Sunday, May 17, 2009

De Novo Generation of Infectious Prions In Vitro Produces a New Disease Phenotype

Sent: Saturday, May 16, 2009 9:49 PM

Subject: De Novo Generation of Infectious Prions In Vitro Produces a New Disease Phenotype

De Novo Generation of Infectious Prions In Vitro Produces a New Disease Phenotype

Marcelo A. Barria1,2, Abhisek Mukherjee1,2, Dennisse Gonzalez-Romero1,2, Rodrigo Morales1,2,3, Claudio Soto1,2*

1 George and Cynthia Mitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, Texas, United States of America, 2 Department of Neurology, University of Texas Houston Medical School, Houston, Texas, United States of America, 3 Facultad de Ciencias, University of Chile, Santiago, Chile

Abstract

Prions are the proteinaceous infectious agents responsible for Transmissible Spongiform Encephalopathies. Compelling evidence supports the hypothesis that prions are composed exclusively of a misfolded version of the prion protein (PrPSc) that replicates in the body in the absence of nucleic acids by inducing the misfolding of the cellular prion protein (PrPC). The most common form of human prion disease is sporadic, which appears to have its origin in a low frequency event of spontaneous misfolding to generate the first PrPSc particle that then propagates as in the infectious form of the disease. The main goal of this study was to mimic an early event in the etiology of sporadic disease by attempting de novo generation of infectious PrPSc in vitro. For this purpose we analyzed in detail the possibility of spontaneous generation of PrPSc by the protein misfolding cyclic amplification (PMCA) procedure. Under standard PMCA conditions, and taking precautions to avoid cross-contamination, de novo generation of PrPSc was never observed, supporting the use of the technology for diagnostic applications. However, we report that PMCA can be modified to generate PrPSc in the absence of pre-existing PrPSc in different animal species at a low and variable rate. De novo generated PrPSc was infectious when inoculated into wild type hamsters, producing a new disease phenotype with unique clinical, neuropathological and biochemical features. Our results represent additional evidence in support of the prion hypothesis and provide a simple model to study the mechanism of sporadic prion disease. The findings also suggest that prion diversity is not restricted to those currently known, and that likely new forms of infectious protein foldings may be produced, resulting in novel disease phenotypes.

Citation: Barria MA, Mukherjee A, Gonzalez-Romero D, Morales R, Soto C (2009) De Novo Generation of Infectious Prions In Vitro Produces a New Disease Phenotype. PLoS Pathog 5(5): e1000421. doi:10.1371/journal.ppat.1000421 Editor: David Westaway, University of Alberta, Canada Received April 7, 2008; Accepted April 9, 2009; Published May 15, 2009 Copyright:  2009 Barria et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Funding: This work was supported by grants from the National Institute of Neurological Disorders (R01 NS49173), the National Institute of Allergy and Infectious Diseases (P01 AI77774) and the National Institute of Aging (P01 AG14359). None of the sponsors or funders played any role in the design and conduct of the study, in the collection, analysis, and interpretation of the data, or in the preparation, review, or approval of the manuscript. Competing Interests: Dr. Soto is an inventor on the PMCA technology and a Founder, Vice-President and Chief Scientific Officer of Amprion Inc, a biotech company focusing on the development of early and sensitive diagnosis for prion diseases and other disorders involving protein misfolding. * E-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000223/!x-usc:mailto:claudio.soto@uth.tmc.edu

Discussion

In this study we report spontaneous generation of PrPSc in vitro using a modified PMCA procedure with brain homogenate substrate. Misfolded protein was produced in two different animal species without the need to add seeds of in vivo generated PrPSc. At present it is unclear whether PMCA replicated a PrPSc intermediate already present in the brain homogenate or rather ‘‘spontaneous’’ misfolding was induced by the amplification cycles. In this context, a recent study reported the presence of small quantities of a PrPSc-like protein in healthy brains [20], but it is yet unknown whether this protein is infectious.

Although de novo prion formation was achieved before by PMCA using purified proteins in the presence of synthetic polyanions [4], the purpose of our study was to evaluate whether de novo generation of prions is possible under standard PMCA conditions. This is important to assess the validity of using PMCA for prion diagnosis. Another aim was to study whether different species of animals have a distinct propensity to form spontaneous prions under a given set of conditions. Finally, we aimed to characterize the newly generated infectivity and to show that the diversity of prions is perhaps larger than we currently think. Our results indicate that standard PMCA rounds consisting of 144 cycles (or less) did not show spontaneous formation of PrPSc, but longer rounds of 240 cycles were successful in replicating or generating misfolded protein. These findings suggest that de novo formation of PrPSc can be experimentally distinguished from replication of pre-formed PrPSc, indicating that the biochemical, conformational or stability properties of the PrP structures involved in both processes are probably different. Therefore, PMCA can be adapted to produce de novo generated PrPSc and it is likely that more drastic modifications of the procedure may lead to higher rates of spontaneous prion formation. Indeed, the higher rate of de novo PrPSc formation reported in the study by Deleault and colleagues, who used only 48 PMCA cycles per round [4], indicates that using polyanions and purified PrPC may favor spontaneous prion formation, suggesting that some factors in brain homogenate may prevent PrP misfolding.

Our data support the use of PMCA, (under conditions in which PrPSc de novo generation does not occur), for biochemical detection of prions and its potential application for TSE diagnosis. The usefulness of PMCA for highly sensitive and specific detection of prions in biological fluids, has been demonstrated by studies from us and other groups [21–25].

Strikingly, the rate and number of PMCA cycles required to produce de novo PrPSc was variable in distinct species. Considering that from the species studied humans are the only one in which sporadic disease is known to occur, we were surprised that de novo PrPSc was never obtained with human brain homogenates under the experimental conditions used. This contrast with the high levels of amplification of human PrPSc observed in samples seeded with vCJD (Fig. S1) or various sCJD brain homogenates (data not shown). The absence of spontaneous formation of PrPres in humans may be due to the different conditions for the preparation of the tissue, including several hours of post-mortem delay or the lack of perfusion before collection of the brain. However, this is unlikely, because similar results were obtained using brains of transgenic mice expressing human PrP subjected to the same conditions to prepare brain than the other rodent species. Our interpretation of these results is that human PrPC has a lower propensity to initiate misfolding than the rodent protein. The alternative explanation that factors present in the human brain may prevent conversion is unlikely considering the experiments with humanized transgenic mice. The appearance of sporadic disease in humans may simply reflect the longer life span that provides greater chances for stochastic processes of spontaneous misfolding. However, it is also possible that sporadic disease is actually more frequent in animals, because the rate of spontaneous illness in animals has not been systematically studied.

Several lines of evidence enable us to rule out the possibility that de novo PrPSc was the result of cross-contamination. First of all, conventional PMCA that allows us to amplify as little as a single particle of PrPSc did not show spontaneous formation of misfolded protein, even after extensive PMCA cycling (Fig. 1). Second, the rate of spontaneous generation of prions in different species does not correlate with the availability of infectious material in our lab. Moreover, the variable rate was surprisingly constant among different experiments, arguing that it is dependent on some intrinsic properties of the protein rather than a stochastic event as cross-contamination. Third, an experiment done using strictly prion-free equipment and reagents, performed in a new laboratory that was never exposed to prions and done by a person who has never been in contact with prion material showed very similar results as the one carried out in our standard facilities. Finally, the biochemical, structural and biological properties of de novo generated PrPSc in hamster were substantially different to those of various conventional hamster prion strains. Although all these evidences strongly indicate that the results are not due to crosscontamination, this possibility cannot entirely be ruled out.

