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

 

FOR IMMEDIATE RELEASE

 

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.

 

snip...

 

###

 

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.

 

snip...

 

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

 

*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD

 


 

Tuesday, July 01, 2014

 

CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND POTENTIAL RISK FACTORS THERE FROM

 


 

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

 


 

10/21/2014

 

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)

 


 

FORGOT TO ADD THIS ONE...

 

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.

 

TSS

 

UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON CWD TRANSMISSION TO CATTLE ;

 

CWD to cattle figures CORRECTION

 

Greetings,

 

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.

 

snip...

 


 

----- 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

 

===========END...TSS==============

 

SNIP...SEE FULL TEXT ;

 


 

UPDATED DATA ON 2ND CWD STRAIN Wednesday, September 08, 2010 CWD PRION CONGRESS SEPTEMBER 8-11 2010

 


 

Sunday, August 19, 2012

 

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

 

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

 


 

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 ???

 

SNIP...SEE FULL TEXT HERE ;

 

 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

 

RESPONSE TO SINGELTARY ON HARVARD BSE RISK ASSESSMENT

 

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

 


 

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

 

REFERENCES

 

Sunday, June 29, 2014

 

Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014

 


 

Tuesday, August 12, 2014

 

MAD COW USDA TSE PRION COVER UP or JUST IGNORANCE, for the record AUGUST 2014

 


 

Terry S. Singeltary Sr.

 

 

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

10/21/2014

 

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)

 


 

FORGOT TO ADD THIS ONE...

 

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.

 

TSS

 

UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON CWD TRANSMISSION TO CATTLE ;

 

CWD to cattle figures CORRECTION

 

Greetings,

 

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.

 

snip...

 


 

----- 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

 

===========END...TSS==============

 

SNIP...SEE FULL TEXT ;

 


 

UPDATED DATA ON 2ND CWD STRAIN Wednesday, September 08, 2010 CWD PRION CONGRESS SEPTEMBER 8-11 2010

 


 

Sunday, August 19, 2012

 

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

 

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

 


 

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 ???

 

*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent

 

*** Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP,

 

*** indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains.

 

PPo2-27:

 

Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions

 

*** Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.

 

PPo2-7:

 

Biochemical and Biophysical Characterization of Different CWD Isolates

 

*** The data presented here substantiate and expand previous reports on the existence of different CWD strains.

 


 

Envt.07:

 

Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease

 

***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.

 


 

>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO CONVERSION OF THE HUMAN PRION PROTEIN<<<

 

*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***

 

Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014

 

Wednesday, January 01, 2014

 

Molecular Barriers to Zoonotic Transmission of Prions

 

*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.

 

*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.

 


 


 

PRION2013 CONGRESSIONAL ABSTRACTS CWD

 

Sunday, August 25, 2013

 

HD.13: CWD infection in the spleen of humanized transgenic mice

 

***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.

 

Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system ***However, they also show that there is no absolute barrier to conversion of human prion protein in the case of chronic wasting disease.

 

PRION2013 CONGRESSIONAL ABSTRACTS CWD

 

Sunday, August 25, 2013

 

***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission

 


 

there is in fact evidence that the potential for cwd transmission to humans can NOT be ruled out.

 

I thought your readers and hunters and those that consume the venison, should have all the scientific facts, personally, I don’t care what you eat, but if it effects me and my family down the road, it should then concern everyone, and the potential of iatrogenic transmission of the TSE prion is real i.e. ‘friendly fire’, medical, surgical, dental, blood, tissue, and or products there from...like deer antler velvet and TSE prions and nutritional supplements there from, all a potential risk factor that should not be ignored or silenced. ...

 

the prion gods at the cdc state that there is ;

 

''no strong evidence''

 

but let's see exactly what the authors of this cwd to human at the cdc state ;

 

now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????

 

“Our conclusion stating that we found no strong evidence of CWD transmission to humans”

 

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

 

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 ;

 


 


 


 

***********CJD REPORT 1994 increased risk for consumption of veal and venison and lamb***********

 

CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994

 

Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss)

 

These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...

 

Table 9 presents the results of an analysis of these data.

 

There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).

 

Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.

 

There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).

 

The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).

 

There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).

 

The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).

 

snip...

 

It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).

 

snip...

 

In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...

 

snip...

 

In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)

 

snip...see full report ;

 


 

Thursday, October 10, 2013

 

*************CJD REPORT 1994 increased risk for consumption of veal and venison and lamb**************

 


 

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.

