Friday, December 20, 2019

Texas TAHC, Administrative Code, Title 4, Part 2, Chapter 40, Chronic Wasting Disease Amendments Open For Comment beginning December 20, 2019 thru January 20, 2020 Terry Singeltary Comments Submission

-----Original Message-----
From: Terry Singeltary
To: comments
Sent: Fri, Dec 20, 2019 3:53 pm
Subject: Texas TAHC, Administrative Code, Title 4, Part 2, Chapter 40, Chronic Wasting Disease Amendments Open For Comment beginning December 20, 2019 thru January 20, 2020 Terry Singeltary Comments Submission

Texas TAHC, Administrative Code, Title 4, Part 2, Chapter 40, Chronic Wasting Disease Amendments Open For Comment beginning December 20, 2019 thru January 20, 2020 Terry Singeltary Comments Submission

December 20, 2019

The Texas Animal Health Commission (TAHC) held a regularly scheduled commission meeting on December 10, 2019, where a proposed rule review was approved.

The following chapters are undergoing the rule reviewal process, and the public is encouraged to comment on and suggest amendments to the TAHC’s rules as they currently exist.

The public may submit comments beginning December 20, 2019 thru January 20, 2020.

Chapter 40, Chronic Wasting Disease - view rule proposal

The Texas Animal Health Commission (commission) proposes the review of Texas Administrative Code, Title 4, Part 2, Chapter 40, concerning Chronic Wasting Disease, in its entirety, in accordance with Texas Government Code, §2001.039. As required by §2001.039 of the Texas Government Code, the commission will accept comments and make a final assessment regarding whether the reasons for initially adopting these rules continues to exist and whether these rules should be revised, readopted or repealed.

Comments on the rule review may be submitted to Amanda Bernhard, Texas Animal Health Commission, 2105 Kramer Lane, Austin, Texas 78758, by fax at (512) 719-0719, or by email at “comments@tahc.texas.gov” no later than 30 days from the date that the proposed review is published in the Texas Register.


CHAPTER 40. CHRONIC WASTING DISEASE  
§ 40.1. Definitions

http://txrules.elaws.us/rule/title4_chapter40_sec.40.1
§ 40.2. General Requirements

http://txrules.elaws.us/rule/title4_chapter40_sec.40.2
§ 40.3. Herd Status Plans for Cervidae

http://txrules.elaws.us/rule/title4_chapter40_sec.40.3
§ 40.4. Entry Requirements

http://txrules.elaws.us/rule/title4_chapter40_sec.40.4
§ 40.5. Surveillance and Movement Requirements for Exotic CWD Susceptible Species

http://txrules.elaws.us/rule/title4_chapter40_sec.40.5
§ 40.6. CWD Movement Restriction Zones

http://txrules.elaws.us/rule/title4_chapter40_sec.40.6
§ 40.7. Executive Director Declaration of a CWD Movement Restriction Zone

http://txrules.elaws.us/rule/title4_chapter40_sec.40.7

Texas TAHC, Administrative Code, Title 4, Part 2, Chapter 40, Chronic Wasting Disease Amendments Open For Comment beginning December 20, 2019 thru January 20, 2020 Terry Singeltary Comments Submission

Greetings TAHC et al,

Thank You Kindly for letting me comment again on cwd tse prion.

My comments 1-8 with updated science in references to back all my concerns up with...

1. ALL CWD TSE PRION RULES MUST BE MADE MANDATORY, voluntary does not work.

2. TAHC MUST BAN THE MOVEMENT OF ALL CERVID BY GAME FARMS, BREEDERS, SPERM MILLS, URINE MILLS, HORN MILLS, VELVET MILLS, HIGH/LOW FENCE, WITH ALL VEHICLES AND FARM EQUIPMENT BEING LIMITED TO ONLY THOSE SITES.

3. ALL CAPTIVE FARMING PUT ON HOLD WITH NO MORE PERMITTED

4. ALL CAPTIVE FARMING CERVID MUST BE TESTED ANNUALLY LIVE AND DEAD AND VERIFIED, THAT OLD BSe of ''just another escapee' does not cut it anymore, see why here;

WEDNESDAY, FEBRUARY 10, 2016

Wisconsin Two deer that escaped farm had chronic wasting disease CWD

http://chronic-wasting-disease.blogspot.com/2016/02/wisconsin-two-deer-that-escaped-farm.html

436 Deer Have Escaped From Farms to Wild

Tuesday, 18 March 2003 00:00

As the DNR prepared to hand over authority for overseeing game farms to the agriculture department, it sent 209 conservation wardens to 550 farms to collect information, attempt to pinpoint the source of the disease and to learn whether other deer had been exposed to it. The audit found that most farms were in compliance, but the DNR found many violations and instances of poor record keeping. Also in numerous instances, fences did not stop wild and captive deer from intermingling. see;

436 Deer Have Escaped From Farms to Wild

Tuesday, 18 March 2003 00:00

http://cwd-info.org/436-deer-have-escaped-from-farms-to-wild/

TUESDAY, JULY 14, 2015

TWO Escaped Captive Deer on the loose in Eau Claire County Wisconsin CWD postive farm Yellow ear tag

http://chronic-wasting-disease.blogspot.com/2015/07/two-escaped-captive-deer-on-loose-in.html

5. ALL CAPTIVE FARMING CERVID ON ANY FARM MUST BE KILLED AND INCINERATED, COMPLETE ERADICATION OF ANY CWD POSITIVE HERD

6. ALL CAPTIVE FARMING CERVID OPERATIONS MUST BE INSURED TO PAY FOR ANY CLEAN UP OF CWD AND QUARANTINE THERE FROM FOR THE STATE, NO MORE ENTITLEMENT PROGRAM FOR CERVID GAME FARMING PAY TO PLAY FOR CWD TSE PRION OFF THE TAX PAYERS BACK, QUARANTINE MUST BE FOR AT LEAST 16 YEARS WITH NO MOVEMENT IN OR OUT OF THAT PREMISES

7. TRUCKING TRANSPORTING CERVID CHRONIC WASTING DISEASE TSE PRION VIOLATING THE LACEY ACT

***> PLEASE SEE HISTORY OF TEXAS TRUCKING CWD TSE PRION DISEASE AT THE BOTTOM OF MY SUBMISSION, TOO LONG TO POST HERE.

8.CONSIDERING RECENT SCIENCE THAT CWD TSE PRION WILL TRANSMIT ORALLY TO PIGS AND ALSO SCRAPIE TO PIGS BY ORAL ROUTES, CONSIDERING CWD TRANSMIT EASILY TO CERVID BY ORAL ROUTE, CONSIDERING A NEW TSE PRION OUTBREAK IN A NEW LIVESTOCK SPECIES, THE CAMEL, CONSIDERING THE FACT THE USA THAT THE 1997 BSE feed regulation at 589.2000, which remains in effect but which applies only to feed for cattle and other ruminants, and specifically, the new section 589.2001, WAS AND STILL IS A TOTAL AND COLOSSAL FAILURE, AND PROVEN TO BE SO BY RECENT COMMENTS COMING FROM THE FDA, BUT FIRST, COMMENTS FROM DEFRA;

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.....


FDA Reports on VFD Compliance 

John Maday 

August 30, 2019 09:46 AM VFD-Form 007 (640x427) 

Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.


SUNDAY, SEPTEMBER 1, 2019 

***> FDA Reports on VFD Compliance 


TUESDAY, APRIL 18, 2017 

*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP *** 


http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html

I STRENUOUSLY URGE TEXAS FDA MODIFY THESE FEED BANS ASAP!

SEE;

Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary

View Attachment:View as format pdf

https://www.regulations.gov/contentStreamer?documentId=APHIS-2018-0011-0003&attachmentNumber=1&contentType=pdf

https://www.regulations.gov/document?D=APHIS-2018-0011-0003

http://chronic-wasting-disease.blogspot.com/2018/03/docket-no-aphis-2018-0011-chronic.html 





if now is not the time to panic, after ignoring cwd for a decade, when should we panic ?

the tse prion aka mad cow type disease is not your normal pathogen.

The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.

you cannot cook the TSE prion disease out of meat.

you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.

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

the TSE prion agent also survives Simulated Wastewater Treatment Processes.

IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.

you can bury it and it will not go away.

The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.

it’s not your ordinary pathogen you can just cook it out and be done with. that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.

CWD WEBINAR CWD YESTERDAY! December 11, 2019

Dr. Mckenzie and CIDRAP on CWD TSE Prion



Texas CWD Symposium: Transmission by Saliva, Feces, Urine & Blood

the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.

https://www.youtube.com/watch?v=bItnEElzuKo&index=6&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj

''On January 21, 2017 a tornado took down thousands of feet of fence for a 420-acre illegal deer enclosure in Lamar County that had been subject to federal and state investigation for illegally importing white-tailed deer into Mississippi from Texas (a CWD positive state). Native deer were free to move on and off the property before all of the deer were able to be tested for CWD. Testing will be made available for a period of three years for CWD on the property and will be available for deer killed within a 5-mile radius of the property on a voluntary basis. ''

Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS

See Wisconsin update...terrible news, right after Texas updated map around 5 minute mark...


WISCONSIN CWD CAPTIVE CWD UPDATE VIDEO


cwd update on Wisconsin from Tammy Ryan...


Wyoming CWD Dr. Mary Wood

''first step is admitting you have a problem''

''Wyoming was behind the curve''

wyoming has a problem...


TEXAS BREEDER DEER ESCAPEE WITH CWD IN THE WILD, or so the genetics would show?

OH NO, please tell me i heard this wrong, a potential Texas captive escapee with cwd in the wild, in an area with positive captive cwd herd?

apparently, no ID though. tell me it ain't so please...

23:00 minute mark

''Free Ranging Deer, Dr. Deyoung looked at Genetics of this free ranging deer and what he found was, that the genetics on this deer were more similar to captive deer, than the free ranging population, but he did not see a significant connection to any one captive facility that he analyzed, so we believe, Ahhhhhh, this animal had some captive ahhh, whatnot.''


Wyoming CWD Dr. Mary Wood

''first step is admitting you have a problem''

''Wyoming was behind the curve''

wyoming has a problem...


the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.


Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS See Wisconsin update...terrible news, right after Texas updated map around 5 minute mark... 


SATURDAY, JANUARY 19, 2019 

Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS 


for those that believe in all things stupid, like ted nugent, and say that cwd is not adversely affecting, look no further than Colorado, here's your sign...

Colorado Chronic Wasting Disease Response Plan December 2018

I. Executive Summary Mule deer, white-tailed deer, elk and moose are highly valued species in North America. Some of Colorado’s herds of these species are increasingly becoming infected with chronic wasting disease (CWD). As of July 2018, at least 31 of Colorado's 54 deer herds (57%), 16 of 43 elk herds (37%), and 2 of 9 moose herds (22%) are known to be infected with CWD. Four of Colorado's 5 largest deer herds and 2 of the state’s 5 largest elk herds are infected. Deer herds tend to be more heavily infected than elk and moose herds living in the same geographic area. Not only are the number of infected herds increasing, the past 15 years of disease trends generally show an increase in the proportion of infected animals within herds as well. Of most concern, greater than a 10-fold increase in CWD prevalence has been estimated in some mule deer herds since the early 2000s; CWD is now adversely affecting the performance of these herds.

snip...

(the map on page 71, cwd marked in red, is shocking...tss)


ORIGIN OF CHRONIC WASTING DISEASE TSE PRION?

COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?

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

IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989


ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;

''it pains me to no end to even contemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end

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


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.....


Here is the latest on the cwd tse prion...terry

FRIDAY, NOVEMBER 08, 2019 

***> EFSA Panel on Biological Hazards (BIOHAZ) Update on chronic wasting disease (CWD) III


***> that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.

1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 

***> Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. 

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. 

Laboratory of Central Nervous System Studies, National Institute of 

Neurological Disorders and Stroke, National Institutes of Health, 

Bethesda, MD 20892. 

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. 

PMID: 8006664 [PubMed - indexed for MEDLINE] 


2018 - 2019

***> This is very likely to have parallels with control efforts for CWD in cervids.

Rapid recontamination of a farm building occurs after attempted prion removal


Kevin Christopher Gough, BSc (Hons), PhD1, Claire Alison Baker, BSc (Hons)2, Steve Hawkins, MIBiol3, Hugh Simmons, BVSc, MRCVS, MBA, MA3, Timm Konold, DrMedVet, PhD, MRCVS3 and Ben Charles Maddison, BSc (Hons), PhD2

Abstract

The transmissible spongiform encephalopathy scrapie of sheep/goats and chronic wasting disease of cervids are associated with environmental reservoirs of infectivity. 

Preventing environmental prions acting as a source of infectivity to healthy animals is of major concern to farms that have had outbreaks of scrapie and also to the health management of wild and farmed cervids. 

Here, an efficient scrapie decontamination protocol was applied to a farm with high levels of environmental contamination with the scrapie agent. 

Post-decontamination, no prion material was detected within samples taken from the farm buildings as determined using a sensitive in vitro replication assay (sPMCA). 

A bioassay consisting of 25 newborn lambs of highly susceptible prion protein genotype VRQ/VRQ introduced into this decontaminated barn was carried out in addition to sampling and analysis of dust samples that were collected during the bioassay. 

Twenty-four of the animals examined by immunohistochemical analysis of lymphatic tissues were scrapie-positive during the bioassay, samples of dust collected within the barn were positive by month 3. 

The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.

snip...

As in the authors' previous study,12 the decontamination of this sheep barn was not effective at removing scrapie infectivity, and despite the extra measures brought into this study (more effective chemical treatment and removal of sources of dust) the overall rates of disease transmission mirror previous results on this farm. With such apparently effective decontamination (assuming that at least some sPMCA seeding ability is coincident with infectivity), how was infectivity able to persist within the environment and where does infectivity reside? Dust samples were collected in both the bioassay barn and also a barn subject to the same decontamination regime within the same farm (but remaining unoccupied). Within both of these barns dust had accumulated for three months that was able to seed sPMCA, indicating the accumulation of scrapie-containing material that was independent of the presence of sheep that may have been incubating and possibly shedding low amounts of infectivity.

This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.

Acknowledgements The authors thank the APHA farm staff, Tony Duarte, Olly Roberts and Margaret Newlands for preparation of the sheep pens and animal husbandry during the study. The authors also thank the APHA pathology team for RAMALT and postmortem examination.

Funding This study was funded by DEFRA within project SE1865. 

Competing interests None declared. 


Saturday, January 5, 2019 

Rapid recontamination of a farm building occurs after attempted prion removal 


THURSDAY, FEBRUARY 28, 2019 

BSE infectivity survives burial for five years with only limited spread


***> CONGRESSIONAL ABSTRACTS PRION CONFERENCE 2018

P69 Experimental transmission of CWD from white-tailed deer to co-housed reindeer 

Mitchell G (1), Walther I (1), Staskevicius A (1), Soutyrine A (1), Balachandran A (1) 

(1) National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada. 

Chronic wasting disease (CWD) continues to be detected in wild and farmed cervid populations of North America, affecting predominantly white-tailed deer, mule deer and elk. Extensive herds of wild caribou exist in northern regions of Canada, although surveillance has not detected the presence of CWD in this population. Oral experimental transmission has demonstrated that reindeer, a species closely related to caribou, are susceptible to CWD. Recently, CWD was detected for the first time in Europe, in wild Norwegian reindeer, advancing the possibility that caribou in North America could also become infected. Given the potential overlap in habitat between wild CWD-infected cervids and wild caribou herds in Canada, we sought to investigate the horizontal transmissibility of CWD from white-tailed deer to reindeer. 

Two white-tailed deer were orally inoculated with a brain homogenate prepared from a farmed Canadian white-tailed deer previously diagnosed with CWD. Two reindeer, with no history of exposure to CWD, were housed in the same enclosure as the white-tailed deer, 3.5 months after the deer were orally inoculated. The white-tailed deer developed clinical signs consistent with CWD beginning at 15.2 and 21 months post-inoculation (mpi), and were euthanized at 18.7 and 23.1 mpi, respectively. Confirmatory testing by immunohistochemistry (IHC) and western blot demonstrated widespread aggregates of pathological prion protein (PrPCWD) in the central nervous system and lymphoid tissues of both inoculated white-tailed deer. Both reindeer were subjected to recto-anal mucosal associated lymphoid tissue (RAMALT) biopsy at 20 months post-exposure (mpe) to the white-tailed deer. The biopsy from one reindeer contained PrPCWD confirmed by IHC. This reindeer displayed only subtle clinical evidence of disease prior to a rapid decline in condition requiring euthanasia at 22.5 mpe. Analysis of tissues from this reindeer by IHC revealed widespread PrPCWD deposition, predominantly in central nervous system and lymphoreticular tissues. Western blot molecular profiles were similar between both orally inoculated white-tailed deer and the CWD positive reindeer. Despite sharing the same enclosure, the other reindeer was RAMALT negative at 20 mpe, and PrPCWD was not detected in brainstem and lymphoid tissues following necropsy at 35 mpe. Sequencing of the prion protein gene from both reindeer revealed differences at several codons, which may have influenced susceptibility to infection. 

Natural transmission of CWD occurs relatively efficiently amongst cervids, supporting the expanding geographic distribution of disease and the potential for transmission to previously naive populations. The efficient horizontal transmission of CWD from white-tailed deer to reindeer observed here highlights the potential for reindeer to become infected if exposed to other cervids or environments infected with CWD. 

https://prion2018.org/

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

***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. 

Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3

Correspondence

Gudmundur Georgsson ggeorgs@hi.is

1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland

2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland

3 Bethesda, Maryland, USA

Received 7 March 2006 Accepted 6 August 2006

In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.

http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A
 
 TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION 

https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261
 
*** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION 

http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article

SEE;

Back around 2000, 2001, or so, I was corresponding with officials abroad during the bse inquiry, passing info back and forth, and some officials from here inside USDA aphis FSIS et al. In fact helped me get into the USA 50 state emergency BSE conference call way back. That one was a doozy. But I always remember what “deep throat” I never knew who they were, but I never forgot;

Some unofficial information from a source on the inside looking out -

Confidential!!!!

As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!

---end personal email---end...tss

http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html

Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).

http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf

Dr. Paul Brown Scrapie Soil Test BSE Inquiry Document

https://web.archive.org/web/20090505211734/http://www.bseinquiry.gov.uk/files/sc/Seac07/tab03.pdf

THURSDAY, FEBRUARY 28, 2019 

BSE infectivity survives burial for five years with only limited spread


Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission. 

Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston. 

Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.

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

***>>> Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.

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

Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis. 

https://prion2015.files.wordpress.com/2015/05/programguide1.pdf


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

http://www.pnas.org/content/97/7/3418.full


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

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/


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

https://www.ncbi...nlm.nih.gov/pmc/articles/PMC2802782/pdf/prion0303_0171.pdf


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

http://onlinelibrary.wiley.com/doi/10.1111/j.1539-6924.2012.01922.x/abstract


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 

http://transmissiblespongiformencephalopathy.blogspot.com/2013/07/rapid-assessment-of-bovine-spongiform.html


PPo4-4: 

Survival and Limited Spread of TSE Infectivity after Burial 

http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html

Discussion Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). 

Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). 

Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23). 

Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. 

Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. 

Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). 

The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. 

When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier. 

This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. 

Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. 

It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. 

Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. 

Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. 

Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions. 

PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. 

In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. 

In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). 

As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. 

False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). 

This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. 

This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. 

In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. 

Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. 

The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. 

In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). 

A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). 

This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. 

Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions. 

In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. 

These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes. 

Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification 

http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full

Wednesday, December 16, 2015 

*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission *** 

http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html

WEDNESDAY, MARCH 13, 2019 

CWD, TSE, PRION, MATERNAL mother to offspring, testes, epididymis, seminal fluid, and blood


Subject: Prion 2019 Conference

See full Prion 2019 Conference Abstracts


see scientific program and follow the cwd studies here;

Thursday, May 23, 2019 

Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts


FRIDAY, MAY 24, 2019 

Assessing chronic wasting disease strain differences in free-ranging cervids across the United States

MONDAY, MAY 20, 2019 

APHIS, USDA, Announces the Finalized Chronic Wasting Disease Herd Certification Program Standards Singeltary Submissions


SUNDAY, JULY 14, 2019 

Korea Chronic Wasting Disease CWD TSE Prion additional cases were observed in red deer, sika deer, and their crossbred deer in 2010 and 2016, beyond that, anyone's guess


Korea Chronic Wasting Disease CWD TSE Prion additional cases were observed in red deer, sika deer, and their crossbred deer in 2010 and 2016

In Korea, CWD was only confirmed in elk in 2001, 2004, and 2005 [13]; however, additional cases were observed in red deer, sika deer, and their crossbred deer in 2010 and 2016 [14]. Therefore, it is important to prevent CWD recurrence in the Republic of Korea, and farmers that have experienced a CWD outbreak are required to disinfect the farm before reintroducing the cervids. Thus, farmers require a disinfectant solution that is marketed and readily available to effectively inactivate prions.

[14] Sohn HJ, Roh IS, Kim HJ, et al. Epidemiology of chronic wasting disease in Korea. Prion. 2106;10 (supp1):S16–S17

WS-03: Epidemiology of chronic wasting disease in Korea
Hyun Joo Sohn
In Soon Roh
Hyo Jin Kim
Tae Young Suh
Kyung Je Park
Hoo Chang Park
Byounghan Kim
Foreign Animal Disease Division (FADD), Animal and Plant Quarantine Agency (QIA), Gimcheon, Korea
Transmissible spongiform encephalopathy (TSE) is a fatal neurodegenerative disorder, which is so-called as prion diseases due to the causative agents (PrPSc). TSEs are believed to be due to the template-directed accumulation of disease-associated prion protein, generally designated PrPSc. Based on export information of Chronic wasting disease (CWD) suspected elk from Canada to Korea, CWD surveilance program was initiated by the Ministry of Agriculture, Food and Rural Affairs (MAFRA) in 2001. CWD control measures included stamping out of all animals in the affected farm, and through cleaning and disinfection of the premises. In addition, nationwide clinical surveillance of Korean native cervid and improved measures to ensure reporting of CWD suspect cases were implemented. Total of 9 elks were found to be affected. CWD was designated as a notifiable disease under the Act for Prevention of Livestock Epidemics in 2002. Additional CWD cases– 12 elks and 2 elks – were diagnosed in 2004 and 2005. On 2010, 6 elks, 7 sika deer, one red deer and 5 cross-breeds were confirmed as positive. Further epidemiological investigations showed that these CWD outbreaks were linked to the importation of elks from Canada in 1994 based on circumstantial evidences. CWD is the prion disease that is known spread horizontally. The experimental studies have shown that PrPCWD is capable of transmitting CWD through saliva and blood. We conducted sPMCA and animal biosassy using contaminated soils in the playground of farm 2 which considered horizontal transmission between cervid and have been confirmed infectious PrPCWD. This result suggests PrPCWD shedding in the CWD contaminated soil is progressive through the disease course.
Keywords: CWD, soil, sPMCA
WEDNESDAY, OCTOBER 16, 2019 

Australia Assessment of bulk wheat from Canada Part B: Animal biosecurity risk advice, CWD TSE Prion concerns are mounting 


THURSDAY, AUGUST 08, 2019 

Raccoons accumulate PrPSc after intracranial inoculation with the agents of chronic wasting disease (CWD) or transmissible mink encephalopathy (TME) but not atypical scrapie 


*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** 




FRIDAY, JULY 26, 2019 

Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species


atypical and typical BSE and Scrapie Zoonosis

CHRONIC WASTING DISEASE CWD TSE PRION TRANSMITS TO PIGS BY ORAL ROUTES!!!

cwd scrapie pigs oral routes
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** 

 >*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** 

***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). 

***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. 

This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. 

Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. 




***> Subject: Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban? <***

Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies 2017 Annual Report

1a. Objectives (from AD-416): 
Objective 1: Investigate the mechanisms of protein misfolding in prion disease, including the genetic determinants of misfolding of the prion protein and the environmental influences on protein misfolding as it relates to prion diseases. Subobjective 1.A: Investigate the differences in the unfolded state of wild-type and disease associated prion proteins to better understand the mechanism of misfolding in genetic prion disease. Subobjective 1.B: Investigate the influence of metal ions on the misfolding of the prion protein in vitro to determine if environmental exposure to metal ions may alter disease progression. Objective 2: Investigate the pathobiology of prion strains in natural hosts, including the influence of prion source genotype on interspecies transmission and the pathobiology of atypical transmissible spongiform encephalopathies (TSEs). Subobjective 2.A: Investigate the pathobiology of atypical TSEs. Subobjective 2.B: Investigate the influence of prion source genotype on interspecies transmission. Objective 3: Investigate sampling methodologies for antemortem detection of prion disease, including the utility of blood sampling as a means to assess prion disease status of affected animals and the utility of environmental sampling for monitoring herd prion disease status. Subobjective 3.A: Investigate the utility of blood sampling as a means to assess prion disease status of affected animals. Subobjective 3.B: Investigate the utility of environmental sampling for monitoring herd prion disease status.
1b. Approach (from AD-416): 

The studies will focus on three animal transmissible spongiform encephalopathy (TSE) agents found in the United States: bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic wasting disease (CWD) of deer, elk, and moose. The research will address sites of protein folding and misfolding as it relates to prion disease, accumulation of misfolded protein in the host, routes of infection, and ante mortem diagnostics with an emphasis on controlled conditions and natural routes of infection. Techniques used will include spectroscopic monitoring of protein folding/misfolding, clinical exams, histopathology, immunohistochemistry, and biochemical analysis of proteins. The enhanced knowledge gained from this work will help understand the underlying mechanisms of prion disease and mitigate the potential for unrecognized epidemic expansions of these diseases in populations of animals that could either directly or indirectly affect food animals.

3. Progress Report: 

All 8 project plan milestones for FY17 were fully met. Research efforts directed toward meeting objective 1 of our project plan center around the production of recombinant prion protein from either bacteria or mammalian tissue culture systems and collection of thermodynamic data on the folding of the recombinant prion protein produced. Both bacterial and mammalian expression systems have been established. Thermodynamic data addressing the denatured state of wild-type and a disease associated variant of bovine prion protein has been collected and a manuscript is in preparation. In research pertaining to objective 2, all studies have been initiated and animals are under observation for the development of clinical signs. The animal studies for this objective are long term and will continue until onset of clinical signs. In vitro studies planned in parallel to the animals studies have similarly been initiated and are ongoing. Objective 3 of the project plan focuses on the detection of disease associated prion protein in body fluids and feces collected from a time course study of chronic wasting disease inoculated animals. At this time samples are being collected as planned and methods for analysis are under development.

4. Accomplishments 

1. Showed that swine are potential hosts for the scrapie agent. A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested. ARS researchers at Ames, Iowa conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Necropsies were done on a subset of animals at approximately 6 months post inoculation (PI): the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of transmissible spongiform encephalopathies (TSE) until study termination at 80 months PI or when removed due to intercurrent disease. Brain samples were examined by multiple diagnostic approaches, and for a subset of pigs in each inoculation group, bioassay in mice expressing porcine prion protein. At 6 months PI, no evidence of scrapie infection was noted by any diagnostic method. However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.

2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.

3. Developed a method for amplification and discrimination of the 3 forms of BSE in cattle. The prion protein (PrP) is a protein that is the causative agent of transmissible spongiform encephalopathies (TSEs). The disease process involves conversion of the normal cellular PrP to a pathogenic misfolded conformation. This conversion process can be recreated in the lab using a misfolding amplification process known as real-time quaking induced conversion (RT-QuIC). RT-QuIC allows the detection of minute amounts of the abnormal infectious form of the prion protein by inducing misfolding in a supplied substrate. Although RT-QuIC has been successfully used to detect pathogenic PrP with substrates from a variety of host species, prior to this work bovine prion protein had not been proven for its practical uses for RT-QuIC. We demonstrated that prions from transmissible mink encephalopathy (TME) and BSE-infected cattle can be detected with using bovine prion proteins with RT-QuIC, and developed an RT-QuIC based approach to discriminate different forms of BSE. This rapid and robust method, both to detect and discriminate BSE types, is of importance as the economic implications for different types of BSE vary greatly.

Review Publications 
Moore, S., Kunkle, R., Greenlee, M., Nicholson, E., Richt, J., Hamir, A., Waters, W., Greenlee, J. 2016. Horizontal transmission of chronic wasting disease in reindeer. Emerging Infectious Diseases. 22(12):2142-2145. doi:10.3201/eid2212.160635.
Moore, S.J., West Greenlee, M.H., Smith, J.D., Vrentas, C.E., Nicholson, E.M., Greenlee, J.J. 2016. A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation. Frontiers in Veterinary Science. 3:78.
Greenlee, J.J., Kunkle, R.A., Smith, J.D., West Greenlee, M.H. 2016. Scrapie in swine: a diagnostic challenge. Food Safety. 4(4):110-114.
Kondru, N., Manne, S., Greenlee, J., West Greenlee, H., Anantharam, V., Halbur, P., Kanthasamy, A., Kanthasamy, A. 2017. Integrated organotypic slice cultures and RT-QuIC (OSCAR) assay: implications for translational discovery in protein misfolding diseases. Scientific Reports. 7:43155. doi:10.1038/srep43155.
Mammadova, N., Ghaisas, S., Zenitsky, G., Sakaguchi, D.S., Kanthasamy, A.G., Greenlee, J.J., West Greenlee, M.H. 2017. Lasting retinal injury in a mouse model of blast-induced trauma. American Journal of Pathology. 187(7):1459-1472. doi:10.1016/j.ajpath.2017.03.005.


FRIDAY, APRIL 20, 2018 

*** Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban? 

Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies


CDC

New Outbreak of TSE Prion in NEW LIVESTOCK SPECIES

Mad Camel Disease

Volume 24, Number 6—June 2018 Research 

Prion Disease in Dromedary Camels, Algeria Abstract

Prions cause fatal and transmissible neurodegenerative diseases, including Creutzfeldt-Jakob disease in humans, scrapie in small ruminants, and bovine spongiform encephalopathy (BSE). After the BSE epidemic, and the associated human infections, began in 1996 in the United Kingdom, general concerns have been raised about animal prions. We detected a prion disease in dromedary camels (Camelus dromedarius) in Algeria. Symptoms suggesting prion disease occurred in 3.1% of dromedaries brought for slaughter to the Ouargla abattoir in 2015–2016. We confirmed diagnosis by detecting pathognomonic neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues from 3 symptomatic animals. Prion detection in lymphoid tissues is suggestive of the infectious nature of the disease. PrPSc biochemical characterization showed differences with BSE and scrapie. Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.

SNIP...

The possibility that dromedaries acquired the disease from eating prion-contaminated waste needs to be considered.

Tracing the origin of prion diseases is challenging. In the case of CPD, the traditional extensive and nomadic herding practices of dromedaries represent a formidable factor for accelerating the spread of the disease at long distances, making the path of its diffusion difficult to determine. Finally, the major import flows of live animals to Algeria from Niger, Mali, and Mauritania (27) should be investigated to trace the possible origin of CPD from other countries. Camels are a vital animal species for millions of persons globally. The world camel population has a yearly growth rate of 2.1% (28). In 2014, the population was estimated at ≈28 million animals, but this number is probably underestimated.. Approximately 88% of camels are found in Africa, especially eastern Africa, and 12% are found in Asia. Official data reported 350,000 dromedaries in Algeria in 2014 (28).

On the basis of phenotypic traits and sociogeographic criteria, several dromedary populations have been suggested to exist in Algeria (29). However, recent genetic studies in Algeria and Egypt point to a weak differentiation of the dromedary population as a consequence of historical use as a cross-continental beast of burden along trans-Saharan caravan routes, coupled with traditional extensive/nomadic herding practices (30).

Such genetic homogeneity also might be reflected in PRNP. Studies on PRNP variability in camels are therefore warranted to explore the existence of genotypes resistant to CPD, which could represent an important tool for CPD management as it was for breeding programs for scrapie eradication in sheep. In the past 10 years, the camel farming system has changed rapidly, with increasing setup of periurban dairy farms and dairy plants and diversification of camel products and market penetration (13). This evolution requires improved health standards for infectious diseases and, in light of CPD, for prion diseases.

The emergence of another prion disease in an animal species of crucial importance for millions of persons worldwide makes it necessary to assess the risk for humans and develop evidence-based policies to control and limit the spread of the disease in animals and minimize human exposure. The implementation of a surveillance system for prion diseases would be a first step to enable disease control and minimize human and animal exposure. Finally, the diagnostic capacity of prion diseases needs to be improved in all countries in Africa where dromedaries are part of the domestic livestock. https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article ;

***> IMPORTS AND EXPORTS <***

***SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN ***


Friday, December 14, 2012

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

snip.....

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

Animals considered at high risk for CWD include:

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

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

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

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

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

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

snip.....

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

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

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

snip.....

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

snip.....

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

snip.....

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

snip.....

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

snip.....


THE USA FDA MAD COW FEED BAN OF 1997 WAS NOTHING MORE THAN INK ON PAPER, NEVER ENFORCED...terry

SUNDAY, SEPTEMBER 1, 2019 

FDA Reports on VFD Compliance

Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary.


WEDNESDAY, JULY 31, 2019 

The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L


TUESDAY, JULY 30, 2019 

Guidelines for reporting surveillance data on Transmissible Spongiform Encephalopathies (TSE) in the EU within the framework of Regulation (EC) No 999/2001 APPROVED: 9 July 2019


In summary, our results establish aerosols as a surprisingly efficient modality of prion transmission. This novel pathway of prion transmission is not only conceptually relevant for the field of prion research, but also highlights a hitherto unappreciated risk factor for laboratory personnel and personnel of the meat processing industry. In the light of these findings, it may be appropriate to revise current prion-related biosafety guidelines and health standards in diagnostic and scientific laboratories being potentially confronted with prion infected materials. While we did not investigate whether production of prion aerosols in nature suffices to cause horizontal prion transmission, the finding of prions in biological fluids such as saliva, urine and blood suggests that it may be worth testing this possibility in future studies.



