Michigan reports more CWD TSE Prion aka mad deer disease 117 cases to date, with 59,870 total tested
Michigan reports more CWD TSE Prion aka mad deer disease 117 cases to date, with 59,870 total tested.
THURSDAY, JANUARY 17, 2019
Michigan reports more CWD TSE Prion aka mad deer disease 115 cases to date
THURSDAY, JANUARY 10, 2019
Michigan reports more CWD TSE Prion aka mad deer disease 111 cases to date
MICHIGAN-SPORTSMAN.COM UPDATE More Ted Nugent CWD TSE Prion science from Michigan-sportsman.com cwd tse prion expert and fake news spreader otcarcher latest update
-----Original Message-----
From:
To: flounder9
Sent: Sun, Jan 20, 2019 6:41 pm
Subject: Michigan-Sportsman.com CWD Otcarcher Update
From:
To: flounder9
Sent: Sun, Jan 20, 2019 6:41 pm
Subject: Michigan-Sportsman.com CWD Otcarcher Update
Dec 19, 2018#13 Joe Archer Joe Archer Staff Member Mods WE LOVE IT! Michigan Sportsman 15 season die hard! Outdoor Photographer
Messages:15,117 Likes Received:6,424 Location:New Baltimore Michigan
Just do what many around here seem to do... Put your hands over your ears and yell "LA LA LA LA LA LA LA LA LA LA LA"! We had our chance as hunters to thin the herd (note THIN, not decimate), while not protecting yearling bucks.... Hunters simply will not do this... end of story. Think of Wisconsin in 50 years.... Michigan in 100. <---- span="">
Joe Archer Staff Member Mods WE LOVE IT! Michigan Sportsman 15 season die hard! Outdoor Photographer
Messages:15,117 Likes Received:6,424 Location:New Baltimore Michigan Hillsdales Most Wanted said:
↑ Well lets see what the dnr does in the UP It really isn't about what the DNR will do... it is about what hunters will NOT do. Hunters in the core and management zones are still going out and seeing 30 - 100 deer in a single filed. <---- span="">
Dec 19, 2018#36 otcarcher otcarcher WE LOVE IT! Michigan Sportsman You've been here one season and counting!
Messages:3,304 Likes Received:2,849 Bucman said: ↑ What is happening that is causing this in Wisconson? Why now? This has been around along time and now its spreading like that?? Im skeptical on all the info out there until there are facts as to what,where and how its spread! I've done more research on this than I care to admit, and share as much as I can, but most times it falls on completely deaf ears. Go to the Wisconsin CWD report page online. Please compare county testing numbers in the SFZ by year and the answer will be very clear.
The point....when you increase testing in those counties of the SFZ with the highest prevalence rates, it is going to increase overall prevalence. Stating the disease is spreading is completely disingenuous.
A quick example and I'll let others look on their own. In 2017, there were 3236 deer tested in the 4 county high prevalence area. In 2018, there have been 4438 in those same counties. It matters, considering a few of those counties have a near 25% prevalence rate, which by adding more of them into testing, skews overall prevalence rates of the SFZ as a whole. But, hey, what the heck do I know? Last edited: Dec 19, 2018
Dec 19, 2018#59 otcarcher otcarcher WE LOVE IT! Michigan Sportsman You've been here one season and counting!
Messages:3,304 Likes Received:2,849 Ken said: ↑ How many deer in Michigan were found dead (not by vehicle, archery, firearm, or accident such as fences) and then were determined to have died from CWD?...……...ZERO.
How many deer in Wisconsin died of CWD? probably not a number they are releasing....I'd bet a drop in the bucket at most.
How many deer died as a result of CWD regulations, such as sharpshooter targeting, increased harvest in CWD areas, etc?
They say the disease is always fatal to deer. How many that tested positive showed signs (either externally or internally)? In Michigan, 1. The first one in the original core area.
It's like testing the NBA for HIV, and then stating they will all die of AIDS because some are positive. Click to expand... Kroll conducted a study in Wisconsin looking for exactly how many deer had been found dead from CWD. After major kickback when requesting reports, he was eventually able to determine it was less than 12 in over a decade. Jan 4, 2019#102 Tracker83 Tracker83 WE LOVE IT! Charter Member 10 season die hard
Messages:2,173 Likes Received:824 Location:Michigan Joe Archer said: ↑
I didn't kill my deer in the CWD zone, so there is really no relevance to any DNR CWD plan. The reason that CWD will continue to spread is plain and simple, has been known since day one, and you seem to echo this constantly; "Hunter harvest decisions depend most heavily on personal attitudes and are relatively unaffected by agency educational efforts" . CWD in Michigan will NEVER end. Any actions taken now are simply to help prevent your grand kids from having to hunt areas with prevalence rates of over 50% or higher. Anyway - preventing the spread of CWD, or limiting the spread is just blowing smoke because nowhere have hunters been willing and able to reduce population densities, while limiting buck age structure. NOWHERE... Why expect anything different here?
<---- 2019="" 3="" 4="" a="" add="" again="" and="" as="" been="" best="" bound="" buckguts1970="" but="" chance="" click="" combat="" continue="" counting="" cwd="" destined="" disclaimer="" every="" expand...="" explain="" fail="" follow="" from="" have="" here="" i="" if="" in="" is="" isn="" it="" jan="" known="" like="" lol.="" love="" m="" manager="" maybe="" michigan="" no="" not="" of="" on="" one="" only="" otcarcher="" others="" over="" paper="" paragraph="" plan="" please="" post="" printed="" professional="" right="" s="" science="" season="" should="" sniper="" span="" sportsman="" start="" success.="" t="" that="" the="" then="" this.="" this="" time="" to="" ve="" way="" we="" why="" wildlife="" will="" worth="" yet="" you="" your="">
Messages:3,304 Likes Received:2,849 The sky is falling, the sky is falling. There's been enough Chicken Little nonsense here over the past three years to last a lifetime. Lightfoot, Musket, HUBBHUNTER and 3 others like this. Jan 6, 2019#103 Luv2hunteup Luv2hunteup WE LOVE IT! Michigan Sportsman 15 season die hard! Outdoor Photographer
Messages:27,490 Likes Received:15,072 Location:Somewhere Near the Tip of the Mitt Wisconsin’s history of great hunting will slowly diminish, it won’t be in my lifetime but it may in my children’s. There is no way any herd can stand a 3 times higher mortality rate over time.
https://www.jsonline.com/story/spor...n-diseased-animals-wisconsin-study/378642002/ Jan 4, 2019#104 sniper sniper WE LOVE IT! Michigan Sportsman 10 season die hard Outdoor Photographer
Messages:6,684 Likes Received:9,715 Location:Livonia-Hillsdale otcarcher said: ↑ The sky is falling, the sky is falling. There's been enough Chicken Little nonsense here over the past three years to last a lifetime. To add, it's sometimes embarrassing that some of these statements are coming from grown men...
