Neuroanatomical Distribution of Disease-Associated Prion Protein in Cases of Bovine Spongiform Encephalopathy Detected by Fallen Stock Surveillance in Japan
Neuroanatomical Distribution of Disease-Associated Prion Protein in Cases of Bovine Spongiform Encephalopathy Detected by Fallen Stock Surveillance in Japan
Hiroyuki OKADA1), Yoshihumi IWAMARU1), Morikazu IMAMURA1), Kentaro MASUJIN1), Yuichi MATSUURA1), Yoshihisa SHIMIZU1), Kazuo KASAI1), Masuhiro TAKATA1), Shigeo FUKUDA2), Satoshi NIKAIDO2), Kei FUJII2), Sadao ONOE2), Shirou MOHRI1) and Takashi YOKOYAMA1)
1) Prion Disease Research Center, National Institute of Animal Health 2) Hokkaido Animal Research Center, Hokkaido Research Organization
(Received 15-Jun-2011) (Accepted 2-Jul-2011)
ABSTRACT.
Bovine spongiform encephalopathy (BSE) is a fatal neurodegenerative disorder of cattle characterized by accumulation of the disease-associated prion protein (PrPSc) in the central nervous system (CNS). The immunohistochemical patterns and distribution of PrPSc were investigated in the CNS, brains, and spinal cords of 7 naturally occurring BSE cases confirmed by the fallen stock surveillance program in Japan. No animals showed characteristic clinical signs of the disease. Coronal slices of 14 different brain areas in each case were immunohistochemically analyzed using an anti-prion protein antibody. Immunolabeled PrPSc deposition was widely observed throughout each brain and spinal cord. Intense PrPSc deposition was greater in the thalamus, brainstem, and spinal cord of the gray matter than in the neocortices. The topographical distribution pattern and severity of PrPSc accumulation were mapped and plotted as immunohistochemical profiles of the different brain areas along the caudal-rostral axis of the brain. The distribution pattern and severity of the immunolabeled PrPSc in the CNS were almost the same among the 7 cases analyzed, suggesting that the naturally occurring cases in this study were at the preclinical stage of the disease. Immunohistochemical mapping of the PrPSc deposits will be used to clarify the different stages of BSE in cattle.
KEY WORDS: BSE, cattle, immunohistochemistry, prion
SNIP...
DISCUSSION
Levels and regional tropism of vacuolar changes, namely the lesion profile in the brain, is considered a reliable indicator for histopathological diagnosis of BSE-affected cattle [26, 32]. However, optimal preservation is required to ensure the identification of vacuolar changes in certain areas of the brainstem devoid of artifactual vacuolations induced by a postmortem delay of tissue sampling that led to autolysis. Although autolysis conditions have been usually encountered in field cases of BSE diagnosis, autolysis and the frozen condition do not significantly influence PrPSc detection by immunohistochemistry [4, 6, 7, 18]. Moreover, PrPSc immunohistochemistry is an essential tool and may contribute to our understanding of the pathogenesis of BSE [6, 12].
All cattle in the present study were field BSE cases confirmed by the fallen stock surveillance program in Japan. Despite the limited number of animals and differences in their ages and breeds, PrPSc topographical distributions and types in the brain were remarkably similar among these cases and to those in published reports in BSE cattle [5, 13, 15, 16, 20, 27, 30]. The severity of PrPSc deposition was variable in
12
the brain regions. Large amounts of PrPSc deposits were present in the brainstem and thalamus, whereas the cerebral cortices and hippocampus were less involved, suggesting that PrPSc accumulation in the brain of BSE-affected cattle is related to area-dependent tropism [5, 30]. These results indicate that most BSE cases that occur in Japan have been caused by a single infectious agent strain identical to the C-BSE prion. Moreover, the lack of apparent differences in PrPSc distribution patterns or deposition intensity among the 7 cases in this study might suggest the same clinical stage of the disease. A greater degree of PrPSc accumulation within the thalamus and brainstem of all animals was obvious compared to the slaughtered cases in Japan that seemed to be at the preclinical stage of the disease [13]. The present cases revealed no clinical signs or symptoms relevant to BSE, but some cases exhibited dystasia. These results might indicate that the 2 BSE cases with the locomotive disability were highly likely to be at an early clinical stage of the disease.
Recently, other phenotypes, namely atypical BSE that differs from C-BSE, have been reported among BSE cases in Europe [2, 21], North America [23] and Japan [11, 34]. Atypical BSE cases are temporally classified into 2 types, namely L- and H-types according to the molecular size of the proteinases K-digested nonglycosylated form of PrPSc [14, 21]. The immunolabeled PrPSc distribution patterns and/or types in the brains of cattle affected with L-BSE [3, 17] and H-BSE [23] differed from those with C-BSE. C-BSE was characterized the presence of stellate and intraneuronal immunolabeled PrPSc [17, 27]. Stellate PrPSc deposition was located mainly in the gray matter neuropils of the cerebral and cerebellar cortices [27] and was reported to deposit to astrocytes stained with glial fibrillary acidic protein [30]. Additionally, coarse granular and coalescing PrPSc deposition was mainly distributed in the brainstem in the
13
present cases as described in an report [30]. On the other hand, a differential PrPSc deposition pattern was detected in atypical BSE cases. L-BSE showed abundant amyloid PrP-plaques and perineural PrPSc in the brain [3, 17]. PrP-positive amyloid plaques up to 25 μm in diameter were present in an atypical BSE case in Japan (BSE/JP24). In the 7 cases studied here, no PrP-positive plaques were demonstrated in the brain. However, it has been reported that plaque-like PrPSc stained with Congo red rarely appeared in the thalamic nuclei of C-BSE–affected cattle [5, 33]. Additionally, in a Swedish H-BSE case, no stellate PrPSc deposits were identified [8]. Therefore, immunohistochemical profile and mapping of the pathologic stage of the disease and confirmation of the infectious agent strain, e.g., C-BSE or atypical BSE [30].
In summary, the types and distribution patterns of immunolabeled PrPSc in the brain and spinal cords of the 7 naturally occurring BSE cases confirmed by the fallen stock surveillance program in Japan were in accordance with published C-BSE cases, indicating that the BSE in the affected animals reported here was caused by a single infectious agent strain identical to the C-BSE prion.
[PDF (934K)]
doi:10.1292/jvms.11-0291 JOI JST.JSTAGE/jvms/11-0291
Copyright(c) 2011 by the Japanese Society of Veterinary Science
http://www.jstage.jst.go.jp/article/jvms/advpub/0/1107110572/_pdf
Bio.040: Phenotypic Variability of Italian BASE Affected Cattle
Cristiano Corona,1,† Chiara Porcario,1 Elena Vallino Costassa,1 Maria Mazza,1 Francesca Martucci,1 Barbara Iulini,1 Marina Gallo,1 Franco Paterlini,2 Maria N. Chieppa,1 Luana Dell’Atti,1 Cristiana Maurella,1 Simone Peletto,1 Pierluigi Acutis,1 Maria Caramelli,1 Gianluigi Zanusso3 and Cristina Casalone1
1Istituto Zooprofilattico Sperimentale del Piemonte Liguria e Valle d’Aosta; Turin, Italy; 2Istituto Zooprofilattico Sperimentale della Lombardia e dell’Emilia Romagna; Bergamo, Italy; 3Università di Verona, Policlinico GB Rossi; Verona, Italy†Presenting author; Email: cristiano.corona@izsto.it
In Italy, in the framework of BSE surveillance program, 145 cases of the disease have been identified so far. Out of 145 BSE positive cases, five cattle were L-type BSE forms, according to the lower electrophoretic migration and the mono-glycosylated dominant glycotype of protease resistant PrP (PrPSc), distinct from classical BSE (C-BSE).
The first three Italian L-type BSE cases were defined "BASE" (bovine amyloidotic spongiform encephalopathy) cases, since the immunohistochemistry showed PrP amyloid deposits in the brain tissue mainly localized in the white matter of thalamus and forebrain areas. Unfortunately, in the fourth Italian L-type case brain sampling was restricted to the brainstem with no evidence of amyloid deposits and the definition of BASE was precluded.
The fifth L-type BSE case was recently confirmed in a 14-year-old regularly slaughtered Alpine Brown cattle free of neurological signs. Immunoblot analysis showed the BSE L-type PrPSc, as in all other four Italian cases. However, in contrast to what observed in the other BASE cases, PrPSc was mainly distributed in the obex compare to the more rostral brain regions. These results were confirmed also by immunohistochemistry (IHC). Furthermore, PrP deposition pattern in the obex was granular and punctate, resembling what we usually observe in C-BSE. Unexpectedly, no PrPSc amyloid plaques were observed but only small scattered PrPSc aggregates in the thalamus as well as in the forebrain. Genetic analysis of the PRNP coding sequence revealed a genotype similar to that of the other atypical cases detected so far, suggesting that an association between the PrP amino acid composition and the observed phenotype should be excluded.
Despite all atypical BSE cases were L-type BSE the neuropathological phenotype showed a slight variability. These differences highlighted might be not related to the animal age, breed or PRNP but to a different stage of the disease. To date, all data indicate that BASE is a sporadic disease in cattle and that disease modifiers, other than those investigated might influence the disease phenotype.
Risk.16: Clinical Disease in Cattle Experimentally Inoculated with All Types of BSE
Catherine Graham,1,† Michel Levy,2 Ed Pajor,2 Garth McGregor,1 Rheana Flitton1 and Stefanie Czub1
1Canadian Food Inspection Agency; Lethbridge, AB Canada; 2Faculty of Veterinary Medicine; University of Calgary; Calgary, AB Canada†Presenting author; Email: catherine.graham@inspection.gc.ca
Background. Classical, or C-type, bovine spongiform encephalopathy (BSE) has been extensively described in the literature. Recently, two novel forms of BSE, termed atypical BSE, have been reported in a number of countries. These new forms show differences in the biochemical characteristics of the prion protein and, where reported, tend to occur in aged animals but descriptions of clinical presentation are incomplete or absent.
Materials and Methods. Female Hereford/Angus cross calves were intracranially challenged at approximately five months of age with 1 ml of a 10% brain homogenate originating from Canadian field cases of BSE which had been previously classified as C-, L-, or H- type.
The animals were monitored during incubation period, and clinical disease is described using a standardized examination protocol. Incubation period, description and progression of clinical signs was recorded and videotaped for objective evaluation.
Results. All L- and H- type atypical BSE challenged animals began to display signs of clinical disease at approximately 11 months post inoculation, and disease progression was slow but constant until animals were euthanized. Clinical signs in all atypical BSE inoculated animals included hesitation at doors and gates, spontaneous muscle fasciculations and sensitivity to touch. Teeth grinding and excessive salivation are occasionally noted. Animals with L-type BSE are very anxious and show high levels of sensitivity to hand movement. One H-type animal shows periods of somnolence. Both H-type inoculated animals go down during handling and have difficulty rising and show sensitivity to movement around their head and neck area, but to a lesser degree than the L-type BSE inoculated animals. Interestingly, no locomotor abnormalities have been observed in either group.
C-type challenged animals remain normal at approximately 18 months post inoculation. Clinical disease in C-type inoculated animals from a previous transmission study was typically slow and intermittently displayed during the initial stages and after a period of two to four months was more consistent and progressive. Clinical signs in C-type BSE were as previously reported in the literature.
Discussion. The spectrum of clinical signs for all three types of BSE examined is similar. Incubation period is shorter for H- and L-type BSE as compared with C-type. Once clinical signs begin, progression is slow but relentless in atypical BSE, and more insidious in classical BSE. A summary of clinical signs presented in the three different types of BSE will be presented, and video of clinical disease will be displayed.
http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf
Thursday, June 23, 2011
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html
Journal of Clinical Microbiology, June 2011,p. 2109-2115, Vol. 49, No. 6 0095-1137/11/$12.00+0 doi:10.1128/JCM.02033-10
Distinct Proteinase K-Resistant Prion Protein Fragment in Goats with No Signs of Disease in a Classical Scrapie Outbreak
Ilias G. Bouzalas1,, Florian Lörtscher3,, Chrysostomos I. Dovas1, Anna Oevermann3, Jan P. M. Langeveld2, Maria Papanastassopoulou1, Orestis Papadopoulos1, Andreas Zurbriggen3 and Torsten Seuberlich3*
Aristotle University of Thessaloniki, Thessaloniki, Greece,1 Central Veterinary Institute of Wageningen UR, Lelystad, Netherlands,2 University of Berne, Berne, Switzerland3
Received 8 October 2010/ Returned for modification 26 November 2010/ Accepted 19 March 2011
Considerable efforts have been directed toward the identification of small-ruminant prion diseases, i.e., classical and atypical scrapie as well as bovine spongiform encephalopathy (BSE). Here we report the in-depth molecular analysis of the proteinase K-resistant prion protein core fragment (PrPres) in a highly scrapie-affected goat flock in Greece. The PrPres profile by Western immunoblotting in most animals was that of classical scrapie in sheep. However, in a series of clinically healthy goats we identified a unique C- and N-terminally truncated PrPres fragment, which is akin but not identical to that observed for atypical scrapie. These findings reveal novel aspects of the nature and diversity of the molecular PrPres phenotypes in goats and suggest that these animals display a previously unrecognized prion protein disorder.
--------------------------------------------------------------------------------
* Corresponding author. Mailing address: NeuroCentre, DCR-VPH, Bremgartenstrasse 109a, CH-3001 Berne, Switzerland. Phone: 41 31 631 2206. Fax: 41 31 631 2538. E-mail: torsten.seuberlich@itn.unibe.ch .
I.G.B. and F.L. contributed equally to this study.
Supplemental material for this article may be found at http://jcm.asm.org/.
Published ahead of print on 30 March 2011.
http://jcm.asm.org/cgi/content/abstract/49/6/2109
Scrapie Nor-98 like case in California FY 2011 AS of December 31, 2010.
Scrapie cases in goats FY 2002 - 2011 AS of December 31, 2010 Total goat cases = 21 Scrapie cases, 0 Nor-98 like Scrapie cases (21 field cases, 0 RSSS cases)
Last herd with infected goats disignated in FY 2008 Michigan 8 cases
http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep
http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html
Sunday, October 3, 2010
Scrapie, Nor-98 atypical Scrapie, and BSE in sheep and goats North America, who's looking ?
http://nor-98.blogspot.com/2010/10/scrapie-nor-98-atypical-scrapie-and-bse.html
http://nor-98.blogspot.com/
FROM THE STUDY ;
Neuroanatomical Distribution of Disease-Associated Prion Protein in Cases of Bovine Spongiform Encephalopathy Detected by Fallen Stock Surveillance in Japan
"Although autolysis conditions have been usually encountered in field cases of BSE diagnosis, autolysis and the frozen condition do not significantly influence PrPSc detection by immunohistochemistry [4, 6, 7, 18]."
maybe that's why the USDA et al likes to use it ;
Completely Edited Version
PRION ROUNDTABLE
2003
Dr. Linda Detwiler
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
=============================
http://madcowtesting.blogspot.com/
http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position-post.html
-------- Original Message --------
Subject: USA BIO-RADs INCONCLUSIVEs
Date: Fri, 17 Dec 2004 15:37:28 -0600 From: "Terry S. Singeltary Sr." To: susan_berg@bio-rad.com
Hello Susan and Bio-Rad,
Happy Holidays!
I wish to ask a question about Bio-Rad and USDA BSE/TSE testing and there inconclusive. IS the Bio-Rad test for BSE/TSE that complicated, or is there most likely some human error we are seeing here?
HOW can Japan have 2 positive cows with No clinical signs WB+, IHC-, HP- , BUT in the USA, these cows are considered 'negative'?
IS there more politics working here than science in the USA?
What am I missing?
-------- Original Message --------
Subject: Re: USDA: More mad cow testing will demonstrate beef's safety
Date: Fri, 17 Dec 2004 09:26:19 -0600
From: "Terry S. Singeltary Sr." snip...end
Experts doubt USDA's mad cow results
snip...END
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''. ...
TSS
-------- Original Message --------
Subject: Your questions
Date: Mon, 27 Dec 2004 15:58:11 -0800
From: To: flounder@wt.net
Hi Terry:
snip...
Let me know your phone number so I can talk to you about the Bio-Rad BSE test.
Thank you
Regards
Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email:
=================================
END...TSS
######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########
Wednesday, July 28, 2010
Atypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA Final report
http://bse-atypical.blogspot.com/2010/07/atypical-prion-proteins-and-ibnc-in.html
IBNC
"All of the 15 cattle tested showed that the brains had abnormally accumulated prion protein."
Saturday, February 28, 2009
NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS "All of the 15 cattle tested showed that the brains had abnormally accumulated PrP" 2009
SEAC 102/2
http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html
ATYPICAL LESION DISTRIBUTION (RBSE 92/21367)
A 6 year old, home bred (HB), Friesian x Holstein cow in a dairy herd in Aberdeenshirer submitted as a suspect BSE case in the negative study (SE0203), has been diagnosed as BSE negative on standard, statutory (obex only), diagnostic criteria at CVL.
Further examination by Dr Jeffrey at Lasswade, as required by the project design, has revealed vacuolar change in the septal nucleus and putamen which co-localised with PrP immunoreactivity. No significant lesions were found in any other part of the brain, neither was PrP found in the medulla.
It is important to note that examination of four brain blocks used earlier in the epidemic would not have detected the lesion but a 16 block study (as used in the very days of BSE) would.
FURTHER INFORMATION
The herd of origin has had 15, HB, suspect cases of BSE since July 1989 and a further case is still alive.
2. Of the 15, eight have been confirmed by standard histopathology and seven diagnosed negative (including the above case).
3. Fixed brain tissue from the negative cases exists at Lasswade (because they always collect whole brain in Scotland) but has not so far been examined further. No frozen tissue was collected so neither SAF nor PrP detection (by immunoblotting) has been attempted.
4. Mr Wells agrees with Dr Jeffrey's and Dr Simmons' findings.
FURTHER ACTION IN PROGRESS
1. The brain tissue from the negative cases will be examined in detail by conventional histopathology and ICC.
2. Kevin Taylor and his veterinary colleagues have been alerted to the situation.
OTHER RECOMMENDED ACTIONS
1. TRANSMISSION Attempt transmission from the 'case' to standard mice strains. (Note: In regard to strain typing, formalin may have modified strain phenotype - we need to discuss with NPU). Further transmission studies (eg in cattle) might be suggested if primary transmission in mice fails. These proposals have funding implications.
CODE 18-77
93/2.17/1.1
2. PrP GENOTYPING - Although only fixed brain tissue is available we are considering genotyping from parents/offspring/fixed brain. As a first step we are attempting to extract DNA from the fixed brain and to amplify the PrP gene by PCR.
3. John Wilesmith has interrogated the data base for the herd history. Other than the high proportion of negative cases nothing significant is apparent.
4. Familial relationships between suspect (including positive and negative) cases in this herd could be examined and tracings of breeding animals initiated.
5. Consideration might be given to collecting frozen spinal cord from new cases in this herd or in dispersals from it for (SAF/PrP examination).
CONCLUSIONS
1. At present it is unclear whether or not this is a singleton incident or whether the other negative cases in this herd show a similar lesion.
2. The discovery might indicate the existence of a different strain of BSE from that present in the general epidemic or an unusual response by an individual host.
3. If further atypical lesion distribution cases are revealed in this herd then implications of misdiagnosis of 'negative' cases in other herds may not be insignificant.
4. If this is a new strain all the implications need to be considered including whether or not to proceed with the further investigation of future cases negative for BSE on obex examination alone and from which whole brains are available (as in Scotland) or collected in the future. Also perhaps investigation of the tissue distribution of infectivity in these animals might be considered.
5. Animal and public health controls in place should be sufficient since all tissues (other than brain for diagnosis) are incinerated.
We observe that Dr Tyrrell would wish to be informed of this at an early opportunity and that the SEAC would wish to discuss it at their meeting in April.
R BRADLEY
M DAWSON
17 February 1993
CVO - for information and comment on further action please
cc Mr K C Taylor
Dr B J Shreeve
93/2.17/1.2
This minute is re-issued with a wider distribution.
The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".
Mr Scudamore
Mr R C Lowson
Dr D Matthews
Mr I Robertson
Dr K MacOwan
Mr C Randall
Mr J W Wilesmith
Mr G A H Wells
Dr M Jeffrey
Dr M Simmons
93/2.17/1.3
http://tna.europarchive.org/20080609145105/http://www.bseinquiry.gov.uk/files/yb/1993/02/17001001.pdf
IN CONFIDENCE
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367)
http://tna.europarchive.org/20080609145105/http://www.bseinquiry.gov.uk/files/yb/1993/03/14001001.pdf
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. ...
http://collections.europarchive.org/tna/20090114131343/http://www.bseinquiry.gov.uk/files/yb/1992/10/26001001.pdf
Tuesday, November 17, 2009
SEAC NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS (IBNC) FROM THE VETERINARY LABORATORIES AGENCY (VLA) SEAC 103/1
http://bse-atypical.blogspot.com/2009/11/seac-new-results-on-idiopathic.html
NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS "All of the 15 cattle tested showed that the brains had abnormally accumulated PrP" 2009
http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html
''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
http://collections.europarchive.org/tna/20080102204938/http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf
http://web.archive.org/web/20030327015011/http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf
NOW, what about the 'obex only' mode of testing used by the USDA et al for TSE, prions $$$ works for them too, a sure fire way NOT TO FIND MAD COW DISEASE $$$
NOW, read the following please, and then ask yourself, WHY the USDA et al were ONLY TESTING THE OBEX PART OF THE BRAIN in USA cattle for BSE $$$
BECAUSE they knew that would be the least likely way to find BSE/TSE in USA cattle $$$...TSS
Tuesday, November 02, 2010
IN CONFIDENCE
The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
Tuesday, July 14, 2009
U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST
WHERE did we go wrong $$$
http://madcowtesting.blogspot.com/2009/07/us-emergency-bovine-spongiform.html
Thursday, July 14, 2011
Histopathological Studies of “CH1641-Like” Scrapie Sources Versus Classical Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html
=========
Discussion
In the five cats in this study with a spongiform encephalopathy, fibrils were observed by electron microscopy and their major protein, Prpsc, was identified by SDS-PAGE and Western blot. The fibrils were similar to those described in sheep with scrapie (Rubenstein and others 1987, Gibson and others 1987, Scott and others 1987, Dawson and others 1987), cattle with bovine spongiform encephalopathy (Wells and others 1987, Hope and others 1988, Scott and others 1990) and humans with Creutzfeldt-Jakob disease (Merz and others 1984).
In sheep with scrapie, fibrils can be readily detected in several areas of the brain, including cerebral cortex (Stack and others 1991).
By contrast, the frequency with which fibrils were detected in cattle with BSE, DEPENDED ON THE REGION OF THE BRAIN SAMPLED; THE HIGHEST YIELD BEING OBTAINED FROM MEDULLA, MIDBRAIN, THALAMUS AND BASAL NUCLEI WHERE VACUOLA CHANGES ARE PRESENT (Scott and others 1990). This correlation between PrPsc accumulation and vacuolar pathology is also well established in laboratory animal models of scrapie (Bruce and others 1989). Because of the widespread distribution of changes in FSE (Whatt and others 1991) and the requirement, in the present study, not to compromise the histopathological examination of the brain, the frontal region of the cerebrum was therefore selected for fibril and PrPsc examinations. However, studies of the sensitivity of fibril detection in different parts of the brain in cats with FSE are required to determine whether detection can be made as readliy in other regions as in the frontal cerebral cortex.
IT IS OF INTEREST, that fibrils were detected in the brains of 3 cats (cases 9, 13, & 18) WITHOUT histopathological evidence of spongiform encephalopathy, and that in only one of them, (case 9), a Western blot for modified PrP was positive. There are precedents for the occurrence of abnormal PrP in the organs of animals incubation scrapie prior to clinical signs and/or spongiform encephalopathy...
snip...
(please see full text (and one might start downloading these documents for future use, as some disappear never to re-appear, as in some of the FDA's. ...TSS)
http://collections.europarchive.org/tna/20090113230941/http://www.bseinquiry.gov.uk/files/sc/seac12/tab04.pdf
PLEASE NOTE *
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
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
FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html
http://www.mail-archive.com/fda-newsdigest-l@list.nih.gov/msg00094.html
THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006
In an article today for United Press International, science reporter Steve Mitchell writes:
Analysis: What that mad cow means
By STEVE MITCHELL UPI Senior Medical Correspondent
WASHINGTON, March 15 (UPI) -- 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 they did before 2005 suspect," Brown said.
Despite this, Brown said the U.S. prevalence of mad cow, formally known as bovine spongiform encephalopathy, or BSE, did not significantly threaten human or cattle health.
"Overall, my view is BSE is highly unlikely to pose any important risk either in cattle feed or human feed," he said.
However, Jean Halloran of Consumers Union in Yonkers, N.Y., said consumers should be troubled by the USDA's secrecy and its apparent plan to dramatically cut back the number of mad cow tests it conducts.
"Consumers should be very concerned about how little we know about the USDA's surveillance program and the failure of the USDA to reveal really important details," Halloran told UPI. "Consumers have to be really concerned if they're going to cut back the program," she added.
Last year the USDA tested more than 300,000 animals for the disease, but it has proposed, even in light of a third case, scaling back the program to 40,000 tests annually.
"They seem to be, in terms of actions and policies, taking a lot more seriously the concerns of the cattle industry than the concerns of consumers," Halloran said. "It's really hard to know what it takes to get this administration to take action to protect the public."
The USDA has insisted that the safeguards of a ban on incorporating cow tissue into cattle feed (which is thought to spread the disease) and removal of the most infectious parts of cows, such as the brain and spinal cord, protect consumers. But the agency glosses over the fact that both of these systems have been revealed to be inadequately implemented.