Adriano Aguzzi ''We even showed that a prion AEROSOL will infect 100% of mice within 10 seconds of exposure''

WOW!...tss

THURSDAY, AUGUST 08, 2019 

Raccoons accumulate PrPSc after intracranial inoculation with the agents of chronic wasting disease (CWD) or transmissible mink encephalopathy (TME) but not atypical scrapie


Bovine spongiform encephalopathy Update

Ray Bradley

Veterinary Laboratories Agency, New Haw, Addlestone, KT15 3NB, United Kingdom, Email: raybradley@btinternet.com

Received 8 July 2002, accepted 24 July 2002

snip...

TSE IN CAPTIVE WILD ANIMALS

TSE almost certainly related to BSE (but as yet not proven by experimental challenge) has been reported in five species of captive wild Felidae in Great Britain (GB) (Bradley 1997). These are: cheetah 5 cases (with five further cases in cheetah exported from the UK to Ireland (1), Australia (1) and France (2+1unknown)), lions 3, ocelots 3, pumas 3 and tigers 3. All of these are assumed to have been exposed following consumption of uncooked cattle carcasses containing infected central nervous tissue. This might have been present in heads, necks or other parts of the vertebral column. Protection was secured by the 1990 SBO ban and there have been very few cases that were born thereafter. TSE has also been reported in captive wild Bovidae in GB (Bradley 1997), but not elsewhere or in any natural environment inhabited by these animals. Eight species have been affected. In two, a nyala and a greater kudu, brain tissue has been inoculated into in-bred strains of mice. This shows the disease is experimentally transmissible and that the agent responsible is biologically indistinguishable from the BSE agent, i.e. it is of the same strain type (Bruce et al. 1994). The number of confirmed TSE by species is: Arabian oryx, bison, gemsbok, nyala and scimitar-horned oryx, one each; ankole, two; eland and greater kudu, six. All these species have presumably been exposed to infected MBM in concentrate diets that had similar formulations to those used in cattle feed before 1988. The reason for the cases occurring after 1988 (BAB cases) is, as in cattle, presumably cross contamination of diets with MBM intended for use in non-ruminant species. So far as records permit, no cases have been reported in animals born after January 1993.


BSE is considered to occur in 16 species: cattle, domestic cats, nyala and greater kudu (types of antelopes), gemsbok, eland, Arabian oryx, scimitar-horned oryx, ankole, bison, cheetah, lion, tiger, puma, ocelot and humans (brains from Variant Creutzfeldt-Jakob Disease (vCJD) patients). Other than feline spongiform encephalopathy (FSE) in domestic cats, all these are rare diseases in captive wild animals in the UK. Cases of FSE have also been found in cheetah in Ireland, France and Australia, but only in captive animals exported from the UK. There have not been any reports of naturally occurring cases of TSE in pigs or poultry. The spread of BSE is associated with concentrate feeding and the vehicle of infectivity was meat and bonemeal (MBM). There is continuing controversy on the origin of BSE. There were changes in rendering practices and evidence suggest this may have changed the evolution of the epidemic. 


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...

10. The case of SE in a cheetah that occurred during the period, involved a 7 year-old female which had been born and lived all her life at Whipsnade (except for the final stages when she was moved to the Animal Hospital at Regent’s Park for diagnosis and treatment). This animal, which died in December 1993, had been fed on cuts of meat and bone from carcases of cattle unfit for human consumption and it was thought likely that she had been exposed to spinal cord (Kirkwood, J.K., Cunningham, A.A., Flach, E.J., Thornton, S.M. & Wells, G.A.H. (1995) Spongiform encephalopathy in another captive cheetah (Acinonyx jubatus): evidence for variation in susceptibility or incubation periods between species. Journal of Zoo and Wildlife Medicine 26, 577-582: J/ZWM/26/577). 

11. During the period we also collated information on cases of SE that occurred in wild animals at or from other zoos in the British Isles. The total number of cases of which I was aware in June 1996, when I presented a review on occurrence of spongiform encephalopathies in zoo animals (at the Royal College of Pathologists’ Symposium on Transmitting prions: BSE, CJD, and other TSEs, The Royal Society, London, 4th July 1996), was 25, involving 10 species. The animals involved were all from the families Bovidae and Felidae, and comprised: 1 Nyala Tragelaphus angasi, 5 Eland Taurotragus oryx, 6 greater kudu Tragelaphus strepsiceros, 1 Gemsbok Oryx gazella, 1 Arabian oryx Oryx leucoryx, 1 Scimitar-horned oryx Oryx dammah, 4 Cheetah Acinonyx jubatus, 3 Puma Felis concolor 2 Ocelot Felis pardalis, and 1 Tiger Panthera tigris. (A spongiform encephalopathy, which was thought probably to have a different aetiology, had also been reported in 3 ostriches Struthio camelus in Germany). This list did not include cases of BSE in domesticated species in zoos (ie BSE in Ankole or other cattle, or SEs, assumed to be scrapie, in mouflon sheep Ovis musimon). 

 
NEW URL ;
 


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...

The BSE Inquiry / Statement No 324

Dr James Kirkwood (not scheduled to give oral evidence)

Statement to the BSE Inquiry

James K Kirkwood BVSc PhD FIBiol MRCVS

[This witness has not been asked to give oral evidence in Phase 1 of the Inquiry]

1. I became involved in the field of TSEs through my work as Head of the Veterinary Science Group at the Zoological Society of London’s Institute of Zoology. I held this post from November 1984 until June 1996, when I took up my present post at UFAW. During this time, concurrent with the BSE epidemic, cases of scrapie-like spongiform encephalopathies occurred in animals at the Zoological Society of London’s collections at Regent’s Park and Whipsnade and in other zoos. It was appropriate to investigate the epidemiology of these cases in order to try to determine the possible impact on zoo animals and breeding programmes, and to consider how the disease in zoo animals might be controlled.

2. Throughout the period from 1985 to March 1996, I worked at the Institute of Zoology (IoZ). I was Head of the Veterinary Science Group of the IoZ and Senior Veterinary Officer of the Zoological Society of London (ZSL). I was responsible for the provision of the veterinary service for the ZSL collections.

3. During the period from 1985 to March 1996, scrapie-like spongiform encephalopathies were diagnosed in the following animals which died, or were euthanased, at London Zoo and Whipsnade:

Animal Sex Date of Death Age (mos)

Arabian Oryx Oryx leucoryx F 24.3.89 38

Greater kudu Tragelaphus strepsiceros (Linda) F 18.8.89 30

Greater kudu (Karla) F 13.11.90 19 Greater kudu (Kaz) M 6.6.91 37

Greater kudu (Bambi) M 24.10.91 36

Greater kudu (346/90) M 26.2.92 18

Greater kudu (324/90) F 22.11.92 38

Cheetah Acinonyx jubatus (Michelle) F 22.12.93 91

All these cases were described in papers published in the scientific literature (as cited below).


Subject: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY 

Date: Thu, 17 Oct 2002 17:04:51 -0700 

From: "Terry S. Singeltary Sr." 

Reply-To: Bovine Spongiform Encephalopathy 

To: BSE-L

Greetings BSE-L,

is there any other CWD surveys/testing in the UK on their deer? what sort of testing has been done to date on UK/EU deer? any input would be helpful... thank you

DEER SPONGIFORM ENCEPHALOPATHY SURVEY

3. This will be a low key study with no publicity to avoid unnecessary media interest. It will be carried out in two stages ;

(I) A small scale examination of around 30 deer brains to establish the normal histology of the healthy brain; and

(II) A larger scale random examination of 300 or more adult deer brains drawn from both deer farms and parks to establish whether there is any evidence of a cervine spongiform encephalopathy. ...


Ministry of Agriculture Fisheries and Food Veterinary Investigation Centre West House. Station Road. Thirsk Y07 IPZ Telephone: 0845·522065 Fax: 0845·525224

Your reference

Our reference RJH/ASB

Date 4 November 1992

DEER SPONGIFORM ENCEPHALOPATHY SURVEY

Dear Paul

I have now found time to review the 10 deer- brains collected from Mr Walker farm··via Winchester Via Winchester VIC. In answer to your specific question was there sufficient difference in preservation of brain tissue to warrant the extra effort involved in rapid brain removal on the farm, the answer is definitely "Yes." The original five brains (Winchester ref M487/11) showed varying degrees of autolytic vacuolation affecting both white and grey matter throughout the brain. vacuolation and separation of Purkinje cells and marked perivascular spaces. These artifacts made interpretation of subtle, specific pathological vacuolation more difficult. By contrast the second submission (Winchester reference N736/2) showed excellent preservation of white and grey matter. Any vacuolar Change present could be confidently interpreted as pathological albeit of unknown pathogenesis.

I can only reiterate the comments made by Gerald Wells and myself at the preliminary discussion at Weybridge in Autumn 1991. If the survey's purpose is an accurate histopathological interpretation of brain tissue. the material must be collected in a pristine state. This is particularly valid when looking for ar unrecognised and undefined spongiform encephalopathy in a new species. Deer brains are very large structures which take a lot of fixation and therefore must be handled sympathetically from the start. We have already seen the problems encountered in comparatively smaller hound brains where delayed fixation was a major limitation on interpretation of true pathological change.

The bottom line must be that if a pathologist's expertise is to be used, it is critical to collect artefact free brain material. If the politics or economics do not allow this, then I would suggest that an electron microscopy survey in­volving detection of scrapie associated fibrils would be much more appropriate.

Best wishes Yours sincerely

R J HIGGINS VIO 92/11.4/2.1


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, identify the three brains that were from the ''POSITIVE'' end of the lesion spectrum.


HOUND SURVEY PATHOLOGICAL REPORT (see positive results) and MAD DOGS AND ENGLISHMAN...

ya'll thought i was making this stuff up didn't ya...i don't make this stuff up!


It is clear that the designing scientists must also have shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.


second supplementary


snip...see history and full text here;

MONDAY, FEBRUARY 25, 2019

***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019


THURSDAY, DECEMBER 19, 2019 

The emergence of classical BSE from atypical/Nor98 scrapie


O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations 

Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France 

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). 

Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. 

*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, 

***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), 

***is the third potentially zoonotic PD (with BSE and L-type BSE), 

***thus questioning the origin of human sporadic cases. 

We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. 

=============== 

***thus questioning the origin of human sporadic cases*** 

=============== 

***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. 

============== 


***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. 

***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 

***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. 

 
PRION 2016 TOKYO

Saturday, April 23, 2016

SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online

Taylor & Francis

Prion 2016 Animal Prion Disease Workshop Abstracts

WS-01: Prion diseases in animals and zoonotic potential

Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,

Natalia Fernandez-Borges a. and Alba Marin-Moreno a

"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France

Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion... Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.

To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.

These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.

Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. 

Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 

These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. 

 
***> 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



Title: Transmission of scrapie prions to primate after an extended silent incubation period) 

*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. 

*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. 

*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. 


***> Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility. <***

Transmission of scrapie prions to primate after an extended silent incubation period 

Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation

Abstract 

Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.

SNIP...

Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.

The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.

We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.

Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.

The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.

Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.

Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.

Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.

Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.

In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free... Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.


