE and Scrapie epidemiology.
As it had been previously impossible to apply histopathological examination due to the advanced degree of autolyisis of the analyzed samples, immunohistochemistry was evidenced as the first and reliable technique to diagnosis of samples included here.

Immunocytochemistry has been demonstrated here as a technique capable to provide final results for bovine samples. Moreover, this study first demonstrates the reliability of this technique established by Monleón et al. [18] since their results have been corroborated by other confirmatory techniques, specifically, by electron microscopy and by in vivo tools (bioassay). Confirmation of the immunocytochemical positive results by electron microscopy clearly discards the possible subjectivity and non-specificity which some authors could state for the immunocytochemical assessment established, since SAF visualization has been demonstrated to be exclusive to TSEs [31]. In spite of the proportion and length of fibrils being lower than those previously described in conventional positive cases [32], the immunolabelling of these fibrils by colloidal gold [33] unequivocally identified PrPsc in all of them. This slight difference in appearance is probably associated with the low PrPsc concentration assumed at the beginning and finally evidenced in this study. Besides, the visualization of paired gold deposits which seem to correspond with PrPsc dimers described by Dourmashkin et al. [34], supports this hypothesis, associating gold deposits to areas of potential formation of fibrils [35]. As a consequence, although it is a technique currently fallen into disuse, SAF visualization by electron microscopy is confirmed in this study as a technique with high sensitivity despite PrPsc concentration and autolysis of the sample, demonstrating to be useful for diagnosing this kind of samples.

On the other hand, although the bioassay presented a transmission rate lower than expected (only 24% of the inoculated mice developing clinical signs), its sensitivity was 100% since it confirmed the positive diagnosis of the bovine samples. The low number of affected mice, expressed in the low percentage of animals which presented clinical signs or positive result by diagnostic techniques, could be explained by several reasons. Despite partly avoiding the problem of species barrier by use of bovinized transgenic mice [36], the autolytic state of samples could have hampered the choice of the area of study where PrPsc was present.

Nevertheless, the main responsible factor for this failure seems to be the low initial PrPsc concentration due to, advancement of the protease digestion associated with the putrefaction process, the serial dilutions and heat treatment which had to be applied on the samples before inoculation. This scarce PrPsc presence could elongate the incubation period and, indirectly, cause false negatives in those mice which died prematurely, by natural death or euthanasia, before presenting clinical signs [37] or not presenting enough concentration of PrPsc to be detected by the applied techniques at that moment [38]. The fact that the only mouse clearly considered positive by rapid tests and the only mouse showing PrPsc plaques (as usually seen in BSE inoculated mice) [39] belonged to the group of animals where the highest concentration was used for inoculation, confirms this theory.
Moreover, the presence of isolated fibrils in the mice analyzed [40] instead of grouped fibrils visualized by electron microscopy in the only positive mouse by rapid tests [41], would, once again, correlate with this hypothesis.

As for the variance between the presence of PrPsc deposits and presentation of clinical signs found in some mice, PrPsc concentration used for inoculation could affect the results but also other explanations arise on this matter [42]. The possibility of a transmission of the disease without neurological signs [43] or a possible non-exclusive relationship between PrPsc and infectivity [44-46] and neurodegeneration [47], among them. Besides, the demonstration of the existence of animals as persistent carriers [48] or with a subclinical state of the disease [47], already described in mice with high titers of infection but no symptoms [49], should be borne in mind. This same lack of correlation between PrPsc and infectivity could be reflecting in the animals with symptoms but no PrPsc deposits [50], considering in this case that the disease might be transmitted without detectable PrPsc [44], even with high titers [51]. Further studies with non-diagnostic aims but for identification of astrocytes co-locating with PrPsc were developed here, as mentioned in Material and Methods section. The relationship between PrPsc and glial cells observed by conventional immunohistochemistry, was confirmed by confocal microscopy showing an evident co-localization. This finding would put in evidence the possibility of the participation of these cells, possibly across the haematoencephalic barrier [27,52], in the prion propagation in the model used here [53]. On this occasion, it was not possible to associate the studied samples to classical or atypical BSE owing to the lack of success to provide a clear banding pattern by Western blotting and/or a characteristic profile by immunohistochemistry, the lack of reference to previous data on incubation periods and the inability to determine lesion profiles in the mouse line. All these facts, as it has been stated, probably due to the very scarce concentration of PrPsc. Otherwise, whether the agent present in samples was atypical BSE or classical BSE with really low PrPsc deposits and low infectivity titers was not possible to be determined.

Conclusions

In conclusion, demonstration of transmission of the disease even with low concentrations of PrPsc [54], highlights BSE’s ability to adopt different behavior, even sometimes similar to Scrapie [55], should reinforce that vigilance is required in interpreting results so that subtle changes do not go unnoticed. Additionally, to maintain a continued supervision of the techniques which are applied in the routine diagnosis would prove essential for the ultimate eradication of the disease. A study of the actual BSE presence should be considered as necessary because a state of sporadic prevalence could exist [56] and samples without a diagnosis [57,58] could reach the food chain, involving therefore a risk for public health.


Keywords

TSEs, BSE, Confirmatory diagnosis, Non-conclusive cases

http://www.biomedcentral.com/content/pdf/1746-6148-9-212.pdf


WOW! holy mad cows, how many more were there, and how many were consumed or put into by-products for consumption, for humans and animals ???
 
 
 

Sent: Tuesday, August 13, 2013 3:58 PM
 
 
Subject: Idiopathic Brainstem Neuronal Chromatolysis (IBNC): a novel prion protein related disorder of cattle?
 
 
Greetings Honorable Science Advisory Council et al @ DEFRA,
 
 
I wish to ask a question about something I have seen no updates on, that concerns me.
 
 
IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS IBNC or what I some times call, IBNC BSE.
 
 
I have seen nothing in the scientific literature updated on this in years, since around 2008, then it was like it fell off the face of the earth ?
 
can you please give me some sort of update on the IBNC BSE science to date ?
 
how many cases of IBNC BSE have been detected ?
 
is there an ongoing surveillance for this the IBNC BSE, and are the BSE test even capable of detecting it ?
 
could the USA and or North America even detect, if they were even looking for it ?
 
latest studies, if any more since "All of the 15 cattle tested showed that the brains had abnormally accumulated PrP" ?
 
 
thank you,
 
kind regards,
terry
 
references as follows ;
 
 
Research article

Idiopathic Brainstem Neuronal Chromatolysis (IBNC): a novel prion protein related disorder of cattle?

Martin Jeffrey1*, Belinda Baquero Perez2, Stuart Martin1, Linda Terry2 and Lorenzo González1
1 Veterinary Laboratories Agency (VLA-Lasswade), Pentlands Science Park, Bush Loan, Midlothian EH26 0PZ, UK
2 VLA-Weybridge, Addlestone, Surrey, KT15 3NB, UK
For all author emails, please log on.

