Tuesday, October 21, 2014

Texas Pair Convicted in Illegal Deer Breeding Operation TPWD

News Release Media Contact: Steve Lightfoot, 512-389-4701, steve.lightfoot@tpwd.texas.gov


Oct. 21, 2014


Pair Convicted in Illegal Deer Breeding Operation AUSTIN – The latest chapter in a decade long series of criminal and wildlife disease investigations involving a former South Texas deer breeder ended recently when a Corpus Christi area couple pleaded guilty to 50 charges of Unlawful Possession and/or Sale of Live Game Animals.


Frank Thomas Shumate Jr., 51, and Kalub Rogers Shumate, 31, were each assessed $14,127.50 in fines and agreed to surrender the ability to apply for a deer breeder permit or a hunting lease license for all time. Mr. Shumate also agreed to surrender his hunting license through the end of the 2015 license year and Ms. Shumate through the end of the 2017 license year.


The criminal cases were adjudicated in the office of Hon. Caroline Korzekwa, Karnes County Justice Court Precinct. 2.


Retired San Antonio attorney Rene Barrientos served as special prosecutor in the case with approval and support from the Karnes County Attorney. He also coordinated a global agreement in Travis County District Court to resolve a pending civil case against Ms. Rogers and recover $34,080 in restitution related to expenses incurred by TPWD staff while conducting a deer herd inventory inspection and disease sampling at a deer breeding facility permitted to Ms. Rogers.


Investigation into Mr. Shumate’s deer breeding activities began in March 2004 and led to multiple charges in three counties. Two years later, his deer breeder violations resulted in 10 convictions on criminal charges in Jim Wells County, 5 convictions in Nueces County and 5 convictions in Webb County. As a result of these findings, Mr. Shumate agreed to relinquish his Scientific Breeder’s Permit and liquidate all deer held in captivity in his deer breeding facility in Nueces County.


In advance of losing his deer breeding privileges, Mr. Shumate allegedly initiated a plan to have a new deer breeding facility permitted in the name of Kalub Rogers on his property in Karnes County, where he then transferred more than 100 deer from his Nueces County facility.


Over time the TPWD Special Operations Unit received numerous reports that Mr. Shumate was reportedly still in the deer business and was buying and selling deer for which he was not legally authorized by TPWD. An investigation revealed that Mr. Shumate conducted sales of at least 78 white-tailed deer from Ms. Rogers’ deer breeding facility to ranches for release into the wild for stocking purposes since September 2010. Mr. Shumate received a minimum of $171,466 in payments for white-tailed deer he unlawfully sold, which according to records submitted to TPWD, were transported from Ms. Rogers’ deer breeding facility. The investigation further indicated that Kalub Rogers was holding a deer breeder permit in her name on behalf of her husband Frank Thomas Shumate Jr.


Ms. Rogers’ facility came under additional scrutiny in 2012, initially as a result of a delinquent annual report required of all permitted deer breeding facilities. Criminal charges were filed when a subsequent herd inspection and inventory revealed significant irregularities and discrepancies, including 162 inventoried deer that were missing from the facility. During the herd inspection, TPWD wildlife biologists noted the remaining deer in the facility to be in poor condition and numerous decayed deer carcasses were observed throughout the pens.


The observation of 142 deer of unknown origin was cause for additional concern and tissue samples from several deer were tested for both Chronic Wasting Disease and Bovine Tuberculosis. Neither disease was detected.


“Unscrupulous actions by these two individuals are not only a threat to all the law-abiding deer breeders who are carefully monitoring and managing their facilities, but also to the state’s free-ranging deer, which can be exposed to unnecessary disease risk from these illegitimate activities,” said Mitch Lockwood, TPWD Big Game Program Director. “Captive and free-ranging deer are too important to our state to have them compromised by the actions of a few.”


SL 2014-10-21



> The observation of 142 deer of unknown origin was cause for additional concern and tissue samples from several deer were tested for both Chronic Wasting Disease and Bovine Tuberculosis. Neither disease was detected.


‘’several deer’’, two deer tested for cwd?...seriously???


they did not want to find cwd apparently.


I am not surprised...tss


MR. KURZAWSKI: Thank you, commissioner.


COMMISSIONER DUGGINS: All right, good. We are at Item 7, Rules Concerning Implementation of Senate Bill 820, Deer Permits, recommended adoption of proposed changes, Mitch Lockwood. Welcome.


