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Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY TESTING

Posted May 02 2013 11:10pm
Important Chronic Wasting Disease (CWD) Program News



The USDA has recently adopted new federal regulations and standards for the National CWD Program. The TAHC is currently working with interested parties to modify current TAHC regulations to be consistent with the new federal regulations and standards.


One major change that was adopted as a result of the new federal regulations is the sample collection for diagnostic testing of CWD.


Under the old regulations, owners were only required to collect and submit a sample of the obex (brainstem) to the laboratory for testing. The new federal changes require owners to collect and submit a sample of both the obex and retropharyngeal lymph nodes for a more complete diagnostic testing.


The TAHC has discussed these changes with the Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL.) Currently the TVMDL has been testing samples of the obex for a lab charge of $40. TVMDL has modified their testing protocol to now test both the obex and retropharyngeal lymph nodes for an additional fee of only $5 for a total lab fee of $45. The request to test both samples must be documented on the form upfront.


If you use another laboratory for your testing it is recommended that you contact the lab to discuss specifics about the testing of both samples and lab charges.


If you have any questions regarding the CWD program please feel free to contact your Regional TAHC office.




image




Stay tuned for more information and details on changes.


Texas Animal Health Commission www.tahc.texas.gov 800-550-8242










Greetings,



Texas and other states are well known for the infamous OBEX ONLY TSE PRION TESTING, and how useless it really has been, but certified to MISS cases, of which is why it has been used for so long. USDA officials have known this for a decade or more.



now, we will stray from CWD here at first and look at past history of testing the obex only TSE prion mad cow type disease, then back to CWD, but first, just out ;





Dissociation between Transmissible Spongiform Encephalopathy (TSE) Infectivity and Proteinase K-Resistant PrPSc Levels in Peripheral Tissue from a Murine Transgenic Model of TSE Disease



Karen Dobie and


Rona Barron


+ Author Affiliations


Neurobiology Division, The Roslin Institute & R(D)SVS, Easter Bush, Midlothian, United Kingdom


ABSTRACT


Most current diagnostic tests for transmissible spongiform encephalopathies (TSE) rely on the presence of proteinase K (PK)-resistant PrPSc (PrP-res) in postmortem tissues as an indication of TSE disease. However, a number of studies have highlighted a discrepancy between TSE infectivity and PrP-res levels in both natural and experimental cases of TSE disease. Previously, we have shown high TSE infectivity levels in the brain tissue of mice that have a clinical TSE disease with associated vacuolar pathology but little or no detectable PrP-res. Here, the levels of TSE infectivity and PrP-res within a peripheral tissue of this mouse model were investigated. Biochemical analysis showed that low levels of PrP-res were present in the spleen tissue in comparison to the levels observed in the spleen of mice infected with ME7 or 79A. However, upon subpassage of brain and spleen tissue from clinically ill mice with little or no PrP-res detectable, similar short incubation periods to disease were observed, indicating that infectivity levels were similarly high in both tissues. Thus, the discrepancy between PrP-res and TSE infectivity was also present in the peripheral tissues of this disease model. This result indicates that peripheral tissues can contain higher levels of infectivity given the correct combination of host species, PrP genotype, and TSE agent. Therefore, the assumption that the levels of peripheral infectivity are lower than those in the central nervous system is not always correct, and this could have implications for current food safety regulations.


FOOTNOTES


Received 19 December 2012.


Accepted 7 March 2013.


Address correspondence to Rona Barron, rona.barron@roslin.ed.ac.uk.


Published ahead of print 13 March 2013


Copyright © 2013, American Society for Microbiology. All Rights Reserved.








Wednesday, April 24, 2013


Dissociation between Transmissible Spongiform Encephalopathy (TSE) Infectivity and Proteinase K-Resistant PrPSc Levels in Peripheral Tissue from a Murine Transgenic Model of TSE Disease







Saturday, December 15, 2012


Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle -- an update 5 December 2012







Tuesday, November 02, 2010



BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992



Greetings BSE-L members et al,



THIS seems to be another lesson on 'how not to find BSE' via the 'statutory (obex only) diagnostic criteria'. However, this was some 10 years before Dr. Detwiler was warning of this very practice, and how they would be 'MISSING' cases of BSE if USED, which the USDA et al seemed to use as the 'GOLD STANDARD'. NOW we see the UK used it. This seems to put a different light on the true numbers of BSE mad cow cases that were documented, or, better yet, how many were NOT documented $$$ IN THE USA AND ABROAD ??



