Wednesday, December 10, 2014
From: Terry S. Singeltary Sr.
Sent: Monday, December 08, 2014 12:34 PM
Cc: mdonoghue@freepressmedia.com ; deb.markowitz@state.vt.us ; justin.johnson@state.vt.us ; penny.percival@state.vt.us ; jon.groveman@state.vt.us ; Leila.LaRosa@state.vt.us
Subject: Burlington Vermont Man Charged With Importing Deer from CWD
Area from a New York captive hunt facility
Greetings Vermont et al,
I would like to kindly enlighten you a bit on the Transmissible Spongiform
Encephalopathy TSE prion disease aka mad cow type disease...as follows...kindest
regards, terry
IN REPLY TO :
News Releases
12-8-2014 Burlington Man Charged With Importing Deer from CWD Area
VERMONT FISH & WILDLIFE
Press Release
For Immediate Release: December 8, 2014
Media Contacts: Warden Robert Currier, 802-497-2126; Maj. Dennis Reinhardt,
802-828-1529;
Wildlife Biologist Adam Murkowski, 802-786-3860
Burlington Man Charged With Importing Deer from CWD Area
BURLINGTON, Vt. – The Vermont Fish & Wildlife Department says a
multi-year investigation has led to the arrest by game wardens of a Burlington
man for importing deer from a chronic wasting disease (CWD) endemic area.
Wardens executed a search warrant on December 2, 2014 at the residence of Alan
Baker in Burlington for evidence of the importation of deer from a New York
captive hunt facility. Wardens obtained evidence of four deer being imported
from the Lowlands Whitetails Hunting Ranch in Lowville, NY.
Evidence obtained through the search warrant as well as information
provided by Environmental Police Officers of the New York Department of
Environmental Conservation and the New York State Police proved that Baker has
imported deer from this facility in 2012, 2013 and 2014. Baker also allegedly
attempted to report the deer as being killed in Vermont.
Baker has been charged with three counts of importing deer from a Chronic
Wasting Disease endemic area and captive hunt facility.
Each charge carries a maximum fine of $1,000 with five points charged
against the offender’s privilege to hunt, fish and trap. Baker will lose his
hunting, fishing and trapping privileges for two years upon conviction and has
been cited to appear in Chittenden County Superior Court on February 10, 2015.
CWD is a fatal disease of the brain and nervous system in deer and elk.
Abnormal prion proteins produce lesions in the brain that cause disorientation
and emaciation. For the latest information on CWD, check www.cwd-info.org and
www.vtfishandwildlife.com.
A Vermont regulation requires special processing of deer or elk carcasses
being imported from states or provinces that have, or have had, CWD. The disease
has been found in more than 20 states and two Canadian provinces, including New
York. Vermont's CWD regulation applies to hunters bringing in deer or elk
carcasses from the following states and provinces:
Alberta, Colorado, Illinois, Iowa, Kansas, Maryland, Michigan, Minnesota,
Missouri, Montana, Nebraska, New Mexico, New York, North Dakota, Ohio, Oklahoma,
Pennsylvania, Saskatchewan, South Dakota, Texas, Utah, Virginia, West Virginia,
Wisconsin, Wyoming.
-30-
Mike Donoghue, Free Press Staff Writer 12:58 p.m. EST December 8,
2014
A retired Burlington Police corporal is facing Vermont charges of illegal
importation of deer from a chronic wasting disease endemic area in New York, the
Vermont Fish and Wildlife Department said Monday. Game wardens raided the home
of Alan Baker, 70, on James Avenue last week and seized evidence of four deer
that were imported from the Lowlands Whitetails Hunting Ranch in Lowville, N.Y.,
officials said
Baker also attempted to report the deer as being killed in Vermont, Game
Warden Robert Currier said.
He said Baker has been ordered to appear in Vermont Superior Court on Feb.
10 to face three counts of importing deer from a Chronic Wasting Disease endemic
area and captive hunt facility.
