Missouri MDC finds seven new cases of ChronicWasting Disease CWD during past‐season testing
MDC finds new cases of chronic wasting disease during past‐season testing
Department will increase CWD monitoring efforts this
fall with mandatory testing in 29 counties during firearms
opening weekend.
JEFFERSON CITY, Mo. ‐‐ The Missouri Department of Conservation (MDC)
received final results from its 2015‐2016 fall and
winter testing of nearly 7,700 free‐ranging deer for
Chronic Wasting Disease (CWD). Seven were confirmed to be positive for the fatal
deer‐disease.
Three were from Adair County, two from Macon County, one from Linn County, and
one from Franklin County (reported earlier in the
year).
The new cases bring the total number of Missouri
free‐ranging deer that have tested positive for CWD to 33
since the disease was first discovered in the state in 2010. Of the 33 cases, 21
have been found in Macon County, 9 in Adair, one in Cole, one in Franklin, and
one in Linn.
Chronic Wasting Disease infects only deer and other
members of the deer family by causing degeneration of the brain. The disease has
no vaccine or cure and is 100‐percent fatal.
According to MDC State Wildlife Veterinarian Kelly
Straka, the Department’s CWD‐testing efforts focus mostly on
deer harvested by hunters and deer removed by MDC staff and landowners from
specific private properties in northeast, central, and
east‐central Missouri around where the disease has
been found, along with a small number of sick and
road‐kill
deer.
Straka added that MDC also conducts broader CWD testing around the
state each year as part of its ongoing monitoring efforts. Nearly 2,700 of the
deer tested last fall and winter were part of this broader CWD monitoring and
the focus was on the southern half of Missouri. No deer from southern Missouri
were found to be positive for CWD.
The Conservation Department has collected more than 51,000 tissue
samples for CWD testing from all around the state since it began testing for the
disease in 2001.
NEW MANDATORY CWD TESTING
This coming fall and winter, MDC will increase its
CWD‐testing efforts in its CWD management zones. The
management zones consist of 29 counties within or that touch a radius of
approximately 25 miles from where the disease has been found. Counties in the
CWD management zones are: Adair, Boone, Callaway, Carroll, Chariton, Crawford,
Cole, Cooper, Franklin, Gasconade, Jefferson, Knox, Linn, Livingston, Macon,
Miller, Moniteau, Morgan, Osage, Putnam, St. Charles, St. Louis, Randolph,
Schuyler, Scotland, Shelby, Sullivan, Washington, and
Warren.
The Department will require hunters to present their deer for CWD
testing at an MDC testing location if they harvest it in one of these 29
counties during the opening weekend of the fall firearms deer season, Nov. 12
and 13. The testing is free and hunters can also get free test
results.
“We are in the process of working out the logistics
for this important CWD‐testing effort and will have more details this summer
and fall,” explained Straka. “We will be providing several locations in each of
the 29 counties to help make getting their deer tested as convenient as possible
for hunters.”
MDC will also continue to work with meat processors
and taxidermists in the 29 counties to provide free CWD testing during other
parts of the upcoming deer‐hunting seasons. The Department will also continue its
broader ongoing CWD monitoring efforts with a focus on the northern half of the
state for the upcoming season.
MDC will increase its CWD-testing efforts this coming fall and
winter in the highlighted counties (shown in orange) that are within or touch a
radius of about 25 miles from where the disease has been
found.
From: Terry S. Singeltary Sr.
Sent: Sunday, March 06, 2016 1:04 PM
To: BSE-L@LISTS.AEGEE.ORG
Subject: [BSE-L] Missouri 2015-2016 CWD Surveillance Summary to Date, with confirmed cases mounting
Sent: Sunday, March 06, 2016 1:04 PM
To: BSE-L@LISTS.AEGEE.ORG
Subject: [BSE-L] Missouri 2015-2016 CWD Surveillance Summary to Date, with confirmed cases mounting
2015-2016 CWD Surveillance Summary to Date
CWD surveillance in Missouri includes two distinct sampling areas: CWD
Management Zones and Statewide. CWD Management Zones include counties within
approximately 25-miles of confirmed CWD detections in free-ranging deer.
Statewide surveillance focuses on counties outside of established CWD Management
Zones, and is designed to detect new areas of infection in the state. To date,
CWD Management Zones include the following counties:
North Management Zone: Adair, Chariton, Knox, Linn, Macon, Putnam,
Randolph, Schuyler, Scotland, Shelby and Sullivan counties
Central Management Zone: Boone, Callaway, Cole, Cooper, Miller, Moniteau,
Morgan and Osage counties
Total CWD Samples Taken To Date Area CWD Not Detected CWD Positive Results
Pending Total
Central CWD Management Zone CWD Management Zone 2162 0 39 2201
North CWD Management Zone CWD Management Zone 2499 6 120 2625
Statewide (Outside of Zone) 2621 1 36 2658
TOTAL 7282 7 195 7484
A CWD surveillance season runs from July 1 through June 30 the following
year.
Surveillance Maps
Can I Get It?
As of 2014, there is no evidence that humans can be infected with CWD.
However, research is ongoing to determine any public health impacts.
HOW BAD CAN IT GET?
As of 2014, no human health risk has been reported.
SYMPTOMS IN HUMANS Currently, CWD is not known to infect people.
Safe for Pets? There is no evidence that CWD can be naturally transmitted
to pets but, to be safe, animals that have tested positive for CWD should not be
fed to pets.