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



ATYPICAL LESION DISTRIBUTION (RBSE 92/21367)


A 6 year old, home bred (HB), Friesian x Holstein cow in a dairy herd in Aberdeenshirer submitted as a suspect BSE case in the negative study (SE0203), has been diagnosed as BSE negative on standard, statutory (obex only), diagnostic criteria at CVL.


Further examination by Dr Jeffrey at Lasswade, as required by the project design, has revealed vacuolar change in the septal nucleus and putamen which co-localised with PrP immunoreactivity. No significant lesions were found in any other part of the brain, neither was PrP found in the medulla.


It is important to note that examination of four brain blocks used earlier in the epidemic would not have detected the lesion but a 16 block study (as used in the very days of BSE) would.


FURTHER INFORMATION


The herd of origin has had 15, HB, suspect cases of BSE since July 1989 and a further case is still alive.


2. Of the 15, eight have been confirmed by standard histopathology and seven diagnosed negative (including the above case).


3. Fixed brain tissue from the negative cases exists at Lasswade (because they always collect whole brain in Scotland) but has not so far been examined further. No frozen tissue was collected so neither SAF nor PrP detection (by immunoblotting) has been attempted.


4. Mr Wells agrees with Dr Jeffrey's and Dr Simmons' findings.


FURTHER ACTION IN PROGRESS


1. The brain tissue from the negative cases will be examined in detail by conventional histopathology and ICC.


2. Kevin Taylor and his veterinary colleagues have been alerted to the situation.


OTHER RECOMMENDED ACTIONS


1. TRANSMISSION Attempt transmission from the 'case' to standard mice strains. (Note: In regard to strain typing, formalin may have modified strain phenotype - we need to discuss with NPU). Further transmission studies (eg in cattle) might be suggested if primary transmission in mice fails. These proposals have funding implications.


CODE 18-77


93/2.17/1.1


2. PrP GENOTYPING - Although only fixed brain tissue is available we are considering genotyping from parents/offspring/fixed brain. As a first step we are attempting to extract DNA from the fixed brain and to amplify the PrP gene by PCR.


3. John Wilesmith has interrogated the data base for the herd history. Other than the high proportion of negative cases nothing significant is apparent.


4. Familial relationships between suspect (including positive and negative) cases in this herd could be examined and tracings of breeding animals initiated.


5. Consideration might be given to collecting frozen spinal cord from new cases in this herd or in dispersals from it for (SAF/PrP examination).


CONCLUSIONS


1. At present it is unclear whether or not this is a singleton incident or whether the other negative cases in this herd show a similar lesion.


2. The discovery might indicate the existence of a different strain of BSE from that present in the general epidemic or an unusual response by an individual host.


3. If further atypical lesion distribution cases are revealed in this herd then implications of misdiagnosis of 'negative' cases in other herds may not be insignificant.


4. If this is a new strain all the implications need to be considered including whether or not to proceed with the further investigation of future cases negative for BSE on obex examination alone and from which whole brains are available (as in Scotland) or collected in the future. Also perhaps investigation of the tissue distribution of infectivity in these animals might be considered.


5. Animal and public health controls in place should be sufficient since all tissues (other than brain for diagnosis) are incinerated.


We observe that Dr Tyrrell would wish to be informed of this at an early opportunity and that the SEAC would wish to discuss it at their meeting in April.


R BRADLEY


M DAWSON


17 February 1993


CVO - for information and comment on further action please


cc Mr K C Taylor


Dr B J Shreeve


93/2.17/1.2


This minute is re-issued with a wider distribution.


The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".


Mr Scudamore


Mr R C Lowson


Dr D Matthews


Mr I Robertson


Dr K MacOwan


Mr C Randall


Mr J W Wilesmith


Mr G A H Wells


Dr M Jeffrey


Dr M Simmons


93/2.17/1.3






IN CONFIDENCE


BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367)






1992


NEW BRAIN DISORDER


3. WHAT ABOUT REPORTS OF NEW FORM OF BSE ?


THE VETERINARY RECORD HAS PUBLISHED AN ARTICLE ON A NEW BRAIN DISORDER OF CATTLE DISCOVERED THROUGH OUR CONTROL MEASURES FOR BSE. ALTHOUGH IT PRESENTS SIMILAR CLINICAL SIGNS TO BSE THERE ARE MAJOR DIFFERENCES IN HISTOPATHOLOGY AND INCUBATION PERIODS BETWEEN THE TWO. MUST EMPHASISE THAT THIS IS _NOT_ BSE.


