Saturday, November 07, 2015

Pennsylvania 2015 September Minutes CWD Urine Scents

 
Sent: Saturday, November 07, 2015 11:54 AM
Subject: re-Pennsylvania 2015 September Minutes CWD Urine Scents
 

Pennsylvania 2015 September Minutes CWD Urine Scents
 
 
Current Status:

Chronic wasting disease (CWD) has been detected in three locations in Pennsylvania: a captive deer farm in Adams County (fall 2012); free-ranging deer in Blair and Bedford counties (2012 firearms season); and a captive deer farm in Jefferson county (spring 2014). Following the detection of CWD in both captive and free-ranging deer in Pennsylvania, an executive order was issued by the Game Commission to establish Disease Management Areas (DMAs). Within DMAs, rehabilitation of cervids (deer, elk and moose); the use or possession of cervid urine-based attractants in an outdoor setting; the removal of high-risk cervid parts; and the feeding of wild, free-ranging cervids are prohibited. Increased testing continues in these areas to determine the distribution of the disease. Newly confirmed cases will alter the boundaries of DMAs as the Game Commission continues to manage the disease and minimize its affect on free ranging cervids.
 
 
 
 
Pennsylvania 2015 September Minutes CWD Urine Scents
 
DAVID J. PUTNAM
 
PRESIDENT PUTNAM:
 
1 Thank you. The time period was such
 
2 that if we waited until today to approve it, they
 
3 would have had a very hard time getting it out by
 
4 October 1st. That's why the notational vote was
 
5 taken. At a prior meeting we asked the staff to look
 
6 into the possible regulations regarding deer urine as
 
7 a lure. And the staff has been working on that. I’m
 
8 going to ask Matt to give us a little update on where
 
9 we're at with that project.
 
10 MR. HOUGH:
 
11 Well, we have been working on that deer
 
12 urine ban and we actually have regulations that are
 
13 proposed sitting back in the Bureau of Wildlife
 
14 Protection. We are meeting with members of the deer
 
15 urine industry. Director Larouche has a meeting
 
16 scheduled with them to meet with them and look at some
 
17 of their operations trying to ensure that CWD prions
 
18 are not being spread around the Commonwealth by deer
 
19 urine. So Wayne's going to meet with them. And from
 
20 what I understand, the industry is now looking at a
 
21 way to certify that the animals that they use for
 
22 urine collection are CWD free and hopefully, that will
 
23 happen in the near future.
 
24 PRESIDENT PUTNAM:
 
 
end...tss
 
 
Pennsylvania 2015 September Minutes CWD Urine Scents
 
 
 
 
Greetings President Putnam et al at PA Gov,
 
I kindly submit
for your info.......kind regards, terry
 
 
***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.
 
========================
 
Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.
 
 
P.141: Abundant prion shedding in CWD-infected deer revealed by Realtime conversion
 
Edward A Hoover,1 Davin M Henderson,1 Nathaniel D Denkers,1 Candace K Mathiason,1 Matteo Manca,2,3 and Byron Caughey2 1Prion Research Center, Colorado State University; Fort Collins, CO USA; 2Laboratory of Persistent Viral Diseases, NI AID; Hamilton, MT USA; 3Department of Biomedical Sciences, University of Cagliari; Monserrato, Italy
 
Background/Introduction. Chronic wasting disease (CWD) is unique among prion diseases in its efficient lateral transmission in nature. While the presence of infectious prions in body fluids and excreta of infected cervids has been demonstrated by bioassay, the dynamics, magnitude, and consequences of prion shedding remain unknown. The present studies were undertaken to determine the kinetics, duration, and magnitude of prion shedding in infected white-tailed deer.
 
Materials and Methods. Longitudinal samples were collected from white-tailed deer over a 2-year span after either oral (n=11)] aerosol (n = 6) CWD exposure. The assay protocol employed phosphotungstic acid precipitation of either whole saliva or the pelleted fraction of urine to seed recombinant Syrian hamster prion PrP substrate in RT-QuIC reactions. Prion seeding activity was assayed in 8 replicates of each sample employing thioflavin T detection in a 96-well plate-based fluorometer. Prion seeding reaction rate was determined by taking the inverse of the time at which samples exceeded a threshold of 5 standard deviations above the mean fluorescence of negative controls (1/time to threshold). Seeding activity was quantitated by comparing the realtime conversion reaction rate to a standard curve derived from a reference bioassayed brain pool homogenate from deer with terminal CWD.
 
Results. We analyzed >200 longitudinally collected, blinded, then randomized saliva and urine samples from 17 CWDinfected and 3 uninfected white-tailed deer. We detected prion shedding as early as 3 months post exposure and sustained thereafter throughout the disease course in both aerosol and orally exposed deer. The incidence of non-specific false positive results from > 500 saliva and urine samples from negative control deer was 0.8%. By comparing real-time reaction rates for these body fluids to a bioassayed serially diluted brain control, we estimated that ≤1 ml of saliva or urine from pre-symptomatic infected deer constitutes a lethal infectious prion dose.
 
Conclusion. CWD prions are shed in saliva and urine of infected deer as early as 3 months post infection and throughout the subsequent >1.5 year course of infection. In current work we are examining the relationship of prionemia to excretion and the impact of excreted prion binding to surfaces and particulates in the environment.
 
Acknowledgments. Support: NIH-RO1-NS-061902; Morris Animal Foundation D12ZO-045
 
P.154: Urinary shedding of prions in Chronic Wasting Disease infected white-tailed deer
 
Nathaniel D Denkers,1 Davin M Henderson, 1 Candace K Mathiason,1 and Edward A Hoover1 1Prion Research Center, Department of Microbiology, Immunology, and Pathology, Colorado State University; Fort Collins, CO USA
 
Background/Introduction. Chronic wasting disease (CWD) is unique among prion diseases in its efficient lateral transmission in nature, yet the dynamics and magnitude of shedding and its immediate and long term consequences remain unknown. The present study was designed to determine the frequency and time span in which CWD prions are shed in urine from infected white-tailed deer using adapted real-time quaking-induced conversion (RT-QuIC) methodology.
 
Materials and Methods. Longitudinal urine samples were collected by free catch or catheterization over a 2-year period from oral-route infected [CWD+ (n = 11)] and aerosol-route-infected [CWD+ (n = 6); CWD- (n = 3)] white-tailed deer. High speed centrifugation pelleted material from 500 µl of urine was treated with sodium phosphotungstic acid (Na-PTA), resuspended in 0.05% SDS buffer, and used as seed in RT-QuIC assays employing recombinant Syrian hamster prion PrP substrate. Eight (8) replicates of each sample were run and prion seeding activity was recorded as thioflavin T binding fluorescence (480 nm emission) using a fluorimeter-shaker. Samples were considered positive if they crossed an established threshold (5 standard deviations above the negative mean fluorescence).
 
Results. In our oral-route inoculation studies, prion seeding activity has been demonstrated in urine collected at 6 months post-inoculation in 6 of 10 deer (11 of 80 replicates; 14%), and intermittently at later time points in all 11 CWD+ exposed deer. Our aerosol-route inoculation studies also showed prion seeding activity in urine collected at 6 months post-inoculation in 1 of 2 deer (3 of 16 replicates; 19%), and intermittently at later time points in 4 of 6 CWD+ exposed deer. Urine from sham-inoculated control deer and all baseline samples yielded 3 false-positive prion seeding activities (3 of 352 replicates; 0.8%).
 
