COLORADO CWD CJD TSE PRION REPORTING 2011
October 2011
Research Looks at Test to Identify Chronic Wasting Disease in Wildlife
Dr. Ed Hoover
A Colorado State University study is developing and evaluating a more sensitive test for chronic wasting disease – including the potential to test for infection in live animals, animal products, and the environment – through a project funded by Denver-based Morris Animal Foundation.
The disease, which affects deer, moose and elk and is related to similar diseases in cattle and sheep, is a primary concern for hunters and wildlife ranchers and now affects wildlife in 19 states, two Canadian provinces and one Asian country.
Prions are rogue proteins that cause the family of diseases that include CWD. The diseases are known as spongiform encephalopathies. While this Morris Animal Foundation-funded study would be the first in several steps to develop and evaluate a potential new test, it will look at a method that shows promise in detecting a wider array of prions at lower levels than are currently detected.
The research into the potential test may allow detection of CWD prions in live animals, animal products and the environment.
“Developing this test may eventually lead to a more rapid and sensitive to test for CWD,” said Dr. Ed Hoover, a Professor in the Department of Microbiology, Immunology and Pathology. “But, just as significantly, it may lead to a substantial gain in our understanding of how prions spread, survive in natural habitats, and impact animal and public health.”
Currently, CWD can only be identified either by testing brain after an animal is deceased or by surgical sampling and testing lymphatic tissues. While researchers don’t know exactly how CWD is passed from animal to animal, CSU scientists discovered that body fluids such as saliva, blood, urine and feces harbor infectious prions. Animals can then be exposed by direct contact with an infected animal or by contact with a contaminated environment.
Current tests also don’t detect all levels of or kinds of infectious prions or prions in the environment, and the test being evaluated in this study has the potential to be developed into a process that would detect those prions.
The test is being researched in collaboration with Dr. Byron Caughey at the National Institutes of Health’s Rocky Mountain Laboratory in Hamilton, Mont. Dr. Caughey’s laboratory developed the strategy for the study. Dr. Hoover, Dr. Caughey and colleagues will focus first on determining if their proposed test detects prions in body fluids with greater sensitivity, accuracy and faster output than is currently possible.
It is unknown why an infectious prion from one species, such as deer or elk, can “jump” to infect another species, and the potential risk to other species such as cattle, or even humans, remains uncertain.
http://www.cvmbs.colostate.edu/ns/pubs/einsight/2011/october/hoover_ed.aspx
For Immediate Release Thursday, September 29, 2011 Contact for Reporters: Dell Rae Moellenberg 970.491.6009 DellRae.Moellenberg@ColoState.EDU
Colorado State University Study Looks at Test to Identify Chronic Wasting Disease in Wildlife
FORT COLLINS - A Colorado State University study is developing and evaluating a more sensitive test for chronic wasting disease – including the potential to test for infection in live animals, animal products and the environment – through a project funded by Denver-based Morris Animal Foundation.
The disease, which affects deer, moose and elk and is related to similar diseases in cattle and sheep, is a primary concern for hunters and wildlife ranchers and now affects wildlife in 19 states, 2 Canadian provinces and one Asian country.
Prions are rogue proteins that cause the family of diseases that include CWD. The diseases are known as spongiform encephalopathies. While this Morris Animal Foundation-funded study would be the first in several steps to develop and evaluate a potential new test, it will look at a method that shows promise in detecting a wider array of prions at lower levels than are currently detected.
The research into the potential test may allow detection of CWD prions in live animals, animal products and the environment.
“Developing this test may eventually lead to a more rapid and sensitive to test for CWD,” said Dr. Ed Hoover, a Colorado State University veterinarian and researcher with 30 years of experience in researching infectious diseases of animals. “But, just as significantly, it may lead to a substantial gain in our understanding of how prions spread, survive in natural habitats, and impact animal and public health.”
Currently, CWD can only be identified either by testing brain after an animal is deceased or by surgical sampling and testing lymphatic tissues. While researchers don’t know exactly how CWD is passed from animal to animal, CSU scientists discovered that body fluids such as saliva, blood, urine and feces harbor infectious prions. Animals can then be exposed by direct contact with an infected animal or by contact with a contaminated environment.
Current tests also don’t detect all levels of or kinds of infectious prions or prions in the environment, and the test being evaluated in this study has the potential to be developed into a process that would detect those prions.
The test is being researched in collaboration with Dr. Byron Caughey at the National Institutes of Health’s Rocky Mountain Laboratory in Hamilton, Mont. Caughey’s laboratory developed the strategy for the study. Hoover, Caughey and colleagues will focus first on determining if their proposed test detects prions in body fluids with greater sensitivity, accuracy and faster output than is currently possible.
It is unknown why an infectious prion from one species, such as deer or elk, can “jump” to infect another species, and the potential risk to other species such as cattle, or even humans, remains uncertain. -30-
http://www.news.colostate.edu/release.aspx?id=5913
Effective April 2010
COLORADO BOARD OF HEALTH CONDITIONS REPORTABLE BY ALL LABORATORIES COLLECTING SPECIMENS OR PERFORMING TESTS IN COLORADO
http://www.cdphe.state.co.us/dc/Reportables%20laboratories%202010.pdf
COLORADO BOARD OF HEALTH CONDITIONS REPORTABLE BY ALL PHYSICIANS AND HEALTH CARE PROVIDERS IN COLORADO
http://www.cdphe.state.co.us/dc/Reportables%20physicians%202010.pdf
http://www.cdphe.state.co.us/dc/reportable.html
Diseases and Conditions Reported to Colorado Public Health Agencies by State Law Important notice for patients receiving health care services in Colorado: The following list of diseases and conditions must be reported to state or county public health agencies by health care providers, hospitals and laboratories, according to Colorado Board of Health regulations
http://www.cdphe.state.co.us/op/regs/diseasecontrol/index.html
By law, this reporting does not require patient consent or notification. The confidentiality of personal health information reported to the Colorado Department of Public Health and Environment (CDPHE) is protected by law. If you have questions regarding these reporting requirements, please call CDPHE at (303) 692-2700. If you have questions about whether you might have a condition that must be reported, discuss this with your health care provider.
Infectious Diseases
Crutchfield-Jacob Disease (CJD) or variant CJD
http://www.cdphe.state.co.us/dc/medlistpatients.pdf
please note, cjd spelling above, that's how it is on the site...really...tss
===============================
CHRONIC WASTING DISEASE IN COLORADO: 2010 & 2011 SURVEILLANCE UPDATE Colorado Division of Parks & Wildlife 9 August 2011
As of July 2011, at least one case of CWD has been detected in 24 of 55 deer (Odocoileus spp.) data analysis units (DAUs), 14 of 46 elk (Cervus elaphus nelsoni) DAUs, and 2 of 5 moose (Alces alces) DAUs. Within affected DAUs, prevalence estimated from 2010ƒ{11 harvest survey data ranged from <1ƒ{25% among male mule deer, <1ƒ{17% among male elk, and <1% among moose; most current prevalence estimates have wide confidence intervals because sample sizes in many sampled DAUs are small. Prevalence appears to be stable or increasing among harvested male mule deer in two DAUs monitored since 1996 (Figure). A more extensive analysis of temporal trends in CWD prevalence in select DAUs is ongoing. Maps showing estimated prevalence by DAU are posted on the Colorado Division of Parks and Wildlife¡¦s web site
http://wildlife.state.co.us/Hunting/BigGame/CWD/
http://wildlife.state.co.us/SiteCollectionDocuments/DOW/Hunting/BigGame/CWD/PDF/TestResults/CWDReport2010-2011.pdf
http://wildlife.state.co.us/hunting/biggame/cwd/Pages/CWDHome.aspx
CWD POSTIVE Elk Meat Sold in Boulder Colorado Recalled
FOR IMMEDIATE RELEASE
Wednesday, Dec. 24, 2008
CONTACT Mark W. Salley Communications Director 303-692-2013
Elk Meat Sold in Boulder Recalled DENVER-The Boulder County Health Department and Colorado Department of Public Health and Environment are issuing an advisory to customers who purchased elk meat at a farmers’ market at the Boulder County Fairgrounds on Dec. 13. Testing has shown that one of the elk sold that day was infected with chronic wasting disease (CWD). Although there is no known human health risk associated with exposure to CWD, as a precaution, the state health department has recommended against consuming meat from animals known to be infected with CWD.
Fifteen elk were purchased from a commercial Colorado elk ranch and processed in early December at a USDA licensed meat-processing plant. All 15 animals were tested for CWD as required under Colorado law. Preliminary testing indicated only one animal of the 15 was infected with CWD. Confirmatory testing is being conducted.
The vendor at the farmers’ market where the meat was sold, indicated that meat from three or four elk, including the infected elk, all was sold on Dec. 13. The labeling on the product would have the following information:
Seller: High Wire Ranch
The type of cut: “chuck roast,” “arm roast,” “flat iron,” “ribeye steak,” “New York steak,” “tenderloin,” “sirloin tip roast,” “medallions” or “ground meat.”
Processor: Cedaredge Processing
The USDA triangle containing the number “34645”
CWD is among several diseases believed to be caused by prions, misshaped proteins that cause damage to nerve cells in the brain. CWD has been found in elk, deer and moose. Other prion diseases include scrapie in sheep, bovine spongiform encephalopathy in cattle and Cruetzfeldt-Jakob disease (CJD) in humans. BSE, also known as mad-cow disease, has been shown to cause disease in people.
Scientific studies over the past 10 years have not found any human health risk from exposure to CWD. But as a precaution, consumers who purchased elk meat at the Boulder farmer’s market on Dec. 13 should consider discarding the meat. There is no way to test the meat, and consumers would be unable to tell whether their meat came from an infected or uninfected animal by looking at it.