Evidence obtained through the search warrant as well as information
provided by Environmental Police Officers of the New York Department of
Environmental Conservation and the New York State Police proved that Baker has
imported deer from this facility in 2012, 2013 and 2014, Currier said.
For each offense, if convicted, Baker could be fined up to $1,000 with five
points charged against his privilege to hunt, fish and trap.
He also could lose his hunting, fishing and trapping privileges for two
years upon conviction, officials said.
CWD is a fatal disease of the brain and nervous system in deer and elk.
Abnormal prion proteins produce lesions in the brain that cause disorientation
and emaciation.
A Vermont regulation requires special processing of deer or elk carcasses
being imported from states or provinces that have, or have had, CWD, the Vermont
Fish and Wildlife Department said.
The disease has been found in more than 20 states and two Canadian
provinces, including New York.
Contact Mike Donoghue at 660-1845 or mdonoghue@freepressmedia.com Follow
Mike on Twitter at www.twitter.com/FreepsMikeD.
>>> A retired Burlington Police corporal is facing Vermont charges
of illegal importation of deer from a chronic wasting disease endemic area in
New York, the Vermont Fish and Wildlife Department said Monday. <<<
I kindly submit the following science, please use as you wish...
PENS, pens, pens, Scrapie vs CWD, is there a difference ??? please see the
science.
cwd to humans ? please see the science. ...
kind regards, terry
From: Terry S. Singeltary Sr. Sent: Monday, November 03, 2014 11:11 AM To:
BSE-L@LISTS.AEGEE.ORG Subject: [BSE-L] Persistence of ovine scrapie infectivity
in a farm environment following cleaning and decontamination
Paper
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
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.
Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD)
Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National
Animal Disease Center, ARS, USDA, Ames, IA
snip...
This highlights the facts that
1) prior to the onset of clinical signs PrPSc is widely distributed in the
CNS and lymphoid tissues and
2) currently used diagnostic methods are sufficient to detect PrPSc prior
to the onset of clinical signs.
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in white-tailed deer 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 consistent with 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 white-tailed deer 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 scrapie by
IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil,
retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and
spleen. While two WB patterns have been detected in brain regions of deer
inoculated by the natural route, unlike the IC inoculated deer, the pattern
similar to the scrapie inoculum predominates.
2011 Annual Report
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Unit
2011 Annual Report
In Objective 1, Assess cross-species transmissibility of transmissible
spongiform encephalopathies (TSEs) in livestock and wildlife, numerous
experiments assessing the susceptibility of various TSEs in different host
species were conducted. Most notable is deer inoculated with scrapie, which
exhibits similarities to chronic wasting disease (CWD) in deer suggestive of
sheep scrapie as an origin of CWD.
snip...
4. Accomplishments
1. Deer inoculated with domestic isolates of sheep scrapie.
Scrapie-affected deer exhibit 2 different patterns of disease associated prion
protein. In some regions of the brain the pattern is much like that observed for
scrapie, while in others it is more like chronic wasting disease (CWD), the
transmissible spongiform encephalopathy typically associated with deer.
his work conducted by ARS scientists at the National Animal Disease Center,
Ames, IA suggests that an interspecies transmission of sheep scrapie to deer may
have been the origin of CWD. This is important for husbandry practices with both
captive deer, elk and sheep for farmers and ranchers attempting to keep their
herds and flocks free of CWD and 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
snip...
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 ;
SEE MORE USAHA REPORTS HERE, 2012 NOT PUBLISHED YET...TSS
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep. ...
also, see where even decades back, the USDA had the same thought as they do
today with CWD, not their problem...see page 27 below as well, where USDA stated
back then, the same thing they stated in the state of Pennsylvania, not their
damn business, once they escape, and they said the same thing about CWD in
general back then ;
”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.
Conclusions. During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature. Acknowledgments.
Supported by NIH grant RO1-NS-061902 and grant D12ZO-045 from the Morris Animal
Foundation.