Sunday, March 06, 2016
Missouri 2015-2016 CWD Surveillance Summary to Date, with confirmed cases
mounting
Thursday, December 03, 2015
Missouri MDC reports CWD found in Franklin County
Saturday, September 05, 2015
Missouri Captive Cervid Industry, CWD TSE Prion, and Procrastinating for
Money, while mad deer and elk disease silently spreads
Tuesday, June 16, 2015
Missouri MDC changes deer hunting regs to help slow CWD
Wednesday, March 11, 2015
MDC reports 11 new cases of Chronic Wasting Disease CWD in Missouri deer
Monday, January 26, 2015
Missouri MDC reports two new cases of CWD found in Adair and Macon counties
Tuesday, December 09, 2014
Missouri MDC reports one new case of CWD, found in Adair County
Friday, October 17, 2014
Missouri Final action on Orders of Rule making Breeders and Big Game
Hunting Preserves
Thursday, September 11, 2014
Missouri Nixon's Veto Stands Overide Fails on Agriculture Legislation
How they voted: attempt to override veto of ag bill fails in the House
Thursday, May 01, 2014
Missouri DNR CWD prevention and captive cervid farming Update
Tuesday, March 26, 2013
CWD Missouri remains confined to Linn-Macon-County Core Area with four new
cases
Wednesday, January 23, 2013
Missouri sixth case CWD documented northwest Macon County
Tuesday, January 24, 2012
CWD found in two free-ranging deer from Macon County Missouri
Friday, February 26, 2010
Chronic wasting disease found in Missouri deer
Sunday, March 25, 2012
Three more cases of CWD found in free-ranging deer in Macon County
From: Terry S. Singeltary Sr.
Sent: Thursday, March 29, 2012 6:26 PM
To: warhovert@missouri.edu
Cc: abbottjm@missouri.edu ; waltermr@missouri.edu ;
John.McLaughlin@missouri.edu ; connerek@missouri.edu ; contact@dnr.mo.gov ;
Shelly.Witt@mda.mo.gov ; Animal.Health@mda.mo.gov ; acfa@mda.mo.gov ;
animalid@mda.mo.gov ; Linda.Hickam@mda.mo.gov
Subject: re-Missouri officials seek states' advice on chronic wasting
disease in deer
Thursday, May 31, 2012
Missouri MDC staff will provide information on five recently found cases of
CWD in free-ranging deer in northwest Macon County June 2, 2012
Wednesday, September 05, 2012
Missouri MDC seeks hunters’ help when processing harvested deer and
preventing CWD
Thursday, December 20, 2012
MISSOURI Initial CWD sampling test results available online from MDC so far
one adult buck has tested positive for the disease
Friday, October 21, 2011
Chronic Wasting Disease Found in Captive Deer Missouri
The Missouri Department of Agriculture discovers the state's first case of
CWD in a captive white-tailed deer.
Friday, February 26, 2010
Chronic wasting disease found in Missouri deer February 25, 2010
Chronic Wasting Disease Found in Captive Deer
The Missouri Departments of Agriculture, Conservation and Health and Senior
Services and the U.S. Department of Agriculture announced today that a captive
white-tailed deer in Linn County, Missouri has tested positive for Chronic
Wasting Disease (CWD). CWD is a neurological disease found in deer, elk and
moose.
"There is no evidence that CWD poses a risk to domestic animals or humans,"
said State Veterinarian Dr. Taylor Woods. "We have protocols in place to quickly
and effectively handle these situations."
The animal that tested positive for CWD was a white-tailed deer inspected
as part of the State's CWD surveillance and testing program. Preliminary tests
were conducted by the USDA National Veterinary Services Laboratory in Ames,
Iowa.
Upon receiving the confirmed CWD positive, Missouri's departments of
Agriculture, Conservation and Health and Senior Services initiated their CWD
Contingency Plan. The plan was developed in 2002 by the Cervid Health Committee,
a task force comprised of veterinarians, animal health officers and conservation
officers from USDA, MDA, MDC and DHSS working together to mitigate challenges
associated with CWD.
CWD is transmitted by live animal to animal contact or soil to animal
contact. The disease was first recognized in 1967 in captive mule deer in the
Colorado Division of Wildlife captive wildlife research facility in Fort
Collins, Colorado. CWD has been documented in deer and/or elk in Colorado,
Illinois, Kansas, Michigan, Minnesota, Montana, Nebraska, New Mexico, New York,
Oklahoma, South Dakota, Utah, Virginia, West Virginia, Wisconsin, and the
Canadian Provinces of Alberta and Saskatchewan. There has been no evidence that
the disease can be transmitted to humans.
"Missouri's proactive steps to put a testing protocol in place and create a
contingency plan years ago is proving beneficial. We are in a solid position to
follow pre-established steps to ensure Missouri's valuable whitetail deer
resource remains healthy and strong," said Jason Sumners Missouri's Deer
Biologist.
For more information regarding CWD, please contact Dr. Taylor Woods at
(573) 751-3377.
Friday, September 20, 2013
*** Missouri State records show gaps in oversight of captive deer farms,
ranches ***
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL
THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
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.
==================
***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
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. 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.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** 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.
Chronic Wasting Disease and Potential Transmission to Humans
Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams,† Michael W.
Miller,‡ Pierluigi Gambetti,§ and Lawrence B. Schonberger*
Chronic wasting disease (CWD) of deer and elk is endemic in a tri-corner
area of Colorado, Wyoming, and Nebraska, and new foci of CWD have been detected
in other parts of the United States. Although detection in some areas may be
related to increased surveillance, introduction of CWD due to translocation or
natural migration of animals may account for some new foci of infection.