Only meat with the above package markings, sold at the Boulder County Fairgrounds farmers’ market on Dec. 13 is affected by this advisory. People with questions about this meat can contact John Pape, epidemiologist at the Colorado Department of Public Health and Environment, 303-692-2628. ---30---
http://www.cdphe.state.co.us/release/2008/122408.html
Oral.40: Monitoring the Potential Transmission of Chronic Wasting Disease to Humans
Ermias D. Belay,1,† Joseph Abrams,1 Janell Kenfield,2 Kelly Weidenbach,3 Ryan A. Maddox,1 Elisabeth Lawaczeck2 and Lawrence B. Schonberger1 1 Centers for Disease Control and Prevention; Atlanta, GA USA; 2 Colorado Department of Public Health and Environment; Denver, CO USA; 3 Wyoming Department of Health; Cheyenne, WY USA†Presenting author; Email: EBelay@cdc.gov Introduction:
Chronic wasting disease (CWD) has been occurring for several decades among wild cervids in Colorado and Wyoming. The increasing detection of CWD in an additional 12 US states and two Canadian provinces may have resulted in increased human exposure to CWD. Although studies have evaluated the possible transmission of CWD to humans in laboratory models, a reliable assessment requires conducting epidemiologic and laboratory studies designed to identify prion disease among humans exposed to CWD and generating scientific evidence causally linking the two illnesses. Methods: In collaboration with the Centers for Disease Control and Prevention, the Wyoming Department of Health and the Colorado Department of Public Health and Environment established a long-term follow-up study of hunter data to monitor the potential CWD transmission to humans. Personal identifiers from deer or elk hunter database are cross-checked with mortality data to determine their mortality status and causes of death. Results: In Colorado, the hunter data include about 4.9 million records of licenses purchased during 1995–2008, representing about 1.1 million hunters. Overall, 48% of hunters purchased a license to hunt in areas that included CWD positive game units and 47% to hunt anywhere in Colorado. In Wyoming, the data include about 1.2 million records of licenses purchased during 1996-2009, representing about 0.5 million hunters; 34% of hunters purchased a license to hunt in areas that included CWD positive game units and 28% to hunt anywhere in Wyoming. During the study period three Colorado hunters (expected number: 3-15 cases) and three Wyoming hunters (expected number: 0-6 cases) were identified to have died of Creutzfeldt-Jakob disease (CJD). Conclusions: No evidence suggests that the CJD incidence is higher than expected among persons who hunted in Colorado or Wyoming. The hunter data are valuable for monitoring the potential transmission of CWD to humans. Ongoing assessment and long-term follow-up of the hunter population is necessary because human prion diseases are associated with long latency periods and the pathogenicity of CWD might change over time.
http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf
Saturday, November 12, 2011
IN REPLY TO ; Human Prion Disease and Relative Risk Associated with Chronic Wasting Disease
Fri, 22 Sep 2006 09:05:59 -0500
http://chronic-wasting-disease.blogspot.com/2011/11/human-prion-disease-and-relative-risk.html
"We used Colorado death certificate data from 1979 through 2001 to evaluate rates of death from the human prion disease Creutzfeldt-Jakob disease (CJD)."
HOW RELIABLE IS REVIEWING DEATH CERTIFICATE DATA FOR SURVIELLANCE OF CJD, instead of making CJD and all Prion disease reportable Nationally ???
it's not reliable at all. PLEASE SEE ;
*** Tuesday, November 08, 2011
Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance? A Study in France from 2000 to 2008
Vol. 37, No. 3-4, 2011 Original Paper
Conclusions:These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.
http://creutzfeldt-jakob-disease.blogspot.com/2011/11/can-mortality-data-provide-reliable.html
Friday, November 04, 2011
Diagnostic accuracy of cerebrospinal fluid protein markers for sporadic Creutzfeldt-Jakob disease in Canada: a 6-year prospective study
Research article
http://creutzfeldt-jakob-disease.blogspot.com/2011/11/diagnostic-accuracy-of-cerebrospinal.html
PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
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
NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.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
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip... full text ;
http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html
CJD9/10022 October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To:
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.
That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From:
Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM
......snip........end..............TSS
http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html
Wednesday, October 12, 2011
White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation
http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html
http://www.mad-cow.org/colorado_exp.html
Wednesday, July 06, 2011
Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation
http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html
THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER
Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011
http://chronic-wasting-disease.blogspot.com/2011/02/role-of-predation-in-disease-control.html
Wednesday, September 21, 2011
Evidence for distinct CWD strains in experimental CWD in ferrets
http://chronic-wasting-disease.blogspot.com/2011/09/evidence-for-distinct-cwd-strains-in.html
Chronic Wasting Disease Susceptibility of Four North American Rodents
Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A. Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI 53706, USA 2US Geological Survey, National Wildlife Health Center, 6006 Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author email: cjohnson@svm.vetmed.wisc.edu
We intracerebrally challenged four species of native North American rodents that inhabit locations undergoing cervid chronic wasting disease (CWD) epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles (Myodes gapperi). The inocula were prepared from the brains of hunter-harvested white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles proved to be most susceptible, with a median incubation period of 272 days. Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the brains of all challenged meadow voles. Subsequent passages in meadow voles lead to a significant reduction in incubation period. The disease progression in red-backed voles, which are very closely related to the European bank vole (M. glareolus) which have been demonstrated to be sensitive to a number of TSEs, was slower than in meadow voles with a median incubation period of 351 days. We sequenced the meadow vole and red-backed vole Prnp genes and found three amino acid (AA) differences outside of the signal and GPI anchor sequences. Of these differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is particularly intriguing due its postulated involvement in “rigid loop” structure and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5 years post-inoculation, but appear to be exhibiting a high degree of disease penetrance. White-footed mice have an even longer incubation period but are also showing high penetrance. Second passage experiments show significant shortening of incubation periods. Meadow voles in particular appear to be interesting lab models for CWD. These rodents scavenge carrion, and are an important food source for many predator species. Furthermore, these rodents enter human and domestic livestock food chains by accidental inclusion in grain and forage. Further investigation of these species as potential hosts, bridge species, and reservoirs of CWD is required.
http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html
please see ;
http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf
Thursday, June 09, 2011
Detection of CWD prions in salivary, urinary, and intestinal tissues of deer: potential mechanisms of prion shedding and transmission
http://chronic-wasting-disease.blogspot.com/2011/06/detection-of-cwd-prions-in-salivary.html
Sunday, November 13, 2011
Atypical Scrapie Isolates Involve a Uniform Prion Species with a Complex Molecular Signature
http://nor-98.blogspot.com/2011/11/atypical-scrapie-isolates-involve.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
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
Sunday, July 27, 2008
DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
-------- Original Message --------
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr."
To: fdadockets@oc.fda.gov
Greetings FDA,
i would kindly like to comment on;
Docket 03D-0186
FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Several factors on this apparent voluntary proposal disturbs me greatly, please allow me to point them out;
1. MY first point is the failure of the partial ruminant-to-ruminant feed ban of 8/4/97. this partial and voluntary feed ban of some ruminant materials being fed back to cattle is terribly flawed. without the _total_ and _mandatory_ ban of all ruminant materials being fed back to ruminants including cattle, sheep, goat, deer, elk and mink, chickens, fish (all farmed animals for human/animal consumption), this half ass measure will fail terribly, as in the past decades...
2. WHAT about sub-clinical TSE in deer and elk? with the recent findings of deer fawns being infected with CWD, how many could possibly be sub-clinically infected. until we have a rapid TSE test to assure us that all deer/elk are free of disease (clinical and sub-clinical), we must ban not only documented CWD infected deer/elk, but healthy ones as well. it this is not done, they system will fail...
3. WE must ban not only CNS (SRMs specified risk materials), but ALL tissues. recent new and old findings support infectivity in the rump or ass muscle. wether it be low or high, accumulation will play a crucial role in TSEs.
4. THERE are and have been for some time many TSEs in the USA. TME in mink, Scrapie in Sheep and Goats, and unidentified TSE in USA cattle. all this has been proven, but the TSE in USA cattle has been totally ignored for decades. i will document this data below in my references.
5. UNTIL we ban all ruminant by-products from being fed back to ALL ruminants, until we rapid TSE test (not only deer/elk) but cattle in sufficient numbers to find (1 million rapid TSE test in USA cattle annually for 5 years), any partial measures such as the ones proposed while ignoring sub-clinical TSEs and not rapid TSE testing cattle, not closing down feed mills that continue to violate the FDA's BSE feed regulation (21 CFR 589.2000) and not making freely available those violations, will only continue to spread these TSE mad cow agents in the USA. I am curious what we will call a phenotype in a species that is mixed with who knows how many strains of scrapie, who knows what strain or how many strains of TSE in USA cattle, and the CWD in deer and elk (no telling how many strains there), but all of this has been rendered for animal feeds in the USA for decades. it will get interesting once someone starts looking in all species, including humans here in the USA, but this has yet to happen...
6. IT is paramount that CJD be made reportable in every state (especially ''sporadic'' cjd), and that a CJD Questionnaire must be issued to every family of a victim of TSE. only checking death certificates will not be sufficient. this has been proven as well (see below HISTORY OF CJD -- CJD QUESTIONNAIRE)
7. WE must learn from our past mistakes, not continue to make the same mistakes...
snip...
Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus ) Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3, Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1
Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1 Department of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, University of Wyoming, Laramie, WY 82070, USA 2 Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, CO 80526-2097, USA3 Colorado State University Veterinary Diagnostic Laboratory, 300 West Drake Road, Fort Collins, CO 80523-1671, USA4 Animal Disease Research Unit, Agricultural Research Service, US Department of Agriculture, 337 Bustad Hall, Washington State University, Pullman, WA 99164-7030, USA5
Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail ehoover@lamar.colostate.edu
Mule deer fawns (Odocoileus hemionus) were inoculated orally with a brain homogenate prepared from mule deer with naturally occurring chronic wasting disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns were necropsied and examined for PrP res, the abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an immunohistochemistry assay modified to enhance sensitivity. PrPres was detected in alimentary-tract-associated lymphoid tissues (one or more of the following: retropharyngeal lymph node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42 days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No PrPres staining was detected in lymphoid tissue of three control fawns receiving a control brain inoculum, nor was PrPres detectable in neural tissue of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue treatment with formic acid, proteinase K and hydrated autoclaving prior to immunohistochemical staining with monoclonal antibody F89/160.1.5. These results indicate that CWD PrP res can be detected in lymphoid tissues draining the alimentary tract within a few weeks after oral exposure to infectious prions and may reflect the initial pathway of CWD infection in deer. The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species.
snip...
These results indicate that mule deer fawns develop detectable PrP res after oral exposure to an inoculum containing CWD prions. In the earliest post-exposure period, CWD PrPres was traced to the lymphoid tissues draining the oral and intestinal mucosa (i.e. the retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and ileocaecal lymph nodes), which probably received the highest initial exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum and spleen in a 10-month-old naturally infected lamb by mouse bioassay. Eight of nine sheep had infectivity in the retropharyngeal lymph node. He concluded that the tissue distribution suggested primary infection via the gastrointestinal tract. The tissue distribution of PrPres in the early stages of infection in the fawns is strikingly similar to that seen in naturally infected sheep with scrapie. These findings support oral exposure as a natural route of CWD infection in deer and support oral inoculation as a reasonable exposure route for experimental studies of CWD.
snip...
http://vir.sgmjournals.org/cgi/content/full/80/10/2757
===================================
now, just what is in that deer feed? _ANIMAL PROTEIN_
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES Date: Sat, 25 May 2002 18:41:46 -0700 From: "Terry S. Singeltary Sr." Reply-To: BSE-L To: BSE-L
8420-20.5% Antler Developer For Deer and Game in the wild Guaranteed Analysis Ingredients / Products Feeding Directions
snip...