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC) are shed in urine of infected deer as early as 6 months post inoculation and throughout the subsequent disease course. Further studies are in progress refining the real-time urinary prion assay sensitivity and we are examining more closely the excretion time frame, magnitude, and sample variables in relationship to inoculation route and prionemia in naturally and experimentally CWD-infected cervids.
 
Acknowledgments. Support: NIH: RO1-NS-061902 and Morris Animal Foundation: D12ZO-045 P.178: Longitudinal quantitative analysis of CWD prions shed in saliva of deer
 
Davin M Henderson, Nina Garbino, Nathaniel D Denkers, Amy V Nalls, Candace K Mathiason, and Edward A Hoover Prion Research Center, College of Veterinary Medicine and Biomedical Sciences, Colorado State University; Fort Collins, CO USA
 
Background/Introduction. Chronic Wasting Disease (CWD) is an emergent rapidly spreading fatal prion disease of cervids (deer, elk and moose). CWD has now been identified in 22 States (including two new states within the last year), 2 Canadian provinces, and South Korea. Shedding of infectious prions in excreta (saliva, urine, feces) may be an important factor in CWD transmission. Here we apply an adapted version of a rapid in vitro assay [real-time quaking-induced conversion (RT-QuIC)] to determine the time of onset, length, pattern, and magnitude of prion shedding in saliva of infected deer.
 
Materials and Methods. The RT-QuIC assay was performed as previously described in Henderson et al. PLoS-One (2013). Saliva samples were quantitated by comparison to a RT-QuIC reaction rate standard curve of a bioassayed obex sample from a terminally ill cervid.
 
Results. To better understand the onset and length of CWD prion shedding we analyzed >150 longitudinally collected, blinded, then randomized saliva samples from 17 CWD-infected and 3 uninfected white-tailed deer. We observed prion shedding, as detected by the RT-QuIC assay, as early as 3 months from inoculation and sustained shedding throughout the disease course in both aerosol and orally exposed deer. We estimated the infectious lethal dose of prions shed in saliva from infected deer by comparing real-time reaction rates of saliva samples to a bioassayed serially diluted brain control. Our results indicate that as little as 1 ml of saliva from pre-symptomatic infected deer constitutes a lethal CWD prion dose.
 
Conclusions. During the pre-symptomatic stage of CWD infection and throughout the course of disease deer may be shedding multiple LD50 doses per day in their saliva. CWD prion shedding through saliva and excreta may account for the unprecedented spread of this prion disease in nature.
 
Acknowledgments. Supported by NIH grant RO1-NS-061902 and grant D12ZO-045 from the Morris Animal Foundation.
 
 
Sunday, September 13, 2015
 
urine, feces, and chronic wasting disease cwd tse prion risk factors, loading up the environment
 
 
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
 
Date: Sat, 20 Jul 2002 09:43:10 -0700
 
From: "Terry S. Singeltary Sr."
 
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
 
Date: Sat, 25 May 2002 18:41:46 -0700
 
From: "Terry S. Singeltary Sr."
 
Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de
 
######## Bovine Spongiform Encephalopathy #########
 
MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
 
snip...
 
now, what about those 'deer scents' of 100% urine', and the prion that is found in urine, why not just pass the prion with the urine to other deer...
 
Mrs. Doe Pee Doe in Estrus Model FDE1 Mrs. Doe Pee's Doe in Estrus is made from Estrus urine collected at the peak of the rut, blended with Fresh Doe Urine for an extremely effective buck enticer. Use pre-rut before the does come into heat. Use during full rut when bucks are most active. Use during post-rut when bucks are still actively looking for does. 1 oz.
 
 
ELK SCENT/SPRAY BOTTLE
 
*
 
Works anytime of the year *
 
100 % Cow Elk-in-Heat urine (2oz.) *
 
Economical - mix with water in spray mist bottle *
 
Use wind to your advantage
 
Product Code WP-ESB $9.95
 
 
prions in urine?
 
[PDF] A URINE TEST FOR THE IN-VIVO DIAGNOSIS OF PRION DISEASES
 
 
Terry S. Singeltary Sr.
 
Thank You For Your Comments Thank you for submitting your comments on the Draft Deer Management Plan.
 
 
DRAFT Virginia Deer Management Plan 2015-2024 (bans urine scents do to CWD 2015)
 
 
Saturday, January 31, 2015
 
European red deer (Cervus elaphus elaphus) are susceptible to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route
 
 
I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...
 
======
 
In the USA, under the Food and Drug Administrations 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.
 
======
 
31 Jan 2015 at 20:14 GMT
 
*** Ruminant feed ban for cervids in the United States? ***
 
31 Jan 2015 at 20:14 GMT
 
 
 
 Monday, October 26, 2015
 
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
 
 
 
 
Sent: Thursday, November 05, 2015 9:18 PM
Subject: [BSE-L] TPW Commission Adopts Interim Deer Breeder Movement Rules
 
News Release Media Contact: Steve Lightfoot, 512-389-4701, steve.lightfoot@tpwd.texas.gov
 
Nov. 5, 2015
 
TPW Commission Adopts Interim Deer Breeder Movement Rules AUSTIN – The Texas Parks and Wildlife Commission at its Thursday public hearing adopted interim rules for captive deer movement requirements to provide the deer breeding industry with continuity and consistency through the 2015-16 hunting season.
 
The interim rules will replace emergency rules currently in effect that were developed as appropriate measures to protect white-tailed and mule deer in Texas in response to the discovery of chronic wasting disease (CWD) in a captive deer breeding facility in Medina County this summer. Those emergency rules would have expired prior to the end of deer season.
 
The new rules allow all deer breeders that met previous movement qualifications, except a CWD-positive facility, the opportunity to continue to move and release breeder deer in an effort to balance the needs of the many and varied landowner, management, and deer hunting interests in the state. The interim rules increase the probability of detecting CWD in permitted deer breeding facilities and release sites where it exists, which would allow TPWD and TAHC to promptly implement a response plan designed to contain the disease to that immediate area.
 
A significant component of the new rules is the requirement that breeder deer may be released (liberated) only on release sites that are surrounded by a fence of at least seven feet in height and that is capable of retaining deer at all times.
 
The interim rules are adopted by the Commission as temporary measures with an Aug. 31, 2016 expiration. The Texas Parks and Wildlife Department plans an extensive review of the interim rules following the conclusion of the current hunting season, and with input from stakeholders will develop new proposed rules for Commission consideration next spring.
 
In conjunction with the review process, TPWD is planning a symposium in January involving nationally-recognized authorities on CWD science and research. Among the issues to be discussed include live testing options for CWD.
 
SL 2015-11-05
 
 
Interim Chronic Wasting Disease Response Rules Comment online through 07:00 a.m. November 5, 2015
 
Interim Chronic Wasting Disease Response Rules
 
 
 
I think the cwd rules could have been more stringent in a variety of ways, but will agree for now with what is proposed. I still think the testing should be increased across the board. I think there is still too much catering to the industry. see why I think this below and latest peer review on cwd sound science. ...
 
Wednesday, October 28, 2015
 
Texas' wild deer herd must be protected
 
 
 
Terry S. Singeltary Sr. Your opinions and comments have been submitted successfully. Thank you for participating in the TPWD regulatory process.
 