*** We conclude that TSE infectivity is likely to survive burial for long
time periods with minimal loss of infectivity and limited movement from the
original burial site. However PMCA results have shown that there is the
potential for rainwater to elute TSE related material from soil which could lead
to the contamination of a wider area. These experiments reinforce the importance
of risk assessment when disposing of TSE risk materials.
*** The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
PRION 2014 CONFERENCE
CHRONIC WASTING DISEASE CWD
A FEW FINDINGS ;
Conclusions. To our knowledge, this is the first established experimental
model of CWD in TgSB3985. We found evidence for co-existence or divergence of
two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice.
Finally, we observed phenotypic differences between cervid-derived CWD and
CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway
to characterize these strains.
We conclude that TSE infectivity is likely to survive burial for long time
periods with minimal loss of infectivity and limited movement from the original
burial site. However PMCA results have shown that there is the potential for
rainwater to elute TSE related material from soil which could lead to the
contamination of a wider area. These experiments reinforce the importance of
risk assessment when disposing of TSE risk materials.
The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
Our data establish that meadow voles are permissive to CWD via peripheral
exposure route, suggesting they could serve as an environmental reservoir for
CWD. Additionally, our data are consistent with the hypothesis that at least two
strains of CWD circulate in naturally-infected cervid populations and provide
evidence that meadow voles are a useful tool for CWD strain typing.
Conclusion. CWD prions are shed in saliva and urine of infected deer as
early as 3 months post infection and throughout the subsequent >1.5 year
course of infection. In current work we are examining the relationship of
prionemia to excretion and the impact of excreted prion binding to surfaces and
particulates in the environment.
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC)
are shed in urine of infected deer as early as 6 months post inoculation and
throughout the subsequent disease course. Further studies are in progress
refining the real-time urinary prion assay sensitivity and we are examining more
closely the excretion time frame, magnitude, and sample variables in
relationship to inoculation route and prionemia in naturally and experimentally
CWD-infected cervids.
Conclusions. Our results suggested that the odds of infection for CWD is
likely controlled by areas that congregate deer thus increasing direct
transmission (deer-to-deer interactions) or indirect transmission
(deer-to-environment) by sharing or depositing infectious prion proteins in
these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely
controlled by separate factors than found in the Midwestern and endemic areas
for CWD and can assist in performing more efficient surveillance efforts for the
region.
Conclusions. During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature.
see full text and more ;
Monday, June 23, 2014
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by
heat treatment in yellow grease produced in the industrial manufacturing process
of meat and bone meals
Sunday, November 3, 2013
*** Environmental Impact Statements; Availability, etc.: Animal Carcass
Management [Docket No. APHIS-2013-0044]
Friday, October 17, 2014
Missouri Final action on Orders of Rule making Breeders and Big Game
Hunting Preserves
Saturday, October 18, 2014
Chronic wasting disease threatens Canadian agriculture, Alberta MLA
says
Thursday, October 23, 2014
*** FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE
PRESERVE
Tuesday, October 21, 2014
*** Pennsylvania Department of Agriculture Tenth Pennsylvania Captive Deer
Tests Positive for Chronic Wasting Disease CWD TSE PRION DISEASE
Tuesday, October 07, 2014
*** Wisconsin white-tailed deer tested positive for CWD on a Richland
County breeding farm, and a case of CWD has been discovered on a Marathon County
hunting preserve
Thursday, October 02, 2014
*** IOWA TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE
RELEASED 79.8 percent of the deer tested positive for the disease
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s the
risk to humans and pets?
Tuesday, July 01, 2014
*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND
POTENTIAL RISK FACTORS THERE FROM
Saturday, October 25, 2014
118th USAHA Annual Meeting CWD and Captive Cerivds
IN THE UNITED STATES DISTRICT COURT FOR THE NORTHERN DISTRICT OF INDIANA
SOUTH BEND DIVISION UNITED STATES OF AMERICA, vs. RUSSELL G. BELLAR, Defendant.