_animal protein_
http://www.surefed.com/deer.htm
BODE'S GAME FEED SUPPLEMENT #400 A RATION FOR DEER NET WEIGHT 50 POUNDS 22.6 KG.
snip...
_animal protein_
http://www.bodefeed.com/prod7.htm
Ingredients
Grain Products, Plant Protein Products, Processed Grain By-Products, Forage Products, Roughage Products 15%, Molasses Products, __Animal Protein Products__, Monocalcium Phosphate, Dicalcium Pyosphate, Salt, Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol (source of Vitamin D3), Vitamin E Supplement, Vitamin B12 Supplement, Riboflavin Supplement, Niacin Supplement, Calcium Panothenate, Choline Chloride, Folic Acid, Menadione Soduim Bisulfite Complex, Pyridoxine Hydorchloride, Thiamine Mononitrate, d-Biotin, Manganous Oxide, Zinc Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried Sacchoromyces Berevisiae Fermentation Solubles, Cellulose gum, Artificial Flavors added.
http://www.bodefeed.com/prod6.htm
===================================
MORE ANIMAL PROTEIN PRODUCTS FOR DEER
Bode's #1 Game Pellets A RATION FOR DEER F3153
GUARANTEED ANALYSIS Crude Protein (Min) 16% Crude Fat (Min) 2.0% Crude Fiber (Max) 19% Calcium (Ca) (Min) 1.25% Calcium (Ca) (Max) 1.75% Phosphorus (P) (Min) 1.0% Salt (Min) .30% Salt (Max) .70%
Ingredients
Grain Products, Plant Protein Products, Processed Grain By-Products, Forage Products, Roughage Products, 15% Molasses Products, __Animal Protein Products__, Monocalcium Phosphate, Dicalcium Phosphate, Salt, Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol (source of Vitamin D3) Vitamin E Supplement, Vitamin B12 Supplement, Roboflavin Supplement, Niacin Supplement, Calcium Pantothenate, Choline Chloride, Folic Acid, Menadione Sodium Bisulfite Complex, Pyridoxine Hydrochloride, Thiamine Mononitrate, e - Biotin, Manganous Oxide, Zinc Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried Saccharyomyces Cerevisiae Fermentation Solubles, Cellulose gum, Artificial Flavors added.
FEEDING DIRECTIONS Feed as Creep Feed with Normal Diet
http://www.bodefeed.com/prod8.htm
INGREDIENTS
Grain Products, Roughage Products (not more than 35%), Processed Grain By-Products, Plant Protein Products, Forage Products, __Animal Protein Products__, L-Lysine, Calcium Carbonate, Salt, Monocalcium/Dicalcium Phosphate, Yeast Culture, Magnesium Oxide, Cobalt Carbonate, Basic Copper Chloride, Manganese Sulfate, Manganous Oxide, Sodium Selenite, Zinc Sulfate, Zinc Oxide, Sodium Selenite, Potassium Iodide, Ethylenediamine Dihydriodide, Vitamin E Supplement, Vitamin A Supplement, Vitamin D3 Supplement, Mineral Oil, Mold Inhibitor, Calcium Lignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium Bisulfite Complex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid, Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate
DIRECTIONS FOR USE
Deer Builder Pellets is designed to be fed to deer under range conditions or deer that require higher levels of protein. Feed to deer during gestation, fawning, lactation, antler growth and pre-rut, all phases which require a higher level of nutrition. Provide adequate amounts of good quality roughage and fresh water at all times.
http://www.profilenutrition.com/Products/Specialty/deer_builder_pellets.html
===================================================
DEPARTMENT OF HEALTH & HUMAN SERVICES PUBLIC HEALTH SERVICE FOOD AND DRUG ADMINISTRATION
April 9, 2001 WARNING LETTER
01-PHI-12 CERTIFIED MAIL RETURN RECEIPT REQUESTED
Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy Lake, PA 16145 PHILADELPHIA DISTRICT
Tel: 215-597-4390
Dear Mr. Raymond:
Food and Drug Administration Investigator Gregory E. Beichner conducted an inspection of your animal feed manufacturing operation, located in Sandy Lake, Pennsylvania, on March 23, 2001, and determined that your firm manufactures animal feeds including feeds containing prohibited materials. The inspection found significant deviations from the requirements set forth in Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant Feed. The regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE) . Such deviations cause products being manufactured at this facility to be misbranded within the meaning of Section 403(f), of the Federal Food, Drug, and Cosmetic Act (the Act).
Our investigation found failure to label your swine feed with the required cautionary statement "Do Not Feed to cattle or other Ruminants" The FDA suggests that the statement be distinguished by different type-size or color or other means of highlighting the statement so that it is easily noticed by a purchaser.
In addition, we note that you are using approximately 140 pounds of cracked corn to flush your mixer used in the manufacture of animal feeds containing prohibited material. This flushed material is fed to wild game including deer, a ruminant animal. Feed material which may potentially contain prohibited material should not be fed to ruminant animals which may become part of the food chain.
The above is not intended to be an all-inclusive list of deviations from the regulations. As a manufacturer of materials intended for animal feed use, you are responsible for assuring that your overall operation and the products you manufacture and distribute are in compliance with the law. We have enclosed a copy of FDA's Small Entity Compliance Guide to assist you with complying with the regulation... blah, blah, blah...
http://www.fda.gov/foi/warning_letters/g1115d.pdf
==================================
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
now, what about those 'deer scents' of 100% urine', and the prion that is found in urine, why not just pass the prion with the urine to other deer...
Mrs. Doe Pee Doe in Estrus Model FDE1 Mrs. Doe Pee's Doe in Estrus is made from Estrus urine collected at the peak of the rut, blended with Fresh Doe Urine for an extremely effective buck enticer. Use pre-rut before the does come into heat. Use during full rut when bucks are most active. Use during post-rut when bucks are still actively looking for does. 1 oz.
www.gamecalls.net/hunting...lures.html
ELK SCENT/SPRAY BOTTLE
snip...
REFERENCES
snip...see full text ;
Sunday, July 27, 2008
DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
-------- Original Message --------
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr."
To: fdadockets@oc.fda.gov
Greetings FDA,
i would kindly like to comment on;
Docket 03D-0186
FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
http://madcowfeed.blogspot.com/2008/07/docket-03d-0186-fda-issues-draft.html
Article
Experimental oral transmission of chronic wasting disease to red deer
(Cervus elaphus elaphus): Early detection and late stage distribution
of protease-resistant prion protein
Aru Balachandran, Noel P. Harrington, James Algire, Andrei Soutyrine, Terry R. Spraker,
Martin Jeffrey, Lorenzo González, Katherine I. O’Rourke
Abstract — Chronic wasting disease (CWD), an important emerging prion disease of cervids, is readily transmitted by intracerebral or oral inoculation from deer-to-deer and elk-to-elk, suggesting the latter is a natural route of exposure. Studies of host range susceptibility to oral infection, particularly of those species found in habitats where CWD currently exists are imperative. This report describes the experimental transmission of CWD to red deer following oral inoculation with infectious CWD material of elk origin. At 18 to 20 months post-inoculation, mild to moderate neurological signs and weight loss were observed and animals were euthanized and tested using 3 conventional immunological assays. The data indicate that red deer are susceptible to oral challenge and that tissues currently used for CWD diagnosis show strong abnormal prion (PrPCWD) accumulation. Widespread peripheral PrPCWD deposition involves lymphoreticular tissues, endocrine tissues, and cardiac muscle and suggests a potential source of prion infectivity, a means of horizontal transmission and carrier state.
SNIP...
There is a strong correlation between the presence of PrPTSE and infectivity in prion diseases. Although the epidemiologic evidence strongly suggests that CWD is not transmissible to humans, this study and others suggest caution in this regard. The finding of PrPCWD in various organs, albeit in clinical CWD, suggests that humans who consume or handle meat from CWD-infected red deer may be at risk of exposure to CWD prions. This study found that red deer tissues other than nervous and lymphoid tissue can support CWD prion replication and accumulation. As a result, the consumption or handling of meat from CWD-infected red deer will put humans at risk of exposure to CWD prions. In spite of a well-documented species barrier, a cautious approach would involve preventing such tissues from entering the animal and human food chains. Future studies will require sensitive and quantitative techniques such as bioassays in transgenic mice that assess tissue infectivity and quantitative immunoassays adapted to PrPCWD detection in peripheral tissues.
SNIP...
The exact mode of transmission of CWD in nature remains unclear but is believed to involve direct animal-to-animal contact or environmental contamination. As TSE agents are extremely resistant in the environment (39), oral exposure is the most plausible pathway by which the CWD prion may be introduced to deer in nature and represents a significant obstacle to eradication of CWD from either farmed or free-ranging cervid populations. The distribution of PrPCWD in gut-associated lymphoid tissues, salivary glands, and nasal mucosa in the red deer of this study suggests potential routes of PrPCWD shedding into the environment via fluids such as saliva or feces. However, this study did not identify the point at which an animal may become infectious during the course of infection. An improved understanding of the mechanisms of shedding and transmission will be important in the future management of CWD.
SNIP...
In summary, this study demonstrates the potential for oral transmission of CWD to red deer and describes the pattern of PrPCWD accumulation for this species. The current surveillance testing regime for cervids would be expected to identify CWD-infected red deer should it occur in North America. These results confirm the usefulness of rapid tests such as ELISA but with generally slightly lower sensitivity when compared with IHC when testing tissues with patchy or sporadic PrPCWD deposition. The finding of PrPCWD in several extraneural tissues including cardiac muscle and the endocrine system suggests that further investigation and monitoring of the potential transmissibility to other species including humans is warranted.
SNIP...
(Traduit par Isabelle Vallières)
Can Vet J 2010;51:169–178
Ottawa Laboratory — Fallowfield, Canadian Food Inspection Agency, Ottawa, Ontario (Balachandran, Harrington, Algire,
Soutyrine); Veterinary Diagnostic Laboratory, Colorado State University, Fort Collins, Colorado, USA (Spraker); Veterinary
Laboratory Agency, Department for the Environment, Food & Rural Affairs, Lasswade, Midlothian, Scotland, United Kingdom
(Jeffrey, González); Animal Disease Research Unit, Agricultural Research Service, United States Department of Agriculture, Pullman,
Washington, USA (O’Rourke).