ZOONOSIS OF CWD, BSE, SCRAPIE, TSE PRION

CWD TSE Prion Zoonosis

i was very surprised that no mention of the study out of Canada with oral transmission of CWD to Macaque. 

i have spoken with Stefanie Czub and Professor Aguzzi, whom toured her lab afterwards, about these studies. the transmission studies were valid. plus, we know that cwd zoonosis would NOT look like nvCJD, but would look like sporadic CJD of some type. see;

> However, to date, no CWD infections have been reported in people.
key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
Chronic Wasting Disease CWD TSE Prion aka mad deer disease zoonosis
We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;
(3) Reliable essays can be established to detect CWD infection in humans; and
(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
Prion 2017 Conference
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen 
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. 
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. 
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. 
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS 
PRION 2018 CONFERENCE
Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).
To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years.
After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.
Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate.
The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.
Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.
The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD..
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;
P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States
Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA..
SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD
states.
AND ANOTHER STUDY;
P172 Peripheral Neuropathy in Patients with Prion Disease
Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio..
IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017,
AND
included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%),
AND
THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.
snip…
see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below…terry
PRION 2019 ABSTRACTS 

1. Interspecies transmission of the chronic wasting disease agent

Justin Greenlee

Virus and Prion Research Unit, National Animal Disease Center, USDA Agriculture Research Service

ABSTRACT

The presentation will summarize the results of various studies conducted at our research center that assess the transmissibility of the chronic wasting disease (CWD) agent to cattle, pigs, raccoons, goats, and sheep. This will include specifics of the relative attack rates, clinical signs, and microscopic lesions with emphasis on how to differentiate cross-species transmission of the CWD agent from the prion diseases that naturally occur in hosts such as cattle or sheep. Briefly, the relative difficulty of transmitting the CWD agent to sheep and goats will be contrasted with the relative ease of transmitting the scrapie agent to white-tailed deer.

53. Evaluation of the inter-species transmission potential of different CWD isolates

Rodrigo Moralesa, Carlos Kramma,b, Paulina Sotoa, Adam Lyona, Sandra Pritzkowa, Claudio Sotoa

aMitchell Center for Alzheimer’s disease and Related Brain Disorders, Dept. of Neurology, McGovern School of Medicine University of Texas Health Science Center at Houston, TX, USA; bFacultad de Medicina, Universidad de los Andes, Santiago, Chile

ABSTRACT

Chronic Wasting Disease (CWD) has reached epidemic proportions in North America and has been identified in South Korea and Northern Europe. CWD-susceptible cervid species are known to share habitats with humans and other animals entering the human food chain. At present, the potential of CWD to infect humans and other animal species is not completely clear. The exploration of this issue acquires further complexity considering the differences in the prion protein sequence due to species-specific variations and polymorphic changes within species. While several species of cervids are naturally affected by CWD, white-tailed deer (WTD) is perhaps the most relevant due to its extensive use in hunting and as a source of food. Evaluation of inter-species prion infections using animals or mouse models is costly and time consuming. We and others have shown that the Protein Misfolding Cyclic Amplification (PMCA) technology reproduces, in an accelerated and inexpensive manner, the inter-species transmission of prions while preserving the strain features of the input PrPSc. In this work, we tested the potential of different WTD-derived CWD isolates to transmit to humans and other animal species relevant for human consumption using PMCA. For these experiments, CWD isolates homozygous for the most common WTD-PrP polymorphic changes (G96S) were used (96SS variant obtained from a pre-symptomatic prion infected WTD). Briefly, 96GG and 96SS CWD prions were adapted in homologous or heterologous substrate by PMCA through several (15) rounds. End products, as well as intermediates across the process, were tested for their inter-species transmission potentials. A similar process was followed to assess seed-templated misfolding of ovine, porcine, and bovine PrPC. Our results show differences on the inter-species transmission potentials of the four adapted materials generated (PrPC/PrPSc polymorphic combinations), being the homologous combinations of seed/substrate the ones with the greater apparent zoonotic potential. Surprisingly, 96SS prions adapted in homologous substrate were the ones showing the easiest potential to template PrPC misfolding from other animal species. In summary, our results show that a plethora of different CWD isolates, each comprising different potentials for inter-species transmission, may exist in the environment. These experiments may help to clarify an uncertain and potentially worrisome public health issue. Additional research in this area may be useful to advise on the design of regulations intended to stop the spread of CWD and predict unwanted zoonotic events.

56. Understanding chronic wasting disease spread potential for at-risk species

Catherine I. Cullingham, Anh Dao, Debbie McKenzie and David W. Coltman

Department of Biological Sciences, University of Alberta, Edmonton AB, Canada

CONTACT Catherine I. Cullingham cathy.cullingham@ualberta.ca

ABSTRACT

Genetic variation can be linked to susceptibility or resistance to a disease, and this information can help to better understand spread-risk in a population. Wildlife disease incidence is increasing, and this is resulting in negative impacts on the economy, biodiversity, and in some instances, human health. If we can find genetic variation that helps to inform which individuals are susceptible, then we can use this information on at-risk populations to better manage negative consequences. Chronic wasting disease, a fatal, transmissible spongiform encephalopathy of cervids (both wild and captive), continues to spread geographically, which has resulted in an increasing host-range. The disease agent (PrPCWD) is a misfolded conformer of native cellular protein (PrPC). In Canada, the disease is endemic in Alberta and Saskatchewan, infecting primarily mule deer and white-tail deer, with a smaller impact on elk and moose populations. As the extent of the endemic area continues to expand, additional species will be exposed to this disease, including bison, bighorn sheep, mountain goat, and pronghorn antelope. To better understand the potential spread-risk among these species, we reviewed the current literature on species that have been orally exposed to CWD to identify susceptible and resistant species. We then compared the amino acid polymorphisms of PrPC among these species to determine whether any sites were linked to susceptibility or resistance to CWD infection. We sequenced the entire PrP coding region in 578 individuals across at-risk populations to evaluate their potential susceptibility. Three amino acid sites (97, 170, and 174; human numbering) were significantly associated with susceptibility, but these were not fully discriminating. All but one species among the resistant group shared the same haplotype, and the same for the susceptible species. For the at-risk species, bison had the resistant haplotype, while bighorn sheep and mountain goats were closely associated with the resistant type. Pronghorn antelope and a newly identified haplotype in moose differed from the susceptible haplotype, but were still closely associated with it. These data suggest pronghorn antelope will be susceptible to CWD while bison are likely to be resistant. Based on this data, recommendations can be made regarding species to be monitored for possible CWD infection.

KEYWORDS: Chronic wasting disease; Prnp; wildlife disease; population genetics; ungulates

Thursday, May 23, 2019 

Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts


see full Prion 2019 Conference Abstracts

THURSDAY, OCTOBER 04, 2018
Cervid to human prion transmission 5R01NS088604-04 Update
snip…full text;
SATURDAY, FEBRUARY 09, 2019
Experts: Yes, chronic wasting disease in deer is a public health issue — for people
SATURDAY, FEBRUARY 23, 2019 

Chronic Wasting Disease CWD TSE Prion and THE FEAST 2003 CDC an updated review of the science 2019


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

Authors, though, acknowledged the study was limited in geography and sample size and so it couldn't draw a conclusion about the risk to humans. They recommended more study. Dr. Ermias Belay was the report's principal author but he said New York and Oneida County officials are following the proper course by not launching a study. "There's really nothing to monitor presently. No one's sick," Belay said, noting the disease's incubation period in deer and elk is measured in years. "

FRIDAY, JULY 26, 2019 

Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species


FRIDAY, OCTOBER 25, 2019 

Experts testify United States is underprepared for bioterrorism threats Transmissible Spongiform Encephalopathy TSE Prion disease 

WEDNESDAY, NOVEMBER 20, 2019 

Sheep Are Susceptible to the Bovine Adapted Transmissible Mink Encephalopathy agent by Intracranial Inoculation and Have Evidence of Infectivity in Lymphoid Tissues

***> ''indicating that sheep inoculated with the bovine TME agent harbor infectivity in their lymph nodes despite a lack of detection with conventional immunoassays.''


WEDNESDAY, NOVEMBER 20, 2019 

Review: Update on Classical and Atypical Scrapie in Sheep and Goats


FRIDAY, NOVEMBER 15, 2019 

Southwest Wisconsin CWD, Deer and Predator Study


THURSDAY, OCTOBER 17, 2019 

Europe's uneven laws threaten scavengers and Spread Transmissible Spongiform Encephalopathy TSE Prion


TUESDAY, OCTOBER 29, 2019 

America BSE 589.2001 FEED REGULATIONS, BSE SURVEILLANCE, BSE TESTING, and CJD TSE Prion


THURSDAY, DECEMBER 19, 2019 

TEXAS Val Verde County White-tailed Deer Tests Positive for Chronic Wasting Disease CWD TSE Prion State Positive NOW at 147 Confirmed


FRIDAY, OCTOBER 18, 2019 

TAHC Exotic CWD Susceptible Species Rules, Regulations, TSE PRION, WHEAT, GRAINS, HAY, STRAY, GLOBAL CONCERNS GROW, UPDATE, October 17, 2019


THURSDAY, DECEMBER 19, 2019 

TSE surveillance statistics exotic species and domestic cats Update December 2019


SATURDAY, FEBRUARY 04, 2012 

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


FRIDAY, DECEMBER 20, 2019 

Missouri MDC Confirms 24 New Cases of Chronic Wasting Disease CWD TSE Prion


FRIDAY, DECEMBER 20, 2019 

Montana White-tailed deer in southwest tests positive for CWD; fifth deer tests positive in southeast MT


TUESDAY, DECEMBER 17, 2019 

Mississippi CWD TSE Prion Two confirmed cases with 10 more suspected this season to date


FRIDAY, DECEMBER 13, 2019 

Wisconsin New CWD Detection in a Wild Deer Harvested in Sheboygan County During the 2019 Archery Deer Season


FRIDAY, DECEMBER 13, 2019 

Tennessee CWD TSE Prion 2019 to 2020 Sample 148 Positive So Far


THURSDAY, DECEMBER 12, 2019 

Michigan Total CWD TSE Prion Positive Suspect-Positive Deer Jump To 162 confirmed to date


WEDNESDAY, DECEMBER 11, 2019 

South Dakota CWD TSE Prion Detected in Harding, Meade and Tripp Counties with 5 confirmed


TUESDAY, DECEMBER 10, 2019 

Minnesota MBAH confirms an 8-year-old white-tailed doe tested positive for CWD from hobbyist herd in Douglas County


FRIDAY, DECEMBER 20, 2019 

Montana White-tailed deer in southwest tests positive for CWD; fifth deer tests positive in southeast MT


SATURDAY, DECEMBER 07, 2019 

Montana Chronic wasting disease CWD TSE Prion explodes to 91 Cases This Year, with 25 of those confirmed last week


WEDNESDAY, NOVEMBER 27, 2019 

Montana records first suspected case of CWD in wild elk 


SATURDAY, DECEMBER 07, 2019 

Arkansas CWD-positive deer found in Independence County


MONDAY, DECEMBER 16, 2019 

Chronic Wasting Disease CWD TSE Prion aka mad cow type disease in cervid Zoonosis Update

***> ''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***

What if?


TRUCKING TRANSPORTING CERVID CHRONIC WASTING DISEASE TSE PRION VIOLATING THE LACEY ACT

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.....