Sent from my LG-H871 using Michigan Sportsman mobile app Last edited: Jan 4, 2019
https://www.michigan-sportsman.com/forum/threads/cwd-in-wisconsin-is-spreading-like-wildfire.630873/
Here's the another update from Michigan-sportsman.com cwd tse prion expert and fake news spreader otcarcher latest update. so damn sad what happened with michigan-sportsman hunting forums. even old joe archer can't talk any sense to them anymore. just a sad state of affairs there imo...terry
SATURDAY, DECEMBER 29, 2018
Michigan CWD TSE Prion Climbs To 109 Cases To Date
otcarcher posted on Michigan-sportsman.com
Michigan-sportsman.com otcarcher This is nothing new Squirrels are known "carriers" of Mad Cow disease
otcarcher Michigan-sportsman.com This is nothing new. Squirrels are known "carriers" of Mad Cow disease.
LMAO! now, michigan-sportsman.com otcarcher and their supposedly new expert on CWD claims the squirrels are to blame because the NYT said so back in 1997...LMAO, God help Michigan and Michigan-sportsman.com...
so, media picks this up and runs with it all the while ignoring the other likely routes and sources of tse prion infection staring them right in the face. Hunter died of mad cow-like disease after eating squirrel's brain!
NO, this has not been confirmed, nor has any other suspect squirrel brain eaters that died from cjd.
cdc has never confirmed this.
there are so many other routes and sources staring us in the face, and unless these squirrels were eating ruminant mammalian feed, then i don't believe this story.
no transmission studies were done, this is just a case of circumstance, imo..
IF this is all that they can come up with in a CJD Questionnaire, God help us...
WEDNESDAY, OCTOBER 17, 2018
Towards Earlier Diagnosis of Transmissible Spongiform Encephalopathies (TSEs): A Case Series, Including One Associated with Squirrel Brain Consumption
Rochester Regional researchers: no clear link between squirrel brain consumption and death
By BRETT DAHLBERG • OCT 19, 2018
Rochester Regional Health cannot directly connect the reported death of a man with Creutzfeldt-Jakob disease to his consumption of squirrel brain, researchers said Friday.
National and international media reports had indicated that the man’s squirrel consumption was linked to his development of the illness, which is similar in symptoms to mad cow disease.
But Emil Lesho, a hospital epidemiologist at Rochester Regional Health, said that’s not the conclusion he and a team of researchers had drawn.
The team presented research at a conference in San Francisco, after which LiveScience ran the initial story. That research did not show causation between squirrel brain consumption and the man’s disease, said Lesho. Instead, it showed an association.
“This is just typical epidemiology,” Lesho said. “You look for anything that could indicate where a disease came from.”
The research was not meant for public consumption, Lesho said. “Our original intent with this report was to present it in front of a jury of our peers at a scientific meeting, to become vetted.”
It started, Lesho said, when he and other researchers noticed what looked like a series of cases where patients had symptoms resembling mad cow disease. Statistically, Lesho said, they should see that disease about once a year. But now they were seeing “what looked like two or three patients over a four-month period.”
That would be concerning, because that family of diseases, caused by malformed proteins called prions, is very difficult to disinfect. Surgical equipment that comes in contact with patients who have prion diseases sometimes can’t be cleaned and need to be disposed of entirely.
“We want to be very careful with this at our hospital,” Lesho said.
In the end, further research showed that some suspected cases were not confirmed, and the frequency of the disease was actually in line with statistical expectations.
Still, though, because prion diseases are transmissible through the consumption of an infected animal’s nerve cells, Lesho says the bottom line is, “be careful if you eat brain tissue.”
WEDNESDAY, OCTOBER 31, 2018
Michigan Chronic Wasting Disease CWD TSE Prion Cases Jump To 69 to Date
***> WISCONSIN SINKS INTO THE ABYSS OF CWD TSE PRION AKA MAD DEER DISEASE
***> SEE WISCONSIN ANIMATED MAP OF THE EXPLOSIVE SPREAD OF CWD TSE PRION, and see just what nonsense that Michigan-Sportsman spokesperson and self posed expert on Chronic Wasting Disease and all things TSE Prion, just ask him...
Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS
https://www.youtube.com/watch?v=y1bsK4Igt1o&index=10&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj
See Wisconsin update...terrible news, right after Texas updated map around 5 minute mark...
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...