4. IS THIS NEW BRAIN DISORDER A THREAT ?


WE DO NOT EVEN KNOW WHETHER THE AGENT OF THIS DISEASE IS TRANSMISSIBLE. IN ANY CASE, CASES SO FAR IDENTIFIED HAD SHOWN SIMILAR SYMPTOMS TO THOSE OF BSE, AND THEREFORE HAVE BEEN SLAUGHTERED AND INCINERATED, SO THAT IF A TRANSMISSIBLE AGENT WERE INVOLVED IT WOULD HAVE BEEN ELIMINATED. ...






Tuesday, November 17, 2009


SEAC NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS (IBNC) FROM THE VETERINARY LABORATORIES AGENCY (VLA) SEAC 103/1







NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS "All of the 15 cattle tested showed that the brains had abnormally accumulated PrP" 2009







========




NOW, what about the 'obex only' mode of testing used by the USDA et al for TSE, prions $$$ works for them too, a sure fire way NOT TO FIND MAD COW DISEASE $$$



NOW, read the following please, and then ask yourself, WHY the USDA et al were ONLY TESTING THE OBEX PART OF THE BRAIN in USA cattle for BSE $$$



BECAUSE they knew that would be the least likely way to find BSE/TSE in USA cattle $$$...TSS



=========



Discussion


In the five cats in this study with a spongiform encephalopathy, fibrils were observed by electron microscopy and their major protein, Prpsc, was identified by SDS-PAGE and Western blot. The fibrils were similar to those described in sheep with scrapie (Rubenstein and others 1987, Gibson and others 1987, Scott and others 1987, Dawson and others 1987), cattle with bovine spongiform encephalopathy (Wells and others 1987, Hope and others 1988, Scott and others 1990) and humans with Creutzfeldt-Jakob disease (Merz and others 1984).


In sheep with scrapie, fibrils can be readily detected in several areas of the brain, including cerebral cortex (Stack and others 1991).


By contrast, the frequency with which fibrils were detected in cattle with BSE, DEPENDED ON THE REGION OF THE BRAIN SAMPLED; THE HIGHEST YIELD BEING OBTAINED FROM MEDULLA, MIDBRAIN, THALAMUS AND BASAL NUCLEI WHERE VACUOLA CHANGES ARE PRESENT (Scott and others 1990). This correlation between PrPsc accumulation and vacuolar pathology is also well established in laboratory animal models of scrapie (Bruce and others 1989). Because of the widespread distribution of changes in FSE (Whatt and others 1991) and the requirement, in the present study, not to compromise the histopathological examination of the brain, the frontal region of the cerebrum was therefore selected for fibril and PrPsc examinations. However, studies of the sensitivity of fibril detection in different parts of the brain in cats with FSE are required to determine whether detection can be made as readliy in other regions as in the frontal cerebral cortex.


IT IS OF INTEREST, that fibrils were detected in the brains of 3 cats (cases 9, 13, & 18) WITHOUT histopathological evidence of spongiform encephalopathy, and that in only one of them, (case 9), a Western blot for modified PrP was positive. There are precedents for the occurrence of abnormal PrP in the organs of animals incubation scrapie prior to clinical signs and/or spongiform encephalopathy...



snip...


(please see full text (and one might start downloading these documents for future use, as some disappear never to re-appear, as in some of the FDA's. ...TSS)






PLEASE NOTE *


Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.


snip...


The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...







AND THE USDA ET AL KNEW IT TOO ;



"These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."


THIS WAS DONE FOR A REASON!


THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine, and these were probably from the most high risk cattle pool, the ones the USDA et al, SHOULD have been testing. ...TSS



USDA 2003



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



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



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



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


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


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



snip...



FULL TEXT;


Completely Edited Version PRION ROUNDTABLE


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


END...TSS



==========



Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE sampling FROM HEALTHY USDA CATTLE)


Date: June 21, 2007 at 2:49 pm PST


Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program


An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.


snip...


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


soundness of BSE maintenance sampling (APHIS),


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


snip...


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


4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half







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


Statement on Texas Cow With Central Nervous System Symptoms


On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.


FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.


FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.










THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;


CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006


In an article today for United Press International, science reporter Steve Mitchell writes:


Analysis: What that mad cow means


By STEVE MITCHELL UPI Senior Medical Correspondent


WASHINGTON, March 15 (UPI) -- The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.