Wednesday, October 28, 2015
 
Interim Chronic Wasting Disease Response Rules Comment online through 07:00 a.m. November 5, 2015
 
 
I am pro-hunt, pro-gun, and I am a meat eater. I am however, anti-stupid, and there is enough of that going around. I do not want prions on or in my meat I eat, or in the hospitals. you should not either, tse prions can kill you, killed my mom, i.e. the Hiedenhain Variant of Creutzfeldt Jakob Disease, confirmed. I submit the following tse prion science for your use. while legislating laws about the cwd tse prion disease, one must have the latest sound science, and some of the old science, ...so soon we can forget. I asked someone recently, what sort of hunting legacy do you want to leave your children, did you want to have where all you have are blind, slobbering, drooling, stumbling, or maybe even healthy looking subclinical cwd infected cervid, to go on and expose who knows what (cause cwd is spreading, it has mutated, and nobody can seem to stop it so far), but is this what we want to leave our children? the only answer I ever seem to get from anyone in the industry, is just let cwd take care of itself. how is that working out for us so far? my opinion, until we have a 100% validated live test for cwd tse prion (and we don’t yet)
 
 
in my opinion, the scorched earth policy is the only policy available. and then what do you do with the land? ($$$) this cwd tse prion must be stopped. the vertical and lateral transmission of this cwd tse prion agent amongst cervids, if cwd jumps species (if it has not already), and transmits the same ways vertical and lateral in other species, and the other species are as susceptible from so many different routes and sources, simply put, we’re screwed, if we are not screwed already, I mean the mad cow bse tse prion been out of the barn here in North America for Decades, just saying. I am not trying to scare anyone, I am simply presenting the facts, you must make your own decision or not. we have ignored these tse prion disease way too long. right now seems policy is just to change the name of them, and call it a day, (that would take to long to explain i.e. ibnc bse tse or the infamous sporadic ffi or sporadic gss that is not tied to any family link...GET OUT OF HERE...iatrogenic maybe from ffi or gss, maybe) but to let lobbyist and their legislators make up the science and the policy making for cwd tse pron there from, and continue to ignore sound science, is a terrible mistake in my opinion. like I said, if and when, a tse mutates into humans like cwd in cervid, we are screwed. we have been extremely lucky so for, with the _documented_ body bag count, with the science to date i.e. the UKBSEnvCJD only theory (I have highly disputed this from day one, and since then have been proven correct by science, but on paper, it’s the same old shit still i.e. UKBSEnvCJD only theory). CHRONIC WASTING DISEASE CWD TSE
 
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
 
you cannot cook the TSE prion disease out of meat.
 
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
 
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
 
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
 
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.
 
you can bury it and it will not go away.
 
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
 
it’s not your ordinary pathogen you can just cook it out and be done with. that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.
 
in my opinion, the scorched earth policy is the only policy available. and then what do you do with the land? ($$$)
 
this cwd tse prion must be stopped. the vertical and lateral transmission of this cwd tse prion agent amongst cervids, if cwd jumps species (if it has not already), and transmits the same ways vertical and lateral in other species, and the other species are as susceptible from so many different routes and sources, simply put, we’re screwed, if we are not screwed already, I mean the mad cow bse tse prion been out of the barn here in North America for Decades, just saying.
 
snip...see updated peer review cwd tse prion science ;
 
Wednesday, October 28, 2015
 
Sanders: Texas' wild deer herd must be protected
 
 
Interim Chronic Wasting Disease Response Rules Comment online through 07:00 a.m. November 5, 2015
 
Interim Chronic Wasting Disease Response Rules
 
 
I think the cwd rules could have been more stringent in a variety of ways, but will agree for now with what is proposed. I still think the testing should be increased across the board. I think there is still too much catering to the industry. see why I think this below and latest peer review on cwd sound science. ...
 
Wednesday, October 28, 2015
 
Texas' wild deer herd must be protected
 
 
Terry S. Singeltary Sr. Your opinions and comments have been submitted successfully. Thank you for participating in the TPWD regulatory process.
 
Wednesday, October 28, 2015
 
Interim Chronic Wasting Disease Response Rules Comment online through 07:00 a.m. November 5, 2015
 
 
*** PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS ***
 
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
 
O18
 
Zoonotic Potential of CWD Prions
 
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA
 
***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***
 
P.105: RT-QuIC models trans-species prion transmission
 
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA
 
Additionally, human rPrP was competent for conversion by CWD and fCWD.
 
***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***
 
 
From: Terry S. Singeltary Sr.
 
Sent: Saturday, November 15, 2014 9:29 PM
 
To: Terry S. Singeltary Sr.
 
Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984
 
THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE
 
R. G. WILL
 
1984
 
*** 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). (SEE LINK IN REPORT HERE...TSS) PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
 
snip...
 
 
*** 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).***
 
 
*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.
 
 
now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”
 
From: TSS (216-119-163-189.ipset45.wt.net)
 
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
 
Date: September 30, 2002 at 7:06 am PST
 
From: "Belay, Ermias"
 
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
 
Sent: Monday, September 30, 2002 9:22 AM
 
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
 
Dear Sir/Madam,
 
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
 
Ermias Belay, M.D. Centers for Disease Control and Prevention
 
-----Original Message-----
 
From: Sent: Sunday, September 29, 2002 10:15 AM
 
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
 
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
 
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
 
Thursday, April 03, 2008
 
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
 
snip...
 
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
 
snip... full text ;
 
 
July's Milwaukee Journal Sentinel article did prod state officials to ask CDC to investigate the cases of the three men who shared wild game feasts. The two men the CDC is still investigating were 55 and 66 years old. But there's also Kevin Boss, a Minnesota hunter who ate Barron County venison and died of CJD at 41. And there's Jeff Schwan, whose Michigan Tech fraternity brothers used to bring venison sausage back to the frat house. His mother, Terry, says that in May 2001, Jeff, 26, began complaining about his vision. A friend noticed misspellings in his e-mail, which was totally unlike him. Jeff began losing weight. He became irritable and withdrawn. By the end of June, he couldn't remember the four-digit code to open the garage door or when and how to feed his parents' cats. At a family gathering in July, he stuck to his parents and girlfriend, barely talking. "On the night we took him to the hospital, he was speaking like he was drunk or high and I noticed his pupils were so dilated I couldn't see the irises," his mother says. By then, Jeff was no longer able to do even simple things on his computer at work, and "in the hospital, he couldn't drink enough water." When he died on September 27, 2001, an autopsy confirmed he had sporadic CJD.
 
In 2000, Belay looked into three CJD cases reported by The Denver Post, two hunters who ate meat from animals killed in Wyoming and the daughter of a hunter who ate venison from a plant that processed Colorado elk. All three died of CJD before they were 30 years old. The CDC asked the USDA to kill 1,000 deer and elk in the area where the men hunted. Belay and others reported their findings in the Archives of Neurology, writing that although "circumstances suggested a link between the three cases and chronic wasting disease, they could find no 'causal' link." Which means, says Belay, "not a single one of those 1,000 deer tested positive for CWD. For all we know, these cases may be CWD. What we have now doesn't indicate a connection. That's reassuring, but it would be wrong to say it will never happen."
 
So far, says NIH researcher Race, the two Wisconsin cases pinpointed by the newspaper look like spontaneous CJD. "But we don't know how CWD would look in human brains. It probably would look like some garden-variety sporadic CJD." What the CDC will do with these cases and four others (three from Colorado and Schwan from Upper Michigan), Race says, is "sequence the prion protein from these people, inject it into mice and wait to see what the disease looks like in their brains. That will take two years."
 