___________________________
)))))))))
Cause No.: 3:04cr00068-AS South Bend, Indiana January 4, 2005 9:30 a.m.
TRANSCRIPT EXCERPT OF JURY TRIAL (TESTIMONY OF: RONNIE DUNN AND RUSTY CAMP)
BEFORE THE HONORABLE ALLEN SHARP
snip...
Ronnie Dunn Cross Examination
Q. Mr. Dunn, at one point I believe you told the federal agents that Mr.
Bellar told you that this was a private deer farm and shooting deer on that farm
was like slaughtering cattle; is that correct?
A. I don't know if I used the word "slaughter," but it was, yeah, like
that.
Q. You don't know if that was your word, "slaughtering cattle"?
A. I don't know that.
Q. Well, did he give you the idea of killing cattle?
A. Yes, it was the same principle.
snip...
see full text ;
BUCK FEVER
*** 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.
These data suggest that recommended current guidelines for the
decontamination of farm buildings following outbreaks of scrapie do little to
reduce the titre of infectious scrapie material and that environmental
recontamination could also be an issue associated with these premises.
Scrapie Sheep Goats Transmissible spongiform encephalopathies (TSE)
Accepted October 12, 2014. Published Online First 31 October 2014
Monday, November 3, 2014
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
cwd exposure, and iatrogenic CJD, what if ???
*** our results raise the possibility that CJD cases classified as VV1 may
include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne
infection by type 1 prions from animals, e.g., chronic wasting disease prions in
cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have
been reported (40, 41). The results of the present study emphasize the need for
traceback studies and careful re-examination of the biochemical properties of
sCJD-VV1 prions. ***
snip...see full text ;
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant
Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
*** We hypothesize that both BSE prions and CWD prions passaged through
felines will seed human recPrP more efficiently than BSE or CWD from the
original hosts, evidence that the new host will dampen the species barrier
between humans and BSE or CWD. The new host effect is particularly relevant as
we investigate potential means of trans-species transmission of prion disease.
Tuesday, November 04, 2014
*** Six-year follow-up of a point-source exposure to CWD contaminated
venison in an Upstate New York community: risk behaviours and health outcomes
2005–2011
Tuesday, November 04, 2014
Towards an Age-Dependent Transmission Model of Acquired and Sporadic
Creutzfeldt-Jakob Disease
Friday, December 5, 2014
*** SPECIAL ALERT The OIE recommends strengthening animal disease
surveillance worldwide
*** OIE BSE TSE PRION AKA MAD COW DISEASE ?
‘’the silence was deafening’’ ...tss
Wednesday, December 3, 2014
Over 200 Groups Urge Congress to Continue Supporting COOL
For Immediate Release
Tuesday, December 2, 2014
UK EXPORTS OF MBM TO WORLD Bovine Spongiform Encephalopathy BSE TSE Prion
aka Mad Cow Disease
USA, NORTH AMERICA, MBM (or any potential TSE prion disease) EXPORTS TO THE
WORLD (?) [protected by the BSE MRR policy] $$$
Monday, December 1, 2014
Germany Bovine Spongiform Encephalopathy BSE CJD TSE Prion disease A Review
December 1, 2014
Friday, November 28, 2014
BOVINE SPONGIFORM ENCEPHALOPATHY BSE AKA MAD COW DISEASE PORTUGAL CONFIRMED
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
Monday, May 5, 2014
Brazil BSE Mad Cow disease confirmed OIE 02/05/2014
*** OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED, WISHES TO
CONTINUE SPREADING IT AROUND THE GLOBE
Monday, November 30, 2009
*** USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL
HEALTH CODE, DOES NOT SURPRISE ME $
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of known
infectious tissues. The asymptomatic incubation period in the one monkey exposed
to the virus of kuru was 36 months; that in the two monkeys exposed to the virus
of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the
two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the monkeys failed
to reveal signs or oral lesions. One additional monkey similarly exposed to kuru
has remained asymptomatic during the 39 months that it has been under
observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie
by natural feeding to squirrel monkeys that we have reported provides further
grounds for concern that scrapie-infected meat may occasionally give rise in
humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
Recently the question has again been brought up as to whether scrapie is
transmissible to man. This has followed reports that the disease has been
transmitted to primates. One particularly lurid speculation (Gajdusek 1977)
conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and
transmissible encephalopathy of mink are varieties of a single "virus". The U.S.