Department of Justice U.S. Attorney’s Office Southern District of Mississippi FOR IMMEDIATE RELEASE Tuesday, September 6, 2016

Three Plead Guilty to Importing White-Tailed Deer in Mississippi

Hattiesburg, Miss. – Coleman Virgil Slade, 70, of Purvis, Mississippi, Don Durrett, 72, of Aspermont, Texas, and Dewayne Slade, 44, of Purvis, Mississippi, pled guilty on Wednesday, August 31, 2016, to conspiracy to violate the Lacey Act by importing live white-tailed deer into Mississippi, announced U.S. Attorney Gregory K. Davis, Special Agent in Charge Luis Santiago with the U.S. Fish and Wildlife Service, and Special Agent in Charge Dax Roberson with the U.S. Department of Agriculture – Office of Inspector General (USDA OIG).

Coleman Virgil Slade pled guilty to a felony conspiracy count. He will be sentenced on November 21, 2016, by U.S. District Judge Keith Starrett and faces a maximum penalty of five years in prison and a $250,000 fine.

Don Durrett and Dewayne Slade pled guilty to a misdemeanor conspiracy count and were each sentenced to a $10,000 fine, placed on three years of probation, and prohibited from hunting for one year.

According to the guilty pleas, from January of 2009 through December of 2012, the Slades and Durrett spent over $100,000 to purchase live white-tailed deer for delivery from Texas to Mississippi. It is illegal to import live white-tailed deer into Mississippi. However, the deer were transported to Lamar County, Mississippi, and placed in a high fence enclosure. The purchases and transportation to Mississippi of the live white-tailed deer were accomplished through false purchase and transportation records.

“The Department of Justice is committed to enforcing the Lacey Act and other federal laws to protect our wildlife resources,” said U.S. Attorney Gregory K. Davis. “We will continue to work closely with USDA OIG, U.S. Fish and Wildlife Service and the Mississippi Department of Wildlife, Fisheries and Parks to enforce the Lacey Act.”

U.S. Fish and Wildlife Service Special Agent in Charge Luis Santiago stated “We take our mission working with the Mississippi Department of Wildlife, Fisheries, and Parks and the citizens of Mississippi in conserving, protecting, and enhancing fish, wildlife, plants and their habitats very seriously. We will continue working vigorously investigating those who choose to violate state and federal laws.”

“I want to thank the US Attorney’s office, OIG special agents, and our law enforcement partners for their hard work on this investigation,” said USDA OIG Special Agent in Charge Dax Roberson, “USDA OIG is committed to pursuing individuals who commit criminal violations of the Lacey Act, which is intended to protect the health and well-being of America’s wildlife.”

This case was investigated by the U.S. Fish and Wildlife Service - Office of Law Enforcement, the U.S. Department of Agriculture – Office of Inspector General, and the Mississippi Department of Wildlife, Fisheries, and Parks. It was prosecuted by Deputy Criminal Division Chief Darren LaMarca.


By: Jacob Edson, D&DH managing editor | February 9, 2012

Texas Deer Breeding - whitetail hunting - white-tailed deerIt’s no secret that white-tailed deer breeding is big business, especially in the Lone Star state. And wherever big money is involved, greed and illegal activity seem to follow. See for example, this story by Molly Hennessy-Fiske of the Los Angeles Times about a Texas deer breeder who chose to ignore importation laws to smuggle his six-figure deer herd into the state.

Even more alarming is the suggestion in the third to last paragraph that many more breeders might be putting profits above the regulations that protect the safety of Texas’ wild whitetails.

NEW SUMMERFIELD, Texas — Texas’ hunting season for white-tailed deer has now ended. Normally, Billy Powell would be counting his profit from catering to “hornographers,” hunters who will pay as much as $100,000 to bag a monster buck with impressive headgear.

Instead, the 78-year-old deer breeder is under house arrest and wearing an ankle monitor.

Meanwhile, hundreds of his deer, part of a herd that had included two big bucks named Hit Man and Barry, have been put down in a scandal that has rocked Texas’ $2.8 billion deer-hunting and -breeding industry, the largest in the nation.

Powell is one of 1,236 registered Texas breeders. Some have paid up to $1 million for first-rate bucks they mate with captive does. Their progeny, 103,155 registered this year, are raised in pens and released on high-fenced ranches for hunting.

But Hit Man and Barry were smuggled into Texas from Northern states where two deer diseases are found.

After a four-year federal investigation, Powell paid $1.5 million in fines and restitution and pleaded guilty to charges of smuggling more than three dozen white-tailed deer worth more than $800,000 from Illinois, Indiana, Ohio and Pennsylvania.

Mitch Lockwood, big-game director for the Texas Parks and Wildlife Department, said Powell put the state’s 4 million wild deer “and the entire Texas deer-breeding industry at risk.”

Powell and other breeders say regulators have become overzealous, out for hefty fines that become their agency’s cut of the burgeoning deer-farming business.

“Parks and Wildlife don’t like deer breeders, and they’ll do anything to get you,” Powell said. “ I did wrong, but they did more wrong.”

Hunters rate trophy bucks according to a scoring system developed by Theodore Roosevelt’s Boone and Crockett Club in 1887. The score includes antler length and circumference, with the best Texas white-tails traditionally scoring 150 to 160.

Today, thanks to breeding, mammoth deerzillas are scoring 200 or more.

Texas outlawed importing out-of-state deer to prevent the introduction of bovine tuberculosis and chronic wasting disease, a neurological disorder similar to mad cow disease.

Still, some breeders have ignored the ban.

Barry was among the bucks Powell had smuggled from Pennsylvania, where he was known as Fat Boy. Hit Man was actually Silver Storm, from Indiana.

Barry and Hit Man died of natural causes before authorities brought charges against Powell last year, but they helped establish the government’s case. Powell pleaded guilty in June to smuggling 37 deer. -

http://www.deeranddeerhunting.com/blogs/deer-breeding-big-business-invites-crooks 

Man admits to snatching “Diablo” the Texas buck’s semen. (updated)

Posted on July 12, 2012 | By Dane Schiller

A breeding deer not related to the investigation. James Nielson/ Houston Chronicle)

Court papers made public Friday offer more details in the case of an an Illinois man pleaded guilty to illegally obtaining deer semen from a Texas buck named “Diablo.”

Raymond Favero, 55, specifically pleaded guilty to the charge of acquisition of wild life in interstate commerce in violation of state law before U.S. Magistrate Judge Judith K. Guthrie.

Court papers state that in February 2007, Favero acquired 184 straws of whitetail deer semen valued at about $92,000 from a buck named “Diablo'” that he knew had been illegally taken out of Texas, and again in January 2008 took another 110 straws of semen from a buck named “Thunderstruck.” (Read more in the court paper posted at the bottom of this entry.)

He faces up to five years in prison at sentencing, according to a the U.S. Attorney for the Eastern District of Texas.

If an agreement with prosecutors is accepted by a judge, he will serve 5 years of probation and pay a fine of $150,000 to the U.S. Fish and Wildlife Lacey Act Reward Account, and another $50,000 in community restitution to the Texas Parks and Wildlife Foundation.

The case was investigated by the Special Operations Unit of the Texas Parks and Wildlife and the U.S. Fish & Wildlife Service and prosecuted by Assistant U.S. Attorney Jim Noble.

UPDATE: This case looks like it is related to the one involving Billy Powell, a Cherokee County deer breeder who agreed in 2011 to pay a $1.5 million fine as part of pleading guilty to illegally transporting wildlife. See the charges against Powell in the document posted below. His plea agreement, however, remains sealed.

(This does not have any apparent ties to the world of narcotics trafficking, but was too unusual to pass up posting in this blog.)

Shannon Tompkins, our resident deer expert, shared some wisdom with me on this matter. Here is what he had to say:

The reason the feds and the state take this so seriously is that unregulated movement of deer and other cervids (elk, sika deer, etc.) can and has spread incredibly destructive, virulent, communicable diseases such as Chronic Wasting Disease – the deer version of Mad Cow.

The prions that cause CWD are found in deer body fluids. The disease can take as much as five years to manifest, during which time the infected deer can infect others or “shed” prions that remain viable for, some research indicates, 15 years or more. There is no live test for the disease. You have to kill a deer and test its brain stem.

This is serious stuff. Not only is an incredible natural resource at risk – CWD rather easily spreads from penned deer into the wild population – but it also threatens recreational deer hunting which is hugely important economically ($2.5 billion or so a year in direct economic impact to Texas from recreational hunting) and socially. Plus, deer are the reason many landowners manage, maintain and improve the environmental quality of their land. Lose the deer, lose incentive to maintain wild places.

Texas has prohibited importing live deer into the state for a decade or so. State and federal officers are constantly working cases of illegal import of deer or other criminal violations of deer-related laws. Many of them are felonies – especially the ones involving violations of the federal Lacey Act.


June 15, 2011

Cherokee County Deer Breeder Pleads Guilty to Smuggling Deer

Prominent breeder Agreed to Pay $1.5 million for Smuggling Deer into East Texas

TYLER – After a lengthy four year investigation a 77-year-old Cherokee County, Texas licensed deer breeder has pleaded guilty to illegally transporting wildlife in the Eastern District of Texas and then lying about it to a U.S. Fish and Wildlife agent, announced U.S. Attorney John M. Bales today.

Billy Powell pleaded guilty on June 14, 2011, to the felony offense of smuggling at least 37 whitetail deer, over a 3 year time span, from Indiana, Illinois, and Ohio into Texas in violation of state and federal laws. Powell also admitted that he made a false statement and submitted a false document to a U.S. Fish and Wildlife special agent who was looking into the matter. Powell has agreed to pay a $1 million fine, to be deposited into the U.S. Fish and Wildlife Lacy Act Reward Fund, as well as $500,000.00 in restitution to Texas Parks and Wildlife, on his sentencing date. Powell’s agreement with the government calls for Powell to serve 3 years probation with six months of home confinement which will be monitored with an electric anklet. During the term of probation, Powell will be prohibited from participating in any manner in commercial deer breeding. Additionally, Powell must forfeit any illegally imported deer, any progeny of those deer, and any biological material derived from said deer, which would include any semen, antlers, mounts, and cloned deer. Powell has already forfeited over 1,300 straws of frozen semen valued at approximately $961,500.00 to U.S. Fish and Wildlife.

According to information presented in court, on at least four separate occasions, spanning from October 2006 through June 2008, Powell knowingly imported at least 37 live whitetail deer, many of whom came from captive deer farms in Ligonier, Indiana, into the state of Texas and to his “5-P Farms”, high fenced deer breeding facility in Cherokee County Texas. These deer included bucks known as “Fat Boy” aka “Barry”, “Silver Storm” aka “Hit Man”, “Y 009", “Eagle Storm” aka “BJ”, “Thunderstruck”, “High Five”, and “Primer” aka “Spikes”. At all times Powell knew that Texas law prohibited any person from possessing a deer acquired from an out-of-state source. In spite of this, Powell agreed to participate in the above-described transactions in which whitetail deer would be secretly transported from Illinois, Indiana, and/or Pennsylvania, to Texas in order to evade Texas laws and regulations.

Powell acknowledged that the fair market value of all of the illegally imported, whitetail deer exceeded approximately $800,000.00, that the value of the illegally accumulated white-tailed deer semen exceeded approximately $961,000.00, and that the value of the progeny exceeded approximately $290,000.00.

