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Federal Court Allows USDA to Suppress Testing for Mad Cow Disease

WASHINGTON (Reuters) - The Agriculture Department is within bounds to bar meatpackers from testing slaughter cattle for mad cow disease, a U.S. Court of Appeals panel said in a 2-1 ruling on Friday.

Creekstone Farms Premium Beef LLC, a small Arkansas packer, filed suit on March 23, 2006, to gain access to mad-cow test kits. It said it wanted to test every animal at its plant to assure foreign buyers that the meat was safe to eat.

Three U.S. cases of mad cow disease, a fatal neurological infection, have been reported, the last in March 2006. People can contract a human version of the disease by eating infected meats. Most nations banned U.S. beef after the first case, in December 2003, but trade has been restored for the most part.

In a 25-page ruling, Appellate Judges Karen Henderson and Judith Rogers said USDA has authority under the 1913 Virus-Serum-Toxin Act to prevent sale of mad-cow test kits to meatpackers. USDA interprets the law to control products for "prevention, diagnosis, management or care of diseases of animals."

David Sentelle, chief judge of the District of Columbia appeals circuit, dissented from the decision. He said USDA "exceeds the bounds of reasonableness" for a law enacted to prevent the sale of ineffective animal medicine.

USDA allows the mad-cow test kits to be sold only to laboratories that it approves. It says the tests should not be used as a marketing tool and the cattle that comprise the bulk of the meat supply are too young to be tested reliably.

Two large export markets, Japan and South Korea, accept beef only from younger U.S. cattle. Mad cow is found mostly in older cattle. Its incubation period is two to eight years.

Creekstone said it lost $200,000 a day due to reduced U.S. beef exports when it filed its lawsuit.

In its lawsuit, Creekstone argued the 1913 law could not be invoked to prevent use of products like "rapid test" kits for mad cow disease and the kits were not a "treatment" for livestock.

U.S. District Judge James Robinson had ruled in March 2007 that USDA could not control mad cow tests because they are not a treatment for animals.

The United States applies a number of safeguards against mad cow, formally named bovine spongiform encephalopathy. They include a ban on using cattle parts in feed and requirements for packers to remove at slaughter the materials most likely to carry the mad-cow agent -- the brain, spinal column and nervous system tissue.

(Editing by Walter Bagley)

For more information on this topic or related issues you can search the thousands of archived articles on the OCA website using keywords:

post Sep 4 2008, 04:45 PM

DOES this surprise anyone $$$

why is the same serum-toxin act not applying to the CWD testing in the States, with deer and elk? or does it? these are not trick questions, i really want to know. you cannot ignore these other TSEs, and the politics that surround them. well, the moderators can ;-) and that's their choice, and i will abide by whatever move they take. i am not trying to get off topic, but, these issues must not be ignored. that must not happen with CWD in Michigan. and remember, in Terms of TSE i.e. prion disease, Michigan has CWD, Scrapie, and the atypical Nor-98 scrapie, Michigan also has cattle$ remember, the first recorded case of scrapie in the US occurred on a ranch in Michigan in 1947, the year of the first TME outbreak in Wisconsin. riddle me this batman, riddle me this ???

see last link at bottome of page ; ''Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?''

kind regards, terry


Prof Collinge old findings, a key issue, the media always seems to forget about, states that BSE propagates as either variant CJD-like or sporadic CJD-like prion strains. funny how our health officials, governments, and such seem to conveniently ignore these findings, let alone the atypical TSE in cattle and sheep that do NOT look like nvCJD in the lab, but some sub-types of the sporadic CJD. all this goes ignored for one reason, and one reason only $$$ it's why the UKBSEnvCJD only theory was put forth in the first place, and it's why it is still set in stone $$$ to much science has been forth to date that proves that theory wrong.

PLEASE NOTE, the last two mad cows documented in the USA were H-type BSE, then the USDA quickly shut the testing down to a level of non-detection. it would be a miracle to find one case, from testing only 40,000 annually, from some 97,000,000 (that's 97 million head), and of that, some 37 million slaughtered, if i am not mistaken. and these cattle are cherry picked brains too, probably calves from USDA grain fed facilities, and don't think these corrupt people are not capable of doing it either. they are very capable. ...

"REDACTED is alleged to have provided possibly inaccurate test results involving diseased sheep. However, because the results were determined to be inconclusive, no actual violation was actually committed.''



Statement on Texas Cow With Central Nervous System Symptoms On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.


I would note that the sample was taken in April, at which time the protocols allowed for a preservative to be used (protocols changed in June 2005). The sample was not submitted to us until last week, because the veterinarian set aside the sample after preserving it and simply forgot to send it in. On that point, I would like to emphasize that while that time lag is not optimal, it has no implications in terms of the risk to human health. The carcass of this animal was destroyed, therefore there is absolutely no risk to human or animal health from this animal.


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.



full text ;


USDA: In 9,200 cases only one type of test could be used

WASHINGTON (AP)--The U.S. Department of Agriculture acknowledged Aug. 17 that its testing options for bovine spongiform encephalopathy were limited in 9,200 cases despite its effort to expand surveillance throughout the U.S. herd.

In those cases, only one type of test was used--one that failed to detect the disease in an infected Texas cow.

The department posted the information on its website because of an inquiry from The Associated Press.