Department of Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed for human
or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is
emphasised by the finding that some strains of scrapie produce lesions identical
to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety of laboratory
personnel requires prompt attention. Second, action such as the "scorched meat"
policy of USDA makes the solution of the acrapie problem urgent if the sheep
industry is not to suffer grievously.
snip...
76/10.12/4.6
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes
of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey
(Macaca fascicularis) with an incubation period of more than 5 yr from the time
of intracerebral inoculation of scrapie-infected mouse brain. The animal
developed a chronic central nervous system degeneration, with ataxia, tremor and
myoclonus with associated severe scrapie-like pathology of intensive astroglial
hypertrophy and proliferation, neuronal vacuolation and status spongiosus of
grey matter. The strain of scrapie virus used was the eighth passage in Swiss
mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral
passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton,
Berkshire).
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
Sunday, December 12, 2010
EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2
December 2010
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
Thursday, December 23, 2010
Molecular Typing of Protease-Resistant Prion Protein in Transmissible
Spongiform Encephalopathies of Small Ruminants, France, 2002-2009
Volume 17, Number 1 January 2011
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform
encephalopathy following passage in sheep
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
*** Canada Increased Atypical Scrapie Detections
Press reports indicate that increased surveillance is catching what
otherwise would have been unreported findings of atypical scrapie in sheep. In
2009, five new cases have been reported in Quebec, Ontario, Alberta, and
Saskatchewan. With the exception of Quebec, all cases have been diagnosed as
being the atypical form found in older animals. Canada encourages producers to
join its voluntary surveillance program in order to gain scrapie-free status.
The World Animal Health will not classify Canada as scrapie-free until no new
cases are reported for seven years. The Canadian Sheep Federation is calling on
the government to fund a wider surveillance program in order to establish the
level of prevalence prior to setting an eradication date. Besides long-term
testing, industry is calling for a compensation program for farmers who report
unusual deaths in their flocks.
Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine
(reticular) deposits, see also ; All of the Heidenhain variants were of the
methionine/ methionine type 1 molecular subtype.
Tuesday, July 29, 2008
Heidenhain Variant Creutzfeldt Jakob Disease Case Report
snip...
Heidenhain Variant Creutzfeldt Jakob Disease autopsy case report 'MOM'
DIVISION OF NEUROPATHOLOGY University of Texas Medical Branch 114 McCullough
Bldg. Galveston, Texas 77555-0785 FAX COVER SHEET DATE: 4-23-98 TO: Mr. Terry
Singeltary @ ------- FROM: Gerald Campbell FAX: (409) 772-5315 PHONE: (409)
772-2881 Number of Pages (including cover sheet): Message: *CONFIDENTIALITY
NOTICE* This document accompanying this transmission contains confidential
information belonging to the sender that is legally privileged. This information
is intended only for the use of the individual or entry names above. If you are
not the intended recipient, you are hereby notified that any disclosure, copying
distribution, or the taking of any action in reliances on the contents of this
telefaxed information is strictly prohibited. If you received this telefax in
error, please notify us by telephone immediately to arrange for return of the
original documents. -------------------------- Patient Account: 90000014-518
Med. Rec. No.: (0160)118511Q Patient Name: POULTER, BARBARA Age: 63 YRS DOB:
10/17/34 Sex: F Admitting Race: C Attending Dr.: Date / Time Admitted : 12/14/97
1228 Copies to: UTMB University of Texas Medical Branch Galveston, Texas
77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report FINAL AUTOPSY
DIAGNOSIS Autopsy' Office (409)772-2858 Autopsy NO.: AU-97-00435 AUTOPSY
INFORMATION: Occupation: Unknown Birthplace: Unknown Residence: Crystal Beach
Date/Time of Death: 12/14/97 13:30 Date/Time of Autopsy: 12/15/97 15:00
Pathologist/Resident: Pencil/Fernandez Service: Private Restriction: Brain only
FINAL AUTOPSY DIAGNOSIS
I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.
