Sunday, December 14, 2014

TEXAS 84th Legislature commencing this January, deer breeders are expected to advocate for bills that will seek to further deregulate their industry

TEXAS 84th Legislature 2015

TEXAS WILDLIFE ASSOCIATION
 

Oct 16, 2014


Legislative Agenda

 

Hunters’ Right to Know- TWA will pursue legislation that provides improved animal identification requirements on white-tailed deer and mule deer that are released from breeder pens. TWA maintains the position that a hunter has the right to know the origin of the deer he or she is hunting in order to make personal ethical and meat safety decisions prior to harvest.

 

10 Day Rule- TWA will pursue legislation that will require a “spring release” of pen-raised deer, as opposed to the current “10 day rule” which allows release of bucks up until 10 days prior to the start of the earliest deer season. This will address concerns related to consumption of deer meat that could have drug residues. A spring release would also provide more time for deer to “re-wild” before being hunted, which will address concerns regarding fair chase and perceptions of canned hunting.

 

Texas Wildlife Association (TWA), a statewide organization consisting of almost 7,000 members, is actively developing its legislative agenda as the 84th Texas Legislature approaches in January 2015. “Our organization’s leadership and committees have spent considerable time and energy over the last several months vetting various issues that we believe deserve legislative attention. Because public policy issues are a significant focus for TWA members, we have increased our governmental affairs capacity by adding personnel to our advocacy support team,” said TWA Chief Executive Officer, David Yeates.

 

TWA engages in a broad range of land, water, and wildlife issues. “The diversity of issues that TWA addresses is often times challenging and complex. However, the ambitious advocacy approach reflects the strength of our organization,” said TWA President, Greg Simons. The broad range of issues that TWA addresses is important as each one has the potential to have a tremendous impact on the members of TWA. “We have a history of serving as an advocacy leader for landowners, hunters, and other wildlife enthusiasts, even when the issues are complex or controversial,” said Simons.

 

Below is a list of key issues that TWA will directly address through legislation and/or will continue to closely monitor prior to and during session.

 

Captive Propagation of Wild Mule Deer- TWA will seek to repeal legislation that was passed in 2011 that provides for possible implementation of Deer Management Permits (DMP) for mule deer, which allow captured wild mule deer to be placed into pens for propagation purposes. With the state’s first cases of Chronic Wasting Disease detected in 2012 in the mule deer country of far West Texas, such DMP practices create unnecessary risk to our state’s deer resources. DMPs for mule deer have yet to be implemented and TWA believes that this “dormant” permit allowance should be repealed in order to address these unnecessary risks to our important wildlife resources.

 

“TWA will work to be first in line to protect the rights of private property owners. We will always be diligent in maintaining the balance of protections between the owners of wildlife habitat, the public’s wildlife, and the hunters of Texas,” said TWA Vice President, Marko Barrett.

 

TWA is a 501(c)4 organization that was formed in 1985 with a mission of serving Texas wildlife and its habitat, while protecting the property rights, hunting heritage, and the conservation efforts of those who value and steward wildlife resources.

 


 

Sanders: Animal husbandry practices threaten hunting heritage

 

By Jenny Sanders | December 13, 2014

 

With white-tailed deer season now in full swing, the debate over deer-ranching practices is erupting and promises to greet state lawmakers when they arrive in Austin next month. Here's the scenario: A "hunter" picks out a deer on the Internet to kill for its prized antlers. The "hunter" flies in on his corporate jet to a Texas ranch, hops in a Jeep and drives up to a genetically engineered trophy buck, released from captivity as little as 10 days before. The "hunter" shoots the deer, loads up the antlers, gives the meat to whomever will take it and gets back on his plane so he is home in time for dinner.

 

With more than 4 million wild deer in Texas, how can we justify these extreme factory farming and put-and-take shooting practices that represent nothing more than a commodification of wildlife and a perversion of our hunting culture? Hunters and Texans agree: This is not hunting.

 

Wildlife conservation and management takes on many forms in Texas, and the vast majority of the 250,000 private landowners that creatively steward our state's wildlife resources are to be commended. Rural Texas is fueled by wildlife and hunting enterprises, which serve as the economic engine that sustains many private landowners and keeps them on the land.

 

White-tailed deer, and all wildlife, belong to all Texans, held in trust and managed on behalf of the people by private landowners, with Texas Parks & Wildlife Department oversight. Texas landowners are able to benefit economically from hunting on their land, but regardless of the property size or height of the fence, the wildlife on private land still belongs to the people of Texas.

 

In contrast to the idea of wildlife stewardship, there are approximately 1,300 deer breeders in Texas who are part of a growing billion-dollar industry that raises deer in pens, employing extreme animal husbandry practices usually reserved for livestock, just to cultivate animals for release on "shooting preserves." These practices include repeated forced semen collection, artificial insemination, and even practices that can determine the sex of the fetus, combined with administration of a long list of pharmaceuticals.

 

Deer breeding in Texas is a cottage industry backed by big dollars and focused almost exclusively on antler size. The genesis of this industry was legitimate enough - a tool to supplement genetics for long-term population enhancement. However, in recent years the industry has shifted much of its focus to supplying the increasing demand for "shooter bucks" and a guaranteed kill as described above.

 

With the 84th Legislature commencing this January, deer breeders are expected to advocate for bills that will seek to further deregulate their industry, transfer regulatory authority and privatize a public resource.

 

Texans for Saving Our Hunting Heritage is a group of concerned sportsmen and landowners formed to expose practices that we believe threaten the future of hunting:

 

Cavalier use of drugs and no safety net to protect human health: Extreme animal husbandry practices that are common in the deer breeding industry lend themselves to the use of a long list of pharmaceuticals. Very few of the commonly used drugs are labeled for white-tailed deer, and unlike the strict controls on pharmaceutical administration and withdrawal intervals in the livestock industry, there is no recognized authority that protects the consumer from potential drug residues in liberated breeder deer.

 

The 10-day rule: Current law allows for captive-raised deer to be "hunted" just 11 days after they are liberated from captivity. This poses threats to food safety because of unknown pharmaceutical withdrawal intervals in liberated breeder deer and promotes a perception of "canned hunting" that most hunters and most Texans cannot support.

 

Lack of consumer protection and disclosure: There is currently no requirement for breeder deer to be clearly and visibly marked upon liberation into the wild. No form of disclosure is required to ensure that the hunter is aware he is hunting a pen-raised deer. Hunters deserve transparency regarding the origin and potential pharmaceutical history of the deer they harvest.

 

Lack of enforced habitat requirements: Deer breeders have used political strong-arming to exempt themselves from the Texas Parks & Wildlife Department "Stocking Policy," allowing them to liberate captive-raised deer into any size "pasture," regardless of habitat availability.

 

Hunting is part of the fabric of Texas. It is about camaraderie, family values, conservation and tradition. Texans for Saving our Hunting Heritage calls on Texans and Texas hunters to unite in opposition to practices that threaten the perception and future of our sport. Please join us as we "Hunt Real. Hunt Wild. Hunt Texas Proud."

 

Sanders is the executive director of Texans for Saving Our Hunting Heritage.

 


 

December 14, 2014 Houston Chronicle

 

Deer breeding practices harm proud Texas sport

 

By Jenny Sanders.

 

Here's the scenario: A "hunter" picks out a deer on the Internet to kill for its prized antlers. The "hunter" flies in on his corporate jet to a Texas ranch, hops in a jeep and drives up to a genetically engineered trophy buck, released from captivity as little as 10 days before. The "hunter" shoots the deer, loads up the antlers, gives the meat to whomever will take it and gets back on his plane so he is home in time for dinner.