Increasing spread of CWD has raised concerns about the potential for increasing
human exposure to the CWD agent. The foodborne transmission of bovine spongiform
encephalopathy to humans indicates that the species barrier may not completely
protect humans from animal prion diseases. Conversion of human prion protein by
CWDassociated prions has been demonstrated in an in vitro cellfree experiment,
but limited investigations have not identified strong evidence for CWD
transmission to humans. More epidemiologic and laboratory studies are needed to
monitor the possibility of such transmissions.
Conclusions
The lack of evidence of a link between CWD transmission and unusual cases
of CJD, despite several epidemiologic investigations, and the absence of an
increase in CJD incidence in Colorado and Wyoming suggest that the risk, if any,
of transmission of CWD to humans is low. Although the in vitro studies
indicating inefficient conversion of human prion protein by CWD-associated
prions raise the possibility of low-level transmission of CWD to humans, no
human cases of prion disease with strong evidence of a link with CWD have been
identified. However, the transmission of BSE to humans and the resulting vCJD
indicate that, provided sufficient exposure, the species barrier may not
completely protect humans from animal prion diseases. Because CWD has occurred
in a limited geographic area for decades, an adequate number of people may not
have been exposed to the CWD agent to result in a clinically recognizable human
disease. The level and frequency of human exposure to the CWD agent may increase
with the spread of CWD in the United States. Because the number of studies
seeking evidence for CWD transmission to humans is limited, more epidemiologic
and laboratory studies should be conducted to monitor the possibility of such
transmissions. Studies involving transgenic mice expressing human and cervid
prion protein are in progress to further assess the potential for the CWD agent
to cause human disease. Epidemiologic studies have also been initiated to
identify human cases of prion disease among persons with an increased risk for
exposure to potentially CWD-infected deer or elk meat (47). If such cases are
identified, laboratory data showing similarities of the etiologic agent to that
of the CWD agent would strengthen the conclusion for a causal link. Surveillance
for human prion diseases, particularly in areas where CWD has been detected,
remains important to effectively monitor the possible transmission of CWD to
humans. Because of the long incubation period associated with prion diseases,
convincing negative results from epidemiologic and experimental laboratory
studies would likely require years of follow-up. In the meantime, to minimize
the risk for exposure to the CWD agent, hunters should consult with their state
wildlife agencies to identify areas where CWD occurs and continue to follow
advice provided by public health and wildlife agencies. Hunters should avoid
eating meat from deer and elk that look sick or test positive for CWD. They
should wear gloves when field-dressing carcasses, boneout the meat from the
animal, and minimize handling of brain and spinal cord tissues. As a precaution,
hunters should avoid eating deer and elk tissues known to harbor the CWD agent
(e.g., brain, spinal cord, eyes, spleen, tonsils, lymph nodes) from areas where
CWD has been identified.
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ???? “Our conclusion stating that we found no
strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008
Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
CJD 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 ***
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C.
Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡,
Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ snip...
Abstract The emergence of chronic wasting disease (CWD) in deer and elk in
an increasingly wide geographic area, as well as the interspecies transmission
of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt
Jakob disease, have raised concerns about the zoonotic potential of CWD. Because
meat consumption is the most likely means of exposure, it is important to
determine whether skeletal muscle of diseased cervids contains prion
infectivity. Here bioassays in transgenic mice expressing cervid prion protein
revealed the presence of infectious prions in skeletal muscles of CWD-infected
deer, demonstrating that humans consuming or handling meat from CWD-infected
deer are at risk to prion exposure.
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures
ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** 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, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==============
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
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
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. ...
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...
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL
THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
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.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by
intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and
the disease is likely to continue to spread geographically [10]. However, the
potential that white-tailed deer may be susceptible to sheep scrapie by a
natural route presents an additional confounding factor to halting the spread of
CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie
offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic
areas, but could occur anywhere that sheep with scrapie and susceptible cervids
cohabitate.
This work demonstrates for the first time that white-tailed deer are
susceptible to sheep scrapie by intracerebral inoculation with a high attack
rate and that the disease that results has similarities to CWD. These
experiments will be repeated with a more natural route of inoculation to
determine the likelihood of the potential transmission of sheep scrapie to
white-tailed deer. If scrapie were to occur in white-tailed deer, results of
this study indicate that it would be detected as a TSE, but may be difficult to
differentiate from CWD without in-depth biochemical analysis.
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in WTD after IC inoculation including early and
widespread presence of PrPSc in lymphoid tissues, clinical signs of depression
and weight loss progressing to wasting, and an incubation time of 21-23 months.
Moreover, western blots (WB) done on brain material from the obex region have a
molecular profile similar to CWD and distinct from tissues of the cerebrum or
the scrapie inoculum. However, results of microscopic and IHC examination
indicate that there are differences between the lesions expected in CWD and
those that occur in deer with scrapie: amyloid plaques were not noted in any
sections of brain examined from these deer and the pattern of immunoreactivity
by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to
scrapie.
Deer developed clinical signs of wasting and mental depression and were
necropsied from 28 to 33 months PI. Tissues from these deer were positive for
PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer
exhibited two different molecular profiles: samples from obex resembled CWD
whereas those from cerebrum were similar to the original scrapie inoculum. On
further examination by WB using a panel of antibodies, the tissues from deer
with scrapie exhibit properties differing from tissues either from sheep with
scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are
strongly immunoreactive when probed with mAb P4, however, samples from WTD with
scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4
or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly
immunoreactive and samples from WTD with scrapie are strongly positive. This
work demonstrates that WTD are highly susceptible to sheep scrapie, but on first
passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
Monday, November 3, 2014
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
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.