Address all correspondence to Dr. Aru Balachandran; e-mail: BalachandranA@inspection.gc.ca
http://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1109&context=zoonoticspub
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation
http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR;
Prion disease update 2010 (11)
PRION DISEASE UPDATE 2010 (11)
http://www.promedmail.org/direct.php?id=20101206.4364
This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
snip...
http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1
http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf
see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html
Thursday, August 4, 2011
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011 (SEE VIDEO)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html
Sunday, August 21, 2011
The British disease, or a disease gone global, The TSE Prion Disease (SEE VIDEO)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.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
Wednesday, November 09, 2011
Case report Sporadic fatal insomnia in a young woman: A diagnostic challenge: Case Report TEXAS
HOW TO TURN A POTENTIAL MAD COW VICTIM IN THE USA, INTO A HAPPENSTANCE OF BAD LUCK, A SPONTANEOUS MUTATION FROM NOTHING.
OR WAS IT $$$
http://creutzfeldt-jakob-disease.blogspot.com/2011/11/case-report-sporadic-fatal-insomnia-in.html
http://chronic-wasting-disease.blogspot.com/
http://bse-atypical.blogspot.com/
http://scrapie-usa.blogspot.com/
http://nor-98.blogspot.com/
http://bseusa.blogspot.com/
http://madporcinedisease.blogspot.com/
http://felinespongiformencephalopathyfse.blogspot.com/
http://caninespongiformencephalopathy.blogspot.com/
http://equinespongiformencephalopathy.blogspot.com/
http://transmissible-mink-encephalopathy.blogspot.com/
http://transmissiblespongiformencephalopathy.blogspot.com/
http://creutzfeldt-jakob-disease.blogspot.com/
http://sporadicffi.blogspot.com/
http://prionpathy.blogspot.com/
http://prionopathy.blogspot.com/
http://vcjd.blogspot.com/
http://vcjdblood.blogspot.com/
http://cjdquestionnaire.blogspot.com/2007/11/cjd-questionnaire.html
http://cjdquestionnaire.blogspot.com/
TSS
layperson
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
Sunday, November 13, 2011
California BSE mad cow beef recall, QFC, CJD, and dead stock downer livestock
California BSE mad cow beef in commerce recall, QFC, and CJD
On January 6, 2004, over 2 weeks from recall initiation, USDA determined that the beef went to only six states—Washington, Oregon, California, Nevada, Idaho, and Montana—and that no beef went to Alaska, Hawaii, or Guam. To reach that conclusion, USDA used the distribution lists, shipping records, and sales invoices that it received from companies to piece together exactly where the recalled beef may have been sent. The lists showed that 713 customers may have received the recalled beef; 6 of those may have received beef from more than one source. USDA determined that 176 customers on the lists did not actually receive recalled beef, including the customers in Guam and Hawaii. USDA’s review also indicated that recalled beef was probably not shipped to Alaska or Utah, and USDA checked 2 retailers in Alaska and 3 retailers in Utah to confirm that was the case. In total, USDA conducted verification checks on 537 of the 713 customers on the lists. USDA’s initial checks identified an additional 45 customers that may have received the recalled beef that were not included on the distribution lists, for a total of 582 verification checks. Figure 4 summarizes USDA’s verification efforts during the recall.
SNIP...
USDA’s press release stated that the recall involved 10,410 pounds of beef products, and the USDA recall coordinator for this recall told us that downstream processors mixed the recalled beef with nonrecalled beef, for a total of more than 38,000 pounds of beef that was distributed at the secondary customer level. According to USDA officials involved with the recall, the precise amount of meat that was sold at the retail level is unknown because retailers at the tertiary level further mixed nonrecalled meat with potentially contaminated meat. USDA told us that more than 64,000 pounds of beef was ultimately returned or destroyed by customers, and that, because of the mixing, it was not able to determine how much of the original 10,410 pounds of recalled beef was contained in the 64,000 pounds that were recovered.
Parts of the BSE-infected animal slaughtered on December 9, 2003, were not used for food, but they were sent to renderers to be separated into raw materials, such as proteins and blood. Rendered materials are used for many purposes, including cosmetics and vaccines. FDA has jurisdiction over renderers.
SNIP...
QFC sued over mad cow case
Grocer negligently exposed them to beef, family claims
Friday, March 5, 2004
By LEWIS KAMB SEATTLE POST-INTELLIGENCER REPORTER
An Eastside family who says they ate beef linked to the nation's only known case of mad cow disease yesterday filed a class-action lawsuit against QFC, claiming the grocery store chain negligently exposed them and others to "highly hazardous" meat and did not properly notify them that they had bought it.
Attorneys for Jill Crowson, a 52-year-old interior designer from Clyde Hill, filed the lawsuit in King County Superior Court on behalf of her family and possibly hundreds of other customers who unwittingly bought and consumed beef potentially exposed to mad cow disease.
"I was pretty upset about it," Crowson said. "I've spent all of my kids' lives trying to be a responsible parent for them to keep them safe. I felt badly that the food I served could be harmful to their health."
The lawsuit is believed to be the first stemming from this country's only confirmed case of mad cow disease, or bovine spongiform encephalopathy, which was detected in a slaughtered Holstein from a Yakima Valley ranch on Dec. 23.
Neither officials at Quality Food Centers' Bellevue headquarters, or Kroger -- the company's Ohio-based corporate parent -- could be reached for comment about the lawsuit yesterday.
The suit contends the family bought and later ate ground beef from their local QFC that was part of a batch processed at Vern's Moses Lake Meats on Dec. 9 and included meat from the diseased Holstein.
The beef was later shipped to wholesalers and retailers in Washington, Oregon, California, Idaho, Montana and Nevada.
On Dec. 23 -- after government scientists confirmed the Holstein was infected with BSE -- businesses began pulling potentially affected beef from store shelves under a voluntary recall.
But the family's suit claims that, although QFC was aware of the recall on Dec. 23, the store did not begin pulling the recalled beef from about 40 of its stores that carried it until Dec. 24.
The company also did not try to warn customers about the recalled beef until Dec. 27 -- and only then with small, inconspicuous signs inside the stores, the suit claims.
Steve Berman, the family's attorney, said the company had "a duty to warn" consumers who bought the beef under terms of the Washington Product Liability Act.
QFC could've easily notified customers by taking out TV, radio or newspaper ads, or by tracking and notifying those who bought the beef through customers' QFC Advantage Cards, Berman said.
At Berman's downtown Seattle firm yesterday, Crowson described how on Dec. 22 and Dec. 23 -- the day of the recall -- she bought single packages of "9 percent leanest ground beef" from her local QFC store at Bellevue Village.
Crowson took the beef home, cooked it and made tacos one night and spaghetti the next -- serving the dinners to herself; her daughter, Laura, 22; son, Nicholas, 19; and her niece, Claire De Winter, 23. Members of the family also ate leftovers from those meals for the next several days, Crowson said.
"When the news about mad cow came out, I instantly became concerned," Crowson said. "But the initial stories didn't mention anything about QFC, so I thought we were OK."
While shopping at the grocery store a few days later, Crowson said she asked a store butcher whether QFC stores had sold any of the recalled beef. The butcher assured her they had not, she said.
The family only learned QFC had sold any of the beef in question after reading a news story Jan. 10 about a Mercer Island man who discovered his family had eaten affected beef that he bought at a local QFC store, Crowson said.
Crowson later called QFC and faxed the company a signed letter asking that it track purchases made on her QFC Advantage Card -- a store discount card issued to customers. On Jan. 12, the company notified Crowson that the beef she bought and served to her family was, in fact, part of the recalled batch, she said.
Scientists believe people who eat beef from infected cows can contract a fatal form of the disease.
The family is "now burdened with the possibility that they presently carry (the disease) that may have an incubation period of up to 30 years," the lawsuit says.
Lawyers for the family say they believe hundreds, if not thousands, of QFC customers, and those of other stores, likely ate beef from the recalled batch -- the reason why Berman filed their legal claim as a class-action lawsuit. A USDA official this week said that up to 17,000 pounds of meat affected by the recall likely was eaten or thrown out by customers.
Berman added that an investigator from his firm learned that QFC buys beef for its "9 percent leanest ground beef" products in large tubs that can weigh several hundred pounds, and then regrinds and packages the meat for sale.
Because QFC stores regrind the beef before selling it, Berman contends that makes the store a manufacturer responsible under the Washington Product Liability Act for not selling any unsafe product.
Scientists believe people who eat beef from cows infected with BSE can contract variant Creutzfeldt-Jakob, a fatal brain-wasting disease that has been detected in about 150 people worldwide.
However, officials with the U.S. Agriculture Department have repeatedly said the risk from eating muscle cuts from an infected cow -- the likely cut of meat processed and sold for hamburger in the recalled batch -- is extremely low.
Although Crowson said she tries not to "obsess over it," she is fearful that her family could one day become sick.
"It's pretty scary," she said.
Because no medical test is available to determine whether a living person is infected with the disease, the couple's "stress and fear cannot be allayed," the lawsuit said.
The family seeks unspecified damages for emotional distress and medical monitoring costs.
Crowson said her reason for bringing the lawsuit isn't about money. "The more I've thought about this, the angrier I've gotten," she said.
snip...
QFC s Delayed Mad Cow Response Draws Lawsuit Family claims QFC should have used customer database to warn those at risk sooner
March 05, 2004
SEATTLE A Bellevue, Wash. family today filed a proposed class-action lawsuit against Quality Food Centers (QFC), a subsidiary of Kroger (NYSE: KR), claiming the grocery store chain should have used information gathered through its customer loyalty program to warn those who purchased beef potentially tainted with mad cow disease.
The suit, filed in King County Superior Court, seeks to represent all Washington residents who purchased the potentially tainted meat, and asks the court to establish a medical monitoring fund.
Jill Crowson purchased the potentially tainted beef from a Bellevue QFC on Dec. 22 and 23, and used her Advantage Card, QFC s customer loyalty program. She served the meat to her husband over Dec. 25 and 26, and later heard of the recall in the newspaper.
Steve Berman, the attorney representing the Crowsons, asserts that since the company tracks purchases, it should have warned the Crowsons and many other customers who purchased the beef at approximately 40 stores across Washington.
If you lose your keys with an Advantage Card attached, QFC will return them to you free of charge, said Berman. If they can contact you over a lost set of car keys, why couldn t they contact you and tell you that the beef you purchased could kill you?
QFC is among the large number of grocers that track customer purchases through loyalty cards like the Advantage Card. Once a customer shares contact information including name, address and phone number they are given discounts on certain items.
Regardless of any discounts offered, the loyalty card tracks customers every purchase and stores them in a central database, the complaint states.
We contend that QFC knew which Advantage Card customers purchased the suspect meat, and could have easily called to warn them, said Berman. Instead, QFC used a series of spurious excuses to hide their failure to act.
On Dec. 23, the U.S. Department of Agriculture ordered the recall of approximately 10,410 pounds of raw beef that may have been infected with bovine spongiform encephalopathy (BSE), which if consumed by humans can lead to the always-fatal Cruetzfeldt-Jakobs Disease (vCJD).