The feed ban, which is enforced by the Food and Drug Administration, has been criticized by the Government Accountability Office in two reports, the most recent coming just last year. The GAO said the FDA's enforcement of the ban continues to have weaknesses that "undermine the nation's firewall against BSE."
USDA documents released last year showed more than 1,000 violations of the regulations requiring the removal of brains and spinal cords in at least 35 states, Puerto Rico and the Virgin Islands, with some plants being cited repeatedly for infractions. In addition, a violation of similar regulations that apply to beef exported to Japan is the reason why Japan closed its borders to U.S. beef in January six weeks after reopening them.
Other experts also question the adequacy of the USDA's surveillance system. The USDA insists the prevalence of mad cow disease is low, but the agency has provided few details of its surveillance program, making it difficult for outside experts to know if the agency's monitoring plan is sufficient.
"It's impossible to judge the adequacy of the surveillance system without having a breakdown of the tested population by age and risk status," Elizabeth Mumford, a veterinarian and BSE expert at Safe Food Solutions in Bern, Switzerland, a company that provides advice on reducing mad cow risk to industry and governments, told UPI.
"Everybody would be happier and more confident and in a sense it might be able to go away a little bit for (the USDA) if they would just publish a breakdown on the tests," Mumford added.
UPI requested detailed records about animals tested under the USDA's surveillance plan via the Freedom of Information Act in May 2004 but nearly two years later has not received any corresponding documents from the agency, despite a federal law requiring agencies to comply within 30 days. This leaves open the question of whether the USDA is withholding the information, does not have the information or is so haphazardly organized that it cannot locate it.
Mumford said the prevalence of the disease in U.S. herds is probably quite low, but there have probably been other cases that have so far gone undetected. "They're only finding a very small fraction of that low prevalence," she said.
Mumford expressed surprise at the lack of concern about the deadly disease from American consumers. "I would expect the U.S. public to be more concerned," she said.
Markus Moser, a molecular biologist and chief executive officer of Prionics, a Swiss firm that manufactures BSE test kits, told UPI one concern is that if people are infected, the mad cow pathogen could become "humanized" or more easily transmitted from person to person.
"Transmission would be much easier, through all kinds of medical procedures" and even through the blood supply, Moser said.
© Copyright 2006 United Press International, Inc. All Rights Reserved
http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r
http://www.upi.com/Science_News/2003/12/30/Mad-Cow-Linked-to-thousands-of-CJD-cases/UPI-47861072816318/
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, ...
http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm
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." ........TSS
http://madcowtesting.blogspot.com/2009/07/mad-cow-cover-up-usa-masked-as-sporadic.html
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
THIS is just ONE month report, of TWO recalls of prohibited banned MBM, which is illegal, mixed with 85% blood meal, which is still legal, but yet we know the TSE/BSE agent will transmit blood. we have this l-BSE in North America that is much more virulent and there is much concern with blood issue and l-BSE as there is with nvCJD in humans. some are even starting to be concerned with sporadic CJD and blood, and there are studies showing transmission there as well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that reaches commerce is ever returned via recall, very, very little. this was 2007, TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow feed that was in ALABAMA in one of the links too, this is where the infamous g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the USA. seems this saga just keeps getting better and better.......$$$
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
Sunday, October 24, 2010
Australia Mad cow assessments come to a standstill, USDA hasn't a clue $
"And then FSANZ received an incomplete application from the US, which says at this stage it doesn't have the resources to provide information."
http://www.abc.net.au/rural/news/content/201010/s3044237.htm
please see full text ;
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
Subject: BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA, A REVIEW OF SORTS
Date: October 18, 2007 at 12:25 pm PST
BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA, A REVIEW OF SORTS
HOW can they find anymore mad cows when the june 2004 enhanced bse cover-up was just that, the testing and protocol for testing was totally flawed, and proven to be so. they floundered every step of the way. and then when the atypicals started showing up, they just shut the testing down. the two suspect cows that samples sat on the shelf for 7+ months that was later confirmed, and the other suspect that sat on the shelf for 4 months, but later thought to be negative UNDER VERY QUESTIONABLE CONDITIONS, but could not have all the proper testing done on it, due to the sample being set in paraffin, which is a no no. they knew that, and that was the end around johanns and dehaven did after fong did the same to them on the 7 month delayed sample. all this done, while GW et al at the USDA were shoving down everyone throats the BSE MRR policy, the legal trading of all strains of TSE globally. ...tss
Subject: USDA BSE inconclusive MRR policy Date: August 25, 2006 at 3:52 pm PST
USDA BSE inconclusive MRR policy
BESIDES THE TEXAS MAD COW THAT WAS RENDERED AND NEVER TESTED;
FDA Statement FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).
FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.
To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.
Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.
FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.
####
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html
USDA orders silence on mad cow in Texas
By Steve Mitchell United Press International Published 5/11/2004 10:16 PM
WASHINGTON, May 11 (UPI) -- The U.S. Department of Agriculture has issued an order instructing its inspectors in Texas, where federal mad cow disease testing policies recently were violated, not to talk about the cattle disorder with outside parties, United Press International has learned.
The order, sent May 6 by e-mail from the USDA's Dallas district office, was issued in the wake of the April 27 case at Lone Star Beef in San Angelo, in which a cow displaying signs of a brain disorder was not tested for mad cow disease despite a federal policy to screen all such animals.
The deadly illness also is known as bovine spongiform encephalopathy.
Both the USDA and its Inspector General -- amid allegations that an offsite supervisor overruled the opinion of the inspectors onsite and made the final decision not to test the animal -- have opened up investigations to determine why agency policy was violated.
The order, which was obtained by UPI, was issued by Ijaz Qazi, circuit supervisor for the USDA's Food Safety and Inspection Service's Dallas district, which covers the entire state. It reads: "All BSE inquiries MUST be directed to Congressional Public Affairs Phone 202-720-9113 attention Rob Larew OR Steve Khon. This is an urgent message. Any question contact me. Ijaz Qazi."
Although the language might sound innocuous, experienced inspectors familiar with USDA parlance have taken to referring to the notice as a "gag order."
The National Joint Council of Food Inspection Locals -- the national inspectors union -- considers the order a violation of inspectors' free speech rights and is considering legal action against the USDA for breaching the labor agreement they have with the agency.
Inspectors alleged the order also suggests the agency is concerned about its personnel leaking damaging information about either the Texas case or the USDA's overall mad cow disease surveillance program, which has come under fire since the discovery of an infected cow in Washington state last December.
"Anytime the government suppresses an individual's freedom of speech, that's unconstitutional," Gary Dahl, president of Local 925, the Colorado inspectors union, told UPI.
Stanley Painter, chairman of the National Joint Council, said the USDA has sent out notices in the past stating inspectors cannot talk to reporters.
"It's an intimidation thing," Painter told UPI. Inspectors have the right to talk to anybody about any subject, as long as they clarify they are not speaking on behalf of the USDA and they are not doing it on government time, he said.
USDA spokesman Steven Cohen said he was not familiar with the notice from the Dallas office. He said he would look into it, but did not respond by UPI's publication time. In general, Cohen said, "There's an expectation any statement on behalf of the agency would come from the office of communications (in Washington.)"
Asked if employees could speak freely as long as they clarified that their views did not reflect those of the agency, Cohen said, "We'd rather that agency policy be communicated by those in a position to speak for the agency."
Qazi told UPI the notice was not issued in conjunction with the Texas case and it was routine agency practice that outside inquiries be referred to the Washington office. He said inspectors are free to talk to outside parties, including reporters, and he did not consider the e-mail a violation of the labor agreement with the inspectors.
Painter said the USDA's efforts to keep its employees from talking about mad cow would be better spent "with issues like protecting the consuming public instead of trying to hide things." He added he would "just about bet his last nickel" agency management was attempting to suppress information about the Texas case.
"To keep federal employees from reporting government waste, misuse of appropriations -- those types of things -- that's not a good thing either," Dahl said. "If there is something wrong, let's get it out in the open -- let's get it fixed. We're working for the public, the American consumers. I think they have the right to know this," he said.
"And believe me there's so many indicators saying that the USDA's mad cow testing program is broken," Dahl added.
At least one member of Congress, Sen. Tom Harkin, D-Iowa, agrees.
Harkin, a long-time critic of the USDA, sent a letter to Agriculture Secretary Ann Veneman on Monday, saying the Texas incident "calls into question the effectiveness and reliability of USDA's current and proposed surveillance system."
The USDA has proposed testing more than 200,000 cows -- or 10 times its current rate -- in an expanded program scheduled to begin June 1. Harkin wrote in the five-page letter, however, that given the realities of the cattle industry, it is "quite doubtful" the USDA will be able to test that many cows, particularly because it had difficulty finding 20,000 last year.
"We simply cannot tolerate a BSE testing system that fails to give valid answers to critical questions for U.S. consumers and foreign customers," Harkin said in the letter, which sharply criticizes the agency's failure to address explicitly how its new surveillance program will be implemented.
"We look forward to receiving (Harkin's) letter and having the opportunity to review it and respond to him," USDA spokesman Ed Loyd told UPI. "USDA has acknowledged there was a failure in not testing that cow in Texas for BSE, so we are all working to ensure that does not occur again."
Jim Rogers, a spokesman for USDA's Animal and Plant Health Inspection Service, which oversees the agency's mad cow surveillance program, told UPI the agency has tested about 15,500 animals since fiscal year 2004 began, on Oct. 1, 2003. However, the agency has refused to identify the states and facilities from which the cows originated. Rogers said UPI would have to seek that information through the Freedom of Information Act.
The question is central to the USDA's implementation of its expanded surveillance program. Downer cows -- those unable to stand or walk -- made up the bulk of the animals the agency tested for mad cow in previous years, but these were banned from being slaughtered for human consumption in December. This means the agency inspectors no longer can obtain brain samples from these cows at slaughterhouses as they could in the past.
Furthermore, the USDA has not provided any evidence it has worked out agreements with rendering facilities or ranchers, where downers and dead cows are now most likely to be found, to obtain the extra animals for testing.
Loyd said the agency is "working very hard to get animals on the farm that would never show up in a processing facility," and he was "not aware of any issues" that would delay the launch of the new program.
However, he was unable to provide the names or locations of the rendering facilities where the agency will be obtaining cow brains for BSE testing. He said he would look into it but did not return two follow-up phone calls from UPI before publication.
--
Steve Mitchell is UPI's Medical Correspondent. E-mail sciencemail@upi.com
Copyright © 2001-2004 United Press International
http://www.upi.com/view.cfm?StoryID=20040511-015527-4917r
Subject: The IHC Test Variables (USA BSE SURVEILLANCE) Date: June 24, 2005 at 7:59 pm PST
The IHC Test Variables:
• IHC has been the primary confirmatory test for
USDA’s BSE surveillance program and is recognized
by the World Organization for Animal Health, or OIE.
• IHC allows scientists to determine if a sample is
positive for BSE in two distinct ways:
1.) A staining technique (presence of abnormal
prion protein) that uses antibodies to detect
abnormal prion protein in the brain.
2.) A visual examination to determine whether there
are lesions (holes or "spongy" appearances)
present in the brain.
• Several variables could yield conflicting results:
o IHC is not a standardized, commercially
available test. It involves variables, including
several options in types of antibodies and other
reactive agents. The sensitivity of any given test
is influenced by those variables.
o If the level of infectivity in the animal is extremely
low, the abnormal prion in the brain will be
minimal and therefore more difficult to detect.
o Variations in the conditions under which the
staining process is performed, such as
chemicals and reactive agents used,
temperature and length of antibody exposure,
can also cause the test to yield different results.
Testing History on This Animal:
• In November 2004, a sample from this animal
returned inconclusive for BSE on a Biorad screening
test.
• The sample was subjected to an IHC confirmatory
test, which returned negative.
• USDA scientists also ran an additional, experimental
IHC "rapid" tissue fixation test for academic purposes,
which can be conducted more quickly than the IHC
confirmatory test and is therefore of interest to the
scientific community, but it has not been approved
internationally.
• While some abnormalities were noted in the
experimental IHC test results, because the test was
not a validated procedure, and because the two
approved IHC tests came back negative, the results
were not considered to be of regulatory significance
and therefore were not reported beyond the
laboratory.
• A Western blot test conducted the week of
June 5, 2005, returned positive for BSE.
• An additional IHC confirmatory test conducted the
week of June 13, 2005, by USDA scientists utilizing
different antibodies from the November 2004 test,
confirmed this case as weakly positive for BSE.
• The Veterinary Laboratories Agency in Weybridge,
England, conducted a series of diagnostic tests
including an IHC, using different antibodies from
those used by USDA in November 2004, which
returned positive results for BSE.
• Experts from the Weybridge lab confirmed the
accuracy of the results of USDA’s November
confirmatory IHC test, concurring that the case could
not have been confirmed on the basis of this sample.
• Weybridge experts also examined the November
experimental IHC test and interpreted the results to
be positive.
Potential Causes of Conflicting Results:
• USDA scientists are consulting with Weybridge
scientists to determine the cause of the conflicting
IHC test results.
• Several factors could cause or contribute to the
discrepancy as follows:
o This animal had a very low level of infectivity and
therefore the sensitivity of USDA’s routine IHC
test might not have been sufficient to detect the
disease.
o Weybridge experts indicate that deposits of
abnormal prion in the brain tissue were not
uniformly distributed and were present at low
concentration, which means that even adjacent
samples of brain tissue might not give identical
results.
Factsheet
Veterinary Services June 2005
APHIS
USDA Protocol Review:
• USDA will develop a protocol to conduct dual
confirmatory tests, the IHC and the Western blot,
when the screening test, the Biorad, returns an
inconclusive result.
• USDA and Weybridge scientists are in agreement
that the Biorad test is a very effective and appropriate
screening test.
• USDA scientists will consult with Weybridge scientists
to assess the array of antibodies available for use in
IHC confirmatory tests to determine the most
appropriate for use in United States confirmatory
tests. Those consultations will be repeated periodically.
The U.S. Department of Agriculture (USDA) prohibits discrimination
in all its programs and activities on the basis of race, color,
national origin, sex, religion, age, disability, political beliefs, sexual
orientation, or marital or family status. (Not all prohibited bases
apply to all programs.) Persons with disabilities who require alternative
means for communication of program information (Braille,
large print, audiotape, etc.) should contact USDA’s TARGET
Center at (202) 720–2600 (voice and TDD).
To file a complaint of discrimination, write USDA, Director, Office
of Civil Rights, Room 326–W, Whitten Building, 1400
Independence Avenue, SW, Washington, DC 20250–9410 or call
(202) 720–5964 (voice and TDD). USDA is an equal opportunity
provider and employer.
Safeguarding American Agriculture Animal and Plant Health Inspection Service • United States Department of Agriculture •
http://www.usda.gov/documents/vs_bse_ihctestvar.pdf
THIS confirms that the June 2004 Enhanced BSE cover-up, was just that. Like i said before, due to this terribly flawed system, those 388,000 testing to date for BSE in the USA were meaningless and should be retested. ...
Subject: USDA JOHANN'S MAD ABOUT FONG, PLANS HIS OWN LAB AND HIS OWN MAD COW ANTIBODIES ;-) Date: July 29, 2005 at 2:35 pm PST
Friday, July 29, 2005
Ames lab to take over testing for mad cow disease Published: 07/29/2005 3:52 PM
By: Associated Press - Associated Press
AMES, IA - Scientists at the National Veterinary Services Laboratories here soon will begin conducting their own Western blot tests, eliminating the need to travel to Weybridge, England, when initial rapid testing detects mad cow disease.
"I think the change is good because we're more likely to know exactly what we're dealing with on each case," said Dr. Randall Levings, director of the labs.
The change is a response to an order from U.S. Agriculture Secretary Mike Johanns.
"We took those as our marching orders," Levings said.
Mad cow disease, formally known as bovine spongiform encephalopathy, or BSE, attacks a cow's nervous system. It is characterized by spongelike holes in the brain, the result of misshapen proteins called prions that kill brain cells.
The only way it is known to spread is by cattle eating infected brain and nerve tissue from other cows. That's why the government in 1997 banned the use of cattle feed that contains remnants of other cows. Of the three cases of mad cow confirmed in the United States, all three cows were born before the feed ban, Levings said.
Since January 2004, the government has tested more than 400,000 cows for the disease, using a rapid screening test and a test known immunohistochemistry, or IHC.
Rapid testing of a sample involves removing normal proteins and adding chemicals that bind to the abnormal proteins, making them visible. The IHC test involves staining paper-thin brain tissue samples to highlight the abnormal protein.
The Western blot test, conducted at Weybridge destroys normal proteins in the brain, leaving only the abnormal prions.
In June, the nation's Office of Inspector General ordered a review of the Ames lab's testing procedures after a sample last fall tested positive in England, but negative in Ames.
A rapid test on the sample in Ames detected the presence of BSE, but the following IHC test was negative. Ames workers also relayed the results of the test, but did not complete formal paperwork.
A version of mad cow disease, known as variant Creutzfeld-Jakob, has killed about 150 people worldwide, most of them in Britain, where there was an outbreak in the 1990s.
"We're taking all of the right steps," Levings said. "It would not be a risk to human or animal health in this country. It's not high. It's very, very low."
http://www.crgazette.com/2005/07/29/Home/News/madcowtesting.htm
SO, Johann's/GW et al have perfected the BSE/TSE testing protocols and they don't need anyone else to tell them what to do. this was proven with the TEXAS mad cow cases alone, r i g h t...... $$$ IF this is the case, why is Weybridge having to confirm our inconclusives ??? this is frightening.
IF not for the Honorable Phyllis Fong, that cow would have never been proven postive, well, documented anyway, it was proven postive time and time again...
The Fong Syndrome strikes again.
GW's BSE/TSE MRR policy a recipe for disaster.
USA in dire straights.
God help us... TSS
Greetings,
"Texas Agriculture Commissioner Susan Combs suggested federal regulators wait until animals are confirmed positive or negative before disclosing results to the public."
"While markets may bounce back, enormous amounts of money can be lost in the interim,"
Combs wrote.
"In fact, during the last inconclusive announcement, it is estimated that the market dropped $25 per head on cattle, resulting in hundreds of millions of dollars in losses to our cattle industry."
Susan Combs by no means has public and consumer health at heart while she is protecting the cattle industry. She is oblivious to mad cow disease. Her soul purpose is to protect the cattle industry at all cost, including my mothers life (DOD 12/14/97), or maybe one of your family members from any strain of mad cow disease in TEXAS. SHE helped cover-up mad cow disease in TEXAS both on that inconclusive that was positive so many times it will make your head spin. PLUS, the other mad cow in TEXAS they rendered without testing at all, that came from the top out of Austin. THEY should be tried for murder. corporate homicide is what i call it. they knew for years, but kept on keeping on. IF, that positive, positive, positive, inconclusive, negative, and then 8 months later POSITIVE BY WEYBRIDGE mad cow in TEXAS would not have been made public back in November, people like myself that KNEW that cow was positive and that the USDA/COMBs et al were covering it up due to lack of proper testing, IF that news would not have been brought fourth to the public, that cow would have NEVER tested positive for mad cow disease. it was the fact that the data that was put forth in the public domain, that the public came forth and demanded that the testing be done properly and retested. THIS is what the industry and Susan Combs does not want to happen. They wish to keep it private and to manipulate the markets to there benefit, and not release the mad cow data to the public. I wrote Susan Combs on many occasions about this positive, positive, positive, incl. neg., and finally POSITIVE TEXAS MAD COW and about the one that got away, but the only thing that Susan Combs does is send me back a bought and paid for rubber stamped letter from the USDA/Industry;
----- Original Message -----
From: SusanCombs
To: Terry S. Singeltary Sr.
Sent: Monday, July 18, 2005 11:56 AM
Subject: RE: no mad cow cover up in TEXAS???
Dear Mr. Singeltary:
Thank you for contacting the Texas Department of Agriculture about the isolated case of bovine spongiform encephalopathy found in a Texas cow. I can assure you there has been no cover up by the state’s cattle industry or the U.S. Department of Agriculture, which has kept the public informed at every step in the process. First and foremost, it is important to remember that the safety procedures worked. This animal was banned from the food or feed supply, and long-standing safeguards have been in place to protect public health. Because the animal was unable to walk, it was removed from the food supply and was processed at a facility that handles animals unsuitable for human consumption. The carcass was incinerated. Texas and American cattle producers are committed to producing and ensuring a safe food product – the same safe product their families are consuming.
As far back as the late 1980s, the cattle industry began working with the U.S. government to take precautions and establish firewalls to protect public and animal health from BSE. The United States has had an active surveillance program for BSE since 1990 to test a representative sample of the adult cattle population in the United States. With the discovery of a Canadian cow in Washington state in 2003, USDA expanded the surveillance program to test hundreds of thousands of high risk animals The surveillance program is designed to specifically determine whether BSE exists in the U.S. cattle population and if so, at what level. The number of tests under the surveillance program far exceeds the level recommend by the World Animal Health Organization. With the original goal of testing 268,000 animals in a year, USDA would be able to find the disease if it occurred in as few as 1 in 10 million adult cattle with a 99 percent confidence level. Since the beginning of the program in June 2004, USDA has tested more than 400,000 animals and found only this one case, which confirms estimates that the prevalence of this disease in the U.S. cattle population is extremely low. In regards to this particular animal, the laboratory in Weybridge, England found a very low level of abnormal prion protein in the brain. In addition, the abnormalities were isolated and not consistent throughout the brain – making it possible for one sample to test negative while another sample might test positive, which was the reason for the varying results.
Our cattle producers are working hard to produce the safest beef product in the world, and their strong vigilance is a solid commitment to American consumers.
Sincerely, Susan Combs Commissioner
--------------------------------------------------------------------------------
From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net]
Sent: Wednesday, July 13, 2005 12:11 PM
To: Susan Combs
Subject: no mad cow cover up in TEXAS???
Greetings Honorable Susan Combs,
no cover-up of mad cow disease in Texas ??? if not, then maybe you can explain the 7+ month delay in the announcement of the secret postive test on that postive, positive, inconclusive, negative, postive, cow that WAS going to be slaughtered for human consumption, but THEN went down and was sent to the champion pet food plant. OR maybe you can explain to me the mad cow that got away. the one MAD COW TEXAS rendered without testing at all. please explain these things to me if there is no cover up of TEXAS MAD COW disease???
thank you,
with kindest regards,
I am sincerely,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
===================
IN TEXAS, we feed our cattle ruminant protein, and lots of it. but remember (the fda cannot seem to get this right) .1 gram is lethal; THE TEXAS GONZALES/PURINA INCIDENT SHOWED THAT 5.5 GRAMS OF RUMINANT PROTEIN WAS FED TO CATTLE ;
FOR IMMEDIATE RELEASE P01-05 January 30, 2001 Print Media: 301-827-6242 Broadcast Media: 301-827-3434 Consumer Inquiries: 888-INFO-FDA
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.
http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html
P03.137
Transmission of BSE to Cynomolgus Macaque, a Non-human Primate; Development of Clinical Symptoms and Tissue Distribution of PrPSC
Yamakawa, Y1; Ono, F2; Tase, N3; Terao, K3; Tannno, J3; Wada, N4; Tobiume, M5; Sato, Y5; Okemoto-Nakamura, Y1; Hagiwara, K1; Sata, T5 1National Institure of Infectious diseases, Cell biology and Biochemistry, Japan; 2Corporation for Production and Research Laboratory Primates., Japan; 3National Institure of Biomedical Innovation, Tsukuba Primate Reserch Center, Japan; 4Yamauchi Univ., Veterinary Medicine, Japan; 5National Institure of Infectious diseases, Pathology, Japan
Two of three cynomolgus monkeys developed abnormal neuronal behavioral signs at 30-(#7) and 28-(#10) months after intracerebral inoculation of 200ul of 10% brain homogenates of BSE affected cattle (BSE/JP6). Around 30 months post inoculation (mpi), they developed sporadic anorexia and hyperekplexia with squeal against environmental stimulations such as light and sound. Tremor, myoclonic jerk and paralysis became conspicuous during 32 to 33-mpi, and symptoms become worsened according to the disease progression. Finally, one monkey (#7) fell into total paralysis at 36-mpi. This monkey was sacrificed at 10 days after intensive veterinary care including infusion and per oral supply of liquid food. The other monkey (#10) had to grasp the cage bars to keep an upright posture caused by the sever ataxia. This monkey was sacrificed at 35-mpi. EEG of both monkeys showed diffuse slowing. PSD characteristic for sporadic CJD was not observed in both monkeys. The result of forearm movement test showed the hypofunction that was observed at onset of clinical symptoms. Their cognitive function determined by finger maze test was maintained at the early stage of sideration. However, it was rapidly impaired followed by the disease progression. Their autopsied tissues were immunochemically investigated for the tissue distribution of PrPSc. Severe spongiform change in the brain together with heavy accumulation of PrPSc having the type 2B/4 glycoform profile confirmed successful transmission of BSE to Cynomolgus macaques. Granular and linear deposition of PrPSC was detected by IHC in the CNS of both monkeys. At cerebral cortex, PrPSC was prominently accumulated in the large plaques. Sparse accumulation of PrPSc was detected in several peripheral nerves of #7 but not in #10 monkey, upon the WB analysis. Neither #7 nor #10 monkey accumulated detectable amounts of PrPSc in their lymphatic organs such as tonsil, spleen, adrenal grands and thymus although PrPSc was barely detected in the submandibular lymph node of #7 monkey. Such confined tissue distribution of PrPSc after intracerebral infection with BSE agent is not compatible to that reported on the Cynomolgus macaques infected with BSE by oral or intra-venous (intra-peritoneal) routs, in which PrPSc was accumulated at not only CNS but also widely distributed lymphatic tissues.