MR. LOCKWOOD: Thank you. Good morning, Mr. Chairman, Commissioners. As we discussed yesterday, the 83rd Texas Legislature enacted Senate Bill 820, which requires the Department to issue a deer breeders permit with a duration of one year, three years, or five years.


Well, we already had the authority to issue a deer breeders permit for multiple years; but as I discussed yesterday, we had opted to limit the duration of those permits to one year and one reason for that was to try and not remove an incentive to submit annual reports in a timely fashion. But I admit that it did not prove to be a very effective incentive.


Nonetheless, Senate Bill 820 did amend Parks and Wildlife Code to ensure that we do issue a three-year or a five-year permit to someone who meets a couple of criteria. But the rule -- the statute also gives the Commission the authority to establish some additional criteria, which is the purpose or the intent of this proposal. In essence, we're proposing only one additional criteria, which is that we would issue a multiyear permit to someone who has been in substantial compliance with the deer breeder regulations and statutes for the previous three years.


The idea behind this is to try an prevent invoking or at least minimize the risk of invoking a very lengthy and inefficient permit revocation process. You know, there may be some instances in which some permitted individuals just refuse to comply with annual reporting requirements, which we find to be very important in order to reconcile these herd inventories that affect the entire industry. And so in the event someone does refuse to comply with those requirements, it may give cause to revoke this longterm or multiyear permit.


We think we can avoid implementing or invoking that lengthy process if we can ensure or at least issue this permit to someone who has demonstrated for the previous three years that they have complied with that reporting requirement and with some other regulations. Again, we don't propose any change to the annual permit fee of $200 and so a three-year permit would that $200 times three years at $600 and a five-year permit would be a thousand dollars.


So with that, staff recommend that the Texas Parks and Wildlife Commission adopts amendments to 53.14 concerning deer management and removal permits and 65.603 concerning application of permit issuance, with changes as necessary to the proposed text as published in the October 4th, 2013, issue of the Texas Register.


We have received two public comments, in addition to some input I received from the breeder user group who is supportive of this proposal. Again, they did want to qualify the term compliance by stating "substantial compliance" and so with that, they're supportive of this proposal. Of the two comments we received, one was in favor, one was in opposition; but the comments that accompanied the opposing view was -- really were not germane to this proposal. He was opposed to the practice of deer breeding altogether.


And so that concludes my presentation, and I'll be glad to entertain any questions you might have.



Singeltary Submission TAHC on CWD rule proposal


Saturday, July 07, 2012


TEXAS Animal Health Commission Accepting Comments on Chronic Wasting Disease Rule Proposal


Considering the seemingly high CWD prevalence rate in the Sacramento and Hueco Mountains of New Mexico, CWD may be well established in the population and in the environment in Texas at this time.



Media Contacts:


Steve Lightfoot, TPWD, 512-389-4701, steve.lightfoot@tpwd.state.tx.us


Yvonne "Bonnie" Ramirez, TAHC, 512-719-0710, bonnie.ramirez@tahc.state.tx.us




July 10, 2012


Chronic Wasting Disease Detected in Far West Texas


AUSTIN -- Samples from two mule deer recently taken in far West Texas have been confirmed positive for Chronic Wasting Disease (CWD). These are the first cases of CWD detected in Texas deer. Wildlife officials believe the event is currently isolated in a remote part of the state near the New Mexico border.






Texas Animal Health Commission (TAHC) 2105 Kramer Lane Austin, Texas 78758 1-800-550-8242


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


News Release


Media Contact: Steve Lightfoot, 512-389-4701, steve.lightfoot@tpwd.state.tx.us


Feb. 11, 2013


Four New Positives Found in Trans Pecos CWD Surveillance


Disease not discovered outside Containment Zone


AUSTIN – Nearly 300 tissue samples were collected from hunter harvested mule deer from the Trans Pecos ecoregion of far West Texas during the 2012-13 season for Chronic Wasting Disease (CWD) testing. Texas A&M Veterinary Medical Diagnostic Laboratory and National Veterinary Services Laboratories (NVSL) have confirmed CWD in four of those samples. All CWD-positive deer were harvested within the CWD Containment Zone.