BMC Veterinary Research 2008, 4:38 doi:10.1186/1746-6148-4-38

The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1746-6148/4/38

Received: 3 April 2008
Accepted: 30 September 2008
Published: 30 September 2008
© 2008 Jeffrey et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background

The epidemic form of Bovine Spongiform Encephalopathy (BSE) is generally considered to have been caused by a single prion strain but at least two strain variants of cattle prion disorders have recently been recognized. An additional neurodegenerative condition, idiopathic brainstem neuronal chromatolysis and hippocampal sclerosis (IBNC), a rare neurological disease of adult cattle, was also recognised in a sub-set of cattle submitted under the BSE Orders in which lesions of BSE were absent. Between the years of 1988 and 1991 IBNC occurred in Scotland with an incidence of 7 cases per 100,000 beef suckler cows over the age of 6 years.

Results

When the brains of 15 IBNC cases were each tested by immunohistochemistry, all showed abnormal labelling for prion protein (PrP). Immunohistological labelling for PrP was also present in the retina of a single case available for examination. The pattern of PrP labelling in brain is distinct from that seen in other ruminant prion diseases and is absent from brains with other inflammatory conditions and from normal control brains. Brains of IBNC cattle do not reveal abnormal PrP isoforms when tested by the commercial BioRad or Idexx test kits and do not reveal PrPres when tested by Western blotting using stringent proteinase digestion methods. However, some weakly protease resistant isoforms of PrP may be detected when tissues are examined using mild proteinase digestion techniques.

Conclusion

The study shows that a distinctive neurological disorder of cattle, which has some clinical similarities to BSE, is associated with abnormal PrP labelling in brain but the pathology and biochemistry of IBNC are distinct from BSE. The study is important either because it raises the possibility of a significant increase in the scope of prion disease or because it demonstrates that widespread and consistent PrP alterations may not be confined to prion diseases. Further studies, including transmission experiments, are needed to establish whether IBNC is a condition in which prion protein is abnormally regulated or it is yet a further example of an infectious cattle prion disease.
1992

 
NEW BRAIN DISORDER
 
3. WHAT ABOUT REPORTS OF NEW FORM OF BSE ?
 
THE VETERINARY RECORD HAS PUBLISHED AN ARTICLE ON A NEW BRAIN DISORDER OF CATTLE DISCOVERED THROUGH OUR CONTROL MEASURES FOR BSE. ALTHOUGH IT PRESENTS SIMILAR CLINICAL SIGNS TO BSE THERE ARE MAJOR DIFFERENCES IN HISTOPATHOLOGY AND INCUBATION PERIODS BETWEEN THE TWO. MUST EMPHASISE THAT THIS IS _NOT_ BSE.
 
4. IS THIS NEW BRAIN DISORDER A THREAT ?
 
WE DO NOT EVEN KNOW WHETHER THE AGENT OF THIS DISEASE IS TRANSMISSIBLE. IN ANY CASE, CASES SO FAR IDENTIFIED HAD SHOWN SIMILAR SYMPTOMS TO THOSE OF BSE, AND THEREFORE HAVE BEEN SLAUGHTERED AND INCINERATED, SO THAT IF A TRANSMISSIBLE AGENT WERE INVOLVED IT WOULD HAVE BEEN ELIMINATED. ...
 
 
 
Tuesday, November 17, 2009
 
SEAC NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS (IBNC) FROM THE VETERINARY LABORATORIES AGENCY (VLA) SEAC 103/1
 
 
 
NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS
 
"All of the 15 cattle tested showed that the brains had abnormally accumulated PrP"
 
2009
 
 
 
''THE LINE TO TAKE'' ON IBNC $$$ 1995 $$$
 
1995
 
page 9 of 14 ;
 
30. The Committee noted that the results were unusual. the questioned whether there could be coincidental BSE infection or contamination with scrapie. Dr. Tyrell noted that the feeling of the committee was that this did not represent a new agent but it was important to be prepared to say something publicly about these findings. A suggested line to take was that these were scientifically unpublishable results but in line with the policy of openness they would be made publicly available and further work done to test their validity. Since the BSE precautions were applied to IBNC cases, human health was protected. Further investigations should be carried out on isolations from brains of IBNC cases with removal of the brain and subsequent handling under strict conditions to avoid the risk of any contamination.
 
31. Mr. Bradley informed the Committee that the CVO had informed the CMO about the IBNC results and the transmission from retina and he, like the Committee was satisfied that the controls already in place or proposed were adequate. ...
 
snip... see full text
 
 
 
 
Wednesday, July 28, 2010
 
Atypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA Final report
 
 
 
IN CONFIDENCE
 
BSE ATYPICAL LESION DISTRIBUTION
 
 
 
Tuesday, November 02, 2010
 
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
 
 
 
Sunday, July 21, 2013
 
Welsh Government and Food Standards Agency Wales Joint Public Consultation on the Proposed Transmissible Spongiform Encephalopathies (Wales) Regulations 2013 Singeltary Submission WG18417
 
 
 
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
 
 
 
Thursday, August 15, 2013
 
Stability properties of PrPSc from cattle with experimental transmissible spongiform encephalopathies: use of a rapid whole homogenate, protease-free assay
 
 

 
Thursday, August 15, 2013
 
The emergence of novel BSE prions by serial passages of H-type BSE in bovinized mice
 
 
 
Monday, September 02, 2013
 
Atypical BSE: role of the E211K prion polymorphism
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
 
Location: Virus and Prion Research Unit
 
 
 
Sunday, September 1, 2013
 
Evaluation of the Zoonotic Potential of Transmissible Mink Encephalopathy
 
We previously described the biochemical similarities between PrPres derived from L-BSE infected macaque and cortical MM2 sporadic CJD: those observations suggest a link between these two uncommon prion phenotypes in a primate model (it is to note that such a link has not been observed in other models less relevant from the human situation as hamsters or transgenic mice overexpressing ovine PrP [28]). We speculate that a group of related animal prion strains (L-BSE, c-BSE and TME) would have a zoonotic potential and lead to prion diseases in humans with a type 2 PrPres molecular signature (and more specifically type 2B for vCJD)
 
snip...
 
Together with previous experiments performed in ovinized and bovinized transgenic mice and hamsters [8,9] indicating similarities between TME and L-BSE, the data support the hypothesis that L-BSE could be the origin of the TME outbreaks in North America and Europe during the mid-1900s.
 