========================
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 ;
Potential role of soil properties in the spread of CWD in western
Canada
Alsu Kuznetsova, Debbie McKenzie, Pamela Banser, Tariq Siddique & Judd
M. Aiken
Estimating Prion Adsorption Capacity of Soil by BioAssay of Subtracted
Infectivity from Complex Solutions (BASICS)
Estimating Prion Adsorption Capacity of Soil by BioAssay of Subtracted
Infectivity from Complex Solutions (BASICS) A. Christy Wyckoff, Krista L.
Lockwood, Crystal Meyerett-Reid, Brady A. Michel, Heather Bender, Kurt C.
VerCauteren, Mark D. Zabel PLOS x Published: March 4, 2013 http://dx.doi.org/10.1371/journal.pone.0058630
Behavior of Prions in the Environment: Implications for Prion Biology
Shannon L. Bartelt-Hunt1*, Jason C. Bartz2*
Prion Amplification and Hierarchical Bayesian Modeling Refine Detection of
Prion Infection A. Christy Wyckoff1, 2 n1 , Nathan Galloway3 n1 , Crystal
Meyerett-Reid1 , Jenny Powers4 , Terry Spraker1 , Ryan J. Monello4 , Bruce
Pulford1 , Margaret Wild4 , Michael Antolin3 , Kurt VerCauteren2 […] & Mark
Zabel1 - Show fewer authors Scientific Reports 5, Article number: 8358 (2015)
doi:10.1038/srep08358 Download Citation
Molecular ecology Proteins Statistics Received: 27 June 2014
CELL REPORTS
Report
Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions
PRION UPDATE VIA VEGETABLE PLANTS FROM THE SOIL
56. Members considered that there is no evidence that crops grown on the
land which received composted excreta from BSE-challenged animals pose a TSE
risk to humans or animals. One member suggested that, as some of these animals
are orally challenged with high doses of BSE-infected materials, and the
distribution of infectivity in the digestive system is not completely
understood, it might be premature to conclude that there is no infective agent
in the manure.
Furthermore, an unpublished study had indicated low level absorption of PrP
from soil by tomato plants although it should be noted that this study had not
been repeated. Details of this work would be sent to the SEAC Secretary. Dr
Matthews explained that most of the manure from animals challenged with high
doses of BSE had already been composted and used for coppicing. Members agreed
that the risks from disposal of residual manure from experimental animals would
be much less than historic risks of on farm contamination from naturally
infected animals at the height of the BSE epidemic. ...SNIP...END
SRM are certain cattle tissues capable of transmitting BSE. There is no
human health risk assessment to indicate the absence of human health concerns
associated with use of composted SRM domestically. To date, scientific evidence
has not been able to demonstrate that composting destroys prions. Although
domestic use would pose a negligible risk to livestock, there is a potential
risk to humans via direct ingestion of the compost or of compost particles
adhered to skin or plant material (e.g. carrots). Another potential route of
exposure is by ingestion of prions that have been taken up by plants. It has
been proven that bacteria are readily taken up by some plants (e.g. E. coli in
lettuce) thus the uptake of prions by plants cannot be precluded or dismissed at
this time. As a science-based regulator, the CFIA cannot change the policy on
this issue without a risk assessment demonstrating that the use of composted SRM
poses an acceptable risk to humans.
The BSE Inquiry / Statement No 19B (supplementary) Dr Alan Colchester
Issued 06/08/1999 (not scheduled to give oral evidence) SECOND STATEMENT TO THE
BSE INQUIRY Dr A Colchester BA BM BCh PhD FRCP Reader in Neurosciences &
Computing, University of Kent at Canterbury; Consultant Neurologist, Guy’s
Hospital London and William Harvey Hospital Ashford April 1999
snip...
88. Natural decay: Infectivity persists for a long time in the environment.
A study by Palsson in 1979 showed how scrapie was contracted by healthy sheep,
after they had grazed on land which had previously been grazed by
scrapie-infected sheep, even though the land had lain fallow for three years
before the healthy sheep were introduced. Brown also quoted an early experiment
of his own (1991), where he had buried scrapie-infected hamster brain and found
that he could still detect substantial infectivity three years later near where
the material had been placed. 89. Potential environmental routes of infection:
Brown discusses the various possible scenarios, including surface or subsurface
deposits of TSE-contaminated material, which would lead to a build-up of
long-lasting infectivity. Birds feeding on animal remains (such as gulls
visiting landfill sites) could disperse infectivity. Other animals could become
vectors if they later grazed on contaminated land. "A further question concerns
the risk of contamination of the surrounding water table or even surface water
channels, by effluents and discarded solid wastes from treatment plants. A
reasonable conclusion is that there is a potential for human infection to result
from environmental contamination by BSE-infected tissue residues. The potential
cannot be quantified because of the huge numbers of uncertainties and
assumptions that attend each stage of the disposal process". These comments,
from a long established authority on TSEs, closely echo my own statements which
were based on a recent examination of all the evidence. 90. Susceptibility: It
is likely that transmissibility of the disease to humans in vivo is probably
low, because sheep that die from scrapie and cattle that die from BSE are
probably a small fraction of the exposed population. However, no definitive data
are available.
91. Recommendations for disposal procedures: Brown recommends that material
which is actually or potentially contaminated by BSE should be: 1) exposed to
caustic soda; 2) thoroughly incinerated under carefully inspected conditions;
and 3) that any residue should be buried in landfill, to a depth which would
minimise any subsequent animal or human exposure, in areas that would not
intersect with any potable water-table source.