SL 2013-02-11



7 MR. BROWN: Madam Chairman, Members, 8 my name is Kirby Brown with the Texas Wildlife 9 Association. We want to thank the Commission and 10 the staff for their efforts in this. And, Madam 11 Chairman, your leadership in this action that's 12 going forward, we appreciate the rapid response, 13 the professionalism and the science being brought 14 to bear on the issue. We think that's all very 15 important. 16 We are continuing to work with the 17 Texas Animal Health Commission on the issue. Our 18 meeting over the next few weeks -- in fact, Monday 19 we have a meeting with Commissioner Wood. And 20 although our membership continues to have real 21 concern about CWD and entry into the wild, we 22 think the voluntary actions that are taking place 23 are proceeding at a rapid pace at this point in 24 time. And we'd like to see that continue. And we 25 believe that's a process, especially with the . 38 1 response that we can get for herd health plans 2 from the Texas Animal Health Commission staff, 3 which is -- they're literally overwhelmed right 4 now with so many issues that they have on their 5 plate. We think this is a good process, we think 6 it's an effective process, and we appreciate your 7 consideration in that regard. So with that, 8 that's all I have to say. Thank you very much. 9 CHAIRMAN IDSAL: After Karl, we have 10 Ellis Gilleland. 11 MR. KINSEL: I second entirely what 12 Kirby just said, but I also wanted to bring it to 13 y'all's attention that the letter is drafted going 14 out to all scientific breeders, all 467, both TWA 15 and TDA have individually drafted that letter. We 16 intend to do that jointly to continue showing our 17 joint support and our joint efforts. As soon as 18 we get clarification from TAHC, that will go as a 19 cover letter on form 0008 of the Texas Animal 20 Health Commission to enroll as many as possible 21 into the program. Thank you. 22 CHAIRMAN IDSAL: We may have some 23 questions. Commissioner Fitzsimons has a question 24 of Mr. Kinsel.




19 The second thing I want to say is, 20 voluntary law does not work. George W. Bush 21 approved that. The cold fired power plants 22 throughout this state that are grandfathered from 23 30, 40 years ago are still belching. They keep 24 the shell, they rebuild the guts and keep the same 25 within the grandfather clause. Voluntary -- you . 43 1 lawyers know that. People will take advantage of 2 voluntary law. It does not work. And it's not in 3 your mission statement. Everybody want to do 4 this? No. Okay. Don't do it. Everybody don't 5 want to do it? Yeah, okay, do it. That's not 6 government. That's not what you're being paid to 7 do. So forget about the voluntary stuff. Make a 8 law. Jerry gave you a good first step. Make a 9 law, there it is. Now, get the voluntary 10 compliance once you've got the law. That's where 11 you want the voluntary. Not voluntary eons and 12 eons. There's no -- that's not law. That's an 13 anarchy. 14 The third thing I want to mention, 15 there's no precedence for voluntary law. The 16 precedence are coherent laws. We are a nation of 17 laws. Rabies -- let's bring it down to home. 18 Rabies in Texas. Take away the rabies law and 19 what have we got? We've got a bunch of dead 20 people without rabies law. There's got to be a 21 CWD law or in a year or two or five years from now 22 we're going to all be in trouble and go back and 23 all these (inaudible), well, let's go back and see 24 what happened. Well, we don't have to do that. 25 Let's take the action now. Get the consensus, get . 44 1 the voluntary, yeah, yeah, yeah, make a law. Now, 2 do it, and there's a penalty. Please, the 3 politics are not a factor in this. The heck with 4 them. They can start dipping ice cream at Dairy 5 Queen or something. They don't have to raise a 6 deer. Thank you. 7 CHAIRMAN IDSAL: Does staff have any 8 comments or response on these comments? Does the 9 Commission have any comments? 10 If there are no comments, is there a 11 motion on this item? 12 COMMISSIONER MONTGOMERY: Joseph. 13 CHAIRMAN IDSAL: Joseph, did you 14 have a comment? 15 COMMISSIONER FITZSIMONS: I would 16 move we would adopt the second recommendation. 17 COMMISSIONER MONTGOMERY: Which is 18 to withdraw -- to postpone it? 19 COMMISSIONER RAMOS: To postpone it. 20 CHAIRMAN IDSAL: To postpone it. 21 COMMISSIONER RAMOS: If that's your 22 motion, I'll second that. 23 CHAIRMAN IDSAL: All in favor? 24 COMMISSIONER FITZSIMONS: And 25 republish.



Monday, February 11, 2013


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



Thursday, October 03, 2013


*** TAHC ADOPTS CWD RULE THAT the amendments __REMOVE__ the requirement for a specific fence height for captives ***


Texas Animal Health Commission (TAHC)


October 3, 2013



Monday, June 23, 2014





Tuesday, July 01, 2014





Thursday, July 03, 2014


How Chronic Wasting Disease is affecting deer population and what’s the risk to humans and pets?