According to the complaint, QFC at first mistakenly believed it did not have any of the affected beef and took no action to remove the product from its shelves. The store later removed the beef on Dec. 24, but then did little to warn those who earlier purchased the meat, the suit claims.
It wasn t until Dec. 27 that the grocery chain posted small signs with information about the recall, the complaint alleges.
The Crowsons contacted QFC when they suspected they had purchased the potentially tainted meat, but QFC would not confirm their suspicions for two more weeks, the suit states. According to Berman, the family had to file a written request before QFC would confirm their fears.
According to health experts, Cruetzfeldt-Jakobs Disease can have an incubation period of as long as 30 years. There is no test to determine if infection took place after possible exposure, nor is there any treatment once one is infected. The condition is always fatal.
If the court grants the suit class-action status, QFC would likely be compelled to turn over the names of those who purchased the potentially tainted beef.
The proposed class-action claims QFC violated provisions of the Washington Product Liability Act by failing to give adequate warning to consumers about the potentially dangerous meat.
The suit seeks unspecified damages for the plaintiffs, as well as the establishment of a medical monitoring fund.
QFC's Delayed Mad Cow Response Draws Lawsuit
... subsidiary of Kroger , claiming the grocery store chain should
... beef potentially tainted with "mad cow disease
... beef at approximately 40 stores across Washington.
040307 Woman Sues QFC Over Mad-Cow Recall ... Jakob disease, the human form of mad-cow, from eating ... QFC is subject to the Washington Product Liability ... been found in a slaughtered Yakima County dairy cow. ...
Subject: GOVERNOR SCHWARZENEGGER PREFERS CALIFORNIANS TO EAT MAD COW BEEF IN SECRECY, VETOED BILL SB 1585
Date: October 1, 2004 at 2:22 pm PST
GOVERNOR SCHWARZENEGGER PREFERS CALIFORNIANS TO EAT MAD COW BEEF IN SECRECY, VETOED BILL SB 1585
Schwarzenegger Vetoes Meat Recall Disclosure Bill
Legislation Would Have Identified Stores that Received Contaminated Meat and Poultry
Governor Arnold Schwarzenegger (R-CA) vetoed a bill yesterday that would have let Californians know whether they ve purchased contaminated meat or poultry. The bill, SB 1585, would have ended a secrecy agreement between the U.S. Department of Agriculture (USDA) and California that prevents the state from disclosing the names and locations of stores that receive shipments of recalled meat.
Consumers have a right to know if they purchased recalled meat or poultry, said Ken Kelly, Staff Attorney at the Center for Science in the Public Interest (CSPI). Why force families to roll the dice when they put food on the table? Governor Schwarzenegger prefers a get-sick-first, ask-questions-later policy.
Earlier this year, California was one of several states that received meat from the Washington State cow that tested positive for mad cow disease. But because California is one of 12 states that have signed a secrecy agreement with USDA, state health officials were prohibited from identifying stores or restaurants that may have received beef from the infected cow. Even recalled meat tainted with deadly E. coli 0157:H7 bacteria would be subject to the secrecy agreement, leaving consumers uncertain as to whether the ground beef in their refrigerator were safe to eat.
In his veto message, Governor Schwarzenegger indicated he would instruct the state s health department to renegotiate an agreement that would allow USDA to share recall information with local public health officials. But according to CSPI, even if USDA agreed to share recall information with local officials, the local officials would be similarly prohibited from disclosing names of retail outlets with consumers. In August, CSPI urged USDA not to force states to sign any such secrecy agreements. Federal and state government should be more concerned with protecting consumers from unnecessary hospitalizations and deaths associated with food-borne illness, and less concerned with protecting grocers and meat producers from bad publicity, Kelly said.
SUPERIOR COURT OF THE STATE OF WASHINGTON FOR KING COUNTY
JILL CROWSON, ET AL., PLAINTIFFS
VS
QUALITY FOOD CENTERS, INC., an Ohio corporation Defendent
NO. 04-2-05608-0 SEA
snip...
The Court hereby GRANTS the defendant's motion to dismiss the plaintiff's claims based on a manufacturer's strict liability (Counts I and II) and DENIES the defendant's motion to dismiss the plaintiff's claim of negligence by a product seller (Count III).
DATED this 14th day of June, 2004
snip...
archived link;
Date Filed: March 5, 2004 Court: King County Superior Court (Washington) Location: Seattle Ticker Symbol: NYSE:KR
Join This Suit Tell a Friend
Consumers filed a proposed class-action lawsuit against Quality Food Centers (QFC), a subsidiary of Kroger (NYSE: KR), claiming the grocery store chain should have used information gathered through its customer loyalty program to warn those who purchased beef potentially tainted with ?mad cow disease.? The USDA issued a recall notice for the meat on December 23, 2003. QFC sold the meat through its approximately 40 stores across Washington.
The suit claims that even though QFC had the ability to quickly warn every customer who purchased the potentially deadly meat if they used the QFC Advantage Card at the time of purchase, the grocery store neglected to do so.
The suit seeks to represent every consumer in Washington state who purchased the recalled meat from QFC.
Recent Updates
June 14, 2004 - the King County Superior Court gave the green light to a suit claiming QFC didn't do enough to warn customers about beef potentially tainted with 'mad cow disease,' finding enough questions about the beef and QFC's responsibility to explore in the courtroom.
Read the court order.
archived url link;
QFC - 'Mad Cow' Frequently Asked Questions
The Suit
What is the key issue in this suit?
On December 23, 2003, the United States Department of Agriculture (USDA) recalled more than 10,000 pounds of raw beef that could have been exposed to bovine spongiform encephalopathy (BSE). Humans consuming BSE-tainted meat can contract Creutzfeldt-Jakob Disease (vCJD), an always-fatal condition.
QFC sold this meat throughout its stores in Washington. Even though QFC had the ability to quickly warn every customer who purchased the potentially deadly meat if they used the QFC advantage card at the time of purchase, the grocery store neglected to do so, the suit alleges.
Who does the suit seek to represent?
The suit seeks to represent all persons who purchased recalled meat from any QFC store in the state of Washington.
Who are the defendants?
Quality Food Centers, or QFC. Once a local, Northwest company, QFC is now a wholly owned subsidiary of the grocery chain giant, Kroger.
What does the suit seek?
The suit asks the court to order QFC to establish a medical monitoring fund which would allow those who purchased and consumed the meat to seek medical care, checking for, and if necessary, treating --- the infection of vCJD. The suit also seeks the creation of a medical notification system, allowing those who may have been exposed to the disease to receive periodic updates on research and treatment of vCJD. The suit also seeks unspecified damages for the plaintiffs.
Does the suit claim QFC violated specific laws?
Yes. The lawsuit claims QFC violated the Washington Product Liability Act. In addition, the suit claims QFC was negligent by not warning consumers of the dangers associated with the affected meat.
Where was the lawsuit filed?
The suit was filed in King County Superior Court on March 4, 2004.
How do I determine if I qualify to join the lawsuit?
If you have a QFC Advantage card and believe that you bought recalled meat from a QFC store, you may be eligible to join the lawsuit. Click here to fill out the sign-up request form, or you can contact Hagens Berman attorneys.
QFC
What is the QFC Advantage Card?
The Advantage Card is known in the grocery industry as a Customer Loyalty Card. Customers who sign up for QFC's Advantage Card receive special discounts on selected items, but gives the grocery store chain the ability to track consumers purchases in order to enhance their marketing efforts. In addition, grocery chains which offer affinity card programs often use the database and shopping pattern data to send users coupons and other marketing material. According to the complaint, QFC tracks every purchase made by consumers presenting the Advantage Card, including product description, date of purchase, store of purchase and the price, and saves that data with customer contact information.
What was QFC's response to the meat recall?
On Dec. 23, 2003, QFC received notice from the U.S. Department of Agriculture (USDA) of a recall of approximately 10,410 lbs. of raw meat that may have been contaminated with the infectious agent that causes mad cow disease. QFC did not act immediately on the recall notice but initially responded by denying that it had any of the tainted meat. On December 24 QFC pulled the meat from its shelves, but the company took no steps to directly warn consumers. It was not until Dec. 27 that QFC posted small signs in its stores recalling the tainted beef, according to the complaint. During that four day period when QFC was silent hundreds of consumers may have eaten the meat.
Can QFC determine if an Advantage Card holder purchased the potentially dangerous meat?
Yes. In fact, consumers can now contact QFC directly and the company will provide information about meat purchases ? but only if you ask. Hundreds of other consumers who purchased the meat and are unaware of the situation have not heard from QFC, the complaint states.
Why was QFC sued even though they pulled the meat? Under Washington law since QFC ground the meat it is deemed a manufacturer and is strictly liable for any unsafe product. In addition QFC possessed specific and easily obtainable information on which customers purchased the recalled meat, but did not act to inform customers, the suit states. Considering the potential danger and risk of worry for consumers, and the ease of contacting consumers using database information, simply pulling the meat from the shelves and belatedly posting small signs was not an adequate response, according to the complaint.
What information on customer purchases does QFC track with the Advantage Card? QFC tracks every purchase that a customer with an Advantage Card makes, regardless of whether discounts are offered or not, according to the complaint.
Does the recently announced larger-than-expected recall of beef affect the lawsuit? No. Regardless of the size of the beef recall, attorneys believe the facts in the case remain the same.
How can I find out if I bought recalled meat from QFC? If you believe that you may have purchased recalled meat from a QFC store, and you have an Advantage Card, you can contact QFC and ask if your record shows you purchased recalled beef. You can contact QFC at 866-221-4141.
Isn't QFC prohibited by privacy laws from contacting consumers with warnings like this? No ? the suit notes that the company will return car keys returned to the store if the keys have an Advantage Card attached. According the complaint, If QFC can return car keys by mail, why can't they send a notice saying the meat a customer purchased in their store could cause an incurable, fatal disease? Further privacy laws would prevent QFC from disclosing information to third parties, disclosing the information to the customer whose card it is does not violate privacy laws. For example, if a trade group wanted to know the names of consumers who purchased a given drug sold at QFC, disclosure of that private information might be a privacy concern. However, disclosure to a consumer of his own records is not.
Mad Cow Disease
What is Mad Cow disease? In cows, mad cow disease is defined as bovine spongiform encephalopathy (BSE), and is a progressive neurological disease. The human disease variant is know as Creutzfeldt-Jakob Disease (vCJD), which is a rare brain disorder that causes a rapid, progressive dementia and is always fatal, according to the complaint.
Where can I get more information on Mad Cow disease? The USDA provides information on the disease at www.usda.gov/.