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background: In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims: The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods: Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results: In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions: Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary
The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
http://www.thelancet.com/journal/journal.isa
It is clear that the designing scientists must also have shared Mr Bradley’s surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://web.archive.org/web/20040523230128/www.bseinquiry.gov.uk/files/ws/s145d.pdf
it is clear that the designing scientists must have also shared Mr Bradleyâs surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://web.archive.org/web/20030526212610/http://www.bseinquiry.gov.uk/files/ws/s147f.pdf
USDA did not test possible mad cows
By Steve Mitchell United Press International
Published 6/8/2004 9:30 PM
WASHINGTON, June 8 (UPI) -- The U.S. Department of Agriculture claims it tested 500 cows with signs of a brain disorder for mad cow disease last year, but agency documents obtained by United Press International show the agency tested only half that number.
USDA officials said the difference is made up in animals tested at state veterinary diagnostic laboratories, but these animals were not tested using the "gold standard" test employed by the agency for confirming a case of the deadly disease. Instead, the state labs used a less sensitive test that experts say could miss mad cow cases.
In addition, the state lab figures were not included in a March 2004 USDA document estimating the number of animals most likely to be infected among U.S. herds, and apparently were not given to a congressional committee that had requested agency data on the number of cows with brain disorder signs that had been tested for the disease. "This is just adding to the demise of USDA's credibility," said Felicia Nestor, senior policy adviser to the Government Accountability Project, a group in Washington, D.C., that works with federal whistleblowers. "If the USDA is going to exclude from testing the animals most likely to have the disease, that would seem to have a very negative impact on the reliability of their conclusion," Nestor told UPI.
Nestor, who has monitored the USDA's mad cow surveillance program closely for several years, asked, "Are they deliberately avoiding testing animals that look like they have the disease?" Concerns about the number of cows in U.S. herds with brain disorder symptoms have been heightened due to the recent case in Texas, in which USDA officials failed to test an animal with such symptoms, also known as central nervous system or CNS signs. This was a violation of USDA policy, which stipulates all CNS cows should be tested because they are considered the most likely to be mad cow infected.
To date, the Washington cow that tested positive last December is the only confirmed case of mad cow disease -- also known as bovine spongiform encephalopathy -- among U.S. herds. The Texas incident has alarmed the public and members of Congress because humans can contract a fatal brain disorder called variant Creutzfeldt-Jakob disease from consuming meat infected with the mad cow pathogen. If the USDA's surveillance program is allowing the riskiest cows to go untested, it raises concerns about the ability of the monitoring system to detect the disease reliably in U.S. herds, Rep. Henry Waxman, D-Calif., charged in a May 13 letter to Agriculture Secretary Ann Veneman. Dr. Peter Lurie, of the consumer group Public Citizen, said CNS cows should be the one category that absolutely has to be tested to have a sound surveillance system. "CNS animals are far and away the most important animals to test," said Lurie, who has done several analyses of the USDA's mad cow surveillance program. "If there's any category that needs 100 percent testing, that's it, because they would be the most likely place to find mad cow in America," he told UPI. "Any CNS cow that slips into the food supply represents a major case of malpractice by USDA, and similarly, the failure to test the brain of that animal to see if it was indeed infected is really a failure to protect the public." USDA officials said the agency has no estimate on how many CNS cows occur in U.S. herds.
But spokesman Ed Loyd has told UPI, and at least one other media outlet, that 500 CNS cows were tested in fiscal year 2003. Yet agency testing records for the first 10 months of FY 2003, obtained by UPI under the Freedom of Information Act, show only 254 animals that fall under the CNS category -- or about half the number Loyd cited.
After failing to respond to repeated requests from UPI for clarification of the apparent discrepancy, Loyd finally offered the explanation that an additional 45 CNS cows were tested by the USDA during the final two months of FY 2003. The remainder, he said, was made up by CNS cases tested at various state veterinary diagnostic laboratories. "We also include data reported to us from state veterinary diagnostic laboratories, and all of these are CNS cases that have been tested for BSE using a histological examination," Loyd said. "We were not using any other labs during this period, other than (the USDA lab), to run the IHC tests for BSE, which is the gold standard," he said. "This (state laboratory) information contributes important data to our surveillance effort."
However, the state labs did not use the immunohistochemistry test, which the USDA has called the "gold standard" for diagnosing mad cow disease. Instead, the labs used a different test called histopathology, which the USDA itself does not use to confirm a case, opting instead for the more sensitive IHC test. The histopathology test, unlike the IHC test, does not detect prions -- misfolded proteins that serve as a marker for infection and can be spotted early on in the course of the illness. Rather, it screens for the microscopic holes in the brain that are characteristic of advanced mad cow disease. According to the USDA's Web site, histopathology proves reliable only if the brain sample is removed soon after the death of the animal. If there is too much of a delay, the Web site states, it can be "very difficult to confirm a diagnosis by histopathology" because the brain structures may have begun to disintegrate. That is one reason the agency began using the IHC test -- it can confirm a diagnosis if the brain has begun disintegrating or been frozen for shipping.
The state labs used histopathology to screen 266 CNS cases in FY 2003, as well as 257 cases in FY 2002, according to Loyd. He did not explain why this information was not included in the testing records the agency provided to UPI and has not responded to requests for the identity of the state labs. Linda Detwiler, a former USDA veterinarian who oversaw the agency's mad cow testing program, told UPI the histopathology test probably is adequate for screening CNS cows. If they have mad cow disease, she said, it would likely be an advanced stage that should be obvious.
Other mad cow disease experts, however, said having a back-up test such as IHC would be advisable, because histopathology tests sometimes can miss evidence of infection. The Food and Agriculture Organization of the United Nations offers similar recommendations in its protocol for conducing a histopathology test. The protocol states that even if histopathology is negative, "further sampling should be undertaken" in cases "where clinical signs have strongly suggested BSE" -- a criteria that includes all of the cows tested at the state labs.
The USDA seems to agree on the need for a back-up test. Its expanded surveillance program, which began June 1, calls for using IHC -- or another test called Western blot -- to confirm any positives found on rapid tests. The March 15 document that describes the new program does not mention using histopathology to confirm cases of mad cow disease. "Subtle changes can be missed on histopathology that would probably not be as easy to miss using IHC," said Elizabeth Mumford, a veterinarian and BSE expert at Safe Food Solutions in Bern, Switzerland, a company that provides advice on reducing mad cow risk to industry and governments. "Therefore I believe it is valuable to run (histopathology)," Mumford told UPI. She noted that in Europe, two tests -- neither one the histopathology test -- are used to ensure no cases are missed. A rapid test is used initially for screening, followed by IHC as a confirmatory test.
Markus Moser, a molecular biologist and chief executive officer of the Swiss firm Prionics, which manufactures tests for detecting mad cow disease, agrees about the possibility of a case being missed by histopathology. "There were cases which were (histopathology) negative but still clearly positive with the other (testing) methods," Moser said. "BSE testing based on histology on sub-optimal tissue was probably one of the reasons why Germany was allegedly BSE-free until our test discovered that they were not" in 2000, Moser told UPI. He agreed with Detwiler that histopathology should be suitable for most cases of CNS cows, but added it still can fail to detect the disease in some CNS cases -- particularly if the sample is not optimum. "It is difficult, if not impossible, to distinguish the subtle changes in a diseased brain from artifacts like ruptures in the tissue due to tissue damage during the sampling, transport or preparation," he said.
Loyd asserted the additional CNS cases from the state labs actually yielded a total of 565 such cows the USDA had tested -- 65 more than his original figure of 500. Whether the USDA considers its total to be 500 or 565, however, either figure would exceed the agency's own estimates for the total number of such cows that it identifies annually.
According to data the USDA provided to the House Committee on Government Reform, and numbers the agency included in the March document about its expanded surveillance plan, only 201 to 249 CNS cows are identified at slaughterhouses. Approximately 129 additional cases occur on farms annually. At most, that yields a combined total of 378 CNS cows, or nearly 200 less than the 565 Loyd claims the agency tested.
The USDA surveillance plan document makes no mention of the number of CNS animals tested at state veterinary diagnostic labs. The figure also does not appear to be included in the agency's estimates of the number of high-risk animals that occur in the United States each year. The latter number was used to help the USDA calculate the number of animals it will screen for mad cow disease in its expanded surveillance plan.
USDA officials also did not include the state lab figures in response to a question from the House Committee on Government Reform, a source close to the issue told UPI. The committee, on which Waxman is the ranking Democrat, had requested in a March 8 letter to Veneman that she provide "the number of BSE tests that were conducted on cattle exhibiting central nervous system symptoms" for each of the last five years.
Loyd did not respond to a request from UPI asking why agency officials did not provide that information to the committee or include it in USDA's explanation of its expanded surveillance plan. The committee has taken note of the CNS issue and plans to delve into it further in a hearing slated for sometime in the next few months. "The committee will explore this and other issues surrounding USDA and BSE testing at a hearing later this summer," Drew Crockett, spokesman for the committee, told UPI.
-- Steve Mitchell is UPI's Medical Correspondent. E-mail sciencemail@upi.com Copyright © 2001-2004 United Press International
http://www.upi.com/view.cfm?StoryID=20040608-014607-3865r
''USDA gets a D or D minus," said Caroline Smith Dewaal of the Center for Science in the Public Interest, an advocacy group based in Washington. ''The best thing that came out of this is the work of the inspector general." It was the department's in-house watchdog, Inspector General Phyllis Fong, who skirted the USDA hierarchy by ordering retesting with a different method more than six months after a routine second-round test, known as the immunohistochemistry, or IHC, test proved negative for the disease. Agriculture Secretary Mike Johanns, who assumed office in January, has said he neither knew about nor authorized the retesting by the National Veterinary Services Laboratories in Ames, Iowa.
BESIDES the Texas mad cow that sat on the shelf for 7+ months before the Honorable Phyllis Fong of the OIG finally did the end around Johanns et al and finally had Weybridge bring that negative cow back from the dead to finally being a confirmed mad cow (hint, hint, getting MRR implemented first), was this simply another bumbling of BSE protocol, or just same old same old;
Jim Rogers (202) 690-4755 USDA Press Office (202) 720-4623 Statement by Chief Veterinary Medical Officer John Clifford Animal and Plant Health Inspection Service Regarding Non-Definitive BSE Test Results July 27, 2005
snip...
Our laboratory ran the IHC test on the sample and received non-definitive results that suggest the need for further testing. As we have previously experienced, it is possible for an IHC test to yield differing results depending on the “slice” of tissue that is tested. Therefore, scientists at our laboratory and at Weybridge will run the IHC test on additional “slices” of tissue from this animal to determine whether or not it was infected with BSE. We will announce results as soon as they are compiled, which we expect to occur by next week. 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.
snip...
http://www.aphis.usda.gov/lpa/news/2005/07/bsestatement_vs.html
Subject: Statement by Dr. John Clifford Regarding Non-Definitive BSE Test Results
Date: July 27, 2005 at 12:37 pm PST
Jim Rogers (202) 690-4755 Jerry Redding (202) 720-6959
Statement by Dr. John Clifford Regarding Non-Definitive BSE Test Results Late yesterday, we received non-definitive test results on an animal sampled as part of a voluntary extension of our enhanced BSE surveillance program. USDA is conducting further testing at the National Veterinary Services Laboratories in Ames, Iowa, in consultation with experts from the international reference laboratory in Weybridge, England.
We are also sending samples from this animal to the Weybridge laboratory for further testing. It is important to note that this animal poses no threat to our food supply because it did not enter the human food or animal feed chains.
The sample was submitted to us by a private veterinarian. As an extension of our enhanced surveillance program, accredited private veterinarians, who often visit farms in remote areas, collect samples when warranted. The sample in question today was taken from a cow that was at least 12 years of age and experienced complications during calving. The veterinarian treated the sample with a preservative, which readies it for testing using the immunohistochemistry (IHC) test - an internationally recognized confirmatory test for BSE.
Neither the rapid screening test nor the Western blot confirmatory test can be conducted on a sample that has been preserved.
Our laboratory ran the IHC test on the sample and received non-definitive results that suggest the need for further testing.
As we have previously experienced, it is possible for an IHC test to yield differing results depending on the slice of tissue that is tested. Therefore, scientists at our laboratory and at Weybridge will run the IHC test on additional slices of tissue from this animal to determine whether or not it was infected with BSE. We will announce results as soon as they are compiled, which we expect to occur by next week.
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. Regardless of the outcome of the further testing, I want to emphasize that human and animal health in the United States are protected by a system of interlocking safeguards.
The most important of these is the ban on specified risk materials from the food supply and the Food and Drug Administrations feed ban. And by any measure, the incidence of BSE in this country is extremely low.
snip...update 2011
Thursday, July 14, 2011
Valley Farm Meats (DBA Strasburg Provision, Inc) Issues Precautionary Recall for Beef Products Due to Possible Contamination with Prohibited Materials SRM
Ohio Department of Agriculture and Ohio Department of Health
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/valley-farm-meats-dba-strasburg.html
snip...continued ;
Our enhanced surveillance program is designed to provide information about the level of prevalence of BSE in the United States. We are extremely gratified that to date, all sectors of the cattle industry have cooperated in this program by submitting samples from more than 419,000 animals from the highest risk populations. To date, only one animal has tested positive for the disease as part of the surveillance program. These interlocking safeguards continue to protect our food supply.
# Note to Reporters: USDA news releases, program announcements and media advisories are available on the Internet. Go to the APHIS home page at http://www.aphis.usda.gov and click on the News button. Also, anyone with an e-mail address can sign up to receive APHIS press releases automatically. Send an e-mail message to lyris@mdrdlyriss10.aphis.usda.gov and leave the subject blank. In the message, type subscribe press_releases. USDA News oc.news@usda.gov 202 720-4623
----------------------------------------------------
"The sample was submitted to us by a private veterinarian. As an extension of our enhanced surveillance program, accredited private veterinarians who often visit farms in remote areas collect samples when warranted. The sample in question today was taken from a cow that was at least 12 years of age and experienced complications during calving. "The veterinarian treated the sample with a preservative which readies it for testing using the immunohistochemistry test, an internationally recognized confirmatory test for BSE. "Neither the rapid screening test nor the Western blot confirmatory test can be conducted on a sample that has been preserved. Our laboratory ran the IHC test on the sample and received non-definitive results that suggest the need for further testing. "As we have previously experienced, it is possible for an IHC test to yield differing results, depending on the slice of tissue that is tested. Therefore scientists at our laboratory and at Weybridge will run the IHC test on additional slices of tissue from this animal to determine whether or not it was infected with BSE. "We will announce results as soon as they are compiled, which we expect to occur by next week.
snip...
http://www.usda.gov/wps/portal/usdahome?contentidonly=true&contentid=2005/07/0280.xml
In Reply to:
Re: Statement by Dr. John Clifford Regarding Non-Definitive BSE Test Results posted by TSS on July 27, 2005 at 12:53 pm:
o.k., let me get this right. i am pondering here;-) all the time this TEXAS positive, positive, (secret) positive, inconclusive, negative, then Weybridge confirmed 2nd BSE documented case (thanks to the Honorable Phyllis Fong), all this time this BSe going on in TEXAS, was plastered all over the news, this guy forgot about that sample, and it just sat up on some shelf wasting away for months, as to be in such bad shape, they now cannot even test it properly. r i g h t ... like ooops, sorry. ...end
============================================
The animal died in April, but the veterinarian forgot to send the sample to USDA until this month, Mr. Clifford said. "While that time lag is not optimal, it has no implications in terms of the risk to human health," he said. IHC tests returned conflicting results on the Texas cow. Use of the preservative means that the other tests commonly done when mad cow is suspected, initial rapid screening and Western blot, can't be performed on this sample, the official said. Mr. Clifford said it's possible to get different results, "depending on the slice of tissue that is tested." The fatal brain-wasting disease is known medically as bovine spongiform encephalopathy, or BSE. In people, eating tainted meat products has been linked to about 150 deaths from a fatal disorder called variant Creutzfeldt-Jakob disease. Most of the deaths were in the United Kingdom, where there was an outbreak in the 1980s and 1990s. The U.S. banned Canadian cattle in May 2003 following Canada's first case of mad-cow disease. The U.S. was about to lift the ban in March when U.S. District Judge Richard Cebull in Billings, Mont., granted an injunction to a ranchers' group called R-CALF United Stockgrowers of America. The ranchers had sued to keep the border closed to Canadian cattle, saying the disease presented a risk to the U.S. beef industry as well as to American consumers. The 9th U.S. Circuit Court of Appeals reversed the injunction earlier this month, allowing cattle shipments from Canada to resume. The lifting of the ban reopens the U.S. to cattle younger than 30 months and expands the list of beef products Canada is allowed to ship to the U.S. Older animals are still banned, because infection levels are believed to increase with age.
Copyright © 2005 Associated Press
http://online.wsj.com/
Greetings, this is what you call the 'FONG' syndrome. make sure she can't make them do a WB on this sample. I BEG THE OIG and the Honorable Phyllis Fong to investigate this blunder too. there is no way that sample sat on a shelf while the world waited on that Texas mad cow blunder dust to settle, and someone just forgets about it. i just don't believe this either...
============================================
From: TSS Subject:
Re: Statement by Dr. John Clifford Regarding Non-Definitive BSE Test Results
Date: July 27, 2005 at 12:53 pm PST
In Reply to:
Statement by Dr. John Clifford Regarding Non-Definitive BSE Test Results posted by TSS on July 27, 2005 at 12:37 pm:
----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Sent: Wednesday, July 27, 2005 2:57 PM
Subject: Re: Statement by Dr. John Clifford Regarding Non-Definitive BSE Test Results
##################### Bovine Spongiform Encephalopathy #####################
Greetings,
with great disgust i must comment on this BSE/USDA/APHIS blunder as well. i swear, larry curly and mo could do a better job at this than is being done right now. for this reason alone the USA BSE GBR risk assessment should be raised immediately to BSE GBR IV; "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."
for Heavens sake, this is July 27, 2005 and we are just now getting this sample to Weybridge. this reeks !
THEN, to think of GWs BSE MRR policy of trading TSEs of all strains globally. again, USA and North America's BSE GBR should be raised to BSE GBR IV immediately. still very disgusted in bacliff, texas...TSS
Faults in USDA testing cited Mad cow case in Texas showed glaring missteps
By Barry Shlachter, Knight Ridder | August 7, 2005
snip...
What Fong and the public were unaware of was that Ames researchers had also used an experimental rapid version of the IHC test on brain tissue from the Texas cow. That proved positive for the disease, but staff members thought the result was technically flawed. The USDA did not disclose until just recently that the Ames lab had conducted the experimental test.
snip...
Months later, Fong stepped in and ordered more tests. A ''Western blot" test proved positive, as did later tests at a lab in Weybridge, England. Finally in June, two days after the Weybridge lab confirmed the mad cow case, a chastened USDA announced that in addition to the routine IHC test, it was adopting the Western blot procedure whenever an initial ''BioRad" screening test indicates mad cow disease is possible. In addition, backup tests will now be conducted at Britain's national veterinary laboratory in Weybridge when earlier test results conflict or are inconclusive.
http://www.boston.com/news/nation/articles/2005/08/07/faults_in_usda_testing_cited/
NOW, all the above announced July 27, 2005. SO, the other 'inconclusive' sample has been sitting on the shelf since April, some 4 months earlier, give or take a few days. NOW, what has been going on while this other inconclusive BSE/BASE mad cow sits on the shelf.
Lets look at that BSE MRR COMMODITY time frame ;-)
7/20/05 USDA, APHIS, Veterinary Services, National Center for Import and Export: Protocol for The Importation of Farm Raised Cervids from Canada PDF USDA, APHIS, Veterinary Services, National Center for Import and Export: Protocol for The Importation of Camelids from Canada PDF
7/15/05 Importation of Bovines (Cattle or Bison) from Canada for Feeding PDF BSE Minimal-Risk Regions and the Importation of Live Animals Importers, Brokers, and Other Interested Parties PDF BSE Minimal-Risk Regions and the Importation of Live Animals Accredited Veterinarians or Other Interested Parties PDF USDA, APHIS, Veterinary Services, National Center for Import and Export: Protocol for The Importation of Cattle or Bison for Feeding from Canada PDF USDA, APHIS, Veterinary Services, National Center for Import and Export: Protocol for the Importation of Cattle, Bison, Sheep and Goats for Immediate Slaughter from Canada PDF USDA, APHIS, Veterinary Services, National Center for Import and Export: Protocol for the Importation of Sheep and Goats for Feeding from Canada PDF Animal Products Implementation: Bovine Spongiform Encephalopathy; Minimal-Risk Regions and Importation of Commodities from Canada PDF Johanns Announces Next Steps for Importing Canadian Cattle Transcript of Tele-News Conference with Agriculture Secretary Mike Johanns Bovine Spongiform Encephalopathy; Minimal-Risk Regions and Importation of Commodities— FINAL RULE— 9 CFR Parts 93, 94, 95, and 96 [Docket No. 03-080-3] Bovine Spongiform Encephalopathy; Minimal-Risk Regions and Importation of Commodities; Partial Delay of Applicability [Docket No. 03-080-6] — Final rule; partial delay of applicability — 9 CFR Parts 94 and 95 Published March 11, 2005 — 70 FR 12112-12113 Text | PDF • Risk Document PDF • Economic Analysis PDF • Appendices to economic analysis PDF • Final environmental assessment PDF • Final Rule on BSE and Minimal-Risk Regions (Factsheet) • Questions and Answers for Minimal Risk/Canada Rule • Port of Entry for Eligible Ruminants
7/14/05 Secretary Johanns Statement on Ninth Circuit Court Ruling
04/01/05 Canada, Mexico And United States Release Harmonized North American BSE Strategy Harmonization of a BSE Strategy (PDF)
03/17/05 U.S. Government Requests Appeal In Minimal-Risk Rule Case
03/04/05 BSE Minimal-Risk Regions and Importation of Live Animals and Commodities From Canada Delay of Effective Date (Memo)
03/03/05 Statement By Agriculture Secretary Mike Johanns Regarding The Temporary Injunction Issued By The U.S. District Court For The District Of Montana Regarding USDA's Minimal-Risk Rule NOT to forget ; It should be noted that since the enhanced surveillance program began, USDA has also conducted approximately 9,200 routine IHC tests on samples that did not first undergo rapid testing. This was done to ensure that samples inappropriate for the rapid screen test were still tested, and also to monitor and improve upon IHC testing protocols. Of those 9,200 routine tests, one test returned a non-definitive result on July 27, 2005. That sample underwent additional testing at NVSL, as well as at the Veterinary Laboratories Agency in Weybridge, England, and results were negative. ......
http://www.aphis.usda.gov/lpa/issues/bse_testing/test_results.html
r i g h t ............
By Steve Mitchell United Press International Published 2/9/2004 7:06 PM
WASHINGTON, Feb. 9 (UPI) -- The federal laboratory in Ames, Iowa, that conducts all of the nation's tests for mad cow disease has a history of producing ambiguous and conflicting results -- to the point where many federal meat inspectors have lost confidence in it, Department of Agriculture veterinarians and a deer rancher told United Press International. The veterinarians also claim the facility -- part of the USDA and known as the National Veterinary Services Laboratories -- has refused to release testing results to them and has been so secretive some suspect it is covering up additional mad cow cases. ...
http://www.upi.com/view.cfm?StoryID=20040209-061848-3665r
-------- Original Message --------
Subject: re-USDA's surveillance plan for BSE aka mad cow disease
Date: Mon, 02 May 2005 16:59:07 -0500
From: "Terry S. Singeltary Sr."
To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov, contactOIG@hhsc.state.tx.us
Greetings Honorable Paul Feeney, Keith Arnold, and William Busby et al at OIG, ...............
snip...
There will be several more emails of my research to follow. I respectfully request a full inquiry into the cover-up of TSEs in the United States of America over the past 30 years. I would be happy to testify...
Thank you,
I am sincerely,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 xxx xxx xxxx
Date: June 14, 2005 at 1:46 pm PST
In Reply to: Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding further analysis of BSE Inconclusive Test Results posted by TSS on June 13, 2005 at 7:33 pm:
Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days later inclusive Mad Cow is announced.
June 7th 2005 Bill Hawks Under Secretary for Marketing and Regulatory Programs resigns.
Three days later same mad cow found in November turns out to be positive. Both resignation are unexpected.
just pondering...
TSS
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 -0600
From: "Terry S. Singeltary Sr."
To: Carla Everett References: log in to unmask]> <[log in to unmask]
Greetings Carla,still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food chain?
and i see the TEXAS department of animal health is ramping up forsomething, but they forgot a url for update?
I HAVE NO ACTUAL CONFIRMATION YET...
can you confirm???
terry
==============================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Fri, 19 Nov 2004 11:38:21 -0600 From: Carla Everett
To: "Terry S. Singeltary Sr." References: log in to unmask]
The USDA has made a statement, and we are referring all callers to the USDA web site. We have no informationabout the animal being in Texas. Carla
At 09:44 AM 11/19/2004, you wrote:
Greetings Carla, i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from TEXAS. can you comment on this either way please? thank you, Terry S. Singeltary Sr.
===================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 18:33:20 -0600
From: Carla Everett
To: "Terry S. Singeltary Sr." References: [log in to unmask] [log in to unmask] [log in to unmask] [log in to unmask] [log in to unmask];
our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something.
At 06:05 PM 11/22/2004,
you wrote:
why was the announcement on your TAHC site removed?
Bovine Spongiform Encephalopathy:
November 22: Press Release title here
star image More BSE information
terry
Carla Everett wrote:
no confirmation on the U.S.'inconclusive test...
no confirmation on location of animal.
==========================
UPI Exclusive: No mad cow tests in Wash.