CJD is so rare in people under age 30, one case in a billion (leaving out medical mishaps), that four cases under 30 is "very high," says Colorado neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in the newspaper], six cases of CJD in people associated with venison is very, very high." Only now, with Mary Riley, there are at least seven, and possibly eight, with Steve, her dining companion. "It's not critical mass that matters," however, Belay says. "One case would do it for me." The chance that two people who know each other would both contact CJD, like the two Wisconsin sportsmen, is so unlikely, experts say, it would happen only once in 140 years.
 
Given the incubation period for TSEs in humans, it may require another generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting disease pass into humans? We'll be able to answer that in 2022," says Race. Meanwhile, the state has become part of an immense experiment.
 
 
I urge everyone to watch this video closely...terry
 
*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***
 
 
*** 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).***
 
 
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
 
Emmanuel Comoy, Jacqueline Mikol, Val erie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
 
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. *** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, ***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold longe incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), ***is the third potentially zoonotic PD (with BSE and L-type BSE), ***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
 
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***thus questioning the origin of human sporadic cases...TSS
 
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Thursday, September 10, 2015
 
25th Meeting of the Transmissible Spongiform Encephalopathies Advisory Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015
 
 
PL1
 
Using in vitro prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.
 
Claudio Soto
 
Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.
 
Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.
 
=========================
 
***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.
 
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Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.
 
 
see ;
 
 
 
 
 
 
98 | Veterinary Record | January 24, 2015
 
EDITORIAL
 
Scrapie: a particularly persistent pathogen
 
Cristina Acín
 
Resistant prions in the environment have been the sword of Damocles for scrapie control and eradication. Attempts to establish which physical and chemical agents could be applied to inactivate or moderate scrapie infectivity were initiated in the 1960s and 1970s,with the first study of this type focusing on the effect of heat treatment in reducing prion infectivity (Hunter and Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate the prion protein are based on the method developed by Kimberlin and collaborators (1983). This procedure consists of treatment with 20,000 parts per million free chlorine solution, for a minimum of one hour, of all surfaces that need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so on). Despite this, veterinarians and farmers may still ask a range of questions, such as ‘Is there an official procedure published somewhere?’ and ‘Is there an international organisation which recommends and defines the exact method of scrapie decontamination that must be applied?’
 
From a European perspective, it is difficult to find a treatment that could be applied, especially in relation to the disinfection of surfaces in lambing pens of affected flocks. A 999/2001 EU regulation on controlling spongiform encephalopathies (European Parliament and Council 2001) did not specify a particular decontamination measure to be used when an outbreak of scrapie is diagnosed. There is only a brief recommendation in Annex VII concerning the control and eradication of transmissible spongiform encephalopathies (TSE s).
 
Chapter B of the regulation explains the measures that must be applied if new caprine animals are to be introduced to a holding where a scrapie outbreak has previously been diagnosed. In that case, the statement indicates that caprine animals can be introduced ‘provided that a cleaning and disinfection of all animal housing on the premises has been carried out following destocking’.
 
Issues around cleaning and disinfection are common in prion prevention recommendations, but relevant authorities, veterinarians and farmers may have difficulties in finding the specific protocol which applies. The European Food and Safety Authority (EFSA ) published a detailed report about the efficacy of certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and even a formulation of copper or iron metal ions in combination with hydrogen peroxide, against prions (EFSA 2009). The report was based on scientific evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006, Solassol and others 2006) but unfortunately the decontamination measures were not assessed under outbreak conditions.
 
The EFSA Panel on Biological Hazards recently published its conclusions on the scrapie situation in the EU after 10 years of monitoring and control of the disease in sheep and goats (EFSA 2014), and one of the most interesting findings was the Icelandic experience regarding the effect of disinfection in scrapie control. The Icelandic plan consisted of: culling scrapie-affected sheep or the whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of stables, sheds, barns and equipment with high pressure washing followed by cleaning with 500 parts per million of hypochlorite; drying and treatment with 300 ppm of iodophor; and restocking was not permitted for at least two years. Even when all of these measures were implemented, scrapie recurred on several farms, indicating that the infectious agent survived for years in the environment, even as many as 16 years after restocking (Georgsson and others 2006).
 
In the rest of the countries considered in the EFSA (2014) report, recommendations for disinfection measures were not specifically defined at the government level. In the report, the only recommendation that is made for sheep is repopulation with sheep with scrapie-resistant genotypes. This reduces the risk of scrapie recurrence but it is difficult to know its effect on the infection.
 
Until the EFSA was established (in May 2003), scientific opinions about TSE s were provided by the Scientific Steering Committee (SSC) of the EC, whose advice regarding inactivation procedures focused on treating animal waste at high temperatures (150°C for three hours) and high pressure alkaline hydrolysis (SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe working and the prevention of TSE infection. Annex C of the ACDP report established that sodium hypochlorite was considered to be effective, but only if 20,000 ppm of available chlorine was present for at least one hour, which has practical limitations such as the release of chlorine gas, corrosion, incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its active chemicals and the stability of dilutions (ACDP 2009).
 
In an international context, the World Organisation for Animal Health (OIE) does not recommend a specific disinfection protocol for prion agents in its Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General recommendations on disinfection and disinsection (OIE 2014), focuses on foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on prion disinfection. Nevertheless, the last update published by the OIE on bovine spongiform encephalopathy (OIE 2012) indicates that few effective decontamination techniques are available to inactivate the agent on surfaces, and recommends the removal of all organic material and the use of sodium hydroxide, or a sodium hypochlorite solution containing 2 per cent available chlorine, for more than one hour at 20ºC.
 
The World Health Organization outlines guidelines for the control of TSE s, and also emphasises the importance of mechanically cleaning surfaces before disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO 1999).
 
Finally, the relevant agencies in both Canada and the USA suggest that the best treatments for surfaces potentially contaminated with prions are sodium hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution, while most commercial household bleaches contain 5.25 per cent sodium hypochlorite. It is therefore recommended to dilute one part 5.25 per cent bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency 2013).
 
So what should we do about disinfection against prions? First, it is suggested that a single protocol be created by international authorities to homogenise inactivation procedures and enable their application in all scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available chlorine seems to be the procedure used in most countries, as noted in a paper summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015). But are we totally sure of its effectiveness as a preventive measure in a scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease be needed?
 
What we can conclude is that, if we want to fight prion diseases, and specifically classical scrapie, we must focus on the accuracy of diagnosis, monitoring and surveillance; appropriate animal identification and control of movements; and, in the end, have homogeneous and suitable protocols to decontaminate and disinfect lambing barns, sheds and equipment available to veterinarians and farmers. Finally, further investigations into the resistance of prion proteins in the diversity of environmental surfaces are required.
 
References
 
snip...
 
98 | Veterinary Record | January 24, 2015
 
 
Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination
 
Steve A. C. Hawkins, MIBiol, Pathology Department1, Hugh A. Simmons, BVSc MRCVS, MBA, MA Animal Services Unit1, Kevin C. Gough, BSc, PhD2 and Ben C. Maddison, BSc, PhD3 + Author Affiliations
 
1Animal and Plant Health Agency, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK 2School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK 3ADAS UK, School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK E-mail for correspondence: ben.maddison@adas.co.uk Abstract Scrapie of sheep/goats and chronic wasting disease of deer/elk are contagious prion diseases where environmental reservoirs are directly implicated in the transmission of disease. In this study, the effectiveness of recommended scrapie farm decontamination regimens was evaluated by a sheep bioassay using buildings naturally contaminated with scrapie. Pens within a farm building were treated with either 20,000 parts per million free chorine solution for one hour or were treated with the same but were followed by painting and full re-galvanisation or replacement of metalwork within the pen. Scrapie susceptible lambs of the PRNP genotype VRQ/VRQ were reared within these pens and their scrapie status was monitored by recto-anal mucosa-associated lymphoid tissue. All animals became infected over an 18-month period, even in the pen that had been subject to the most stringent decontamination process. These data suggest that recommended current guidelines for the decontamination of farm buildings following outbreaks of scrapie do little to reduce the titre of infectious scrapie material and that environmental recontamination could also be an issue associated with these premises.
 