snip...see full text ;
P.5.21 Parallels between different forms of sheep scrapie and types of
Creutzfeldt-Jakob disease (CJD)
Wiebke M. Wemheuer1, Sylvie L. Benestad2, Arne Wrede1, Wilhelm E.
Wemheuer3, Tatjana Pfander1, Bjørn Bratberg2, Bertram Brenig3,Walter J.
Schulz-Schaeffer1 1University Medical Center Goettingen, Germany; 2Institute of
Veterinary Medicine Oslo, Norway; 3Institute of Veterinary Medicine Goettingen,
Germany
Background: Scrapie in sheep and goats is often regarded as the archetype
of prion diseases. In 1998, a new form of scrapie - atypical/Nor98 scrapie - was
described that differed from classical scrapie in terms of epidemiology, Western
blot profile, the distribution of pathological prion protein (PrPSc) in the body
and its stability against proteinase K. In a similar way, distinct disease types
exist in sporadic Creutzfeldt-Jakob disease (CJD). They differ with regard to
their clinical outcome, Western blot profile and PrPSc deposition pattern in the
central nervous system (CNS). Objectives: The comparison of PrPSc deposits in
sheep scrapie and human sporadic CJD.
Methods: Tissues of the CNS of sheep with classical scrapie, sheep with
atypical/Nor98 scrapie and 20 patients with sporadic CJD were examined using the
sensitive Paraffin Embedded Tissue (PET) blot method. The results were compared
with those obtained by immunohistochemistry. With the objective of gaining
information on the protein conformation, the PrPSc of classical and
atypical/Nor98 sheep scrapie and sporadic CJD was tested for its stability
against denaturation with guanidine hydrochloride (GdnHCl) using a Membrane
Adsorption Assay.
Results: The PrPSc of atypical/Nor98 scrapie cases and of CJD prion type 1
patients exhibits a mainly reticular/synaptic deposition pattern in the brain
and is relatively sensitive to denaturation with GdnHCl. In contrast classical
scrapie cases and CJD prion type 2 patients have a more complex PrPSc deposition
pattern in common that consists of larger PrPSc aggregates and the PrPSc itself
is comparatively stable against denaturation.
Discussion: The similarity between CJD types and scrapie types indicates
that at least two comparable forms of the misfolded prion protein exist beyond
species barriers and can elicit prion diseases. It seems therefore reasonable to
classify classical and atypical/Nor98 scrapie - in analogy to the existing CJD
types - as different scrapie types.
What if you can catch old-fashioned CJD by eating meat from a sheep
infected with scrapie?
28 Mar 01
Like lambs to the slaughter 31 March 2001 by Debora MacKenzie Magazine
issue 2284. Subscribe and get 4 free issues. FOUR years ago, Terry Singeltary
watched his mother die horribly from a degenerative brain disease. Doctors told
him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit
her violent symptoms, and he demanded an autopsy. It showed she had died of
sporadic Creutzfeldt-Jakob disease.