By Steve Mitchell United Press International Published 1/15/2004 2:46 PM
WASHINGTON, Jan. 15 (UPI) -- Federal agriculture officials did not test any commercial cattle for mad cow disease through the first seven months of 2003 in Washington state -- where the first U.S. case of the disease was detected last month -- according to records obtained by United Press International.
The U.S. Department of Agriculture's records of mad cow screenings, conducted on 35,000 animals between 2001 to 2003, also reveal no animals were tested for the past two years at Vern's Moses Lake Meats, the Washington slaughterhouse where the mad cow case was first detected.
In addition, no mad cow tests were conducted during the two-year period at any of the six federally registered slaughterhouses in Washington state. This includes Washington's biggest slaughterhouse, Washington Beef in Toppeni$h -- the 17th largest in the country, which slaughters 290,000 head per year -- and two facilities in Pasco that belong to Tyson, the largest beef slaughtering company in the United States.
In 2002, nearly every test conducted in Washington was on animals from Midway Meats in Centralia, the packing plant where Vern's Moses sent the infected cow carcass. The meat was distributed to several states where some people apparently consumed it, raising concerns about the possibility of contracting the human equivalent of mad cow, an always fatal, brain-wasting condition known as variant Creutzfeldt-Jakob disease. ...
http://www.upi.com/view.cfm?StoryID=20040114-041124-1470r
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
Subject: Canada’s Protocols for BSE Surveillance DOES NOT MANDATE WB CONFIRMATION Date: August 4, 2005 at 1:16 pm PST
Canadian Food Inspection Agency Factsheet
Canada’s Protocols for BSE Surveillance Printer-Friendly PDF version
BSE testing in Canada is in full accordance with the guidelines recommended by the World Organisation for Animal Health (OIE).
The samples collected target the highest risk cattle. This includes animals over 30 months of age that are dead, down, dying or diseased. In addition, any cattle that are exhibiting symptoms consistent with BSE must be reported to the Canadian Food Inspection Agency. This targeted surveillance program is crucial to defining the level of BSE in Canada and to confirming the effectiveness of the measures in place to protect human and animal health from the disease. A robust surveillance program, with strong producer participation, gives domestic and international consumers confidence that Canada is taking responsible actions to monitor the health of the national herd.
In June 2005, Canada exceeded its minimum testing target of 30,000 animals for the year and, as of August 1, more than 36,000 cattle had been tested. The Government of Canada continues to work with provincial governments to support and encourage the participation of Canadian cattle producers in the surveillance program.
Preliminary Testing Procedures In Canada, two rapid BSE screening tests are used for routine surveillance - the Prionics®- Check Western and the Bio-Rad TeSeE®.
Evaluations conducted by the CFIA and agencies in other governments have found the tests to be 100% accurate for detecting BSE in cattle in later stages of the incubation period. Due to the high sensitivity of the tests, there are rare instances in which samples not infected with BSE may produce an initial reaction, thus necessitating re-testing.
Second Round of Testing Initially reactive samples are referred to as “non-negatives”and require that the same test be repeated in duplicate by the screening laboratory.
If the repeat tests are reactive, the sample is considered “inconclusive” for BSE, and the tissue from the animal is forwarded to the National BSE Reference Laboratory, National Centre for Foreign Animal Disease (NCFAD) in Winnipeg for confirmatory testing.
The rapid test on an inconclusive sample is repeated at the National BSE Reference Laboratory and if the test is again reactive, the sample is considered to be a BSE “suspect” and is subject to confirmatory testing. Even if this third rapid test is negative, a confirmatory test (immunohistochemistry or OIE Western Blot) is run for quality assurance purposes.
Confirmatory Testing The immunohistochemistry (IHC) and the OIE Western Blot, also called the SAF Immunoblot, are internationally recognized confirmatory tests for BSE. The IHC is the principle confirmatory test used at NCFAD.
The OIE Western Blot test may be performed on the sample in addition to, or as an alternative to, the IHC test. It is always used on poor quality tissue samples when it may not be possible to conduct the IHC test, or on suspect samples where the IHC is negative.
http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/bseesbsurve.shtml
THIS protocol has a flaw, the word ''or'' should be changed to ''and'';
(immunohistochemistry or OIE Western Blot)
should read ;
(immunohistochemistry AND OIE Western Blot)
WHY ASK for the blunders and the risks by not using WB, as been documented by the USDA et al in the USA???
WHY even go there???
IF the WB picks up detection where the IHC does not, then why are we even discussing this, IF they were truly trying to find and eradicate BSE/TSE$$$
IHC AND WB should be used for confirmation of any inconclusive.
anything less is not a confirmation, it's a guess.
still disgusted in Sunny Bacliff, Texas USA...TSS
Subject: Re: Canada’s Protocols for BSE Surveillance DOES NOT MANDATE WB CONFIRMATION
Date: August 6, 2005 at 10:05 am PST
In Reply to: Canada’s Protocols for BSE Surveillance DOES NOT MANDATE WB CONFIRMATION
posted by TSS on August 4, 2005 at 1:16 pm:
##################### Bovine Spongiform Encephalopathy #####################
Hello Karin,
indeed i did read the last line, i just think any confusion should be eliminated. i think with the word 'or' is just asking for trouble. one persons opinion on a 'poor quality' tissue sample, may not be the same as the next persons opinion. so why even have the potential for confusion there? i am sure you are aware of this, but maybe some other newer members on the list have not read this study;
Effect of Tissue Deterioration on Postmortem BSE Diagnosis by Immunobiochemical Detection of an Abnormal Isoform of Prion Protein
Hiroko HAYASHI1), Masuhiro TAKATA1), Yoshifumi IWAMARU1), Yuko USHIKI1)2), Kumiko M. KIMURA1), Yuichi TAGAWA1), Morikazu SHINAGAWA1) and Takashi YOKOYAMA1)
1) Prion Disease Research Center, National Institute of Animal Health 2) Nippi Research Institute of Biomatrix (Received 25-Aug-2003) (Accepted 14-Jan-2004)
ABSTRACT.
Surveillance for bovine spongiform encephalopathy (BSE) in fallen stock in Japan is conducted with a commercial enzyme-linked immunosorbent assay (ELISA) for mass screening, with Western blotting (WB) and immunohistochemistry performed for confirmation of the ELISA. All tests are based on immunological detection of an abnormal isoform of the prion protein (PrPSc) in brain tissues, which have sometimes deteriorated by the time samples from fallen stock reach a diagnostic laboratory. To evaluate BSE surveillance procedures for fallen stock, we examined PrPSc detection from artificially deteriorated BSE-affected bovine brain tissues with a commercial ELISA kit and compared the results with those of WB. The optical density (OD) values of the ELISA decreased with advancing deterioration of the tissues, whereas no reduction in the signal for PrPSc was observed in WB, even when performed after 4 days of incubation at 37°C. The progressive decrease in the OD values in the ELISA appear to be caused by a partial loss of the N-terminal moiety of PrPSc due to digestion by endogeneous and/or contaminated microbial enzymes, and by the presence of ELISA inhibitors that are generated in deteriorated tissues. These results suggest that WB is the most reliable test for fallen stock, especially for cattle brains within decaying carcasses. KEY WORDS: BSE, ELISA, PrPSc, Western blot
[PDF (96K)] [References]
To cite this article: Hiroko HAYASHI, Masuhiro TAKATA, Yoshifumi IWAMARU, Yuko USHIKI, Kumiko M. KIMURA, Yuichi TAGAWA, Morikazu SHINAGAWA and Takashi YOKOYAMA “Effect of Tissue Deterioration on Postmortem BSE Diagnosis by Immunobiochemical Detection of an Abnormal Isoform of Prion Protein”. J. Vet. Med. Sci.. Vol. 66: 515-520. (2004) .
http://www.jstage.jst.go.jp/article/jvms/66/5/66_515/_article
FULL TEXT PDF;
Another problem in testing fallen stock for BSE may arise from unequal distribution of PrPSc in BSE-affected brains. Spongiform changes and accumulation of PrPSc are most frequently observed in the obex region [15, 18], but, it could be quite difficult to collect the obex region precisely from extensively deteriorated and liquefied brain tissue. Furthermore, in such cases it would be difficult to perform IHC as a confirmation test.
It has been shown that sample autolysis does not affect detection of PrPSc by means of WB [3, 5, 13]. Our WB results also demonstrated no reduction in the PrPSc signal as a result of deterioration at 30*C or 37*C for up to 4 days, as so far examined (Figs. 2A and 3A). In this study, we showed that several problems undermine the utility of the ELISA with deteriorated samples, whereas WB remains very dependable. Therefore, WB might be the only reliable procedure to detect PrPSc in severely damaged samples from fallen stock...
FULL TEXT 6 PAGES;
http://www.jstage.jst.go.jp/article/jvms/66/5/515/_pdf
Karin writes;
I would be more worried about the latest USA suspect where no WB can be done, due to formalin fixation of the sample. I don’t know if the “reference” laboratory in Weybridge has ever missed any BSE-positive cattle (or atypical bovine TSEs), but they have certainly failed to confirm several cases of atypical scrapie, because they insisted on using the so-called validated methods recommended by the OIE before 2003. I hope they now have solved this problem.
===
i agree with this. in fact, the OIE since adhering to GWs BSE MRR policy (minimal risk region), and doing away with the USA, Canada, and Mexico BSE GBR Risk assessments, was anything but 'sound science'. by the OIE adhering to this 'junk science' of this administrations corporate scientists, the OIE has done nothing more than become a commodity brokerage for the legal trading of all phenotypes of TSEs Globally. THEY have in essence done away with 30 years of trying to eradicate TSEs globally. MILLIONS and millions of dollars down the drain, with MILLIONS and millions of humans and animals now becoming exposed even more than before, due to nothing more than greed and the almighty buck. as GW says, ''bring em on''. he will get exactly what he asks for again in the years and decades to come. but, as my birthday card today states;
This birthday you have something to be thankful for (with a picture of GW on the front), I CAN'T RUN AGAIN....................amen!
SO why should he care, he will not be in office, but the markets will be o.k. for now, borders open, and the list of demented and dead will continue to slowly grow even more, with more strains of TSE mutating and being exported throughout the globe... gee thanks GW/OIE!
==============================================
5.1.3. National TSE Veterinary Diagnostic Laboratory Network
The CFIA created a National TSE Veterinary Diagnostic Laboratory Network in 2001 to ensure consistency of diagnostic testing nationally. The network includes CFIA TSE reference laboratories, CFIA and provincial network laboratories. Standard operating procedures (Appendix 4), control material and panels are provided by the federal laboratories as part of a Quality Assurance Program. Training and research are also provided. Quality assurance and biosafety guidelines were distributed early in 2002.
5.2. Diagnostic Tests
All samples are tested by histopathology (H&E) and some are tested by IHC (see Appendix 4 for test standard operating procedures). According to the OIE Manual of Standards (OIE, 2000), surveillance for BSE requires laboratory examination of brain from clinically suspect animals by histopathology and, if necessary, other methods described in the manual (i.e. western blot, scrapie-associated-fibril examination and detection of abnormal PrP by immunohistochemistry).
Prior to the opening of the NCFAD laboratory (1997), testing for BSE was performed at the ADRI, Ottawa. At this laboratory, the validation of IHC using a polyclonal antibody on central nervous tissue began in 1994 and was completed in 1995. Validation of the IHC test for BSE using a monoclonal antibody was carried out at the National BSE Reference Laboratory at NCFAD/CFIA in Winnipeg in 2001 (Czub 2002).
As of January 2002, the provinces of Alberta, Ontario and Saskatchewan have introduced IHC testing in their laboratories. The province of Manitoba has the option to send samples to Saskatchewan for IHC, and the province of Quebec is currently acquiring laboratory capability for IHC testing (Greenwood 2002). To ensure consistency of diagnostic testing across all laboratories, the CFIA initiated a National TSE Veterinary Diagnostic Laboratory Network in 2001 (see Section 5.1.3 for details).
While less than half of Canada’s BSE surveillance samples have historically been tested by IHC (see Table 2), by the end of 2002 more than 90% of all BSE samples will be tested by this method.
Confirmatory testing of a BSE suspect sample is carried out at the National BSE Reference Laboratory at NCFAD/CFIA in Winnipeg.
Rapid Tests:
Rapid tests for BSE diagnosis are not currently used in Canada; however, the CFIA is evaluating certain rapid tests used in Europe. Once the technology has been obtained and standardized in the National BSE Reference Laboratory in Winnipeg, the CFIA will consider application of these tests in the Canadian BSE Surveillance Program.
2In some countries, the terminology “fallen stock” is used for animals described herein as “non-ambulatory” or “animals found dead.”
3Total Cow Population 5,574,000 (dairy cows 1,122,400, beef cows 4,451,600) Source: 1996 Agricultural Census.
http://www.inspection.gc.ca/english/sci/ahra/bseris/bserisb1e.shtml
----- Original Message -----
From: Terry S. Singeltary Sr.
To: Debra.Beasley@aphis.usda.gov
Sent: Tuesday, November 24, 2009 11:01 AM
Subject: OIE has recently published its proposed animal welfare guidelines for public comment
Greetings USDA/APHIS et al,
I would kindly like to comment on OIE proposed guidelines.
AS I said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization. THE reason most every country around the globe came down with BSE/TSE in their cattle, were due to the failed and flawed BSE/TSE testing and surveillance policy of the O.I.E. NOW, they don't even acknowledge atypical scrapie it seems, as one for concern $
Monday, November 23, 2009
BSE GBR RISK ASSESSMENTS UPDATE NOVEMBER 23, 2009 COMMISSION OF THE EUROPEAN COMMUNITIES AND O.I.E.
http://docket-aphis-2006-0041.blogspot.com/2009/11/bse-gbr-risk-assessments-update.html
Tuesday, May 24, 2011 2:24 PM
O.I.E. Terrestrial Animal Health Standards Commission and prion (TSE) disease reporting 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/oie-terrestrial-animal-health-standards.html
IN A NUT SHELL ;
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to then Central Bureau............
http://www.oie.int/eng/Session2007/RF2006.pdf
SO, the OIE BSE MRR status, is based on whatever information and data the given BSE countries give them to go by.
LIKE i have stated time and time again, OIE BSE MRR policy is bought and paid for by your local cattle dealer.
THE BSE MRR policy is nothing more than a legal tool to trade TSE globally.
I urge that the BSE MRR policy be repealed, and the BSE GBR risk assessments be upgraded to include all strains of TSE, including the USA H-BASE, but to even go further, and include all TSE in ALL species. ...TSS
http://madcowtesting.blogspot.com/
Wednesday, November 17, 2010
MAD COW TESTING FAKED IN USA BY Nebraska INSPECTOR Senator Mike Johanns STATE Neb. inspector accused of faking mad cow tests
Published November 17, 2010
http://madcowtesting.blogspot.com/2010/11/mad-cow-testing-faked-in-usa-by.html
Thursday, November 18, 2010
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS
http://bse-atypical.blogspot.com/2010/11/united-states-of-america-vs-galen-j.html
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html
Sunday, June 26, 2011
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html
Thursday, June 2, 2011
USDA scrapie report for April 2011 NEW ATYPICAL NOR-98 SCRAPIE CASES Pennsylvania AND California
http://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html
Monday, June 20, 2011 2011
Annual Conference of the National Institute for Animal Agriculture ATYPICAL NOR-98 LIKE SCRAPIE UPDATE USA
http://nor-98.blogspot.com/2011/06/2011-annual-conference-of-national.html
Monday, June 27, 2011
Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease
http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE
http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html
I strenuously urge the USDA and the OIE et al to revoke the exemption of the legal global trading of atypical Nor-98 scrapie TSE. ...TSS
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep
http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html
Sunday, October 3, 2010
Scrapie, Nor-98 atypical Scrapie, and BSE in sheep and goats North America, who's looking ?
http://nor-98.blogspot.com/2010/10/scrapie-nor-98-atypical-scrapie-and-bse.html
Wednesday, July 06, 2011
Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation
(see tonnage of mad cow feed in commerce USA...tss)
http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html
Monday, June 27, 2011
Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates
http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html
Please see the following warning from CDC about prion TSE consumption in North America ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.
http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html
CANADA GREENS CALL FOR 100% BSE MAD COW TESTING
Greens call for ban on federal GMO research Apr 10, 2011 11:45 PM
snip...
The party said it would also aim to tighten Canada's testing net for bovine spongiform encephalopathy (BSE) in slaughter cattle by implementing "100 per cent" testing of all slaughtered animals, but only "as soon as the process of detecting BSE in blood samples is perfected." The party also calls for ensuring no "animal byproducts" are used in ruminant animal feed....
snip...
http://www.albertafarmexpress.ca/issues/story.aspx?aid=1000407400
Green Party MPs will develop a National Agricultural and Food Policy which:
Improves Food Safety by:
• Amending the Canadian Food Inspection Agency mandate to remove any obligation to promote Canadian agri-business, ensuring the focus is on food safety and food safety only, with enhanced resources for inspection and monitoring.
• Ensuring the quality and wholesomeness of food by strengthening the monitoring of pesticides, herbicides, fungicides, growth hormones, non-therapeutic antibiotics and insecticides in food production, processing and storage, with the goal of an orderly reduction in detectable residues of these substances until they reach undetectable limits.
• Establishing federally funded, community-guided school lunch programs across Canada to ensure that our children have daily access to healthy local food and can learn about sustainable food production and healthy eating.
• Strengthening Plant Protection and Health of Animals Programs with measures to ensure the integrity of farm food products.
• Improving and strengthening the Canadian Organic Standard.
• Providing transitional assistance for those switching to certified organic farming practices.
• Ensuring that no animal by-products are used in ruminant animal feed.
• Strengthen testing for BSE by implementing 100% testing (testing of every slaughtered animal) as soon as the process of detecting BSE in blood samples is perfected.
Vision Green April 2011
http://greenparty.ca/files/attachments/april_2011_vision_green.pdf
THANK YOU !!!
IN THE USA, we use the SSS policy, or the 'don't look, don't find' policy, or what i also call the ''obex only'' diagnostic criteria for how not to find a mad cow. The USA pollutes its oceans, bays, gulf, and rivers, and allows others to pollute them too. Allows industry to pollute the air we breath. Texas has now become the USA nuclear dumping grounds, thanks to our good gov perry. the USA federal gov. dumps all funding for the mad cow TSE prion diseases, while at the same time, human and animal TSE in North America are mutating, spreading, and cpsCJD (classification pending sporadic creutzfeldt jakob disease) is rising in young and old. i don't understand the insanity of it all. ...
All Other Emerging and Zoonotic Infectious Diseases CDC's FY 2012 request of $52,658,000 for all other emerging and zoonotic infectious disease activities is a decrease of $13,607,000 below the FY 2010 level,
which includes the elimination of Prion activities ($5,473,000),
a reduction for other cross-cutting infectious disease activities, and administrative savings. These funds support a range of critical emerging and zoonotic infectious disease programs such Lyme Disease, Chronic Fatigue Syndrome, and Special Pathogens, as well as other activities described below.
http://www.cdc.gov/fmo/topic/Budget%20Information/appropriations_budget_form_pdf/FY2012_CDC_CJ_Final.pdf
" the FY 2010 level, which includes the elimination of Prion activities ($5,473,000), "
USDA MAD COW PROBLEMS SOLVED $$$
Canadian Researchers Receive $2.9 Million to Protect Against Prion Disease Outbreaks, Develop Novel Therapies to Treat Alzheimer’s, Parkinson’s and ALS
Scientists find increasing connection between development of prion disease and common human neurodegenerative disorders
July 13, 2011 (Vancouver, BC) – Collaborative research groups at nine different universities, involving 55 different investigators across Canada, are poised to make significant advances in the understanding of prion and prion-like diseases in humans and animals. These include the development of an oral vaccine to help stop the spread of chronic wasting disease (CWD) in wild deer and elk populations and novel approaches to treat human neurodegenerative disorders like ALS (Lou Gehrig's disease), Alzheimer’s and Parkinson’s diseases, thanks to $2.9 million in funding announced by PrioNet Canada.
The goal of the funding which supports 11 projects is two-fold, explains Dr. Neil Cashman, Scientific Director of PrioNet Canada, one of Canada’s Network of Centres of Excellence. “By working with our partners, we aim to continue to protect Canada against classical prion diseases like chronic wasting disease and mad cow disease (bovine spongiform encephalopathy or BSE), and we’re also providing benefit to Canadians through the development of innovative therapeutics to treat neurodegenerative diseases like Alzheimer’s, Parkinson’s and ALS.”
The researchers will use the funds to better understand the biology of prion disease, to develop strategies to manage prion disease outbreaks and minimize the impacts, and to apply learnings of prion diseases to the treatment of human neurodegenerative disorders.
Prion diseases are fatal, infectious and transmissible diseases of humans and animals associated with a ‘sponge-like’ degeneration of brain tissue. In animals, the most common prion diseases include BSE, scrapie in sheep and goats, and CWD in deer and elk. In 2003, Canada’s beef and related industries were faced with worldwide closing of trade after a domestic case of BSE was found in Alberta. Canada’s economic loss stemming from this event is estimated at more than $6 billion. Some examples of prion diseases in humans include fatal and sporadic familial insomnia, Creutzfeldt-Jakob disease (CJD) and its many varieties, and Kuru. Some examples of the ground-breaking work supported by PrioNet’s recent funding include:
• Immunotherapies to treat ALS: Five PrioNet researchers at the University of British Columbia, University of Alberta and University of Toronto are focusing on a newly-recognized molecular mechanism of ALS, a misfolded protein called SOD-1. By identifying the parts of the protein that are exposed when it is misfolded in disease, researchers are able to design immunotherapies that can target those areas, interrupting the slow progression of paralysis and eventual death characterized by the disorder. Two animal models have already demonstrated responsiveness to the new immunotherapies and work is now underway to develop a therapy for humans. “We are hoping these discoveries could prove to be a magic bullet for ALS,” said Dr. Cashman, who serves as principal investigator for the multi-disciplinary research team.
• Oral vaccine to control chronic wasting disease in the wild: Prion diseases like chronic wasting disease are continuing to spread throughout the Canadian prairie’s wild deer and elk populations and ten PrioNet researchers in Saskatoon and British Columbia are working on an oral vaccine to stop the spread. “The danger is that prion diseases are evolving and new strains are emerging,” noted Dr. Scott Napper, a Research Scientist with the Vaccine and Infectious Disease Organization in Saskatoon and principal investigator on the project. Dr. Napper’s group is focusing on an oral vaccine that can withstand extreme temperatures and will effectively attract elk and deer in the wild. Similar oral vaccines are already used to control rabies in Eastern Canada, where food packets containing the vaccine are widely distributed for consumption by fox and raccoon populations.
• Framework to minimize the impact of chronic wasting disease: Principal investigator Dr. Ellen Goddard from the University of Alberta along with nine co-investigators are working to identify the risk factors associated with chronic wasting disease in wild deer and elk populations, how they can be managed and what public policy recommendations should be put in place to try and mitigate the effects. The primary goal is to monitor the many unknowns that remain about the impact of CWD in the wild, such as the potential risk to hunters who consume infected animals and the potential interface between wild and domestic animals. “The risk management framework around BSE showed that even though countries were aware of the disease in their cattle, they completely underestimated the economic impact and the public response,” notes Dr. Goddard. “We’re doing the work ahead of the game while CWD is still manageable and while effective policies can be put into place to control it, to help anticipate and prevent the impacts.”
• Understanding ‘good versus bad’ prions in order to develop drugs: The first step to designing drugs to treat prion and prion-like diseases is to understand how prion proteins change shape when they become “misfolded” in disease. Dr. Christoph Borchers, a Professor in the Department of Biochemistry and Microbiology and Director of the University of Victoria-Genome BC Proteomics Centre is collaborating with researchers from the University of Alberta and University of Western Ontario to characterize the changes that occur to the three-dimensional structure of prion fibrils (small, nerve-like fibres) as well as the molecular mechanisms that lead to those changes. Using a combination of protein chemistry and mass spectrometry, they are working to explain what occurs when a ‘good’ prion protein changes to a ‘bad’ one during disease development. The information is crucial to designing drugs that can interfere with those changes, effectively curbing the spread of prion and prion-like diseases.
About PrioNet Canada (www.prionetcanada.ca) One of Canada’s Networks of Centres of Excellence, PrioNet Canada is a pan-Canadian research network that is developing strategies to help solve the food, health safety, and socioeconomic problems associated with prion diseases. The network brings together academia, industry, and public sector partners through its multidisciplinary research projects, training programs, events, and commercialization activities to help derive maximum socioeconomic benefits for Canadians. PrioNet is hosted by the University of British Columbia and the Vancouver Coastal Health Research Institute in Vancouver.
- 30 -
Media information or to set up interviews: Gail Bergman or Christina Vetro Gail Bergman PR Tel: (905) 886-1340 or (905) 886-3345 E-mail: info@gailbergmanpr.com
Last Updated: 7/13/2011 11:27:59 AM
http://www.prionetcanada.ca/detail.aspx?menu=12&dt=293779&app=70&cat1=211&tp=12&lk=no
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.html
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bse-atypical.blogspot.com/2010/08/report-on-investigation-of-sixteenth.html
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bseusa.blogspot.com/2010/08/report-on-investigation-of-seventeenth.html
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31
http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html
Wednesday, December 22, 2010
Manitoba veterinarian has been fined $10,000 for falsifying certification documents for U.S. bound cattle and what about mad cow disease ?
http://usdameatexport.blogspot.com/2010/12/manitoba-veterinarian-has-been-fined.html
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
TSS
Hiroyuki OKADA1), Yoshihumi IWAMARU1), Morikazu IMAMURA1), Kentaro MASUJIN1), Yuichi MATSUURA1), Yoshihisa SHIMIZU1), Kazuo KASAI1), Masuhiro TAKATA1), Shigeo FUKUDA2), Satoshi NIKAIDO2), Kei FUJII2), Sadao ONOE2), Shirou MOHRI1) and Takashi YOKOYAMA1)
1) Prion Disease Research Center, National Institute of Animal Health 2) Hokkaido Animal Research Center, Hokkaido Research Organization
(Received 15-Jun-2011) (Accepted 2-Jul-2011)
ABSTRACT.