 
 
Tuesday, September 24, 2013
 
NORDION (US), INC., AND BIOAXONE BIOSCIENCES, INC., Settles $90M Mad Cow TSE prion Contamination Suit Cethrin(R)
 
Case 0:12-cv-60739-RNS Document 1 Entered on FLSD Docket 04/26/2012 Page 1 of 15
 
 
 
Sunday, November 13, 2011

California BSE mad cow beef recall, QFC, CJD, and dead stock downer livestock
http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/california-bse-mad-cow-beef-recall-qfc.html
 
 
Wednesday, September 25, 2013
 
Inspections, Compliance, Enforcement, and Criminal Investigations BSE TSE PRION 2013
 
 
 
Monday, September 2, 2013
 
PRION2013 AD.22: Bovine spongiform encephalopathy, chronic wasting disease and scrapie (TSE surveillance) programs in Alberta, Canada
 
 
 
Tuesday, May 21, 2013
 
Canada, USA, Bad feed, mad cows: Why we know three BSE cases had a common origin and why the SSS policy is in full force $$$
 
 
 
Monday, August 26, 2013
 
***The Presence of Disease-Associated Prion Protein in Skeletal Muscle of Cattle Infected with Classical Bovine Spongiform Encephalopathy
 
 
 
Tuesday, April 24, 2012

MAD COW DISEASE USA 4TH CASE DOCUMENTED ATYPICAL BSE CALIFORNIA

 
 
Thursday, April 26, 2012
 
Update from USDA Regarding a Detection of Bovine Spongiform Encephalopathy
 
(BSE) in the United States WASHINGTON bulletin at 04/26/2012 10:11 PM EDT
 
 
 
 
atypical L-type BASE BSE California
 
 
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE INVESTIGATION JULY 2012
 
 
Summary Report BSE 2012
 
Executive Summary
 
 
 
Saturday, August 4, 2012
 
*** Final Feed Investigation Summary - California BSE Case - July 2012
 
 
 
Saturday, August 4, 2012
 
Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation
 
 
 
Wednesday, September 25, 2013
 
Inspections, Compliance, Enforcement, and Criminal Investigations BSE TSE PRION 2013
 
 
 
Tuesday, July 2, 2013
 
APHIS USDA Administrator Message to Stakeholders: Agency Vision and Goals Eliminating ALL remaining BSE barriers to export market
 
 
 
 
 

FDA STATEMENT

FOR IMMEDIATE RELEASE
May 4, 2004
Media Inquiries: 301-827-6242
Consumer Inquiries: 888-INFO-FDA

 

Statement on Texas Cow With Central Nervous System Symptoms


 
On Friday, April 30th, the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).
FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.
To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.
Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.
FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.
 
 
FOR IMMEDIATE RELEASE P01-05 January 30, 2001
Print Media : 301-827-6242 Consumer Inquiries: 888-INFO-FDA
 
Note: On Dec. 23, 2003, the U.S. Department of Agriculture reported that a cow in Washington state had tested positive for bovine spongiform encephalopathy (BSE, or mad cow disease). As a result, information on this Web page stating that no BSE cases had been found in the United States is now incorrect. However, because other information on this page continues to have value, the page will remain available for viewing.

FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT

Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.

FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.

It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.

According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."

Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.

FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.

This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.

FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.

Office of Public Affairs 2001-JAN-30
http://www.fda.gov/bbs/topics/news/2001/new00752.html



''FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.'' ???
http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html
 
 
ONE HUNDRED EIGHTH CONGRESS

COMMITTEE ON GOVERNMENT REFORM

May 13,2004

The Honorable Ann M. Veneman Secretary of Agriculture Department of Agriculture1400 Independence Avenue, SW Washington, DC 20250

Dear Madam Secretary:

I am writing to express concern that the recent failure of the U.S. Department of Agriculture (USDA) to test a Texas cow with neurological syrnptoms for bovine spongifonnencephalopathy (BSE) may reflect wider problems in the surveillance program. USDA apparently does not keep track of how many cows condemned for central nervous system symptoms are tested for BSE nor does it require that suspect carcasses be held pending testing...
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

snip...

We attribute the failure to identify the BSE positive sample to rigid protocols, as well as the lack of adequate quality assurance controls over its testing program. Details of our concerns are discussed in Findings 3 and 4.

snip...

Section 2. Testing Protocols and Quality Assurance Controls

In November 2004, USDA announced that its rapid screening test, Bio-Rad Enzyme Linked Immunosorbent Assay (ELISA), produced an inconclusive BSE test result as part of its enhanced BSE surveillance program. The ELISA rapid screening test performed at a BSE contract laboratory produced three high positive reactive results.40 As required,41 the contract laboratory forwarded the inconclusive sample to the APHIS National Veterinary Services Laboratories (NVSL) for confirmatory testing. NVSL repeated the ELISA testing and again produced three high positive reactive results.42 In accordance with its established protocol, NVSL ran its confirmatory test, an immunohistochemistry (IHC) test, which was interpreted as negative for BSE. In addition, NVSL performed a histological43 examination of the tissue and did not detect lesions44 consistent with BSE.

Faced with conflicting results, NVSL scientists recommended additional testing to resolve the discrepancy but APHIS headquarters officials concluded no further testing was necessary because testing protocols were followed. In our discussions with APHIS officials, they justified their decision not to do additional testing because the IHC is internationally recognized as the “gold standard.” Also, they believed that conducting additional tests would undermine confidence in USDA’s established testing protocols. However, OIG obtained evidence that indicated additional testing was prudent to ensure that USDA’s testing protocols were effective in detecting BSE and that confidence in USDA’s testing procedures was maintained. OIG came to this conclusion because the rapid tests produced six high positive reactive results, confirmatory testing conflicted with the rapid test results, and various standard operating procedures were not followed. Also, our review of scientific literature, other country protocols, as well as discussions with internationally recognized experts led us to conclude that confirmatory testing should not be limited when conflicting test results are obtained. To maintain objectivity and independence in our assessment, we requested the USDA Agricultural Research Service (ARS) perform the Office International des Epizooties (OIE) Scrapie-Associated Fibrils (SAF)

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.

USDA/OIG-A/50601-10-KC Page 31

immunoblot.45 ARS performed the test at the National Animal Disease Center because NVSL did not have the necessary equipment46 (ultracentrifuge) to do the test. APHIS scientists observed and participated, as appropriate, in this effort.

The additional tests conducted by ARS produced positive results. To confirm this finding, the Secretary requested the internationally recognized BSE reference laboratory in Weybridge, England, (Weybridge) to perform additional confirmatory testing. Weybridge conducted various tests, including their own IHC methods, as well as three Western blot methods. The tests confirmed that the suspect cow was infected with BSE. Also, Weybridge confirmed this case as an unequivocal positive case of BSE on the basis of IHC. As a result of this finding, the Secretary immediately directed USDA scientists to work with international experts to develop a new protocol that includes performing dual confirmatory tests in the event of another inconclusive BSE screening test.

snip...

http://www.usda.gov/oig/webdocs/50601-10-KC.pdf

Tuesday, August 22, 2006

BSE ATYPICAL TEXAS AND ALABAMA UPDATE JANUARY 20, 2007
2009 UPDATE ON ALABAMA MAD COW FOUND IN 2006

http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
I ask Professor Kong ;
Thursday, December 04, 2008 3:37 PM
Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment
''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''
 
Professor Kong reply ;
 
 
.....snip
 
 
''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''
 
Best regards, Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA
 
END...TSS
 
 
Thursday, December 04, 2008 2:37 PM
 
"we have found that H-BSE can infect humans."
 
personal communication with Professor Kong. ...TSS
 
BSE-H is also transmissible in our humanized Tg mice.
 