Saturday, July 07, 2012


TEXAS Animal Health Commission Accepting Comments on Chronic Wasting Disease Rule Proposal


Considering the seemingly high CWD prevalence rate in the Sacramento and Hueco Mountains of New Mexico, CWD may be well established in the population and in the environment in Texas at this time.



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



Thursday, October 03, 2013


*** TAHC ADOPTS CWD RULE THAT the amendments __REMOVE__ the requirement for a specific fence height for captives ***


Texas Animal Health Commission (TAHC)


October 3, 2013



Saturday, October 18, 2014


Chronic wasting disease threatens Canadian agriculture, Alberta MLA says





Tenth Pennsylvania Captive Deer Tests Positive for Chronic Wasting Disease


​News for Immediate Release Oct. 21, 2014 Harrisburg – The Pennsylvania Department of Agriculture today announced a tenth captive deer has tested positive for Chronic Wasting Disease in Pennsylvania since the disease was discovered on a captive deer farm in 2012. The seven year old white-tailed deer died at a farm in Reynoldsville, Jefferson County, on Sept. 18, and tested positive for the disease at the Pennsylvania Veterinary Laboratory in Harrisburg. Four Jefferson County deer farms where the deer had lived are under quarantine. Currently 31 captive deer farms across the state are quarantined, where deer cannot be moved on or off the properties. The investigation continues and additional herds may be quarantined. There is no evidence that humans or livestock can get the disease, according to the Centers for Disease Control and Prevention. Chronic Wasting Disease attacks the brain of infected deer, elk and moose, producing small lesions that eventually result in death. Animals can get the disease through direct contact with saliva, feces and urine from an infected animal. Symptoms include weight loss, excessive salivation, increased drinking and urination, and abnormal behavior like stumbling, trembling and depression. Infected deer and elk may also allow unusually close approach by humans or natural predators. The disease is fatal and there is no known treatment or vaccine. The first cases of CWD in Pennsylvania were detected when two Adams County deer tested positive for Chronic Wasting Disease in 2012. Surveillance for the disease has been ongoing in Pennsylvania since 1998. The Department of Agriculture coordinates a mandatory surveillance program for more than 23,000 captive deer on 1,100 breeding farms, hobby farms and shooting preserves. Ten captive deer have tested positive since 2012. The Pennsylvania Game Commission collects samples from hunter-harvested deer and elk and those that appear sick or behave abnormally. Since 1998, the commission has tested more than 48,000 free-ranging deer and elk for the disease. Six wild deer have tested positive for the disease since 2013. For more information, visit www.agriculture.state.pa.us and click on the “Chronic Wasting Disease Information” button. Media contact: Samantha Elliott Krepps, 717-787-5085 ###​



>>> There is no evidence that humans or livestock can get the disease, according to the Centers for Disease Control and Prevention.


hang on now, what do you call this ;


> First transmission of CWD to transgenic mice over-expressing bovine prion protein gene (TgSB3985)


PRION 2014 - PRIONS: EPIGENETICS and NEURODEGENERATIVE DISEASES – Shaping up the future of prion research


Animal TSE Workshop 10.40 – 11.05 Talk Dr. L. Cervenakova First transmission of CWD to transgenic mice over-expressing bovine prion protein gene (TgSB3985)





P.126: Successful transmission of chronic wasting disease (CWD) into mice over-expressing bovine prion protein (TgSB3985)


Larisa Cervenakova,1 Christina J Sigurdson,2 Pedro Piccardo,3 Oksana Yakovleva,1 Irina Vasilyeva,1 Jorge de Castro,1 Paula Saá,1 and Anton Cervenak1 1American Red Cross, Holland Laboratory; Rockville, MD USA; 2University of California; San Diego, CA USA; 3Lab TSE/OBRR /CBER/FDA; Rockville, MD USA


Keywords: chronic wasting disease, transmission, transgenic mouse, bovine prion protein


Background. CWD is a disease affecting wild and farmraised cervids in North America. Epidemiological studies provide no evidence of CWD transmission to humans. Multiple attempts have failed to infect transgenic mice expressing human PRNP gene with CWD. The extremely low efficiency of PrPCWD to convert normal human PrPC in vitro provides additional evidence that transmission of CWD to humans cannot be easily achieved. However, a concern about the risk of CWD transmission to humans still exists. This study aimed to establish and characterize an experimental model of CWD in TgSB3985 mice with the following attempt of transmission to TgHu mice.