 

With more than 4 million wild deer in Texas, how can we justify these extreme factory farming and put-and-take shooting practices that represent nothing more than a commodification of wildlife and a perversion of our hunting culture? Hunters and Texans agree: This is not hunting.

 

Wildlife conservation and management takes on many forms in Texas, and the vast majority of the 250,000 private landowners that creatively steward our state's wild- life resources are to be commended. Rural Texas is fueled by wildlife and hunting enterprises, which serve as the economic engine that sustains many private landowners and keeps them on the land. White-tailed deer, and all wild- life, belong to all Texans, held in trust and managed on behalf of the people by private landowners, with Texas Parks & Wildlife Department oversight. Texas landowners are able to benefit economically from hunting on their land, but regard- less of the property size or height of the fence, the wildlife on private land still belongs to the people of Texas.

 

In contrast to the idea of wildlife stewardship, there are approximately 1,300 deer breeders in Texas who are part of a growing billion- dollar industry that raises deer in pens, employing extreme animal husbandry practices usually re- served for livestock, just to cultivate animals for release on "shooting preserves." These practices include repeated forced semen collection, artificial insemination, and even practices that can determine the sex of the fetus, combined with administration of a long list of pharmaceuticals.

 

Deer breeding in Texas is a cottage industry backed by big dollars and focused almost exclusively on antler size. The genesis of this industry was legitimate enough - a tool to supplement genetics for long-term population enhancement. However, in recent years the industry has shifted much of its focus to supplying the increasing demand for "shooter bucks" and a guaranteed kill as described above.

 

 With the 84th Legislature commencing this January, deer breeders are expected to advocate for bills that will seek to further deregulate their industry, transfer regulatory authority and privatize a public resource,

 

Texans for Saving Our Hunting Heritage is a group of concerned sportsmen and landowners formed to expose practices that we believe threaten the future of hunting:

 

Cavalier use of drugs and no

 

Breeding continues on B13

 

Breeding rules allow industry to run rampant

 

Breeding from page B13

 

safety net to protect human health: Extreme animal husbandry practices that are common in the deer breeding industry lend themselves to the use of a long list of pharmaceuticals. Very few of the commonly used drugs are labeled for white-tailed deer, and unlike the strict controls on pharmaceutical administration and withdrawal intervals in the livestock industry, there is no recognized authority that protects the consumer from potential drug residues in liberated breeder deer.

 

 •• The to-day rule: Current law allows for captive-raised deer to be "hunted" just 11 days after they are liberated from captivity. This poses threats to food safety because of unknown pharmaceutical withdrawal intervals in liberated breeder deer and promotes a perception of "canned hunting" that most hunters and most Texans cannot support .

 

•• Lack of consumer protection and disclosure: There is currently no requirement for breeder deer to be clearly and visibly marked upon liberation into the wild. No form of disclosure is required to ensure that the hunter is aware he is hunting a pen-raised deer. Hunters deserve transparency regarding the origin and potential pharmaceutical history of the deer they harvest.

 

•• Lack of enforced habitat requirements: Deer breeders have used political strong-arming to exempt themselves from the Texas Parks & Wildlife Department "Stocking Policy," allowing them to liberate captive-raised deer into any size "pasture," regard- less of habitat availability.

 

Hunting is part of the fabric of Texas. It is about camaraderie, family values, conservation and tradition, Texans for Saving our Hunting Heritage calls on Texans and Texas hunters to unite in opposition to practices that threaten the perception and future of our sport. Please join us as we "Hunt Real. Wild. Hunt Texas Proud."

 

==========

 

COUNTERPOINT

 

Responsible management preserves hunting legacy

 

snip...see ;

 


 

also see ;

 

Keep our Texas Wildlife Wild

 


 

When Hunting Isn’t Very Sporting

 



83R30157 BPG-D By: Kuempel H.R. No. 2597

R E S O L U T I O N

 WHEREAS, Texas is home to the largest population of white-tailed deer in the nation, and deer breeding and hunting make important contributions to the state's economy; and
 WHEREAS, A Texas A&M University study conducted in 2007 found that deer breeding and ranching generated over $650 million annually and supported more than 7,300 jobs; as land ownership becomes increasingly fragmented, deer breeding is particularly well suited to the utilization of smaller tracts, and the industry is now one of the fastest growing in rural America; by 2012, Texas had permitted over 1,200 breeder facilities containing over 100,000 breeder deer in nearly 200 counties; and

 WHEREAS, Disease issues that arise in the deer industry are handled by the Texas Animal Health Commission, but most industry activities fall under the purview of the wildlife division of the Texas Parks and Wildlife Department; although TPWD is noted for its vast knowledge of wildlife biology, it is the TAHC that maintains expertise in agriculture, animal husbandry, and related matters of genetics, health, nutrition, breeding, and marketability; moreover, the TAHC manages certain breeds of cervid animals, including red deer and sika deer; and

 WHEREAS, Properly managing this growing industry is of long-term importance, and an in-depth consideration of relevant issues would be beneficial to this state; now, therefore, be it
 RESOLVED, That the House of Representatives of the 83rd Texas Legislature hereby request the speaker of the house to create a select interim committee to study regulatory oversight of the deer breeding industry in order to ensure that the industry is served by the state agency tasked with promoting and ensuring animal health and productivity; and, be it further

 RESOLVED, That the study include recommendations on measures to ensure the vitality of the industry and encompass assurances that the Texas Parks and Wildlife Department will remain involved in the industry through its responsibility for issuing hunting licenses and providing game wardens; and, be it further

 RESOLVED, That the committee submit a full report, including findings and recommendations for legislation, to the speaker and the members of the house of the 84th Texas Legislature when it convenes in January 2015.



http://www.legis.state.tx.us/tlodocs/83R/billtext/html/HR02597I.htm


 

Greetings Texans for Saving Our Hunting Heritage et al.

 

I saw your piece in the Houston Chronicle today, POINT ‘Deer breeding practices harm proud Texas sport’. I was glad to see it, but disturbed that you did not bring up Chronic Wasting Disease CWD, considering it has been documented in Texas. I tried telling the TAHC 10 years before it was discovered, where it was, and where to go look, but they ignored my warning. I kindly wish to submit the following for your files. a bit of history first, and then some recent science on the CWD TSE prion disease, and my concerns therefrom. ...

 

thank you for your work!

 

kindes tegards, terry

 

I kindly wish to submit the following ;

 

a few examples of the overuse of antibiotics in farming agriculture practice with other species ;

 

Our investigation also found that you hold animals under conditions that are so inadequate that medicated animals bearing potentially harmful drug residues are likely to enter the food supply. For example, you failed to maintain complete treatment records. Food from animals held under such conditions is adulterated within the meaning of section 402(a)(4) of the FD&C Act, 21 U.S.C. § 342(a)(4).

 


 


 

Tuesday, September 17, 2013

 

Antibiotic resistance threats in the United States, 2013 THREAT REPORT

 

“We continue to promote the concept that, if an animal is sick, using antibiotics to treat that animal is obviously important,” said CDC Director Dr. Tom Frieden. “We also know that there are specific situations in which the widespread use of antimicrobials in agriculture has resulted in an increase in resistant infections in humans.”