SNIP...
 
Discussion
 
Thorough pressure washing of a pen had no effect on the amount of bioavailable scrapie infectivity (pen B). The routine removal of prions from surfaces within a laboratory setting is treatment for a minimum of one hour with 20,000 ppm free chlorine, a method originally based on the use of brain macerates from infected rodents to evaluate the effectiveness of decontamination (Kimberlin and others 1983). Further studies have also investigated the effectiveness of hypochlorite disinfection of metal surfaces to simulate the decontamination of surgical devices within a hospital setting. Such treatments with hypochlorite solution were able to reduce infectivity by 5.5 logs to lower than the sensitivity of the bioassay used (Lemmer and others 2004). Analogous treatment of the pen surfaces did not effectively remove the levels of scrapie infectivity over that of the control pens, indicating that this method of decontamination is not effective within a farm setting. This may be due to the high level of biological matrix that is present upon surfaces within the farm environment, which may reduce the amount of free chlorine available to inactivate any infectious prion. Remarkably 1/5 sheep introduced into pen D had also became scrapie positive within nine months, with all animals in this pen being RAMALT positive by 18 months of age. Pen D was no further away from the control pen (pen A) than any of the other pens within this barn. Localised hot spots of infectivity may be present within scrapie-contaminated environments, but it is unlikely that pen D area had an amount of scrapie contamination that was significantly different than the other areas within this building. Similarly, there were no differences in how the biosecurity of pen D was maintained, or how this pen was ventilated compared with the other pens. This observation, perhaps, indicates the slower kinetics of disease uptake within this pen and is consistent with a more thorough prion removal and recontamination. These observations may also account for the presence of inadvertent scrapie cases within other studies, where despite stringent biosecurity, control animals have become scrapie positive during challenge studies using barns that also housed scrapie-affected animals (Ryder and others 2009). The bioassay data indicate that the exposure of the sheep to a farm environment after decontamination efforts thought to be effective in removing scrapie is sufficient for the animals to become infected with scrapie. The main exposure routes within this scenario are likely to be via the oral route, during feeding and drinking, and respiratory and conjunctival routes. It has been demonstrated that scrapie infectivity can be efficiently transmitted via the nasal route in sheep (Hamir and others 2008), as is the case for CWD in both murine models and in white-tailed deer (Denkers and others 2010, 2013). Recently, it has also been demonstrated that CWD prions presented as dust when bound to the soil mineral montmorillonite can be infectious via the nasal route (Nichols and others 2013). When considering pens C and D, the actual source of the infectious agent in the pens is not known, it is possible that biologically relevant levels of prion survive on surfaces during the decontamination regimen (pen C). With the use of galvanising and painting (pen D) covering and sealing the surface of the pen, it is possible that scrapie material recontaminated the pens by the movement of infectious prions contained within dusts originating from other parts of the barn that were not decontaminated or from other areas of the farm.
 
Given that scrapie prions are widespread on the surfaces of affected farms (Maddison and others 2010a), irrespective of the source of the infectious prions in the pens, this study clearly highlights the difficulties that are faced with the effective removal of environmentally associated scrapie infectivity. This is likely to be paralleled in CWD which shows strong similarities to scrapie in terms of both the dissemination of prions into the environment and the facile mode of disease transmission. These data further contribute to the understanding that prion diseases can be highly transmissible between susceptible individuals not just by direct contact but through highly stable environmental reservoirs that are refractory to decontamination.
 
The presence of these environmentally associated prions in farm buildings make the control of these diseases a considerable challenge, especially in animal species such as goats where there is lack of genetic resistance to scrapie and, therefore, no scope to re-stock farms with animals that are resistant to scrapie.
 
Scrapie Sheep Goats Transmissible spongiform encephalopathies (TSE) Accepted October 12, 2014. Published Online First 31 October 2014
 
 
Monday, November 3, 2014
 
Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination
 
 
PPo3-22:
 
Detection of Environmentally Associated PrPSc on a Farm with Endemic Scrapie
 
Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University of Nottingham; Sutton Bonington, Loughborough UK
 
Key words: scrapie, evironmental persistence, sPMCA
 
Ovine scrapie shows considerable horizontal transmission, yet the routes of transmission and specifically the role of fomites in transmission remain poorly defined. Here we present biochemical data demonstrating that on a scrapie-affected sheep farm, scrapie prion contamination is widespread. It was anticipated at the outset that if prions contaminate the environment that they would be there at extremely low levels, as such the most sensitive method available for the detection of PrPSc, serial Protein Misfolding Cyclic Amplification (sPMCA), was used in this study. We investigated the distribution of environmental scrapie prions by applying ovine sPMCA to samples taken from a range of surfaces that were accessible to animals and could be collected by use of a wetted foam swab. Prion was amplified by sPMCA from a number of these environmental swab samples including those taken from metal, plastic and wooden surfaces, both in the indoor and outdoor environment. At the time of sampling there had been no sheep contact with these areas for at least 20 days prior to sampling indicating that prions persist for at least this duration in the environment. These data implicate inanimate objects as environmental reservoirs of prion infectivity which are likely to contribute to disease transmission.
 
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
 
Title: Transmission of scrapie prions to primate after an extended silent incubation period
 
Authors
 
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire, Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron, Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item Deslys, Jean-Philippe -
 
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015 Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E., Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C., Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J. 2015. Transmission of scrapie prions to primate after an extended silent incubation period. Scientific Reports. 5:11573. Interpretive Summary: The transmissible spongiform encephalopathies (also called prion diseases) are fatal neurodegenerative diseases that affect animals and humans. The agent of prion diseases is a misfolded form of the prion protein that is resistant to breakdown by the host cells. Since all mammals express prion protein on the surface of various cells such as neurons, all mammals are, in theory, capable of replicating prion diseases. One example of a prion disease, bovine spongiform encephalopathy (BSE; also called mad cow disease), has been shown to infect cattle, sheep, exotic undulates, cats, non-human primates, and humans when the new host is exposed to feeds or foods contaminated with the disease agent. The purpose of this study was to test whether non-human primates (cynomologous macaque) are susceptible to the agent of sheep scrapie. After an incubation period of approximately 10 years a macaque developed progressive clinical signs suggestive of neurologic disease. Upon postmortem examination and microscopic examination of tissues, there was a widespread distribution of lesions consistent with a transmissible spongiform encephalopathy. ***This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.
 
Technical Abstract: Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the past decades, c-BSE's zoonotic potential has been the driving force in establishing extensive protective measures for animal and human health. In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
 
***This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
 
 
why do we not want to do TSE transmission studies on chimpanzees $
 
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
 
snip...
 
R. BRADLEY
 
 
Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasized by the finding that some strains of scrapie produce lesions identical to the once which characterize the human dementias"
 
Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the scrapie problem urgent if the sheep industry is not to suffer grievously.
 
snip...
 
76/10.12/4.6
 
 
Saturday, January 31, 2015
 
European red deer (Cervus elaphus elaphus) are susceptible to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route
 
 
I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...
 
======
 
In the USA, under the Food and Drug Administrations 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.
 