Materials and Methods. TgSB3985 mice and wild-type FVB/ NCrl mice were intracranially injected with 1% brain homogenate from a CWD-infected Tga20 mouse (CWD/Tga20). TgSB3985 and TgRM (over-expressing human PrP) were similarly injected with 5% brain homogenates from CWD-infected white-tailed deer (CWD/WTD) or elk (CWD/Elk). Animals were observed for clinical signs of neurological disease and were euthanized when moribund. Brains and spleens were removed from all mice for PrPCWD detection by Western blotting (WB). A histological analysis of brains from selected animals was performed: brains were scored for the severity of spongiform change, astrogliosis, and PrPCWD deposition in ten brain regions.


Results. Clinical presentation was consistent with TSE. More than 90% of TgSB3985 and wild-type mice infected with CWD/Tga20, tested positive for PrPres in the brain but only mice in the latter group carried PrPCWD in their spleens. We found evidence for co-existence or divergence of two CWD/ Tga20 strains based on biochemical and histological profiles. In TgSB3985 mice infected with CWD-elk or CWD-WTD, no animals tested positive for PrPCWD in the brain or in the spleen by WB. However, on neuropathological examination we found presence of amyloid plaques that stained positive for PrPCWD in three CWD/WTD- and two CWD/Elk-infected TgSB3985 mice. The neuropathologic profiles in CWD/WTD- and CWD/Elkinfected mice were similar but unique as compared to profiles of BSE, BSE-H or CWD/Tg20 agents propagated in TgSB3985 mice. None of CWD-infected TgRM mice tested positive for PrPCWD by WB or by immunohistochemical detection.


Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.






CWD to cattle figures CORRECTION




I believe the statement and quote below is incorrect ;


"CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures."


Please see ;


Within 26 months post inoculation, 12 inoculated animals had lost weight, revealed abnormal clinical signs, and were euthanatized. Laboratory tests revealed the presence of a unique pattern of the disease agent in tissues of these animals. These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.



" although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). "


shouldn't this be corrected, 86% is NOT a low rate. ...


kindest regards,


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


Thank you!


Thanks so much for your updates/comments. We intend to publish as rapidly as possible all updates/comments that contribute substantially to the topic under discussion.



re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations


1Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, California 94143 2Department of Neurology, University of California, San Francisco, San Francisco, California 94143 Correspondence: stanley@ind.ucsf.edu



Mule deer, white-tailed deer, and elk have been reported to develop CWD. As the only prion disease identified in free-ranging animals, CWD appears to be far more communicable than other forms of prion disease. CWD was first described in 1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of histopathology of the brain. Originally detected in the American West, CWD has spread across much of North America and has been reported also in South Korea. In captive populations, up to 90% of mule deer have been reported to be positive for prions (Williams and Young 1980). The incidence of CWD in cervids living in the wild has been estimated to be as high as 15% (Miller et al. 2000). The development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible to CWD, has enhanced detection of CWD and the estimation of prion titers (Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces, even in presymptomatic deer, has been identified as a likely source of infection for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures.





----- Original Message -----


From: David Colby To: flounder9@verizon.net


Cc: stanley@XXXXXXXX


Sent: Tuesday, March 01, 2011 8:25 AM


Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations


Dear Terry Singeltary,


Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor Department of Chemical Engineering University of Delaware










Sunday, August 19, 2012


Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation 2012





Thursday, November 21, 2013


*** Assessing the susceptibility of transgenic mice over-expressing deer prion protein to bovine spongiform encephalopathy


The present study was designed to assess the susceptibility of the prototypic mouse line, Tg(CerPrP)1536+/- to bovine spongiform encephalopathy (BSE) prions, which have the ability to overcome species barriers. Tg(CerPrP)1536+/- mice challenged with red deer-adapted BSE resulted in a 90-100% attack rates, BSE from cattle failed to transmit, indicating agent adaptation in the deer.



*** 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.



NOW, what is the latest on human risk factors to CWD strains ???




 Tuesday, October 21, 2014


Pennsylvania Department of Agriculture Tenth Pennsylvania Captive Deer Tests Positive for Chronic Wasting Disease CWD TSE PRION DISEASE



Singeltary Response to USDA, and USDA




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






Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014


Transmissible Spongiform Encephalopathy TSE Prion Disease have now been discovered in a wide verity of species across North America. typical C-BSE, atypical L-type BASE BSE, atypical H-type BSE, atypical H-G BSE, of the bovine, typical and atypical Scrapie strains, in sheep and goats, with atypical Nor-98 Scrapie spreading coast to coast in about 5 years. Chronic Wasting Disease CWD in cervid is slowly spreading without any stopping it in Canada and the USA and now has mutated into many different strains. Transmissible Mink Encephalopathy TME outbreaks. These Transmissible Spongiform Encephalopathy TSE Prion Disease have been silently mutating and spreading in different species in North America for decades.