92. This review and recommendations from Brown have particular importance.
Brown is one of the world's foremost authorities on TSEs and is a senior
researcher in the US National Institutes of Health (NIH). It is notable that
such a respected authority is forthright in acknowledging the existence of
potential risks, and in identifying the appropriate measures necessary to
safeguard public health. Paper by SM Cousens, L Linsell, PG Smith, Dr M
Chandrakumar, JW Wilesmith, RSG Knight, M Zeidler, G Stewart, RG Will,
"Geographical distribution of variant CJD in the UK (excluding Northern
Ireland)". Lancet 353:18-21, 2 nd January 1999 93. The above paper {Appendix 41
(02/01/99)} (J/L/353/18) examined the possibility that patients with vCJD
(variant CJD) might live closer to rendering factories than would be expected by
chance. All 26 cases of vCJD in the UK with onset up to 31 st August 1998 were
studied. The incubation period of vCJD is not known but by analogy with other
human TSEs could lie within the range 5-25 years. If vCJD had arisen by exposure
to rendering products, such exposure might plausibly have occurred 8-10 years
before the onset of symptoms. The authors were able to obtain the addresses of
all rendering plants in the UK which were in production in 1988. For each case
of vCJD, the distance from the place of residence on 1st January 1998 to the
nearest rendering plant was calculated
snip...
Friday, February 08, 2013
*** Behavior of Prions in the Environment: Implications for Prion Biology
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it
has been reported in naïve, supposedly previously unexposed sheep placed in
pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the
vector for disease transmission is not known, soil is likely to be an important
reservoir for prions (2) where – based on studies in rodents – prions can adhere
to minerals as a biologically active form (21) and remain infectious for more
than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in
mule deer housed in paddocks used by infected deer 2 years earlier, which was
assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was
greater through exposure to contaminated wooden, plastic, and metal surfaces via
water or food troughs, fencing, and hurdles than through grazing. Drinking from
a water trough used by the scrapie flock was sufficient to cause infection in
sheep in a clean building. Exposure to fences and other objects used for rubbing
also led to infection, which supported the hypothesis that skin may be a vector
for disease transmission (9). The risk of these objects to cause infection was
further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid
tissue after grazing on one of the paddocks, which contained metal hurdles, a
metal lamb creep and a water trough in contact with the scrapie flock up to 8
weeks earlier, whereas no infection had been demonstrated previously in sheep
grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate
dropped significantly to 8% of 12 sheep, with soil of the paddock as the most
likely source of infection caused by shedding of prions from the
scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field
furniture sufficient to cause infection was dependent on two factors: stage of
incubation period and time of last use by scrapie-infected sheep. Drinking from
a water trough that had been used by scrapie sheep in the predominantly
pre-clinical phase did not appear to cause infection, whereas infection was
shown in sheep drinking from the water trough used by scrapie sheep in the later
stage of the disease. It is possible that contamination occurred through
shedding of prions in saliva, which may have contaminated the surface of the
water trough and subsequently the water when it was refilled. Contamination
appeared to be sufficient to cause infection only if the trough was in contact
with sheep that included clinical cases. Indeed, there is an increased risk of
bodily fluid infectivity with disease progression in scrapie (24) and CWD (25)
based on PrPSc detection by sPMCA. Although ultraviolet light and heat under
natural conditions do not inactivate prions (26), furniture in contact with the
scrapie flock, which was assumed to be sufficiently contaminated to cause
infection, did not act as vector for disease if not used for 18 months, which
suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for
infectivity measurements by bioassay in sheep or mice. In this reported study,
however, the levels of PrPSc present in the environment were below the limit of
detection of the sPMCA method, yet were still sufficient to cause infection of
in-contact animals. In the present study, the outdoor objects were removed from
the infected flock 8 weeks prior to sampling and were positive by sPMCA at very
low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive
reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay
could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo
formation of infectious prions have been reported (27, 28). This is in contrast
to our previous study where we demonstrated that outdoor objects that had been
in contact with the scrapie-infected flock up to 20 days prior to sampling
harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions
(12)] and was significantly more positive by the assay compared to analogous
samples from the scrapie-free farm. This discrepancy could be due to the use of
a different sPMCA substrate between the studies that may alter the efficiency of
amplification of the environmental PrPSc. In addition, the present study had a
longer timeframe between the objects being in contact with the infected flock
and sampling, which may affect the levels of extractable PrPSc. Alternatively,
there may be potentially patchy contamination of this furniture with PrPSc,
which may have been missed by swabbing. The failure of sPMCA to detect
CWD-associated PrP in saliva from clinically affected deer despite confirmation
of infectivity in saliva-inoculated transgenic mice was associated with as yet
unidentified inhibitors in saliva (29), and it is possible that the sensitivity
of sPMCA is affected by other substances in the tested material. In addition,
sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more
difficult from furniture exposed to weather, which is supported by the
observation that PrPSc was detected by sPMCA more frequently in indoor than
outdoor furniture (12). A recent experimental study has demonstrated that
repeated cycles of drying and wetting of prion-contaminated soil, equivalent to
what is expected under natural weathering conditions, could reduce PMCA
amplification efficiency and extend the incubation period in hamsters inoculated
with soil samples (30). This seems to apply also to this study even though the
reduction in infectivity was more dramatic in the sPMCA assays than in the sheep
model. Sheep were not kept until clinical end-point, which would have enabled us
to compare incubation periods, but the lack of infection in sheep exposed to
furniture that had not been in contact with scrapie sheep for a longer time
period supports the hypothesis that prion degradation and subsequent loss of
infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of
furniture that had been in contact with scrapie-infected animals should be
recommended, particularly since cleaning and decontamination may not effectively
remove scrapie infectivity (31), even though infectivity declines considerably
if the pasture and the field furniture have not been in contact with
scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in
furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible spongiform
encephalopathy, sheep, field furniture, reservoir, serial protein misfolding
cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission ***
Circulation of prions within dust on a scrapie affected farm
Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben
C Maddison2*
Abstract
Prion diseases are fatal neurological disorders that affect humans and
animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk
are contagious prion diseases where environmental reservoirs have a direct link
to the transmission of disease. Using protein misfolding cyclic amplification we
demonstrate that scrapie PrPSc can be detected within circulating dusts that are
present on a farm that is naturally contaminated with sheep scrapie. The
presence of infectious scrapie within airborne dusts may represent a possible
route of infection and illustrates the difficulties that may be associated with
the effective decontamination of such scrapie affected premises.
snip...