 


 

*** our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions. ***

 


 

snip...see full text ;

 


 

Thursday, January 2, 2014

 

*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***

 


 

*** We hypothesize that both BSE prions and CWD prions passaged through felines will seed human recPrP more efficiently than BSE or CWD from the original hosts, evidence that the new host will dampen the species barrier between humans and BSE or CWD. The new host effect is particularly relevant as we investigate potential means of trans-species transmission of prion disease.

 


 

Monday, August 8, 2011

 

*** Susceptibility of Domestic Cats to CWD Infection ***

 

Oral.29: Susceptibility of Domestic Cats to CWD Infection

 

Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason†

 

Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu

 

Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness.

 

*** Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.

 


 


 

AD.63:

 

Susceptibility of domestic cats to chronic wasting disease

 

Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN USA

 

Domestic and nondomestic cats have been shown to be susceptible to feline spongiform encephalopathy (FSE), almost certainly caused by consumption of bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and free-ranging nondomestic felids scavenge cervid carcasses, including those in areas affected by chronic wasting disease (CWD), we evaluated the susceptibility of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated cats developed signs consistent with prion disease, including a stilted gait, weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from these two cats were pooled and inoculated into cohorts of cats by IC, PO, and intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the symptomatic cats by western blotting and immunohistochemistry and abnormalities were seen in magnetic resonance imaging, including multifocal T2 fluid attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4 IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns consistent with the early stage of feline CWD.

 

*** These results demonstrate that CWD can be transmitted and adapted to the domestic cat, thus raising the issue of potential cervid-to- feline transmission in nature.

 


 

www.landesbioscience.com

 

PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)

 


 


 

FELINE SPONGIFORM ENCEPHALOPATHY FSE

 


 


 

Singeltary submission ;

 

Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose

 

DOCUMENT ID: APHIS-2006-0118-0411

 

***Singeltary submission

 

Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program Standards

 

>>>The CWD herd certification program is a voluntary, cooperative program that establishes minimum requirements for the interstate movement of farmed or captive cervids, provisions for participating States to administer Approved State CWD Herd Certification Programs, and provisions for participating herds to become certified as having a low risk of being infected with CWD<<<

 

Greetings USDA/APHIS et al,

 

I kindly would like to comment on Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program Standards.

 

I believe, and in my opinion, and this has been proven by scientific facts, that without a validated and certified test for chronic wasting disease cwd, that is 100% sensitive, and in use, any voluntary effort will be futile. the voluntary ban on mad cow feed and SRMs have failed terribly, the bse mad cow surveillance program has failed terribly, as well as the testing for bse tse prion in cattle, this too has failed terrible. all this has been proven time and time again via OIG reports and GOA reports.

 

I believe that until this happens, 100% cwd testing with validated test, ALL MOVEMENT OF CERVIDS BETWEEN STATES MUST BE BANNED, AND THE BORDERS CLOSED TO INTERSTATE MOVEMENT OF CERVIDS. there is simply to much at risk.

 

In my opinion, and the opinions of many scientists and DNR officials, that these so called game farms are the cause of the spreading of chronic wasting disease cwd through much negligence. the game farms in my opinion are not the only cause, but a big factor. I kindly wish to submit the following to show what these factors are, and why interstate movement of cervids must be banned. ...

 

snip...see full text and PDF ATTACHMENT HERE ;

 


 


 

Sunday, June 23, 2013

 

National Animal Health Laboratory Network Reorganization Concept Paper (Document ID APHIS-2012-0105-0001)

 

***Terry S. Singeltary Sr. submission

 


 

Friday, November 22, 2013

 

Wasting disease is threat to the entire UK deer population CWD TSE PRION disease in cervids

 

***SINGELTARY SUBMISSION

 

The Scottish Parliament’s Rural Affairs, Climate Change and Environment Committee has been looking into deer management, as you can see from the following press release,

 

***and your email has been forwarded to the committee for information:

 


 


 

Friday, November 22, 2013

 

Wasting disease is threat to the entire UK deer population

 


 

Sunday, July 21, 2013

 

Welsh Government and Food Standards Agency Wales Joint Public Consultation on the Proposed Transmissible Spongiform Encephalopathies (Wales) Regulations 2013

 

*** Singeltary Submission WG18417

 


 

Quantitative Assessment of Prion Infectivity in Tissues and Body Fluids by RT-QuIC

 

Davin M. Henderson1, Kristen A. Davenport1, Nicholas J. Haley2, Nathaniel D. Denkers1, Candace K. Mathiason1 and Edward A. Hoover Jr1,3

 

+ Author Affiliations 1 Prion Research Center, Colorado State University, USA; 2 Department of Diagnostic Medicine and Pathobiology, Kansas State University, USA ↵3 E-mail: edward.hoover@colostate.edu Received 8 July 2014. Accepted 6 October 2014.