======
 
31 Jan 2015 at 20:14 GMT
 
*** Ruminant feed ban for cervids in the United States? ***
 
31 Jan 2015 at 20:14 GMT
 
 
Monday, October 26, 2015
 
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
 
 
Sunday, October 25, 2015
 
USAHA Detailed Events Schedule – 119th USAHA Annual Meeting CAPTIVE LIVESTOCK CWD SCRAPIE TSE PRION
 
 
Monday, October 26, 2015
 
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
 
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Title: Transmission of scrapie prions to primate after an extended silent incubation period Authors
 
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire, Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron, Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item Deslys, Jean-Philippe -
 
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015 Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E., Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C., Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J. 2015. Transmission of scrapie prions to primate after an extended silent incubation period. Scientific Reports. 5:11573. Interpretive Summary: The transmissible spongiform encephalopathies (also called prion diseases) are fatal neurodegenerative diseases that affect animals and humans. The agent of prion diseases is a misfolded form of the prion protein that is resistant to breakdown by the host cells. Since all mammals express prion protein on the surface of various cells such as neurons, all mammals are, in theory, capable of replicating prion diseases. One example of a prion disease, bovine spongiform encephalopathy (BSE; also called mad cow disease), has been shown to infect cattle, sheep, exotic undulates, cats, non-human primates, and humans when the new host is exposed to feeds or foods contaminated with the disease agent. The purpose of this study was to test whether non-human primates (cynomologous macaque) are susceptible to the agent of sheep scrapie. After an incubation period of approximately 10 years a macaque developed progressive clinical signs suggestive of neurologic disease. Upon postmortem examination and microscopic examination of tissues, there was a widespread distribution of lesions consistent with a transmissible spongiform encephalopathy. This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.
 
Technical Abstract: Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the past decades, c-BSE's zoonotic potential has been the driving force in establishing extensive protective measures for animal and human health. In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
 
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Title: Transmission of the agent of sheep scrapie to deer results in PrPSc with two distinct molecular profiles Authors
 
item Greenlee, Justin item Moore, Sarah - item Smith, Jodi item West Greenlee, Mary - item Kunkle, Robert
 
Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: March 31, 2015 Publication Date: May 25, 2015 Citation: Greenlee, J., Moore, S.J., Smith, J.., West Greenlee, M.H., Kunkle, R. 2015.
 
Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease and distinct from the scrapie inoculum. Prion 2015. p. S62. Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes reveal PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile type readily passes to deer.
 
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease Authors
 
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle, Robert item West Greenlee, M -
 
Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 Publication Date: N/A
 
Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.
 
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Title: Detection of PrP**CWD in retinal tissues in white-tailed deer (Odocoileus virginianus) and Rocky Mountain elk (Cervus elaphus nelsoni) with CWD Authors
 
item Spraker, Terry - COLORADO STATE UNIVERSITY item Gidleweski, Thomas - APHIS-VS, FORT COLLINS item Greenlee, Justin item Keane, Delwyn - WISCONSIN DIAGNOSTIC LAB item Hamir, Amirali item O'Rourke, Katherine
 
Submitted to: American Association of Veterinary Laboratory Diagnosticians Publication Type: Abstract Only Publication Acceptance Date: July 15, 2007 Publication Date: October 18, 2007 Citation: Spraker, T., Gidleweski, T., Greenlee, J., Keane, D., Hamir, A., Orourke, K. 2007. Detection of PrP**CWD in retinal tissues in white-tailed deer (Odocoileus virginianus) and Rocky Mountain elk (Cervus elaphus nelsoni) with CWD [abstract]. American Association of Veterinary Laboratory Diagnosticians 50th Annual Meeting. p. 47.
 
Technical Abstract: Introduction. Chronic wasting disease (CWD), a transmissible spongiform encephalopathy, has been reported in captive and free-ranging mule deer (Odocoileus hemionus hemionus), white-tailed deer (Odocoileus virginianus) and Rocky Mountain elk (Cervus elaphus nelsoni). An abnormal isoform of a prion protein (PrP**CWD) that has been associated with CWD has been reported in numerous internal organs other than the brain and lymphoid tissues, including the retina of mule deer. The objective of this project was to investigate the possibility of PrP**CWD in the retina of white-tailed deer and Rocky Mountain elk with CWD.
 
Materials and methods. Eyes from 80 captive white-tailed deer that were killed during a depopulation program were collected and placed in 10% neutral buffered formalin. None of these 80 white-tailed deer showed any clinical signs suggestive of CWD prior to euthanasia (gun shot); however 79% were positive for CWD by using immunohistochemical staining of the brain stem and head lymphoid tissues. Eyes from 7 captive and 2 research elk were collected and placed in Davison’s fixative. Clinical signs typical of CWD were observed in 5 elk (3 with M/M genotype, 1 M/L and 1 L/L). The other 4 were non-clinical (3 with genotype M/M and 1 L/L), but did have a previous positive rectal biopsy. The globe from each animal was trimmed and embedded in a single paraffin block and sectioned at 5 µm. Tissue sections were stained with H&E and immunostained with Anti-Prion 99 and P4 for the detection of PrP**CWD.
 
Results. Prion was only found in the retina, all other regions of the eye (cornea, lens, ciliary body, iris, choroid, sclera) were free of PrP**CWD in the deer. Examination of the eyes from the white-tailed deer revealed 4 to have detectable PrP**CWD within the retina. PrP**CWD was restricted to the inner and outer plexiform layers of these deer. Sections from all 9 elk had PrP**CWD in 8 of the 10 retinal layers and in the optic nerve. All other regions of the eye were free of PrP**CWD. The most prominent features in the elk were heavy PrP**CWD staining in the inner and outer plexiform layers with minimal intracytoplasmic staining in ganglion cells in the M/M and M/L elk. The 2 L/L elk had minimal PrP**CWD staining in the plexiform layers, but relatively heavy staining in the cytoplasm of ganglion cells and an unusual accumulation of PrP**CWD just inside outer limiting membrane layer. An occasional ganglion cell within the ganglion cell layer contained an intracytoplasmic vacuole in the M/M elk.
 
Discussion/Conclusion. Deer and elk do have an abundance of PrP**CWD in retinal tissues and optic nerve (elk). This accumulation of PrP**CWD may affect vision especially in elk. Genotypes did result in different patterns of PrP**CWD accumulation in elk. The LL genotype at codon 132, which has a prolonged incubation period, had much less PrP**CWD in the retina, especially within the inner and outer plexiform layers. In addition, the LL elk seemed to have more intracytoplasmic staining within ganglion cells as compared to the MM and ML elk.
 