What should I do if I believe that I've eaten recalled meat? According to the complaint, no screening tests or treatments have been found for Creutzfeldt-Jakob disease. Those who suspect they've eaten recalled meat should contact their physician for more information.
http://www.hagens-berman.com/files/madcowfaq1-13-051105661006369.html
archived url link;
Do Stores That Offer Loyalty Cards Have a Duty to Notify Customers of Product Safety Recalls? A Recent Suit Raises This Novel Question By ANITA RAMASASTRY ----
Thursday, Aug. 05, 2004
An interesting new Washington state court suit raises an important question: If a retailer benefits from collecting personally identifiable information about its customers, does it have a corresponding duty to use such data to alert its customers that products they've bought have been recalled for health or safety reasons? And if so, could turning over private data to companies actually create benefits, as well as privacy risks, for the consumer?
In the suit, consumer Jill Crowson is suing her grocery store -- Quality Food Center (QFC), a subsidiary of Kroger -- for negligent infliction of emotional distress and disregard of a "duty to warn" under the Washington Product Liability Act. Crowson alleges in her complaint that QFC failed to alert her family that ground beef it had sold them had been recalled in December's mad-cow scare.
Yet, Crowson says, QFC easily could have done so through information it maintained connected with her Advantage card - a "loyalty card" that meant QFC had Crowson's name, address and purchasing information. According to her complaint, QFC tracks every purchase made by consumers presenting the Advantage Card, including product description, date of purchase, store of purchase and the price, and saves that data alongside customer contact information.
Now, Crowson says, her family members "feel like walking time bombs" knowing they may be infected with the human form of mad-cow disease which the complaint states may have an up-to-30-year incubation period. And they are not the only ones: Crowson is seeking class action status for herself and what she believes are "hundreds" of similarly-situated Washington customers at QFC's approximately 40 stores in the state.
Some lawyers think Crowson's suit is a stretch. Federal law does not impose on companies a specific duty to notify consumers when tainted meat is recalled under the direction of the U.S. Department of Agriculture (USDA), as was the case here. Also, Crowson and her family, and the class she seeks to represent, are suing based on fear (and possible future harm), not current illness. Moreover, the chance they will actually get Mad Cow Disease some time in the future are apparently remote.
Nevertheless, the lawsuit has strong intuitive appeal: QFC could have saved the Crowsons and others like them a lot of worry, and perhaps sleepless nights, with what appears would have been minimal effort, using information at its digital fingertips. And the court has already once refused to dismiss it - finding that there were sufficient factual questions about the beef and about QFC's responsibility to the Crowsons, to merit further exploration of the evidence, through discovery and in the courtroom.
Regardless of the outcome of Crowson's suit, it underscores the need for retailers and policymakers to examine what sort of responsibilities come with private data gathering under loyalty card schemes.
The Lawsuit: The Chronology of Facts Alleged, and the Loyalty Card at Issue
On December 22 and 23, 2003, Crowson bought ground beef from a QFC store. Also on December 23, 2003, the USDA recalled Washington beef after it confirmed that a cow slaughtered in Washington had been infected with Mad Cow Disease. But Crowson says QFC did not pull the affected meat from its shelves until December 24, and did not post signs in its stores announcing the recall until December 27. By then, the Crowson family had eaten the meat.
Crowson states that she only learned of the recall by reading an article in her local newspaper. She said she subsequently called the supermarket chain, then faxed QFC a letter asking that her purchase be traced through her QFC Advantage card. On January 10, she was notified that her ground beef purchase was indeed from the recalled batch.
Crowson says that what QFC allegedly did in response to the recall - pulling the beef from shelves the next day, and posting signs three days after that -- was far from enough. She says it should have immediately warned customers who had bought possibly tainted meat through newspaper, radio and television advertising -- and by contacting individually those who, like her, had Advantage cards. Its failure to do so, she says, is what makes the company liable to her and other shoppers.
The Advantage Card is known in the retail industry as a customer "loyalty card" - providing discounts on specific items, in exchange for consumer information that will aid in better tailoring the company's marketing efforts. Combining the data from one's loyalty card application with data from other commercial databases or public records (for examples, mortgage records, or court filings) can often allow a very specific profile of each consumer.
Some states limit the types of information that a grocery store can collect from you when you register for a loyalty card. For example, California state law prohibits a grocery store from requiring that you turn over your social security or your driver's license number.
Companies, of course, stress the potential savings that might result from use of a loyalty card. Consider, for instance, the sales pitch on the QFC website it reads: "If you don't have a QFC Advantage Card, you're missing out! The Advantage Card is a powerful new way to save on the groceries you buy every day. It gives you the best of all possible worlds: premium quality, superb service and lower prices. That's something no other grocery store can match. So make sure you take advantage of the big savings."
Privacy advocates complain that loyalty cards result in the improper use - and, often, sale to third parties - of customers' private information. QFC apparently doesn't sell customers' data to third parties, however. Its website promises that "QFC will not release your name to any list service or manufacturer, and that such information will be held in the strictest of confidence-even within our company."
Privacy advocates also warn, however, that even if third-party sales of data are not allowed, the data compiled can always be accessed with a subpoena or warrant and used against the customer in court proceedings. Meanwhile, consumer advocates claim that certain loyalty cards don't really offer the savings they promise. Nevertheless, numerous stores employ loyalty cards.
Turning the Privacy Debate on Its Head: With Great Information, Comes Great Responsibility?
The Crowson lawsuit turns the privacy debate on its head. Typically, privacy advocates ask retailers to safeguard the personal information they collect about their shoppers. In this case, in contrast, plaintiff is asking that QFC delve into its database to notify her about a meat recall.
QFC does this very thing if a consumer loses his or her keys with an Advantage Card attached to them - returning the keys free of charge. So Crowson's attorney, Steve Berman, asks: "If they can contact you over a lost set of car keys, why couldn't they contact you and tell you that the beef you purchased could kill you?"
According to some news reports, QFC was reluctant to call customers regarding the recall based on privacy concerns. But in this case, the concerns seem misplaced. No privacy law is violated when a consumer communicates with the customer herself regarding private information - indeed, every offer the customer receives is, in a sense, this kind of communication. When the customer is receiving personalized discounts based on her purchase history, why can't she receive personalized health and safety warnings based on that history, too?
Was There a Duty to Warn Here?
From the law's perspective, the question will be not whether QFC ideally should have warned the Crowsons - of course it should have. The question will be if it had a legal duty to do so. Such a duty would come from either the common law of torts, which allows claims where there is a duty to behave reasonably to prevent foreseeable harm to others. . Or it might come from the Washington product liability statute - which, as noted above, creates a "duty to warn" in certain situations.
And of course, if there is no current duty, the legislature may see fit to pass a statute creating such a duty. :It may seem more prudent, however, for retailers to voluntarily assume such a responsibility. When companies benefit from collecting customer information, shouldn't they also assume a duty to protect customers from known risks associated with that very information? Some risks, of course, may be a matter of opinion. But this one was not: The fact of the risk was acknowledged by the USDA recall of the meat. With this kind of clear notice of the risk, it seems that QFC either does - or ought to - have a duty to protect customers from this risk.
Of course, should a retailer not wish to take on this responsibility, it can also change its loyalty program. QFC and other retailers could still track consumer purchases without asking them for personally identifiable information.
http://writ.corporate.findlaw.com/ramasastry/20040805.html
archived url link;
FindLaw's Writ - Ramasastry: Mad Cow in the USA
http://writ.corporate.findlaw.com/ramasastry/20031230.html
Family to sue grocery chain
A Seattle family that ate beef linked to the US's only known case of BSE has filed a classaction lawsuit against the grocery chain QFC, claiming the company negligently exposed them and others to "highly hazardous" meat and did not properly notify them that they had bought it.34 The suit contends that Jill Crowson and her family bought and later ate ground beef from their local QFC that was part of a batch processed at Vern's Moses Lake Meats on 9 December 2003 and included meat from the diseased Holstein. The beef was later shipped to wholesalers and retailers in Washington, Oregon, California, Idaho, Montana and Nevada.
After government scientists confirmed on 23 December that the Holstein was infected with BSE, businesses began pulling potentially affected beef from store shelves under a voluntary recall. But, the family's suit claims, although QFC was aware of the recall, the store did not begin pulling the beef from about 40 of its stores until 24 December. The company also did not try to warn customers about the recalled beef until 27 December – and only then with small, inconspicuous signs inside the stores, the suit claims. The family only learned QFC had
9
sold any of the beef in question after reading a news story on 10 January about a man who discovered his family had eaten affected beef that he bought at a local QFC store, Crowson said. She later called QFC and faxed the company a signed letter asking that it track purchases made on her QFC Advantage Card, and on 12 January the company notified Crowson that the beef she bought and served to her family was, in fact, part of the recalled batch, she said.
The family seeks unspecified damages for emotional distress and medical monitoring costs. Crowson said her reason for bringing the lawsuit is not about money. "The more I've thought about this, the angrier I've gotten," she said. Neither the company nor its parent corporation, Kroger, have commented.
http://www.which.net/campaigns/food/safety/bse_reports/bserep0304.pdf
archived url link;
please see full text ;
CALIFORNIA CREUTZFELDT JAKOB DISEASE TSE PRION DISEASE STATISTICS ???
there seems to be no data on CJD cases in California ???
http://ceip.us/cjd.htm
archived url link;
California Case Report Form ;
http://www.cdph.ca.gov/pubsforms/forms/CtrldForms/cdph9002.pdf
archived url link;
now this form would probably go straight to Gambetti et al and CDC.
CWRU Gambetti et al surveillance program for CJD is lacking significantly. so your guess is as good as mine on CJD cases in California.
Gambetti's case files on CJD has not been updated since August of 2011. ...
http://www.cjdsurveillance.com/pdf/case-table.pdf
archived url link;
Barriers to Creutzfeldt-Jakob Disease Autopsies, California
Janice K. Louie,*† Shilpa S. Gavali,* Ermias D. Belay,‡ Rosalie Trevejo,† Lucinda H. Hammond,* Lawrence B. Schonberger,‡ and Duc J. Vugia*†
Creutzfeldt-Jakob disease (CJD) surveillance relies on autopsy and neuropathologic evaluation. The 1990–2000 CJD autopsy rate in California was 21%. Most neurologists were comfortable diagnosing CJD (83%), but few pathologists felt comfortable diagnosing CJD (35%) or performing autopsy (29%). Addressing obstacles to autopsy is necessary to improve CJD surveillance. Transmissible spongiform encephalopathies (TSEs) are rare, progressively fatal, neurodegenerative illnesses. Human TSEs include classic Creutzfeldt-Jakob disease (CJD) and the recently described variant CJD associated with eating bovine spongiform encephalopathy–infected cattle products in Europe (1). The recent identification of bovine spongiform encephalopathy in the United States underscores the importance of maintaining enhanced surveillance to monitor for the possible occurrence of variant CJD in this country (2,3). In California, CJD is not reportable. Since 1999, the California CJD Surveillance Project of the California Emerging Infections Program, a collaboration of the California Department of Health Services and the U.S. Centers for Disease Control and Prevention, has conducted enhanced surveillance for classic and variant CJD. Methods include review of state mortality data and followup investigation of CJD-related deaths that occur in persons <55 years of age, since >98% of cases of variant CJD in the United Kingdom have occurred in this age group. As part of this enhanced surveillance, medical records for 33 deceased California residents <55 years old from 1996 through 2003 have been investigated with criteria for CJD developed by the World Health Organization and Centers for Disease Control and Prevention; none met the criteria for variant CJD.
snip...