 

Abstract

 

Prions are amyloid-forming proteins that cause transmissible spongiform encephalopathies through a process involving the templated conversion of the normal cellular prion protein (PrPC) to a pathogenic misfolded conformation. Templated conversion has been modeled in several in vitro assays, including serial protein misfolding amplification (sPMCA), amyloid seeding, and real time quaking induced conversion (RT-QuIC). Because RT-QuIC measures formation of amyloid fibrils in real time, it can be used to estimate the rate of seeded conversion. Here we use samples from deer infected with chronic wasting disease (CWD) in RT-QuIC to show that serial dilution of prion seed is linearly related to the rate of amyloid formation over a range of 10-3 to 10-8 µg. We then used an amyloid formation rate standard curve derived from a bioassayed reference sample (CWD+ brain homogenate) to estimate the prion seed concentration and infectivity in tissues, body fluids and excreta. Using these methods we estimate that urine and saliva from CWD-infected deer contain between 1 and 5 LD50 per 10 ml, respectively. Thus, over the 1 to 2 year course of infection, a substantial environmental reservoir of CWD prion contamination accumulates.

 

Amyloid Quantitation CWD Prion RT-QuIC TSE

 


 

P.141: Abundant prion shedding in CWD-infected deer revealed by Realtime conversion

 

Edward A Hoover,1 Davin M Henderson,1 Nathaniel D Denkers,1 Candace K Mathiason,1 Matteo Manca,2,3 and Byron Caughey2

 

1Prion Research Center, Colorado State University; Fort Collins, CO USA; 2Laboratory of Persistent Viral Diseases, NI AID; Hamilton, MT USA; 3Department of Biomedical Sciences, University of Cagliari; Monserrato, Italy

 

Background/Introduction. Chronic wasting disease (CWD) is unique among prion diseases in its efficient lateral transmission in nature. While the presence of infectious prions in body fluids and excreta of infected cervids has been demonstrated by bioassay, the dynamics, magnitude, and consequences of prion shedding remain unknown. The present studies were undertaken to determine the kinetics, duration, and magnitude of prion shedding in infected white-tailed deer.

 

Materials and Methods. Longitudinal samples were collected from white-tailed deer over a 2-year span after either oral (n=11)] aerosol (n = 6) CWD exposure. The assay protocol employed phosphotungstic acid precipitation of either whole saliva or the pelleted fraction of urine to seed recombinant Syrian hamster prion PrP substrate in RT-QuIC reactions. Prion seeding activity was assayed in 8 replicates of each sample employing thioflavin T detection in a 96-well plate-based fluorometer. Prion seeding reaction rate was determined by taking the inverse of the time at which samples exceeded a threshold of 5 standard deviations above the mean fluorescence of negative controls (1/time to threshold). Seeding activity was quantitated by comparing the realtime conversion reaction rate to a standard curve derived from a reference bioassayed brain pool homogenate from deer with terminal CWD.

 

Results. We analyzed >200 longitudinally collected, blinded, then randomized saliva and urine samples from 17 CWDinfected and 3 uninfected white-tailed deer. We detected prion shedding as early as 3 months post exposure and sustained thereafter throughout the disease course in both aerosol and orally exposed deer. The incidence of non-specific false positive results from >500 saliva and urine samples from negative control deer was 0.8%. By comparing real-time reaction rates for these body fluids to a bioassayed serially diluted brain control, we estimated that ≤1 ml of saliva or urine from pre-symptomatic infected deer constitutes a lethal infectious prion dose.

 

Conclusion. CWD prions are shed in saliva and urine of infected deer as early as 3 months post infection and throughout the subsequent >1.5 year course of infection. In current work we are examining the relationship of prionemia to excretion and the impact of excreted prion binding to surfaces and particulates in the environment.

 

Acknowledgments. Support: NIH-RO1-NS-061902; Morris Animal Foundation D12ZO-045

 

P.154: Urinary shedding of prions in Chronic Wasting Disease infected white-tailed deer

 

Nathaniel D Denkers,1 Davin M Henderson, 1 Candace K Mathiason,1 and Edward A Hoover1 1Prion Research Center, Department of Microbiology, Immunology, and Pathology, Colorado State University; Fort Collins, CO USA

 

Background/Introduction. Chronic wasting disease (CWD) is unique among prion diseases in its efficient lateral transmission in nature, yet the dynamics and magnitude of shedding and its immediate and long term consequences remain unknown. The present study was designed to determine the frequency and time span in which CWD prions are shed in urine from infected white-tailed deer using adapted real-time quaking-induced conversion (RT-QuIC) methodology.