Inoculation of wild type hamsters with de novo generated PrPSc produced disease in all animals. Strikingly, many of the disease characteristics were substantially different to those observed with several other hamster prion strains. In this study we directly compared PGP-h1 with 3 well-established strains (263K, HY and DY) and literature comparisons with other strains such as Sc237, SHa(Me7), MT-C5, SHa(RML), 139H and Me7-H, also show substantial differences [26,27]. It is important to note that PMCA amplification of PrPSc from various strains (of hamsters, mice, human or deer origin) faithfully propagates the strain characteristics [8–10,28,29]. Thus, the differences observed in the de novo generated material are not attributable to PMCA amplification, but to intrinsic differences of this new prion strain. In our direct comparisons the incubation time of PGP-h1 was significantly larger than 263K and HY strains, but much shorter than DY. Clinical signs were also clearly distinguishable from those observed in animals affected by other strains (see Video S1 and Video S2 in supporting online material). The animals inoculated with PGP-h1 were not hyperactive or aggressive, but not lethargic either. They exhibited a social withdrawal and lack of interest for the surroundings, which reflected in a much reduced horizontal and vertical activity and increased extent of inactive time in an open field test. The clinical differences on the PGP-h1 induced disease were likely the result of the severe brain damage produced, including extensive spongiform degeneration, PrPSc accumulation and brain inflammation. Remarkably, the brain areas targeted by vacuolation damage were significantly different from all other hamster strains studied and included a substantially greater extent of spongiosis in colliculus and a much reduced level of injury in cerebellum and cortex. The biochemical characteristics of PrPSc were also different in PGP-h1, mostly in terms of the higher quantity of PrPSc accumulated in the brain and the lower relative resistance to proteolytic degradation than the other hamster strains analyzed. Taken together this data demonstrate that de novo generated prions correspond to a novel strain of infectious material, able to generate a new disease in wild type animals. We are currently assessing the infectious properties of some of the other de novo generated PrPSc obtained in this study to examine whether or not new strains and new diseases are produced also in other species.

Our findings provide a model to study the possible origins of sporadic TSEs and a new avenue to investigate the mechanism and factors controlling spontaneous formation of infectious material. For example, using the modified PMCA reaction described in this study we could assess the sequence determinants of the variable propensity of PrPC in distinct species to undergo conversion into the pathological form. We could also study the contribution of other factors in brain to alter the rate of de novo generation of PrPSc. Finally, our data provides further support for the prion hypothesis, since misfolded and infectious protein was generated in vitro, without the need for addition of pre-existing PrPSc. The fact that the de novo generated PrPSc corresponds to a new strain of infectious material suggest that the diversity of alternative and transmissible foldings that PrPSc can adopt is much larger than usually thought. This is worrisome, because it raises the possibility that novel and perhaps more aggressive infectious prion foldings may spontaneously originate in diverse species, leading to the emergence of new and unpredictable forms of transmissible diseases.


http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2675078&blobtype=pdf



Subject: USDA, SPONTANEOUS MAD COW DISEASE, THE TOOTH FAIRY AND SANTA CLAUS

Date: June 12, 2006 at 5:18 am PST

IF we all believe the BSe that the USDA is trying to put out now about atypical BSE in USA cattle just arising spontaneously, then we all should believe in the tooth fairy and santa claus as well.

IF USA scrapie transmitted to USA cattle long ago in experiments in a lab in Mission Texas did not produce UK BSE, but something very different, then why would USA TSE cattle produce the UK human version of mad cow i.e. nvCJD? IT wouldn't. USA sporadic cjd is increasing, the USA also has atypical human cases of unknown origin as well?

THERE are over 20 strains of scrapie, plus the atypical in sheep, and these strains are increasing in numbers.

SCRAPIE, CWD, AND TSE IN CATTLE i.e. ANIMAL TSE RAMPANT IN USA FOR DECADES, and amplified via rendering and feeding practices, where USDA triple firewalls against BSE were nothing more than a mere smoke screen.

NO test tube TSE by either Prusiner or Soto, to date, have ever produced a TSE identical to the sporadic CJD. IN fact, no test tube TSE has ever been produced that resembles _any_ natural field TSE.

IF you feed BSE tainted materials to cattle and primate, you have BSE and nvCJD. IF you feed USA sheep strain to USA cattle, you get USA TSE. IF you feed USA tainted cattle to humans, you get USA mad cow disease. IF you feed sporadic CJD to primate you get a CJD infected primate. NOTHING spontaneous about it at all.

USA is in a very unique situation. there are more documented TSE in different species than any other country, all of which have been rendered and fed back to animals for human and animal consumption, for decades. Millions exposed, and of these Millions, how many surgical and dental procedures have been done on these exposed, to pass on to others, via the 'friendly fire' mode of transmission?

IF, the spontaneous TSE was true, then this would be Prusiner and everyone else that is trying to cash in on this agent with there TSE rapid test, this would be there dream come true. IT would require mandatory BSE/TSE testing of all species, due to the fact you could not ever eradicate it through any intervention. BUT, then again, the spontaneous TSE is like believing in the tooth fairy or santa clause will be arriving at your house this year.

How long can this sharade continue $

How many more will become exposed and have to die $

snip...


http://www.prwatch.org/node/4883



http://scienceblogs.com/aetiology/2006/06/emerging_disease_and_zoonoses_8.php



DEADLY FEAST RICHARD RHODES 1997

EVEN the origin of sporadic CJD continues to be debated. A British researcher, Dr. Richard Kimberlin, points out that the age-specific incidence of sporadic CJD: is similar to the age-specific incidence of BSE.

snip...

Kimberlin argues that the bell curve of sporadic CJD indicates that this seemingly random human disease is probably also caused by infection: "The shape of the age-specific incidence curve... implies that infection with [a] common strain [of CJD] occurs in childhood or adolescence, and that the median incubation period is 40 to 50 years."

German researcher Dr. Heino Diringer similarly defends an infectious cause: "It seems more than likely that ... the sporadic cases of CJD always originate from direct or indirect transmission from animals to man."

END

1: EMBO J. 2002 Dec 2;21(23):6358-66. Links BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein.Asante EA, Linehan JM, Desbruslais M, Joiner S, Gowland I, Wood AL, Welch J, Hill AF, Lloyd SE, Wadsworth JD, Collinge J. MRC Prion Unit, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK.