The Study Data from the 1990–2000 Death Public Use File (underlying cause of death only) and 1990–1999 Multiple Cause-of-Death Data (underlying or contributing causes of death) were obtained from the Center for Health Statistics, California Department of Health Services (5). Deaths among California residents with an International Classification of Diseases, 9th Revision, code 046.1 or 10th Revision, code A81.0 listed anywhere on the death record were included in our analysis. Both data files included report of autopsy as a variable, with the exception of the Multiple Cause-of-Death Data for 1997 to 1999, when autopsy performance was not recorded. Statistical analysis was performed by using SAS software (SAS Institute, Cary, NC). From July to December 2002, questionnaires regarding experience with diagnosing CJD were sent to 1,241 California neurologists identified as members of the American Academy of Neurology and 574 pathologists identified as members of the California Society of Pathologists and the American Association of Neuropathologists. Approval was obtained from the Committee for the Protection of Human Subjects of the State of California.
Review of mortality data identified 263 CJD-related deaths in California from 1990 through 2000. Of these, 244 were identified from the 1990–1999 Multiple Causeof- Death Data, and an additional 19 deaths were identified from the 1990–2000 Death Public Use File. A total of 42 (16%) cases identified by the Multiple Cause-of-Death Data were not detected in the Death Public Use File. Overall, 26 (10%) of the 263 CJD-related deaths were in persons <55 years of age. Only two deaths occurred in persons <30 years of age. The overall autopsy rate, which for 1997 to 2000 only includes autopsies performed on persons for whom CJD was recorded as the underlying cause of death, was 53 (21%) of 251 persons: 11 (44%) of 25 persons <55 years of age, and 42 (19%) of 226 persons 55 years of age. For two deaths, autopsy performance was not recorded.
Of 1,241 questionnaires mailed to neurologists, 428 (34%) were completed, including 310 (25%) from respondents involved in patient care. Responses regarding the neurologists’ experience with diagnosing CJD and performing autopsy are summarized in Tables 1 and 2. Most neurologists (83%, 255/307) felt comfortable clinically recognizing classic CJD. More than one third (36%, 74/207) had not considered arranging for autopsy in their CJD patients, although most reported access to histopathologic services (75%, 223/297). The most commonly cited barrier to obtaining autopsy was family reluctance to give consent (79%, 192/242). Of 574 questionnaires mailed to pathologists, 284 (49%) were completed. Tables 1 and 2 summarize the responses. Thirty-five percent (96/273) and 15% (40/274) of pathologists were comfortable recognizing the neuropathologic features of classic CJD and variant CJD, respectively. Infection control concerns (77%, 143/185), lack of experience (62%, 69/111), and institutional limitations (53%, 111/210) were cited as major obstacles to autopsy performance, and less than half of respondents reported that confirming the diagnosis of CJD (47%, 92/197) or ruling out variant CJD (45%, 87/193) was an important reason to pursue autopsy.
Conclusions
Our analysis suggests that autopsy rates for CJD in California are low. The results of our surveys, which attempted to discern the reasons for this low rate, imply that both neurologists and pathologists have similar perceptions of the value of obtaining histopathologic evaluation for CJD but for different reasons. Most neurologists appeared to be comfortable clinically diagnosing CJD, with more than one third reporting they had never considered pursuing autopsy for CJD cases. In contrast, pathologists appeared to be less comfortable making a histopathologic diagnosis, indicating that autopsy performance was limited by infection control concerns, lack of experience with CJD cases, and institutional restrictions.
Our results have some limitations. Approximately 10% of CJD cases may have atypical signs and symptoms that can obscure the diagnosis. To the extent that these cases are misdiagnosed and not autopsied, they could contribute to overestimation of the autopsy rate. On the other hand, death certificate analysis can be an insensitive indicator of the true rate of autopsy, and autopsy performance information was unavailable for 1997 to 2000 from the Multiple Cause-of-Death Data. Both factors could lead to possible underestimation of the true autopsy rate. Given that some CJD cases will have had confirmatory brain biopsy or strongly suggestive clinical features and diagnostic studies, the autopsy rates cited may apply mostly to patients for whom a satisfactory antemortem diagnosis could not be made. Interpreting survey results is limited by the low response rate; neurologists and pathologists who are experienced in diagnosing CJD may be more likely to respond, which would introduce bias.
The public health benefits of performing autopsy on patients with suspected CJD should not be underestimated. Autopsy and histopathologic analysis remain important ways to confirm a diagnosis of CJD and help define the usual occurrence of subtypes of classic CJD, thereby facil-itating the recognition of emerging TSEs (1,6,7). Autopsy rates for nonforensic deaths have declined dramatically during the past 40 years, with national hospital rates currently <5%, possibly resulting in missed diagnoses of the actual cause of death in 8% to 25% of cases (8–11). The reasons for the decline are multifaceted and include escalating cost of autopsy borne by hospitals and county medical examiners, lack of direct reimbursement, fear of litigation, and increasing reliance on modern technology to determine a diagnosis antemortem (10).
Our survey results suggest that infection control concerns play a role in low autopsy rates for CJD, whether because of fears about the risk of acquiring CJD from handling contaminated tissue or because of liability considerations at the institutional level. More realistically, brain autopsy can be performed safely as long as CJD-specific infection control guidelines are strictly followed (12–13). Nonetheless, concerns about potentially acquiring CJD through autopsy procedures should be acknowledged and recognized as an opportunity to address proper infection control techniques.
Enhancing surveillance for variant CJD and other emerging prion diseases will require educating neurologists and pathologists, addressing the perceived obstacles to obtaining autopsy, and encouraging the use of available resources that provide expertise and technical assistance in evaluating CJD. For example, brain tissue can be submitted to the National Prion Disease Pathology Surveillance Center (NPDPSC) in Cleveland, Ohio, for free state-ofthe- art diagnostic testing (14). The availability of a national center of expertise may facilitate obtaining tissue evaluation; since the inception of NPDPSC, the number of referrals to the facility has more than doubled, from 104 in 1997 to 265 in 2002, and the number of TSE cases confirmed from those referrals increased from 60 in 1997 to 151 in 2002 (14). Regional academic institutions, such as the University of California, San Francisco, Memory and Aging Center, can also provide expertise and assistance with diagnostic testing. Such resources are vital to maintaining vigilance for cases of CJD and potentially emerging human TSEs, such as variant CJD or possibly a human form of chronic wasting disease in the United States.
Title 17, California Code of Regulations (CCR) §2500, §2593, §2641.5-2643.20, and §2800-2812 Reportable Diseases and Conditions*
REPORTABLE COMMUNICABLE DISEASES §2500(j)(1)
Creutzfeldt-Jakob Disease (CJD) Spongiform Encephalopathies (TSE)
URGENCY REPORTING REQUIREMENTS [17 CCR §2500(h)(i)] . ! = Report immediately by telephone (designated by a . in regulations).
http://www.cdph.ca.gov/HealthInfo/Documents/Reportable_Diseases_Conditions.pdf
archived url link;
http://www.cdph.ca.gov/HealthInfo/Documents/TITLE_17_SECTION_2505.pdf
archived url link;
http://www.ceip.us/cjd_lhd.htm
latest link;
2011
Tuesday, November 08, 2011
Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance? A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011
Original Paper
Conclusions: These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.
PLEASE NOTE, cjd or any prion disease is still NOT a Nationally Notifiable Infectious Disease, which in my mind boggles the imagination, considering ramifications from Iatrogenic CJD TSE Prion disease. ...
NATIONALLY NOTIFIABLE INFECTIOUS CONDITIONS
UNITED STATES 2011
CALIFORNIA CJD Sonoma County 2011
Local cases of rare brain disease draw scrutiny
By CATHY BUSSEWITZ THE PRESS DEMOCRAT
Published: Saturday, May 28, 2011 at 3:00 a.m.
Last Modified: Saturday, May 28, 2011 at 10:30 p.m.
Page 3 of 5
Dr. Michael Geschwind, neurologist at UC San Francisco, who has treated CJD patients from Sonoma County, ran the first U.S. treatment study for CJD. Geschwind said he and other scientists expect another outbreak of variant Creutzfeldt-Jakob disease to occur because the disease has a long incubation period, and there likely are people who have been exposed but have not yet come down with disease.
Geschwind said researchers are investigating potential connections between sporadic CJD, mad cow disease and the chronic wasting disease that afflicts wild deer and elk.
“It's possible, and that's why we're doing these cases,” Geschwind said. “We call it ‘sporadic' almost out of ignorance. We call it sporadic because we don't know what causes it.”
Over the past 18 years, 19 people have died in Sonoma County of CJD, an average of one case per year in a county with a population of about 483,000 — about twice the national average.
Geschwind said it's hard to know whether Sonoma County's higher infection rate is significant because the diagnosis can be difficult. Unless those cases of CJD are confirmed by an autopsy or specialist, the number could be overreported, he said.
Becky Weislow of Santa Rosa, whose sister-in-law in San Carlos died of CJD this month, said her “biggest concern is to make sure that we aren't in some way or another contracting it from our food source.”
“How can you say it's not, if you don't know how it is contracted?” she said. “Especially because it seems like the people who have contracted it have been lovers of food. My sister-in-law loved to experience new food, and Ric Collins had traveled to Europe extensively.”
Weislow and Lorraine Collins recently walked in the Human Race and raised $11,000 for research at UCSF, where their family members were treated, she said.
Collins, through her network, identified a third Sonoma County person who died of CJD last year.
Wednesday, November 09, 2011
Case report Sporadic fatal insomnia in a young woman: A diagnostic challenge: Case Report TEXAS
HOW TO TURN A POTENTIAL MAD COW VICTIM IN THE USA, INTO A HAPPENSTANCE OF BAD LUCK, A SPONTANEOUS MUTATION FROM NOTHING.
OR WAS IT $$$
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
Thursday, November 10, 2011
National Meat Association v. Harris Docket No., 10-224
DEADSTOCK DOWNER PIGS AND PORCINE SPONGIFORM ENCEPHALOPATHY PSE
Court Likely to Overturn CALIFORNIA Law on Livestock
WHO WILL FOLLOW THE CHILDREN FOR CJD SYMPTOMS ???