 

Materials and Methods. Longitudinal urine samples were collected by free catch or catheterization over a 2-year period from oral-route infected [CWD+ (n = 11)] and aerosol-route-infected [CWD+ (n = 6); CWD- (n = 3)] white-tailed deer. High speed centrifugation pelleted material from 500 µl of urine was treated with sodium phosphotungstic acid (Na-PTA), resuspended in 0.05% SDS buffer, and used as seed in RT-QuIC assays employing recombinant Syrian hamster prion PrP substrate. Eight (8) replicates of each sample were run and prion seeding activity was recorded as thioflavin T binding fluorescence (480 nm emission) using a fluorimeter-shaker. Samples were considered positive if they crossed an established threshold (5 standard deviations above the negative mean fluorescence).

 

Results. In our oral-route inoculation studies, prion seeding activity has been demonstrated in urine collected at 6 months post-inoculation in 6 of 10 deer (11 of 80 replicates; 14%), and intermittently at later time points in all 11 CWD+ exposed deer. Our aerosol-route inoculation studies also showed prion seeding activity in urine collected at 6 months post-inoculation in 1 of 2 deer (3 of 16 replicates; 19%), and intermittently at later time points in 4 of 6 CWD+ exposed deer. Urine from sham-inoculated control deer and all baseline samples yielded 3 false-positive prion seeding activities (3 of 352 replicates; 0.8%).

 

Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC) are shed in urine of infected deer as early as 6 months post inoculation and throughout the subsequent disease course. Further studies are in progress refining the real-time urinary prion assay sensitivity and we are examining more closely the excretion time frame, magnitude, and sample variables in relationship to inoculation route and prionemia in naturally and experimentally CWD-infected cervids.

 

Acknowledgments. Support: NIH: RO1-NS-061902 and Morris Animal Foundation: D12ZO-045

 

P.121: Efficient transmission of prion disease through environmental contamination

 

Sandra Pritzkow, Rodrigo Morales, and Claudio Soto Mitchell Center for Alzheimer’s disease and related Brain disorders; University of Texas Medical School at Houston; Hourston, TX USA

 

Chronic wasting disease (CWD) is a prion disorder effecting captive and free-ranging deer and elk. The efficient propagation suggests that horizontal transmission through contaminated environment may play an important role. It has been shown that infectious prions enter the environment through saliva, feces, urine, blood or placenta tissue from infected animals, as well as by carcasses from diseased animals and can stay infectious inside soil over several years.

 

We hypothesize that environmental components getting in contact with infectious prions can also play a role for the horizontal transmission of prion diseases. To study this issue, surfaces composed of various environmentally relevant materials were exposed to infectious prions and the attachment and retention of infectious material was studied in vitro and in vivo. We analyzed polypropylene, glass, stainless steel, wood, stone, aluminum, concrete and brass surfaces exposed to 263K-infected brain homogenate. For in vitro analyses, the material was incubated in serial dilutions of 263K-brain homogenate, washed thoroughly and analyzed for the presence of PrPSc by PMCA. The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.

 

In addition, in order to study the transmission in a more natural setting, we exposed a group of hamster to habit in the presence of spheres composed of various materials that were pretreated with 263K prions. Many of the hamsters exposed to these contaminated materials developed typical signs of the disease that were confirmed by immunohistological and biochemical analyses.

 

These findings suggest that various surfaces can efficiently bind infectious prions and act as carriers of infectivity, suggesting that diverse elements in the environment may play an important role in horizontal prion transmission.

 

P.138: Phenotypic diversity in meadow vole (Microtus pennsylvanicus) prion diseases following challenge with chronic wasting disease isolates

 

Christopher J Johnson,1 Christina M Carlson,1,2 Jay R Schneider,1 Jamie K Wiepz,1 Crystal L Meyerett-Reid,3 Mark D Zabel,3 Joel A Pedersen,2 and Dennis M Heisey1 1USGS National Wildlife Health Center; Madison, WI USA; 2University of Wisconsin— Madison; Madison, WI USA; 3Colorado State University; Fort Collins, CO USA

 