Variant Creutzfeldt-Jakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrP(Sc) type 2. These data suggest that more than one BSE-derived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure.


http://www.ncbi.nlm.nih.gov/pubmed/12456643



http://www.neurology.org/cgi/eletters/60/2/176



2009

Monday, May 11, 2009

Rare BSE mutation raises concerns over risks to public health


http://bse-atypical.blogspot.com/2009/05/rare-bse-mutation-raises-concerns-over.html



Rare BSE mutation raises concerns over risks to public health

SIR - Atypical forms (known as H- and L-type) of bovine spongiform encephalopathy (BSE) have recently appeared in several European countries as well as in Japan, Canada and the United States. This raises the unwelcome possibility that variant Creutzfeldt-Jakob disease (vCJD) could increase in the human population. Of the atypical BSE cases tested so far, a mutation in the prion protein gene (PRNP) has been detected in just one, a cow in Alabama with BSE; her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008). This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine-human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks. Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000223/!x-usc:mailto:maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA

NATUREVol 45726 February 2009


http://www.nature.com/nature/journal/v457/n7233/full/4571079b.html



Sunday, May 10, 2009

Identification and characterization of bovine spongiform encephalopathy cases diagnosed and not diagnosed in the United States


http://bse-atypical.blogspot.com/2009/05/identification-and-characterization-of.html



Wednesday, February 11, 2009

Atypical BSE North America Update

February 2009

Both of the BSE cases ascertained in the US native-born cattle were atypical cases (H-type), which contributed to the initial ambiguity of the diagnosis. 174, 185 In Canada, there have been 2 atypical BSE cases in addition to the 14 cases of the classic UK strain of BSE2: one was the H-type, and the other was of the L-type.198 snip...end source : Enhanced Abstract Journal of the American Veterinary Medical Association January 1, 2009, Vol. 234, No. 1, Pages 59-72 Bovine spongiform encephalopathy Jane L. Harman, DVM, PhD; Christopher J. Silva, PhD


http://avmajournals.avma.org/doi/ref/10.2460/javma.234.1.59



Atypical BSE North America Update February 2009


http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.html



Thursday, April 30, 2009 FDA Issues Final Guidance for Renderers on Substances Prohibited From Use in Animal Food or Feed CVM Update Back April 30, 2009


http://madcowfeed.blogspot.com/2009/04/fda-issues-final-guidance-for-renderers.html



Sunday, May 10, 2009

Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)


http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html



April 20, 2009

National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)

National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)

Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD 1996 & earlier 42 32 28 4 0 0 1997 115 68 59 9 0 0 1998 93 53 45 7 1 0 1999 115 69 61 8 0 0 2000 151 103 89 14 0 0 2001 210 118 108 9 0 0 2002 258 147 123 22 2 0 2003 273 176 135 41 0 0 2004 335 184 162 21 0 13 2005 346 193 154 38 1 0 2006 380 192 159 32 0 14 2007 370 212 185 26 0 0 2008 383 228 182 23 0 0 TOTAL 30715 17756 1490 254 4 2 1 Listed based on the year of death or, if not available, on year of referral; 2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted; 3 Disease acquired in the United Kingdom; 4 Disease acquired in Saudi Arabia; 5 Includes 20 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 25 cases with type determination pending in which the diagnosis of vCJD has been excluded. Rev 2/13/09 National


http://www.cjdsurveillance.com/pdf/case-table.pdf



http://www.cjdsurveillance.com/resources-casereport.html



http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45



*5 Includes 20 cases in which the diagnosis is pending, and 17 inconclusive cases; *6 Includes 25 cases with type determination pending in which the diagnosis of vCJD has been excluded.


Greetings,

it would be interesting to know what year these atypical cases occurred, as opposed to lumping them in with the totals only.

are they accumulating ?

did they occur in one year, two years, same state, same city ?

location would be very interesting ?

age group ?

sex ?

how was it determined that nvCJD was ruled out ?

from 1997, the year i started dealing with this nightmare, there were 28 cases (per this report), up until 2007 where the total was 185 cases (per this report), and to date 2008 is at 182. a staggering increase in my opinion, for something that just happens spontaneously as some would have us believe. i don't believe it, not in 85%+ of all sporadic CJD cases. actually, i do not believe yet that anyone has proven that any of the sporadic CJD cases have been proven to be a spontaneous misfolding of a protein. there are many potential routes and sources for the sporadic CJD's. ...TSS


Sunday, April 12, 2009

r-calf and the USA mad cow problem, don't look, don't find, and then blame Canada


http://prionunitusaupdate2008.blogspot.com/2009/04/r-calf-and-usa-mad-cow-problem-dont.html



snip...


SEE FULL TEXT BELOW !

Monday, April 20, 2009 National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)


http://prionunitusaupdate2008.blogspot.com/2009/04/national-prion-disease-pathology.html



Friday, November 30, 2007

CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION

snip...

i am reminded of a few things deep throat told me years ago;


=================================================2001


The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people......... Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie..... why???? than the UK... then would the same mechanisms that make different strains of scrapie here make different strains of BSE... if the patterns are different in sheep and mice for scrapie..... could not the BSE be different in the cattle, in the mink, in the humans....... I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........ bse..... scrapie


Scrape the damn slide and put it into mice..... wait..... chop up the mouse brain and and spinal cord........ put into some more mice..... dammit amplify the thing and start the damned research..... This is NOT rocket science... we need to use what we know and get off our butts and move.... the whining about how long everything takes..... well it takes a whole lot longer if you whine for a year and then start the research!!!



Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde..... for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a year....... it is a big fat sponge... the agent continues to eat the brain ...... you can't make slides anymore because the agent has never stopped........ and the old slides that are stained with Hemolysin and Eosin...... they get holier and holier and degenerate and continue... what you looked at 6 months ago is not there........ Gambetti better be photographing every damned thing he is looking at.....



Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at.......... USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........ if you want to move this thing along and shake the earth.... then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........ I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........ forget any action........ it is ALL gonna be sporadic!!! And, if there is a case....... there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats.... and this may be their biggest downfall...



Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here.......... knocked me out of my chair........ you must keep pushing. If I was a power person.... I would be demanding that there be at least a million bovine tested as soon as possible and agressively seeking this disease. The big players are coming out of the wood work as there is money to be made!!!



In short: "FIRE AT WILL"!!! for the very dumb.... who's "will"! "Will be the burden to bare if there is any coverup!"



again it was said years ago and it should be taken seriously.... BSE will NEVER be found in the US!



As for the BSE conference call... I think you did agreat service to freedom of information and making some people feign integrity... I find it scary to see that most of the "experts" are employed by the federal government or are supported on the "teat" of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.



You need to watch your back........ but keep picking at them....... like a buzzard to the bone... you just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself... you ask the questions that everyone else is too afraid to ask.)



================================================



greetings again voice,

then i remind everyone to read this;

'As implied in the Inset 25 we must not assume that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.'



http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf



Saturday, May 2, 2009

U.S. GOVERNMENT SUES WESTLAND/HALLMARK MEAT OVER USDA CERTIFIED DEADSTOCK DOWNER COW SCHOOL LUNCH PROGRAM



http://downercattle.blogspot.com/2009/05/us-government-sues-westlandhallmark.html



Sunday, May 17, 2009

WHO WILL WATCH THE CHILDREN ? SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE



http://downercattle.blogspot.com/2009/05/who-will-watch-children.html



CWRU CJD QUESTIONNAIRE HISTORY


http://cjdquestionnaire.blogspot.com/



Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

Labels: , , , , ,

Monday, May 11, 2009

Rare BSE mutation raises concerns over risks to public health

Rare BSE mutation raises concerns over risks to public health

SIR — Atypical forms (known as H- and L-type) of bovine spongiform encephalopathy (BSE) have recently appeared in several European countries as well as in Japan, Canada and the United States. This raises the unwelcome possibility that variant Creutzfeldt–Jakob disease (vCJD) could increase in the human population. Of the atypical BSE cases tested so far, a mutation in the prion protein gene (PRNP) has been detected in just one, a cow in Alabama with BSE; her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008). This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine–human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks. Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA

NATUREVol 45726 February 2009


http://www.nature.com/nature/journal/v457/n7233/full/4571079b.html



Sunday, May 10, 2009

Identification and characterization of bovine spongiform encephalopathy cases diagnosed and not diagnosed in the United States


http://bse-atypical.blogspot.com/2009/05/identification-and-characterization-of.html