Saturday, May 2, 2009
U.S. GOVERNMENT SUES WESTLAND/HALLMARK MEAT OVER USDA CERTIFIED DEADSTOCK DOWNER COW SCHOOL LUNCH PROGRAM
DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ???
you can check and see here ;
http://www.fns.usda.gov/fns/safety/pdf/Hallmark-Westland_byState.pdf
see archived link;
Thursday, June 2, 2011
USDA scrapie report for April 2011 NEW ATYPICAL NOR-98 SCRAPIE CASES Pennsylvania AND *CALIFORNIA
Sunday, November 13, 2011
Atypical Scrapie Isolates Involve a Uniform Prion Species with a Complex Molecular Signature
PrPres peptides of low molecular mass have also been described in other types of prion disease, such as Gerstmann-Sträussler-Scheinker disease [32], [33] and Creutzfeldt-Jakob disease [34], [35] in humans as well as in H-BSE in cattle [36], [37].
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
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"
EFSA Journal 2011 The European Response to BSE: A Success Story
This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
snip...
see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;
Wednesday, March 31, 2010
Atypical BSE in Cattle
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE.
In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
http://www.neuroprion.org/en/np-neuroprion.html
archived link;
Rural and Regional Affairs and Transport References Committee
The possible impacts and consequences for public health, trade and agriculture of the Government's decision to relax import restrictions on beef Final report June 2010
2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo-has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50
http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf
archived url link;
[Terry S. Singeltary Sr. has added the following comment:
"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed.
http://whqlibdoc.who.int/publications/2003/9241545887.pdf
archived url link;
https://web.archive.org/web/20051105100237/http://whqlibdoc.who.int/publications/2003/9241545887.pdf
Terry S. Singeltary Sr. has added the following comment:
"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed.
The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"
http://www.promedmail.org/direct.php?id=20100405.1091
archived url link;
When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
archived link;
The conclusions state that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Active screening has allowed the identification of 3 new forms of animal TSEs (H-type atypical BSE, L-type atypical BSE, and atypical scrapie), but the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs. There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential. Transmission experiments to human PrP transgenic mice or primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential and indicate that that of the L-type atypical BSE agent appears similar or even higher than that of the classical BSE agent. A single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.
Commentary ---------- Following to a request from the European Commission, the Panel on Biological Hazards (BIOHAZ) and the European Centre for Disease Prevention and Control (ECDC) were asked to deliver a scientific opinion on any possible epidemiological or molecular association between transmissible spongiform encephalopathies (TSEs) in animals and humans. The opinion reviews and discusses the existing scientific evidence that links animal and human TSEs currently known.
The opinion first considers the definition of zoonoses and the principles for the identification of zoonotic diseases, which can be based on evidence gathered from both epidemiological and laboratory studies. The opinion describes the challenges involved in identifying TSEs as zoonoses, due to the specific characteristics of TSE infections/diseases, such as the nature of TSE agents, the occurrence of animal and human TSEs, and the type of monitoring applied, the long incubation period of TSEs etc. The example of the process that led to establishing a link between bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (vCJD) is reviewed. The epidemiological and laboratory criteria that can be used to investigate such a link are described in detail, since those criteria might be useful for the identification of links between other animal and human TSEs.
The opinion discusses the strain diversity of the TSE agents described in sheep, goats, cattle, cervids, and humans, based on the current knowledge, which highlights that multiple TSE agents exist in each species. The factors influencing the capacity of TSE agents to cross the species transmission barrier are then considered in detail, including the variability in host and donor PrP gene and protein, the TSE strain type involved and its interaction with the host PrP, and the route of infection.
The opinion critically assesses the tools and methodologies currently available to study and evaluate the possible association between animal and human TSEs. The use of epidemiology is discussed for TSEs in both animals and humans, and the possibility to compare the 2 sources of information is presented as a possible method to study the possible links.
Both in vivo and in vitro laboratory methods are considered and discussed, including neuropathology, transmission experiments involving different animal models (wild type and transgenic mice, primates and other species), biochemical methods, cell-free conversion assays, protein misfolding cyclic amplification (PMCA), and cell culture assays. Characteristics, advantages, and disadvantages of the different methods are reviewed, including the opportunity to collate data from different types of experiments for the study of potential associations between animal and human TSEs.
The opinion then reviews the scientific evidence currently available for the different animal and human TSEs, including classical BSE, atypical BSE (H-type and L-type), classical scrapie, atypical scrapie, chronic wasting disease (CWD), transmissible mink encephalopathy (TME), and human TSEs. In particular, the following aspects are systematically discussed for each TSE agent: epidemiology, pathogenesis, and in vivo and in vitro transmission experiments.
The opinion concludes that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. With regard to human TSEs, detected cases of sporadic CJD are randomly distributed in time and geographical location. These observations have been interpreted as a supportive argument that sporadic CJD is not environmentally acquired. However, the epidemiological evidence in relation to sporadic CJD cannot be regarded as definitive, and the possibility that a small proportion of cases are zoonotic cannot be excluded.
It also concludes that a series of uncertainties in relation to the epidemiological patterns of animal and human TSEs indicate that even a rough comparison of the present epidemiological patterns of human and animal TSEs other than classical BSE is unlikely to be informative. Because of these uncertainties, it is an imperative to continue to carry out systematic surveillance of human TSE diseases, and to continue and improve the surveillance of animal TSE diseases.
The opinion highlights that the active screening has allowed the identification of 3 new forms of animal TSEs (L-type atypical BSE, H-type atypical BSE, and atypical scrapie), but that the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs.
There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential.
Transmission experiments to human PrP transgenic mice suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE and classical BSE in sheep agents) might have zoonotic potential, whereas for other agents there is no evidence provided of a zoonotic potential (H-type atypical BSE and CWD), or no published studies are available (classical and atypical scrapie). In addition, transmission experiments to primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential. In particular, primates are highly permissive to L-type atypical BSE, even by the oral route.
The opinion emphasizes that laboratory transmission experiments indicate that the L-type atypical BSE agent has a significant zoonotic potential, which appears similar or even higher than that of the classical BSE agent. While transmission data for evaluating the zoonotic potential of classical scrapie in primates and human PrP transgenic mice are extremely limited or not yet available, a single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.
The opinion concludes that human PrP transgenic mice and primates are currently the most relevant models for investigating the human transmission barrier, but the extent to which such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. It is unpredictable whether a TSE agent will transmit to a new host, and if the transmission principally occurs, what the transmission rate will be.
Based on the results obtained with in vitro conversion assays, the opinion concludes that there is probably no absolute molecular barrier to transmission of TSE agents between mammalian species. Results also suggest that these assays may be developed as a tool for quantifying the transmission barriers between species for different TSE agent strains; however, there is no means at the moment to transpose in vitro results into the likelihood of in vivo interspecies transmission.
-- Communicated by: Terry S Singeltary Sr
[ProMED-mail thanks Terry S Singeltary Sr for drawing attention to this comprehensive document which provides a current evaluation of experimental work designed to explore the zoonotic potential of the various recently recognised TSEs of domestic and other animals.
It is concluded that at present the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Nor can it be entirely excluded at the present time that a small proportion of cases of sporadic CJD may be environmentally acquired. - Mod.CP]
******
http://www.promedmail.org/direct.php?id=20110607.1736
USDA FDA FAILED BSE TRIPLE FIRE WALLS, a feed ban and surveillance system that was nothing more than ink on paper ;
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
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
archived url link;
Monday, September 12, 2011
BSE PRION Agriculture Animal Feed Question House of Lords Thursday, 8 September 2011
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)
PRION DISEASE UPDATE 2010 (11)
Thursday, August 4, 2011
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011 (SEE VIDEO)
Sunday, August 21, 2011
The British disease, or a disease gone global, The TSE Prion Disease (SEE VIDEO)
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
Friday, November 04, 2011
Diagnostic accuracy of cerebrospinal fluid protein markers for sporadic Creutzfeldt-Jakob disease in Canada: a 6-year prospective study Research article
Tuesday, October 4, 2011
De novo induction of amyloid-ß deposition in vivo
Molecular Psychiatry advance online publication 4 October 2011; doi: 10.1038/mp.2011.120
Molecular Psychiatry advance online publication 4 October 2011; doi: 10.1038/mp.2011.120
De novo induction of amyloid-ß deposition in vivo
R Morales1,2, C Duran-Aniotz1,3, J Castilla2,4, L D Estrada2,5 and C Soto1,2
1Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, University of Texas Houston Medical School, Houston, TX, USA 2University of Texas Medical Branch at Galveston, Galveston, TX, USA 3Universidad de Los Andes, Facultad de Medicina. Av. San Carlos de Apoquindo 2200, Las Condes, Santiago, Chile 4CIC bioGUNE, Parque Tecnologico de Biskaia, Ed 800, 48160 Derio and IKERBASQUE, Basque Foundation for Science, 48011 Bilbao, Spain
Correspondence: Dr C Soto, Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, University of Texas Houston Medical School, 6431 Fannin St, Houston, TX 77030, USA. E-mail: Claudio.Soto@uth.tmc.edu
5Current address: Laboratorio de Señalización Celular, Centro de Envejecimiento y Regeneración. P. Universidad Catolica de Chile, Santiago, Chile.
Received 8 March 2011; Revised 15 August 2011; Accepted 25 August 2011; Published online 4 October 2011.
Abstract
Alzheimer's disease (AD), the most common type of senile dementia, is associated to the build-up of misfolded amyloid-ß (Aß) in the brain. Although compelling evidences indicate that the misfolding and oligomerization of Aß is the triggering event in AD, the mechanisms responsible for the initiation of Aß accumulation are unknown. In this study, we show that Aß deposition can be induced by injection of AD brain extracts into animals, which, without exposure to this material, will never develop these alterations. The accumulation of Aß deposits increased progressively with the time after inoculation, and the Aß lesions were observed in brain areas far from the injection site. Our results suggest that some of the typical brain abnormalities associated with AD can be induced by a prion-like mechanism of disease transmission through propagation of protein misfolding. These findings may have broad implications for understanding the molecular mechanisms responsible for the initiation of AD, and may contribute to the development of new strategies for disease prevention and intervention.
Keywords:
amyloid; prion; protein misfolding; disease transmission
see more here ;
Wednesday, September 21, 2011
PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)
POLITICAL BSe and CJD and THE WOW FACTOR $$$
Monday, September 26, 2011
Variably Protease-Sensitive Prionopathy, Prionpathy, Prionopathy, FFI, GSS, gCJD, hvCJD, sCJD, TSE, PRION, update 2011
Sunday, September 25, 2011
Mad Cow Scaremongers
Mad Cow Scaremongers by Terry S. Singeltary Sr. a review of the TSE prion agent 2003-2011
TSS
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