Conducted over the past 14 months, the tests have not been included in the department's running tally of BSE tests since last summer. That total reached 439,126 on Aug. 17.

"There's no secret program," the department's chief veterinarian, John Clifford, said in an interview. "There has been no hiding, I can assure you of that."

Officials intended to report the tests later in an annual report, Clifford said.

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.

In the Texas case, officials had declared the cow free of disease in November after an IHC test came back negative. The department's inspector general ordered an additional kind of test, which confirmed the animal was infected.

Veterinarians in remote locations have used the preservative on tissue to keep it from degrading on its way to the department's laboratory in Ames, Iowa. Officials this year asked veterinarians to stop using preservative and send fresh or chilled samples within 48 hours.

The department recently investigated a possible case of BSE that turned up in a preserved sample. Further testing ruled out the disease two weeks ago.

Scientists used two additional tests--rapid screening and Western blot--to help detect BSE in the country's second confirmed case, in a Texas cow in June. They used IHC and Western blot to confirm the first case, in a Washington state cow in December 2003.

"The IHC test is still an excellent test," Clifford said. "These are not simple tests, either."

Clifford pointed out that scientists reran the IHC several times and got conflicting results. That happened, too, with the Western blot test. Both tests are accepted by international animal health officials.

Date: 8/25/05

""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."


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.


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.



Completely Edited Version PRION ROUNDTABLE

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




The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.

The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.

These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.

"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."

Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.

USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.

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

CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...


179 Page 10 of 17

BSE cattle may need to be reexamined.

T. Kitamoto (Ed.) PRIONS Food and Drug Safety


ALSO from the International Symposium of Prion Diseases held in Sendai, October 31, to November 2, 2004; Bovine spongiform encephalopathy (BSE) in Japan


"Furthermore, current studies into transmission of cases of BSE that are atypical or that develop in young cattle are expected to amplify the BSE prion" NO. Date conf. Farm Birth place and Date Age at diagnosis 8. 2003.10.6. Fukushima Tochigi 2001.10.13. 23 9. 2003.11.4. Hiroshima Hyogo 2002.1.13. 21

Test results # 8b, 9c cows Elisa Positive, WB Positive, IHC negative, histopathology negative b = atypical BSE case c = case of BSE in a young animal b,c, No PrPSc on IHC, and no spongiform change on histology International Symposium of Prion Diseases

held in Sendai, October 31, to November 2, 2004. Tetsuyuki Kitamoto Professor and Chairman Department of Prion Research Tohoku University School of Medicine 2-1 SeiryoAoba-ku, Sendai 980-8575, JAPAN TEL +81-22-717-8147 FAX +81-22-717-8148 e-mail; Symposium Secretariat Kyomi Sasaki TEL +81-22-717-8233 FAX +81-22-717-7656 e-mail: ================================= 9/13/2005 -------------------------------------------------------------------------------- Page 11 of 17 From: TSS () Subject: Atypical Proteinase K-Resistant Prion Protein (PrPres) observed in an Apparently Healthy 23-Month-Old Holstein Steer Date: August 26, 2005 at 10:24 am PST Atypical Proteinase K-Resistant Prion Protein (PrPres) observed in an Apparently Healthy 23-Month-Old Holstein Steer Jpn. J. Infect. Dis., 56, 221-222, 2003 Laboratory and Epidemiology Communications Atypical Proteinase K-Resistant Prion Protein (PrPres) Observed in an Apparently Healthy 23-Month-Old Holstein Steer Yoshio Yamakawa*, Ken�ichi Hagiwara, Kyoko Nohtomi, Yuko Nakamura, Masahiro Nishizima ,Yoshimi Higuchi1, Yuko Sato1, Tetsutaro Sata1 and the Expert Committee for BSE Diagnosis, Ministry of Health, Labour and Welfare of Japan2 Department of Biochemistry & Cell Biology and 1Department of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640 and 2Miistry of Health, Labour and Welfare, Tokyo 100-8916 Communicated by Tetsutaro Sata (Accepted December 2, 2003) *Corresponding author: Mailing address: Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 1628640, Japan. Tel: +81-3-5285-1111, Fax: +81-3-5285-1157, E-mail:

Since October 18, 2001, 'bovine spongiform encephalopathy (BSE) examination for all cattle slaughtered at abattoirs in the country' has been mandated in Japan by the Ministry of Health, Labour and Welfare (MHLW). 'Plateria' ELISA-kit (Bio-Rad Laboratories, Hercules, Calif., USA) is routinely used at abattoirs for detecting proteinase K (PK)-resistant prion protein (PrPSc) in the obex region. Samples positive according to the ELISA screening are further subjected to Western blot (WB) and histologic and immunohistochemical examination (IHC) at the National Institute of Infectious Diseases (NIID) or Obihiro University. If PrPSc is detected either by WB or by IHC, the cattle are diagnosed as BSE. The diagnosis is approved by the Expert Committee for BSE Diagnosis, MHLW. From October 18, 2001 to September 30, 2003, approximately 2.5 million cattle were screened at abattoirs. A hundred and ten specimens positive according to ELISA were subjected to WB/IHC. Seven showed positive by both WB and IHC, all exhibiting the typical electrophoretic profile of a high content of the di-glycosylated molecular form of PrPSc (1-3) and the distinctive granular deposition of PrPSc in neuronal cells and neuropil of the dorsal nucleus of vagus. An ELISA-positive specimen from a 23 month-old Holstein steer slaughtered on September 29, 2003, in Ibaraki Prefecture (Ibaraki case) was sent to the NIID for confirmation. The animal was reportedly healthy before slaughter. The OD titer in ELISA was slightly higher than the 'cut-off' level given by the manufacturer. The histology showed no spongiform changes and IHC revealed no signal of PrPSc accumulation typical for BSE. However, WB analysis of the homogenate that was prepared from the obex region and used for ELISA revealed a small amount of PrPSc with an electrophoretic profile different from that of typical BSE-associated PrPSc (1-3). The characteristics were (i) low content of the di-glycosylated molecular form of PrPSc, (ii) a faster migration of the non-glycosylated form of PrPSc on SDS-PAGE, and (iii) less resistance against PK digestion as compared with an authentic PrPSc specimen derived from an 83-month-old Holstein (Wakayama case) (Fig. 1). Table 1 summarizes the relative amounts of three distinctive glycoforms (di-, mono, non-glycosylated) of PrPSc calculated by densitometric analysis of the blot shown in Fig. 1. As 2.5 mg wet weight obex-equivalent homogenate of the Ibaraki case (Fig. 1, lane 4) gave slightly stronger band intensities of PrPSc than an 8 mg wet weight obex-equivqlent homogenate of a typical BSE-affected Wakayama case (Fig. 1, lane 2), the amount of PrPSc accumulated in the Ibaraki case was calculated to be 1/500 - 1/1000 of the Wakayama case. In the Ibaraki case, the PrPSc bands were not detectable in the homogenates of the proximal surrounding region of the obex. These findings were consistent with the low OD value in ELISA, i.e., 0.2 -0.3 for the Ibaraki case versus over 3.0 for the Wakayama case. The DNA sequence of the PrP coding region of the Ibaraki case was the same as that appearing in the database (GenBank accession number: AJ298878). More recently, we encountered another case that resembled the Ibaraki case. It was a 21-monthold Holstein steer from Hiroshima Prefecture. WB showed typical BSE-specific PrPSc deposition though IHC did not detect positive signals of PrPSc (data not shown). Though the clinical onset of BSE is usually at around 5 years of age or later, a 20-month-old case showing the clinical signs has been reported (4). Variant forms of BSE similar to our cases, i.e., with atypical histopathological and/or biochemical phenotype, have been recently reported in Italy (5) and in France (6). Such variant BSE was not associated with mutations in the prion protein (PrP) coding region as in our case (5,6). The Ministry of Agriculture, Forestry and Fisheries of Japan (MAFF) announced a ban of feeding ruminants with meat bone meal (MBM) on September 18, 2001, and a complete ban was made on October 15 of the same year. According to the recent MAFF report, the p vious seven cases of BSE in Japan were cattle born in 1995 - 1996 and possibly fed with cross-contaminated feed. However, the two cattle in this report were born after the complete ban. Whether contaminated MBM was implicated in the present cases remains to be investigated.

REFERENCES Collinge, J., Sidle, K. C. L., Meads, J., Ironside, J. and Hill, A. F. (1996): Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD. Nature, 383, 685690. Bruce, M. E., Will, R. G., Ironside, J. W., McConnell, I., Drummond, D., Suttie, A., McCardle, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser, H. and Bostock, C. J. (1997): Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent. Nature, 389, 498-501. Hill, A. F., Desbruslais, M., Joiner, S., Sidle, K. C. L., Gowland, I. and Collinge, J. (1997): The same prion strain causes vCJD and BSE. Nature, 389, 448-450. Matravers, W., Bridgeman, J. and Smith, M.-F. (ed.)(2000): The BSE Inquiry. p. 37. vol. 16. The Stationery Office Ltd., Norwich, UK. Casalone, C., Zanusso, G., Acutis, P. L., Crescio, M. I., Corona, C., Ferrari, S., Capobianco, R., Tagliavini, F., Monaco, S. and Caramelli, M. (2003): Identification of a novel molecular and neuropathological BSE phenotype in Italy. International Conference on Prion Disease: from basic research to intervention concepts. Gasreig, Munhen, October 8-10. Bicaba, A. G., Laplanche, J. L., Ryder, S. and Baron, T. (2003): A molecular variant of bovine spongiform encephalopatie. International Conference on Prion Disease: from basic research to intervention concepts. Gasreig, Munhen, October 8-10. Asante, E. A., Linehan, J. M., Desbruslais, M., Joiner, S., Gowland, I., Wood, A. L., Welch, J., Hill, A. F., Lloyd, S. E., Wadsworth, J. D. F. and Collinge, J. (2002). BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein. EMBO J., 21, 6358-6366. 9/13/2005 Page 12 of 17 SEE SLIDES IN PDF FILE;



WELL, someone did call me from Bio-Rad about this, however it was not Susan Berg. but i had to just about take a blood oath not to reveal there name. IN fact they did not want me to even mention this, but i feel it is much much to important. I have omitted any I.D. of this person, but thought I must document this ;

Bio-Rad, TSS phone conversation 12/28/04

Finally spoke with ;

Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: XXXXXXXXXXXXXXXXXX

at approx. 14:00 hours 12/28/04, I had a very pleasant phone conversation with XXXX XXXXX about the USDA and the inconclusive BSE testing problems they seem to keep having. X was very very cautious as to speak directly about USDA and it's policy of not using WB. X was very concerned as a Bio-Rad official of retaliation of some sort. X would only speak of what other countries do, and that i should take that as an answer. I told X I understood that it was a very loaded question and X agreed several times over and even said a political one.

my question;

Does Bio-Rad believe USDA's final determination of False positive, without WB, and considering the new atypical TSEs not showing positive with -IHC and -HP ???

ask if i was a reporter. i said no, i was with CJD Watch and that i had lost my mother to hvCJD. X did not want any of this recorded or repeated.

again, very nervous, will not answer directly about USDA for fear of retaliation, but again said X tell me what other countries are doing and finding, and that i should take it from there. "very difficult to answer"

"very political"

"very loaded question"

outside USA and Canada, they use many different confirmatory tech. in house WB, SAF, along with IHC, HP, several times etc. you should see at several talks meetings (TSE) of late Paris Dec 2, that IHC- DOES NOT MEAN IT IS NEGATIVE. again, look what the rest of the world is doing. said something about Dr. Houston stating; any screening assay, always a chance for human error. but with so many errors (i am assuming X meant inconclusive), why are there no investigations, just false positives? said something about ''just look at the sheep that tested IHC- but were positive''. ...


-------- Original Message -------- Subject: Your questions Date: Mon, 27 Dec 2004 15:58:11 -0800 From: To:

Hi Terry:

............................................snip Let me know your phone number so I can talk to you about the Bio-Rad BSE test. Thank you


Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: =================================


######### ##########

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.

i hope i have not lost you. i know how some don't like to get political, but cwd, mad cow disease (all strains), TME, Scrapie, and cjd i.e. human and animal TSE, that's all they are are political. bush has failed us terribly, clinton before him failed us terribly, and whomever gets in office next will do the same damn thing, in terms of human and animal TSE. it was said long ago ;

In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells

3. Prof. A Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. BSE was not reported in the USA.


and they meant it. ...TSS

The EMBO Journal Vol. 21 No. 23 pp. 6358�6366, 2002

BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein

Emmanuel A.Asante, Jacqueline M.Linehan, Melanie Desbruslais, Susan Joiner, Ian Gowland, Andrew L.Wood, Julie Welch, Andrew F.Hill, Sarah E.Lloyd, Jonathan D.F.Wadsworth and John Collinge1 MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK 1Corresponding author e-mail: Variant Creutzfeldt�Jakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2. These data suggest that more than one BSEderived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure. ...snip...end...TSS

Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE

Biacabe, A-G1; Jacobs, JG2; Gavier-Wid�n, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden

Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK�resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Str�ussler-Scheinker (GSS) syndrome in humans. ...end


18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7 December 2006 are now available.


64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE.

Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. *** A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD.


AND WHAT ABOUT THOSE atypical NOR-98 scrapie cases in the USA, now documented at 6 cases in the past two years, and the risk thereof to humans as sporadic CJD ???


Aspects of the Cerebellar Neuropathology in Nor98

Gavier-Wid�n, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,

Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.


There were 20 scrapie infected and source flocks with open statuses (Figure 3) as of April, 30, 2008. Twenty eight new infected and source flocks have been designated in FY 2008 (Figure 4); three source flocks were reported in April. ...snip


As of April 30, 2008, 122 new scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL) in FY 2008 (Figure 6). Of these, 103 were field cases and 19* were Regulatory Scrapie Slaughter Surveillance (RSSS) cases (collected in FY 2008 and reported by May 20, 2008). Positive cases reported for April 2008 are depicted in Figure 7. Eighteen cases of scrapie in goats have been confirmed by NVSL since implementation of the regulatory changes in FY 2002 (Figure 8). The most recent positive goat case was confirmed in February 2008 and originated from the same herd in Michigan as the other FY 2008 goat cases. ...snip



However, four positive goats have been identified this fiscal year through field investigations. One was a clinical suspect submitted for testing and the other three originated from the birth herd of the clinical case.


As of April 30, 2008, 26,703 animals have been sampled for scrapie testing: 23,378 RSSS, 1,517 goats for the CSPS study, 1,466 regulatory field cases, 270 regulatory third eyelid biopsies, and 72 regulatory rectal biopsies (chart 8).


PLEASE NOTE, (FIGURE 6), Scrapie Confirmed Cases in FY 2008 MAP, PA 3, 1**, Two cases-state of ID UNKNOWN, 1 case Nor98-like**

NOT to forget the 5 cases of the NOR-98 atypical scrapie documented in the USA in 2007, in five different states. WHICH pathologically looks like some sub-types of sporadic CJD, of which Stanely Prusiner warns of a public health risk ;

***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.

Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005)


NOR-98 ATYPICAL SCRAPIE 5 cases documented in USA in 5 different states USA 007

Nonambulatory Cattle as a Potential Source of TSE

In this study, Wisconsin was the only State in which mink producers were reported to receive nonambulatory cows directly from dairies. However, given the small number of surveyed herds this finding is likely a result of the sampling design. Because mink producers pay a premium for nonambulatory cows, it appears reasonable that the practice of feeding nonambulatory cows to mink could occur wherever both large numbers of dairy cows and mink are found. As many as 2,157(3) nonambulatory cows per million milk cows, or a total of 9,482 nonambulatory cows, could have been fed to mink in the 7 surveyed States in 1992. Based on the sample response, only half of those cows would have had an identifiable reason for being nonambulatory. This equates to an estimated 4,741 nonambulatory cows that were, hypothetically, a potential source of TSE in the surveyed States.