 
Research Project: TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES: THE ROLE OF GENETICS, STRAIN VARIATION, AND ENVIRONMENTAL CONTAMINATION IN DISEASE CONTROL Title: Molecular genealogy tools for white-tailed deer with chronic wasting disease Authors
 
item Ernest, H - UC DAVIS item Hoar, B - UC DAVIS item Well, J - UC DAVIS item O'Rourke, Katherine
 
Submitted to: Canadian Journal of Veterinary Research Publication Type: Peer Reviewed Journal Publication Acceptance Date: October 14, 2009 Publication Date: May 4, 2010 Citation: Ernest, H., Hoar, B.R., Well, J.A., Orourke, K.I. 2010. Molecular genealogy tools for white-tailed deer with chronic wasting disease. Canadian Journal of Veterinary Research. 74(2):152-156. Interpretive
 
Summary: Chronic wasting disease (CWD) is a fatal degenerative brain disorder of deer, elk, and moose. The disease appears to be caused by prions, which are abnormally folded proteins formed in the lymph nodes and brain of infected deer after contact with an infected animal. The amount of time needed for transmission of disease is not known. White tailed deer live in family groups, with adult females and their female offspring spending much of the year together. Males leave the family group at adolescence and travel among groups during the breeding season. This social pattern supports a model in which disease is spread among females by repeated contact during the year and among groups by males visiting many groups during each breeding season. In this study, we developed a set of genetic tools to examine the family groups in a herd of white tailed deer in a fenced area in Nebraska. The density of deer was unusually high (more than 200 deer in 1.2 square miles, compared to less than 30 deer per square mile in forested areas of Wisconsin. Also, the rate of CWD was 50%, much higher than the 5% to 20% found in free ranging deer. We also tested a sample of deer ranging within 20 km of the fenced area. We tested the hypothesis that female deer within a family unit with a CWD-positive animal would have higher disease rates than male deer and that pairs of related animals would be more likely to have disease than unrelated deer. We used a large set of DNA markers to identify parents, siblings, aunts, and grandparents of the infected deer. Under these conditions, we did not see an increased rate of CWD among related deer. This finding may be due to the high density of deer or to the practice of providing food and water for the deer at various times of the year, encouraging the tight grouping of multiple families at the common feed and water areas. The DNA markers will be useful in examining herds of wild deer in more typical social groups.
 
Technical Abstract: Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy or prion disease of deer, elk, and moose. CWD is a fatal neurologic disease with a long preclinical incubation period, during which the disease is probably transmitted to healthy animals through direct exposure or environmental contamination by the causative agent. Although the routes of infection are not known, the saliva and blood of deer contain the agent. Deer live in matrilineal groups as fawns, with males leaving the group at adolescence. The does and female progeny remain together much of the year. Adult males travel among groups during the breeding season, visiting as many groups as possible. This spatial grouping supports a model in which disease is spread by repeated exposure among females in a matrilineal group and transmitted among groups by males during the breeding season. In this study, we applied molecular genetic tools to reconstruct family relationship for a fenced herd of deer with a high CWD prevalence and for nearby free-ranging herds. We tested the hypotheses that females within first order (full sibs or parent-offspring) kin groups containing a CWD-positive adult female were more likely than males to test CWD positive and that dyads of CWD-positive individuals related in first order occurred at a higher frequency than predicted by chance alone. WE used a panel of 39 microsatellite markers and a set of mitochondrial sequences to provide kinship data for all deer in the fenced facility (n=200) and a sample of deer generally ranging within 20 km of the facility. In this system, we found no association between kinship and CWD status, although it is likely that the results were impacted by the high population density (200 deer in 1.2 square miles), the concentrated sources of feed and water during some times of the year, and the high disease prevalence. However, the study identifies a panel of genetic markers suitable for identifying first degree and second degree relatives. This panel will be useful in examining the disease patterns in the more typical settings of free ranging deer in areas with a density of fewer than 30 deer per square mile and disease prevalence of 15% to 30%.
 
 
SINGELTARY PEER REVIEW
 
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
 
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
 
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
 
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
 
Terry S. Singeltary, Sr Bacliff, Tex
 
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
 
 
26 March 2003
 
Terry S. Singeltary, retired (medically) CJD WATCH
 
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
 
 
2 January 2000
 
British Medical Journal
 
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
 
 
15 November 1999
 
British Medical Journal
 
vCJD in the USA * BSE in U.S.
 
 
The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
 
Tracking spongiform encephalopathies in North America
 
Original
 
Xavier Bosch
 
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt—Jakob ...
 
 
Suspect symptoms
 
What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?
 
28 Mar 01
 
Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America. Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.
 
"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb...
 
 
***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.
 
***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.
 
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
 
Posted by flounder on 03 Jul 2015 at 16:53 GMT
 
 
AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.
 
snip...
 
 
OR-09: Canine spongiform encephalopathy—A new form of animal prion disease
 
Monique David, Mourad Tayebi UT Health; Houston, TX USA
 
snip...see letter to me from DEFRA on the hound study and tse prion aka bse mad cow disease ;
 
Monday, March 26, 2012
 
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE
 
 
Monday, March 8, 2010
 
Canine Spongiform Encephalopathy aka MAD DOG DISEASE
 
 
31 Jan 2015 at 20:14 GMT
 
*** Ruminant feed ban for cervids in the United States? ***
 
Singeltary et al
 
31 Jan 2015 at 20:14 GMT
 
 
Thursday, July 24, 2014
 
*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations
 
 
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
 
 
SNIP... PLEASE SEE FULL TEXT SUBMISSION HERE ;
 
re-Human Prion Diseases in the United States
 
Posted by flounder on 01 Jan 2010 at 18:11 GMT I kindly disagree with your synopsis for the following reasons ;
 
 
Tuesday, October 20, 2015
 
FBI: Agroterrorism not likely, but very possible, Dr. Stephen Gold­smith FBI Laboratory Division, here's your sign
 
CC-Dr. Steve Goldsmith, FBI Laboratory Division
 
please note, I tried to forward this to the FBI, spoke with several folks at FBI headquarters, and they were not interested...just saying...terry
 
 
Sunday, October 25, 2015
 
USAHA Detailed Events Schedule – 119th USAHA Annual Meeting CAPTIVE LIVESTOCK CWD SCRAPIE TSE PRION
 
 
Thursday, October 22, 2015
 
Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened
 
 
Sunday, October 18, 2015
 
World Organisation for Animal Health (OIE) and the Institut Pasteur Cooperating on animal disease and zoonosis research
 
 
Thursday, October 1, 2015
 
H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism: clinical and pathologic features in wild-type and E211K cattle following intracranial inoculation
 
Master Obi-Wan Kenobi, Kemosabe...THIS IS NOT GOOD GOOSE!...grasshopper...tonto...tss
 
 
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle
 
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
 
snip...
 
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
 
 
In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
 
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...
 
 
Wednesday, July 15, 2015
 
*** Additional BSE TSE prion testing detects pathologic lesion in unusual brain location and PrPsc by PMCA only, how many cases have we missed?
 
 
Saturday, June 25, 2011
 
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
 
"BSE-L in North America may have existed for decades"
 
 
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
 
 
Comments on technical aspects of the risk assessment were then submitted to FSIS.
 
Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary.
 
This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:
 
 
Owens, Julie
 
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
 
Sent: Monday, July 24, 2006 1:09 PM
 
To: FSIS RegulationsComments
 
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
 
Page 1 of 98
 
 
FSIS, USDA, REPLY TO SINGELTARY
 
 
2004, highly suspect stumbling and staggering mad cow reported, however, NO TESTING DONE, ON ORDERS FROM AUSTIN $
 
May 4, 2004
 
Statement on Texas Cow With Central Nervous System Symptoms
 
On Friday, April 30th, the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
 
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
 
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
 
Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison)...
 
 
USDA regulations, any cow that exhibits signs of central nervous system (CNS)
 
According to a 1997 Animal and Plant Health Inspection Service (NHIS) Memorandum, brain samples all of such animals should be sent for BSE testing.2 The memorandum notes that "it is essential that brain specimens be collected from adult cattle condemned for CNS signs as part of our national surveillance of BSE."
 
The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5
 
May 13,2004
 
Page 2
 
snip...
 