13:26 Texas CWD Symposium: Welcome and Introductions Texas Parks and Wildlife
1:00:49 Texas CWD Symposium: CWD Overview Texas Parks and Wildlife
28:04 Texas CWD Symposium: Myths, Facts, and Legends Texas Parks and Wildlife
26:42 Texas CWD Symposium: CWD Drives population decline Texas Parks and Wildlife
31:08 Texas CWD Symposium: Pre-symptomatic prion detection Texas Parks and Wildlife
26:58 Texas CWD Symposium: Transmission by Saliva, Feces, Urine & Blood Texas Parks and Wildlife
31:06 Texas CWD Symposium: Sampling CWD Texas Parks and Wildlife
24:10 Texas CWD Symposium: Advantages and Limitations Texas Parks and Wildlife
27:06 Texas CWD Symposium: Diagnostics and Detection Texas Parks and Wildlife
28:56 Texas CWD Symposium: CWD in Wyoming 30+ Yrs Later Texas Parks and Wildlife
31:40 Texas CWD Symposium: CWD Management & Response in Wisconsin Texas Parks and Wildlife
31:46 Texas CWD Symposium: Missouri's Approach to CWD Surveillance Texas Parks and Wildlife
33:35 Texas CWD Symposium: CWD Management in Texas Texas Parks and Wildlife
27:24 Texas CWD Symposium: Report on Ante-Mortem Testing in Texas Texas Parks and Wildlife
47:11 Texas CWD Symposium: Overview of CWD Positive Breeder Facilities Texas Parks and Wildlife
30:43 Texas CWD Symposium: What we have learned after 21 years Texas Parks and Wildlife
25:09 Texas CWD Symposium: Hunter/Landowner Perspective Texas Parks and Wildlife
1:38:33 Texas CWD Symposium: Panel Discussion: Challenges in Texas Texas Parks and Wildlife
MONDAY, JANUARY 14, 2019
Evaluation of iatrogenic risk of CJD transmission associated with Chronic Wasting Disease TSE Prion in Texas TAHC TPWD
It is a dimension as vast as space and as timeless as infinity. It is the middle ground between light and shadow, between science and superstition, and it lies between the pit of man's fears and the summit of his knowledge. This is the dimension of imagination. It is NOT, an area which we call the Twilight Zone, but an area that believes junk science, and the very industries and lobbyist some Texas Hunters, the cervid industry, that insist on shoving the fake news down their throats, we call this ted nugent junk science, and in TEXAS, sometimes you just can't fix stupid, this is where the rubber meets the road, here's your sign!
chronic wasting disease cwd tse prion aka mad deer elk disease, if you consume a cwd tse prion positive cervid, then months, years, decades later, go on to have surgery, dental, ophthalmology, endoscopy, donate tissue, blood, organs, you then expose those medical theaters and tissue, blood, organs, that are incubating the infectious cwd tse prion disease, to everyone that comes in contact.
these are not memes, these are actual statements from hunters/industry in Texas about CWD tse prion.
God help them, and us...terry
''Got a call today from TPWD, I’ve got a mule deer that tested early positive for CWD. I’m soon to turn into a zombie because I have already been eating it. They advised not to consume any of the meat...too late! They want to come confiscate what meat is left once they get more results back from another lab.''
snip...
FRIDAY, JANUARY 04, 2019
TEXAS TPWD CONFIRMED CWD TSE PRION 3 WTD in Medina, Dallam, and Hartley Counties, and in 3 MD in Hudspeth, Hartley, and El Paso Counties
*** Hartley County Sheep with Scrapie, and CWD in Hartley county ???
*** Friday, April 22, 2016
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer
SUNDAY, MAY 14, 2017
85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play
Wednesday, May 04, 2016
TPWD proposes the repeal of §§65.90 -65.94 and new §§65.90 -65.99 Concerning Chronic Wasting Disease - Movement of Deer Singeltary Comment Submission
TUESDAY, DECEMBER 16, 2014
Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry TAHC TPWD CWD TSE PRION
SUNDAY, DECEMBER 14, 2014
TEXAS 84th Legislature commencing this January, deer breeders are expected to advocate for bills that will seek to further deregulate their industry
***> TEXAS HISTORY OF CHRONIC WASTING DISEASE CWD TSE PRION
***> Singeltary on Texas Chronic Wasting Disease CWD TSE Prion History
SATURDAY, JANUARY 19, 2019
Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS
TUESDAY, JANUARY 22, 2019
TEXAS REPORTS 6 MORE CWD TSE PRION ALL WILD CERVID TOTAL TO DATE 139
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
Author affiliations
School of Veterinary Medicine and Science, The University of Nottingham, Loughborough, UK ADAS, School of Veterinary Medicine and Science, The University of Nottingham, Loughborough, UK Animal Sciences Unit, Pathology Department, Animal & Plant Health Agency Weybridge, New Haw, Addlestone, Surrey, UK E-mail for correspondence; ben.maddison@adas.co.uk
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...
PrPC is ubiquitous in its distribution in vivo2 and with both scrapie and CWD the in vivo dissemination of infectivity is also widespread with PrPSc usually accumulating within peripheral lymphatic tissues before the CNS.3 4 With scrapie, PrPSc can be secreted/ excreted via a multiplicity of routes including saliva,5 6 milk,7 faeces,8 skin9 and urine.10 The accumulation of this material within the environment (particularly the built farm environment),11 12 creates levels of infectivity that can be transmitted to naïve animals. These reservoirs of infectivity can remain infectious for prolonged periods of time, in one such recorded incident at least 16 years.13 The advent of high sensitivity prion replication assays such as protein misfolding cyclic amplification (PMCA) with application to sheep/goat scrapie14 15 has allowed the monitoring of prions within environments.11
Attempts to decontaminate pens on a scrapie-affected farm and measuring efficacy using a sheep bioassay were previously reported.12 It was concluded that the failure of effective decontamination within that study was likely to have been due to the incomplete farm decontamination and the presence of dust containing infectious prions that recontaminated the pen surfaces. The serial protein misfolding cyclic amplification (sPMCA) technique was recently used to confirm the presence of prions within extracts prepared from dust samples that had settled on sterile surfaces.16 Given the presence of mobile infectious prions within dust, it was proposed that for effective scrapie decontamination emphasis should be given to the removal of all sources of dust within the decontamination strategy for a farm. More recently, the sPMCA technique has been used by the authors' laboratory to look at effective methods of decontaminating prions bound to concrete surfaces within the laboratory setting.17 This study demonstrated that current methodology based on a one-hour exposure to 20000 ppm free chlorine was likely to be ineffective at removing surface-bound scrapie prion. However, there was an enhanced effectiveness of this chemical decontamination when using multiple applications over four hours. Here, a study is described where a scrapie-affected farm was decontaminated using four applications of 20000 ppm free chlorine to livestock barns and concreted areas. The decontamination also included a high-level clean of the buildings that had housed sheep to remove all traces of dust as far as practicable before the chemical decontamination procedure. Following these treatments the surfaces within the barn were demonstrably free from prion using a sensitive sPMCA assay. The presence of any residual infectivity was then evaluated by sheep bioassay and dust samples collected during the bioassay were assayed for prion seeding activity by sPMCA.
snip...