Chronic wasting disease (CWD), a prion disease of cervids (deer, elk and moose), is spreading unchecked through large sections of North America. Transmission of CWD among cervids is especially facile and can occur through direct animal-toanimal contact and indirectly through contact with prions shed from infected animals. The disease transmission threat posed by CWD to other wildlife species remains unknown, but other species are inevitably exposed to CWD by consumption of infectious materials and through contact with environmental CWD contamination. In this study, we investigated the transmission and adaptation of various white-tailed deer CWD isolates in the meadow vole (Microtus pennsylvanicus), a native North American rodent that is sympatric with current CWD epizootics that we have previously established is susceptible to CWD. We found that serial subpassage of CWD from white-tailed deer homozygous for glycine at position 96 (96GG) of the prion protein in meadow voles resulted in the selection of a single prion strain that was characterized by homogeneity in incubation period, abnormal prion protein (PrPTSE) glycoform ratio, lesion profile and PrPTSE deposition pattern. In contrast, passage of CWD from heterozygous 96GS genotype deer produced four unique disease phenotypes upon first passage. Subpassage of these types ultimately resulted in selection of a single strain by third passage that was distinct from the 96GG genotype CWD-derived strain. We also establish that meadow voles are susceptible to CWD via peripheral challenge, albeit with lower attack rates and longer incubation periods. Interestingly, oral challenge of meadow voles with CWD resulted in subclinical infection in primary passage animals, but manifested as clinical prion disease upon subpassage. Our data establish that meadow voles are permissive to CWD via peripheral exposure route, suggesting they could serve as an environmental reservoir for CWD. Additionally, our data are consistent with the hypothesis that at least two strains of CWD circulate in naturally-infected cervid populations and provide evidence that meadow voles are a useful tool for CWD strain typing.

 

P.146: Kinetics and cell association of chronic wasting disease prions shed in saliva and urine of white-tailed deer

 

Nicholas J Haley,1,2 Scott Carver,3 Clare E Hoover,1 Kristen A Davenport,1 Candace K Mathiason,1 Glenn C Telling,1 and Edward A Hoover1

 

1Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences; Colorado State University; Fort Collins, CO USA; 2Department of Diagnostic Medicine and Pathobiology, College of Veterinary Medicine; Kansas State University; Manhattan, KS USA; 3School of Zoology; University of Tasmania; Hobart, Tasmania, Australia

 

Chronic wasting disease, a transmissible spongiform encephalopathy (TSE) of deer, elk, and moose, is unique among prion diseases in its relatively efficient horizontal transmissibility. Recent studies have shown that excreta—saliva, urine, and feces—from CWD-positive cervids may play an important role in horizontal transmission of CWD, and although the precise onset of shedding in these excreta is unknown, it is thought to occur long before the onset of clinical symptoms. High levels of prion seeding activity have been demonstrated in excretory tissues of deer, including tongue, salivary glands, kidney, and urinary bladder, though the origin(s) and cellular nature of infectious prions in excreta is unknown. We hypothesized that excretory shedding of CWD prions in saliva and urine would coincide with the appearance of PrPd appearance in peripheral lymphatic tissues, and that infectivity would associate with cellular preparations of these excreta. Following intracerebral inoculation of susceptible Tg[CerPrP] mice, we observed efficient transmission in saliva collected as early as 12 months post-exposure, coinciding with peripheral PrPd appearance in tonsil biopsies; while urine collected at terminal disease was only minimally infectious in transgenic mice. We also found that acellular preparations of saliva, and cellular preparations of urine, were capable of transmitting CWD infection to transgenic Tg[CerPrP] mice with incubation periods similar to that of whole saliva or urine; saliva and urine from CWD-negative deer failed to induce prion disease in these mice. Infectious titers were determined for obex and bodily fluids, and were similar to those previously described. These findings extend our understanding of CWD shedding in white-tailed deer, and offer insight into the source and cellular associations of infectious CWD prions in excreta.

 

P.178: Longitudinal quantitative analysis of CWD prions shed in saliva of deer

 

Davin M Henderson, Nina Garbino, Nathaniel D Denkers, Amy V Nalls, Candace K Mathiason, and Edward A Hoover Prion Research Center, College of Veterinary Medicine and Biomedical Sciences, Colorado State University; Fort Collins, CO USA

 

Background/Introduction. Chronic Wasting Disease (CWD) is an emergent rapidly spreading fatal prion disease of cervids (deer, elk and moose). CWD has now been identified in 22 States (including two new states within the last year), 2 Canadian provinces, and South Korea. Shedding of infectious prions in excreta (saliva, urine, feces) may be an important factor in CWD transmission. Here we apply an adapted version of a rapid in vitro assay [real-time quaking-induced conversion (RT-QuIC)] to determine the time of onset, length, pattern, and magnitude of prion shedding in saliva of infected deer.

 

Materials and Methods. The RT-QuIC assay was performed as previously described in Henderson et al. PLoS-One (2013). Saliva samples were quantitated by comparison to a RT-QuIC reaction rate standard curve of a bioassayed obex sample from a terminally ill cervid.

 

Results. To better understand the onset and length of CWD prion shedding we analyzed >150 longitudinally collected, blinded, then randomized saliva samples from 17 CWD-infected and 3 uninfected white-tailed deer. We observed prion shedding, as detected by the RT-QuIC assay, as early as 3 months from inoculation and sustained shedding throughout the disease course in both aerosol and orally exposed deer. We estimated the infectious lethal dose of prions shed in saliva from infected deer by comparing real-time reaction rates of saliva samples to a bioassayed serially diluted brain control. Our results indicate that as little as 1 ml of saliva from pre-symptomatic infected deer constitutes a lethal CWD prion dose.