Discussion
We present biochemical data illustrating the airborne movement of scrapie
containing material within a contaminated farm environment. We were able to
detect scrapie PrPSc within extracts from dusts collected over a 70 day period,
in the absence of any sheep activity. We were also able to detect scrapie PrPSc
within dusts collected within pasture at 30 m but not at 60 m distance away from
the scrapie contaminated buildings, suggesting that the chance of contamination
of pasture by scrapie contaminated dusts decreases with distance from
contaminated farm buildings. PrPSc amplification by sPMCA has been shown to
correlate with infectivity and amplified products have been shown to be
infectious [14,15]. These experiments illustrate the potential for low dose
scrapie infectivity to be present within such samples. We estimate low ng levels
of scrapie positive brain equivalent were deposited per m2 over 70 days, in a
barn previously occupied by sheep affected with scrapie. This movement of dusts
and the accumulation of low levels of scrapie infectivity within this
environment may in part explain previous observations where despite stringent
pen decontamination regimens healthy lambs still became scrapie infected after
apparent exposure from their environment alone [16]. The presence of sPMCA
seeding activity and by inference, infectious prions within dusts, and their
potential for airborne dissemination is highly novel and may have implications
for the spread of scrapie within infected premises. The low level circulation
and accumulation of scrapie prion containing dust material within the farm
environment will likely impede the efficient decontamination of such scrapie
contaminated buildings unless all possible reservoirs of dust are removed.
Scrapie containing dusts could possibly infect animals during feeding and
drinking, and respiratory and conjunctival routes may also be involved. It has
been demonstrated that scrapie can be efficiently transmitted via the nasal
route in sheep [17], as is also the case for CWD in both murine models and in
white tailed deer [18-20].
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
Thursday, April 07, 2016
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
Sheep and cattle may be exposed to CWD via common grazing areas with
affected deer but so far, appear to be poorly susceptible to mule deer CWD
(Sigurdson, 2008).
***In contrast, cattle are highly susceptible to white-tailed deer CWD and
mule deer CWD in experimental conditions but no natural CWD infections in cattle
have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how
susceptible humans are to CWD but given that the prion can be present in muscle,
it is likely that humans have been exposed to the agent via consumption of
venison (Sigurdson, 2008). Initial experimental research, however, suggests that
human susceptibility to CWD is low and there may be a robust species barrier for
CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD
is affecting wild and farmed cervid populations in endemic areas with some deer
populations decreasing as a result.
snip...
For the purpose of the qualitative risk assessment developed here it is
necessary to estimate the probability that a 30-ml bottle of lure contains urine
from an infected deer. This requires an estimate of the proportion of deer herds
in the USA which are infected with CWD together with the within herd
prevalence.
The distribution map of CWD in US shows it is present mainly in central
states (Figure 1). However, Virginia in the east of the country has recorded
seven recent cases of CWD (Anon 2015a). Some US manufacturers claim to take
steps to prevent urine being taken from infected animals eg by sourcing from
farms where the deer are randomly tested for CWD (Anon 2015a). However, if
disease is already present and testing is not carried out regularly, captive
populations are not necessarily disease free (Strausser 2014). Urine-based deer
lures have been known to be collected from domestic white-tailed deer herds and
therefore there is a recognised risk. This is reflected by 6 US States which
have
14
banned the use of natural deer urine for lures, as the deer urine may be
sourced from CWD-endemic areas in the USA as well as from areas free of CWD. For
example, the US State of Virginia is banning the use of urine-based deer lures
on July 2015 and Vermont from 2016 due to the risk of spread of CWD. Alaska
banned their use in 2012 (Anon 2015a). Pennsylvania Game Commission has banned
urine-based deer lures and acknowledged that there is no way to detect their use
(Strausser 2014). On the basis of unpublished data (J. Manson, Pers. Comm.) it
appears that up to 50% of deer herds can be infected with 80-90% of animals
infected within some herds.
*** It is therefore assumed that probability that a 30-ml bottle of deer
urine lure imported from the USA is sources from an infected deer is
medium.
SNIP...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. ***For elk and deer
considered at high risk for CWD, the FDA recommends that these animals do not
enter the animal feed system. ***However, this recommendation is guidance and
not a requirement by law.
***Animals considered at high risk for CWD include:
***1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
***2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
***Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants. The
amount of animal PAP that is of deer and/or elk origin imported from the USA to
GB cannot be determined, however, as it is not specified in TRACES. It may
constitute a small percentage of the very low tonnage of non-fish origin
processed animal proteins that were imported from US into GB.
*** Overall, therefore, it is considered there is a greater than negligible
risk that (non-ruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB. There is uncertainty associated with this estimate
given the lack of data on the amount of deer and/or elk protein possibly being
imported in these products.
SNIP...
Summary and MORE HERE ;
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
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
see Singeltary comment ;
Monday, March 28, 2016
National Scrapie Eradication Program February 2016 Monthly Report
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
Greetings again FDA and Mr. Pritchett et al,
I would kindly like to comment on ;
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
#158
Guidance for Industry
Use of Material from Deer and Elk in Animal Feed
This version of the guidance replaces the version made available
September15, 2003.