 


 


 

Chronic Wasting Disease CWD of Cervids Transmissible Spongiform Encephalopathy TSE Prion disease aka mad cow type disease

 

my concerns with Chronic Wasting Disease CWD TSE prion disease in cervids, recent and old history and science, source references as follows, please use as you wish. science on the TSE prion disease is very political, you must divulge the science, and then make your mind up, and a lot of times, folks just don’t know about all the science, ...good luck!

 

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

 

From: "Terry S. Singeltary Sr." <[log in to unmask]>

 

To: <[log in to unmask]>

 

Sent: Saturday, December 23, 2006 1:47 PM

 

Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing sampling figures -- what gives TAHC ???

 

Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing sampling figures -- what gives TAHC ???

 

Date: December 23, 2006 at 11:25 am PST

 

Greetings BSE-L members,

 

i never know if i am going crazy or just more of the same BSe. several years ago i brought up the fact to the TAHC that CWD was literally at the Texas borders and that the sample size for cwd testing was no where near enough in the location of that zone bordering NM. well, i just wrote them another letter questioning this again on Dec. 14, 2006 (see below) and showed them two different pdf maps, one referencing this url, which both worked just fine then. since then, i have NOT received a letter from them answering my question, and the url for the map i used as reference is no longer working? i had reference this map several times from the hunter-kill cwd sampling as of 31 August 2005 pdf which NO longer works now??? but here are those figures for that zone bordering NM, for those that were questioning the url. the testing samples elsewhere across Texas where much much more than that figure in the zone bordering NM where CWD has been documented bordering TEXAS, near the White Sands Missile Range. SO, why was the Texas hunter-kill cwd sampling as of 31 August 2005 document removed from the internet??? you know, this reminds me of the infamous TEXAS MAD COW that i documented some 7 or 8 months before USDA et al documented it, when the TAHC accidentally started ramping up for the announcement on there web site, then removed it (see history at bottom). i am not screaming conspiracy here, but confusious is confused again on the ciphering there using for geographical distribution of cwd tissue sample size survey, IF they are serious about finding CWD in TEXAS. common sense would tell you if cwd is 35 miles from the border, you would not run across state and have your larger samples there, and least samples 35 miles from where is what found..........daaa..........TSS

 

THEN NOTICE CWD sample along that border in TEXAS, Three Year Summary of Hunter-Kill CWD sampling as of 31 August 2005 of only 191 samples, then compare to the other sample locations ;

 


 


 

 TPWD has been conducting surveys of hunter-kill animals since 2002 and has collected more than 7300 samples (as of 31 August 2005). In total, there have been over 9400 samples, both hunter-kill and private samples, tested in Texas to date, and no positives have been found.

 


 

 SO, out of a total of 9,400 samples taken for CWD surveillance in TEXAS since 2002 of both hunter-kill and private kill, ONLY 191 samples have been taken in the most likely place one would find CWD i.e. the border where CWD has been documented at TEXAS and New Mexico

 

latest map NM cwd old data

 


 


 

 CWD in New Mexico ;

 

What is the Department doing to

 

prevent the spread of CWD?

 

Chronic wasting disease (CWD) was recently

 

detected in a mule deer from

 

Unit 34. Until 2005, CWD had only been found

 

in Unit 19. With this discovery, the Department

 

will increase its surveillance of deer and elk

 

harvested in Units 29, 30 and 34.

 

Lymph nodes and/or brain stems from every

 

harvested deer and brain stems from all elk

 

taken in Unit 34 will be sampled.

 

snip...

 


 


 


 


 


 


 

 CWD SURVEILLANCE TEXAS

 


 

 IMPLEMENTATION OF A GEOGRAPHICALLY FOCUSED CWD SURVEILLANCE PROGRAM FOR FREE-RANGING CERVIDS A geographically-focused free-ranging cervid Monitoring Program was implemented during the fall 2002 deer-hunting season. Brain stem samples from hunter-killed deer will be obtained from TPWD Wildlife Management Areas (WMA), State Parks, and where otherwise available with hunter and/or landowner permission, from deer taken on private land. Volume 1, Sixth Edition of United States Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services, Regulatory Statistics (Appendix D1) indicates that 148 samples is sufficient to detect disease at two per-cent prevalence, regardless of the population size. Therefore the goal is to acquire 148 samples from each of the State's ten ecoregions provided adequate sampling distribution is achieved across each ecoregion. The five year 2002 -2006, goal is to cumulatively collect 459 samples from each of the ten ecoregions. The cumulative sample would be used statistically to detect CWD at one per-cent prevalence level with 99 per-cent confidence. However, funding from APHIS/USDA could provide the necessary funds for sampling at the one per-cent prevalence level each year. TAHC conducted a risk assessment of counties where deer and elk have been imported and where high densities of free-ranging deer occur. The assessment was conducted for USDA funding consideration. The risk assessment was based on limited number of criteria. Since CWD could potentially occur anywhere in Texas, monitoring efforts would be focused to achieve a stratified sampling scheme across each ecoregion of the State.

 

Confidentiality laws restrict the type of data TPWD personnel can collect as it relates to a specific parcel of land. Therefore, personnel will ensure that no property specific information is collected (i.e. ranch name or exact location) without the landowner's written permission. The following are guidelines for data and sample collection distributed to TPWD personnel prior to sample collection:

 

A Texas Veterinary Medical Diagnostic Laboratory (TVMDL) Accession Form must be submitted with brain stem samples. The most important items to be filled out are the TPWD employee name, address and phone number, and "Patient/Deer ID". County of Kill can be recorded on the bottom of the form, but DO NOT report any information that identifies the specific parcel of land. The "Patient/Deer ID" number MUST BE specific to the field data sheet the employee is using to record data. Specific CWD field data sheets will not be provided, as current field data sheets (i.e. Age/Weight Antler Data Sheets, Hunter Check Station Data Sheets, etc.) will be appropriate in most cases. Field staff may produce their own CWD data sheet if necessary. The field data sheet must contain: Employee Name Sample Number (same as Patient/Deer ID on TVMDL Accession Form Sample Date Deer Age Deer Sex County of Kill Hunter Name Hunting License Number Ranch name or tract name/location ONLY with landowner permission. Should a CWD positive be detected, TAHC will use hunter contact information to conduct CWD investigation under their regulatory authority. Make sure the container containing the brain stem sample is legibly identified with the sample number, deer age and sex, county of kill and date. Although the sample number is all that is needed, additional information will help resolve any problems should batches of samples be combined. Should a landowner retain deer heads for our sampling purposes, remind the landowner to issue the hunters a proof of sex document as provided for in TAHC 65.10 (c). In addition, a Wildlife resource document (PWD 905) must accompany the head until the carcass reaches a final destination and finally processed. Samples MAY NOT be taken from legally harvested deer without the hunter's consent.

 


 

 ACTIONS SHOULD A CWD POSITIVE BE DETECTED Should sampling detect a CWD positive animal, TAHC and TPWD would activate the Media Response Plan (Appendix F). TAHC and TPWD would immediately begin review of the information at hand and determine the action to be taken within the Response Plan (Appendix C.) The first action should be to inform landowners adjacent to the property containing the CWD positive and hold a meeting with advisory committees and affected landowner to discuss plans for secondary sampling. Planning for secondary sampling, investigating movements of deer into and away from property for further actions would then be the next step. The secondary sampling is critical for determining distribution and prevalence of the disease.

 

As distribution and prevalence is being determined, information review and discussions with TPWD advisory committees (e.g., Private Lands Advisory Board, Hunting Advisory Committee, White-tailed Deer Advisory Committee etc.) and landowners would take place in order to determine the appropriate management action to be taken.