The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5
 
This sequence of events is troubling, and it raises the question of whether this is an isolated incident. In 1997, USDA noted a major gap between the number of cattle condemned for CNS symptoms and the number of these cows actually tested for mad cow disease. The Department found:
 
 
-------- Original Message --------
 
Subject: re-USDA's surveillance plan for BSE aka mad cow disease
 
Date: Mon, 02 May 2005 16:59:07 -0500
 
From: "Terry S. Singeltary Sr."
 
To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov, contactOIG@hhsc.state.tx.us
 
Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at OIG, ...............
 
snip...
 
There will be several more emails of my research to follow. I respectfully request a full inquiry into the cover-up of TSEs in the United States of America over the past 30 years. I would be happy to testify...
 
Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 xxx xxx xxxx
 
Date: June 14, 2005 at 1:46 pm PST In
 
Reply to: Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding further analysis of BSE Inconclusive Test Results posted by TSS on June 13, 2005 at 7:33 pm:
 
Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary for Marketing and Regulatory Programs resigns. Three days later same mad cow found in November turns out to be positive. Both resignation are unexpected. just pondering... TSS
 
MAD COW IN TEXAS NOVEMBER 2004. ...TSS
 
-------- Original Message --------
 
Director, Public Information Carla Everett ceverett@tahc.state.tx.us
 
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
 
Date: Mon, 22 Nov 2004 17:12:15 –0600
 
From: "Terry S. Singeltary Sr."
 
To: Carla Everett References: <[log in to unmask]> <[log in to unmask] us>
 
Greetings Carla,still hear a rumor;
 
Texas single beef cow not born in Canada no beef entered the food chain?
 
and i see the TEXAS department of animal health is ramping up forsomething, but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???
 
terry
 
-------- Original Message --------
 
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
 
Date: Fri, 19 Nov 2004 11:38:21 –0600
 
From: Carla Everett
 
To: "Terry S. Singeltary Sr." References: <[log in to unmask]>
 
The USDA has made a statement, and we are referring all callers to the USDA web site. We have no information about the animal being in Texas. Carla At 09:44 AM 11/19/2004, you wrote:>Greetings Carla,>>i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from>TEXAS. can you comment on this either way please?>>thank you,>Terry S. Singeltary Sr.>>
 
-------- Original Message --------
 
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
 
Date: Mon, 22 Nov 2004 18:33:20 -0600 From: Carla Everett
 
To: "Terry S. Singeltary Sr."
 
References: ...sniptss
 
our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something. At 06:05 PM 11/22/2004,
 
you wrote:
 
>why was the announcement on your TAHC site removed?
 
>>Bovine Spongiform Encephalopathy:
 
>November 22: Press Release title here
 
>>star image More BSE information
 
>>>>terry
 
>>Carla Everett wrote:
 
>>>no confirmation on the U.S.' inconclusive test...
 
>>no confirmation on location of animal.>>>>>>
 
==========================
 
-------- Original Message --------
 
Director, Public Information Carla Everett ceverett@tahc.state.tx.us
 
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
 
Date: Mon, 22 Nov 2004 17:12:15 –0600
 
From: "Terry S. Singeltary Sr."
 
To: Carla Everett References: <[log in to unmask]> <[log in to unmask] us>
 
Greetings Carla,still hear a rumor;
 
Texas single beef cow not born in Canada no beef entered the food chain?
 
and i see the TEXAS department of animal health is ramping up forsomething, but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???
 
terry
 
==============================
 
 
 
Monday, October 26, 2015
 
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
 
 
Friday, October 09, 2015
 
An alarming presentation level II trauma center of Creutzfeldt-Jakob disease following a self-inflicted gunshot wound to the head
 
 
Friday, October 23, 2015
 
CJD FOUNDATION CREUTZFELDT JAKOB DISEASE TSE PRION QUESTIONNAIRE UPDATE OCTOBER 2015
 
 
the tse prion aka mad cow type disease is not your normal pathogen.
 
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
 
you cannot cook the TSE prion disease out of meat. you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
 
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
 
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
 
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.
 
you can bury it and it will not go away.
 
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
 
it’s not your ordinary pathogen you can just cook it out and be done with.
 
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.
 
cwd to humans, consumption, exposure, sub-clinical, iatrogenic, what if ?
 
to the breeders and industry that care more about their bottom dollar, ignore science, and the ones crying about their poor deer being slaughtered...crying me a river$$$
 
CENSORED, RAW, AND UNCUT...
 
Sunday, August 23, 2015
 
TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig and take her to the dance in Texas
 
from the other side of the fence... today’s Singeltary Sunday School class ‘thinking outside of the box, God’s Wrath’ at the bottom. ...tss
 
 
TEXAS DEER CZAR SENT TO WISCONSIN TO SOLVE CWD CRISIS, WHILE ROME (TEXAS) BURNS
 
Tuesday, August 11, 2015
 
Wisconsin doing what it does best, procrastinating about CWD yet again thanks to Governor Walker
 
 
Wednesday, March 18, 2015
 
*** Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015
 
 
Wednesday, March 25, 2015
 
*** Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015
 
 
Wednesday, July 01, 2015
 
*** TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer
 
 
Tuesday, July 21, 2015
 
*** Texas CWD Medina County Herd Investigation Update July 16, 2015 ***
 
 
Thursday, August 06, 2015
 
*** WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY
 
 
Friday, August 07, 2015
 
*** Texas CWD Captive, and then there were 4 ?
 
 
Thursday, September 24, 2015
 
TEXAS Hunters Asked to Submit Samples for Chronic Wasting Disease CWD TSE Prion Testing
 
*** I cannot stress enough to all of you, for the sake of your family and mine, before putting anything in the freezer, have those deer tested for CWD. ...terry
 
 
Saturday, October 03, 2015
 
TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO 2015
 
 
Friday, October 09, 2015
 
Texas TWA Chronic Wasting Disease TSE Prion Webinars and Meeting October 2015
 
 
Friday, October 23, 2015
 
*** Ohio Wildlife Council Passes Rule to Help Monitor CWD
 
 
Monday, August 24, 2015
 
Ohio wildlife officials ramp up fight against fatal deer brain disease after 17 more positive tests CWD
 
 
Sunday, October 18, 2015
 
*** Pennsylvania Game Commission Law and Law Makers CWD TSE PRION Bans Singeltary 2002 from speaking A smelly situation UPDATED 2015
 
 
Monday, August 31, 2015
 
Illinois Loosing Ground to Chronic Wasting Disease CWD cases mounting with 71 confirmed in 2015 and 538 confirmed cases to date
 
 
Saturday, September 05, 2015
 
Missouri Captive Cervid Industry, CWD TSE Prion, and Procrastinating for Money, while mad deer and elk disease silently spreads
 
 
Friday, August 14, 2015
 
*** Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation
 
 
Friday, August 14, 2015
 
*** Carcass Management During a Mass Animal Health Emergency Draft Programmatic Environmental Impact Statement—August 2015
 
 
Tuesday, September 22, 2015
 
*** Host Determinants of Prion Strain Diversity Independent of Prion Protein Genotype
 
 
Friday, August 28, 2015
 
*** Chronic Wasting Disease CWD TSE Prion Diagnostics and subclinical infection ***
 
 
 
just made a promise to mom DOD 12/14/97 confirmed hvCJD. never forget, and never let them forget. ...
 
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
 
Galveston Bay, on the bottom...
 
wasted days and wasted nights...Freddy Fender
 
 
Thursday, November 05, 2015
 
TPW Commission Adopts Interim Deer Breeder Movement Rules
 
 

posted by Terry S. Singeltary Sr. at 11:57 AM

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