(3)This estimate does not account for any nonambulatory cows received from slaughter plants.

Page 23

The five reported outbreaks of TME in the U.S. reveal no discernable trend. Assuming an average of 2,000 mink farms in the U.S. during the last 50 years, one outbreak of TME has occurred per 20,000 mink farm-years. Extrapolating from the data gathered in this study, 66,374 nonambulatory cows have been fed to mink in the 7 surveyed States since the last reported outbreak of TME in 1985. Of those, 33,187 would have had no identifiable reason for being nonambulatory and were hypothetically a potential source of TSE. Given the severity of signs and number of mink affected by TME it is unlikely that outbreaks have gone unreported. If any form Of a TSE (infectious, spontaneous, or other) occurs in U.S. cattle that is transmissible to mink in the form of TME, then it must be exceedingly rare or the conditions for its transmission must be highly specific and unusual. Nonetheless, studies are underway at the State and Federal levels to further characterize the disposition of nonambulatory cows and usage on mink farms.


An estimated 4,741 nonambulatory cows hypothetically considered to be potential sources of TSE may have been fed to mink in the 7 surveyed States in 1992. This equates to 33,187 such cows fed to mink since the last reported outbreak of TME in mink. Given this large number of nonambulatory cows fed to mink, the historic and current mink population, and the infrequent occurrence of TME, if TSE exists in cattle in the U.S. it must be very rare or transmissible to mink only under very unusual conditions.

To be published in the Proceedings of the Fourth International Scientific Congress in Fur Animal Production. Toronto, Canada, August 21-28, 1988

Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle

R.F. Marsh* and G.R. Hartsough

�Department of Veterinary Science, University of Wisconsin-Madison, Madison, Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092


Epidemiologic investigation of a new incidence of transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin suggests that the disease may have resulted from feeding infected cattle to mink. This observation is supported by the transmission of a TME-like disease to experimentally inoculated cattle, and by the recent report of a new bovine spongiform encephalopathy in England.



A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin reported that many of his mink were �acting funny??, and some had died. At this time, we visited the farm and found that approximately 10% of all adult mink were showing typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of normal habits of cleanliness, deposition of droppings throughout the pen rather than in a single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over their _backs like squirrels. These signs were followed by progressive deterioration of neurologic function beginning with locomoior incoordination, long periods of somnolence in which the affected mink would stand motionless with its head in the corner of the cage, complete debilitation, and death.

Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. Since previous incidences of TME were associated with common or shared feeding practices, we obtained a careful history of feed ingredients used over the past 12-18 months. ***The rancher was a �dead stock?? feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed.***


Epidemiology Epidemiologic studies suggest that animals contract the disease by external exposure to the infectious agent, such as by eating contaminated feed. No evidence suggests that the TME agent spreads by contact between unrelated mink or from mother to nursing young. The disease has been identified in both genders and all color phases in animals greater than 1 year old. The first documented TME outbreak in the United States occurred in 1947 on one ranch in Wisconsin and then on a ranch in Minnesota that had received mink from the Wisconsin ranch. In 1961, TME outbreaks occurred on five ranches in Wisconsin. In Factsheet Veterinary Services February 2002 APHIS 1963, outbreaks occurred in Idaho, Minnesota, and Wisconsin. Epidemiologic data from the Minnesota and Wisconsin outbreaks trace the cases in those States to one common purchased food source.


The 1985 Stetsonville Outbreak The most recent TME outbreak occurred on one mink ranch in Stetsonville, WI, in 1985. In the herd of 7,300 adult mink, 60 percent of the animals died. Clinical signs included tail arching, incoordination, and hyperexcitability. At the most advanced stages of the disease, the animals were in trancelike states and eventually died. The outbreak lasted 5 months. Microscopic examination of sections of the brain confirmed the spongelike changes characteristic of TME. Diagnostic tests identified the prion protein. The following year, mink born during the outbreak showed no signs of TME. The late Richard Marsh, a veterinary virologist at the University of Wisconsin who studied the transmission of TME and other TSE�s, investigated this outbreak. Marsh learned that the mink were fed a diet composed of fresh meat products from �downer cattle?? and commercial sources of fish, poultry, and cereal. Downer cattle are nonambulatory and cannot rise because they are affected with a condition such as a metabolic disease, broken limbs, or a central nervous system disorder. Marsh theorized that the meat from these downer cattle introduced a TSE agent to the mink in which TME resulted. Although Marsh�s hypothesis is based on speculation and anecdotal evidence, in 1993 APHIS adjusted its national BSE surveillance program to include testing downer cattle for evidence of a TSE. The brains of more than 20,141 cattle have been examined at APHIS� National Veterinary Services Laboratories and other State diagnostic laboratories. Not a single tissue sample has revealed evidence of BSE or another TSE in cattle.