 

Conclusions. During the pre-symptomatic stage of CWD infection and throughout the course of disease deer may be shedding multiple LD50 doses per day in their saliva. CWD prion shedding through saliva and excreta may account for the unprecedented spread of this prion disease in nature. Acknowledgments. Supported by NIH grant RO1-NS-061902 and grant D12ZO-045 from the Morris Animal Foundation.

 


 

*** We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.

 

*** The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.

 

PRION 2014 CONFERENCE

 

CHRONIC WASTING DISEASE CWD

 

A FEW FINDINGS ;

 

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.

 

We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.

 

The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.

 

Our data establish that meadow voles are permissive to CWD via peripheral exposure route, suggesting they could serve as an environmental reservoir for CWD. Additionally, our data are consistent with the hypothesis that at least two strains of CWD circulate in naturally-infected cervid populations and provide evidence that meadow voles are a useful tool for CWD strain typing.

 

Conclusion. CWD prions are shed in saliva and urine of infected deer as early as 3 months post infection and throughout the subsequent >1.5 year course of infection. In current work we are examining the relationship of prionemia to excretion and the impact of excreted prion binding to surfaces and particulates in the environment.

 

Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC) are shed in urine of infected deer as early as 6 months post inoculation and throughout the subsequent disease course. Further studies are in progress refining the real-time urinary prion assay sensitivity and we are examining more closely the excretion time frame, magnitude, and sample variables in relationship to inoculation route and prionemia in naturally and experimentally CWD-infected cervids.

 

Conclusions. Our results suggested that the odds of infection for CWD is likely controlled by areas that congregate deer thus increasing direct transmission (deer-to-deer interactions) or indirect transmission (deer-to-environment) by sharing or depositing infectious prion proteins in these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely controlled by separate factors than found in the Midwestern and endemic areas for CWD and can assist in performing more efficient surveillance efforts for the region.

 

Conclusions. During the pre-symptomatic stage of CWD infection and throughout the course of disease deer may be shedding multiple LD50 doses per day in their saliva. CWD prion shedding through saliva and excreta may account for the unprecedented spread of this prion disease in nature.

 

see full text and more ;

 

Monday, June 23, 2014

 

*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD

 


 


 

*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years***

 

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

 


 

New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication

 


 

Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production

 


 

Detection of protease-resistant cervid prion protein in water from a CWD-endemic area

 


 

A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing

 


 

Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals

 


 

spreading cwd around...tss

 

Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of farmed elk in Saskatchewan in a single epidemic. All of these herds were depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease eradication program. Animals, primarily over 12 mo of age, were tested for the presence CWD prions following euthanasia. Twenty-one of the herds were linked through movements of live animals with latent CWD from a single infected source herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily infected herds.

 

***The source herd is believed to have become infected via importation of animals from a game farm in South Dakota where CWD was subsequently diagnosed (7,4). A wide range in herd prevalence of CWD at the time of herd depopulation of these herds was observed. Within-herd transmission was observed on some farms, while the disease remained confined to the introduced animals on other farms.

 


 

spreading cwd around...tss

 

Friday, May 13, 2011

 

Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea

 

Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim, Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research Division, National Veterinary Research and Quarantine Service, Republic of Korea

 

Chronic wasting disease (CWD) has been recognized as an important prion disease in native North America deer and Rocky mountain elks. The disease is a unique member of the transmissible spongiform encephalopathies (TSEs), which naturally affects only a few species. CWD had been limited to USA and Canada until 2000.

 

On 28 December 2000, information from the Canadian government showed that a total of 95 elk had been exported from farms with CWD to Korea. These consisted of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72 elk in 1997, which had been held in pre export quarantine at the “source farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD surveillance program was initiated by the Ministry of Agriculture and Forestry (MAF) in 2001.

 

All elks imported in 1997 were traced back, however elks imported in 1994 were impossible to identify. CWD control measures included stamping out of all animals in the affected farm, and thorough cleaning and disinfection of the premises. In addition, nationwide clinical surveillance of Korean native cervids, and improved measures to ensure reporting of CWD suspect cases were implemented.

 

Total of 9 elks were found to be affected. CWD was designated as a notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.

 

Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and 2005.

 

Since February of 2005, when slaughtered elks were found to be positive, all slaughtered cervid for human consumption at abattoirs were designated as target of the CWD surveillance program. Currently, CWD laboratory testing is only conducted by National Reference Laboratory on CWD, which is the Foreign Animal Disease Division (FADD) of National Veterinary Research and Quarantine Service (NVRQS).