Wednesday, February 11, 2009 Atypical BSE North America Update February 2009 Both of the BSE cases ascertained in the US native-born cattle were atypical cases (H-type), which contributed to the initial ambiguity of the diagnosis. 174, 185 In Canada, there have been 2 atypical BSE cases in addition to the 14 cases of the classic UK strain of BSE2: one was the H-type, and the other was of the L-type.198 snip...end source : Enhanced Abstract Journal of the American Veterinary Medical Association January 1, 2009, Vol. 234, No. 1, Pages 59-72 Bovine spongiform encephalopathy Jane L. Harman, DVM, PhD; Christopher J. Silva, PhD


http://avmajournals.avma.org/doi/ref/10.2460/javma.234.1.59



Atypical BSE North America Update February 2009


http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.html



Thursday, April 30, 2009 FDA Issues Final Guidance for Renderers on Substances Prohibited From Use in Animal Food or Feed CVM Update Back April 30, 2009


http://madcowfeed.blogspot.com/2009/04/fda-issues-final-guidance-for-renderers.html



Sunday, May 10, 2009

Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)


http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html




April 20, 2009

National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)

National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)

Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD 1996 & earlier 42 32 28 4 0 0 1997 115 68 59 9 0 0 1998 93 53 45 7 1 0 1999 115 69 61 8 0 0 2000 151 103 89 14 0 0 2001 210 118 108 9 0 0 2002 258 147 123 22 2 0 2003 273 176 135 41 0 0 2004 335 184 162 21 0 13 2005 346 193 154 38 1 0 2006 380 192 159 32 0 14 2007 370 212 185 26 0 0 2008 383 228 182 23 0 0 TOTAL 30715 17756 1490 254 4 2 1 Listed based on the year of death or, if not available, on year of referral; 2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted; 3 Disease acquired in the United Kingdom; 4 Disease acquired in Saudi Arabia; 5 Includes 20 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 25 cases with type determination pending in which the diagnosis of vCJD has been excluded. Rev 2/13/09 National


http://www.cjdsurveillance.com/pdf/case-table.pdf



http://www.cjdsurveillance.com/resources-casereport.html



http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45



*5 Includes 20 cases in which the diagnosis is pending, and 17 inconclusive cases; *6 Includes 25 cases with type determination pending in which the diagnosis of vCJD has been excluded. Greetings, it would be interesting to know what year these atypical cases occurred, as opposed to lumping them in with the totals only. are they accumulating ? did they occur in one year, two years, same state, same city ? location would be very interesting ? age group ? sex ? how was it determined that nvCJD was ruled out ? from 1997, the year i started dealing with this nightmare, there were 28 cases (per this report), up until 2007 where the total was 185 cases (per this report), and to date 2008 is at 182. a staggering increase in my opinion, for something that just happens spontaneously as some would have us believe. i don't believe it, not in 85%+ of all sporadic CJD cases. actually, i do not believe yet that anyone has proven that any of the sporadic CJD cases have been proven to be a spontaneous misfolding of a protein. there are many potential routes and sources for the sporadic CJD's. ...TSS Sunday, April 12, 2009 r-calf and the USA mad cow problem, don't look, don't find, and then blame Canada


http://prionunitusaupdate2008.blogspot.com/2009/04/r-calf-and-usa-mad-cow-problem-dont.html



snip...


SEE FULL TEXT BELOW ! Monday, April 20, 2009 National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)


http://prionunitusaupdate2008.blogspot.com/2009/04/national-prion-disease-pathology.html



Friday, November 30, 2007


CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION


snip...


i am reminded of a few things deep throat told me years ago;


=================================================2001


The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people......... Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie..... why???? than the UK... then would the same mechanisms that make different strains of scrapie here make different strains of BSE... if the patterns are different in sheep and mice for scrapie..... could not the BSE be different in the cattle, in the mink, in the humans....... I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........ bse..... scrapie

Scrape the damn slide and put it into mice..... wait..... chop up the mouse brain and and spinal cord........ put into some more mice..... dammit amplify the thing and start the damned research..... This is NOT rocket science... we need to use what we know and get off our butts and move.... the whining about how long everything takes..... well it takes a whole lot longer if you whine for a year and then start the research!!!

Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde..... for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a year....... it is a big fat sponge... the agent continues to eat the brain ...... you can't make slides anymore because the agent has never stopped........ and the old slides that are stained with Hemolysin and Eosin...... they get holier and holier and degenerate and continue... what you looked at 6 months ago is not there........ Gambetti better be photographing every damned thing he is looking at.....

Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at.......... USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........ if you want to move this thing along and shake the earth.... then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........ I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........ forget any action........ it is ALL gonna be sporadic!!! And, if there is a case....... there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats.... and this may be their biggest downfall...

Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here.......... knocked me out of my chair........ you must keep pushing. If I was a power person.... I would be demanding that there be at least a million bovine tested as soon as possible and agressively seeking this disease. The big players are coming out of the wood work as there is money to be made!!!

In short: "FIRE AT WILL"!!! for the very dumb.... who's "will"! "Will be the burden to bare if there is any coverup!"

again it was said years ago and it should be taken seriously.... BSE will NEVER be found in the US!

As for the BSE conference call... I think you did agreat service to freedom of information and making some people feign integrity... I find it scary to see that most of the "experts" are employed by the federal government or are supported on the "teat" of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.

You need to watch your back........ but keep picking at them....... like a buzzard to the bone... you just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself... you ask the questions that everyone else is too afraid to ask.)


================================================


greetings again voice,

then i remind everyone to read this;

'As implied in the Inset 25 we must not assume that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.'


http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf



CWRU CJD QUESTIONNAIRE HISTORY


http://cjdquestionnaire.blogspot.com/




Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518

Labels: , , , , ,

Sunday, May 10, 2009

Identification and characterization of bovine spongiform encephalopathy cases diagnosed and not diagnosed in the United States

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Diseases of Livestock

Title: Identification and characterization of two bovine spongiform encephalopathy cases diagnosed in the United States

Authors

Richt, Juergen Kunkle, Robert Alt, David Nicholson, Eric Hamir, Amirali Czub, Stefanie - NATL BSE REF LAB,MANITOBA Kluge, John - NVSL, APHIS, USDA, AMES, Davis, Arthur - NVSL, APHIS, USDA, AMES, Hall, S Mark - NVSL, APHIS, USDA, AMES,

Submitted to: Journal of Veterinary Diagnostic Investigation Publication Type: Peer Reviewed Journal Publication Acceptance Date: October 20, 2006 Publication Date: March 1, 2007 Citation: Richt, J.A., Kunkle, R.A., Alt, D., Nicholson, E.M., Hamir, A.N., Czub, S., Kluge, J., Davis, A.J., Hall, S.M. 2007. Identification and characterization of two bovine spongiform encephalopathy cases diagnosed in the United States. Journal of Veterinary Diagnostic Investigation. 19(2):142-154.