 


 

 and the discovery of several CWD positive mule deer in New Mexico, approximately 35 miles north of the Texas border were well out of the known boundaries of the disease.

 

The disease prevalence appears to be increasing in localized areas, although it is not clear whether this is due to increased incidence, or increased surveillance, reporting, and testing. Information from states with direct experience in managing CWD is being used for developing Texas plans as we learn from their experiences.

 

TPWD and TAHC are developing stepped up targeted and geographically-focused surveillance plans to monitor free-ranging deer for the presence of the disease and a rapid response plan to guide both TPWD and TAHC should CWD be detected in the State. TPWD and TAHC are also evaluating cervid management laws, rules, and policies for free ranging and scientific breeder permitted cervids under their authority to identify issues and potential weaknesses related to disease management. In these efforts, TPWD and TAHC will work with other agencies and organizations responsible for or are concerned about cervid disease management in an attempt to ensure comprehensive approaches to effective management of CWD risks (see Appendix C: Importation of Susceptible Cervids).

 


 

 ----- Original Message -----

 

From: Terry S. Singeltary Sr. To: [log in to unmask]

 

Sent: Thursday, December 14, 2006 9:52 PM

 

Subject: cwd at Texas border and low sampling figures ???

 

Greetings TAHC,

 

can someone please explain to me any reasoning at all for the very low sampling for CWD which have been taken where CWD is literally right at the steps of one of Texas borders, but yet across the state elsewhere, the numbers for testing increases ???

 

i do not understand the low sampling for cwd size where it is at our borders, compared to the highter numbers elsewhere???

 

see Texas hunter kill sample for CWD to Aug 31, 2005

 


 

 see map where CWD has been documented at Texas border in free ranging deer and elk

 


 

kind regards,

 

Terry

 

snip...

 

 IS and or HAS Texas really been looking for CWD ??? or is it kinda like the Texas BSE mad cow triple SSS policy ???

 

you be the judge.

 

Texas would not know if they had CWD, if it were spreading from this area, in my opinion.

 

PLUS, stupidity and greed like this does not helps us. see also;

 

see full text ;

 

Sunday, October 04, 2009

 

CWD NEW MEXICO SPREADING SOUTH TO TEXAS 2009

 


 

TEXAS 6 CASES OF CWD CONFIRMED TO DATE

 

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.

 


 

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.

 


 

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

 


 

Thursday, October 23, 2014

 

*** FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE PRESERVE

 


 

Tuesday, October 21, 2014

 

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

 


 

Tuesday, October 07, 2014

 

*** Wisconsin white-tailed deer tested positive for CWD on a Richland County breeding farm, and a case of CWD has been discovered on a Marathon County hunting preserve

 


 

Thursday, October 02, 2014

 

*** IOWA TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease

 


 

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

 


 

Saturday, November 23, 2013

 

TAHC REMINDS MULE DEER HUNTERS OF CWD TESTING REQUIREMENTS & CHECK STATIONS November 22, 2013

 


 

Thursday, March 14, 2013

 

TEXAS DEER BREEDERS CHEER TWO NEW BILLS SB 1444 AND HB 2092 THAT COULD HELP POTENTIALLY ENHANCE CHRONIC WASTING DISEASE CWD

 


 

 

Saturday, February 04, 2012

 

*** Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised

 

Approximately 4,200 fawns, defined as deer under 1 year of age, were sampled from the eradication zone over the last year. The majority of fawns sampled were between the ages of 5 to 9 months, though some were as young as 1 month.

 

*** Two of the six fawns with CWD detected were 5 to 6 months old.

 

All six of the positive fawns were taken from the core area of the CWD eradication zone where the highest numbers of positive deer have been identified. ...

 

snip...

 

"Finding CWD prions in both lymph and brain tissues of deer this young is slightly surprising," said Langenberg, "and provides information that CWD infection and illness may progress more rapidly in a white-tailed deer than previously suspected. Published literature suggests that CWD doesn't cause illness in a deer until approximately 16 months of age. Our fawn data shows that a few wild white-tailed deer may become sick from CWD or may transmit the disease before they reach that age of 16 months." ... see full text and more here ; Saturday, February 04, 2012

 

Wisconsin 16 MONTH age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised

 


 

 

Houston Chronicle CWD TEXAS, what happened ? the silence is deafening. ...tss

 

Thursday, October 30, 2014

 

A cool start to deer season, but challenges linger By Shannon Tompkins

 


 


 

Thursday, November 14, 2013

 

Deer don't disappoint after hunters' early optimism Houston Chronicle By Shannon Tompkins November 13, 2013

 


 

CWD, Houston Chronicle, and CWD reporting, what happened ???

 

Thursday, December 27, 2012

 

CWD TSE PRION, dr. deer, shooting pen type game farms and ranchers, Texas, TAHC, Houston Chronicle, all silent about disease ?

 


 

Thursday, December 13, 2012

 

HUNTERS FEELING THE HEAT Houston Chronicle December 13, 2012 OUTDOORS not talking about CWD in Texas

 


 

Wednesday, November 07, 2012

 

Chronic Wasting Disease CWD, Texas, Houston Chronicle Shannon Thomkins 1998 - 2012 what happened ???

 


 

Thursday, July 12, 2012

 

CWD aka MAD DEER, ELK DISEASE TEXAS HOUSTON CHRONICLE Wednesday, July 11, 2012

 


 

CWD TSE PRION disease aka mad cow type disease

 

a recent report I sent to TAHC ;

 

From: Terry S. Singeltary Sr.

 

Sent: Monday, December 08, 2014 3:55 PM

 

To: Dee.Ellis@tahc.texas.gov

 

Cc: steve.lightfoot@tpwd.state.tx.us ; Mitch Lockwood ; execdir@tahc.texas.gov ; prdir@tahc.texas.gov ; comments@tahc.texas.gov ; stateepi@tahc.texas.gov ; labdir@tahc.texas.gov

 

Subject: Texas Animal Health Commission Chronic Wasting Disease CWD TSE PRION Update December 2014

 

Greetings Gentlemen et al at the TAHC;

 

Thank you kindly for the two updates on the facebook page about CWD, the importance of proper carcass disposal, and CWD testing.

 

I would kindly like to update you all on the TSE prion disease, for any one person out there that might still be interested.

 

Wishing you all a very Merry Christmas, and a very Healthy and Peaceful New Year. ...warmest regards, terry

 

in reply to ;

 

Texas Animal Health Commission December 5 at 3:01pm · Hunters and landowners in far West Texas:

 

The TAHC and Texas Parks and Wildlife have mandatory check stations for susceptible species like elk and mule deer that are taken inside the CWD Containment Zone, which covers portions of Hudspeth, Culberson, and El Paso counties.

 

The map of the check stations can be viewed on the TPWD website:

 


 

Texas Animal Health Commission

 

Our friends at the Texas Deer Association published a great article explaining how to properly dispose carcasses from harvested deer to help prevent the spread of infectious diseases. Read more at

 


 

I wish to kindly further elaborate on this please, as follows ;

 

***Given that scrapie prions are widespread on the surfaces of affected farms (Maddison and others 2010a), irrespective of the source of the infectious prions in the pens, this study clearly highlights the difficulties that are faced with the effective removal of environmentally associated scrapie infectivity.

 

***This is likely to be paralleled in CWD which shows strong similarities to scrapie in terms of both the dissemination of prions into the environment and the facile mode of disease transmission. These data further contribute to the understanding that prion diseases can be highly transmissible between susceptible individuals not just by direct contact but through highly stable environmental reservoirs that are refractory to decontamination.