The USDA, FDA, et al have assured us of a robust Triple BSE TSE prion Firewall, of which we now know without a doubt, that it was nothing but ink on paper. Since the 1997 mad cow feed ban in the USA, literally tons and tons of banned mad cow feed has been put out into commerce, never to return, as late as December of 2013, serious, serious breaches in the FDA mad cow feed ban have been documented. The 2004 enhanced BSE surveillance program was so flawed, that one of the top TSE prion Scientist for the CDC, Dr. Paul Brown stated ; 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.


see ;



The BSE surveillance and testing have also been proven to be flawed, and the GAO and OIG have both raised serious question as to just how flawed it has been (see GAO and OIG reports). North America has more documented TSE prion disease, in different documented species (excluding the Zoo BSE animals in the EU), then any other place on the Globe. This does not include the very likelihood that TSE prion disease in the domestic feline and canine have been exposed to high doses of the TSE prion disease vid pet food. To date, it’s still legal to include deer from cwd zone into pet food or deer food. Specified Risk Material i.e. SRM bans still being breach, as recently as just last month.


nvCJD or what they now call vCJD, another case documented in Texas last month, with very little information being released to the public on about this case? with still the same line of thought from federal officials, ‘it can’t happen here’, so another vCJD blamed on travel of a foreign animal disease from another country, while ignoring all the BSE TSE Prion risk factors we have here in the USA and Canada, and the time that this victim and others, do spend in the USA, and exposed to these risk factors, apparently do not count in any way with regard to risk factor. a flawed process of risk assessment.


sporadic CJD, along with new TSE prion disease in humans, of which the young are dying, of which long duration of illness from onset of symptoms to death have been documented, only to have a new name added to the pot of prion disease i.e. sporadic GSS, sporadic FFI, and or VPSPR. I only ponder how a familial type disease could be sporadic with no genetic link to any family member? when the USA is the only documented Country in the world to have documented two different cases of atypical H-type BSE, with one case being called atypical H-G BSE with the G meaning Genetic, with new science now showing that indeed atypical H-type BSE is very possible transmitted to cattle via oral transmission (Prion2014). sporadic CJD and VPSPR have been rising in Canada, USA, and the UK, with the same old excuse, better surveillance. You can only use that excuse for so many years, for so many decades, until one must conclude that CJD TSE prion cases are rising. a 48% incease in CJD in Canada is not just a blip or a reason of better surveillance, it is a mathematical rise in numbers. More and more we are seeing more humans exposed in various circumstance in the Hospital, Medical, Surgical arenas to the TSE Prion disease, and at the same time in North America, more and more humans are becoming exposed to the TSE prion disease via consumption of the TSE prion via deer and elk, cattle, sheep and goats, and for those that are exposed via or consumption, go on to further expose many others via the iatrogenic modes of transmission of the TSE prion disease i.e. friendly fire. I pondered this mode of transmission via the victims of sporadic FFI, sporadic GSS, could this be a iatrogenic event from someone sub-clinical with sFFI or sGSS ? what if?


Two decades have passed since Dr. Ironside first confirmed his first ten nvCJD victims in 1995. Ten years later, 2005, we had Dr. Gambetti and his first ten i.e. VPSPR in younger victims. now we know that indeed VPSPR is transmissible. yet all these TSE prion disease and victims in the USA and Canada are being pawned off as a spontaneous event, yet science has shown, the spontaneous theory has never been proven in any natural case of TSE prion disease, and scientist have warned, that they have now linked some sporadic CJD cases to atypical BSE, to atypical Scrapie, and to CWD, yet we don’t here about this in the public domain. We must make all human and animal TSE prion disease reportable in every age group, in ever state and internationally, we must have a serious re-evaluation and testing of the USA cattle herds, and we must ban interstate movement of all cervids. Any voluntary effort to do any of this will fail. Folks, we have let the industry run science far too long with regards to the TSE prion disease. While the industry and their lobbyist continues to funnel junk science to our decision policy makers, Rome burns. ...end




Sunday, June 29, 2014


Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014



Tuesday, August 12, 2014





Terry S. Singeltary Sr.




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