Powell further admitted that he lied to a U.S. Fish and Wildlife Special Agent during a voluntary statement at the U.S. Attorney’s Office in Tyler, Texas. Powell told the agent that he had illegally imported approximately 35 white-tailed deer into the state of Texas when in fact he knew that he had illegally imported no less than 41 white-tailed deer, including 6 white-tail deer fawns. During the same statement, Powell also submitted lists identifying 35 white-tailed deer as the total number of white-tailed deer that he had illegally imported into the state of Texas when he knew that he had actually illegally imported no less than 41 white-tailed, including 6 white-tail deer fawns.

Findings of the investigation also prompted the Wildlife Division of Texas Parks and Wildlife Department to conduct an epidemiological investigation in consultation with veterinarians and wildlife disease experts from Texas Animal Health Commission, Texas Department of State Health Services, and Texas ­A&M College of Veterinary Medicine and accredited veterinarians actively involved in the deer breeding industry. This process was carried out in three separate phases. Ultimately all 334 deer contained in Powell’s deer breeding facility were euthanized to facilitate testing for chronic wasting disease (CWD) and bovine tuberculosis (TB). This process was necessary in order to provide an acceptable level of assurance that neither disease was prevalent in Powell’s deer breeding facility nor in any deer breeding facility that had received deer from Powell’s facility since October 2004.

Texas Parks and Wildlife Department has had an intensive CWD surveillance program since 2002, and this disease has yet to be detected in Texas. Likewise, bovine tuberculosis has not been detected in any Texas deer population. However, illegal entry of white-tailed deer from other states poses a serious risk of introducing these diseases and others into Texas. Introduction of these diseases into Texas could have a detrimental impact on the longtime cultural tradition of deer hunting, which generates an estimated $1.2 billion in retail sales and has a total economic output of more than $2 billion in Texas each year. Disease monitoring is also necessary to protect legal deer breeding activity from risk of disease exposure. Furthermore, bovine tuberculosis could have a significant impact on the Texas livestock industry. Prevention is the most effective tool to combat diseases because once established in wild populations, these diseases are extremely difficult, if not impossible to eradicate.

Since no live-animal test for CWD exists, TPWD consulted with trained experts to ensure the most humane euthanasia method and treatment of the animals was used. Texas Parks and Wildlife officials are presently awaiting the test results for the tissue samples submitted to the Texas Veterinarian Medical Diagnostic Laboratory located in College Station, TX

This case was investigated by the Special Operations Unit of the Texas Parks and Wildlife and U.S. Fish and Wildlife Service and prosecuted by Assistant U.S. Attorney Jim Noble.


Texas deer breeder sentenced for smuggling

Aug. 18, 2010 at 3:18 a.m.

TYLER, Texas (AP) - A licensed deer breeder from Austin must serve three years of probation for illegally transporting wildlife in east Texas.

U.S. Attorney John Bales says 41-year-old Lance Clawson was sentenced Wednesday in Tyler.

Clawson on April 14 pleaded guilty to smuggling whitetail deer from Oklahoma into Texas. He also was fined $15,000 and must pay $7,250 in restitution to the Texas Parks and Wildlife Foundation.

Investigators say Clawson, who operates a ranch and deer breeding facility near Goldthwaite, traveled to Muskogee, Okla., on Oct. 15, 2008, to buy fawns from a breeder.

Clawson's vehicle was stopped the following day by Texas game wardens as he returned with eight fawns.

Texas law bans importing live whitetail or mule deer due to the threat of transmittable diseases.


News Release Media Contact: Mike Cox, 512-389-8046, mike.cox@tpwd.texas.gov

Feb. 5, 2010

Texas Men Sentenced to Federal Prison for Deer Trafficking, Stolen Property

AUSTIN — A four-year, multi-agency investigation that began when two Texas Parks and Wildlife Department Game Wardens received information about possible stolen property on two Northeast Texas ranches has ended with federal prison sentences for a father and son who pled guilty to transporting stolen property and wildlife trafficking.

Forty-nine-year-old James Dwayne Anderton and his 26-year-old son Jimmie Wallace Anderton, both of Quinlan in Hunt County, Texas were sentenced Tuesday in U.S. District Court in Sherman by Judge Marcia Crone.

"This case is an excellent example of a joint effort on the part of local, state and federal law enforcement," said Col. Pete Flores, TPWD’s law enforcement director. "We’re proud of the work our Game Wardens put in on this case, but everyone involved did a great job in pursuing a complicated investigation that not only resulted in the recovery of thousands of dollars worth of stolen property, it will help keep our Texas deer herd safe from disease by ending an illegal importation operation."

The elder Anderton drew 30 months in federal prison for interstate transportation of stolen property and was ordered to pay $180,952 restitution. His son will serve 27 months in federal prison for interstate transportation and will be jointly responsible for making restitution. In addition, both men got 12 months federal confinement for violations of the Federal Lacey Act involving the illegal transportation of deer across state lines. These sentences will be served concurrently with their other sentence, but they also face 36 months of supervised release following their discharge from prison.

Benjamin Tuggle, Regional Director for the U.S. Fish and Wildlife Service, agrees with Col. Flores, adding, "We appreciate these kinds of collaborative efforts. It is all about wildlife conservation and to be successful we need to work together. All of the law enforcement agents working on this case are to be commended for their dedication and hard work."

The Andertons operate a turf grass and landscaping business and hold a TPWD permit to breed captive deer. In the spring of 2006 Game Wardens Dale Waters and Eric Collins were looking into some possible deer breeding violations when they received information that the Andertons might be in possession of stolen heavy equipment and trailers.

The wardens relayed this information to Texas Department of Public Safety Motor Vehicle Theft Division Sgts. John Murphy and Rex Wilemon, who drew up a search warrant executed on two pieces of land owned by the Andertons, one in Delta County and the other in Hunt County near Quinlan. Six Game Wardens and Sgt. Brad Chappell of the TPWD Special Operations Unit participated in the search, which resulted in the recovery of stolen farm machinery and construction equipment. Deputies with the Delta and Hunt county sheriff’s departments and members of the Northeast Texas Auto Theft Task Force also assisted in the search.

The two DPS investigators presented the findings from their stolen equipment investigation to FBI Special Agent Ken Paith who furthered the investigation and developed sufficient evidence to indict the Andertons on July 8, 2009 for interstate transportation of stolen property. Also indicted on the same charge was Timothy Shane Peavler, 37, of Lone Oak, Texas.

During this time Chappell received information that the Andertons had been unlawfully importing white-tailed deer from Arkansas. The Game Warden sergeant contacted U.S. Fish and Wildlife Service Special Agent Mike Merida and began a joint investigation along with Little Rock-based Fish and Wildlife Special Agent Glen Pye and investigators with Arkansas Fish and Game Commission.

This cooperative effort eventually revealed the source of the deer the Andertons were illegally importing. Merida and Chappell determined the Andertons had paid more than $63,000 for at least 125 white-tailed deer and imported them to Texas in violation of a state statute which restricts deer importation.

The two officers eventually learned that the Andertons had hired people to travel to a deer breeder’s facility in northern Arkansas, load deer and return to Texas where they delivered the illegal cargo to both the Anderton’s properties.

Peavler pled guilty on July 27 last year to interstate transportation of stolen property and was sentenced to six months in federal prison and ordered to pay $42,403 restitution. The Andertons pled guilty Aug. 31.

"TPWD began limiting importation of live white-tailed deer and mule deer into Texas in the spring of 2002 due to concerns over potential spread of two diseases that could be devastating to our deer population, chronic wasting disease (CWD) and bovine tuberculosis," Flores said. "We have worked hard to prevent CWD from being introduced into Texas and so far our state has remained CWD free."

Assistant United States Attorney Randall Blake prosecuted the case.


Appeal from the United States District Court for the Northern District of Texas No. 3:13-CV-01641

JAMES ANDERTON; JIMMIE ANDERTON,

Plaintiffs – Appellants

v.

TEXAS PARKS AND WILDLIFE DEPARTMENT; TEXAS ANIMAL HEALTH COMMISSION; CARTER SMITH, Executive Director, Texas Parks and Wildlife Department; CRAIG HUNTER, Director, Texas Parks and Wildlife Department; L. DAVID SINCLAIR, Chief Game Warden, Texas Parks and Wildlife Department; MITCH LOCKWOOD, Big Game Warden, Texas Parks and Wildlife Department; DALE WATERS, Game Warden, Texas Parks and Wildlife Department; GARY COLLINS, Game Warden, Texas Parks and Wildlife Department; BRAD CHAPPELL, Investigator, Texas Parks and Wildlife Department; AMBER ANDEL, Deer Breeders Program, Texas Parks and Wildlife Department, Defendants – Appellees

SNIP...

FACTUAL AND PROCEDURAL BACKGROUND

From 2000 until 2010, the Andertons possessed a current permit issued by the Department that authorized them to breed deer. Their breeding ranch was located east of Dallas in Quinlan, Texas. In 2010, 2011, and 2012, the Andertons submitted applications for renewal of the permit. The Department denied those applications without explanation.

It has been alleged in this litigation that the Andertons’s permit was not renewed because they had illegally imported deer from another state. The Andertons had pled guilty, as shown in a federal court judgment of February 2, 2010, to the offense of conspiring to transport wildlife in interstate commerce in violation of Texas law. The Andertons were charged under the general federal conspiracy statute, 18 U.S.C. § 371. The substantive federal statutes setting forth the offense were 16 U.S.C. §§ 3372(a)(2)(A) and 3373(d)(2). Those are sections of what is called the Lacey Act. 16 U.S.C. §§ 3371-3378. The Texas laws they were charged in an information with violating were 31 Texas Administration Code Sections 65.609(b)(2), 65.611(h), and 65.611(i). The Department may refuse permit issuance or renewal to any person convicted of a violation of the Lacey Act. 31 TEX. ADMIN. CODE § 65.603(g)(2) (2010).

As mentioned above, the Andertons deer-breeding permit was not renewed in 2010. Such a permit is valid from the date of issuance until the immediately following July 1. 31 TEX. ADMIN. CODE 65.603(c). Apparently, then, as of July 1, 2010, four months after their February convictions, they no longer had a current permit to maintain breeder deer. On December 6, 2010,

2

Case: 14-10297 Document: 00512982550 Page: 2 Date Filed: 03/26/2015

No. 14-10297

and May 1, 2011, Department officials entered and shot breeder deer on the Andertons’ land. The Andertons allege the officials killed the deer in front of their family and several witnesses. In April 2013, the Andertons brought suit in the United States District Court for the Northern District of Texas against the Texas Animal Health Commission and the Department for violations of the Fourth, Fifth, and Fourteenth Amendments, and the Racketeer Influenced and Corrupt Organizations Act (“RICO”). They also sued several Department officials in their official and individual capacities under 42 U.S.C. § 1983 and RICO. Additionally, they brought claims for injunctive and declaratory relief against all parties. The district court dismissed the Andertons’ Section 1983 and RICO claims against the officials in their individual capacities under Federal Rule of Civil Procedure 12(b)(6), and dismissed the remaining claims under Rule 12(b)(1). The Andertons appealed.

DISCUSSION

SNIP...

The Andertons argue that the breeder-deer industry is not a closely regulated industry.

SNIP...

The Andertons argue the killing of the deer “shocks the conscience.” Even if there were a protected property interest in the deer – an issue we will analyze in the next section on procedural rights – Department officials were acting pursuant to state law, not violating it. The Andertons failed to allege facts that established the conduct of the officials was intended to injure them unjustifiably. The district court stated that though the allegations “may raise questions related to the most humane ways to kill deer, [they] do not plausibly establish that the officials’ conduct was so egregious, so outrageous, that it may fairly be said to shock the contemporary conscience.”