Interpretive Summary: Bovine spongiform encephalopathy (BSE), also known as "mad cow disease," is a transmissible spongiform encephalopathy of cattle, first detected in 1986 in the United Kingdom and subsequently in other countries. Here we report the identification and characterization the two cases of BSE diagnosed in the United States. BSE case 1 (12/2003) and BSE case 2 (11/2004) were identified and characterized using various diagnostic methods specific for BSE (rapid test, Western blot, immunohistochemistry). Sequencing of the prion protein gene of both BSE-positive animals revealed that the sequences of both cattle were similar as previously reported for cattle. These results confirm that two cases of BSE have been identified in the United States so far: one in a cow imported from Canada and one in a cow born and raised in Texas. Technical Abstract: Bovine spongiform encephalopathy (BSE) is a transmissible spongiform encephalopathy of cattle, first detected in 1986 in the United Kingdom and subsequently in other countries. It is the most likely cause of variant Creutzfeldt-Jakob disease (vCJD) in humans, but the origin of BSE has not been elucidated so far. Here we report the identification and characterization of the two cases of BSE diagnosed in the United States. Case 1 (12/2003) revealed spongiform changes in the obex area of the brainstem and the presence of the abnormal form of the prion protein, PrP**Sc, in the same brain area, by immunohistochemistry and Western blot analysis. Initial suspect diagnosis of BSE for case 2 (11/2004) was made by a rapid ELISA-based BSE test. Case 2 did not reveal unambiguous spongiform changes in the obex area, but PrP**Sc was detected by immunohistochemistry and enrichment Western Blot analysis in the obex. Using Western blot analysis, PrP**Sc from case 1 showed molecular features similar to typical BSE isolates, whereas PrP**Sc from case 2 revealed an unusual molecular PrP**Sc pattern: molecular mass of the unglycosylated and monoglycosylated isoform was higher than that of typical BSE isolates and case 2 was strongly labeled with antibody P4, which is consistent with a higher molecular mass. Sequencing of the prion protein gene of both BSE-positive animals revealed that the sequences of both animals were within the range of the prion protein gene sequence diversity previously reported for cattle.

Project Team

Kunkle, Robert Kehrli, Marcus Nicholson, Eric Greenlee, Justin Hamir, Amirali

Publications

Publications

Related National Programs

Animal Health (103)

Patents

Method For Detecting A Gene Linked To Mad Cow Disease

Last Modified: 05/09/2009



http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=193457



Research Project: Genetic and Biological Determinants of Respiratory Disease Susceptibility Location: Animal Health Systems Research

Title: Association of a bovine prion gene haplotype with atypical BSE

Author

Clawson, Michael

Submitted to: Meeting Abstract Publication Type: Abstract Publication Acceptance Date: December 2, 2008 Publication Date: January 1, 2009 Citation: Clawson, M.L. 2009. Association of a bovine prion gene haplotype with atypical BSE [abstract]. Plant and Animal Genomes XVII Conference. Abstract No. W091. Available: http://www.intl-pag.org/17/abstracts/

Technical Abstract: Transmissible spongiform encephalopathies (TSEs), also known as prion diseases, are a class of fatal neurodegenerative disorders that occur in humans, ruminants, cats, and mink. Three distinct TSEs afflict cattle: classical bovine spongiform encephalopathy (BSE), atypical H-type BSE, and atypical L-type BSE. Classical BSE was identified in the 1980s and is acquired by cattle through the consumption of feed contaminated with the infectious prion agent. Atypical BSEs have only recently been recognized as distinct cattle prion diseases and are extremely rare. The full extent of genetic susceptibilities to atypical BSEs is unknown; however, one atypical H-type case identified in the United States (2006) was most likely caused by a genetic mutation in the prion gene, E211K. We have identified an association of a bovine prion DNA haplotype with atypical BSE that is independent of E211K. The haplotype spans a portion of the prion gene that includes part of intron 2, the entire coding region of exon 3, and part of the three prime untranslated region of exon 3 (13 kb). Despite the low frequency of this haplotype among general cattle populations, it was present in a majority of H- and L-type atypical BSE cases from Canada, France, and the United States. This result indicates that there is a genetic component to atypical BSE susceptibility in addition to E211K.



http://www.ars.usda.gov/research/publications/Publications.htm?seq_no_115=234699



BSE in an Alabama cow

On March 13, 2006, the U.S. Department of Agriculture (USDA) announced the confirmation of bovine spongiform encephalopathy (BSE) in a cow in Alabama. This is the eighth confirmed case of BSE in North American cattle and the second case since the beginning of 2006. Three cases were detected in the United States and five in Canada. One of the two previous U.S. cases was of Canadian origin, and the first of the five cases detected in Canada was in a cow that had been imported from the United Kingdom.

The newly confirmed case was identified in a non-ambulatory (downer) cow on a farm in Alabama. The animal was euthanized by a local veterinarian and buried on the farm. USDA surveillance is targeted at those animal populations in which BSE would most likely be found. These animals primarily include clinically abnormal or deceased cattle, which would not be expected to enter the human food supply. The cow in Alabama did not enter either the animal or the human food chains, according to the USDA announcement. USDA is working with Alabama animal health officials to conduct an epidemiologic investigation to gather additional information about the age and herd of origin of this animal, which had resided on the Alabama farm for less than a year.

The agency also will work to identify other cows born in the same herd within one year of the affected animal, and any offspring. In addition, USDA is working with Food and Drug Administration (FDA) officials to determine any feed history that may be relevant to the investigation. "Experience worldwide has shown us that it is highly unusual to find BSE in more than one animal in a herd or in an affected animal's offspring. Nevertheless, all animals of interest will be tested for BSE," according to the USDA statement.

BSE is a progressive neurological disorder of cattle that results from infection by an unconventional transmissible agent. Strong evidence indicates that BSE has been transmitted to humans, primarily in the United Kingdom, causing a variant form of Creutzfeldt-Jakob disease (vCJD). As of March 2006, a total of 190 cases of vCJD have been reported worldwide; of these, 160 occurred in the United Kingdom. Two cases have been reported in the United States; for both of these cases, there was clear epidemiologic evidence that the disease was acquired in the United Kingdom.

For additional information about the newly confirmed BSE case, see the USDA announcement available on the USDA website at www.usda.gov.

Date: March 15, 2006 Content source: National Center for Infectious Diseases



http://www.cdc.gov/ncidod/dvrd/bse/news/alabama_cow_031506.htm



BSE ALABAMA



http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/EPI_Final5-2-06.pdf



BSE Case Associated with Prion Protein Gene Mutation

Jürgen A. Richt1¤*, S. Mark Hall2

1 National Animal Disease Center, United States Department of Agriculture, Agriculture Research Service, Ames, Iowa, United States of America, 2 National Veterinary Services Laboratories, Pathobiology Laboratory, Animal and Plant Health Inspection Service, United States Department of Agriculture, Ames, Iowa, United States of America

Abstract Top Bovine spongiform encephalopathy (BSE) is a transmissible spongiform encephalopathy (TSE) of cattle and was first detected in 1986 in the United Kingdom. It is the most likely cause of variant Creutzfeldt-Jakob disease (CJD) in humans. The origin of BSE remains an enigma. Here we report an H-type BSE case associated with the novel mutation E211K within the prion protein gene (Prnp). Sequence analysis revealed that the animal with H-type BSE was heterozygous at Prnp nucleotides 631 through 633. An identical pathogenic mutation at the homologous codon position (E200K) in the human Prnp has been described as the most common cause of genetic CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. A recent epidemiological study revealed that the K211 allele was not detected in 6062 cattle from commercial beef processing plants and 42 cattle breeds, indicating an extremely low prevalence of the E211K variant (less than 1 in 2000) in cattle.

Author Summary Top Bovine spongiform encephalopathy (BSE or Mad Cow Disease), a transmissible spongiform encephalopathy (TSE) or prion disease of cattle, was first discovered in the United Kingdom in 1986. BSE is most likely the cause of a human prion disease known as variant Creutzfeldt Jakob Disease (vCJD). In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in “the approximately 10-year-old cow” carrying the E221K mutation.