 

***The presence of these environmentally associated prions in farm buildings make the control of these diseases a considerable challenge, especially in animal species such as goats where there is lack of genetic resistance to scrapie and, therefore, no scope to re-stock farms with animals that are resistant to scrapie.

 

***These data suggest that recommended current guidelines for the decontamination of farm buildings following outbreaks of scrapie do little to reduce the titre of infectious scrapie material and that environmental recontamination could also be an issue associated with these premises.

 

Scrapie Sheep Goats Transmissible spongiform encephalopathies (TSE) Accepted October 12, 2014. Published Online First 31 October 2014

 


 

Monday, November 3, 2014

 

Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination

 


 

PPo3-22:

 

Detection of Environmentally Associated PrPSc on a Farm with Endemic Scrapie

 

Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University of Nottingham; Sutton Bonington, Loughborough UK

 

Key words: scrapie, evironmental persistence, sPMCA

 

Ovine scrapie shows considerable horizontal transmission, yet the routes of transmission and specifically the role of fomites in transmission remain poorly defined. Here we present biochemical data demonstrating that on a scrapie-affected sheep farm, scrapie prion contamination is widespread. It was anticipated at the outset that if prions contaminate the environment that they would be there at extremely low levels, as such the most sensitive method available for the detection of PrPSc, serial Protein Misfolding Cyclic Amplification (sPMCA), was used in this study. We investigated the distribution of environmental scrapie prions by applying ovine sPMCA to samples taken from a range of surfaces that were accessible to animals and could be collected by use of a wetted foam swab. Prion was amplified by sPMCA from a number of these environmental swab samples including those taken from metal, plastic and wooden surfaces, both in the indoor and outdoor environment. At the time of sampling there had been no sheep contact with these areas for at least 20 days prior to sampling indicating that prions persist for at least this duration in the environment. These data implicate inanimate objects as environmental reservoirs of prion infectivity which are likely to contribute to disease transmission.

 


 

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.

 


 

*** 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.

 


 

Veterinary Pathology Onlinevet.sagepub.com Published online before print February 27, 2014, doi: 10.1177/0300985814524798 Veterinary Pathology February 27, 2014 0300985814524798

 

Lesion Profiling and Subcellular Prion Localization of Cervid Chronic Wasting Disease in Domestic Cats

 

D. M. Seelig1⇑ A. V. Nalls1 M. Flasik2 V. Frank1 S. Eaton2 C. K. Mathiason1 E. A. Hoover1 1Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO, USA 2Department of Biomedical Sciences, Colorado State University, Fort Collins, CO, USA D. M. Seelig, University of Minnesota, Department of Veterinary Clinical Sciences, Room 339 VetMedCtrS, 6192A (Campus Delivery Code), 1352 Boyd Ave, St Paul, MN 55108, USA. Email address: dseelig@umn.edu

 

Abstract

 

Chronic wasting disease (CWD) is an efficiently transmitted, fatal, and progressive prion disease of cervids with an as yet to be fully clarified host range. While outbred domestic cats (Felis catus) have recently been shown to be susceptible to experimental CWD infection, the neuropathologic features of the infection are lacking. Such information is vital to provide diagnostic power in the event of natural interspecies transmission and insights into host and strain interactions in interspecies prion infection. Using light microscopy and immunohistochemistry, we detail the topographic pattern of neural spongiosis (the “lesion profile”) and the distribution of misfolded prion protein in the primary and secondary passage of feline CWD (FelCWD). We also evaluated cellular and subcellular associations between misfolded prion protein (PrPD) and central nervous system neurons and glial cell populations. From these studies, we (1) describe the novel neuropathologic profile of FelCWD, which is distinct from either cervid CWD or feline spongiform encephalopathy (FSE), and (2) provide evidence of serial passage-associated interspecies prion adaptation. In addition, we demonstrate through confocal analysis the successful co-localization of PrPD with neurons, astrocytes, microglia, lysosomes, and synaptophysin, which, in part, implicates each of these in the neuropathology of FelCWD. In conclusion, this work illustrates the simultaneous role of both host and strain in the development of a unique FelCWD neuropathologic profile and that such a profile can be used to discriminate between FelCWD and FSE.

 

prion chronic wasting disease immunohistochemistry interspecies cat feline spongiform encephalopathy transmissible spongiform encephalopathy adaptation species barrier

 


 

Sunday, March 09, 2014

 

Lesion Profiling and Subcellular Prion Localization of Cervid Chronic Wasting Disease in Domestic Cats

 


 

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

 


 


 

From: Terry S. Singeltary Sr.

 

Sent: Sunday, October 12, 2014 2:15 PM

 

Subject: CWD TSE PRION, TISSUE, BODY FLUIDS, AND ENVIRONMENTAL CONTAMINATION

 

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

 


 

Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute and R(D)SVS; University of Edinburgh; Roslin, Scotland UK

 

Scrapie and chronic wasting disease probably spread via environmental routes, and there are also concerns about BSE infection remaining in the environment after carcass burial or waste 3disposal. In two demonstration experiments we are determining survival and migration of TSE infectivity when buried for up to five years, as an uncontained point source or within bovine heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters containing either sandy or clay soil. Migration from the boluses is being assessed from soil cores taken over time. With the exception of a very small amount of infectivity found 25 cm from the bolus in sandy soil after 12 months, no other infectivity has been detected up to three years. Secondly, ten bovine heads were spiked with TSE infected mouse brain and buried in the two soil types. Pairs of heads have been exhumed annually and assessed for infectivity within and around them. After one year and after two years, infectivity was detected in most intracranial samples and in some of the soil samples taken from immediately surrounding the heads. The infectivity assays for the samples in and around the heads exhumed at years three and four are underway. These data show that TSE infectivity can survive burial for long periods but migrates slowly. Risk assessments should take into account the likely long survival rate when infected material has been buried.

 

The authors gratefully acknowledge funding from DEFRA.

 


 


 

Sunday, November 3, 2013

 

*** Environmental Impact Statements; Availability, etc.: Animal Carcass Management [Docket No. APHIS-2013-0044] ***

 


 

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

 


 

Sunday, November 10, 2013

 

*** LARGE CJD TSE PRION POTENTIAL CASE STUDY AMONG HUMANS WHO TAKE DEER ANTLER VELVET WILL BE ONGOING FOR YEARS IF NOT DECADES, but who's cares $

 


 

Sunday, July 07, 2013

 

*** Could avian scavengers translocate infectious prions to disease-free areas initiating new foci of chronic wasting disease? Prion. 2013 Jul 3;7(4). [Epub ahead of print]

 


 

Monday, February 14, 2011

 

*** THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER

 

NO, NO, NOT NO, BUT HELL NO !

 

Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011

 


 

OR-09: Canine spongiform encephalopathy—A new form of animal prion disease

 

Monique David, Mourad Tayebi UT Health; Houston, TX USA

 

It was also hypothesized that BSE might have originated from an unrecognized sporadic or genetic case of bovine prion disease incorporated into cattle feed or even cattle feed contaminated with prion-infected human remains.1 However, strong support for a genetic origin of BSE has recently been demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2 Furthermore, a specific prion protein strain causing BSE in cattle is believed to be the etiological agent responsible for the novel human prion disease, variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in a number countries, including France, Italy, Ireland, the Netherlands, Canada, Japan, US and the UK with the largest number of cases. Naturally occurring feline spongiform encephalopathy of domestic cats4 and spongiform encephalopathies of a number of zoo animals so-called exotic ungulate encephalopathies5,6 are also recognized as animal prion diseases, and are thought to have resulted from the same BSE-contaminated food given to cattle and humans, although and at least in some of these cases, a sporadic and/or genetic etiology cannot be ruled out. The canine species seems to display resistance to prion disease and no single case has so far been reported.7,8 Here, we describe a case of a 9 week old male Rottweiler puppy presenting neurological deficits; and histological examination revealed spongiform vacuolation characteristic of those associated with prion diseases.9 Initial biochemical studies using anti-PrP antibodies revealed the presence of partially proteinase K-resistant fragment by western blotting. Furthermore, immunohistochemistry revealed spongiform degeneration consistent with those found in prion disease and displayed staining for PrPSc in the cortex.