This document has been revised to update the docket number, contact
information, and standard disclosures. Submit comments on this guidance at any
time.
Submit electronic comments to http://www.regulations.gov. Submit written
comments to the Division of Dockets Management (HFA-305), Food and Drug
Administration, 5630 Fishers Lane, Rm. 1061, Rockville, MD 20852. All comments
should be identified with the Docket No. FDA-2003-D-0432 (formerly 03D-0186).
For further information regarding this guidance, contact Burt Pritchett,
Center for Veterinary Medicine (HFV-222), Food and Drug Administration, 7519
Standish Place, Rockville, MD 20855, 240-402-6276, E-mail:
burt.pritchett@fda.hhs.gov.
Additional copies of this guidance document may be requested from the
Policy and Regulations Staff (HFV-6), Center for Veterinary Medicine, Food and
Drug Administration, 7519 Standish Place, Rockville, MD 20855, and may be viewed
on the Internet at either http://www.fda.gov/AnimalVeterinary/default.htm
or http://www.regulations.gov.
U.S. Department of Health and Human Services Food and Drug Administration
Center for Veterinary Medicine March 2016
Contains Nonbinding Recommendations
2
Guidance for Industry Use of Material from Deer and Elk in Animal Feed
This guidance represents the current thinking of the Food and Drug
Administration (FDA or Agency) on this topic. It does not establish any rights
for any person and is not binding on FDA or the public. You can use an
alternative approach if it satisfies the requirements of the applicable statutes
and regulations. To discuss an alternative approach, contact the FDA office
responsible for this guidance as listed on the title page.
I. Introduction
Under FDA’s BSE feed regulation (21 CFR 589.2000) most material from deer
and elk is prohibited for use in feed for ruminant animals. This guidance
document describes FDA’s recommendations regarding the use in all animal feed of
all material from deer and elk that are positive for Chronic Wasting Disease
(CWD) or are considered at high risk for CWD. The potential risks from CWD to
humans or non-cervid animals such as poultry and swine are not well understood.
However, because of recent recognition that CWD is spreading rapidly in
white-tailed deer, and because CWD’s route of transmission is poorly understood,
FDA is making recommendations regarding the use in animal feed of rendered
materials from deer and elk that are CWD-positive or that are at high risk for
CWD.
In general, FDA’s guidance documents do not establish legally enforceable
responsibilities. Instead, guidances describe the Agency’s current thinking on a
topic and should be viewed only as recommendations, unless specific regulatory
or statutory requirements are cited. The use of the word should in Agency
guidances means that something is suggested or recommended, but not required.
II. Background
CWD is a neurological (brain) disease of farmed and wild deer and elk that
belong in the animal family cervidae (cervids). Only deer and elk are known to
be susceptible to CWD by natural transmission. The disease has been found in
farmed and wild mule deer, white-tailed deer, North American elk, and in farmed
black-tailed deer. CWD belongs to a family of animal and human diseases called
transmissible spongiform encephalopathies (TSEs). These include bovine
spongiform encephalopathy (BSE or “mad cow” disease) in cattle; scrapie in sheep
and goats; and classical and variant Creutzfeldt-Jakob diseases (CJD and vCJD)
in humans. There is no known treatment for these diseases, and there is no
vaccine to prevent them. In addition, although validated postmortem diagnostic
tests are available, there are no validated diagnostic tests for CWD that can be
used to test for the disease in live animals.
Contains Nonbinding Recommendations
III. Use in animal feed of material from CWD-positive deer and elk
Material from CWD-positive animals may not be used in any animal feed or
feed ingredients. Pursuant to Sec. 402(a)(5) of the Federal Food, Drug, and
Cosmetic Act, animal feed and feed ingredients containing material from a
CWD-positive animal would be considered adulterated. FDA recommends that any
such adulterated feed or feed ingredients be recalled or otherwise removed from
the marketplace.
IV. Use in animal feed of material from deer and elk considered at high
risk for CWD Deer and elk considered at high risk for CWD include: (1) animals
from areas declared by State officials to be endemic for CWD and/or to be CWD
eradication zones; and (2) deer and elk that at some time during the 60-month
period immediately before the time of slaughter were in a captive herd that
contained a CWD-positive animal.
FDA recommends that materials from deer and elk considered at high risk for
CWD no longer be entered into the animal feed system. Under present
circumstances, FDA is not recommending that feed made from deer and elk from a
non-endemic area be recalled if a State later declares the area endemic for CWD
or a CWD eradication zone. In addition, at this time, FDA is not recommending
that feed made from deer and elk believed to be from a captive herd that
contained no CWD-positive animals be recalled if that herd is subsequently found
to contain a CWD-positive animal.
V. Use in animal feed of material from deer and elk NOT considered at high
risk for CWD FDA continues to consider materials from deer and elk NOT
considered at high risk for CWD to be acceptable for use in NON-RUMINANT animal
feeds in accordance with current agency regulations, 21 CFR 589.2000. Deer and
elk not considered at high risk include: (1) deer and elk from areas not
declared by State officials to be endemic for CWD and/or to be CWD eradication
zones; and (2) deer and elk that were not at some time during the 60-month
period immediately before the time of slaughter in a captive herd that contained
a CWD-positive animal.
3
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
Greetings again FDA and Mr. Pritchett et al,
MY comments and source reference of sound science on this very important
issue are as follows ;
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
I kindly wish to once again submit to Docket No. FDA-2003-D-0432 (formerly
03D-0186) Use of Material from Deer and Elk in Animal Feed.