The possibility of more than two atypical BSE strains will be discussed.
 
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
 
 
 
 
 
 
 
please see below from PRION2013 ;
 
 
 
*** This study imply the possibility that the novel BSE prions with high virulence in cattle will be emerged during intraspecies transmission.
 
 
AD.56: The emergence of novel BSE prions by serial passages of H-type BSE in bovinized mice
 
Kentaro Masujin, Naoko Tabeta, Ritsuko Miwa, Kohtaro Miyazawa, Hiroyuki Okada, Shirou Mohri and Takashi Yokoyama
 
National Institute of Animal Health; Tsukuba, Japan
 
H-type bovine spongiform encephalopathy (BSE) is an atypical form of BSE, and has been detected in several European countries, and North America. Transmission studies of H-type BSE led to the emergence of the classical BSE (C-BSE) phenotypes during passages in inbred wild type and bovinized PrP-overexpressing transgenic mice. In this study, we conducted serial passages of Canadian H-type BSE isolate in bovinized PrP-overexpressing transgenic mice (TgBoPrP). H-type BSE isolate was transmitted to TgBoPrP with incubation periods of 320 ± 12.2 d at primary passage. The incubation period of 2nd and 3rd passage were constant (~= 220 d), no clear differences were observed in their biological and biochemical properties. However, at the forth passage, 2 different BSE phenotypes were confirmed; one is shorter survival times (109 ± 4 d) and the other is longer survival times. TgBoPrP mice with longer incubation period showed the H-type phenotype of PrPsc profile and pathology. However, those of shorter incubation period were different phenotypes from previously existed BSE prions (C-BSE, L-type BSE, and H-type BSE). *** This study imply the possibility that the novel BSE prions with high virulence in cattle will be emerged during intraspecies transmission.
 
 
 
 
 
 
please see ;
 
 
Thursday, August 15, 2013
 
The emergence of novel BSE prions by serial passages of H-type BSE in bovinized mice
 
 
 
Wednesday, September 25, 2013
 
Presence of subclinical infection in gene-targeted human prion protein transgenic mice exposed to atypical BSE
 
 
 

TEST, TEST, TEST, TEST ALL LIVESTOCK PRODUCING ANIMALS FOR TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY, and let the chips fall where they may. ...

Subject: USDA VS CREEKSTONE BSE/BASE/TSE TESTING Civil Action No. 06-0544 Date: September 4, 2007 at 9:47 am PST USDA

AUGUST 21, 2007

Mr. Terry S. Singeltary Sr. Post Office Box 42 Bacliff, Texas 77518-0042

Dear Mr. Singeltary:

This is in response to your e-mails to Secretary Johanns concerning private testing for bovine spongiform encephalopathy (BSE) and a ruling by the U.S. District Court for the District of Columbia involving Creekstone Farms Premium Beef, LLC. We regret the delay in responding.

As you may know, the U.S. Department of Agriculture (USDA) filed an appeal of the U.S. District Court's order on June 15,2007. While we recognize your views, we cannot comment on any matters at issue in the pending litigation. However, we can assure you that USDA remains committed to ensuring effective, scientifically sound testing for significant animal diseases and to protecting U.S. animal and public health from BSE.

We understand that the effects of Creutzfeldt-Jakob disease (CJD) are devastating, and we are sorry to learn of the loss of your mother. Some of us at USDA have also lost family members to CJD and other degenerative neurological diseases. Although it is rare, the classical form of CJD does occur sporadically in the United States and worldwide. However, no cases of vCJD-the form of BSE that can be transmitted from animals to humans-are known to have originated in the United States. Because the U.S. Department of Health and Human Services' (HHS) Centers for Disease Control and Prevention (CDC) is responsible for addressing concerns about CJD and other human health issues, you may wish to contact that agency directly. The address is CDC, HHS, 200 Independence Avenue, SW., Washington, D.C. 20201.

We also wish to clarify that the U.S. Food and Drug Administration's 1997 ban on ruminant-to-ruminant feeding is the primary measure in place to protect animal health with regard to BSE. Protection of public health from BSE is achieved by the removal from the human food supply of the animal tissues-often referred to as specified risk

Mr. Terry S. Singeltary, Sr. Page 2

materials-in which the BSE infective agent would be found if present, and by other controls imposed at the slaughter level. These additional controls include the Food Safety and Inspection Services' ban on nonambulatory cattle from the human food chain; a prohibition on air-injection stunning of slaughter cattle; the requirement of additional process controls in advanced meat recovery systems; and, a prohibition on the use of mechanically separated beef in human food. Additionally, protection from BSE and other diseases is achieved by conducting antemortem inspections of slaughter cattle and excluding any animals that display clinical signs of neurological disease or other abnormalities.

We appreciate the opportunity to address your concerns. To learn more about USDA's BSE surveillance and safeguarding activities, please visit our Web site at
www.aphis.usda.gov/newsroom/hot_issues/bse/index.shtml.


Sincerely,

Jere L. Dick Associate Deputy Administrator National Animal Health Policy and Programs Veterinary Services


============================END=========================


we all know the infamous ENHANCE BSE SURVEILLANCE PROGRAM you speak of where some 800,000 plus animals were tested, was so flawed, it was a joke. nobody with believes it, not even CONGRESS OIG/GAO. NOR did Paul Brown, one of the leading TSE scientist at the NIH/CDC. I quote ;

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

snip...end

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


PAUL BROWN COMMENT TO ME ON THIS ISSUE

Tuesday, September 12, 2006 11:10 AM

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

OR, what the Honorable Phyllis Fong of the OIG found ;

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

Report No. 50601-10-KC January 2006

Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf


”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

USDA 2003

We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back. Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS.

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.

snip.............

Dr. Detwiler: It seems a good idea, but I'm not aware of it. Another important thing to get across to the public is that the negatives do not guarantee absence of infectivity. The animal could be early in the disease and the incubation period. Even sample collection is so important. If you're not collecting the right area of the brain in sheep, or if collecting lymphoreticular tissue, and you don't get a good biopsy, you could miss the area with the PRP in it and come up with a negative test. There's a new, unusual form of Scrapie that's been detected in Norway. We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back.

Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS .

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.

snip...

FULL TEXT;

Completely Edited Version PRION ROUNDTABLE

Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado

2005
http://madcowtesting.blogspot.com/2009/02/report-on-testing-ruminants-for-tses-in.html


Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE sampling FROM HEALTHY USDA CATTLE) Date: June 21, 2007 at 2:49 pm PST

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.

snip...