 

Of major importance, PrPSc isolated from the Rottweiler was able to cross the species barrier transmitted to hamster in vitro with PMCA and in vivo (one hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100% attack rate (n = 4) and animals displayed untypical lesional profile and shorter incubation period.

 

In this study, we show that the canine species might be sensitive to prion disease and that PrPSc isolated from a dog can be transmitted to dogs and hamsters in vitro using PMCA and in vivo to hamsters.

 

If our preliminary results are confirmed, the proposal will have a major impact on animal and public health and would certainly lead to implementing new control measures for ‘canine spongiform encephalopathy’ (CSE).

 

References 1. Colchester AC, Colchester NT. The origin of bovine spongiform encephalopathy: the human prion disease hypothesis. Lancet 2005; 366:856-61; PMID:16139661; http:// dx.doi.org/10.1016/S0140-6736(05)67218-2.

 

2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation. PLoS Pathog 2008; 4:e1000156; PMID:18787697; http://dx.doi.org/10.1371/journal. ppat.1000156.

 

3. Collinge J. Human prion diseases and bovine spongiform encephalopathy (BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662; http://dx.doi.org/10.1093/ hmg/6.10.1699.

 

4. Wyatt JM, Pearson GR, Smerdon TN, Gruffydd-Jones TJ, Wells GA, Wilesmith JW. Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Vet Rec 1991; 129:233-6; PMID:1957458; http://dx.doi.org/10.1136/vr.129.11.233.

 

5. Jeffrey M, Wells GA. Spongiform encephalopathy in a nyala (Tragelaphus angasi). Vet Pathol 1988; 25:398-9; PMID:3232315; http://dx.doi.org/10.1177/030098588802500514.

 

6. Kirkwood JK, Wells GA, Wilesmith JW, Cunningham AA, Jackson SI. Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu (Tragelaphus strepsiceros). Vet Rec 1990; 127:418-20; PMID:2264242.

 

7. Bartz JC, McKenzie DI, Bessen RA, Marsh RF, Aiken JM. Transmissible mink encephalopathy species barrier effect between ferret and mink: PrP gene and protein analysis. J Gen Virol 1994; 75:2947-53; PMID:7964604; http://dx.doi.org/10.1099/0022-1317- 75-11-2947.

 

8. Lysek DA, Schorn C, Nivon LG, Esteve-Moya V, Christen B, Calzolai L, et al. Prion protein NMR structures of cats, dogs, pigs, and sheep. Proc Natl Acad Sci U S A 2005; 102:640-5; PMID:15647367; http://dx.doi.org/10.1073/pnas.0408937102.

 

9. Budka H. Neuropathology of prion diseases. Br Med Bull 2003; 66:121-30; PMID:14522854; http://dx.doi.org/10.1093/bmb/66.1.121.

 


 

Monday, March 26, 2012

 

CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE

 


 

2005

 

DEFRA Department for Environment, Food & Rural Affairs

 

Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904 6287 E-mail: h.mcdonagh.defra.gsi.gov.uk

 

GTN: FAX:

 

Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518

 

21 November 2001

 

Dear Mr Singeltary

 

TSE IN HOUNDS

 

Thank you for e-mail regarding the hounds survey. I am sorry for the long delay in responding.

 

As you note, the hound survey remains unpublished. However the Spongiform Encephalopathy Advisory Committee (SEAC), the UK Government's independent Advisory Committee on all aspects related to BSE-like disease, gave the hound study detailed consideration at their meeting in January 1994. As a summary of this meeting published in the BSE inquiry noted, the Committee were clearly concerned about the work that had been carried out, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.

 

Later, at their meeting in June 95, The Committee re-evaluated the hound study to see if any useful results could be gained from it. The Chairman concluded that there were varying opinions within the Committee on further work. It did not suggest any further transmission studies and thought that the lack of clinical data was a major weakness.

 

Overall, it is clear that SEAC had major concerns about the survey as conducted. As a result it is likely that the authors felt that it would not stand up to r~eer review and hence it was never published. As noted above, and in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether additional work should be performed to examine dogs for evidence of TSE infection. Although the Committee had mixed views about the merits of conducting further work, the Chairman noted that when the Southwood Committee made their recommendation to complete an assessment of possible spongiform disease in dogs, no TSEs had been identified in other species and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less

 

critical. For more details see- http://www.bseinquiry, gov.uk/files/yb/1995/06/21005001 .pdf

 

As this study remains unpublished, my understanding is that the ownership of the data essentially remains with the original researchers. Thus unfortunately, I am unable to help with your request to supply information on the hound survey directly. My only suggestion is that you contact one of the researchers originally involved in the project, such as Gerald Wells. He can be contacted at the following address.

 

Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, KT 15 3NB, UK

 

You may also wish to be aware that since November 1994 all suspected cases of spongiform encephalopathy in animals and poultry were made notifiable. Hence since that date there has been a requirement for vets to report any suspect SE in dogs for further investigation. To date there has never been positive identification of a TSE in a dog.

 

I hope this is helpful

 

Yours sincerely 4

 

HUGH MCDONAGH BSE CORRESPONDENCE SECTION

 

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

 

HOUND SURVEY

 

I am sorry, but I really could have been a co-signatory of Gerald's minute.

 

I do NOT think that we can justify devoting any resources to this study, especially as larger and more important projects such as the pathogenesis study will be quite demanding.

 

If there is a POLITICAL need to continue with the examination of hound brains then it should be passed entirely to the VI Service.

 

J W WILESMITH Epidemiology Unit 18 October 1991

 

Mr. R Bradley

 

cc: Mr. G A H Wells

 


 

3.3. Mr R J Higgins in conjunction with Mr G A Wells and Mr A C Scott would by the end of the year, indentify the three brains that were from the ''POSITIVE'' end of the lesion spectrum.

 


 

TSE in dogs have not been documented simply because OF THE ONLY STUDY, those brain tissue samples were screwed up too. see my investigation of this here, and to follow, later follow up, a letter from defra, AND SEE SUSPICIOUS BRAIN TISSUE SAF's. ...TSS

 


 

TSE & HOUNDS

 

GAH WELLS (very important statement here...TSS)

 

HOUND STUDY

 

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

 

snip...

 


 

76 pages on hound study;

 

snip...

 


 

The spongiform changes were not pathognomonic (ie. conclusive proof) for prion disease, as they were atypical, being largely present in white matter rather than grey matter in the brain and spinal cord. However, Tony Scott, then head of electron microscopy work on TSEs, had no doubt that these SAFs were genuine and that these hounds therefore must have had a scrapie-like disease. I reviewed all the sections myself (original notes appended) and although the pathology was not typical, I could not exclude the possibility that this was a scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian degeneration was also present in the white matter of the hounds, another feature of scrapie.