Discussion
The authors' previous work on this farm indicated that dust harbours low levels of mobile scrapie prions that can accumulate on surfaces16 and this is likely to perpetuate transmission of scrapie within such a farm environment.12 In addition, previous in vitro modelling of scrapie prions bound to a concrete ‘fomite’ demonstrated that prion seeding activity could be inactivated by four applications of 20,000 ppm free chlorine as measured by a sPMCA assay. This previous modelling demonstrated that residual contamination of the swab extract with hypochlorite at levels which would inhibit the sPMCA are unlikely, and the authors consider these results as reduction in seeding titre.17 Here, this same decontamination methodology was tested within a farm-scale study which also included steps to remove dust within the barns. This study demonstrated that this thorough decontamination method applied to a farm with a high incidence of naturally acquired scrapie was sufficient to remove scrapie prions on surfaces to levels that were undetectable by sPMCA, one of the most sensitive biochemical assays for prions. The authors' sPMCA assay has an limit of detection of around 1–10pg scrapie-infected sheep brain per sPMCA reaction. The authors assume that the samples negative by sPMCA had less than this amount (of brain equivalent) within the extracts that were prepared. This treatment together with measures designed to minimise the amount of dust retained within the buildings (vacuuming all surfaces, pressure washing and then hypochlorite treatment) was expected to have removed all infectivity from the buildings and the concrete areas surrounding them, and it was anticipated that the sheep bioassay would confirm absence of infective prion.
However, the introduction into this decontaminated barn of 25 VRQ/VRQ sheep (a genotype highly susceptible to classical scrapie) demonstrated that all animals, with the exception of 1 lamb that died at 122 dpe, had detectable PrPSc in lymphoid tissue, indicating infection with the scrapie agent. This included 14 animals (54 per cent) that were PrPSc-positive on the first RAMALT analysis at 372 dpe or 419 dpe. Although infected sheep were removed based on a positive RAMALT result, it is possible that lateral transmission or subsequent contamination of the environment from infected sheep had contributed to the rapid spread of scrapie in nearly all sheep. It has been shown previously that objects in contact with scrapie-infected sheep, such as water troughs and fence posts, can act as a reservoir for infection.23 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.
***> see more of study here;
Wednesday, January 16, 2019
Early preclinical detection of prions in the skin of prion-infected animals
Michigan-sportsman.com cwd tse prion expert and fake news spreader otcarcher latest update
SATURDAY, DECEMBER 29, 2018
Michigan CWD TSE Prion Climbs To 109 Cases To Date
FRIDAY, DECEMBER 28, 2018
***> Chronic Wasting Disease CWD TSE Prion 2019 Where The Rubber Meets The Road
FRIDAY, JANUARY 04, 2019 TEXAS TPWD CONFIRMED CWD TSE PRION 3 WTD in Medina, Dallam, and Hartley Counties, and in 3 MD in Hudspeth, Hartley, and El Paso Counties
Wednesday, May 04, 2016
TPWD proposes the repeal of §§65.90 -65.94 and new §§65.90 -65.99 Concerning Chronic Wasting Disease - Movement of Deer Singeltary Comment Submission
*** Hartley County Sheep with Scrapie, and CWD in Hartley county ???
*** Friday, April 22, 2016
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer
SUNDAY, MAY 14, 2017
85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play
TUESDAY, DECEMBER 16, 2014
Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry TAHC TPWD CWD TSE PRION
SUNDAY, DECEMBER 14, 2014
TEXAS 84th Legislature commencing this January, deer breeders are expected to advocate for bills that will seek to further deregulate their industry
MONDAY, AUGUST 14, 2017
***> Singeltary on Texas Chronic Wasting Disease CWD TSE Prion History
THURSDAY, OCTOBER 04, 2018
Cervid to human prion transmission 5R01NS088604-04 Update
FRIDAY, DECEMBER 28, 2018
***> Chronic Wasting Disease CWD TSE Prion 2019 Where The Rubber Meets The Road
Saturday, December 15, 2018
***> ADRD Summit RFI Singeltary COMMENT SUBMISSION BSE, SCRAPIE, CWD, AND HUMAN TSE PRION DISEASE December 14, 2018
SATURDAY, JANUARY 5, 2019
Low levels of classical BSE infectivity in rendered fat tissue
FRIDAY, DECEMBER 14, 2018 MAD COW USA FLASHBACK
FRIDAY DECEMBER 14, 2018
THURSDAY, JANUARY 3, 2019
MAD COW USDA DISEASE BSE TSE Prion
THURSDAY, JANUARY 17, 2019
Missouri MDC reports 28 more deer with CWD TSE Prion total now stands at 103 confirmed cases
MONDAY, JANUARY 14, 2019
Evaluation of iatrogenic risk of CJD transmission associated with Chronic Wasting Disease TSE Prion in Texas TAHC TPWD
It is a dimension as vast as space and as timeless as infinity. It is the middle ground between light and shadow, between science and superstition, and it lies between the pit of man's fears and the summit of his knowledge. This is the dimension of imagination. It is NOT, an area which we call the Twilight Zone, but an area that believes junk science, and the very industries and lobbyist some Texas Hunters, the cervid industry, that insist on shoving the fake news down their throats, we call this ted nugent junk science, and in TEXAS, sometimes you just can't fix stupid, this is where the rubber meets the road, here's your sign!
chronic wasting disease cwd tse prion aka mad deer elk disease, if you consume a cwd tse prion positive cervid, then months, years, decades later, go on to have surgery, dental, ophthalmology, endoscopy, donate tissue, blood, organs, you then expose those medical theaters and tissue, blood, organs, that are incubating the infectious cwd tse prion disease, to everyone that comes in contact.
these are not memes, these are actual statements from hunters/industry in Texas about CWD tse prion.