AND as everyone knows, the rest is history, those dead-stock downers, the most high risk cattle, were NOT tested, and in FACT, was a major source of YOUR CHILDRENS SCHOOL LUNCH PROGRAM, all across the Nation. sorry, these are the most high risk cattle for TSE aka mad cow disease, and i am a bit touchy about this topic. ...sorry. ...terry



In April of 1985, a mink rancher in Wisconsin reported a debilitating neurologic disease in his herd which we diagnosed as TME by histopathologic findings confirmed by experimental transmission to mink and squirrel monkeys. The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle and a few horses. She had never been fed.

We believe that these findings may indicate the presence of a previously unrecognized scrapie-like disease in cattle and wish to alert dairy practitioners to this possibility.



NOW, back to those mad mink i.e. TME. let me throw a curve ball here ;

Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model Thierry Baron,* Anna Bencsik,* Anne-Ga�lle Biacabe,* Eric Morignat,* and Richard A. Bessen� Emerging Infectious

Transmissible mink encepholapathy (TME) is a foodborne transmissible spongiform encephalopathy (TSE) of ranch-raised mink; infection with a ruminant TSE has been proposed as the cause, but the precise origin of TME is unknown. To compare the phenotypes of each TSE, bovine- passaged TME isolate and 3 distinct natural bovine spongiform encephalopathy (BSE) agents (typical BSE, Htype BSE, and L-type BSE) were inoculated into an ovine transgenic mouse line (TgOvPrP4). Transgenic mice were susceptible to infection with bovine-passaged TME, typical BSE, and L-type BSE but not to H-type BSE. Based on survival periods, brain lesions profi les, disease-associated prion protein brain distribution, and biochemical properties of protease-resistant prion protein, typical BSE had a distint phenotype in ovine transgenic mice compared to L-type BSE and bovine TME. The similar phenotypic properties of L-type BSE and bovine TME in TgOvPrP4 mice suggest that L-type BSE is a much more likely candidate for the origin of TME than is typical BSE. Transmissible mink encephalopathy (TME) is a rare prion disease in ranch-raised mink (Mustela vison) in North America and Europe (1�4). Six outbreaks have been reported from 1947 through 1985 in North America, and several have been linked to contaminated commercial feed (1). Although contamination of feed with scrapie-infected sheep parts has been proposed as the cause of TME, the origin of the disease remains elusive. The idea that scrapie in sheep may be a source of TME infection is supported by fi ndings that scrapie-infected mink have a similar distribution of vacuolar pathologic features in the brain and the same clinical signs as mink with natural and experimental TME (5). However, mink are not susceptible to scrapie infection following oral exposure for up to 4 years postinoculation, which suggests that either the scrapie agent may not be the source of natural TME infection or that only specifi c strains of the scrapie agent are able to induce TME (6,7). Epidemiologic investigations in the Stetsonville, Wisconsin, outbreak of TME in 1985 suggested a possible cattle origin, since mink were primarily fed downer or dead dairy cattle but not sheep products (8). Experimental transmission of Stetsonville TME into cattle resulted in transmissible spongiform encephalopathy (TSE) disease with an incubation period of 18.5 months. Back passage of bovine TME into mink resulted in incubation periods of 4 and 7 months after oral or intracerebral inoculation, respectively, which was similar to that found following inoculation of Stetsonville TME into mink by these same routes (8). These fi ndings indicated that cattle are susceptible to TME, and that bovine-passaged TME did not result in a reduced pathogenicity for mink. These studies raised the question as to whether an unknown TSE in cattle was the source of TME infection in the Stetsonville outbreak. Several additional TME outbreaks in the United States have been associated with mink diet that contained downer or dead cattle (9). ...

snip...full text ;

CWD, is but a small piece, of a very big puzzle. and one of the main reasons this puzzle has not been solved, is the secrecy, cover-ups, and such. you must not ignore these facts. i did not want to believe this either. for years i was naive, but the facts speak for themselves.

it goes way back ;

Wednesday, August 20, 2008

Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?

August 20, 2008

Wednesday, September 03, 2008

Accelerated High Fidelity Prion Amplification Within and Across Prion Species Barriers

to be continued. ...TSS

post Sep 5 2008, 08:29 AM

My mother in law is dying from CJD as I write this.
From doing reasearch into this disease, I have learned a lot about just how much we do not know about the whole thing. This latest action is absolutely unacceptable. The whole premise that we are actually doing anything to prevent or detect mad cow in the US is a lie. Who knows how many infected cows have acually entered the food chain? The downer cow videos show that slaughter houses are not being held to any sort of standards, regardless of what the law states. My family is now officially swearing off beef forever. Unfortunately, this may be way too late. In addition, the fact that the prions can survive and find their way into fertilizer, etc means even lifetime vegetarians may be at risk. The reported rate of 1 case per million is total bunk. The incidence rate of CJD is much higher. The disease is not even one of the reportable ones in many states in the US, so we don't know how many people actually have it. Also, the incubation period is up to 40 years, so again a major unknown. I have no faith in our government to protect us from this disease at all. Kudos to South Koreans for trying to keep our beef out of their country.

post Today, 02:09 PM

-------------------- BSE-L@LISTS.AEGEE.ORG --------------------


The identification of disease-induced biomarkers in the urine of BSE infected cattle

Sharon LR Simon , Lise Lamoureux , Margot Plews , Micheal Stobart , Jillian LeMaistre , Ute Ziegler , Catherine Graham , Stefanie Czub , Martin Groschup and J. David Knox

Proteome Science 2008, 6:23doi:10.1186/1477-5956-6-23

Published: 5 September 2008

Abstract (provisional)


The bovine spongiform encephalopathy (BSE) epidemic and the emergence of a new human variant of Creutzfeldt-Jakob Disease (vCJD) have led to profound changes in the production and trade of agricultural goods. The rapid tests currently approved for BSE monitoring in slaughtered cattle are all based on the detection of the disease related isoform of the prion protein, PrPd, in brain tissue and consequently are only suitable for post-mortem diagnosis.