Topics that will be covered in ongoing or planned reviews under Goal 1 include:

soundness of BSE maintenance sampling (APHIS),

implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),

snip...

The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.

4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
http://www.usda.gov/oig/webdocs/sarc070619.pdf


-MORE Office of the United States Attorney District of Arizona FOR IMMEDIATE RELEASE For Information Contact Public Affairs February 16, 2007
 
WYN HORNBUCKLE Telephone: (602) 514-7625 Cell: (602) 525-2681

CORPORATION AND ITS PRESIDENT PLEAD GUILTY TO DEFRAUDING GOVERNMENT’S MAD COW DISEASE SURVEILLANCE PROGRAM

PHOENIX -- Farm Fresh Meats, Inc. and Roland Emerson Farabee, 55, of Maricopa, Arizona, pleaded guilty to stealing $390,000 in government funds, mail fraud and wire fraud, in federal district court in Phoenix. U.S. Attorney Daniel Knauss stated, “The integrity of the system that tests for mad cow disease relies upon the honest cooperation of enterprises like Farm Fresh Meats. Without that honest cooperation, consumers both in the U.S. and internationally are at risk. We want to thank the USDA’s Office of Inspector General for their continuing efforts to safeguard the public health and enforce the law.” Farm Fresh Meats and Farabee were charged by Information with theft of government funds, mail fraud and wire fraud. According to the Information, on June 7, 2004, Farabee, on behalf of Farm Fresh Meats, signed a contract with the U.S. Department of Agriculture (the “USDA Agreement”) to collect obex samples from cattle at high risk of mad cow disease (the “Targeted Cattle Population”). The Targeted Cattle Population consisted of the following cattle: cattle over thirty months of age; nonambulatory cattle; cattle exhibiting signs of central nervous system disorders; cattle exhibiting signs of mad cow disease; and dead cattle. Pursuant to the USDA Agreement, the USDA agreed to pay Farm Fresh Meats $150 per obex sample for collecting obex samples from cattle within the Targeted Cattle Population, and submitting the obex samples to a USDA laboratory for mad cow disease testing. Farm Fresh Meats further agreed to maintain in cold storage the sampled cattle carcasses and heads until the test results were received by Farm Fresh Meats.

Evidence uncovered during the government’s investigation established that Farm Fresh Meats and Farabee submitted samples from cattle outside the Targeted Cattle Population. Specifically, Farm Fresh Meats and Farabee submitted, or caused to be submitted, obex samples from healthy, USDA inspected cattle, in order to steal government moneys.

Evidence collected also demonstrated that Farm Fresh Meats and Farabee failed to maintain cattle carcasses and heads pending test results and falsified corporate books and records to conceal their malfeasance. Such actions, to the extent an obex sample tested positive (fortunately, none did), could have jeopardized the USDA’s ability to identify the diseased animal and pinpoint its place of origin. On Wednesday, February 14, 2007, Farm Fresh Meats and Farabee pleaded guilty to stealing government funds and using the mails and wires to effect the scheme. According to their guilty pleas:

(a) Farm Fresh Meats collected, and Farabee directed others to collect, obex samples from cattle outside the Targeted Cattle Population, which were not subject to payment by the USDA;

(b) Farm Fresh Meats 2 and Farabee caused to be submitted payment requests to the USDA knowing that the requests were based on obex samples that were not subject to payment under the USDA Agreement;

(c) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Data Collection Forms to the USDA’s testing laboratory that were false and misleading;

(d) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Submission Forms filed with the USDA that were false and misleading;

(e) Farm Fresh Meats falsified, and Farabee directed others to falsify, internal Farm Fresh Meats documents to conceal the fact that Farm Fresh Meats was seeking and obtaining payment from the USDA for obex samples obtained from cattle outside the Targeted Cattle Population; and

(f) Farm Fresh Meats failed to comply with, and Farabee directed others to fail to comply with, the USDA Agreement by discarding cattle carcasses and heads prior to receiving BSE test results. A conviction for theft of government funds carries a maximum penalty of 10 years imprisonment. Mail fraud and wire fraud convictions carry a maximum penalty of 20 years imprisonment. Convictions for the above referenced violations also carry a maximum fine of $250,000 for individuals and $500,000 for organizations. In determining an actual sentence, Judge Earl H. Carroll will consult the U.S. Sentencing Guidelines, which provide appropriate sentencing ranges. The judge, however, is not bound by those guidelines in determining a sentence.

Sentencing is set before Judge Earl H. Carroll on May 14, 2007. The investigation in this case was conducted by Assistant Special Agent in Charge Alejandro Quintero, United States Department of Agriculture, Office of Inspector General. The prosecution is being handled by Robert Long, Assistant U.S. Attorney, District of Arizona, Phoenix. CASE NUMBER: CR-07-00160-PHX-EHC RELEASE NUMBER: 2007-051(Farabee) # # #
http://www.usdoj.gov/usao/az/press_releases/2007/2007-051(Farabee).pdf


The beef import forecast for the second quarter was unchanged from last month’s, despite pressure from higher-than-expected domestic cow slaughter that has remained high through most of this period. Beef imports into the United States from Australia, New Zealand, and Uruguay provide additional processing beef that, along with domestic cow and bull beef, is mixed with 50-percent trim from fed cattle to make ground beef. Forecast beef exports were raised slightly, mainly on continued (though gradual) improvements in sales to major Asian markets. In late May the World Animal Health Organization – known by its French acronym, OIE – designated the United States as having “controlled risk status” for bovine spongiform encephalopathy, or BSE. This designation reflects the OIE’s view that beef produced in the United States is safe for export, since BSE control measures such as feed bans and removal of specified risk materials result in negligible risk to consumers. However, the OIE standards are only guidelines. Individual countries may adopt differing standards, and those countries that do accept OIE standards must still undertake the bureaucratic processes to revise their rules and procedures.http://www.ers.usda.gov/publications/ldp/2007/06Jun/ldpm156.pdf


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

11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to then Central Bureau............
http://www.oie.int/eng/Session2007/RF2006.pdf
 
 
Saturday, October 19, 2013
 
ACA Council Meets to Endorse Several Proposed USAHA Resolutions (CWD TSE PRION DISEASE)
 
 

Friday, August 16, 2013
 
*** Creutzfeldt-Jakob disease (CJD) biannual update August 2013 U.K. and *** Contaminated blood products induce a highly atypical prion disease devoid of PrPres in primates
 
 
 
Monday, October 14, 2013
 
Researchers estimate one in 2,000 people in the UK carry variant CJD proteins
 
 
 
Sunday, August 11, 2013
 
Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013
 
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010
 
 


Sunday, October 13, 2013

CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-tse-prion-disease-cases-in-texas-by.html