God help them, and us...terry
''Got a call today from TPWD, I’ve got a mule deer that tested early positive for CWD. I’m soon to turn into a zombie because I have already been eating it. They advised not to consume any of the meat...too late! They want to come confiscate what meat is left once they get more results back from another lab.''
snip...
TUESDAY, JANUARY 1, 2019
CHILDHOOD EXPOSURE TO CADAVERIC DURA
***> 2018 URGENT DATA <***
***2018***
Cervid to human prion transmission
Kong, Qingzhong
Case Western Reserve University, Cleveland, OH, United States
Abstract
Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans.
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.
Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of humanized Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental human CWD samples will also be generated for Aim 3.
Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1.
Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental human CWD samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.
Public Health Relevance
There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.
Funding Agency
Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Project (R01)
Project #
5R01NS088604-04
Application #
9517118
Study Section
Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)
Program Officer Wong, May
Project Start 2015-09-30 Project End 2019-07-31 Budget Start 2018-08-01 Budget End 2019-07-31 Support Year 4 Fiscal Year 2018 Total Cost Indirect Cost Institution Name Case Western Reserve University Department Pathology Type Schools of Medicine DUNS # 077758407 City Cleveland State OH Country United States Zip Code 44106
Related projects
NIH 2018 R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University
NIH 2017 R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University
NIH 2016 R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University
NIH 2015 R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University $337,507
ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
here is the latest;
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
just out CDC...see;
Research Susceptibility of Human Prion Protein to Conversion by Chronic Wasting Disease Prions
Marcelo A. Barria
Adriana Libori, Gordon Mitchell, and Mark W. Head Author affiliations: National CJD Research and Surveillance Unit, University of Edinburgh, Edinburgh, Scotland, UK (M.A. Barria, A. Libori, M.W. Head); National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada (G. Mitchell) M. A. Barria et al.
ABSTRACT
Chronic wasting disease (CWD) is a contagious and fatal neurodegenerative disease and a serious animal health issue for deer and elk in North America. The identification of the first cases of CWD among free-ranging reindeer and moose in Europe brings back into focus the unresolved issue of whether CWD can be zoonotic like bovine spongiform encephalopathy. We used a cell-free seeded protein misfolding assay to determine whether CWD prions from elk, white-tailed deer, and reindeer in North America can convert the human prion protein to the disease-associated form.
We found that prions can convert, but the efficiency of conversion is affected by polymorphic variation in the cervid and human prion protein genes. In view of the similarity of reindeer, elk, and white-tailed deer in North America to reindeer, red deer, and roe deer, respectively, in Europe, a more comprehensive and thorough assessment of the zoonotic potential of CWD might be warranted.
Molecular Barriers to Zoonotic Transmission of Prions
Marcelo A. Barria, Aru Balachandran, Masanori Morita, Tetsuyuki Kitamoto, Rona Barron, Jean Manson, Richard Knight, James W. Ironside, and Mark W. Headcorresponding author
snip...
The conversion of human PrPC by CWD brain homogenate in PMCA reactions was less efficient when the amino acid at position 129 was valine rather than methionine.
***Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
snip...
However, we can say with confidence that under the conditions used here, none of the animal isolates tested were as efficient as C-type BSE in converting human PrPC, which is reassuring.
***Less reassuring is the finding that there is no absolute barrier to the conversion of human PrPC by CWD prions in a protocol using a single round of PMCA and an entirely human substrate prepared from the target organ of prion diseases, the brain.
Prion 2017 Conference Abstracts
CWD 2017 PRION 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
Subject: PRION 2017 CONFERENCE
DECIPHERING NEURODEGENERATIVE DISORDERS
VIDEO PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS
*** PRION 2017 CONFERENCE VIDEO
ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION
10. ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD DEER ELK DISEASE IN HUMANS, has it already happened, that should be the question...
''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)
EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ... See all authors
First published: 17 January 2018 https://doi.org/10.2903/j.efsa.2018.5132 ;
also, see;
8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. 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. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers.. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.
snip...
The tissue distribution of infectivity in CWD‐infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure.
zoonosis zoonotic cervid tse prion cwd to humans, preparing for the storm
***An alternative to modeling the species barrier is the cell-free conversion assay which points to CWD as the animal prion disease with the greatest zoonotic potential, after (and very much less than) BSE..116***
To date there is no direct evidence that CWD has been or can be transmitted from animals to humans.
However, initial findings from a laboratory research project funded by the Alberta Prion Research Institute (APRI) and Alberta Livestock Meat Agency (ALMA), and led by a Canadian Food Inspection Agency (CFIA) scientist indicate that CWD has been transmitted to cynomolgus macaques (the non-human primate species most closely related to humans that may be used in research), through both the intracranial and oral routes of exposure.
Both infected brain and muscle tissues were found to transmit disease.
Health Canada’s Health Products and Food Branch (HPFB) was asked to consider the impact of these findings on the Branch’s current position on CWD in health products and foods.
Summary and Recommendation:
snip...
Health Portfolio partners were recently made aware of initial findings from a research project led by a CFIA scientist that have demonstrated that cynomolgus macaques can be infected via intracranial exposure and oral gavage with CWD infected muscle.
These findings suggest that CWD, under specific experimental conditions, has the potential to cross the human species barrier, including by enteral feeding of CWD infected muscle.
*** WDA 2016 NEW YORK ***
We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions.
In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species.
***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions.
Student Presentations Session 2
The species barriers and public health threat of CWD and BSE prions
Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University
Chronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein.
These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans. On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species.
The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time.
We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations.
We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species.
***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD. Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders
TUESDAY, SEPTEMBER 12, 2017
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
SATURDAY, JANUARY 27, 2018
CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018
Subject: CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018
CHRONIC WASTING DISEASE CWD TSE PRION IS THE USA AND NORTH AMERICA'S MAD COW DISEASE.
THE USDA INC ET AL WORKED VERY HARD CONCEALING BSE TSE PRION IN CATTLE. they almost succeeded $$$
BUT CWD TSE PRION IN CERVIDS IS A DIFFERENT BEAST, THE COVER UP THERE, USDA INC COULD NOT CONTAIN.