In instances such as assessing the health of breeding stock for export purposes where post-mortem testing is not an option, there is a demand for an ante-mortem test based on a matrix or body fluid that would permit easy access and repeated sampling. Urine and urine based analyses would meet these requirements.


Two dimensional differential gel eletrophoresis (2D-DIGE) and mass spectrometry analyses were used to identify proteins exhibiting differential abundance in the urine of BSE infected cattle and age matched controls over the course of the disease. Multivariate analyses of protein expression data identified a single protein able to discriminate, with 100% accuracy, control from infected samples. In addition, a subset of proteins were able to predict with 85% +/- 13.2 accuracy the time post infection that the samples were collected.

Conclusions These results suggest that in principle it is possible to identify biomarkers in urine useful in the diagnosis, prognosis and monitoring of disease progression of transmissible spongiform encephalopathy diseases (TSEs).

BUT, will the USDA et al let any test be used to detect BSE or any TSE in the USA bovine ???

i doubt it $$$

Sunday, September 07, 2008
CWD LIVE TEST, and the political aspects or fallout of live testing for BSE in cattle in the USA

Friday, August 29, 2008



5.289 We have concluded, for the reasons given above, that Dr Narang's work received fair consideration by MAFF scientists. While we would pay tribute to Dr Narang's dedication to research into TSEs, we feel that he had a fair opportunity to demonstrate the validity of his work but did not succeed in doing so.

No way to treat a pioneer Apr 20 2003 By Phil Doherty

A leading charity has called for a public inquiry into the way a top mad cow disease expert has been treated by the establishment. Harash Narang was the first scientist to make the link between the illness and its human equivalent- variant Creutzfeldt-Jakob disease - in 1990. Dr Narang says he was made redundant from his job at Newcastle's Public Health Laboratory Services after making his findings known. He claims that he lost his post after the then Health Minister Stephen Dorrell ordered all the lab's work on the killer disease to cease. Since he became a whistle-blower, he says, he has not been able to get lab time in the UK to continue his work.

Dr Narang has since moved to the United States. He is now working at the CJD surveillance unit based at Case Western Reserve University in Cleveland, Ohio.

CJD Foundation head Noel Baldwin, who lost his son Patrick to the killer disease, said: "There is more and more information coming out that proves Dr Narang was right all along.


"He said years ago that CJD could be found in blood and passed on by transfusions and medical instruments. This has now been accepted.

"He argued that BSE could cause both sporadic as well as vCJD, and recent research has shown this to be correct. He also invented a urine test which shows if someone is harbouring the disease."

Mr Baldwin also rued the Government's decision to pull Medical Research Council funding from Dr Narang.

He said: "Now it looks as if the US will benefit financially from this ground-breaking research. "The UK establishment has ignored him for more than 10 years. We believe those responsible should be made accountable for this because if they had listened to Dr Narang maybe some of those poor people wouldn't have died from this terrible disease.


"This is a national scandal that needs to be fully addressed by a public inquiry. "We are planning to launch this campaign in the next few months and will be involving sympathetic MPs to get this issue aired in the House of Commons."


CJD doc jets off

Mar 9 2003

By Phil Doherty, Sunday Sun

The North scientist who first established a link between mad cow disease and its human form is quitting Britain.

Harash Narang has been head-hunted by a top US university to continue his research into variant Creutzfeldt-Jakob disease.

He was working for the Government's Public Health Laboratory Service in Newcastle when he revealed the link and later lost his job.

Dr Narang claimed he was made redundant because he went public with his findings, an allegation which has always been denied. He said: "I now have a job at the United States CJD Surveillance Centre based in Case Western Reserve University, Cleveland, Ohio.

"I'm very excited because it has excellent facilities and is one of the best CJD surveillance centres in the world.

The university is examining a urine test pioneered by Dr Narang which can show whether someone has CJD.

Currently only a post-mortem diagnosis can be made.

Dr Narang said: "Early indications show that my test has performed even better than anticipated. It is expected to be validated very shortly."

And he revealed: "I do not regret telling the truth all those years ago. If I had to do it again then I would."

Ken Bell, a financial backer of Dr Narang's work, claimed he had been forced to go abroad because he cannot get laboratory time in the UK.

He said: "Harash has been blackballed in the UK because he told the public the truth. "The establishment will try anything to stop him working here. It's a disgrace."

Noel Baldwin, of the CJD Foundation charity, said: "He has been proved right about so many things . . . that CJD can be transmitted through blood, that BSE can cause both variant and sporadic CJD and that you can test for the disease through urine samples."