Thank you kindly for allowing me to comment again, ...and again...and
again, on a topic so important, why it is ‘NON-BINDING’ is beyond me.
this should have been finalized and made ‘BINDING’ or MANDATORY OVER A
DECADE AGO.
but here lay the problem, once made ‘BINDING’ or ‘MANDATORY’, it is still
nothing but ink on paper.
we have had a mad cow feed ban in place since August 1997, and since then,
literally 100s of millions of pounds BANNED MAD COW FEED has been sent out to
commerce and fed out (see reference materials).
ENFORCEMENT OF SAID BINDING REGULATIONS HAS FAILED US TOO MANY TIMES.
so, in my opinion, any non-binding or voluntary regulations will not work,
and to state further, ‘BINDING’ or MANDATORY regulations will not work unless
enforced.
with that said, we know that Chronic Wasting Disease CWD TSE Prion easily
transmits to other cervid through the oral route.
the old transmission studies of BSE TSE floored scientist once they figured
out what they had, and please don’t forget about those mink that were fed 95%+
dead stock downer cow, that all came down with TME. please see ;
It is clear that the designing scientists must also have shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
it is clear that the designing scientists must have also shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
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...
*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***
Sunday, March 20, 2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission
Saturday, April 16, 2016
APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal
Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
Comment from Terry S. Singeltary Sr.
|
This is a
Comment on the Food and Drug Administration (FDA) Notice:
Risk Assessment of Foodborne Illness
Associated With Pathogens From Produce Grown in Fields Amended With Untreated
Biological Soil Amendments of Animal Origin; Request for Scientific Data,
Information, and Comments
For
related information, Open Docket Folder
 Comment
Greetings FDA et al, I kindly would like to make
comment submission to ;
Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated with Pathogens from Produce Grown in Fields Amended with Untreated Biological Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and Information A Notice by the Food and Drug Administration on 03/04/2016 MY comment as follows, There has been proven documented risk for Untreated Biological Soil Amendments of Animal Origin and risk of transmitting Transmissible Spongiform Encephalopathy TSE Prion disease aka mad cow type disease such as the typical and atypical Bovine Spongiform Encephalopathy strains, typical and atypical Scrapie strains, typical and atypical Chronic Wasting Disease CWD strains, and even the Transmissible Mink Encephalopathy TME Prion disease. Science has shown that infected deer harbor and shed high levels of infectious prions in saliva, blood, urine, and feces thereby leading to transmission by direct contact and environmental contamination. Ingestion of prion contaminated 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. Plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves) [please see data from Soto et al Prion2015 Conference below in Science reference data]. Also, Detection of protease-resistant cervid prion protein in water from a CWD-endemic area is very concerning. Science has shown that soil plays a role in the spreading and transmission of the CWD and Scrapie TSE prion agent. For these reason and more (see reference materials) I urge the FDA to stop this practice of Untreated Biological Soil Amendments of Animal Origin, including blood, for use on our produce grown in fields, for the following reasons, please see attachments and updated TSE Prion science on these very important matters here (I do not advertise or make money the science is there for educational use for Transmissible Spongiform Encephalopathy TSE Prion disease. just made a promise to mom dod 12/14/97 confirmed Heidenhain Variant Creutzfeldt Jakob Disease, hvCJD. ... Attachments(1)Comment from Terry S Singeltary Sr
View
Attachment:
 |
Tuesday, March 15, 2016
Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated
with Pathogens from Produce Grown in Fields Amended with Untreated Biological
Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and
Information Singeltary Submission
Friday, April 22, 2016
COLORADO CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING
PROGRAM IS MINIMAL AND LIMITED
Wednesday, April 20, 2016
UTAH CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING PROGRAM
70 mule deer and two elk have tested positive
Friday, April 22, 2016
Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in
a Mule Deer
Saturday, April 02, 2016
TEXAS TAHC BREAKS IT'S SILENCE WITH TWO MORE CASES CWD CAPTIVE DEER
BRINGING TOTAL TO 10 CAPTIVES REPORTED TO DATE
Friday, February 26, 2016
TEXAS Hartley County Mule Deer Tests Positive for Chronic Wasting Disease
CWD TSE Prion
Friday, February 05, 2016
TEXAS NEW CHRONIC WASTING DISEASE CWD CASE DISCOVERD AT CAPTIVE DEER
RELEASE SITE
Tuesday, April 19, 2016
Arkansas First Phase of CWD sampling reveals 23 percent prevalence rate in
focal area With 82 Confirmed to Date
Friday, April 08, 2016
Arkansas AGFC Chronic Wasting Disease CWD TSE Prion Confirms 23 Additional
Cases Total At 79 To Date
Friday, April 01, 2016
ARKANSAS CHRONIC WASTING DISEASE CWD TSE PRION CASES EXPLODE BY 27 NEW
CASES WITH 50 CASES TOTAL TO DATE
WISCONSIN CWD CASES OUT OF CONTROL
Wednesday, March 16, 2016 Wisconsin CWD sample survey 2015 confirms 290
cases of Chronic Wasting Disease TSE Prion
KANSAS CWD CASES ALARMING
Wednesday, March 02, 2016 Kansas Chronic Wasting Disease CWD TSE Prion 52
cases 2015 updated report 'ALARMING'
Tuesday, February 02, 2016
Illinois six out of 19 deer samples tested positive for CWD in the Oswego
zone of Kendall County
I could go on, for more see ;
Thursday, March 31, 2016
*** Chronic Wasting Disease CWD TSE Prion Roundup USA 2016 ***
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
9:35 PM
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