SPORADIC CJD IS 85%+ OF ALL HUMAN TSE PRION DISEASE.
SPORADIC CJD HAS NOW BEEN LINKED TO TYPICAL AND ATYPICAL BSE, SCRAPIE, AND CWD.
SPORADIC/SPONTANEOUS TSE HAS NEVER BEEN PROVEN.
***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.***
CDC CWD TSE PRION UPDATE USA JANUARY 2018
As of January 2018, CWD in free-ranging deer, elk and/or moose has been reported in at least 22 states in the continental United States, as well as two provinces in Canada. In addition, CWD has been reported in reindeer and moose in Norway, and a small number of imported cases have been reported in South Korea. The disease has also been found in farmed deer and elk. CWD was first identified in captive deer in the late 1960s in Colorado and in wild deer in 1981. By the 1990s, it had been reported in surrounding areas in northern Colorado and southern Wyoming. Since 2000, the area known to be affected by CWD in free-ranging animals has increased to at least 22 states, including states in the Midwest, Southwest, and limited areas on the East Coast.. It is possible that CWD may also occur in other states without strong animal surveillance systems, but that cases haven’t been detected yet. Once CWD is established in an area, the risk can remain for a long time in the environment. The affected areas are likely to continue to expand. Nationwide, the overall occurrence of CWD in free-ranging deer and elk is relatively low. However, in several locations where the disease is established, infection rates may exceed 10 percent (1 in 10), and localized infection rates of more than 25 percent (1 in 4) have been reported. The infection rates among some captive deer can be much higher, with a rate of 79% (nearly 4 in 5) reported from at least one captive herd. As of January 2018, there were 186 counties in 22 states with reported CWD in free-ranging cervids...
Chronic Wasting Disease Among Free-Ranging Cervids by County, United States, January 2018
snip....
*** 2017-2018 CWD TSE Prion UPDATE
*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.
you can see more evidence here ;
Wednesday, May 24, 2017
PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1
WEDNESDAY, SEPTEMBER 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
PRION 2010
International Prion Congress: From agent to disease September 8–11, 2010 Salzburg, Austria
Transmission Studies
Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS
resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.
snip....
Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿
Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations
In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease
Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.
*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip... full text ;
> 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).***
SEE; Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Monday, May 23, 2011
CDC Assesses Potential Human Exposure to Prion Diseases Travel Warning
Public release date: 23-May-2011
Contact: Francesca Costanzo adajmedia@elsevier.com 215-239-3249 Elsevier Health Sciences
CDC assesses potential human exposure to prion diseases Study results reported in the Journal of the American Dietetic Association
Philadelphia, PA, May 23, 2011 – Researchers from the Centers for Disease Control and Prevention (CDC) have examined the potential for human exposure to prion diseases, looking at hunting, venison consumption, and travel to areas in which prion diseases have been reported in animals. Three prion diseases in particular – bovine spongiform encephalopathy (BSE or “Mad Cow Disease”), variant Creutzfeldt-Jakob disease (vCJD), and chronic wasting disease (CWD) – were specified in the investigation. The results of this investigation are published in the June issue of the Journal of the American Dietetic Association.
“While prion diseases are rare, they are generally fatal for anyone who becomes infected. More than anything else, the results of this study support the need for continued surveillance of prion diseases,” commented lead investigator Joseph Y. Abrams, MPH, National Center for Emerging and Zoonotic Infectious Diseases, CDC, Atlanta.”But it’s also important that people know the facts about these diseases, especially since this study shows that a good number of people have participated in activities that may expose them to infection-causing agents.”
Although rare, human prion diseases such as CJD may be related to BSE. Prion (proteinaceous infectious particles) diseases are a group of rare brain diseases that affect humans and animals. When a person gets a prion disease, brain function is impaired. This causes memory and personality changes, dementia, and problems with movement. All of these worsen over time. These diseases are invariably fatal. Since these diseases may take years to manifest, knowing the extent of human exposure to possible prion diseases could become important in the event of an outbreak.
CDC investigators evaluated the results of the 2006-2007 population survey conducted by the Foodborne Diseases Active Surveillance Network (FoodNet). This survey collects information on food consumption practices, health outcomes, and demographic characteristics of residents of the participating Emerging Infections Program sites. The survey was conducted in Connecticut, Georgia, Maryland, Minnesota, New Mexico, Oregon, and Tennessee, as well as five counties in the San Francisco Bay area, seven counties in the Greater Denver area, and 34 counties in western and northeastern New York.
Survey participants were asked about behaviors that could be associated with exposure to the agents causing BSE and CWD, including travel to the nine countries considered to be BSE-endemic (United Kingdom, Republic of Ireland, France, Portugal, Switzerland, Italy, the Netherlands, Germany, Spain) and the cumulative length of stay in each of those countries. Respondents were asked if they ever had hunted for deer or elk, and if that hunting had taken place in areas considered to be CWD-endemic (northeastern Colorado, southeastern Wyoming or southwestern Nebraska). They were also asked if they had ever consumed venison, the frequency of consumption, and whether the meat came from the wild.
The proportion of survey respondents who reported travel to at least one of the nine BSE endemic countries since 1980 was 29.5%. Travel to the United Kingdom was reported by 19.4% of respondents, higher than to any other BSE-endemic country. Among those who traveled, the median duration of travel to the United Kingdom (14 days) was longer than that of any other BSE-endemic country.. Travelers to the UK were more likely to have spent at least 30 days in the country (24.9%) compared to travelers to any other BSE endemic country. The prevalence and extent of travel to the UK indicate that health concerns in the UK may also become issues for US residents.
The proportion of survey respondents reporting having hunted for deer or elk was 18.5% and 1.2% reported having hunted for deer or elk in CWD-endemic areas. Venison consumption was reported by 67.4% of FoodNet respondents, and 88.6% of those reporting venison consumption had obtained all of their meat from the wild. These findings reinforce the importance of CWD surveillance and control programs for wild deer and elk to reduce human exposure to the CWD agent. Hunters in CWD-endemic areas are advised to take simple precautions such as: avoiding consuming meat from sickly deer or elk, avoiding consuming brain or spinal cord tissues, minimizing the handling of brain and spinal cord tissues, and wearing gloves when field-dressing carcasses.