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


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


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


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


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


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


Despite this, Brown said the U.S. prevalence of mad cow, formally known as bovine spongiform encephalopathy, or BSE, did not significantly threaten human or cattle health.


"Overall, my view is BSE is highly unlikely to pose any important risk either in cattle feed or human feed," he said.


However, Jean Halloran of Consumers Union in Yonkers, N.Y., said consumers should be troubled by the USDA's secrecy and its apparent plan to dramatically cut back the number of mad cow tests it conducts.


"Consumers should be very concerned about how little we know about the USDA's surveillance program and the failure of the USDA to reveal really important details," Halloran told UPI. "Consumers have to be really concerned if they're going to cut back the program," she added.


Last year the USDA tested more than 300,000 animals for the disease, but it has proposed, even in light of a third case, scaling back the program to 40,000 tests annually.


"They seem to be, in terms of actions and policies, taking a lot more seriously the concerns of the cattle industry than the concerns of consumers," Halloran said. "It's really hard to know what it takes to get this administration to take action to protect the public."


The USDA has insisted that the safeguards of a ban on incorporating cow tissue into cattle feed (which is thought to spread the disease) and removal of the most infectious parts of cows, such as the brain and spinal cord, protect consumers. But the agency glosses over the fact that both of these systems have been revealed to be inadequately implemented.


The feed ban, which is enforced by the Food and Drug Administration, has been criticized by the Government Accountability Office in two reports, the most recent coming just last year. The GAO said the FDA's enforcement of the ban continues to have weaknesses that "undermine the nation's firewall against BSE."


USDA documents released last year showed more than 1,000 violations of the regulations requiring the removal of brains and spinal cords in at least 35 states, Puerto Rico and the Virgin Islands, with some plants being cited repeatedly for infractions. In addition, a violation of similar regulations that apply to beef exported to Japan is the reason why Japan closed its borders to U.S. beef in January six weeks after reopening them.


Other experts also question the adequacy of the USDA's surveillance system. The USDA insists the prevalence of mad cow disease is low, but the agency has provided few details of its surveillance program, making it difficult for outside experts to know if the agency's monitoring plan is sufficient.


"It's impossible to judge the adequacy of the surveillance system without having a breakdown of the tested population by age and risk status," Elizabeth Mumford, a veterinarian and BSE expert at Safe Food Solutions in Bern, Switzerland, a company that provides advice on reducing mad cow risk to industry and governments, told UPI.


"Everybody would be happier and more confident and in a sense it might be able to go away a little bit for (the USDA) if they would just publish a breakdown on the tests," Mumford added.


UPI requested detailed records about animals tested under the USDA's surveillance plan via the Freedom of Information Act in May 2004 but nearly two years later has not received any corresponding documents from the agency, despite a federal law requiring agencies to comply within 30 days. This leaves open the question of whether the USDA is withholding the information, does not have the information or is so haphazardly organized that it cannot locate it.


Mumford said the prevalence of the disease in U.S. herds is probably quite low, but there have probably been other cases that have so far gone undetected. "They're only finding a very small fraction of that low prevalence," she said.


Mumford expressed surprise at the lack of concern about the deadly disease from American consumers. "I would expect the U.S. public to be more concerned," she said.


Markus Moser, a molecular biologist and chief executive officer of Prionics, a Swiss firm that manufactures BSE test kits, told UPI one concern is that if people are infected, the mad cow pathogen could become "humanized" or more easily transmitted from person to person.


"Transmission would be much easier, through all kinds of medical procedures" and even through the blood supply, Moser said.


© Copyright 2006 United Press International, Inc. All Rights Reserved









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







PAUL BROWN COMMENT TO ME ON THIS ISSUE



Tuesday, September 12, 2006 11:10 AM


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






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


Audit Report Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy (BSE) Surveillance Program ­ Phase II and Food Safety and Inspection Service


Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III


Report No. 50601-10-KC January 2006


Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain






THIS is just ONE month report, of TWO recalls of prohibited banned MBM, which is illegal, mixed with 85% blood meal, which is still legal, but yet we know the TSE/BSE agent will transmit blood. we have this l-BSE in North America that is much more virulent and there is much concern with blood issue and l-BSE as there is with nvCJD in humans. some are even starting to be concerned with sporadic CJD and blood, and there are studies showing transmission there as well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that reaches commerce is ever returned via recall, very, very little. this was 2007, TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow feed that was in ALABAMA in one of the links too, this is where the infamous g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the USA. seems this saga just keeps getting better and better.......$$$



10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007




snip...see full text ;



Tuesday, November 02, 2010


IN CONFIDENCE


The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".


BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992







2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006






Comments on technical aspects of the risk assessment were then submitted to FSIS.


Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary.


This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:






Owens, Julie


From: Terry S. Singeltary Sr. [flounder9@verizon.net]


Sent: Monday, July 24, 2006 1:09 PM


To: FSIS RegulationsComments


Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)


Page 1 of 98






FSIS, USDA, REPLY TO SINGELTARY






Friday, April 19, 2013


APHIS 2013 Stakeholder Meeting (March 2013) BSE TSE PRION






Saturday, December 15, 2012


Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle -- an update 5 December 2012






Friday, April 19, 2013


FDA BSE TSE PRION NEWS FEED AND ANNUAL INSPECTION OF FEED MILLS REPORTS HAS CEASED TO EXIST






Monday, March 25, 2013


Minnesota Firm Recalls Bone-In Ribeye That May Contain Specified Risk Materials Recall Release CLASS II RECALL FSIS-RC-024-2013






Tuesday, March 5, 2013


Use of Materials Derived From Cattle in Human Food and Cosmetics; Reopening of the Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION)


FDA believes current regulation protects the public from BSE but reopens comment period due to new studies






Wednesday, March 20, 2013


GAO-13-244, Mar 18, 2013 Dietary Supplements FDA May Have Opportunities to Expand Its Use of Reported Health Problems to Oversee Product


From: Terry S. Singeltary Sr.


Sent: Tuesday, March 19, 2013 2:46 PM


To: gomezj@gao.gov


Cc: siggerudk@gao.gov ; youngc1@gao.gov ; oighotline@gao.gov






Wednesday, February 20, 2013


World Organization for Animal Health Recommends United States' BSE Risk Status Be Upgraded


Statement from Agriculture Secretary Tom Vilsack:






Thursday, February 14, 2013


The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and TSE prion disease






Friday, April 19, 2013


Bovine Spongiform Encephalopathy (BSE) Feed Safety Support Program Grants Fiscal Year 2011: October 1, 2010 - September 30, 2011 FDA







USDA-APHIS-VS Chronic Wasting Disease National Program


Patrice N. Klein of USDA APHIS VS – National Center for Animal Health Programs provided an update on the agency’s CWD–related activities:


CWD Rule Update: The amended final rule on chronic wasting disease (CWD) is currently in departmental clearance. The rule will set minimum standards for interstate movement and establish the national voluntary Herd Certification Program (HCP). Farmed/captive cervid surveillance testing: Through FY2010, VS conducted surveillance testing on approximately 20,000 farmed /captive cervids by the immunohistochemistry (IHC) standard protocol. As of September 15, 2011, approximately 19,000 farmed /captive cervids were tested by IHC for CWD with funding to cover lab costs provided through NVSL.


Farmed/captive cervid CWD status: The CWD positive captive white-tailed deer (WTD) herd reported in Missouri (February 2010) was indemnified and depopulation activities were completed in June 2011. All depopulated animals were tested for CWD and no additional CWD positive animals were found.


In FY 2011, CWD was reported in two captive elk herds in Nebraska (December, 2010 and April 2011, respectively).


To date, 52 farmed/captive cervid herds have been identified in 11 states: CO, KS, MI, MN, MO, MT, NE, NY, OK, SD, WI.


Thirty-nine were elk herds and 13 were WTD herds. At this time, eight CWD positive herds remain – six elk herds in Colorado and the two elk herds in Nebraska.


Wild Cervid surveillance: In FY 2009 funding supported surveillance in approximately 74,330 wild cervids in 47 cooperating States. Wild cervid CWD surveillance totals are pending for fiscal year 2010 (2010 – 2011 calendar year) due to seasonal surveillance activities and completion of final cooperative agreement reporting to APHIS.


In fiscal year 2011, there are 15 ‘tier 1’ States, 20 ‘tier 2’ States, and 15 ‘tier 3’ States. Two new ‘tier 1’ States, Minnesota and Maryland, were added in fiscal year 2011 based on the new CWD detections in a free-ranging white-tailed deer in southeastern Minnesota and in western Maryland. Consequently, Delaware was upgraded to ‘tier 2’ status as an adjacent State to Maryland. For FY 2011, 45 States and 32 Tribes will receive cooperative agreement funds to complete wild cervid surveillance and other approved work plan activities. Based on FY 2012 projected budget reductions, future cooperative agreement funds will be eliminated.