Sunday, October 13, 2013

Prion Disease Cases in Texas by Year, 2003-2012
http://cjdtexas.blogspot.com/2013/10/prion-disease-cases-in-texas-by-year_13.html


Wednesday, October 09, 2013

WHY THE UKBSEnvCJD ONLY THEORY IS SO POPULAR IN IT'S FALLACY, £41,078,281 in compensation REVISED
http://creutzfeldt-jakob-disease.blogspot.com/2013/10/why-ukbsenvcjd-only-theory-is-so.html
 
Sunday, March 31, 2013
 
Creutzfeldt Jakob Disease CJD worlds youngest documented victim, 11 years old, shall we pray
 
 
 
Monday, January 14, 2013
 
Gambetti et al USA Prion Unit change another highly suspect USA mad cow victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes along with this BSe
 
 
 
Monday, December 31, 2012
 
Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State, 2006–2011-2012
 
 
 
Saturday, December 29, 2012
 
MAD COW USA HUMAN TSE PRION DISEASE DECEMBER 29 2012 CJD CASE LAB REPORT
 
 
 
MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...
 
 
 
Tuesday, November 6, 2012
 
Transmission of New Bovine Prion to Mice, Atypical Scrapie, BSE, and Sporadic CJD, November-December 2012 update
 
 
 
Tuesday, June 26, 2012
 
Creutzfeldt Jakob Disease Human TSE report update North America, Canada, Mexico, and USDA PRION UNIT as of May 18, 2012
 
type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the rise in Canada and the USA
 
 
 
Saturday, March 5, 2011
 
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
 
 
 
Sunday, February 12, 2012
 
National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas
 
 
 
Monday, August 9, 2010
 
Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more Prionbaloney ?
 
 
 
Wednesday, March 28, 2012
 
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion poker goes up again $
 
OR-10 15:25 - 15:40 VARIABLY PROTEASE-SENSITIVE PRIONOPATHY IS TRANSMISSIBLE IN BANK VOLES Nonno
 
 
 
 
=====================================
 
 
>>>We previously described the biochemical similarities between PrPres derived from L-BSE infected macaque and cortical MM2 sporadic CJD: those observations suggest a link between these two uncommon prion phenotypes in a primate model (it is to note that such a link has not been observed in other models less relevant from the human situation as hamsters or transgenic mice overexpressing ovine PrP [28]). We speculate that a group of related animal prion strains (L-BSE, c-BSE and TME) would have a zoonotic potential and lead to prion diseases in humans with a type 2 PrPres molecular signature (and more specifically type 2B for vCJD)<<<
 
 
=====================================
 
 
2003 Singeltary Submission to FDA ;
 
 
Asante/Collinge et al have major findings on sporadic CJD, why in the hell is this not making big news in the USA? ($$$) the fact that with the new findings from Collinge et al, that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc, the commonest sporadic CJD, i only ponder how many of the sporadic CJDs in the USA are tied to this alternate phenotype? these new findings are very serious, and should have a major impact on the way sporadic CJDs are now treated as opposed to the vCJD that was thought to be the only TSE tied to ingesting beef, in the medical/surgical arena. these new findings should have a major impact on the way sporadic CJD is ignored, and should now be moved to the forefront of research as with vCJD/nvCJD. the USA has many TSEs, the USA lacks sufficient testing for TSEs in cattle, and the USA still refuses to rapid TSE test USA cattle in sufficient numbers to find, when the late Dr. Richard Marsh had proven that mink had gone down with a TSE (TME), from being fed on 95%+ downer cattle.
 
 
 
 
From: Terry S. Singeltary Sr. [flounder@wt.net]
 
Sent: Tuesday, July 29, 2003 1:03 PM
 
 
 
Subject: Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION TO DOCKET 2003N-0312]
 
Greetings FDA,
 
my name is Terry S. Singeltary Sr., i lost my mother to hvCJD (Heidenhain Variant Creutzfeldt Jakob Disease).
 
i would kindly like to comment on the proposed HACCP method of detecting and or preventing TSEs in the human/animal feed supply.
 
it seems to me by implementing something that was designed for Astronauts instead of cattle, something that the GAO has already stated is terribly flawed (HACCP), i find it very disturbing to continue to insist on refusing to use rapid TSE TESTING in sufficient numbers to find TSEs, as with other Countries that they too once thought they were BSE free. for example, it took Italy 1 MILLION rapid TSE tests since 2001 to find 102 cases of BSE. THE USA has only tested 48,000 cattle in the 14 years of surveillance. there is documented proof that indeed the USA cattle have been infected with a TSE for decades, but the FDA/USDA and other USA Gov. agencies continue to conveniently ignore these findings. YOU must not ignore what Richard Marsh found. Plus, you must not ignore Asante/Collinge new findings that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD. The USA has been feeding ruminant by-products back to cattle, deer, elk and sheep for decades, and TSEs in these species have been recycled for feed for decades in the USA. The rendering process here in the USA will not kill this agent. to implement any HACCP over massive rapid TSE testing is only prolonging the inevitable, and will only allow the agent to spread further. it is simply a band-aid approach to something that needs a tourniquet...
 
 
 
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 ;
 
 
 
 
response to Singeltary et al ;
 
 
 
 
 
Monday, January 08, 2001 3:03 PM
 
 
 
A kind greetings from Bacliff, Texas !
 
I have often pondered if the whole damn mad cow follies started over here in the USA, and somehow, the USA shipped it over to the UK ?
 
It happened with S. Korea and CWD, via Canada. see ;
 
The disease was confirmed only in elk in the Republic of Korea in 2001, 2004 and 2005. Epidemiological investigations showed that CWD was introduced via importation of infected elk from Canada between 1994 and 1997.
 
 
 
but I still am not so sure that the mad cow follies did not start long ago right here in the USA i.e. Richard Marsh and deadstock downer cattle to those mink, and then the USA shipped it to hell and back. just pondering out loud here. ...tss
 
 
The exact same recipe for B.S.E. existed in the U.S. for years
 
and years. In reading over the Qualitative Analysis of BSE
 
Risk Factors-1, this is a 25 page report by the
 
USDA:APHIS:VS. It could have been done in one page. The
 
first page, fourth paragraph says it all;
 
"Similarities exist in the two countries usage of continuous
 
rendering technology and the lack of usage of solvents,
 
however, large differences still remain with other risk factors
 
which greatly reduce the potential risk at the national level."
 
Then, the next 24 pages tries to down-play the high risks of
 
B.S.E. in the U.S., with nothing more than the cattle to sheep
 
ratio count, and the geographical locations of herds and flocks.
 
That's all the evidence they can come up with, in the next 24
 
pages.
 
Something else I find odd, page 16;
 
"In the United Kingdom there is much concern for a specific
 
continuous rendering technology which uses lower
 
temperatures and accounts for 25 percent of total output. This
 
technology was _originally_ designed and imported from the
 
United States. However, the specific application in the
 
production process is _believed_ to be different in the two
 
countries."
 