Bovine spongiform encephalopathy (BSE) is a fatal neurodegenerative disorder of cattle characterized by accumulation of the disease-associated prion protein (PrPSc) in the central nervous system (CNS). The immunohistochemical patterns and distribution of PrPSc were investigated in the CNS, brains, and spinal cords of 7 naturally occurring BSE cases confirmed by the fallen stock surveillance program in Japan. No animals showed characteristic clinical signs of the disease. Coronal slices of 14 different brain areas in each case were immunohistochemically analyzed using an anti-prion protein antibody. Immunolabeled PrPSc deposition was widely observed throughout each brain and spinal cord. Intense PrPSc deposition was greater in the thalamus, brainstem, and spinal cord of the gray matter than in the neocortices. The topographical distribution pattern and severity of PrPSc accumulation were mapped and plotted as immunohistochemical profiles of the different brain areas along the caudal-rostral axis of the brain. The distribution pattern and severity of the immunolabeled PrPSc in the CNS were almost the same among the 7 cases analyzed, suggesting that the naturally occurring cases in this study were at the preclinical stage of the disease. Immunohistochemical mapping of the PrPSc deposits will be used to clarify the different stages of BSE in cattle.
KEY WORDS: BSE, cattle, immunohistochemistry, prion
SNIP...
DISCUSSION
Levels and regional tropism of vacuolar changes, namely the lesion profile in the brain, is considered a reliable indicator for histopathological diagnosis of BSE-affected cattle [26, 32]. However, optimal preservation is required to ensure the identification of vacuolar changes in certain areas of the brainstem devoid of artifactual vacuolations induced by a postmortem delay of tissue sampling that led to autolysis. Although autolysis conditions have been usually encountered in field cases of BSE diagnosis, autolysis and the frozen condition do not significantly influence PrPSc detection by immunohistochemistry [4, 6, 7, 18]. Moreover, PrPSc immunohistochemistry is an essential tool and may contribute to our understanding of the pathogenesis of BSE [6, 12].
All cattle in the present study were field BSE cases confirmed by the fallen stock surveillance program in Japan. Despite the limited number of animals and differences in their ages and breeds, PrPSc topographical distributions and types in the brain were remarkably similar among these cases and to those in published reports in BSE cattle [5, 13, 15, 16, 20, 27, 30]. The severity of PrPSc deposition was variable in
12
the brain regions. Large amounts of PrPSc deposits were present in the brainstem and thalamus, whereas the cerebral cortices and hippocampus were less involved, suggesting that PrPSc accumulation in the brain of BSE-affected cattle is related to area-dependent tropism [5, 30]. These results indicate that most BSE cases that occur in Japan have been caused by a single infectious agent strain identical to the C-BSE prion. Moreover, the lack of apparent differences in PrPSc distribution patterns or deposition intensity among the 7 cases in this study might suggest the same clinical stage of the disease. A greater degree of PrPSc accumulation within the thalamus and brainstem of all animals was obvious compared to the slaughtered cases in Japan that seemed to be at the preclinical stage of the disease [13]. The present cases revealed no clinical signs or symptoms relevant to BSE, but some cases exhibited dystasia. These results might indicate that the 2 BSE cases with the locomotive disability were highly likely to be at an early clinical stage of the disease.
Recently, other phenotypes, namely atypical BSE that differs from C-BSE, have been reported among BSE cases in Europe [2, 21], North America [23] and Japan [11, 34]. Atypical BSE cases are temporally classified into 2 types, namely L- and H-types according to the molecular size of the proteinases K-digested nonglycosylated form of PrPSc [14, 21]. The immunolabeled PrPSc distribution patterns and/or types in the brains of cattle affected with L-BSE [3, 17] and H-BSE [23] differed from those with C-BSE. C-BSE was characterized the presence of stellate and intraneuronal immunolabeled PrPSc [17, 27]. Stellate PrPSc deposition was located mainly in the gray matter neuropils of the cerebral and cerebellar cortices [27] and was reported to deposit to astrocytes stained with glial fibrillary acidic protein [30]. Additionally, coarse granular and coalescing PrPSc deposition was mainly distributed in the brainstem in the
13
present cases as described in an report [30]. On the other hand, a differential PrPSc deposition pattern was detected in atypical BSE cases. L-BSE showed abundant amyloid PrP-plaques and perineural PrPSc in the brain [3, 17]. PrP-positive amyloid plaques up to 25 μm in diameter were present in an atypical BSE case in Japan (BSE/JP24). In the 7 cases studied here, no PrP-positive plaques were demonstrated in the brain. However, it has been reported that plaque-like PrPSc stained with Congo red rarely appeared in the thalamic nuclei of C-BSE–affected cattle [5, 33]. Additionally, in a Swedish H-BSE case, no stellate PrPSc deposits were identified [8]. Therefore, immunohistochemical profile and mapping of the pathologic stage of the disease and confirmation of the infectious agent strain, e.g., C-BSE or atypical BSE [30].
In summary, the types and distribution patterns of immunolabeled PrPSc in the brain and spinal cords of the 7 naturally occurring BSE cases confirmed by the fallen stock surveillance program in Japan were in accordance with published C-BSE cases, indicating that the BSE in the affected animals reported here was caused by a single infectious agent strain identical to the C-BSE prion.
[PDF (934K)]
doi:10.1292/jvms.11-0291 JOI JST.JSTAGE/jvms/11-0291
Copyright(c) 2011 by the Japanese Society of Veterinary Science
http://www.jstage.jst.go.jp/article/jvms/advpub/0/1107110572/_pdf
Bio.040: Phenotypic Variability of Italian BASE Affected Cattle
Cristiano Corona,1,† Chiara Porcario,1 Elena Vallino Costassa,1 Maria Mazza,1 Francesca Martucci,1 Barbara Iulini,1 Marina Gallo,1 Franco Paterlini,2 Maria N. Chieppa,1 Luana Dell’Atti,1 Cristiana Maurella,1 Simone Peletto,1 Pierluigi Acutis,1 Maria Caramelli,1 Gianluigi Zanusso3 and Cristina Casalone1
1Istituto Zooprofilattico Sperimentale del Piemonte Liguria e Valle d’Aosta; Turin, Italy; 2Istituto Zooprofilattico Sperimentale della Lombardia e dell’Emilia Romagna; Bergamo, Italy; 3Università di Verona, Policlinico GB Rossi; Verona, Italy†Presenting author; Email: cristiano.corona@izsto.it
In Italy, in the framework of BSE surveillance program, 145 cases of the disease have been identified so far. Out of 145 BSE positive cases, five cattle were L-type BSE forms, according to the lower electrophoretic migration and the mono-glycosylated dominant glycotype of protease resistant PrP (PrPSc), distinct from classical BSE (C-BSE).
The first three Italian L-type BSE cases were defined "BASE" (bovine amyloidotic spongiform encephalopathy) cases, since the immunohistochemistry showed PrP amyloid deposits in the brain tissue mainly localized in the white matter of thalamus and forebrain areas. Unfortunately, in the fourth Italian L-type case brain sampling was restricted to the brainstem with no evidence of amyloid deposits and the definition of BASE was precluded.
The fifth L-type BSE case was recently confirmed in a 14-year-old regularly slaughtered Alpine Brown cattle free of neurological signs. Immunoblot analysis showed the BSE L-type PrPSc, as in all other four Italian cases. However, in contrast to what observed in the other BASE cases, PrPSc was mainly distributed in the obex compare to the more rostral brain regions. These results were confirmed also by immunohistochemistry (IHC). Furthermore, PrP deposition pattern in the obex was granular and punctate, resembling what we usually observe in C-BSE. Unexpectedly, no PrPSc amyloid plaques were observed but only small scattered PrPSc aggregates in the thalamus as well as in the forebrain. Genetic analysis of the PRNP coding sequence revealed a genotype similar to that of the other atypical cases detected so far, suggesting that an association between the PrP amino acid composition and the observed phenotype should be excluded.
Despite all atypical BSE cases were L-type BSE the neuropathological phenotype showed a slight variability. These differences highlighted might be not related to the animal age, breed or PRNP but to a different stage of the disease. To date, all data indicate that BASE is a sporadic disease in cattle and that disease modifiers, other than those investigated might influence the disease phenotype.
Risk.16: Clinical Disease in Cattle Experimentally Inoculated with All Types of BSE
Catherine Graham,1,† Michel Levy,2 Ed Pajor,2 Garth McGregor,1 Rheana Flitton1 and Stefanie Czub1
1Canadian Food Inspection Agency; Lethbridge, AB Canada; 2Faculty of Veterinary Medicine; University of Calgary; Calgary, AB Canada†Presenting author; Email: catherine.graham@inspection.gc.ca
Background. Classical, or C-type, bovine spongiform encephalopathy (BSE) has been extensively described in the literature. Recently, two novel forms of BSE, termed atypical BSE, have been reported in a number of countries. These new forms show differences in the biochemical characteristics of the prion protein and, where reported, tend to occur in aged animals but descriptions of clinical presentation are incomplete or absent.
Materials and Methods. Female Hereford/Angus cross calves were intracranially challenged at approximately five months of age with 1 ml of a 10% brain homogenate originating from Canadian field cases of BSE which had been previously classified as C-, L-, or H- type.
The animals were monitored during incubation period, and clinical disease is described using a standardized examination protocol. Incubation period, description and progression of clinical signs was recorded and videotaped for objective evaluation.
Results. All L- and H- type atypical BSE challenged animals began to display signs of clinical disease at approximately 11 months post inoculation, and disease progression was slow but constant until animals were euthanized. Clinical signs in all atypical BSE inoculated animals included hesitation at doors and gates, spontaneous muscle fasciculations and sensitivity to touch. Teeth grinding and excessive salivation are occasionally noted. Animals with L-type BSE are very anxious and show high levels of sensitivity to hand movement. One H-type animal shows periods of somnolence. Both H-type inoculated animals go down during handling and have difficulty rising and show sensitivity to movement around their head and neck area, but to a lesser degree than the L-type BSE inoculated animals. Interestingly, no locomotor abnormalities have been observed in either group.
C-type challenged animals remain normal at approximately 18 months post inoculation. Clinical disease in C-type inoculated animals from a previous transmission study was typically slow and intermittently displayed during the initial stages and after a period of two to four months was more consistent and progressive. Clinical signs in C-type BSE were as previously reported in the literature.
Discussion. The spectrum of clinical signs for all three types of BSE examined is similar. Incubation period is shorter for H- and L-type BSE as compared with C-type. Once clinical signs begin, progression is slow but relentless in atypical BSE, and more insidious in classical BSE. A summary of clinical signs presented in the three different types of BSE will be presented, and video of clinical disease will be displayed.
http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf
Thursday, June 23, 2011
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html
Journal of Clinical Microbiology, June 2011,p. 2109-2115, Vol. 49, No. 6 0095-1137/11/$12.00+0 doi:10.1128/JCM.02033-10
Distinct Proteinase K-Resistant Prion Protein Fragment in Goats with No Signs of Disease in a Classical Scrapie Outbreak
Ilias G. Bouzalas1,, Florian Lörtscher3,, Chrysostomos I. Dovas1, Anna Oevermann3, Jan P. M. Langeveld2, Maria Papanastassopoulou1, Orestis Papadopoulos1, Andreas Zurbriggen3 and Torsten Seuberlich3*
Aristotle University of Thessaloniki, Thessaloniki, Greece,1 Central Veterinary Institute of Wageningen UR, Lelystad, Netherlands,2 University of Berne, Berne, Switzerland3
Received 8 October 2010/ Returned for modification 26 November 2010/ Accepted 19 March 2011
Considerable efforts have been directed toward the identification of small-ruminant prion diseases, i.e., classical and atypical scrapie as well as bovine spongiform encephalopathy (BSE). Here we report the in-depth molecular analysis of the proteinase K-resistant prion protein core fragment (PrPres) in a highly scrapie-affected goat flock in Greece. The PrPres profile by Western immunoblotting in most animals was that of classical scrapie in sheep. However, in a series of clinically healthy goats we identified a unique C- and N-terminally truncated PrPres fragment, which is akin but not identical to that observed for atypical scrapie. These findings reveal novel aspects of the nature and diversity of the molecular PrPres phenotypes in goats and suggest that these animals display a previously unrecognized prion protein disorder.
--------------------------------------------------------------------------------
* Corresponding author. Mailing address: NeuroCentre, DCR-VPH, Bremgartenstrasse 109a, CH-3001 Berne, Switzerland. Phone: 41 31 631 2206. Fax: 41 31 631 2538. E-mail: torsten.seuberlich@itn.unibe.ch .
I.G.B. and F.L. contributed equally to this study.
Supplemental material for this article may be found at http://jcm.asm.org/.
Published ahead of print on 30 March 2011.
http://jcm.asm.org/cgi/content/abstract/49/6/2109
Scrapie Nor-98 like case in California FY 2011 AS of December 31, 2010.
Scrapie cases in goats FY 2002 - 2011 AS of December 31, 2010 Total goat cases = 21 Scrapie cases, 0 Nor-98 like Scrapie cases (21 field cases, 0 RSSS cases)
Last herd with infected goats disignated in FY 2008 Michigan 8 cases
http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep
http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html
Sunday, October 3, 2010
Scrapie, Nor-98 atypical Scrapie, and BSE in sheep and goats North America, who's looking ?
http://nor-98.blogspot.com/2010/10/scrapie-nor-98-atypical-scrapie-and-bse.html
http://nor-98.blogspot.com/
FROM THE STUDY ;
Neuroanatomical Distribution of Disease-Associated Prion Protein in Cases of Bovine Spongiform Encephalopathy Detected by Fallen Stock Surveillance in Japan
"Although autolysis conditions have been usually encountered in field cases of BSE diagnosis, autolysis and the frozen condition do not significantly influence PrPSc detection by immunohistochemistry [4, 6, 7, 18]."
maybe that's why the USDA et al likes to use it ;
Completely Edited Version
PRION ROUNDTABLE
2003
Dr. Linda Detwiler
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
=============================
http://madcowtesting.blogspot.com/
http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position-post.html
-------- Original Message --------
Subject: USA BIO-RADs INCONCLUSIVEs
Date: Fri, 17 Dec 2004 15:37:28 -0600 From: "Terry S. Singeltary Sr." To: susan_berg@bio-rad.com
Hello Susan and Bio-Rad,
Happy Holidays!
I wish to ask a question about Bio-Rad and USDA BSE/TSE testing and there inconclusive. IS the Bio-Rad test for BSE/TSE that complicated, or is there most likely some human error we are seeing here?
HOW can Japan have 2 positive cows with No clinical signs WB+, IHC-, HP- , BUT in the USA, these cows are considered 'negative'?
IS there more politics working here than science in the USA?
What am I missing?
-------- Original Message --------
Subject: Re: USDA: More mad cow testing will demonstrate beef's safety
Date: Fri, 17 Dec 2004 09:26:19 -0600
From: "Terry S. Singeltary Sr." snip...end
Experts doubt USDA's mad cow results
snip...END
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''. ...
TSS
-------- Original Message --------
Subject: Your questions
Date: Mon, 27 Dec 2004 15:58:11 -0800
From: To: flounder@wt.net
Hi Terry:
snip...
Let me know your phone number so I can talk to you about the Bio-Rad BSE test.
Thank you
Regards
Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email:
=================================
END...TSS
######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########
Wednesday, July 28, 2010
Atypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA Final report
http://bse-atypical.blogspot.com/2010/07/atypical-prion-proteins-and-ibnc-in.html
IBNC
"All of the 15 cattle tested showed that the brains had abnormally accumulated prion protein."
Saturday, February 28, 2009
NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS "All of the 15 cattle tested showed that the brains had abnormally accumulated PrP" 2009
SEAC 102/2
http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html
ATYPICAL LESION DISTRIBUTION (RBSE 92/21367)
A 6 year old, home bred (HB), Friesian x Holstein cow in a dairy herd in Aberdeenshirer submitted as a suspect BSE case in the negative study (SE0203), has been diagnosed as BSE negative on standard, statutory (obex only), diagnostic criteria at CVL.
Further examination by Dr Jeffrey at Lasswade, as required by the project design, has revealed vacuolar change in the septal nucleus and putamen which co-localised with PrP immunoreactivity. No significant lesions were found in any other part of the brain, neither was PrP found in the medulla.
It is important to note that examination of four brain blocks used earlier in the epidemic would not have detected the lesion but a 16 block study (as used in the very days of BSE) would.
FURTHER INFORMATION
The herd of origin has had 15, HB, suspect cases of BSE since July 1989 and a further case is still alive.
2. Of the 15, eight have been confirmed by standard histopathology and seven diagnosed negative (including the above case).
3. Fixed brain tissue from the negative cases exists at Lasswade (because they always collect whole brain in Scotland) but has not so far been examined further. No frozen tissue was collected so neither SAF nor PrP detection (by immunoblotting) has been attempted.
4. Mr Wells agrees with Dr Jeffrey's and Dr Simmons' findings.
FURTHER ACTION IN PROGRESS
1. The brain tissue from the negative cases will be examined in detail by conventional histopathology and ICC.
2. Kevin Taylor and his veterinary colleagues have been alerted to the situation.
OTHER RECOMMENDED ACTIONS
1. TRANSMISSION Attempt transmission from the 'case' to standard mice strains. (Note: In regard to strain typing, formalin may have modified strain phenotype - we need to discuss with NPU). Further transmission studies (eg in cattle) might be suggested if primary transmission in mice fails. These proposals have funding implications.
CODE 18-77
93/2.17/1.1
2. PrP GENOTYPING - Although only fixed brain tissue is available we are considering genotyping from parents/offspring/fixed brain. As a first step we are attempting to extract DNA from the fixed brain and to amplify the PrP gene by PCR.
3. John Wilesmith has interrogated the data base for the herd history. Other than the high proportion of negative cases nothing significant is apparent.
4. Familial relationships between suspect (including positive and negative) cases in this herd could be examined and tracings of breeding animals initiated.
5. Consideration might be given to collecting frozen spinal cord from new cases in this herd or in dispersals from it for (SAF/PrP examination).
CONCLUSIONS
1. At present it is unclear whether or not this is a singleton incident or whether the other negative cases in this herd show a similar lesion.
2. The discovery might indicate the existence of a different strain of BSE from that present in the general epidemic or an unusual response by an individual host.
3. If further atypical lesion distribution cases are revealed in this herd then implications of misdiagnosis of 'negative' cases in other herds may not be insignificant.
4. If this is a new strain all the implications need to be considered including whether or not to proceed with the further investigation of future cases negative for BSE on obex examination alone and from which whole brains are available (as in Scotland) or collected in the future. Also perhaps investigation of the tissue distribution of infectivity in these animals might be considered.
5. Animal and public health controls in place should be sufficient since all tissues (other than brain for diagnosis) are incinerated.
We observe that Dr Tyrrell would wish to be informed of this at an early opportunity and that the SEAC would wish to discuss it at their meeting in April.
R BRADLEY
M DAWSON
17 February 1993
CVO - for information and comment on further action please
cc Mr K C Taylor
Dr B J Shreeve
93/2.17/1.2
This minute is re-issued with a wider distribution.
The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".
Mr Scudamore
Mr R C Lowson
Dr D Matthews
Mr I Robertson
Dr K MacOwan
Mr C Randall
Mr J W Wilesmith
Mr G A H Wells
Dr M Jeffrey
Dr M Simmons
93/2.17/1.3
http://tna.europarchive.org/20080609145105/http://www.bseinquiry.gov.uk/files/yb/1993/02/17001001.pdf
IN CONFIDENCE
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367)
http://tna.europarchive.org/20080609145105/http://www.bseinquiry.gov.uk/files/yb/1993/03/14001001.pdf
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. ...
http://collections.europarchive.org/tna/20090114131343/http://www.bseinquiry.gov.uk/files/yb/1992/10/26001001.pdf
Tuesday, November 17, 2009
SEAC NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS (IBNC) FROM THE VETERINARY LABORATORIES AGENCY (VLA) SEAC 103/1
http://bse-atypical.blogspot.com/2009/11/seac-new-results-on-idiopathic.html
NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS "All of the 15 cattle tested showed that the brains had abnormally accumulated PrP" 2009
http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html
''THE LINE TO TAKE'' ON IBNC $$$ 1995 $$$
1995
page 9 of 14 ;
30. The Committee noted that the results were unusual. the questioned whether there could be coincidental BSE infection or contamination with scrapie. Dr. Tyrell noted that the feeling of the committee was that this did not represent a new agent but it was important to be prepared to say something publicly about these findings. A suggested line to take was that these were scientifically unpublishable results but in line with the policy of openness they would be made publicly available and further work done to test their validity. Since the BSE precautions were applied to IBNC cases, human health was protected. Further investigations should be carried out on isolations from brains of IBNC cases with removal of the brain and subsequent handling under strict conditions to avoid the risk of any contamination.
31. Mr. Bradley informed the Committee that the CVO had informed the CMO about the IBNC results and the transmission from retina and he, like the Committee was satisfied that the controls already in place or proposed were adequate. ...
snip... see full text
http://collections.europarchive.org/tna/20080102204938/http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf
http://web.archive.org/web/20030327015011/http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf
NOW, what about the 'obex only' mode of testing used by the USDA et al for TSE, prions $$$ works for them too, a sure fire way NOT TO FIND MAD COW DISEASE $$$
NOW, read the following please, and then ask yourself, WHY the USDA et al were ONLY TESTING THE OBEX PART OF THE BRAIN in USA cattle for BSE $$$
BECAUSE they knew that would be the least likely way to find BSE/TSE in USA cattle $$$...TSS
Tuesday, November 02, 2010
IN CONFIDENCE
The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
Tuesday, July 14, 2009
U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST
WHERE did we go wrong $$$
http://madcowtesting.blogspot.com/2009/07/us-emergency-bovine-spongiform.html
Thursday, July 14, 2011
Histopathological Studies of “CH1641-Like” Scrapie Sources Versus Classical Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html
=========
Discussion
In the five cats in this study with a spongiform encephalopathy, fibrils were observed by electron microscopy and their major protein, Prpsc, was identified by SDS-PAGE and Western blot. The fibrils were similar to those described in sheep with scrapie (Rubenstein and others 1987, Gibson and others 1987, Scott and others 1987, Dawson and others 1987), cattle with bovine spongiform encephalopathy (Wells and others 1987, Hope and others 1988, Scott and others 1990) and humans with Creutzfeldt-Jakob disease (Merz and others 1984).
In sheep with scrapie, fibrils can be readily detected in several areas of the brain, including cerebral cortex (Stack and others 1991).
By contrast, the frequency with which fibrils were detected in cattle with BSE, DEPENDED ON THE REGION OF THE BRAIN SAMPLED; THE HIGHEST YIELD BEING OBTAINED FROM MEDULLA, MIDBRAIN, THALAMUS AND BASAL NUCLEI WHERE VACUOLA CHANGES ARE PRESENT (Scott and others 1990). This correlation between PrPsc accumulation and vacuolar pathology is also well established in laboratory animal models of scrapie (Bruce and others 1989). Because of the widespread distribution of changes in FSE (Whatt and others 1991) and the requirement, in the present study, not to compromise the histopathological examination of the brain, the frontal region of the cerebrum was therefore selected for fibril and PrPsc examinations. However, studies of the sensitivity of fibril detection in different parts of the brain in cats with FSE are required to determine whether detection can be made as readliy in other regions as in the frontal cerebral cortex.
IT IS OF INTEREST, that fibrils were detected in the brains of 3 cats (cases 9, 13, & 18) WITHOUT histopathological evidence of spongiform encephalopathy, and that in only one of them, (case 9), a Western blot for modified PrP was positive. There are precedents for the occurrence of abnormal PrP in the organs of animals incubation scrapie prior to clinical signs and/or spongiform encephalopathy...
snip...
(please see full text (and one might start downloading these documents for future use, as some disappear never to re-appear, as in some of the FDA's. ...TSS)
http://collections.europarchive.org/tna/20090113230941/http://www.bseinquiry.gov.uk/files/sc/seac12/tab04.pdf
PLEASE NOTE *
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
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
FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html
http://www.mail-archive.com/fda-newsdigest-l@list.nih.gov/msg00094.html
THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006
In an article today for United Press International, science reporter Steve Mitchell writes:
Analysis: What that mad cow means
By STEVE MITCHELL UPI Senior Medical Correspondent
WASHINGTON, March 15 (UPI) -- 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 they did before 2005 suspect," Brown said.
Despite this, Brown said the U.S. prevalence of mad cow, formally known as bovine spongiform encephalopathy, or BSE, did not significantly threaten human or cattle health.
"Overall, my view is BSE is highly unlikely to pose any important risk either in cattle feed or human feed," he said.
However, Jean Halloran of Consumers Union in Yonkers, N.Y., said consumers should be troubled by the USDA's secrecy and its apparent plan to dramatically cut back the number of mad cow tests it conducts.
"Consumers should be very concerned about how little we know about the USDA's surveillance program and the failure of the USDA to reveal really important details," Halloran told UPI. "Consumers have to be really concerned if they're going to cut back the program," she added.
Last year the USDA tested more than 300,000 animals for the disease, but it has proposed, even in light of a third case, scaling back the program to 40,000 tests annually.
"They seem to be, in terms of actions and policies, taking a lot more seriously the concerns of the cattle industry than the concerns of consumers," Halloran said. "It's really hard to know what it takes to get this administration to take action to protect the public."