Pathog 4(9): e1000156. doi:10.1371/journal.ppat.1000156

Editor: David Westaway, University of Alberta, Canada

Received: June 5, 2008; Accepted: August 15, 2008; Published: September 12, 2008

This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

Funding: This work was supported by the USDA-ARS-National Animal Disease Center (NADC) and USDA-APHIS-National Veterinary Services Laboratories (NVSL) and by the NIAID-NIH PO1 AI 77774-01 “Pathogenesis, Transmission and Detection of Zoonotic Prion Diseases”.

Competing interests: Patent pending: Dr. Jürgen A. Richt submitted a patent application entitled “Novel Polymorphism in Bovine Prion Protein Gene Sequence” (Docket Number 0078.06; Serial No. 11/787,784) on April 18, 2006.

* E-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000388/!x-usc:mailto:jricht@vet.k-state.edu

¤ Current address: Kansas State University, College of Veterinary Medicine, DM/P, Manhattan, Kansas, United States of America

Introduction Top Transmissible spongiform encephalopathy (TSE) agents induce fatal neurodegenerative diseases in humans and in some mammalian species [1]. According to the prion-only hypothesis, infectious prions are composed of an abnormal isoform of a host-encoded glycoprotein, called prion protein (PrPc). The disease-associated form, PrPd, is derived from PrPc by a post-translational mechanism that involves conformational change [1]. Human TSEs include Creutzfeldt–Jakob disease (CJD), Gerstmann–Sträussler–Scheinker syndrome, Kuru and Fatal Familial Insomnia [1]. In animals, several distinct TSE diseases are recognized: Scrapie in sheep and goats, transmissible mink encephalopathy in mink, chronic wasting disease in cervids, and bovine spongiform encephalopathy (BSE) in cattle [2]. BSE was first detected in 1986 in the United Kingdom and is the most likely cause of variant CJD (vCJD) in humans. The origin of the original case(s) of BSE still remains an enigma. Hypotheses include (i) sheep- or goat-derived scrapie-infected tissues included in meat and bone meal fed to cattle, (ii) a previously undetected sporadic or genetic bovine TSE contaminating cattle feed or (iii) origination from a human TSE through animal feed contaminated with human remains [3]. This study will provide support to the hypothesis that BSE originated from a previously undetected genetic bovine TSE contaminating cattle feed in the U.K.

Results


Here we report a case of bovine BSE associated with a mutation within the prion protein gene (Prnp) sequence, not previously described for the bovine Prnp. The animal (called “U.S. BSE Alabama”) was an approximately 10 year-old red crossbred (Bos indicus×Bos taurus) hybrid beef cow from Alabama (see Materials and Methods). The ELISA-based BSE test (see Materials and Methods) on brainstem from this animal was repeated five times and revealed a strongly positive reaction with mean optical density (OD) value of 2.40±0.57, whereas the OD value of bovine control obex was <0.04. href="mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000388/!x-usc:http://www.aphis.usda.gov/newsroom/hot_i?ssues/bse/downloads/EPI_Final5-2-06.pdf">http://www.aphis.usda.gov/newsroom/hot_i?ssues/bse/downloads/EPI_Final5-2-06.pdf ). There are several possibilities for the origin of the Prnp K211 allele in animal B14842: (i) it arose de novo in a germ line cell from the U.S. BSE Alabama animal or one of its parents; (ii) it arose as a somatic mutation in the U.S. BSE Alabama animal (rather unlikely), and (iii) it is present in a cattle population or breed yet to be found. Recently, it was determined that the 2-year-old heifer offspring of the U.S. BSE Alabama cow also carries the E211K polymorphism, indicating that the allele is heritable and may persist within the cattle population (11) In a recent epidemiological study which included 6062 cattle from 5 commercial beef processing plants (3892 carcasses) and 2170 registered cattle from 42 breeds., the K211 allele was not detected using a newly developed mass spectrometry assay specific for the E211K variant [12]. These data indicate a rather low prevalence of the E211K variant of less than 1 in 2000 cattle when using Bayesian analysis [12]. This newly developed assay system for K211 [12] will offer the possibility for genetic surveillance of cattle for rare pathogenic mutations that may be associated with BSE.


SNIP...


FULL TEXT ;



http://www.plospathogens.org/article/info:doi%2F10.1371%2Fjournal.ppat.1000156



Texas BSE Investigation Final Epidemiology Report August 2005

Executive Summary

In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample from November 2004, that had originally been classified as negative on the immunohistochemistry test, was confirmed positive on SAF immunoblot (Western blot). The U.S. Department of Agriculture (USDA) identified the herd of origin for the index cow in Texas; that identification was confirmed by DNA analysis. USDA, in close cooperation with the Texas Animal Health Commission (TAHC), established an incident command post (ICP) and began response activities according to USDA’s BSE Response Plan of September 2004. Response personnel removed at-risk cattle and cattle of interest (COI) from the index herd, euthanized them, and tested them for BSE; all were negative. USDA and the State extensively traced all at-risk cattle and COI that left the index herd. The majority of these animals entered rendering and/or slaughter channels well before the investigation began. USDA’s response to the Texas finding was thorough and effective.

Background of the Investigation

On June 10, 2005, USDA announced that the November 2004 inconclusive BSE sample tested positive on SAF immunoblot. The SAF immunoblot was run at USDA’s National Animal Disease Center (NADC) upon the recommendation of USDA’s Office of the Inspector General. Samples were sent to a World Organization for Animal Health (OIE) reference laboratory for BSE in Weybridge, England, for confirmatory tests. Farm A, located in Texas, was the suspected farm of origin for the index cow and was placed under hold order on June 20, 2005 pending confirmation of the positive results and DNA analysis of the herd. Weybridge confirmed the BSE positive on June 24, 2005. The carcass of the index cow had been disposed of by incineration in November 2004.



http://www.aphis.usda.gov/newsroom/hot_issues/bse/downloads/bse_final_epi_report8-05.pdf



News Release

Texas Animal Health Commission

Box l2966 * Austin, Texas 78711 * (800) 550-8242 * FAX (512) 719-0719

Bob Hillman, DVM * Executive Director

For info, contact Carla Everett, information officer, at 1-800-550-8242, ext. 710, or mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000388/!x-usc:mailto:ceverett@tahc.state.tx.us

For immediate release---

State-Federal Team Responds to Texas BSE Case

The US Department of Agriculture announced June 29 that genetic testing has verified that an aged cow that tested positive for Bovine Spongiform Encephalopathy or BSE originated from a Texas beef cattle herd. Tissues for laboratory testing were initially collected from the animal in November 2004, and the carcass was incinerated and did not enter the human food, animal feed or fertilizer supply system. While tests in November indicated the animal did not have BSE, retesting in England in June confirmed the animal had the disease. The Texas Animal Health Commission (TAHC), the state’s livestock and poultry health regulatory agency, and USDA have jointly assigned a state-federal team to conduct the epidemiological investigation and response.

“The TAHC and US Department of Agriculture’s Veterinary Services are working with a complement of experts from federal and state animal health, food safety, public health and feed regulatory agencies to ensure the continued safety and wholesomeness of our meat supply,” said Dr. Bob Hillman, Texas state veterinarian and executive director of the TAHC, the state’s livestock and poultry health regulatory agency. “Epidemiological investigations are thorough and focus on verifying the herd of origin, and when, where and how the animal and potentially, any herd mates, were exposed to the abnormal prion, or disease agent, that causes BSE. Additionally, epidemiology investigations trace the infected animal’s movement and herd mates. Animals potentially exposed to the disease will be depopulated, with proper disposal. The animals will not be introduced into the human or animal food chain.”