 

In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the human consumption was confirmed as positive. Consequently, all cervid – 54 elks, 41 Sika deer and 5 Albino deer – were culled and one elk was found to be positive. Epidemiological investigations were conducted by Veterinary Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary services.

 

Epidemiologically related farms were found as 3 farms and all cervid at these farms were culled and subjected to CWD diagnosis. Three elks and 5 crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.

 

All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and confirmed as negative.

 

Further epidemiological investigations showed that these CWD outbreaks were linked to the importation of elks from Canada in 1994 based on circumstantial evidences.

 

In December 2010, one elk was confirmed as positive at Farm 5. Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer – were culled and one Manchurian Sika deer and seven Sika deer were found to be positive. This is the first report of CWD in these sub-species of deer. Epidemiological investigations found that the owner of the Farm 2 in CWD outbreaks in July 2010 had co-owned the Farm 5.

 

In addition, it was newly revealed that one positive elk was introduced from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed (species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as negative.

 

: Corresponding author: Dr. Hyun-Joo Sohn (+82-31-467-1867, E-mail: shonhj@korea.kr) 2011 Pre-congress Workshop: TSEs in animals and their environment 5

 


 


 

***raising the possibility that deer may be susceptible to multiple scrapie strains. ***

 

Saturday, August 02, 2014

 

Structural effects of PrP polymorphisms on intra- and inter-species prion transmission

 

*** Finally, our findings showing that Tg(DeerPrP), but not Tg(ElkPrP) are sensitive to infection with SSBP/1 belie previously published results showing that SSBP/1 of the same provenance caused disease in two lines of Tg mice expressing elk PrP (13). However, our results appear to be consistent with the reported susceptibilities of elk and deer to sheep prions. In previous studies, of six elk inoculated with scrapie, three presented with neurological signs and neuropathology, but only after long and variable times to disease onset ranging from 25 to 46 months (29). In contrast, our results with SSBP/1 demonstrate relatively facile transmission of scrapie to deer, with all inoculated animals developing within 19 to 20 months, which is in accordance with susceptibility of deer to a US scrapie isolate with a similar time to disease onset (24). Polymorphisms ovine PrP add a further level of complexity, since they control the propagation scrapie strains. Occupancy of residue 136 by A or V is of particular importance. Our previous results indicated that SSBP/1 is comprised of a dominant strain that is preferentially propagated by sheep PrP encoding V at 136 (12). In contrast, the scrapie prions used in the deer transmission studies of Greenlee and colleagues were isolated from a sheep encoding A136, ***raising the possibility that deer may be susceptible to multiple scrapie strains. ***

 

Significance

 

The unpredictable recurrences of prion epidemics, their incurable lethality, and the capacity of animal prions to infect humans, provide significant motivation to ascertain the parameters governing disease transmission. The unprecedented spread, and uncertain zoonotic potential of chronic wasting disease (CWD), a contagious epidemic among deer, elk, and other cervids, is of particular concern. Here we demonstrate that naturally occurring primary structural differences in cervid PrPs differentially impact the efficiency of intra- and interspecies prion transmission. Our results not only deliver new information about the role of primary structural variation on prion susceptibility, but also provide functional support to a mechanism in which plasticity of a tertiary structural epitope governs prion protein conversion and intra- and inter-species susceptibility to prions.-

 

snip...

 

Saturday, August 02, 2014

 

Structural effects of PrP polymorphisms on intra- and inter-species prion transmission

 


 

now, decades later ;

 

2012

 

PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer

 

Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA

 

snip...

 

The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD 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 similar to 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 WTD 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 PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.

 


 

2011

 

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

 


 

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

 

snip...

 

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.

 


 

2011 Annual Report

 

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

 

2011 Annual Report

 

In Objective 1, Assess cross-species transmissibility of transmissible spongiform encephalopathies (TSEs) in livestock and wildlife, numerous experiments assessing the susceptibility of various TSEs in different host species were conducted. Most notable is deer inoculated with scrapie, which exhibits similarities to chronic wasting disease (CWD) in deer suggestive of sheep scrapie as an origin of CWD.

 

snip...

 

4. Accomplishments

 

1. Deer inoculated with domestic isolates of sheep scrapie. Scrapie-affected deer exhibit 2 different patterns of disease associated prion protein. In some regions of the brain the pattern is much like that observed for scrapie, while in others it is more like chronic wasting disease (CWD), the transmissible spongiform encephalopathy typically associated with deer.