The USDA has insisted that the safeguards of a ban on incorporating cow tissue into cattle feed (which is thought to spread the disease) and removal of the most infectious parts of cows, such as the brain and spinal cord, protect consumers. But the agency glosses over the fact that both of these systems have been revealed to be inadequately implemented.
The feed ban, which is enforced by the Food and Drug Administration, has been criticized by the Government Accountability Office in two reports, the most recent coming just last year. The GAO said the FDA's enforcement of the ban continues to have weaknesses that "undermine the nation's firewall against BSE."
USDA documents released last year showed more than 1,000 violations of the regulations requiring the removal of brains and spinal cords in at least 35 states, Puerto Rico and the Virgin Islands, with some plants being cited repeatedly for infractions. In addition, a violation of similar regulations that apply to beef exported to Japan is the reason why Japan closed its borders to U.S. beef in January six weeks after reopening them.
Other experts also question the adequacy of the USDA's surveillance system. The USDA insists the prevalence of mad cow disease is low, but the agency has provided few details of its surveillance program, making it difficult for outside experts to know if the agency's monitoring plan is sufficient.
"It's impossible to judge the adequacy of the surveillance system without having a breakdown of the tested population by age and risk status," Elizabeth Mumford, a veterinarian and BSE expert at Safe Food Solutions in Bern, Switzerland, a company that provides advice on reducing mad cow risk to industry and governments, told UPI.
"Everybody would be happier and more confident and in a sense it might be able to go away a little bit for (the USDA) if they would just publish a breakdown on the tests," Mumford added.
UPI requested detailed records about animals tested under the USDA's surveillance plan via the Freedom of Information Act in May 2004 but nearly two years later has not received any corresponding documents from the agency, despite a federal law requiring agencies to comply within 30 days. This leaves open the question of whether the USDA is withholding the information, does not have the information or is so haphazardly organized that it cannot locate it.
Mumford said the prevalence of the disease in U.S. herds is probably quite low, but there have probably been other cases that have so far gone undetected. "They're only finding a very small fraction of that low prevalence," she said.
Mumford expressed surprise at the lack of concern about the deadly disease from American consumers. "I would expect the U.S. public to be more concerned," she said.
Markus Moser, a molecular biologist and chief executive officer of Prionics, a Swiss firm that manufactures BSE test kits, told UPI one concern is that if people are infected, the mad cow pathogen could become "humanized" or more easily transmitted from person to person.
"Transmission would be much easier, through all kinds of medical procedures" and even through the blood supply, Moser said.
© Copyright 2006 United Press International, Inc. All Rights Reserved
http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r
http://www.upi.com/Science_News/2003/12/30/Mad-Cow-Linked-to-thousands-of-CJD-cases/UPI-47861072816318/
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, ...
http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm
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." ........TSS
http://madcowtesting.blogspot.com/2009/07/mad-cow-cover-up-usa-masked-as-sporadic.html
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
THIS is just ONE month report, of TWO recalls of prohibited banned MBM, which is illegal, mixed with 85% blood meal, which is still legal, but yet we know the TSE/BSE agent will transmit blood. we have this l-BSE in North America that is much more virulent and there is much concern with blood issue and l-BSE as there is with nvCJD in humans. some are even starting to be concerned with sporadic CJD and blood, and there are studies showing transmission there as well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that reaches commerce is ever returned via recall, very, very little. this was 2007, TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow feed that was in ALABAMA in one of the links too, this is where the infamous g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the USA. seems this saga just keeps getting better and better.......$$$
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
Sunday, October 24, 2010
Australia Mad cow assessments come to a standstill, USDA hasn't a clue $
"And then FSANZ received an incomplete application from the US, which says at this stage it doesn't have the resources to provide information."
http://www.abc.net.au/rural/news/content/201010/s3044237.htm
please see full text ;
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
Subject: BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA, A REVIEW OF SORTS
Date: October 18, 2007 at 12:25 pm PST
BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA, A REVIEW OF SORTS
HOW can they find anymore mad cows when the june 2004 enhanced bse cover-up was just that, the testing and protocol for testing was totally flawed, and proven to be so. they floundered every step of the way. and then when the atypicals started showing up, they just shut the testing down. the two suspect cows that samples sat on the shelf for 7+ months that was later confirmed, and the other suspect that sat on the shelf for 4 months, but later thought to be negative UNDER VERY QUESTIONABLE CONDITIONS, but could not have all the proper testing done on it, due to the sample being set in paraffin, which is a no no. they knew that, and that was the end around johanns and dehaven did after fong did the same to them on the 7 month delayed sample. all this done, while GW et al at the USDA were shoving down everyone throats the BSE MRR policy, the legal trading of all strains of TSE globally. ...tss
Subject: USDA BSE inconclusive MRR policy Date: August 25, 2006 at 3:52 pm PST
USDA BSE inconclusive MRR policy
BESIDES THE TEXAS MAD COW THAT WAS RENDERED AND NEVER TESTED;
FDA Statement FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).
FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.
To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.
Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.
FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.
####
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html
USDA orders silence on mad cow in Texas
By Steve Mitchell United Press International Published 5/11/2004 10:16 PM
WASHINGTON, May 11 (UPI) -- The U.S. Department of Agriculture has issued an order instructing its inspectors in Texas, where federal mad cow disease testing policies recently were violated, not to talk about the cattle disorder with outside parties, United Press International has learned.
The order, sent May 6 by e-mail from the USDA's Dallas district office, was issued in the wake of the April 27 case at Lone Star Beef in San Angelo, in which a cow displaying signs of a brain disorder was not tested for mad cow disease despite a federal policy to screen all such animals.
The deadly illness also is known as bovine spongiform encephalopathy.
Both the USDA and its Inspector General -- amid allegations that an offsite supervisor overruled the opinion of the inspectors onsite and made the final decision not to test the animal -- have opened up investigations to determine why agency policy was violated.
The order, which was obtained by UPI, was issued by Ijaz Qazi, circuit supervisor for the USDA's Food Safety and Inspection Service's Dallas district, which covers the entire state. It reads: "All BSE inquiries MUST be directed to Congressional Public Affairs Phone 202-720-9113 attention Rob Larew OR Steve Khon. This is an urgent message. Any question contact me. Ijaz Qazi."
Although the language might sound innocuous, experienced inspectors familiar with USDA parlance have taken to referring to the notice as a "gag order."
The National Joint Council of Food Inspection Locals -- the national inspectors union -- considers the order a violation of inspectors' free speech rights and is considering legal action against the USDA for breaching the labor agreement they have with the agency.
Inspectors alleged the order also suggests the agency is concerned about its personnel leaking damaging information about either the Texas case or the USDA's overall mad cow disease surveillance program, which has come under fire since the discovery of an infected cow in Washington state last December.
"Anytime the government suppresses an individual's freedom of speech, that's unconstitutional," Gary Dahl, president of Local 925, the Colorado inspectors union, told UPI.
Stanley Painter, chairman of the National Joint Council, said the USDA has sent out notices in the past stating inspectors cannot talk to reporters.
"It's an intimidation thing," Painter told UPI. Inspectors have the right to talk to anybody about any subject, as long as they clarify they are not speaking on behalf of the USDA and they are not doing it on government time, he said.
USDA spokesman Steven Cohen said he was not familiar with the notice from the Dallas office. He said he would look into it, but did not respond by UPI's publication time. In general, Cohen said, "There's an expectation any statement on behalf of the agency would come from the office of communications (in Washington.)"
Asked if employees could speak freely as long as they clarified that their views did not reflect those of the agency, Cohen said, "We'd rather that agency policy be communicated by those in a position to speak for the agency."
Qazi told UPI the notice was not issued in conjunction with the Texas case and it was routine agency practice that outside inquiries be referred to the Washington office. He said inspectors are free to talk to outside parties, including reporters, and he did not consider the e-mail a violation of the labor agreement with the inspectors.
Painter said the USDA's efforts to keep its employees from talking about mad cow would be better spent "with issues like protecting the consuming public instead of trying to hide things." He added he would "just about bet his last nickel" agency management was attempting to suppress information about the Texas case.
"To keep federal employees from reporting government waste, misuse of appropriations -- those types of things -- that's not a good thing either," Dahl said. "If there is something wrong, let's get it out in the open -- let's get it fixed. We're working for the public, the American consumers. I think they have the right to know this," he said.
"And believe me there's so many indicators saying that the USDA's mad cow testing program is broken," Dahl added.
At least one member of Congress, Sen. Tom Harkin, D-Iowa, agrees.
Harkin, a long-time critic of the USDA, sent a letter to Agriculture Secretary Ann Veneman on Monday, saying the Texas incident "calls into question the effectiveness and reliability of USDA's current and proposed surveillance system."
The USDA has proposed testing more than 200,000 cows -- or 10 times its current rate -- in an expanded program scheduled to begin June 1. Harkin wrote in the five-page letter, however, that given the realities of the cattle industry, it is "quite doubtful" the USDA will be able to test that many cows, particularly because it had difficulty finding 20,000 last year.
"We simply cannot tolerate a BSE testing system that fails to give valid answers to critical questions for U.S. consumers and foreign customers," Harkin said in the letter, which sharply criticizes the agency's failure to address explicitly how its new surveillance program will be implemented.
"We look forward to receiving (Harkin's) letter and having the opportunity to review it and respond to him," USDA spokesman Ed Loyd told UPI. "USDA has acknowledged there was a failure in not testing that cow in Texas for BSE, so we are all working to ensure that does not occur again."
Jim Rogers, a spokesman for USDA's Animal and Plant Health Inspection Service, which oversees the agency's mad cow surveillance program, told UPI the agency has tested about 15,500 animals since fiscal year 2004 began, on Oct. 1, 2003. However, the agency has refused to identify the states and facilities from which the cows originated. Rogers said UPI would have to seek that information through the Freedom of Information Act.
The question is central to the USDA's implementation of its expanded surveillance program. Downer cows -- those unable to stand or walk -- made up the bulk of the animals the agency tested for mad cow in previous years, but these were banned from being slaughtered for human consumption in December. This means the agency inspectors no longer can obtain brain samples from these cows at slaughterhouses as they could in the past.
Furthermore, the USDA has not provided any evidence it has worked out agreements with rendering facilities or ranchers, where downers and dead cows are now most likely to be found, to obtain the extra animals for testing.
Loyd said the agency is "working very hard to get animals on the farm that would never show up in a processing facility," and he was "not aware of any issues" that would delay the launch of the new program.
However, he was unable to provide the names or locations of the rendering facilities where the agency will be obtaining cow brains for BSE testing. He said he would look into it but did not return two follow-up phone calls from UPI before publication.
--
Steve Mitchell is UPI's Medical Correspondent. E-mail sciencemail@upi.com
Copyright © 2001-2004 United Press International
http://www.upi.com/view.cfm?StoryID=20040511-015527-4917r
Subject: The IHC Test Variables (USA BSE SURVEILLANCE) Date: June 24, 2005 at 7:59 pm PST
The IHC Test Variables:
• IHC has been the primary confirmatory test for
USDA’s BSE surveillance program and is recognized
by the World Organization for Animal Health, or OIE.
• IHC allows scientists to determine if a sample is
positive for BSE in two distinct ways:
1.) A staining technique (presence of abnormal
prion protein) that uses antibodies to detect
abnormal prion protein in the brain.
2.) A visual examination to determine whether there
are lesions (holes or "spongy" appearances)
present in the brain.
• Several variables could yield conflicting results:
o IHC is not a standardized, commercially
available test. It involves variables, including
several options in types of antibodies and other
reactive agents. The sensitivity of any given test
is influenced by those variables.
o If the level of infectivity in the animal is extremely
low, the abnormal prion in the brain will be
minimal and therefore more difficult to detect.
o Variations in the conditions under which the
staining process is performed, such as
chemicals and reactive agents used,
temperature and length of antibody exposure,
can also cause the test to yield different results.
Testing History on This Animal:
• In November 2004, a sample from this animal
returned inconclusive for BSE on a Biorad screening
test.
• The sample was subjected to an IHC confirmatory
test, which returned negative.
• USDA scientists also ran an additional, experimental
IHC "rapid" tissue fixation test for academic purposes,
which can be conducted more quickly than the IHC
confirmatory test and is therefore of interest to the
scientific community, but it has not been approved
internationally.
• While some abnormalities were noted in the
experimental IHC test results, because the test was
not a validated procedure, and because the two
approved IHC tests came back negative, the results
were not considered to be of regulatory significance
and therefore were not reported beyond the
laboratory.
• A Western blot test conducted the week of
June 5, 2005, returned positive for BSE.
• An additional IHC confirmatory test conducted the
week of June 13, 2005, by USDA scientists utilizing
different antibodies from the November 2004 test,
confirmed this case as weakly positive for BSE.
• The Veterinary Laboratories Agency in Weybridge,
England, conducted a series of diagnostic tests
including an IHC, using different antibodies from
those used by USDA in November 2004, which
returned positive results for BSE.
• Experts from the Weybridge lab confirmed the
accuracy of the results of USDA’s November
confirmatory IHC test, concurring that the case could
not have been confirmed on the basis of this sample.
• Weybridge experts also examined the November
experimental IHC test and interpreted the results to
be positive.
Potential Causes of Conflicting Results:
• USDA scientists are consulting with Weybridge
scientists to determine the cause of the conflicting
IHC test results.
• Several factors could cause or contribute to the
discrepancy as follows:
o This animal had a very low level of infectivity and
therefore the sensitivity of USDA’s routine IHC
test might not have been sufficient to detect the
disease.
o Weybridge experts indicate that deposits of
abnormal prion in the brain tissue were not
uniformly distributed and were present at low
concentration, which means that even adjacent
samples of brain tissue might not give identical
results.
Factsheet
Veterinary Services June 2005
APHIS
USDA Protocol Review:
• USDA will develop a protocol to conduct dual
confirmatory tests, the IHC and the Western blot,
when the screening test, the Biorad, returns an
inconclusive result.
• USDA and Weybridge scientists are in agreement
that the Biorad test is a very effective and appropriate
screening test.
• USDA scientists will consult with Weybridge scientists
to assess the array of antibodies available for use in
IHC confirmatory tests to determine the most
appropriate for use in United States confirmatory
tests. Those consultations will be repeated periodically.
The U.S. Department of Agriculture (USDA) prohibits discrimination
in all its programs and activities on the basis of race, color,
national origin, sex, religion, age, disability, political beliefs, sexual
orientation, or marital or family status. (Not all prohibited bases
apply to all programs.) Persons with disabilities who require alternative
means for communication of program information (Braille,
large print, audiotape, etc.) should contact USDA’s TARGET
Center at (202) 720–2600 (voice and TDD).
To file a complaint of discrimination, write USDA, Director, Office
of Civil Rights, Room 326–W, Whitten Building, 1400
Independence Avenue, SW, Washington, DC 20250–9410 or call
(202) 720–5964 (voice and TDD). USDA is an equal opportunity
provider and employer.
Safeguarding American Agriculture Animal and Plant Health Inspection Service • United States Department of Agriculture •
http://www.usda.gov/documents/vs_bse_ihctestvar.pdf
THIS confirms that the June 2004 Enhanced BSE cover-up, was just that. Like i said before, due to this terribly flawed system, those 388,000 testing to date for BSE in the USA were meaningless and should be retested. ...
Subject: USDA JOHANN'S MAD ABOUT FONG, PLANS HIS OWN LAB AND HIS OWN MAD COW ANTIBODIES ;-) Date: July 29, 2005 at 2:35 pm PST
Friday, July 29, 2005
Ames lab to take over testing for mad cow disease Published: 07/29/2005 3:52 PM
By: Associated Press - Associated Press
AMES, IA - Scientists at the National Veterinary Services Laboratories here soon will begin conducting their own Western blot tests, eliminating the need to travel to Weybridge, England, when initial rapid testing detects mad cow disease.
"I think the change is good because we're more likely to know exactly what we're dealing with on each case," said Dr. Randall Levings, director of the labs.
The change is a response to an order from U.S. Agriculture Secretary Mike Johanns.
"We took those as our marching orders," Levings said.
Mad cow disease, formally known as bovine spongiform encephalopathy, or BSE, attacks a cow's nervous system. It is characterized by spongelike holes in the brain, the result of misshapen proteins called prions that kill brain cells.
The only way it is known to spread is by cattle eating infected brain and nerve tissue from other cows. That's why the government in 1997 banned the use of cattle feed that contains remnants of other cows. Of the three cases of mad cow confirmed in the United States, all three cows were born before the feed ban, Levings said.
Since January 2004, the government has tested more than 400,000 cows for the disease, using a rapid screening test and a test known immunohistochemistry, or IHC.
Rapid testing of a sample involves removing normal proteins and adding chemicals that bind to the abnormal proteins, making them visible. The IHC test involves staining paper-thin brain tissue samples to highlight the abnormal protein.
The Western blot test, conducted at Weybridge destroys normal proteins in the brain, leaving only the abnormal prions.
In June, the nation's Office of Inspector General ordered a review of the Ames lab's testing procedures after a sample last fall tested positive in England, but negative in Ames.
A rapid test on the sample in Ames detected the presence of BSE, but the following IHC test was negative. Ames workers also relayed the results of the test, but did not complete formal paperwork.
A version of mad cow disease, known as variant Creutzfeld-Jakob, has killed about 150 people worldwide, most of them in Britain, where there was an outbreak in the 1990s.
"We're taking all of the right steps," Levings said. "It would not be a risk to human or animal health in this country. It's not high. It's very, very low."
http://www.crgazette.com/2005/07/29/Home/News/madcowtesting.htm
SO, Johann's/GW et al have perfected the BSE/TSE testing protocols and they don't need anyone else to tell them what to do. this was proven with the TEXAS mad cow cases alone, r i g h t...... $$$ IF this is the case, why is Weybridge having to confirm our inconclusives ??? this is frightening.
IF not for the Honorable Phyllis Fong, that cow would have never been proven postive, well, documented anyway, it was proven postive time and time again...
The Fong Syndrome strikes again.
GW's BSE/TSE MRR policy a recipe for disaster.
USA in dire straights.
God help us... TSS
Greetings,
"Texas Agriculture Commissioner Susan Combs suggested federal regulators wait until animals are confirmed positive or negative before disclosing results to the public."
"While markets may bounce back, enormous amounts of money can be lost in the interim,"
Combs wrote.
"In fact, during the last inconclusive announcement, it is estimated that the market dropped $25 per head on cattle, resulting in hundreds of millions of dollars in losses to our cattle industry."
Susan Combs by no means has public and consumer health at heart while she is protecting the cattle industry. She is oblivious to mad cow disease. Her soul purpose is to protect the cattle industry at all cost, including my mothers life (DOD 12/14/97), or maybe one of your family members from any strain of mad cow disease in TEXAS. SHE helped cover-up mad cow disease in TEXAS both on that inconclusive that was positive so many times it will make your head spin. PLUS, the other mad cow in TEXAS they rendered without testing at all, that came from the top out of Austin. THEY should be tried for murder. corporate homicide is what i call it. they knew for years, but kept on keeping on. IF, that positive, positive, positive, inconclusive, negative, and then 8 months later POSITIVE BY WEYBRIDGE mad cow in TEXAS would not have been made public back in November, people like myself that KNEW that cow was positive and that the USDA/COMBs et al were covering it up due to lack of proper testing, IF that news would not have been brought fourth to the public, that cow would have NEVER tested positive for mad cow disease. it was the fact that the data that was put forth in the public domain, that the public came forth and demanded that the testing be done properly and retested. THIS is what the industry and Susan Combs does not want to happen. They wish to keep it private and to manipulate the markets to there benefit, and not release the mad cow data to the public. I wrote Susan Combs on many occasions about this positive, positive, positive, incl. neg., and finally POSITIVE TEXAS MAD COW and about the one that got away, but the only thing that Susan Combs does is send me back a bought and paid for rubber stamped letter from the USDA/Industry;
----- Original Message -----
From: SusanCombs
To: Terry S. Singeltary Sr.
Sent: Monday, July 18, 2005 11:56 AM
Subject: RE: no mad cow cover up in TEXAS???
Dear Mr. Singeltary:
Thank you for contacting the Texas Department of Agriculture about the isolated case of bovine spongiform encephalopathy found in a Texas cow. I can assure you there has been no cover up by the state’s cattle industry or the U.S. Department of Agriculture, which has kept the public informed at every step in the process. First and foremost, it is important to remember that the safety procedures worked. This animal was banned from the food or feed supply, and long-standing safeguards have been in place to protect public health. Because the animal was unable to walk, it was removed from the food supply and was processed at a facility that handles animals unsuitable for human consumption. The carcass was incinerated. Texas and American cattle producers are committed to producing and ensuring a safe food product – the same safe product their families are consuming.
As far back as the late 1980s, the cattle industry began working with the U.S. government to take precautions and establish firewalls to protect public and animal health from BSE. The United States has had an active surveillance program for BSE since 1990 to test a representative sample of the adult cattle population in the United States. With the discovery of a Canadian cow in Washington state in 2003, USDA expanded the surveillance program to test hundreds of thousands of high risk animals The surveillance program is designed to specifically determine whether BSE exists in the U.S. cattle population and if so, at what level. The number of tests under the surveillance program far exceeds the level recommend by the World Animal Health Organization. With the original goal of testing 268,000 animals in a year, USDA would be able to find the disease if it occurred in as few as 1 in 10 million adult cattle with a 99 percent confidence level. Since the beginning of the program in June 2004, USDA has tested more than 400,000 animals and found only this one case, which confirms estimates that the prevalence of this disease in the U.S. cattle population is extremely low. In regards to this particular animal, the laboratory in Weybridge, England found a very low level of abnormal prion protein in the brain. In addition, the abnormalities were isolated and not consistent throughout the brain – making it possible for one sample to test negative while another sample might test positive, which was the reason for the varying results.
Our cattle producers are working hard to produce the safest beef product in the world, and their strong vigilance is a solid commitment to American consumers.
Sincerely, Susan Combs Commissioner
--------------------------------------------------------------------------------
From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net]
Sent: Wednesday, July 13, 2005 12:11 PM
To: Susan Combs
Subject: no mad cow cover up in TEXAS???
Greetings Honorable Susan Combs,
no cover-up of mad cow disease in Texas ??? if not, then maybe you can explain the 7+ month delay in the announcement of the secret postive test on that postive, positive, inconclusive, negative, postive, cow that WAS going to be slaughtered for human consumption, but THEN went down and was sent to the champion pet food plant. OR maybe you can explain to me the mad cow that got away. the one MAD COW TEXAS rendered without testing at all. please explain these things to me if there is no cover up of TEXAS MAD COW disease???
thank you,
with kindest regards,
I am sincerely,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
===================
IN TEXAS, we feed our cattle ruminant protein, and lots of it. but remember (the fda cannot seem to get this right) .1 gram is lethal; THE TEXAS GONZALES/PURINA INCIDENT SHOWED THAT 5.5 GRAMS OF RUMINANT PROTEIN WAS FED TO CATTLE ;
FOR IMMEDIATE RELEASE P01-05 January 30, 2001 Print Media: 301-827-6242 Broadcast Media: 301-827-3434 Consumer Inquiries: 888-INFO-FDA
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.
http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html
P03.137
Transmission of BSE to Cynomolgus Macaque, a Non-human Primate; Development of Clinical Symptoms and Tissue Distribution of PrPSC
Yamakawa, Y1; Ono, F2; Tase, N3; Terao, K3; Tannno, J3; Wada, N4; Tobiume, M5; Sato, Y5; Okemoto-Nakamura, Y1; Hagiwara, K1; Sata, T5 1National Institure of Infectious diseases, Cell biology and Biochemistry, Japan; 2Corporation for Production and Research Laboratory Primates., Japan; 3National Institure of Biomedical Innovation, Tsukuba Primate Reserch Center, Japan; 4Yamauchi Univ., Veterinary Medicine, Japan; 5National Institure of Infectious diseases, Pathology, Japan
Two of three cynomolgus monkeys developed abnormal neuronal behavioral signs at 30-(#7) and 28-(#10) months after intracerebral inoculation of 200ul of 10% brain homogenates of BSE affected cattle (BSE/JP6). Around 30 months post inoculation (mpi), they developed sporadic anorexia and hyperekplexia with squeal against environmental stimulations such as light and sound. Tremor, myoclonic jerk and paralysis became conspicuous during 32 to 33-mpi, and symptoms become worsened according to the disease progression. Finally, one monkey (#7) fell into total paralysis at 36-mpi. This monkey was sacrificed at 10 days after intensive veterinary care including infusion and per oral supply of liquid food. The other monkey (#10) had to grasp the cage bars to keep an upright posture caused by the sever ataxia. This monkey was sacrificed at 35-mpi. EEG of both monkeys showed diffuse slowing. PSD characteristic for sporadic CJD was not observed in both monkeys. The result of forearm movement test showed the hypofunction that was observed at onset of clinical symptoms. Their cognitive function determined by finger maze test was maintained at the early stage of sideration. However, it was rapidly impaired followed by the disease progression. Their autopsied tissues were immunochemically investigated for the tissue distribution of PrPSc. Severe spongiform change in the brain together with heavy accumulation of PrPSc having the type 2B/4 glycoform profile confirmed successful transmission of BSE to Cynomolgus macaques. Granular and linear deposition of PrPSC was detected by IHC in the CNS of both monkeys. At cerebral cortex, PrPSC was prominently accumulated in the large plaques. Sparse accumulation of PrPSc was detected in several peripheral nerves of #7 but not in #10 monkey, upon the WB analysis. Neither #7 nor #10 monkey accumulated detectable amounts of PrPSc in their lymphatic organs such as tonsil, spleen, adrenal grands and thymus although PrPSc was barely detected in the submandibular lymph node of #7 monkey. Such confined tissue distribution of PrPSc after intracerebral infection with BSE agent is not compatible to that reported on the Cynomolgus macaques infected with BSE by oral or intra-venous (intra-peritoneal) routs, in which PrPSc was accumulated at not only CNS but also widely distributed lymphatic tissues.