The USDA’s BSE testing protocol requires testing of emaciated or injured cattle, cattle that exhibit central nervous system disorder, cattle unable to rise or to walk normally, and cattle that die of unknown causes. Since June 1, 2004, brain tissue samples from more than 394,000 cattle have been tested in the U.S. and were negative for BSE. Of those, 38,320 were tested in Texas, Dr. Hillman noted. BSE surveillance has been conducted in the U.S. since l990.

The U.S. has taken preventive measures against the introduction of BSE since l989, when prohibitions were placed on cattle and other ruminants from BSE-affected countries, noted Dr. Hillman. In 1997, the importation ban was extended to all of Europe.

Dr. Hillman said the U.S. Food and Drug Administration (FDA) in 1997 banned the use of ruminant-derived protein (from animals such as cattle and sheep) in feed for cattle and other ruminants. There is no evidence that BSE spreads from live animal to animal in the herd, but cattle can be exposed by eating feed that contains rendered protein from infected animals. “These measures taken by the USDA and the FDA are safeguards that work to protect livestock, and ultimately, our meat supply,” he said.

--30--



http://www.tahc.state.tx.us/news/pr/2005/2005Jun30_BSE_Positive_Results.pdf



Second BSE case occurred in Texas, USDA says Jun 30, 2005 (CIDRAP News) – The United States' second case of bovine spongiform encephalopathy (BSE) was in a 12-year-old cow that came from a Texas herd and would have been made into pet food if it hadn't been flagged for BSE testing, federal officials announced yesterday evening.

US Department of Agriculture (USDA) officials said the cow was to be processed at a pet food plant in Waco, Tex., when it was diverted for testing because it couldn't walk. Officials didn't name the plant or say exactly where the cow came from. But an Associated Press (AP) report today identified the plant as Champion Pet Food in Waco and said the cow was already dead when brought there last November.

"The source herd is now under a hold order as we identify animals of interest within the herd," USDA Chief Veterinarian John Clifford said in a prepared statement. Investigators will look for cattle born within a year before or after the BSE-infected cow and any of the cow's offspring born within the past 2 years, he explained.

"If the age of the animal cannot be pinpointed, then we may expand our inquiry to include all animals in this herd before the feed ban went into place in 1997," Clifford said. To prevent BSE, the government banned putting cattle protein into cattle feed in August 1997.

The infected cow was incinerated, and no parts were used in human food or animal feed, according to the USDA. "The safety of our food supply is not in question," Clifford stated.

Because of the cow's age, the USDA suspects it became infected by eating contaminated feed before the government ban began in 1997. The USDA and the Food and Drug Administration (FDA) will try to trace the source herd's feed history, officials said.

The FDA will also check whether firms that may have processed meat-and-bone meal from animals from that herd have complied with the 1997 feed ban, Dr. Steve Sundlof, director of the FDA's Center for Veterinary Medicine, said at a news conference last night.

The Texas case is the first US BSE case in a native-born animal; Clifford said the cow lived on one farm all its life. The previous US case, found in December 2003, involved a Canadian-born dairy cow in Washington state.

An initial screening test on the Texas cow last November was inconclusive, and two confirmatory immunohistochemistry tests were negative. But early this month the USDA's inspector general ordered a Western blot test, which came back positive. Further confirmatory tests at an international reference lab in Britain were also positive, prompting the USDA to announce the findings last week.

The USDA waited for the results of DNA tests before announcing that the infected cow came from Texas. The step was necessary because parts of the infected cow were stored with those of four other cattle, causing some uncertainty, officials said.

"We felt that we had the correct herd; we wanted to identify that appropriately with DNA," Clifford said at the news conference. Investigators analyzed DNA from the infected animal and then looked for relatives in the presumed source herd by analyzing DNA from members of the herd, he said. The investigation turned up two cattle that are related to the infected cow, he added.

The AP report said Champion Pet Food is under contract to take samples from animals in poor health. The company's owner, Benjy Bauer, told the AP that his workers took samples from the cow and sent them to the Texas Veterinary Diagnostic Laboratory at Texas A&M University. The lab is one of several the USDA uses to screen cattle for BSE, the story said.

See also:

USDA news release http://www.aphis.usda.gov/lpa/issues/bse/BSE_statement6-29-05.pdf



USDA fact sheet on BSE epidemiologic investiation

http://www.usda.gov/documents/FactSheetbse062905.pdf



USDA press conference transcript



https://www.cidrap.umn.edu/cidrap/content/other/bse/news/june3005bse.html



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



Correspondence Nature 457, 1079 (26 February 2009) doi:10.1038/4571079b;


Published online 25 February 2009


Rare BSE mutation raises concerns over risks to public health


Malcolm A. Ferguson-Smith1 & Jürgen A. Richt2

Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK Email: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000388/!x-usc:mailto:maf12@cam.ac.uk College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA

Atypical forms (known as H- and L-type) of bovine spongiform encephalopathy (BSE) have recently appeared in several European countries as well as in Japan, Canada and the United States. This raises the unwelcome possibility that variant Creutzfeldt–Jakob disease (vCJD) could increase in the human population. ...



http://www.nature.com/nature/journal/v457/n7233/full/4571079b.html



Thursday, July 10, 2008 A Novel Human Disease with Abnormal Prion Protein Sensitive to Protease update July 10, 2008



http://cjdmadcowbaseoct2007.blogspot.com/2008/07/novel-human-disease-with-abnormal-prion.html



Thursday, July 10, 2008


A New Prionopathy update July 10, 2008



http://cjdmadcowbaseoct2007.blogspot.com/2008/07/new-prionopathy-update-july-10-2008.html



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



''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://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf



LINE TO TAKE

18. There is nothing to add to CMO's statement in January 1994, in relation to both the safety of meat and to the diagnosis in the 16 year old girl.

snip...



http://www.bseinquiry.gov.uk/files/yb/1995/08/01006001.pdf



IMPORTANT - CONFIDENTIAL

LINE TO TAKE



http://www.bseinquiry.gov.uk/files/yb/1995/08/17006001.pdf



CJD FOURTH FARMER LINE TO TAKE, preparing for media storm ;



http://www.bseinquiry.gov.uk/files/yb/1995/09/29009001.pdf



http://www.bseinquiry.gov.uk/files/yb/1995/09/29013001.pdf



LINE TO TAKE ;



http://www.bseinquiry.gov.uk/files/yb/1995/10/23010001.pdf



IN CONFIDENCE


CJD IN YOUNG PEOPLE

* in the USA, a 16 year old in 1978

* in France, a 19 year old in 1982

* in Canada, a 14 year old of UK origin in 1988

* in Poland, cases in people aged 19, 23 and 27 were identified in a retrospective study (published 1991), having been originally misdiagnosed with a viral encephalitis;


++++++++++++++++++++


* Creutzfeldt's first patient in 1920 was aged 23


++++++++++++++++++++


snip...


http://www.bseinquiry.gov.uk/files/yb/1995/10/26005001.pdf



April 20, 2009

National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)

National Prion Disease Pathology Surveillance Center Cases Examined1

(December 31, 2008)

Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD

1996 & earlier 42 32 28 4 0 0

1997 115 68 59 9 0 0

1998 93 53 45 7 1 0

1999 115 69 61 8 0 0

2000 151 103 89 14 0 0

2001 210 118 108 9 0 0

2002 258 147 123 22 2 0

2003 273 176 135 41 0 0

2004 335 184 162 21 0 13

2005 346 193 154 38 1 0

2006 380 192 159 32 0 14

2007 370 212 185 26 0 0

2008 383 228 182 23 0 0

TOTAL 30715 17756 1490 254 4 2

1 Listed based on the year of death or, if not available, on year of referral; 2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted; 3 Disease acquired in the United Kingdom; 4 Disease acquired in Saudi Arabia; 5 Includes 20 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 25 cases with type determination pending in which the diagnosis of vCJD has been excluded.