APHIS CWD Funding: In FY2011, APHIS received approximately $15.8 million in appropriated funding for the CWD Program. The President’s FY 2012 budget proposes to reduce program funding for CWD by $13.9 million, leaving the program with a request of $1.925 million to provide some level of Federal coordination for the national herd certification program (HCP).


Consequently, APHIS is planning to amend its role in the program to one of Federal coordination. Based on the projected FY 2012 budget, funding for CWD cooperative agreements and indemnity funding for States and Tribes will be eliminated. Under this scenario, the States or cervid industry producers will likely be responsible for the costs of surveillance testing and indemnity for appraisal, depopulation, and disposal of CWD-positive animals.


Commodity Health Line Structure: In the FY 2012 budget, livestock commodities regulated by USDA have been organized into ‘Commodity Health Line’ structures or groupings. APHIS’ Equine, Cervid and Small Ruminant (ECSR) Health line supports efforts to protect the health and thereby improve the quality and productivity of the equine, cervid and small ruminant industries. Activities supported by the ECSR Health line range from monitoring and surveillance to investigation and response actions undertaken when health issues relevant to the industry are identified. APHIS also maintains regulations and program standards which guide ECSR activities at both the Federal and State/Tribal level.


The ECSR Health line funds essential activities necessary to maintain current ECSR surveillance and program operations while providing the flexibility to respond to new and emerging industry-specific health concerns. APHIS’ current activities include Scrapie, Chronic Wasting Disease (CWD), Slaughter Horse Transport, and Brucellosis/Tuberculosis in cervids. Overall, APHIS will use funding from the ECSR Health Line Item to support Agency efforts in the following mission areas: prevention, preparedness and communication; monitoring, surveillance and detection; response and containment; and continuity of business, mitigation and recovery


Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD)


Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National Animal Disease Center, ARS, USDA, Ames, IA provided a presentation on scrapie and CWD in inoculated deer. Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. We inoculated white-tailed deer intracranially (IC) and by a natural route of exposure (concurrent oral and intranasal inoculation) with a US scrapie isolate. All deer inoculated by the intracranial route had evidence of PrPSc accumulation and those necropsied after 20 months post-inoculation (PI) (3/5) had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. A single deer that was necropsied at 15.6 months PI did not have clinical signs, but had widespread distribution of PrPSc. This highlights the facts that 1) prior to the onset of clinical signs PrPSc is widely distributed in the CNS and lymphoid tissues and 2) currently used diagnostic methods are sufficient to detect PrPSc prior to the onset of clinical signs. The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in white-tailed deer after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile consistent with CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like. After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie. Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. While two WB patterns have been detected in brain regions of deer inoculated by the natural route, unlike the IC inoculated deer, the pattern similar to the scrapie inoculum predominates.


Committee Business:


The Committee discussed and approved three resolutions regarding CWD. They can be found in the report of the Reswolutions Committee. Essentially the resolutions urged USDA-APHIS-VS to:


Continue to provide funding for CWD testing of captive cervids


Finalize and publish the national CWD rule for Herd Certification and Interstate Movement


Evaluate live animal test, including rectal mucosal biopsy, for CWD in cervids







how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms ??


? game farms in a state X $465,000., do all these game farms have insurance to pay for this risk of infected the wild cervid herds, in each state ??


Tuesday, December 20, 2011


CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011


The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.


RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.


Form 1100-001


(R 2/11)


NATURAL RESOURCES BOARD AGENDA ITEM


SUBJECT: Information Item: Almond Deer Farm Update


FOR: DECEMBER 2011 BOARD MEETING


TUESDAY


TO BE PRESENTED BY TITLE: Tami Ryan, Wildlife Health Section Chief



SUMMARY:











*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.







2011


*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.








Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions


Marcelo A. Barria1, Glenn C. Telling2, Pierluigi Gambetti3, James A. Mastrianni4 and Claudio Soto1,* 1Mitchell Center for Alzheimer’s disease and related Brain disorders, Dept of Neurology, University of Texas Houston Medical School, Houston, TX 77030, USA 2Dept of Microbiology, Immunology & Molecular Genetics, and Neurology, Sanders Brown Center on Aging, University of Kentucky Medical Center, Lexington, KY, USA 3Institute of Pathology, Case Western Reserve University, Cleveland, OH, USA 4Dept of Neurology, University of Chicago, Chicago, IL, USA. Running Title: Conversion of human PrPC by cervid PrPSc Keywords: Prion / transmissible spongiform encephalopathy / infectivity / misfolded prion protein / prion strains * To whom correspondence should be addressed. University of Texas Houston Medical School, 6431 Fannin St, Houston, TX 77030. Tel 713-5007086; Fax 713-5000667; E-mail Claudio.Soto@uth.tmc.edu The latest version is at http://www.jbc.org/cgi/doi/10.1074/jbc.M110.198465 JBC Papers in Press.