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background: In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims: The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods: Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results: In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions: Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary
The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
http://www.thelancet.com/journal/journal.isa
It is clear that the designing scientists must also have shared Mr Bradley’s surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://web.archive.org/web/20040523230128/www.bseinquiry.gov.uk/files/ws/s145d.pdf
it is clear that the designing scientists must have also shared Mr Bradleyâs surprise at the results because all the dose levels right down to 1 gram triggered infection.
http://web.archive.org/web/20030526212610/http://www.bseinquiry.gov.uk/files/ws/s147f.pdf
USDA did not test possible mad cows
By Steve Mitchell United Press International
Published 6/8/2004 9:30 PM
WASHINGTON, June 8 (UPI) -- The U.S. Department of Agriculture claims it tested 500 cows with signs of a brain disorder for mad cow disease last year, but agency documents obtained by United Press International show the agency tested only half that number.
USDA officials said the difference is made up in animals tested at state veterinary diagnostic laboratories, but these animals were not tested using the "gold standard" test employed by the agency for confirming a case of the deadly disease. Instead, the state labs used a less sensitive test that experts say could miss mad cow cases.
In addition, the state lab figures were not included in a March 2004 USDA document estimating the number of animals most likely to be infected among U.S. herds, and apparently were not given to a congressional committee that had requested agency data on the number of cows with brain disorder signs that had been tested for the disease. "This is just adding to the demise of USDA's credibility," said Felicia Nestor, senior policy adviser to the Government Accountability Project, a group in Washington, D.C., that works with federal whistleblowers. "If the USDA is going to exclude from testing the animals most likely to have the disease, that would seem to have a very negative impact on the reliability of their conclusion," Nestor told UPI.
Nestor, who has monitored the USDA's mad cow surveillance program closely for several years, asked, "Are they deliberately avoiding testing animals that look like they have the disease?" Concerns about the number of cows in U.S. herds with brain disorder symptoms have been heightened due to the recent case in Texas, in which USDA officials failed to test an animal with such symptoms, also known as central nervous system or CNS signs. This was a violation of USDA policy, which stipulates all CNS cows should be tested because they are considered the most likely to be mad cow infected.
To date, the Washington cow that tested positive last December is the only confirmed case of mad cow disease -- also known as bovine spongiform encephalopathy -- among U.S. herds. The Texas incident has alarmed the public and members of Congress because humans can contract a fatal brain disorder called variant Creutzfeldt-Jakob disease from consuming meat infected with the mad cow pathogen. If the USDA's surveillance program is allowing the riskiest cows to go untested, it raises concerns about the ability of the monitoring system to detect the disease reliably in U.S. herds, Rep. Henry Waxman, D-Calif., charged in a May 13 letter to Agriculture Secretary Ann Veneman. Dr. Peter Lurie, of the consumer group Public Citizen, said CNS cows should be the one category that absolutely has to be tested to have a sound surveillance system. "CNS animals are far and away the most important animals to test," said Lurie, who has done several analyses of the USDA's mad cow surveillance program. "If there's any category that needs 100 percent testing, that's it, because they would be the most likely place to find mad cow in America," he told UPI. "Any CNS cow that slips into the food supply represents a major case of malpractice by USDA, and similarly, the failure to test the brain of that animal to see if it was indeed infected is really a failure to protect the public." USDA officials said the agency has no estimate on how many CNS cows occur in U.S. herds.
But spokesman Ed Loyd has told UPI, and at least one other media outlet, that 500 CNS cows were tested in fiscal year 2003. Yet agency testing records for the first 10 months of FY 2003, obtained by UPI under the Freedom of Information Act, show only 254 animals that fall under the CNS category -- or about half the number Loyd cited.
After failing to respond to repeated requests from UPI for clarification of the apparent discrepancy, Loyd finally offered the explanation that an additional 45 CNS cows were tested by the USDA during the final two months of FY 2003. The remainder, he said, was made up by CNS cases tested at various state veterinary diagnostic laboratories. "We also include data reported to us from state veterinary diagnostic laboratories, and all of these are CNS cases that have been tested for BSE using a histological examination," Loyd said. "We were not using any other labs during this period, other than (the USDA lab), to run the IHC tests for BSE, which is the gold standard," he said. "This (state laboratory) information contributes important data to our surveillance effort."
However, the state labs did not use the immunohistochemistry test, which the USDA has called the "gold standard" for diagnosing mad cow disease. Instead, the labs used a different test called histopathology, which the USDA itself does not use to confirm a case, opting instead for the more sensitive IHC test. The histopathology test, unlike the IHC test, does not detect prions -- misfolded proteins that serve as a marker for infection and can be spotted early on in the course of the illness. Rather, it screens for the microscopic holes in the brain that are characteristic of advanced mad cow disease. According to the USDA's Web site, histopathology proves reliable only if the brain sample is removed soon after the death of the animal. If there is too much of a delay, the Web site states, it can be "very difficult to confirm a diagnosis by histopathology" because the brain structures may have begun to disintegrate. That is one reason the agency began using the IHC test -- it can confirm a diagnosis if the brain has begun disintegrating or been frozen for shipping.
The state labs used histopathology to screen 266 CNS cases in FY 2003, as well as 257 cases in FY 2002, according to Loyd. He did not explain why this information was not included in the testing records the agency provided to UPI and has not responded to requests for the identity of the state labs. Linda Detwiler, a former USDA veterinarian who oversaw the agency's mad cow testing program, told UPI the histopathology test probably is adequate for screening CNS cows. If they have mad cow disease, she said, it would likely be an advanced stage that should be obvious.
Other mad cow disease experts, however, said having a back-up test such as IHC would be advisable, because histopathology tests sometimes can miss evidence of infection. The Food and Agriculture Organization of the United Nations offers similar recommendations in its protocol for conducing a histopathology test. The protocol states that even if histopathology is negative, "further sampling should be undertaken" in cases "where clinical signs have strongly suggested BSE" -- a criteria that includes all of the cows tested at the state labs.
The USDA seems to agree on the need for a back-up test. Its expanded surveillance program, which began June 1, calls for using IHC -- or another test called Western blot -- to confirm any positives found on rapid tests. The March 15 document that describes the new program does not mention using histopathology to confirm cases of mad cow disease. "Subtle changes can be missed on histopathology that would probably not be as easy to miss using IHC," said Elizabeth Mumford, a veterinarian and BSE expert at Safe Food Solutions in Bern, Switzerland, a company that provides advice on reducing mad cow risk to industry and governments. "Therefore I believe it is valuable to run (histopathology)," Mumford told UPI. She noted that in Europe, two tests -- neither one the histopathology test -- are used to ensure no cases are missed. A rapid test is used initially for screening, followed by IHC as a confirmatory test.
Markus Moser, a molecular biologist and chief executive officer of the Swiss firm Prionics, which manufactures tests for detecting mad cow disease, agrees about the possibility of a case being missed by histopathology. "There were cases which were (histopathology) negative but still clearly positive with the other (testing) methods," Moser said. "BSE testing based on histology on sub-optimal tissue was probably one of the reasons why Germany was allegedly BSE-free until our test discovered that they were not" in 2000, Moser told UPI. He agreed with Detwiler that histopathology should be suitable for most cases of CNS cows, but added it still can fail to detect the disease in some CNS cases -- particularly if the sample is not optimum. "It is difficult, if not impossible, to distinguish the subtle changes in a diseased brain from artifacts like ruptures in the tissue due to tissue damage during the sampling, transport or preparation," he said.
Loyd asserted the additional CNS cases from the state labs actually yielded a total of 565 such cows the USDA had tested -- 65 more than his original figure of 500. Whether the USDA considers its total to be 500 or 565, however, either figure would exceed the agency's own estimates for the total number of such cows that it identifies annually.
According to data the USDA provided to the House Committee on Government Reform, and numbers the agency included in the March document about its expanded surveillance plan, only 201 to 249 CNS cows are identified at slaughterhouses. Approximately 129 additional cases occur on farms annually. At most, that yields a combined total of 378 CNS cows, or nearly 200 less than the 565 Loyd claims the agency tested.
The USDA surveillance plan document makes no mention of the number of CNS animals tested at state veterinary diagnostic labs. The figure also does not appear to be included in the agency's estimates of the number of high-risk animals that occur in the United States each year. The latter number was used to help the USDA calculate the number of animals it will screen for mad cow disease in its expanded surveillance plan.
USDA officials also did not include the state lab figures in response to a question from the House Committee on Government Reform, a source close to the issue told UPI. The committee, on which Waxman is the ranking Democrat, had requested in a March 8 letter to Veneman that she provide "the number of BSE tests that were conducted on cattle exhibiting central nervous system symptoms" for each of the last five years.
Loyd did not respond to a request from UPI asking why agency officials did not provide that information to the committee or include it in USDA's explanation of its expanded surveillance plan. The committee has taken note of the CNS issue and plans to delve into it further in a hearing slated for sometime in the next few months. "The committee will explore this and other issues surrounding USDA and BSE testing at a hearing later this summer," Drew Crockett, spokesman for the committee, told UPI.
-- Steve Mitchell is UPI's Medical Correspondent. E-mail sciencemail@upi.com Copyright © 2001-2004 United Press International
http://www.upi.com/view.cfm?StoryID=20040608-014607-3865r
''USDA gets a D or D minus," said Caroline Smith Dewaal of the Center for Science in the Public Interest, an advocacy group based in Washington. ''The best thing that came out of this is the work of the inspector general." It was the department's in-house watchdog, Inspector General Phyllis Fong, who skirted the USDA hierarchy by ordering retesting with a different method more than six months after a routine second-round test, known as the immunohistochemistry, or IHC, test proved negative for the disease. Agriculture Secretary Mike Johanns, who assumed office in January, has said he neither knew about nor authorized the retesting by the National Veterinary Services Laboratories in Ames, Iowa.
BESIDES the Texas mad cow that sat on the shelf for 7+ months before the Honorable Phyllis Fong of the OIG finally did the end around Johanns et al and finally had Weybridge bring that negative cow back from the dead to finally being a confirmed mad cow (hint, hint, getting MRR implemented first), was this simply another bumbling of BSE protocol, or just same old same old;
Jim Rogers (202) 690-4755 USDA Press Office (202) 720-4623 Statement by Chief Veterinary Medical Officer John Clifford Animal and Plant Health Inspection Service Regarding Non-Definitive BSE Test Results July 27, 2005
snip...
Our laboratory ran the IHC test on the sample and received non-definitive results that suggest the need for further testing. As we have previously experienced, it is possible for an IHC test to yield differing results depending on the “slice” of tissue that is tested. Therefore, scientists at our laboratory and at Weybridge will run the IHC test on additional “slices” of tissue from this animal to determine whether or not it was infected with BSE. We will announce results as soon as they are compiled, which we expect to occur by next week. 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.
snip...
http://www.aphis.usda.gov/lpa/news/2005/07/bsestatement_vs.html
Subject: Statement by Dr. John Clifford Regarding Non-Definitive BSE Test Results
Date: July 27, 2005 at 12:37 pm PST
Jim Rogers (202) 690-4755 Jerry Redding (202) 720-6959
Statement by Dr. John Clifford Regarding Non-Definitive BSE Test Results Late yesterday, we received non-definitive test results on an animal sampled as part of a voluntary extension of our enhanced BSE surveillance program. USDA is conducting further testing at the National Veterinary Services Laboratories in Ames, Iowa, in consultation with experts from the international reference laboratory in Weybridge, England.
We are also sending samples from this animal to the Weybridge laboratory for further testing. It is important to note that this animal poses no threat to our food supply because it did not enter the human food or animal feed chains.
The sample was submitted to us by a private veterinarian. As an extension of our enhanced surveillance program, accredited private veterinarians, who often visit farms in remote areas, collect samples when warranted. The sample in question today was taken from a cow that was at least 12 years of age and experienced complications during calving. The veterinarian treated the sample with a preservative, which readies it for testing using the immunohistochemistry (IHC) test - an internationally recognized confirmatory test for BSE.
Neither the rapid screening test nor the Western blot confirmatory test can be conducted on a sample that has been preserved.
Our laboratory ran the IHC test on the sample and received non-definitive results that suggest the need for further testing.
As we have previously experienced, it is possible for an IHC test to yield differing results depending on the slice of tissue that is tested. Therefore, scientists at our laboratory and at Weybridge will run the IHC test on additional slices of tissue from this animal to determine whether or not it was infected with BSE. We will announce results as soon as they are compiled, which we expect to occur by next week.
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. Regardless of the outcome of the further testing, I want to emphasize that human and animal health in the United States are protected by a system of interlocking safeguards.
The most important of these is the ban on specified risk materials from the food supply and the Food and Drug Administrations feed ban. And by any measure, the incidence of BSE in this country is extremely low.
snip...update 2011
Thursday, July 14, 2011
Valley Farm Meats (DBA Strasburg Provision, Inc) Issues Precautionary Recall for Beef Products Due to Possible Contamination with Prohibited Materials SRM
Ohio Department of Agriculture and Ohio Department of Health
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/valley-farm-meats-dba-strasburg.html
snip...continued ;
Our enhanced surveillance program is designed to provide information about the level of prevalence of BSE in the United States. We are extremely gratified that to date, all sectors of the cattle industry have cooperated in this program by submitting samples from more than 419,000 animals from the highest risk populations. To date, only one animal has tested positive for the disease as part of the surveillance program. These interlocking safeguards continue to protect our food supply.
# Note to Reporters: USDA news releases, program announcements and media advisories are available on the Internet. Go to the APHIS home page at http://www.aphis.usda.gov and click on the News button. Also, anyone with an e-mail address can sign up to receive APHIS press releases automatically. Send an e-mail message to lyris@mdrdlyriss10.aphis.usda.gov and leave the subject blank. In the message, type subscribe press_releases. USDA News oc.news@usda.gov 202 720-4623
----------------------------------------------------
"The sample was submitted to us by a private veterinarian. As an extension of our enhanced surveillance program, accredited private veterinarians who often visit farms in remote areas collect samples when warranted. The sample in question today was taken from a cow that was at least 12 years of age and experienced complications during calving. "The veterinarian treated the sample with a preservative which readies it for testing using the immunohistochemistry test, an internationally recognized confirmatory test for BSE. "Neither the rapid screening test nor the Western blot confirmatory test can be conducted on a sample that has been preserved. Our laboratory ran the IHC test on the sample and received non-definitive results that suggest the need for further testing. "As we have previously experienced, it is possible for an IHC test to yield differing results, depending on the slice of tissue that is tested. Therefore scientists at our laboratory and at Weybridge will run the IHC test on additional slices of tissue from this animal to determine whether or not it was infected with BSE. "We will announce results as soon as they are compiled, which we expect to occur by next week.
snip...
http://www.usda.gov/wps/portal/usdahome?contentidonly=true&contentid=2005/07/0280.xml
In Reply to:
Re: Statement by Dr. John Clifford Regarding Non-Definitive BSE Test Results posted by TSS on July 27, 2005 at 12:53 pm:
o.k., let me get this right. i am pondering here;-) all the time this TEXAS positive, positive, (secret) positive, inconclusive, negative, then Weybridge confirmed 2nd BSE documented case (thanks to the Honorable Phyllis Fong), all this time this BSe going on in TEXAS, was plastered all over the news, this guy forgot about that sample, and it just sat up on some shelf wasting away for months, as to be in such bad shape, they now cannot even test it properly. r i g h t ... like ooops, sorry. ...end
============================================
The animal died in April, but the veterinarian forgot to send the sample to USDA until this month, Mr. Clifford said. "While that time lag is not optimal, it has no implications in terms of the risk to human health," he said. IHC tests returned conflicting results on the Texas cow. Use of the preservative means that the other tests commonly done when mad cow is suspected, initial rapid screening and Western blot, can't be performed on this sample, the official said. Mr. Clifford said it's possible to get different results, "depending on the slice of tissue that is tested." The fatal brain-wasting disease is known medically as bovine spongiform encephalopathy, or BSE. In people, eating tainted meat products has been linked to about 150 deaths from a fatal disorder called variant Creutzfeldt-Jakob disease. Most of the deaths were in the United Kingdom, where there was an outbreak in the 1980s and 1990s. The U.S. banned Canadian cattle in May 2003 following Canada's first case of mad-cow disease. The U.S. was about to lift the ban in March when U.S. District Judge Richard Cebull in Billings, Mont., granted an injunction to a ranchers' group called R-CALF United Stockgrowers of America. The ranchers had sued to keep the border closed to Canadian cattle, saying the disease presented a risk to the U.S. beef industry as well as to American consumers. The 9th U.S. Circuit Court of Appeals reversed the injunction earlier this month, allowing cattle shipments from Canada to resume. The lifting of the ban reopens the U.S. to cattle younger than 30 months and expands the list of beef products Canada is allowed to ship to the U.S. Older animals are still banned, because infection levels are believed to increase with age.
Copyright © 2005 Associated Press
http://online.wsj.com/
Greetings, this is what you call the 'FONG' syndrome. make sure she can't make them do a WB on this sample. I BEG THE OIG and the Honorable Phyllis Fong to investigate this blunder too. there is no way that sample sat on a shelf while the world waited on that Texas mad cow blunder dust to settle, and someone just forgets about it. i just don't believe this either...
============================================
From: TSS Subject:
Re: Statement by Dr. John Clifford Regarding Non-Definitive BSE Test Results
Date: July 27, 2005 at 12:53 pm PST
In Reply to:
Statement by Dr. John Clifford Regarding Non-Definitive BSE Test Results posted by TSS on July 27, 2005 at 12:37 pm:
----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Sent: Wednesday, July 27, 2005 2:57 PM
Subject: Re: Statement by Dr. John Clifford Regarding Non-Definitive BSE Test Results
##################### Bovine Spongiform Encephalopathy #####################
Greetings,
with great disgust i must comment on this BSE/USDA/APHIS blunder as well. i swear, larry curly and mo could do a better job at this than is being done right now. for this reason alone the USA BSE GBR risk assessment should be raised immediately to BSE GBR IV; "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."
for Heavens sake, this is July 27, 2005 and we are just now getting this sample to Weybridge. this reeks !
THEN, to think of GWs BSE MRR policy of trading TSEs of all strains globally. again, USA and North America's BSE GBR should be raised to BSE GBR IV immediately. still very disgusted in bacliff, texas...TSS
Faults in USDA testing cited Mad cow case in Texas showed glaring missteps
By Barry Shlachter, Knight Ridder | August 7, 2005
snip...
What Fong and the public were unaware of was that Ames researchers had also used an experimental rapid version of the IHC test on brain tissue from the Texas cow. That proved positive for the disease, but staff members thought the result was technically flawed. The USDA did not disclose until just recently that the Ames lab had conducted the experimental test.
snip...
Months later, Fong stepped in and ordered more tests. A ''Western blot" test proved positive, as did later tests at a lab in Weybridge, England. Finally in June, two days after the Weybridge lab confirmed the mad cow case, a chastened USDA announced that in addition to the routine IHC test, it was adopting the Western blot procedure whenever an initial ''BioRad" screening test indicates mad cow disease is possible. In addition, backup tests will now be conducted at Britain's national veterinary laboratory in Weybridge when earlier test results conflict or are inconclusive.
http://www.boston.com/news/nation/articles/2005/08/07/faults_in_usda_testing_cited/
NOW, all the above announced July 27, 2005. SO, the other 'inconclusive' sample has been sitting on the shelf since April, some 4 months earlier, give or take a few days. NOW, what has been going on while this other inconclusive BSE/BASE mad cow sits on the shelf.
Lets look at that BSE MRR COMMODITY time frame ;-)
7/20/05 USDA, APHIS, Veterinary Services, National Center for Import and Export: Protocol for The Importation of Farm Raised Cervids from Canada PDF USDA, APHIS, Veterinary Services, National Center for Import and Export: Protocol for The Importation of Camelids from Canada PDF
7/15/05 Importation of Bovines (Cattle or Bison) from Canada for Feeding PDF BSE Minimal-Risk Regions and the Importation of Live Animals Importers, Brokers, and Other Interested Parties PDF BSE Minimal-Risk Regions and the Importation of Live Animals Accredited Veterinarians or Other Interested Parties PDF USDA, APHIS, Veterinary Services, National Center for Import and Export: Protocol for The Importation of Cattle or Bison for Feeding from Canada PDF USDA, APHIS, Veterinary Services, National Center for Import and Export: Protocol for the Importation of Cattle, Bison, Sheep and Goats for Immediate Slaughter from Canada PDF USDA, APHIS, Veterinary Services, National Center for Import and Export: Protocol for the Importation of Sheep and Goats for Feeding from Canada PDF Animal Products Implementation: Bovine Spongiform Encephalopathy; Minimal-Risk Regions and Importation of Commodities from Canada PDF Johanns Announces Next Steps for Importing Canadian Cattle Transcript of Tele-News Conference with Agriculture Secretary Mike Johanns Bovine Spongiform Encephalopathy; Minimal-Risk Regions and Importation of Commodities— FINAL RULE— 9 CFR Parts 93, 94, 95, and 96 [Docket No. 03-080-3] Bovine Spongiform Encephalopathy; Minimal-Risk Regions and Importation of Commodities; Partial Delay of Applicability [Docket No. 03-080-6] — Final rule; partial delay of applicability — 9 CFR Parts 94 and 95 Published March 11, 2005 — 70 FR 12112-12113 Text | PDF • Risk Document PDF • Economic Analysis PDF • Appendices to economic analysis PDF • Final environmental assessment PDF • Final Rule on BSE and Minimal-Risk Regions (Factsheet) • Questions and Answers for Minimal Risk/Canada Rule • Port of Entry for Eligible Ruminants
7/14/05 Secretary Johanns Statement on Ninth Circuit Court Ruling
04/01/05 Canada, Mexico And United States Release Harmonized North American BSE Strategy Harmonization of a BSE Strategy (PDF)
03/17/05 U.S. Government Requests Appeal In Minimal-Risk Rule Case
03/04/05 BSE Minimal-Risk Regions and Importation of Live Animals and Commodities From Canada Delay of Effective Date (Memo)
03/03/05 Statement By Agriculture Secretary Mike Johanns Regarding The Temporary Injunction Issued By The U.S. District Court For The District Of Montana Regarding USDA's Minimal-Risk Rule NOT to forget ; It should be noted that since the enhanced surveillance program began, USDA has also conducted approximately 9,200 routine IHC tests on samples that did not first undergo rapid testing. This was done to ensure that samples inappropriate for the rapid screen test were still tested, and also to monitor and improve upon IHC testing protocols. Of those 9,200 routine tests, one test returned a non-definitive result on July 27, 2005. That sample underwent additional testing at NVSL, as well as at the Veterinary Laboratories Agency in Weybridge, England, and results were negative. ......
http://www.aphis.usda.gov/lpa/issues/bse_testing/test_results.html
r i g h t ............
By Steve Mitchell United Press International Published 2/9/2004 7:06 PM
WASHINGTON, Feb. 9 (UPI) -- The federal laboratory in Ames, Iowa, that conducts all of the nation's tests for mad cow disease has a history of producing ambiguous and conflicting results -- to the point where many federal meat inspectors have lost confidence in it, Department of Agriculture veterinarians and a deer rancher told United Press International. The veterinarians also claim the facility -- part of the USDA and known as the National Veterinary Services Laboratories -- has refused to release testing results to them and has been so secretive some suspect it is covering up additional mad cow cases. ...
http://www.upi.com/view.cfm?StoryID=20040209-061848-3665r
-------- Original Message --------
Subject: re-USDA's surveillance plan for BSE aka mad cow disease
Date: Mon, 02 May 2005 16:59:07 -0500
From: "Terry S. Singeltary Sr."
To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov, contactOIG@hhsc.state.tx.us
Greetings Honorable Paul Feeney, Keith Arnold, and William Busby et al at OIG, ...............
snip...
There will be several more emails of my research to follow. I respectfully request a full inquiry into the cover-up of TSEs in the United States of America over the past 30 years. I would be happy to testify...
Thank you,
I am sincerely,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 xxx xxx xxxx
Date: June 14, 2005 at 1:46 pm PST
In Reply to: Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding further analysis of BSE Inconclusive Test Results posted by TSS on June 13, 2005 at 7:33 pm:
Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days later inclusive Mad Cow is announced.
June 7th 2005 Bill Hawks Under Secretary for Marketing and Regulatory Programs resigns.
Three days later same mad cow found in November turns out to be positive. Both resignation are unexpected.
just pondering...
TSS
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 -0600
From: "Terry S. Singeltary Sr."
To: Carla Everett References: log in to unmask]> <[log in to unmask]
Greetings Carla,still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food chain?
and i see the TEXAS department of animal health is ramping up forsomething, but they forgot a url for update?
I HAVE NO ACTUAL CONFIRMATION YET...
can you confirm???
terry
==============================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Fri, 19 Nov 2004 11:38:21 -0600 From: Carla Everett
To: "Terry S. Singeltary Sr." References: log in to unmask]
The USDA has made a statement, and we are referring all callers to the USDA web site. We have no informationabout the animal being in Texas. Carla
At 09:44 AM 11/19/2004, you wrote:
Greetings Carla, i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from TEXAS. can you comment on this either way please? thank you, Terry S. Singeltary Sr.
===================
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 18:33:20 -0600
From: Carla Everett
To: "Terry S. Singeltary Sr." References: [log in to unmask] [log in to unmask] [log in to unmask] [log in to unmask] [log in to unmask];
our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something.
At 06:05 PM 11/22/2004,
you wrote:
why was the announcement on your TAHC site removed?
Bovine Spongiform Encephalopathy:
November 22: Press Release title here
star image More BSE information
terry
Carla Everett wrote:
no confirmation on the U.S.'inconclusive test...
no confirmation on location of animal.