Rev 2/13/09 National


http://www.cjdsurveillance.com/pdf/case-table.pdf



http://www.cjdsurveillance.com/resources-casereport.html



http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45


+++++++++++++++++++++++


*5 Includes 20 cases in which the diagnosis is pending, and 17 inconclusive cases; *6 Includes 25 cases with type determination pending in which the diagnosis of vCJD has been excluded.


+++++++++++++++++++++++


Greetings,

it would be interesting to know what year these atypical cases occurred, as opposed to lumping them in with the totals only.

are they accumulating ?

did they occur in one year, two years, same state, same city ?

location would be very interesting ?

age group ?

sex ?

how was it determined that nvCJD was ruled out ?

from 1997, the year i started dealing with this nightmare, there were 28 cases (per this report), up until 2007 where the total was 185 cases (per this report), and to date 2008 is at 182. a staggering increase in my opinion, for something that just happens spontaneously as some would have us believe. i don't believe it, not in 85%+ of all sporadic CJD cases. actually, i do not believe yet that anyone has proven that any of the sporadic CJD cases have been proven to be a spontaneous misfolding of a protein. there are many potential routes and sources for the sporadic CJD's. ...TSS

Sunday, April 12, 2009

r-calf and the USA mad cow problem, don't look, don't find, and then blame Canada



http://prionunitusaupdate2008.blogspot.com/2009/04/r-calf-and-usa-mad-cow-problem-dont.html



Monday, April 20, 2009

National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)



http://prionunitusaupdate2008.blogspot.com/2009/04/national-prion-disease-pathology.html



Thursday, April 9, 2009

Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed



http://madcowfeed.blogspot.com/2009/04/docket-no-fda2002n0031-formerly-docket.html



TSS COMMENT SUBMISSION # 5

Docket ID FDA-2002-N-0031 Docket Title Animal Proteins Prohibited in Ruminant Feed Document ID FDA-2002-N-0031-0132 Document Title Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed Delay of Effective Date

Completely Edited Version

PRION ROUNDTABLE

2003

page 29

Dr. Linda Detwiler

The UK imports into the US.

There were 496 total, and 173 of the UK imports could have entered the US feed system. People don't like to hear this, but it's possible that one of the UK imports in the US entered the animal feed system and was exported to Canada. That's a possibility, because they import 50% of their feed from the US.

From 1994, we imported 11 million head of cattle from Canada. Most of these were feedlot animals for slaughter, but there were about 500,000 breeding animals. A number of Canada's cull cows were slaughtered here and could have introduced infectivity into our system. Even today we have Canadian imports in the country, breeding animals that were brought in prior to the ban and reside here.

We have feed ban exemptions: plate waste, poultry litter. We still allow that if it comes off a human plate, or if it's trimmings, it can be palletized and fed to ruminants. That might be a small amount, but it could allow spinal cord in certain cuts to be fed back to ruminants. Poultry litter or feather meal could be significant. Poultry is getting quite a bit of ruminant material in the US because it cannot go back to ruminants. Poultry and pigs are getting a substantial amount. Poultry litter is not only what passes through the chicken, but think about how chickens eat. They spill a lot on the floor. That stuff is still allowed to be fed back to cattle. That's a direct break in the ban, except that it's legal. Ruminants are getting ruminant material.

Unfiltered tallow: tallow is a lipid material. However, if it's not filtered, there are protein residues. That's meat and bone meal. That's allowed to be fed, so that's another legal exception where you can feed ruminant meat and bone meal through unfiltered tallow. We don't have an SRM ban and the 40 animals are the ones that if you have the agent, they introduce the most infectivity back into the animal food chain when they're rendered.

What's our on-farm compliance? We really don't know. ...

snip...end...Dr. Linda Detwiler



http://madcowfeed.blogspot.com/2009/04/docket-no-fda2002n0031-formerly-docket.html#comments



Thursday, April 9, 2009

Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed



http://madcowfeed.blogspot.com/2009/04/docket-no-fda2002n0031-formerly-docket.html



http://prionunitusaupdate2008.blogspot.com/2009/04/r-calf-and-usa-mad-cow-problem-dont.html#comments



Sunday, April 12, 2009


r-calf and the USA mad cow problem, don't look, don't find, and then blame Canada



http://prionunitusaupdate2008.blogspot.com/2009/04/r-calf-and-usa-mad-cow-problem-dont.html



http://prionunitusaupdate2008.blogspot.com/2009/04/cjd-foundation-sides-with-r-calfers-no.html#comments



Sunday, May 10, 2009

Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)


http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html




Sunday, August 10, 2008 A New Prionopathy OR more of the same old BSe and sporadic CJD



http://creutzfeldt-jakob-disease.blogspot.com/2008/08/new-prionopathy-or-more-of-same-old-bse.html



HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008

snip...

Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...

snip...



http://cjdmadcowbaseoct2007.blogspot.com/2008/06/human-and-animal-tse-classifications-ie.html



Elsevier Editorial System(tm) for The Lancet Infectious Diseases Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary

Abstract:

TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2007. snip...

see full text 31 pages ;



http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf



Saturday, April 04, 2009

An unusually presenting case of sCJD-The VV1 subtype



http://creutzfeldt-jakob-disease.blogspot.com/2009/04/unusually-presenting-case-of-scjdthe.html



Saturday, January 24, 2009

Bovine Spongiform Encephalopathy h-BSE ATYPICAL USA 2008 Annual Report Research Project: Study of Atypical Bse

Location: Virus and Prion Diseases of Livestock

2008 Annual Report



http://bse-atypical.blogspot.com/2009/01/bovine-spongiform-encephalopathy-h-bse.html



Saturday, May 2, 2009

U.S. GOVERNMENT SUES WESTLAND/HALLMARK MEAT OVER USDA CERTIFIED DEADSTOCK DOWNER COW SCHOOL LUNCH PROGRAM



http://downercattle.blogspot.com/2009/05/us-government-sues-westlandhallmark.html




Thursday, December 04, 2008 2:37 PM


"we have found that H-BSE can infect humans."

personal communication with Professor Kong. ...TSS


see full text ;



http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.html



Friday, November 30, 2007

CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION



http://cjdquestionnaire.blogspot.com/



Sunday, April 12, 2009 BSE MAD COW TESTING USA 2009 FIGURES Month Number of Tests

Feb 2009 -- 1,891

Jan 2009 -- 4,620



http://www.aphis.usda.gov/newsroom/hot_issues/bse/surveillance/ongoing_surv_results.shtml



see full text ;



http://madcowtesting.blogspot.com/2009/04/bse-mad-cow-testing-usa-2009-figures.html



Monday, May 4, 2009

Back to the Past With New TSE Testing Agricultural Research/May-June 2009



http://madcowtesting.blogspot.com/2009/05/back-to-past-with-new-tse-testing.html




Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518

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