The Andertons have failed to demonstrate a violation of substantive due process under the Fourteenth Amendment.

SNIP...

Under Texas law, though, breeder deer belong to the state, not the permittee. See, e.g., TEX. PARKS & WILD. CODE §§ 1.011 (“All wild animals . . . inside the borders of this state are the property of the people of this state.”); 43.364 (“All breeder deer . . . are under the full force of the laws of [Texas] pertaining to deer . . . .”). While a permittee may have possession of the breeder deer, the deer are only “held under a permit[.]” Id. § 43.351. Nowhere do the statutes or regulations state that breeder deer become the property of a permit holder.4 Regardless, even if they did give ownership of breeder deer to permit holders, the Andertons were not permit holders when the deer were killed.


While a permittee may have possession of the breeder deer, the deer are only “held under a permit[.]” Id. § 43.351


S.B. No. 820



Texas Senate Bill

Relating to the management, breeding, and destruction of deer and to procedures regarding certain deer permits.

View latest bill text Session:83rd Legislature (2013)


Deer Smugglers Go to Prison

A Texas man and a Minnesota man have been sent to prison for transporting wild deer across state lines. You may not have known that is illegal, but it is, and the Texas Parks and Wildlife Department takes it very seriously, as Jim Bell reports.

By: Jim Bell, December 29th, 2008 08:21 PM

00:00 00:00

Everyone knows it's legal to hunt wild deer in Texas under controlled and licensed conditions. It's also legal for people to get a license to breed deer on private property and use them for private hunts. What's not legal is for the deer breeders to bring deer in from other states. Greg Williford is in the Texas Parks and Wildlife Department's Special Operations Unit, and he says deer from other states could bring a very serious animal disease into the state. It's called Chronic Wasting Disease.

"Similar to Mad Cow Disease but it affects deer and elk. It's been found in Wisconsin and I believe Colorado had it in their elk population at one point.ξ It completely decimates the native deer population."

Deer hunting is a huge industry in Texas. Add up the money hunters spend year round on hunting rifles, hunting and camping clothing and equipment, deer leases, everything related to traveling to hunting areas, hotels, motels, campgrounds, and you're talking about hundreds of millions of dollars. A sick deer from another state could start an epizootic that could spread and kill thousands of deer, and do serious damage to the state's hunting economy.ξ

What were those two men doing that got them in so much trouble?ξ Williford says it started when Robert Eichenour of Houston bought mature trophy bucks with big racks from a rogue breeder named Brian Becker in Minnesota.

"Mr. Eichenour was able to buy them from Mr. Becker in Minnesota for approximately 1500 dollars a buck.ξ Mr. Becker would bring the animals down, they'd be placed on Mr. Eichenour's ranch in Grimes County and then he would sell the hunt for this animal for anywhere between five and ten thousand dollars."ξ

And that's per hunter. Over a four year period, Eichenour smuggled up to $300 thousand dollars worth of deer to his ranch for these hunts. The question arises: since he could breed deer legally as a licensed breeder, why did he need to import deer?ξ Williford says:

"It was more economically advantageous for him to import these deer than it was to try to raise these deer. It would take four to five years to raise a deer with antlers of this quality anyway."

Williford says the Texas breeder just didn't want to spend the time and money it takes to raise trophy deer to adulthood. Both men were caught after an undercover investigation by Parks and Wildlife Department Game Wardens, and both were charged with illegally transporting illegally captured animals across state lines, which is a federal crime. Last month, both pleaded guilty and both are headed for a federal prison. Williford says they can blame it on greed.ξ

im Bell, KUHF, Houston Public Radio News.


Owner of Sandia Deer Breeding Facility Bonded Out of Jail

Posted: May 08, 2014 6:07 PM CDT

Updated: May 16, 2014 6:54 PM CDT

SANDIA (Kiii News) - Fred Rich, the man arrested Wednesday for allowing someone to enter a deer breeding facility and kill a 22-point buck while it was still inside a pen, bonded out of jail on Thursday.

Rich is said to be the owner of the breeding facility at the Lonesome Bull Ranch near Sandia, Texas. That facility is currently being investigated by Texas Parks and Wildlife, and that's how the incident was discovered.

Parks and Wildlife officers are also testing whitetail dear from that ranch for an infectious disease. More than 200 of the deer had to be euthanized to allow for that testing, and the results are expected back in a few weeks. As for Rich, if convicted in aiding the slaughtering of that deer, he could face up to six months in jail.

It's not his first run-in with the law. Rich received time in prison for federal charges that he scammed insurance companies out of thousands of dollars in fraudulent mold claims.

Prosecutors said Rich, who owned a company called Mold Inc., and two other men pled guilty to suing a technique called "cooking houses." It involved wetting down the inside of a home, shutting doors and windows, and then cranking up the heat to create mold.

The alleged incidents happened in Corpus Christi and in Portland between 2000-2002.


Geneticist Fined in Texas Deer Semen Case

An Illinois geneticist must pay $30,000 and serve three years of probation for illegally obtaining valuable semen from whitetail deer in East Texas. A federal judge in Tyler sentenced 55-year-old Raymond Favero of Braidwood, Ill. Favero in...


Subject: Texas 85th Legislative Session 2017, bathroom politics, while Rome burns, CWD detected in 5th captive breeding facility

thought i might comment on the bathroom politics in Austin, while Rome Burns...

Subject: Texas 85th Legislative Session 2017, bathroom politics, while Rome burns, CWD detected in 5th captive breeding facility

Subject: TEXAS CWD POLITICIANS, AND CORPORATE GREED

MONDAY, MAY 15, 2017 

TEXAS New CWD TSE PRION Case Discovered at Fifth Captive Deer Breeding Facility


SUNDAY, MAY 14, 2017 

85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play $$$


FRIDAY, OCTOBER 09, 2015

Texas TWA Chronic Wasting Disease TSE Prion Webinars and Meeting October 2015
http://chronic-wasting-disease.blogspot.com/2015/10/texas-twa-chronic-wasting-disease-tse.html

Thursday, August 20, 2015

*** TEXAS TAHC DEER BREEDER CWD PERMIT RULES EMERGENCY ADOPTION PREAMBLE ***

http://chronic-wasting-disease.blogspot.com/2015/08/texas-tahc-deer-breeder-cwd-permit.html

Under Texas law, though, breeder deer belong to the state, not the permittee. See, e.g., TEX. PARKS & WILD. CODE §§ 1.011 (“All wild animals . . . inside the borders of this state are the property of the people of this state.”); 43.364 (“All breeder deer . . . are under the full force of the laws of [Texas] pertaining to deer . . . .”). While a permittee may have possession of the breeder deer, the deer are only “held under a permit[.]” Id. § 43.351. Nowhere do the statutes or regulations state that breeder deer become the property of a permit holder.4 Regardless, even if they did give ownership of breeder deer to permit holders, the Andertons were not permit holders when the deer were killed.

http://www.ca5.uscourts.gov/opinions%5Cunpub%5C14/14-10297.0.pdf

While a permittee may have possession of the breeder deer, the deer are only “held under a permit[.]” Id. § 43.351

http://www.statutes.legis.state.tx.us/Docs/PW/htm/PW.43.htm

S.B. No. 820

http://www.legis.state.tx.us/tlodocs/83R/billtext/html/SB00820F.HTM

http://openstates.org/tx/bills/83/SB820/

Texas Senate Bill

Relating to the management, breeding, and destruction of deer and to procedures regarding certain deer permits.

View latest bill text Session:83rd Legislature (2013)

http://openstates.org/tx/bills/83/SB820/
Thursday, August 20, 2015

TEXAS CAPTIVE Deer Industry, Pens, Breeding, Big Business, Invites Crooks and CWD

http://chronic-wasting-disease.blogspot.com/2015/08/texas-captive-deer-industry-pens.html

Thursday, August 20, 2015

*** TEXAS TAHC DEER BREEDER CWD PERMIT RULES EMERGENCY ADOPTION PREAMBLE ***



Wednesday, October 28, 2015

Texas' wild deer herd must be protected


Terry S. Singeltary Sr. Your opinions and comments have been submitted successfully. Thank you for participating in the TPWD regulatory process.

Wednesday, October 28, 2015

Interim Chronic Wasting Disease Response Rules Comment online through 07:00 a.m. November 5, 2015


SATURDAY, OCTOBER 03, 2015 

TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO 2015


TEXAS HISTORY OF CWD Singeltary telling TAHC, that CWD was waltzing into Texas from WSMR around Trans Pecos region, starting around 2001, 2002, and every year, there after, until New Mexico finally shamed TAHC et al to test where i had been telling them to test for a decade. 2012 cwd was detected first right there where i had been trying to tell TAHC for 10 years. 

***> Singeltary on Texas Chronic Wasting Disease CWD TSE Prion History <***


***> TRUCKING AND TRANSPORTATION OF CWD TSE PRION

ALABAMA 

Relevant Case: Skinner Illegal Import Case 

 6 live deer from Indiana were imported into Alabama. 

 In addition to violations of state law, Lacey Act (federal) violations were made. 

 A federal judge sentenced Skinner to pay $750,000 ($650,000 to WFF and $100,000 to the Lacey Act Fund) in restitution monies for the possible introduction of CWD to the native deer herd, surrender all animals, and forfeit his game breeder license. 

 USDA in partnership with WFF will depopulate the breeding facility as well as the enclosure, and all deer were tested for the presence of CWD and other diseases. Relevant Case: Canned Hunt Case 

 A canned hunt for a captive buck purchased from a licensed game breeder. 

 The buck was advertised and sold on Facebook as a guaranteed hunt. 

 The deer was accidently overdosed when being moved to the shooting pen, placed in a cooler, and propped up for a staged spot and stalk archery hunt. 

 Three men were arrested in the case of the Popsicle buck. Relevant Case: Canned Hunt Case 

 Multiple violations of 9-11-.501 and 9-11-.502  Hunting of a tame game animal for a fee. 

 Hunting of a game animal within 10 days of release. 

 Hunting of a game animal without a reasonable chance of escape. 

 Violations of 9-11-.501 and 9-11- .502 are misdemeanors and, upon conviction, first offense carries a fine of no less than $2000 nor more than $5000 and no more than 30 days in jail for each offense. 

 They were fined $750 by the local judge, and the Department was ordered to return the antlers. 

https://www.dot.state.al.us/maweb/pdf/chuckSykeDCNandChronicWastingDisease.pdf

SUNDAY, AUGUST 02, 2015 

TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if?


SHOCKING ONES CONSCIENCE VIDEO

*** Danger of Canned Hunting Indiana Wildlife VIDEO ***


THURSDAY, DECEMBER 12, 2019 

Heidenhain Variant Creutzfeldt Jakob Disease hvCJD, sporadic spontaneous CJD and the TSE Prion December 14, 2019

22 years, rip mom dod 12/14/97 confirmed hvcjd, just made a promise to mom, and you don't break those promises, never forget, and never let them forget, before we all do...this pearl's for you mom... love terry


P.S. TAHC, i'm still waiting for my hat lol...?

Terry S. Singeltary Sr.
Bacliff, Texas USA 77518
Galveston Bay...on the bottom!


posted by Terry S. Singeltary Sr. at 3:58 PM

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