A few more factors to consider, page 15;
 
"Figure 26 compares animal protein production for the two
 
countries. The calculations are based on slaughter numbers,
 
fallen stock estimates, and product yield coefficients. This
 
approach is used due to variation of up to 80 percent from
 
different reported sources. At 3.6 million tons, the United
 
States produces 8 times more animal rendered product than
 
the United Kingdom."
 
"The risk of introducing the BSE agent through sheep meat and
 
bone meal is more acute in both relative and absolute terms in
 
the United Kingdom (Figures 27 and 28). Note that sheep
 
meat and bone meal accounts for 14 percent, or 61 thousand
 
tons, in the United Kingdom versus 0.6 percent or 22 thousand
 
tons in the United States. For sheep greater than 1 year, this is
 
less than one-tenth of one percent of the United States supply."
 
"The potential risk of amplification of the BSE agent through
 
cattle meat and bone meal is much greater in the United States
 
where it accounts for 59 percent of total product or almost 5
 
times more than the total amount of rendered product in the
 
United Kingdom."
 
Considering, it would only take _one_ scrapie infected sheep
 
to contaminate the feed. Considering Scrapie has run rampant
 
in the U.S. for years, as of Aug. 1999, 950 scrapie infected
 
flocks. Also, Considering only one quarter spoonful of scrapie
 
infected material is lethal to a cow. Considering all this, the
 
sheep to cow ration is meaningless. As I said, it's 24 pages of
 
B.S.e.
 
To be continued...
 
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA
 
_____________________________________________________________________
 
 
 
 
 
snip...see full text ;
 
 
Monday, June 3, 2013
 
Unsuccessful oral transmission of scrapie from British sheep to cattle
 
 
 
Thursday, August 15, 2013
 
Stability properties of PrPSc from cattle with experimental transmissible spongiform encephalopathies: use of a rapid whole homogenate, protease-free assay
 
 
 
Sunday, July 21, 2013
 
Welsh Government and Food Standards Agency Wales Joint Public Consultation on the Proposed Transmissible Spongiform Encephalopathies (Wales) Regulations 2013 Singeltary Submission WG18417
 
 
 
Saturday, July 6, 2013
 
Small Ruminant Nor98 Prions Share Biochemical Features with Human Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive Prionopathy
 
Research Article
 
 
 
Tuesday, July 21, 2009
 
Transmissible mink encephalopathy - review of the etiology
 
 
 
Saturday, December 01, 2007
 
Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model
 
 
 
Sunday, December 10, 2006
 
Transmissible Mink Encephalopathy TME
 
 
 
 
Thursday, March 29, 2012
 
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
 
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
 
 
 
Friday, July 26, 2013
 
Voluntary Scrapie Program USA UPDATE July 26, 2013 increase in FY 2013 is not statistically meaningful due to the sample size
 
 
 
Sunday, August 25, 2013
 
Prion2013 Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission
 
 
 
AD.63: Susceptibility of domestic cats to chronic wasting disease
 
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1
 
1Colorado State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN USA
 
Domestic and nondomestic cats have been shown to be susceptible to feline spongiform encephalopathy (FSE), almost certainly caused by consumption of bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and free-ranging nondomestic felids scavenge cervid carcasses, including those in areas affected by chronic wasting disease (CWD), we evaluated the susceptibility of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated cats developed signs consistent with prion disease, including a stilted gait, weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from these two cats were pooled and inoculated into cohorts of cats by IC, PO, and intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the symptomatic cats by western blotting and immunohistochemistry and abnormalities were seen in magnetic resonance imaging, including multifocal T2 fluid attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4 IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns consistent with the early stage of feline CWD. These results demonstrate that CWD can be transmitted and adapted to the domestic cat, thus raising the issue of potential cervid-to- feline transmission in nature.
 
 
 
 
 
 
PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)
 
 
 
 
 
 
 
 
 
 
PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)
 
 
 
 
 
 
Thursday, May 31, 2012
 
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more
 
 
 
Monday, August 8, 2011
 
Susceptibility of Domestic Cats to CWD Infection
 
 
 
Sunday, August 25, 2013
 
***Prion2013 Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission
 
 
 
 
Feline Spongiform Encephalopathy (FSE) FSE was first identified in the UK in 1990. Most cases have been reported in the UK, where the epidemic has been consistent with that of the BSE epidemic. Some other countries (e.g. Norway, Liechtenstein and France) have also reported cases.
 
Most cases have been reported in domestic cats but there have also been cases in captive exotic cats (e.g. Cheetah, Lion, Asian leopard cat, Ocelot, Puma and Tiger). The disease is characterised by progressive nervous signs, including ataxia, hyper-reactivity and behavioural changes and is fatal.
 
The chemical and biological properties of the infectious agent are identical to those of the BSE and vCJD agents. These findings support the hypothesis that the FSE epidemic resulted from the consumption of food contaminated with the BSE agent.
 
The FSE epidemic has declined as a result of tight controls on the disposal of specified risk material and other animal by-products.
 
References: Leggett, M.M. et al.(1990) A spongiform encephalopathy in a cat. Veterinary Record. 127. 586-588
 
Synge, B.A. et al. (1991) Spongiform encephalopathy in a Scottish cat. Veterinary Record. 129. 320
 
Wyatt, J. M. et al. (1991) Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Veterinary Record. 129. 233.
 
Gruffydd-Jones, T. J.et al.. (1991) Feline spongiform encephalopathy. J. Small Animal Practice. 33. 471-476.
 
Pearson, G. R. et al. (1992) Feline spongiform encephalopathy: fibril and PrP studies. Veterinary Record. 131. 307-310.
 
Willoughby, K. et al. (1992) Spongiform encephalopathy in a captive puma (Felis concolor). Veterinary Record. 131. 431-434.
 
Fraser, H. et al. (1994) Transmission of feline spongiform encephalopathy to mice. Veterinary Record 134. 449.
 
Bratberg, B. et al. (1995) Feline spongiform encephalopathy in a cat in Norway. Veterinary Record 136. 444
 
Baron, T. et al. (1997) Spongiform encephalopathy in an imported cheetah in France. Veterinary Record 141. 270-271
 
Zanusso, G et al. (1998) Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy. Lancet, V352, N9134, OCT 3, Pp 1116-1117.
 
Ryder, S.J. et al. (2001) Inconsistent detection of PrP in extraneural tissues of cats with feline spongiform encephalopathy. Veterinary Record 146. 437-441
 
Kelly, D.F. et al. (2005) Neuropathological findings in cats with clinically suspect but histologically unconfirmed feline spongiform encephalopathy. Veterinary Record 156. 472-477.
 