Most doctors believe that sCJD is caused by a prion protein deforming by
chance into a killer. But Singeltary thinks otherwise. He is one of a number of
campaigners who say that some sCJD, like the variant CJD related to BSE, is
caused by eating meat from infected animals. Their suspicions have focused on
sheep carrying scrapie, a BSE-like disease that is widespread in flocks across
Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight
to the campaigners' fears. To their complete surprise, the researchers found
that one strain of scrapie causes the same brain damage in mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by
some strains of scrapie," says team member Jean-Philippe Deslys of the French
Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses,
south-west of Paris. Hans Kretschmar of the University of Göttingen, who
coordinates CJD surveillance in Germany, is so concerned by the findings that he
now wants to trawl back through past sCJD cases to see if any might have been
caused by eating infected mutton or lamb.
Scrapie has been around for centuries and until now there has been no
evidence that it poses a risk to human health. But if the French finding means
that scrapie can cause sCJD in people, countries around the world may have
overlooked a CJD crisis to rival that caused by BSE.
Deslys and colleagues were originally studying vCJD, not sCJD. They
injected the brains of macaque monkeys with brain from BSE cattle, and from
French and British vCJD patients. The brain damage and clinical symptoms in the
monkeys were the same for all three. Mice injected with the original sets of
brain tissue or with infected monkey brain also developed the same
symptoms.
As a control experiment, the team also injected mice with brain tissue from
people and animals with other prion diseases: a French case of sCJD; a French
patient who caught sCJD from human-derived growth hormone; sheep with a French
strain of scrapie; and mice carrying a prion derived from an American scrapie
strain. As expected, they all affected the brain in a different way from BSE and
vCJD. But while the American strain of scrapie caused different damage from
sCJD, the French strain produced exactly the same pathology.
"The main evidence that scrapie does not affect humans has been
epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute
for Animal Health in Edinburgh, who was a member of the same team as Deslys.
"You see about the same incidence of the disease everywhere, whether or not
there are many sheep, and in countries such as New Zealand with no scrapie." In
the only previous comparisons of sCJD and scrapie in mice, Bruce found they were
dissimilar.
But there are more than 20 strains of scrapie, and six of sCJD. "You would
not necessarily see a relationship between the two with epidemiology if only
some strains affect only some people," says Deslys. Bruce is cautious about the
mouse results, but agrees they require further investigation. Other trials of
scrapie and sCJD in mice, she says, are in progress.
People can have three different genetic variations of the human prion
protein, and each type of protein can fold up two different ways. Kretschmar has
found that these six combinations correspond to six clinical types of sCJD: each
type of normal prion produces a particular pathology when it spontaneously
deforms to produce sCJD.
But if these proteins deform because of infection with a disease-causing
prion, the relationship between pathology and prion type should be different, as
it is in vCJD. "If we look at brain samples from sporadic CJD cases and find
some that do not fit the pattern," says Kretschmar, "that could mean they were
caused by infection."
There are 250 deaths per year from sCJD in the US, and a similar incidence
elsewhere. Singeltary and other US activists think that some of these people
died after eating contaminated meat or "nutritional" pills containing dried
animal brain. Governments will have a hard time facing activists like Singeltary
if it turns out that some sCJD isn't as spontaneous as doctors have
insisted.
Deslys's work on macaques also provides further proof that the human
disease vCJD is caused by BSE. And the experiments showed that vCJD is much more
virulent to primates than BSE, even when injected into the bloodstream rather
than the brain. This, says Deslys, means that there is an even bigger risk than
we thought that vCJD can be passed from one patient to another through
contaminated blood transfusions and surgical instruments.
Monday, December 1, 2008
When Atypical Scrapie cross species barriers
lost my mom to hvCJD ‘confirmed’ December 14, 1997, just made a promise,
never forget, and never let them forget...
MOM
Sunday, November 23, 2014
*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas
in June 2014 confirmed as USA case NOT European
‘’The specific overseas country where this patient’s infection occurred is
less clear largely because the investigation did not definitely link him to a
country where other known vCJD cases likely had been infected.’’
‘’IN STRICT CONFIDENCE’’
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
Singeltary comment ;
Sunday, December 7, 2014
Scientific update on the potential for transmissibility of non-prion
protein misfolding diseases PRIONOIDS
Terry S. Singeltary Sr.
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