 

38.I reviewed the literature on hound neuropathology, and discovered that micrographs and descriptive neuropathology from papers on 'hound ataxia' mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had done much of this work, and I obtained original sections from hound ataxia cases from him. This enabled me provisionally to conclude that Robert Higgins had in all probability detected hound ataxia, but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination of single restricted microscopic fields that there was no distinction between the white matter vacuolation present in BSE and scrapie cases, and that occurring in hound ataxia and the hound survey cases.

 

39.Hound ataxia had reportedly been occurring since the 1930's, and a known risk factor for its development was the feeding to hounds of downer cows, and particularly bovine offal. Circumstantial evidence suggests that bovine offal may also be causal in FSE, and TME in mink. Despite the inconclusive nature of the neuropathology, it was clearly evident that this putative canine spongiform encephalopathy merited further investigation.

 

40.The inconclusive results in hounds were never confirmed, nor was the link with hound ataxia pursued. I telephoned Robert Higgins six years after he first sent the slides to CVL. I was informed that despite his submitting a yearly report to the CVO including the suggestion that the hound work be continued, no further work had been done since 1991. This was surprising, to say the very least.

 

41.The hound work could have provided valuable evidence that a scrapie-like agent may have been present in cattle offal long before the BSE epidemic was recognised. The MAFF hound survey remains unpublished.

 

Histopathological support to various other published MAFF experiments

 

42.These included neuropathological examination of material from experiments studying the attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice (RVC 1994).

 


 

It was thought likely that at least some, and probably all, of the cases in zoo animals were caused by the BSE agent. Strong support for this hypothesis came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and scrapie to mice: strain variation and species barrier. Philosophical Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation period and lesion profile in six strains of mice inoculated with brain homogenates from an affected kudu and the nyala, was similar to that seen when this panel of mouse strains was inoculated with brain from cattle with BSE. The affected zoo bovids were all from herds that were exposed to feeds that were likely to have contained contaminated ruminant-derived protein and the zoo felids had been exposed, if only occasionally in some cases, to tissues from cattle unfit for human consumption.

 

snip...

 


 

NEW URL ;

 


 

Friday, March 8, 2013

 

Dogs may have been used to make Petfood and animal feed

 


 


 

Chronic Wasting Disease Susceptibility of Four North American Rodents

 

Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A. Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI 53706, USA 2US Geological Survey, National Wildlife Health Center, 6006 Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author email: cjohnson@svm.vetmed.wisc.edu

 

We intracerebrally challenged four species of native North American rodents that inhabit locations undergoing cervid chronic wasting disease (CWD) epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles (Myodes gapperi). The inocula were prepared from the brains of hunter-harvested white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles proved to be most susceptible, with a median incubation period of 272 days. Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the brains of all challenged meadow voles. Subsequent passages in meadow voles lead to a significant reduction in incubation period. The disease progression in red-backed voles, which are very closely related to the European bank vole (M. glareolus) which have been demonstrated to be sensitive to a number of TSEs, was slower than in meadow voles with a median incubation period of 351 days. We sequenced the meadow vole and red-backed vole Prnp genes and found three amino acid (AA) differences outside of the signal and GPI anchor sequences. Of these differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is particularly intriguing due its postulated involvement in "rigid loop" structure and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5 years post-inoculation, but appear to be exhibiting a high degree of disease penetrance. White-footed mice have an even longer incubation period but are also showing high penetrance. Second passage experiments show significant shortening of incubation periods. Meadow voles in particular appear to be interesting lab models for CWD. These rodents scavenge carrion, and are an important food source for many predator species. Furthermore, these rodents enter human and domestic livestock food chains by accidental inclusion in grain and forage. Further investigation of these species as potential hosts, bridge species, and reservoirs of CWD is required.

 


 

Monday, March 8, 2010

 

Canine Spongiform Encephalopathy aka MAD DOG DISEASE

 


 

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.

 


 

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...

 


 

NEW URL LINK ;

 


 

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

 


 

*** 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.

 


 

cwd exposure, and iatrogenic CJD, what if ???

 

*** 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.

 


 

Tuesday, November 04, 2014

 

*** Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011

 


 

Tuesday, November 04, 2014

 

Towards an Age-Dependent Transmission Model of Acquired and Sporadic Creutzfeldt-Jakob Disease

 


 


 

*** URGENT UPDATE ***

 

Friday, December 5, 2014

 

*** SPECIAL ALERT The OIE recommends strengthening animal disease surveillance worldwide ***

 

OIE BSE TSE PRION AKA MAD COW DISEASE ?

 

‘’the silence was deafening’’ ...tss

 


 


 

Wednesday, December 3, 2014

 

Over 200 Groups Urge Congress to Continue Supporting COOL

 

For Immediate Release

 


 

Tuesday, December 2, 2014

 

UK EXPORTS OF MBM TO WORLD Bovine Spongiform Encephalopathy BSE TSE Prion aka Mad Cow Disease

 

USA, NORTH AMERICA, MBM (or any potential TSE prion disease) EXPORTS TO THE WORLD (?) [protected by the BSE MRR policy] $$$

 


 

Monday, December 1, 2014

 

Germany Bovine Spongiform Encephalopathy BSE CJD TSE Prion disease A Review December 1, 2014

 


 

Friday, November 28, 2014

 

BOVINE SPONGIFORM ENCEPHALOPATHY BSE AKA MAD COW DISEASE PORTUGAL CONFIRMED

 


 

Sunday, October 5, 2014

 

France stops BSE testing for Mad Cow Disease

 


 

Monday, May 5, 2014

 

Brazil BSE Mad Cow disease confirmed OIE 02/05/2014

 


 

*** OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED, WISHES TO CONTINUE SPREADING IT AROUND THE GLOBE

 


 

Monday, November 30, 2009

 

*** USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE, DOES NOT SURPRISE ME $

 


 

why do we not want to do TSE transmission studies on chimpanzees $

 

5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

 

snip...

 

R. BRADLEY

 


 

1: J Infect Dis 1980 Aug;142(2):205-8

 

Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.

 

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

 

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.

 

snip...

 

The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.

 

PMID: 6997404

 


 

Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"

 

Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.

 

snip...

 

76/10.12/4.6

 


 

Nature. 1972 Mar 10;236(5341):73-4.

 

Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).

 

Gibbs CJ Jr, Gajdusek DC.

 

Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0

 

Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)

 

C. J. GIBBS jun. & D. C. GAJDUSEK

 

National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland

 

SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).

 


 


 

Wednesday, February 16, 2011

 

IN CONFIDENCE

 

SCRAPIE TRANSMISSION TO CHIMPANZEES

 

IN CONFIDENCE

 


 

Sunday, December 12, 2010

 

EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010

 


 

Sunday, April 18, 2010

 

SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010

 


 

Thursday, December 23, 2010

 

Molecular Typing of Protease-Resistant Prion Protein in Transmissible Spongiform Encephalopathies of Small Ruminants, France, 2002-2009

 

Volume 17, Number 1 January 2011

 


 

Thursday, November 18, 2010

 

Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep

 


 

Monday, April 25, 2011

 

Experimental Oral Transmission of Atypical Scrapie to Sheep

 

Volume 17, Number 5-May 2011

 


 

Friday, February 11, 2011

 

Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues

 


 

Thursday, March 29, 2012

 

atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012

 

NIAA Annual Conference April 11-14, 2011San Antonio, Texas

 


 

*** Canada Increased Atypical Scrapie Detections

 

Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.

 


 

Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine (reticular) deposits, see also ; All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.

 


 

Tuesday, July 29, 2008

 

Heidenhain Variant Creutzfeldt Jakob Disease Case Report

 

snip...