 

his work conducted by ARS scientists at the National Animal Disease Center, Ames, IA suggests that an interspecies transmission of sheep scrapie to deer may have been the origin of CWD. This is important for husbandry practices with both captive deer, elk and sheep for farmers and ranchers attempting to keep their herds and flocks free of CWD and scrapie.

 


 

White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection

 

Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS

 

snip...

 

This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.

 

see full text ;

 


 

SEE MORE USAHA REPORTS HERE, 2012 NOT PUBLISHED YET...TSS

 


 


 


 

Thursday, June 20, 2013

 

atypical, BSE, CWD, Scrapie, Captive Farmed shooting pens (livestock), Wild Cervids, Rectal Mucosa Biopsy 2012 USAHA Proceedings, and CJD TSE prion Update

 


 

*** We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.

 

*** The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.

 

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

 


 

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

 

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.

 

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

 

Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. *** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. *** It also suggests a similar cause or source for atypical BSE in these countries. ***

 

see page 176 of 201 pages...tss

 


 

*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;

 


 

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

 


 

2013

 

Sunday, December 15, 2013

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE

 


 

Susceptibility of UK red deer (Cervus alaphus elaphus) to oral BSE transmission Project Code: M03024

 

02/08/2011

 

The project confirmed that U.K red deer are susceptible to both oral and intra-cerebral inoculation with the cattle BSE agent. Six clinically positive (from 26-42 months post inoculation) i.c inoculated and one (56 months post inoculation) orally dosed deer that tested positive for TSE by immunohistochemistry and Western blotting using several primary antibodies demonstrated widespread accumulation of disease specific prion protein in the central nervous system, peripheral nervous system and enteric nervous system but none in lymphoreticular system. All showed several brain sites positive for disease specific prion protein and presented immunohistochemistry and Western blotting phenotypes with similarities to BSE in sheep, goats and cattle but unlike those seen in chronic wasting disease (CWD) in elk or scrapie in sheep. The vacuolar pathology and distribution of disease specific prion protein in red deer resembled that of CWD in most major respects however we have shown that BSE can be clearly differentiated from CWD by existing immunohistochemical and biochemical methods that are in routine use. The knowledge gained as a result of this work will permit rapid and accurate diagnosis should a TSE ever be detected in European red deer and will also enable effective disease control methods to be quickly put in place.

 


 

Friday, September 05, 2014

 

*** CFIA CWD and Grain Screenings due to potential risk factor of spreading via contamination of grain, oil seeds, etc. ***

 


 

Wednesday, September 17, 2014

 

*** Cervid Health Business Plan Fiscal Years 2014 to 2018 Animal and Plant Health Inspection Service Veterinary Services ***

 


 

The deer from an infected Reynoldsville, Jefferson County farm tested positive for Chronic Wasting Disease. Two other white-tailed deer died in April on the farm and tested positive for the disease. This marks the 14th white-tailed deer in the state to test positive for the disease since 2012.

 

snip

 

“This is an unprecedented level of infection in a captive deer herd,” said Greig. “The department and deer farmers worked together to accommodate the requests of these researchers. The more we know, the greater the chance we can eradicate the disease.”

 


 


 

Sunday, July 13, 2014

 

Louisiana deer mystery unleashes litigation 6 does still missing from CWD index herd in Pennsylvania Great Escape

 


 

Saturday, June 29, 2013

 

PENNSYLVANIA CAPTIVE CWD INDEX HERD MATE YELLOW *47 STILL RUNNING LOOSE IN INDIANA, YELLOW NUMBER 2 STILL MISSING, AND OTHERS ON THE RUN STILL IN LOUISIANA

 


 

Tuesday, June 11, 2013

 

*** CWD GONE WILD, More cervid escapees from more shooting pens on the loose in Pennsylvania

 


 

Tuesday, May 28, 2013

 

Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd Pennsylvania Update May 28, 2013

 

*** 6 doe from Pennsylvania CWD index herd still on the loose in Louisiana, quarantine began on October 18, 2012, still ongoing, Lake Charles premises.

 


 

Sunday, January 06, 2013

 

USDA TO PGC ONCE CAPTIVES ESCAPE

 

*** "it‘s no longer its business.”

 


 

”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” page 26.

 


 

Wednesday, November 14, 2012

 

PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD INVESTIGATION MOVES INTO LOUISIANA and INDIANA

 


 

Tuesday, October 23, 2012

 

PA Captive deer from CWD-positive farm roaming free

 


 

Monday, June 23, 2014

 

PRION 2014 CHRONIC WASTING DISEASE CWD

 


 

Thursday, July 03, 2014

 

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

 


 

Tuesday, July 01, 2014

 

*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND POTENTIAL RISK FACTORS THERE FROM

 


 

 

tss