According to Abrams, “The 2006-2007 FoodNet population survey provides useful information should foodborne prion infection become an increasing public health concern in the future. The data presented describe the prevalence of important behaviors and their associations with demographic characteristics. Surveillance of BSE, CWD, and human prion diseases are critical aspects of addressing the burden of these diseases in animal populations and how that may relate to human health.”
###
The article is “Travel history, hunting, and venison consumption related to prion disease exposure, 2006-2007 FoodNet population survey” by Joseph Y. Abrams, MPH; Ryan A. Maddox, MPH; Alexis R Harvey, MPH; Lawrence B. Schonberger, MD; and Ermias D. Belay, MD. It appears in the Journal of the American Dietetic Association, Volume 111, Issue 6 (June 2011) published by Elsevier.
In an accompanying podcast CDC’s Joseph Y. Abrams discusses travel, hunting, and eating venison in relation to prion diseases. It is available at http://adajournal.org/content/podcast. ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Joseph Y. Abrams, MPH, Ryan A. Maddox, MPH , Alexis R. Harvey, MPH , Lawrence B. Schonberger, MD , Ermias D. Belay, MD
Accepted 15 November 2010. Abstract Full Text PDF References .
Abstract
The transmission of bovine spongiform encephalopathy (BSE) to human beings and the spread of chronic wasting disease (CWD) among cervids have prompted concerns about zoonotic transmission of prion diseases. Travel to the United Kingdom and other European countries, hunting for deer or elk, and venison consumption could result in the exposure of US residents to the agents that cause BSE and CWD. The Foodborne Diseases Active Surveillance Network 2006-2007 population survey was used to assess the prevalence of these behaviors among residents of 10 catchment areas across the United States. Of 17,372 survey respondents, 19.4% reported travel to the United Kingdom since 1980, and 29.5% reported travel to any of the nine European countries considered to be BSE-endemic since 1980. The proportion of respondents who had ever hunted deer or elk was 18.5%, and 1.2% had hunted deer or elk in a CWD–endemic area. More than two thirds (67.4%) reported having ever eaten deer or elk meat. Respondents who traveled spent more time in the United Kingdom (median 14 days) than in any other BSE-endemic country. Of the 11,635 respondents who had consumed venison, 59.8% ate venison at most one to two times during their year of highest consumption, and 88.6% had obtained all of their meat from the wild. The survey results were useful in determining the prevalence and frequency of behaviors that could be important factors for foodborne prion transmission.
PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.
NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
Transmissible Spongiform Encephalopathies
Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY
BSE INQUIRY
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane
BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02)..
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
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It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
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In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
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In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
https://web.archive.org/web/20170126073306/http://collections..europarchive..org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf
PRION 2018 CONFERENCE
O3 Experimental studies on prion transmission barrier and TSE pathogenesis in large animals
Rosa Bolea(1), Acín C(1)Marín B(1), Hedman C(1), Raksa H(1), Barrio T(1), Otero A(1), LópezPérez O(1), Monleón E(1),Martín-Burriel(1), Monzón M(1), Garza MC(1), Filali H(1),Pitarch JL(1), Garcés M(1), Betancor M(1), GuijarroIM(1), GarcíaM(1), Moreno B(1),Vargas A(1), Vidal E(2), Pumarola M(2), Castilla J(3), Andréoletti O(4), Espinosa JC(5), Torres JM(5), Badiola JJ(1).
1Centro de Investigación en Encefalopatías y Enfermedades Transmisibles Emergentes, VeterinaryFaculty, Universidad de Zaragoza; Zaragoza,Spain.2 RTA, Centre de Recerca en Sanitat Animal (CReSA, IRTA-UAB) 3 4 INRA, ÉcoleVétérinaire, Toulouse, France.5CIC bioGUNE, Prion researchlab, Derio, Spain CISA- INIA, Valdeolmos, Madrid 28130, Spain.
Experimental transmission of Transmissible Spongiform Encephalopathies (TSE) has been understood and related with several factors that could modify the natural development of these diseases. In fact, the behaviour of the natural disease does not match exactly in each animal, being modified by parameters such as the age at infection, the genotype, the breed or the causative strain. Moreover, different TSE strains can target different animal species or tissues, what complicate the prediction of its transmissibility when is tested in a different species of the origin source. The aim of the experimental studies in large animals is to homogenize all those factors, trying to minimize as much as possible variations between individuals. These effects can be flattened by experimental transmission in mice, in which a specific strain can be selected after several passages. With this objective, several experimental studies in large animals have been developed by the presenter research team.
Classical scrapie agent has been inoculated in cow, with the aim of demonstrate the resistance or susceptibility of this species to the first well known TSE; Atypical scrapie has been inoculated in sheep (using several routes of infection), cow and pig, with the objective of evaluating the potential pathogenicity of this strain; Classical Bovine Spongiform Encephalopathy (BSE) has been inoculated in goats aiming to demonstrate if the genetic background of this species could protect against this strain; goat BSE and sheep BSE have been inoculated in goats and pigs respectively to evaluate the effect of species barrier; and finally atypical BSE has been inoculated in cattle to assess the transmissibility properties of this newly introduced strain.
Once the experiments have been carried out on large animal species, a collection of samples from animals studied were inoculated in different types of tg mice overexpressing PrPcin order to study the infectivity of the tissues, and also were studied using PMCA.
In summary, the parameters that have been controlled are the species, the strain, the route of inoculation, the time at infection, the genotype, the age, and the environmental conditions.
To date,
***> eleven of the atypical scrapie intracerebrally inoculated sheep have succumbed to atypical scrapie disease;
***> six pigs to sheep BSE;
***> one cow to classical scrapie;
***> nine goats to goat BSE and
***> five goats to classical BSE.
***> PrPSC has been demonstrated in all cases by immunohistochemistry and western blot.
=====> PRION CONFERENCE 2018
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.