 
 
 
 
3 further cheetah cases have occured, plus 1 lion, plus all the primates, and 20 additional house cats. Nothing has been published on any of these UK cases either. One supposes the problem here with publishing is that many unpublished cases were _born_ long after the feed "ban". Caught between a rock and a hard place: leaky ban or horizontal transmission (or both).
 
 
 
 
YOU explained that imported crushed heads were extensively used in the petfood industry...
 
 
 
In particular I do not believe one can say that the levels of the scrapie agent in pet food are so low that domestic animals are not exposed...
 
 
 
 
 
 
 
on occasions, materials obtained from slaughterhouses will be derived from sheep affected with scrapie or cattle that may be incubating BSE for use in pet food manufacture...
 
 
 
 
*** Meldrum's notes on pet foods and materials used
 
 
 
 
*** BSE & Pedigree Petfoods ***
 
 
 
Friday, March 8, 2013
 
Dogs may have been used to make Petfood and animal feed
 
 
 
 
Monday, March 26, 2012
 
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE
 
OR-09 15:10 - 15:25 CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE David
 
 
 
OR-09: Canine spongiform encephalopathy—A new form of animal prion disease
 
Monique David, Mourad Tayebi UT Health; Houston, TX USA
 
It was also hypothesized that BSE might have originated from an unrecognized sporadic or genetic case of bovine prion disease incorporated into cattle feed or even cattle feed contaminated with prion-infected human remains.1 However, strong support for a genetic origin of BSE has recently been demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2 Furthermore, a specific prion protein strain causing BSE in cattle is believed to be the etiological agent responsible for the novel human prion disease, variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in a number countries, including France, Italy, Ireland, the Netherlands, Canada, Japan, US and the UK with the largest number of cases. Naturally occurring feline spongiform encephalopathy of domestic cats4 and spongiform encephalopathies of a number of zoo animals so-called exotic ungulate encephalopathies5,6 are also recognized as animal prion diseases, and are thought to have resulted from the same BSE-contaminated food given to cattle and humans, although and at least in some of these cases, a sporadic and/or genetic etiology cannot be ruled out. The canine species seems to display resistance to prion disease and no single case has so far been reported.7,8
 
Here, we describe a case of a 9 week old male Rottweiler puppy presenting neurological deficits; and histological examination revealed spongiform vacuolation characteristic of those associated with prion diseases.9 Initial biochemical studies using anti-PrP antibodies revealed the presence of partially proteinase K-resistant fragment by western blotting. Furthermore, immunohistochemistry revealed spongiform degeneration consistent with those found in prion disease and displayed staining for PrPSc in the cortex.
 
Of major importance, PrPSc isolated from the Rottweiler was able to cross the species barrier transmitted to hamster in vitro with PMCA and in vivo (one hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100% attack rate (n = 4) and animals displayed untypical lesional profile and shorter incubation period.
 
In this study, we show that the canine species might be sensitive to prion disease and that PrPSc isolated from a dog can be transmitted to dogs and hamsters in vitro using PMCA and in vivo to hamsters.
 
If our preliminary results are confirmed, the proposal will have a major impact on animal and public health and would certainly lead to implementing new control measures for ‘canine spongiform encephalopathy’ (CSE).
 
References
 
1. Colchester AC, Colchester NT. The origin of bovine spongiform encephalopathy: the human prion disease hypothesis. Lancet 2005; 366:856-61; PMID:16139661; http:// dx.doi.org/10.1016/S0140-6736(05)67218-2.
 
2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation. PLoS Pathog 2008; 4:e1000156; PMID:18787697; http://dx.doi.org/10.1371/journal. ppat.1000156.
 
3. Collinge J. Human prion diseases and bovine spongiform encephalopathy (BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662; http://dx.doi.org/10.1093/ hmg/6.10.1699.
 
4. Wyatt JM, Pearson GR, Smerdon TN, Gruffydd-Jones TJ, Wells GA, Wilesmith JW. Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Vet Rec 1991; 129:233-6; PMID:1957458; http://dx.doi.org/10.1136/vr.129.11.233.
 
5. Jeffrey M, Wells GA. Spongiform encephalopathy in a nyala (Tragelaphus angasi). Vet Pathol 1988; 25:398-9; PMID:3232315; http://dx.doi.org/10.1177/030098588802500514.
 
6. Kirkwood JK, Wells GA, Wilesmith JW, Cunningham AA, Jackson SI. Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu (Tragelaphus strepsiceros). Vet Rec 1990; 127:418-20; PMID:2264242.
 
7. Bartz JC, McKenzie DI, Bessen RA, Marsh RF, Aiken JM. Transmissible mink encephalopathy species barrier effect between ferret and mink: PrP gene and protein analysis. J Gen Virol 1994; 75:2947-53; PMID:7964604; http://dx.doi.org/10.1099/0022-1317- 75-11-2947.
 
8. Lysek DA, Schorn C, Nivon LG, Esteve-Moya V, Christen B, Calzolai L, et al. Prion protein NMR structures of cats, dogs, pigs, and sheep. Proc Natl Acad Sci U S A 2005; 102:640-5; PMID:15647367; http://dx.doi.org/10.1073/pnas.0408937102.
 
9. Budka H. Neuropathology of prion diseases. Br Med Bull 2003; 66:121-30; PMID:14522854; http://dx.doi.org/10.1093/bmb/66.1.121.
 
 
 
 
 
 
 
 
Tuesday, June 11, 2013
 
Weld County Bi-Products dba Fort Morgan Pet Foods 6/1/12 significant deviations from requirements in FDA regulations that are intended to reduce the risk of bovine spongiform encephalopathy (BSE) within the United States
 
 
 
Friday, July 19, 2013
 
PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED Revised as of April 1, 2013 50# Regular Chicken Feed was found to contain mammalian protein label does not contain the warning statement
 
 
 
 
FELINE SPONGIFORM ENCEPHALOPATHY FSE
 
 
 
 
 
Friday, November 09, 2012
 
*** Chronic Wasting Disease CWD in cervidae and transmission to other species
 
 
 
Sunday, November 11, 2012
 
*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease November 2012
 
 
 
Friday, December 14, 2012
 
Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005 - December 14, 2012
 
 
 
Sunday, August 09, 2009
 
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
 
 
 
Tuesday, August 18, 2009
 
BSE-The Untold Story - joe gibbs and singeltary 1999 – 2009
 
 
 
Saturday, September 21, 2013
 
Westland/Hallmark: 2008 Beef Recall A Case Study by The Food Industry Center January 2010 THE FLIM-FLAM REPORT
 
FOR 4 YEARS, THE USDA NSLP fed our children all across the USA, from school to school, county to county, state to state, the most high rish cattle for mad cow type disease i.e. the TSE prion disease, they fed our children dead stock downer cows. did your children consume this, and will you have to wait 5 decades to see if they become exposed and go clinical with CJD TSE prion disease ???
 
 

 
 
 
TSS

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