 

Heidenhain Variant Creutzfeldt Jakob Disease autopsy case report

 

'MOM' DOD December 14, 1997, CONFIRMED hvCJD...just made a promise to mom. never forget, and never let them forget. be sure to read ;

 

*** URGENT UPDATE ***

 

Friday, December 5, 2014

 

*** SPECIAL ALERT The OIE recommends strengthening animal disease surveillance worldwide ***

 

OIE BSE TSE PRION AKA MAD COW DISEASE ?

 

‘’the silence was deafening’’ ...tss

 


 


 

P.5.21 Parallels between different forms of sheep scrapie and types of Creutzfeldt-Jakob disease (CJD)

 

Wiebke M. Wemheuer1, Sylvie L. Benestad2, Arne Wrede1, Wilhelm E. Wemheuer3, Tatjana Pfander1, Bjørn Bratberg2, Bertram Brenig3,Walter J. Schulz-Schaeffer1 1University Medical Center Goettingen, Germany; 2Institute of Veterinary Medicine Oslo, Norway; 3Institute of Veterinary Medicine Goettingen, Germany

 

Background: Scrapie in sheep and goats is often regarded as the archetype of prion diseases. In 1998, a new form of scrapie - atypical/Nor98 scrapie - was described that differed from classical scrapie in terms of epidemiology, Western blot profile, the distribution of pathological prion protein (PrPSc) in the body and its stability against proteinase K. In a similar way, distinct disease types exist in sporadic Creutzfeldt-Jakob disease (CJD). They differ with regard to their clinical outcome, Western blot profile and PrPSc deposition pattern in the central nervous system (CNS). Objectives: The comparison of PrPSc deposits in sheep scrapie and human sporadic CJD.

 

Methods: Tissues of the CNS of sheep with classical scrapie, sheep with atypical/Nor98 scrapie and 20 patients with sporadic CJD were examined using the sensitive Paraffin Embedded Tissue (PET) blot method. The results were compared with those obtained by immunohistochemistry. With the objective of gaining information on the protein conformation, the PrPSc of classical and atypical/Nor98 sheep scrapie and sporadic CJD was tested for its stability against denaturation with guanidine hydrochloride (GdnHCl) using a Membrane Adsorption Assay.

 

Results: The PrPSc of atypical/Nor98 scrapie cases and of CJD prion type 1 patients exhibits a mainly reticular/synaptic deposition pattern in the brain and is relatively sensitive to denaturation with GdnHCl. In contrast classical scrapie cases and CJD prion type 2 patients have a more complex PrPSc deposition pattern in common that consists of larger PrPSc aggregates and the PrPSc itself is comparatively stable against denaturation.

 

Discussion: The similarity between CJD types and scrapie types indicates that at least two comparable forms of the misfolded prion protein exist beyond species barriers and can elicit prion diseases. It seems therefore reasonable to classify classical and atypical/Nor98 scrapie - in analogy to the existing CJD types - as different scrapie types.

 


 

What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?

 

28 Mar 01

 

Like lambs to the slaughter 31 March 2001 by Debora MacKenzie Magazine issue 2284. Subscribe and get 4 free issues. FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.

 

Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.

 

Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.

 

"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.

 

Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.

 

Deslys and colleagues were originally studying vCJD, not sCJD. They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.

 

As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. As expected, they all affected the brain in a different way from BSE and vCJD. But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology.

 

"The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. "You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie." In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar.

 

But there are more than 20 strains of scrapie, and six of sCJD. "You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. Bruce is cautious about the mouse results, but agrees they require further investigation. Other trials of scrapie and sCJD in mice, she says, are in progress.

 

People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD.

 

But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. "If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."

 

There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.

 

Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.

 


 

Monday, December 1, 2008

 

When Atypical Scrapie cross species barriers

 


 

Sunday, November 23, 2014

 

Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case NOT European

 

‘’The specific overseas country where this patient’s infection occurred is less clear largely because the investigation did not definitely link him to a country where other known vCJD cases likely had been infected.’’

 


 

Monday, November 3, 2014

 

USA CJD TSE PRION UNIT, TEXAS, SURVEILLANCE UPDATE NOVEMBER 2014

 

National Prion Disease Pathology Surveillance Center Cases Examined1 (October 7, 2014)

 

***6 Includes 11 cases in which the diagnosis is pending, and 19 inconclusive cases;

 

***7 Includes 12 (11 from 2014) cases with type determination pending in which the diagnosis of vCJD has been excluded.

 

***The sporadic cases include 2660 cases of sporadic Creutzfeldt-Jakob disease (sCJD),

 

***50 cases of Variably Protease-Sensitive Prionopathy (VPSPr)

 

***and 21 cases of sporadic Fatal Insomnia (sFI).

 


 

Sunday, November 23, 2014

 

*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case NOT European

 

‘’The specific overseas country where this patient’s infection occurred is less clear largely because the investigation did not definitely link him to a country where other known vCJD cases likely had been infected.’’

 


 

Sunday, December 14, 2014

 

*** ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD strains, TSE prion aka Mad Cow Disease United States of America Update December 14, 2014 Report

 


 

‘’IN STRICT CONFIDENCE’’

 

Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease

 

Received July 24, 2014; Accepted September 16, 2014; Published November 3, 2014

 


 

*** Singeltary comment ;

 


 

Sunday, December 7, 2014

 

Scientific update on the potential for transmissibility of non-prion protein misfolding diseases PRIONOIDS

 


 

MOM...

 

DIVISION OF NEUROPATHOLOGY University of Texas Medical Branch 114 McCullough Bldg. Galveston, Texas 77555-0785 FAX COVER SHEET DATE: 4-23-98 TO: Mr. Terry Singeltary @ ------- FROM: Gerald Campbell FAX: (409) 772-5315 PHONE: (409) 772-2881 Number of Pages (including cover sheet): Message: *CONFIDENTIALITY NOTICE* This document accompanying this transmission contains confidential information belonging to the sender that is legally privileged. This information is intended only for the use of the individual or entry names above. If you are not the intended recipient, you are hereby notified that any disclosure, copying distribution, or the taking of any action in reliances on the contents of this telefaxed information is strictly prohibited. If you received this telefax in error, please notify us by telephone immediately to arrange for return of the original documents. -------------------------- Patient Account: 90000014-518 Med. Rec. No.: (0160)118511Q Patient Name: POULTER, BARBARA Age: 63 YRS DOB: 10/17/34 Sex: F Admitting Race: C Attending Dr.: Date / Time Admitted : 12/14/97 1228 Copies to: UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report FINAL AUTOPSY DIAGNOSIS Autopsy' Office (409)772-2858 Autopsy NO.: AU-97-00435 AUTOPSY INFORMATION: Occupation: Unknown Birthplace: Unknown Residence: Crystal Beach Date/Time of Death: 12/14/97 13:30 Date/Time of Autopsy: 12/15/97 15:00 Pathologist/Resident: Pencil/Fernandez Service: Private Restriction: Brain only

 

FINAL AUTOPSY DIAGNOSIS

 

I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.

 

snip...see full text ;

 


 

lost my mom to hvCJD ‘confirmed’ December 14, 1997, just made a promise, never forget, and never let them forget...

 

with kindest regards,

 

layperson

 

Terry S. Singeltary Sr.

 

Bacliff, Texas USA 77518

 

 

posted by Terry S. Singeltary Sr. at 4:08 PM

0 Comments:

Post a Comment

Subscribe to Post Comments [Atom]

<< Home