Early preclinical detection of prions in the skin of prion-infected animals
Zerui Wang1,2, Matteo Manca3, Aaron Foutz4, Manuel V. Camacho1 , Gregory J. Raymond3, Brent Race3, Christina D. Orru3, Jue Yuan1 , Pingping Shen1,2, Baiya Li1,5, Yue Lang1,2, Johnny Dang1 , Alise Adornato1 , Katie Williams3, Nicholas R. Maurer1 , Pierluigi Gambetti1 , Bin Xu6, Witold Surewicz7, Robert B. Petersen1,8, Xiaoping Dong9, Brian S. Appleby1,4,10, Byron Caughey 3, Li Cui2, Qingzhong Kong1,4,10,11 & Wen-Quan Zou1,2,4,9,10,11
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Although the reasons for early and widespread presence of PrPSc in the skin remain unclear, possibilities include the spread of the prion inoculum itself, or endogenously replicating prions, from the brain through the peripheral nerves to the skin within the 2–3 weeks required for the first detection by our ultrasensitive
sPMCA and RT-QuIC assays. PrP seeding activity has been detected in the blood in the prion-infected hamsters and deer immediately after peripheral inoculation including oral, nasal, or blood route30. However, no reports have shown that PrPSc is consistently detectable in the blood of prion-infected hamsters within 2 weeks post intracerebral inoculation. Thus, the early spread of PrPSc from the brain-to-the skin in the intracerebrally 263K-inoculated hamsters is likely either not through the blood or, if initially from the blood, requires time-dependent concentration or replication in the skin to become detectable.
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Skin PrPSc may derive from urine or fecal prion contamination in addition to possible skin shedding due to scratching or biting each other. Indeed, scrapie infectivity was reported in the urine of prion-infected mice coincident with lymphocytic nephritis during their preclinical and clinical stages of prion infection35,36. It was also observed in their urine in intracerebrally inoculated hamsters even without any apparent inflammation21. In addition, deer with clinical CWD and mild to moderate nephritis were found to have sPMCA-detectable PrPSc and CWD-infectivity in urine22. Using sPMCA, PrPSc was detected in urine of ~80% of the hamsters intraperitoneally inoculated with 263K prions at the symptomatic stage23. Notably, PrPSc was detected in urine, but only at the terminal stage of disease in intracerebrally inoculated hamsters, except for a few days immediately after oral administration24. Similar to the observations by Gonzalez-Romero et al.23, Murayama et al. also found that not all infected hamsters had detectable urine PrPSc even at the terminal stage24. The skin PrPSc detected early in the intracerebrally infected hamsters, but not in the co-habitated-negative controls, at 2 wpi suggests that skin prions may not result from urine at the early stage of infection.
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.
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TUESDAY, MAY 31, 2011
Chronic Wasting Disease DOI: 10.1007/128_2011_159 # Springer-Verlag Berlin Heidelberg 2011
Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) A TOTAL FAILURE $$$
Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿
Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations
In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease
Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.
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.....
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
SUNDAY, DECEMBER 02, 2018
CWD TSE PRION, REGULATORY LEGISLATION, PAY TO PLAY, and The SPREAD of Chronic Wasting Disease
Prion Conference 2018
O5 Prion Disease in Dromedary Camels
Babelhadj B (1), Di Bari MA (2), Pirisinu L (2), Chiappini B (2), Gaouar SB (3), Riccardi G (2), Marcon S (2), Agrimi U (2), Nonno R (2), Vaccari G (2) (1) École Normale Supérieure Ouargla. Laboratoire de protection des écosystèmes en zones arides et semi arides University Kasdi Merbah Ouargla, Ouargla, Algeria; (2) Istituto Superiore di Sanità, Department of Food Safety, Nutrition and Veterinary Public Health, Rome, Italy (3) University Abou Bekr Bélkaid, Tlemcen, Algeria.
Prions are responsible for fatal and transmissible neurodegenerative diseases including CreutzfeldtJakob disease in humans, scrapie in small ruminants and bovine spongiform encephalopathy (BSE). Following the BSE epidemic and the demonstration of its zoonotic potential, general concerns have been raised on animal prions.
Here we report the identification of a prion disease in dromedary camels (Camelus dromedarius) in Algeria and designate it as Camel Prion Disease (CPD). In the last years, neurological symptoms have been observed in adult male and female dromedaries presented for slaughter at the Ouargla abattoir. The symptoms include weight loss, behavioral abnormalities and neurological symptoms such as tremors, aggressiveness, hyper-reactivity, typical down and upwards movements of the head, hesitant and uncertain gait, ataxia of the hind limbs, occasional falls and difficult getting up. During 2015 and 2016, symptoms suggestive of prion disease were observed in 3.1% of 2259 dromedaries presented at ante-mortem examination. Laboratory diagnosis was obtained in three symptomatic dromedaries, sampled in 2016 and 2017, by the detection of typical neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues.
Histopathological examination revealed spongiform change, gliosis and neuronal loss preferentially in grey matter of subcortical brain areas. Abundant PrPSc deposition was detected in the same brain areas by immunohistochemistry and PET-blot. Western blot analysis confirmed the presence of PK-resistant PrPSc, whose N-terminal cleaved PK-resistant core was characterized by a mono-glycosylated dominant form and by a distinctive N-terminal cleavage, different from that observed in BSE and scrapie.
PrPSc was also detected, by immunohistochemistry, in all sampled lymph nodes (cervical, prescapular and lumbar aortic) of the only animal from which they were collected.
The PRNP sequence of the two animals for which frozen material was available, showed 100% nucleotide identity with the PRNP sequence already reported for dromedary camel.
Overall, these data demonstrate the presence of a prion disease in dromedary camelswhose nature, origin and spread need further investigations. However, our preliminary observations on the rather high prevalence of symptomatic dromedaries and the involvement of lymphoid tissues, are consistent with CPD being an infectious disease. In conclusion, the emergence of a new prion disease in a livestock species of crucial importance for millions of people around the world, makes urgent to assess the risk for humans and to develop policies able to control the spread of the disease in animals and to minimize human exposure.
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.
***> IMPORTS AND EXPORTS <***
***SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN ***
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
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