Dr Narang starts work at Case University later this month. Shu Chen, one of his future colleagues, said: "He will be a great asset to our CJD research.";siteid=50081

Edmonton company boasts cheap BSE test Duncan Thorne , CanWest News Service; Edmonton Journal Published: Friday, July 21, 2006 EDMONTON -- An Edmonton company is confident it has a cheap, ground-breaking test for mad cow disease, but the test's British inventor who claims to have first made the link between BSE and the disease's human form insists he still holds the rights.

Despite their differences, inventor Harash Narang and BSE Prion Solutions Inc. agree the test holds amazing potential to quickly and inexpensively test live cattle for bovine spongiform encephalopathy better known as mad-cow disease. The only approved tests so far for mad cow and its human equivalent depend on removing brain samples after death. A test on live animals would open the way to guaranteeing disease-free herds.

"We have a test that not only works, but works each and every time," said Ron Arnold of BSE Prion Solutions Inc., adding formal validation may take up to two years and regulatory approval. Narang, a former British government scientist who went public about human risks from BSE in 1990, started developing tests for detecting the disease in the late 1980s while at a public health laboratory. He had been studying cases of a fatal but rare human brain illness, Creutzfeldt-Jakob disease (CJD), when he started noticing some cases were different. He has said he was well on the way to establishing a link between BSE and the unusual CJD cases when he was ordered to stop his research. He has also claimed officials rejected his calls for increased testing for BSE and the new form of CJD, now known as variant CJD.

Narang developed three diagnostic tests, including an early version of the urine test that BSE Prion intends to bring to market.

A wide-ranging 1998 inquiry into Britain's response to the mad cow crisis found problems with Narang's claims. It cited evidence that fellow scientists could not get his test to work. Even so, Narang continued development of the urine test. A British company, Biotec Global, sponsored much of his work. He is no longer part of the research, but work on it continues at the United States National Prion Disease Pathology Surveillance Center at Case Western Reserve University in Cleveland. Narang and Case Western researchers reported in 2005 that the urine test could reliably detect a harmless form of the prion protein that is blamed for BSE and variant CJD. It could also detect the bad form if the prion was first added directly to the urine.

They said their findings "may lay the foundation for a future technique," if in fact the bad prion can turn up naturally in urine.

"It needs a lot of work still," Ayuna Dagdanova, one of the test's researchers at the U.S. prion surveillance centre, said from Cleveland.

Without solid data it's not possible to say if they are close to detecting BSE in urine, she said. "No one actually knows, but preliminary experiments show the possibility."

Arnold, a partner in Biotec, said Narang gave Biotec the patent rights in 2003 and it in turn gave BSE Prion the licence for the Americas and Europe.

"We've talked with patent attorneys in London and also in Newcastle. Everyone agrees that the documents and the transfer of ownership of the patents was done judiciously and was extremely well put together by the solicitors," said Arnold.

Edmonton company boasts cheap BSE test Duncan Thorne , CanWest News Service; Edmonton Journal Published: Friday, July 21, 2006 Narang, speaking from Newcastle, acknowledged signing papers, but said it was not clear what he was signing. He said he continues to pay the patent renewal fees.

Biotec has sunk more than $2 million into the research, but BSE Prion has not had to pay a licence fee, Arnold said. That's because the project is humanitarian, with plans to hand over any earnings for research purposes, in the form of grants and scholarships.

Narang, who holds shares in Biotec despite the ownership dispute, also said he also wants any profits to go into further research. Meanwhile, he said he's owed back pay and expenses for work he did over the past five years a claim Arnold rejects.

Edmonton Journal � CanWest News Service 2006;k=6995&p=2

Experimental Biology and Medicine 230:343-349 (2005) � 2005 Society for Experimental Biology and Medicine



Sensitive Detection of Prion Protein in Human Urine

Harash K. Narang*,2, Ayuna Dagdanova, Zhiliang Xie, Qiwei Yang and Shu G. Chen,1 * BioTech Global, 22-40 Brentwood Avenue, Newcastle Upon Tyne, NE2 3DH, UK; and Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, Ohio 44106 1To whom requests for reprints should be addressed at Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106. E-mail:


Transmissible spongiform encephalopathies are a group of infectious diseases typically associated with the accumulation of a protease-resistant and �-sheet-rich prion protein, PrPSc, in affected brains. PrPSc is an altered isoform derived from the host-encoded glycoprotein, PrPC. The expression of PrPC is the highest in brain tissue, but it can also be detected at low levels in peripheral tissue. However, it is unclear whether a significant amount of PrPC is released into body fluid and excreted into urine. We have developed a simple, rapid method for the reliable detection of PrPC in urine from normal subjects by Western blotting. Our method can easily and reliably detect PrPC in apparently healthy individuals using less than 1 ml of urine in which the amount of urinary PrPC is estimated to be in the range of low micrograms/liter.

SIMPLE FACT, if you don't test, you don't find.

WHERE might we have been if Narang's research (and others that were not 'in the round'), would have been supported from the start ???

WHY were there just these 'chosen few' that recieved funding and got into the 'peer review round' ???

(please note, i have heard through the grapevine that Narang has recently past away, i have not confirmed this, (came from a good source though), and i never saw this in the news, but i hope that i am wrong. if true, this would be a great loss to the TSE science). ...TSS


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