Published on January 4, 2011 as Manuscript M110.198465 Copyright 2011 by The American Society for Biochemistry and Molecular Biology, Inc. 5, Downloaded from www.jbc.org by guest, on November 11, 2012 2


Prion diseases are infectious neurodegenerative disorders affecting humans and animals that result from the conversion of normal prion protein (PrPC) into the misfolded prion protein (PrPSc). Chronic wasting disease (CWD) is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. Determining the risk of transmission of CWD to humans is of utmost importance, considering that people can be infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the misfolded form by CWD PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification (PMCA) technique, which mimic in vitro the process of prion replication. Our results show that cervid PrPSc can induce the conversion of human PrPC, but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, the newly generated human PrPSc exhibits a distinct biochemical pattern that differs from any of the currently known forms of human PrPSc. Our results also have profound implications for understanding the mechanisms of prion species barrier and indicate that the transmission barrier is a dynamic process that depend on the strain and moreover the degree of adaptation of the strain. If our findings are corroborated by infectivity assays, they will imply that CWD prions have the potential to infect humans, and that this ability depends on CWD strain adaptation.


Various studies aimed to analyze the transmission of CWD to transgenic mice expressing human PrP have consistently given negative results (9-11), indicating a strong species barrier. This conclusion is consistent with our many failed experiments to attempt converting human PrPC with natural CWD, even after pushing the PMCA conditions (see figure 1). We found successful conversion only after adaptation of the CWD prion strain by successive passages in vitro or in cervid transgenic mice. We are not aware that in any of the transgenic mice studies the inoculum used was a previously stabilized CWD strain. Although, it has been shown that strain stabilization in vitro by PMCA (17;26) and in vivo using experimental rodents (36) has similarities with the strain adaptation process occurring in natural hosts, we cannot rule out that the type of CWD strain adaptation that is required to produce strains transmissible to humans may take much longer time in cervids or not occur at all. An important experiment will be to study transmissibility to humanized transgenic mice of CWD passed experimentally in deer several times. Besides the importance of our results for public health in relation to the putative transmissibility of CWD to humans, our data also illustrate a very important and novel scientific concept related to the mechanism of prion transmission across species barriers. Today the view is that species barrier is mostly controlled by the degree of similarity on the sequence of the prion protein between the host and the infectious material (4). In our study we show that the strain and moreover the stabilization of the strain plays a major role in the inter-species transmission. In our system there is no change on the protein sequence, but yet strain adaptation results in a complete change on prion transmissibility with potentially dramatic consequences. Therefore, our findings lead to a new view of the species barrier that should not be seen as a static process, but rather a dynamic biological phenomenon that can change over time when prion strains mature and evolve. It remains to be investigated if other species barriers also change upon progressive strain adaptation of other prion forms (e.g. the sheep/human barrier).


Our results have far-reaching implications for human health, since they indicate that cervid PrPSc can trigger the conversion of human PrPC into PrPSc, suggesting that CWD might be infectious to humans. Interestingly our findings suggest that unstable strains from CWD affected animals might not be a problem for humans, but upon strain stabilization by successive passages in the wild, this disease might become progressively more transmissible to man.








Generation of a New Form of Human PrPScin Vitro by Interspecies Transmission from Cervid Prions*


Marcelo A. Barria‡, Glenn C. Telling§, Pierluigi Gambetti¶, James A. Mastrianni‖ and Claudio Soto‡,1 + Author Affiliations


From the ‡Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, University of Texas Medical School at Houston, Houston, Texas 77030, the §Departments of Microbiology, Immunology, and Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of Kentucky Medical Center, Lexington, Kentucky 40506, the ¶Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, and the ‖Department of Neurology, The University of Chicago, Chicago, Illinois 60637 1 To whom correspondence should be addressed: University of Texas Medical School at Houston, 6431 Fannin St., Houston, TX 77030. Tel.: 713-500-7086; Fax: 713-500-0667; E-mail: claudio.soto@uth.tmc.edu.