==========================
UPI Exclusive: No mad cow tests in Wash.
By Steve Mitchell United Press International Published 1/15/2004 2:46 PM
WASHINGTON, Jan. 15 (UPI) -- Federal agriculture officials did not test any commercial cattle for mad cow disease through the first seven months of 2003 in Washington state -- where the first U.S. case of the disease was detected last month -- according to records obtained by United Press International.
The U.S. Department of Agriculture's records of mad cow screenings, conducted on 35,000 animals between 2001 to 2003, also reveal no animals were tested for the past two years at Vern's Moses Lake Meats, the Washington slaughterhouse where the mad cow case was first detected.
In addition, no mad cow tests were conducted during the two-year period at any of the six federally registered slaughterhouses in Washington state. This includes Washington's biggest slaughterhouse, Washington Beef in Toppeni$h -- the 17th largest in the country, which slaughters 290,000 head per year -- and two facilities in Pasco that belong to Tyson, the largest beef slaughtering company in the United States.
In 2002, nearly every test conducted in Washington was on animals from Midway Meats in Centralia, the packing plant where Vern's Moses sent the infected cow carcass. The meat was distributed to several states where some people apparently consumed it, raising concerns about the possibility of contracting the human equivalent of mad cow, an always fatal, brain-wasting condition known as variant Creutzfeldt-Jakob disease. ...
http://www.upi.com/view.cfm?StoryID=20040114-041124-1470r
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
Subject: Canada’s Protocols for BSE Surveillance DOES NOT MANDATE WB CONFIRMATION Date: August 4, 2005 at 1:16 pm PST
Canadian Food Inspection Agency Factsheet
Canada’s Protocols for BSE Surveillance Printer-Friendly PDF version
BSE testing in Canada is in full accordance with the guidelines recommended by the World Organisation for Animal Health (OIE).
The samples collected target the highest risk cattle. This includes animals over 30 months of age that are dead, down, dying or diseased. In addition, any cattle that are exhibiting symptoms consistent with BSE must be reported to the Canadian Food Inspection Agency. This targeted surveillance program is crucial to defining the level of BSE in Canada and to confirming the effectiveness of the measures in place to protect human and animal health from the disease. A robust surveillance program, with strong producer participation, gives domestic and international consumers confidence that Canada is taking responsible actions to monitor the health of the national herd.
In June 2005, Canada exceeded its minimum testing target of 30,000 animals for the year and, as of August 1, more than 36,000 cattle had been tested. The Government of Canada continues to work with provincial governments to support and encourage the participation of Canadian cattle producers in the surveillance program.
Preliminary Testing Procedures In Canada, two rapid BSE screening tests are used for routine surveillance - the Prionics®- Check Western and the Bio-Rad TeSeE®.
Evaluations conducted by the CFIA and agencies in other governments have found the tests to be 100% accurate for detecting BSE in cattle in later stages of the incubation period. Due to the high sensitivity of the tests, there are rare instances in which samples not infected with BSE may produce an initial reaction, thus necessitating re-testing.
Second Round of Testing Initially reactive samples are referred to as “non-negatives”and require that the same test be repeated in duplicate by the screening laboratory.
If the repeat tests are reactive, the sample is considered “inconclusive” for BSE, and the tissue from the animal is forwarded to the National BSE Reference Laboratory, National Centre for Foreign Animal Disease (NCFAD) in Winnipeg for confirmatory testing.
The rapid test on an inconclusive sample is repeated at the National BSE Reference Laboratory and if the test is again reactive, the sample is considered to be a BSE “suspect” and is subject to confirmatory testing. Even if this third rapid test is negative, a confirmatory test (immunohistochemistry or OIE Western Blot) is run for quality assurance purposes.
Confirmatory Testing The immunohistochemistry (IHC) and the OIE Western Blot, also called the SAF Immunoblot, are internationally recognized confirmatory tests for BSE. The IHC is the principle confirmatory test used at NCFAD.
The OIE Western Blot test may be performed on the sample in addition to, or as an alternative to, the IHC test. It is always used on poor quality tissue samples when it may not be possible to conduct the IHC test, or on suspect samples where the IHC is negative.
http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/bseesbsurve.shtml
THIS protocol has a flaw, the word ''or'' should be changed to ''and'';
(immunohistochemistry or OIE Western Blot)
should read ;
(immunohistochemistry AND OIE Western Blot)
WHY ASK for the blunders and the risks by not using WB, as been documented by the USDA et al in the USA???
WHY even go there???
IF the WB picks up detection where the IHC does not, then why are we even discussing this, IF they were truly trying to find and eradicate BSE/TSE$$$
IHC AND WB should be used for confirmation of any inconclusive.
anything less is not a confirmation, it's a guess.
still disgusted in Sunny Bacliff, Texas USA...TSS
Subject: Re: Canada’s Protocols for BSE Surveillance DOES NOT MANDATE WB CONFIRMATION
Date: August 6, 2005 at 10:05 am PST
In Reply to: Canada’s Protocols for BSE Surveillance DOES NOT MANDATE WB CONFIRMATION
posted by TSS on August 4, 2005 at 1:16 pm:
##################### Bovine Spongiform Encephalopathy #####################
Hello Karin,
indeed i did read the last line, i just think any confusion should be eliminated. i think with the word 'or' is just asking for trouble. one persons opinion on a 'poor quality' tissue sample, may not be the same as the next persons opinion. so why even have the potential for confusion there? i am sure you are aware of this, but maybe some other newer members on the list have not read this study;
Effect of Tissue Deterioration on Postmortem BSE Diagnosis by Immunobiochemical Detection of an Abnormal Isoform of Prion Protein
Hiroko HAYASHI1), Masuhiro TAKATA1), Yoshifumi IWAMARU1), Yuko USHIKI1)2), Kumiko M. KIMURA1), Yuichi TAGAWA1), Morikazu SHINAGAWA1) and Takashi YOKOYAMA1)
1) Prion Disease Research Center, National Institute of Animal Health 2) Nippi Research Institute of Biomatrix (Received 25-Aug-2003) (Accepted 14-Jan-2004)
ABSTRACT.
Surveillance for bovine spongiform encephalopathy (BSE) in fallen stock in Japan is conducted with a commercial enzyme-linked immunosorbent assay (ELISA) for mass screening, with Western blotting (WB) and immunohistochemistry performed for confirmation of the ELISA. All tests are based on immunological detection of an abnormal isoform of the prion protein (PrPSc) in brain tissues, which have sometimes deteriorated by the time samples from fallen stock reach a diagnostic laboratory. To evaluate BSE surveillance procedures for fallen stock, we examined PrPSc detection from artificially deteriorated BSE-affected bovine brain tissues with a commercial ELISA kit and compared the results with those of WB. The optical density (OD) values of the ELISA decreased with advancing deterioration of the tissues, whereas no reduction in the signal for PrPSc was observed in WB, even when performed after 4 days of incubation at 37°C. The progressive decrease in the OD values in the ELISA appear to be caused by a partial loss of the N-terminal moiety of PrPSc due to digestion by endogeneous and/or contaminated microbial enzymes, and by the presence of ELISA inhibitors that are generated in deteriorated tissues. These results suggest that WB is the most reliable test for fallen stock, especially for cattle brains within decaying carcasses. KEY WORDS: BSE, ELISA, PrPSc, Western blot
[PDF (96K)] [References]
To cite this article: Hiroko HAYASHI, Masuhiro TAKATA, Yoshifumi IWAMARU, Yuko USHIKI, Kumiko M. KIMURA, Yuichi TAGAWA, Morikazu SHINAGAWA and Takashi YOKOYAMA “Effect of Tissue Deterioration on Postmortem BSE Diagnosis by Immunobiochemical Detection of an Abnormal Isoform of Prion Protein”. J. Vet. Med. Sci.. Vol. 66: 515-520. (2004) .
http://www.jstage.jst.go.jp/article/jvms/66/5/66_515/_article
FULL TEXT PDF;
Another problem in testing fallen stock for BSE may arise from unequal distribution of PrPSc in BSE-affected brains. Spongiform changes and accumulation of PrPSc are most frequently observed in the obex region [15, 18], but, it could be quite difficult to collect the obex region precisely from extensively deteriorated and liquefied brain tissue. Furthermore, in such cases it would be difficult to perform IHC as a confirmation test.
It has been shown that sample autolysis does not affect detection of PrPSc by means of WB [3, 5, 13]. Our WB results also demonstrated no reduction in the PrPSc signal as a result of deterioration at 30*C or 37*C for up to 4 days, as so far examined (Figs. 2A and 3A). In this study, we showed that several problems undermine the utility of the ELISA with deteriorated samples, whereas WB remains very dependable. Therefore, WB might be the only reliable procedure to detect PrPSc in severely damaged samples from fallen stock...
FULL TEXT 6 PAGES;
http://www.jstage.jst.go.jp/article/jvms/66/5/515/_pdf
Karin writes;
I would be more worried about the latest USA suspect where no WB can be done, due to formalin fixation of the sample. I don’t know if the “reference” laboratory in Weybridge has ever missed any BSE-positive cattle (or atypical bovine TSEs), but they have certainly failed to confirm several cases of atypical scrapie, because they insisted on using the so-called validated methods recommended by the OIE before 2003. I hope they now have solved this problem.
===
i agree with this. in fact, the OIE since adhering to GWs BSE MRR policy (minimal risk region), and doing away with the USA, Canada, and Mexico BSE GBR Risk assessments, was anything but 'sound science'. by the OIE adhering to this 'junk science' of this administrations corporate scientists, the OIE has done nothing more than become a commodity brokerage for the legal trading of all phenotypes of TSEs Globally. THEY have in essence done away with 30 years of trying to eradicate TSEs globally. MILLIONS and millions of dollars down the drain, with MILLIONS and millions of humans and animals now becoming exposed even more than before, due to nothing more than greed and the almighty buck. as GW says, ''bring em on''. he will get exactly what he asks for again in the years and decades to come. but, as my birthday card today states;
This birthday you have something to be thankful for (with a picture of GW on the front), I CAN'T RUN AGAIN....................amen!
SO why should he care, he will not be in office, but the markets will be o.k. for now, borders open, and the list of demented and dead will continue to slowly grow even more, with more strains of TSE mutating and being exported throughout the globe... gee thanks GW/OIE!
==============================================
5.1.3. National TSE Veterinary Diagnostic Laboratory Network
The CFIA created a National TSE Veterinary Diagnostic Laboratory Network in 2001 to ensure consistency of diagnostic testing nationally. The network includes CFIA TSE reference laboratories, CFIA and provincial network laboratories. Standard operating procedures (Appendix 4), control material and panels are provided by the federal laboratories as part of a Quality Assurance Program. Training and research are also provided. Quality assurance and biosafety guidelines were distributed early in 2002.
5.2. Diagnostic Tests
All samples are tested by histopathology (H&E) and some are tested by IHC (see Appendix 4 for test standard operating procedures). According to the OIE Manual of Standards (OIE, 2000), surveillance for BSE requires laboratory examination of brain from clinically suspect animals by histopathology and, if necessary, other methods described in the manual (i.e. western blot, scrapie-associated-fibril examination and detection of abnormal PrP by immunohistochemistry).
Prior to the opening of the NCFAD laboratory (1997), testing for BSE was performed at the ADRI, Ottawa. At this laboratory, the validation of IHC using a polyclonal antibody on central nervous tissue began in 1994 and was completed in 1995. Validation of the IHC test for BSE using a monoclonal antibody was carried out at the National BSE Reference Laboratory at NCFAD/CFIA in Winnipeg in 2001 (Czub 2002).
As of January 2002, the provinces of Alberta, Ontario and Saskatchewan have introduced IHC testing in their laboratories. The province of Manitoba has the option to send samples to Saskatchewan for IHC, and the province of Quebec is currently acquiring laboratory capability for IHC testing (Greenwood 2002). To ensure consistency of diagnostic testing across all laboratories, the CFIA initiated a National TSE Veterinary Diagnostic Laboratory Network in 2001 (see Section 5.1.3 for details).
While less than half of Canada’s BSE surveillance samples have historically been tested by IHC (see Table 2), by the end of 2002 more than 90% of all BSE samples will be tested by this method.
Confirmatory testing of a BSE suspect sample is carried out at the National BSE Reference Laboratory at NCFAD/CFIA in Winnipeg.
Rapid Tests:
Rapid tests for BSE diagnosis are not currently used in Canada; however, the CFIA is evaluating certain rapid tests used in Europe. Once the technology has been obtained and standardized in the National BSE Reference Laboratory in Winnipeg, the CFIA will consider application of these tests in the Canadian BSE Surveillance Program.
2In some countries, the terminology “fallen stock” is used for animals described herein as “non-ambulatory” or “animals found dead.”
3Total Cow Population 5,574,000 (dairy cows 1,122,400, beef cows 4,451,600) Source: 1996 Agricultural Census.
http://www.inspection.gc.ca/english/sci/ahra/bseris/bserisb1e.shtml
----- Original Message -----
From: Terry S. Singeltary Sr.
To: Debra.Beasley@aphis.usda.gov
Sent: Tuesday, November 24, 2009 11:01 AM
Subject: OIE has recently published its proposed animal welfare guidelines for public comment
Greetings USDA/APHIS et al,
I would kindly like to comment on OIE proposed guidelines.
AS I said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization. THE reason most every country around the globe came down with BSE/TSE in their cattle, were due to the failed and flawed BSE/TSE testing and surveillance policy of the O.I.E. NOW, they don't even acknowledge atypical scrapie it seems, as one for concern $
Monday, November 23, 2009
BSE GBR RISK ASSESSMENTS UPDATE NOVEMBER 23, 2009 COMMISSION OF THE EUROPEAN COMMUNITIES AND O.I.E.
http://docket-aphis-2006-0041.blogspot.com/2009/11/bse-gbr-risk-assessments-update.html
Tuesday, May 24, 2011 2:24 PM
O.I.E. Terrestrial Animal Health Standards Commission and prion (TSE) disease reporting 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/oie-terrestrial-animal-health-standards.html
IN A NUT SHELL ;
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to then Central Bureau............
http://www.oie.int/eng/Session2007/RF2006.pdf
SO, the OIE BSE MRR status, is based on whatever information and data the given BSE countries give them to go by.
LIKE i have stated time and time again, OIE BSE MRR policy is bought and paid for by your local cattle dealer.
THE BSE MRR policy is nothing more than a legal tool to trade TSE globally.
I urge that the BSE MRR policy be repealed, and the BSE GBR risk assessments be upgraded to include all strains of TSE, including the USA H-BASE, but to even go further, and include all TSE in ALL species. ...TSS
http://madcowtesting.blogspot.com/
Wednesday, November 17, 2010
MAD COW TESTING FAKED IN USA BY Nebraska INSPECTOR Senator Mike Johanns STATE Neb. inspector accused of faking mad cow tests
Published November 17, 2010
http://madcowtesting.blogspot.com/2010/11/mad-cow-testing-faked-in-usa-by.html
Thursday, November 18, 2010
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS
http://bse-atypical.blogspot.com/2010/11/united-states-of-america-vs-galen-j.html
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html
Sunday, June 26, 2011
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html
Thursday, June 2, 2011
USDA scrapie report for April 2011 NEW ATYPICAL NOR-98 SCRAPIE CASES Pennsylvania AND California
http://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html
Monday, June 20, 2011 2011
Annual Conference of the National Institute for Animal Agriculture ATYPICAL NOR-98 LIKE SCRAPIE UPDATE USA
http://nor-98.blogspot.com/2011/06/2011-annual-conference-of-national.html
Monday, June 27, 2011
Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease
http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE
http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html
I strenuously urge the USDA and the OIE et al to revoke the exemption of the legal global trading of atypical Nor-98 scrapie TSE. ...TSS
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep
http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html
Sunday, October 3, 2010
Scrapie, Nor-98 atypical Scrapie, and BSE in sheep and goats North America, who's looking ?
http://nor-98.blogspot.com/2010/10/scrapie-nor-98-atypical-scrapie-and-bse.html
Wednesday, July 06, 2011
Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation
(see tonnage of mad cow feed in commerce USA...tss)
http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html
Monday, June 27, 2011
Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates
http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html
Please see the following warning from CDC about prion TSE consumption in North America ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.
http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html
CANADA GREENS CALL FOR 100% BSE MAD COW TESTING
Greens call for ban on federal GMO research Apr 10, 2011 11:45 PM
snip...
The party said it would also aim to tighten Canada's testing net for bovine spongiform encephalopathy (BSE) in slaughter cattle by implementing "100 per cent" testing of all slaughtered animals, but only "as soon as the process of detecting BSE in blood samples is perfected." The party also calls for ensuring no "animal byproducts" are used in ruminant animal feed....
snip...
http://www.albertafarmexpress.ca/issues/story.aspx?aid=1000407400
Green Party MPs will develop a National Agricultural and Food Policy which:
Improves Food Safety by:
• Amending the Canadian Food Inspection Agency mandate to remove any obligation to promote Canadian agri-business, ensuring the focus is on food safety and food safety only, with enhanced resources for inspection and monitoring.
• Ensuring the quality and wholesomeness of food by strengthening the monitoring of pesticides, herbicides, fungicides, growth hormones, non-therapeutic antibiotics and insecticides in food production, processing and storage, with the goal of an orderly reduction in detectable residues of these substances until they reach undetectable limits.
• Establishing federally funded, community-guided school lunch programs across Canada to ensure that our children have daily access to healthy local food and can learn about sustainable food production and healthy eating.
• Strengthening Plant Protection and Health of Animals Programs with measures to ensure the integrity of farm food products.
• Improving and strengthening the Canadian Organic Standard.
• Providing transitional assistance for those switching to certified organic farming practices.
• Ensuring that no animal by-products are used in ruminant animal feed.
• Strengthen testing for BSE by implementing 100% testing (testing of every slaughtered animal) as soon as the process of detecting BSE in blood samples is perfected.
Vision Green April 2011
http://greenparty.ca/files/attachments/april_2011_vision_green.pdf
THANK YOU !!!
IN THE USA, we use the SSS policy, or the 'don't look, don't find' policy, or what i also call the ''obex only'' diagnostic criteria for how not to find a mad cow. The USA pollutes its oceans, bays, gulf, and rivers, and allows others to pollute them too. Allows industry to pollute the air we breath. Texas has now become the USA nuclear dumping grounds, thanks to our good gov perry. the USA federal gov. dumps all funding for the mad cow TSE prion diseases, while at the same time, human and animal TSE in North America are mutating, spreading, and cpsCJD (classification pending sporadic creutzfeldt jakob disease) is rising in young and old. i don't understand the insanity of it all. ...
All Other Emerging and Zoonotic Infectious Diseases CDC's FY 2012 request of $52,658,000 for all other emerging and zoonotic infectious disease activities is a decrease of $13,607,000 below the FY 2010 level,
which includes the elimination of Prion activities ($5,473,000),
a reduction for other cross-cutting infectious disease activities, and administrative savings. These funds support a range of critical emerging and zoonotic infectious disease programs such Lyme Disease, Chronic Fatigue Syndrome, and Special Pathogens, as well as other activities described below.
http://www.cdc.gov/fmo/topic/Budget%20Information/appropriations_budget_form_pdf/FY2012_CDC_CJ_Final.pdf
" the FY 2010 level, which includes the elimination of Prion activities ($5,473,000), "
USDA MAD COW PROBLEMS SOLVED $$$
Canadian Researchers Receive $2.9 Million to Protect Against Prion Disease Outbreaks, Develop Novel Therapies to Treat Alzheimer’s, Parkinson’s and ALS
Scientists find increasing connection between development of prion disease and common human neurodegenerative disorders
July 13, 2011 (Vancouver, BC) – Collaborative research groups at nine different universities, involving 55 different investigators across Canada, are poised to make significant advances in the understanding of prion and prion-like diseases in humans and animals. These include the development of an oral vaccine to help stop the spread of chronic wasting disease (CWD) in wild deer and elk populations and novel approaches to treat human neurodegenerative disorders like ALS (Lou Gehrig's disease), Alzheimer’s and Parkinson’s diseases, thanks to $2.9 million in funding announced by PrioNet Canada.
The goal of the funding which supports 11 projects is two-fold, explains Dr. Neil Cashman, Scientific Director of PrioNet Canada, one of Canada’s Network of Centres of Excellence. “By working with our partners, we aim to continue to protect Canada against classical prion diseases like chronic wasting disease and mad cow disease (bovine spongiform encephalopathy or BSE), and we’re also providing benefit to Canadians through the development of innovative therapeutics to treat neurodegenerative diseases like Alzheimer’s, Parkinson’s and ALS.”
The researchers will use the funds to better understand the biology of prion disease, to develop strategies to manage prion disease outbreaks and minimize the impacts, and to apply learnings of prion diseases to the treatment of human neurodegenerative disorders.
Prion diseases are fatal, infectious and transmissible diseases of humans and animals associated with a ‘sponge-like’ degeneration of brain tissue. In animals, the most common prion diseases include BSE, scrapie in sheep and goats, and CWD in deer and elk. In 2003, Canada’s beef and related industries were faced with worldwide closing of trade after a domestic case of BSE was found in Alberta. Canada’s economic loss stemming from this event is estimated at more than $6 billion. Some examples of prion diseases in humans include fatal and sporadic familial insomnia, Creutzfeldt-Jakob disease (CJD) and its many varieties, and Kuru. Some examples of the ground-breaking work supported by PrioNet’s recent funding include:
• Immunotherapies to treat ALS: Five PrioNet researchers at the University of British Columbia, University of Alberta and University of Toronto are focusing on a newly-recognized molecular mechanism of ALS, a misfolded protein called SOD-1. By identifying the parts of the protein that are exposed when it is misfolded in disease, researchers are able to design immunotherapies that can target those areas, interrupting the slow progression of paralysis and eventual death characterized by the disorder. Two animal models have already demonstrated responsiveness to the new immunotherapies and work is now underway to develop a therapy for humans. “We are hoping these discoveries could prove to be a magic bullet for ALS,” said Dr. Cashman, who serves as principal investigator for the multi-disciplinary research team.
• Oral vaccine to control chronic wasting disease in the wild: Prion diseases like chronic wasting disease are continuing to spread throughout the Canadian prairie’s wild deer and elk populations and ten PrioNet researchers in Saskatoon and British Columbia are working on an oral vaccine to stop the spread. “The danger is that prion diseases are evolving and new strains are emerging,” noted Dr. Scott Napper, a Research Scientist with the Vaccine and Infectious Disease Organization in Saskatoon and principal investigator on the project. Dr. Napper’s group is focusing on an oral vaccine that can withstand extreme temperatures and will effectively attract elk and deer in the wild. Similar oral vaccines are already used to control rabies in Eastern Canada, where food packets containing the vaccine are widely distributed for consumption by fox and raccoon populations.
• Framework to minimize the impact of chronic wasting disease: Principal investigator Dr. Ellen Goddard from the University of Alberta along with nine co-investigators are working to identify the risk factors associated with chronic wasting disease in wild deer and elk populations, how they can be managed and what public policy recommendations should be put in place to try and mitigate the effects. The primary goal is to monitor the many unknowns that remain about the impact of CWD in the wild, such as the potential risk to hunters who consume infected animals and the potential interface between wild and domestic animals. “The risk management framework around BSE showed that even though countries were aware of the disease in their cattle, they completely underestimated the economic impact and the public response,” notes Dr. Goddard. “We’re doing the work ahead of the game while CWD is still manageable and while effective policies can be put into place to control it, to help anticipate and prevent the impacts.”
• Understanding ‘good versus bad’ prions in order to develop drugs: The first step to designing drugs to treat prion and prion-like diseases is to understand how prion proteins change shape when they become “misfolded” in disease. Dr. Christoph Borchers, a Professor in the Department of Biochemistry and Microbiology and Director of the University of Victoria-Genome BC Proteomics Centre is collaborating with researchers from the University of Alberta and University of Western Ontario to characterize the changes that occur to the three-dimensional structure of prion fibrils (small, nerve-like fibres) as well as the molecular mechanisms that lead to those changes. Using a combination of protein chemistry and mass spectrometry, they are working to explain what occurs when a ‘good’ prion protein changes to a ‘bad’ one during disease development. The information is crucial to designing drugs that can interfere with those changes, effectively curbing the spread of prion and prion-like diseases.
About PrioNet Canada (www.prionetcanada.ca) One of Canada’s Networks of Centres of Excellence, PrioNet Canada is a pan-Canadian research network that is developing strategies to help solve the food, health safety, and socioeconomic problems associated with prion diseases. The network brings together academia, industry, and public sector partners through its multidisciplinary research projects, training programs, events, and commercialization activities to help derive maximum socioeconomic benefits for Canadians. PrioNet is hosted by the University of British Columbia and the Vancouver Coastal Health Research Institute in Vancouver.
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Media information or to set up interviews: Gail Bergman or Christina Vetro Gail Bergman PR Tel: (905) 886-1340 or (905) 886-3345 E-mail: info@gailbergmanpr.com
Last Updated: 7/13/2011 11:27:59 AM
http://www.prionetcanada.ca/detail.aspx?menu=12&dt=293779&app=70&cat1=211&tp=12&lk=no
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.html
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bse-atypical.blogspot.com/2010/08/report-on-investigation-of-sixteenth.html
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bseusa.blogspot.com/2010/08/report-on-investigation-of-seventeenth.html
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31
http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html
Wednesday, December 22, 2010
Manitoba veterinarian has been fined $10,000 for falsifying certification documents for U.S. bound cattle and what about mad cow disease ?
http://usdameatexport.blogspot.com/2010/12/manitoba-veterinarian-has-been-fined.html
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
TSS
Labels: atypical bse, cattle, immunohistochemistry, prion
posted by Terry S. Singeltary Sr. at
4:11 PM
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