Abstract


Prion diseases are infectious neurodegenerative disorders that affect humans and animals and that result from the conversion of normal prion protein (PrPC) into the misfolded prion protein (PrPSc). Chronic wasting disease (CWD) is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. Determining the risk of transmission of CWD to humans is of utmost importance, considering that people can be infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the misfolded form by CWD PrPSc, we performed experiments using the protein misfolding cyclic amplification technique, which mimics in vitro the process of prion replication. Our results show that cervid PrPSc can induce the conversion of human PrPC but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, the newly generated human PrPSc exhibits a distinct biochemical pattern that differs from that of any of the currently known forms of human PrPSc. Our results also have profound implications for understanding the mechanisms of the prion species barrier and indicate that the transmission barrier is a dynamic process that depends on the strain and moreover the degree of adaptation of the strain. If our findings are corroborated by infectivity assays, they will imply that CWD prions have the potential to infect humans and that this ability progressively increases with CWD spreading.










UPDATED DATA ON 2ND CWD STRAIN


Wednesday, September 08, 2010 CWD PRION CONGRESS SEPTEMBER 8-11 2010








Tuesday, June 05, 2012


Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012 Legislative Session







Friday, August 31, 2012


COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a review








Friday, August 24, 2012


Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting disease within white-tailed deer (Odocoileus virginianus) herds in North America


The overall diagnostic specificity was 99.8%. Selective use of antemortem rectal biopsy sample testing would provide valuable information during disease investigations of CWD-suspect deer herds.








Tuesday, April 09, 2013


EFFICACY OF ANTEMORTEM RECTAL BIOPSIES TO DIAGNOSE AND ESTIMATE PREVALENCE OF CHRONIC WASTING DISEASE IN FREE-RANGING COW ELK (CERVUS ELAPHUS NELSONI)









Monday, March 18, 2013


PROCEEDINGS ONE HUNDRED AND FIFTEENTH ANNUAL MEETING of the UNITED STATES ANIMAL HEALTH ASSOCIATION September 29 – October 5, 2011


see updated 2012 RESOLUTIONS








Monday, April 01, 2013


Dr. Deer/Dough from Texas on Wisconsin’s CWD implementation survey, is now available









Friday, June 01, 2012


*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS








Tuesday, April 02, 2013


IMPORTANT: Cervid Industry and State Veterinarians on Rewriting Chronic Wasting Disease Rule








Friday, April 12, 2013


Federal Protocol on Chronic Wasting Disease (CWD) - Darrel Rowledge, Alliance for Public Wildlife








Saturday, April 13, 2013


Tennessee Launches CWD Herd Certification Program in the wake of legislation for game farms








Thursday, March 29, 2012


TEXAS DEER CZAR SAYS WISCONSIN DNR NOT DOING ENOUGH ABOUT CWD LIKE POT CALLING KETTLE BLACK









Tuesday, July 10, 2012


Chronic Wasting Disease Detected in Far West Texas












Monday, February 11, 2013


TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos












Tuesday, December 18, 2012


A Growing Threat How deer breeding could put public trust wildlife at risk







Friday, December 14, 2012


DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012


snip...


In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.


Animals considered at high risk for CWD include:


1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and


2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.


Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.


The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.


Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.


There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.


snip...


36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).


The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).


Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.


snip...


The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).


snip...


In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.


snip...


In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.


snip...


Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.


snip...








SNIP...SEE ;




Friday, December 14, 2012


DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012







Tuesday, April 16, 2013


*** Cervid Industry Unites To Set Direction for CWD Reform and seem to ignore their ignorance and denial in their role in spreading Chronic Wasting Disease








*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.







Friday, November 09, 2012


*** Chronic Wasting Disease CWD in cervidae and transmission to other species






Sunday, November 11, 2012


*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease November 2012







Friday, December 14, 2012


Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005 - December 14, 2012







Wednesday, April 24, 2013


Dissociation between Transmissible Spongiform Encephalopathy (TSE) Infectivity and Proteinase K-Resistant PrPSc Levels in Peripheral Tissue from a Murine Transgenic Model of TSE Disease







Tuesday, April 16, 2013


Cervid Industry Unites To Set Direction for CWD Reform and seem to ignore their ignorance and denial in their role in spreading Chronic Wasting Disease







Thursday, May 02, 2013


Pennsylvania Game Commission has established the state’s second Disease Management Area in parts of four counties in response to three hunter-killed deer that tested positive for CWD


FOR IMMEDIATE RELEASE: May 01, 2013











TSS


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