Current as of: 2015-01-31
Domestic cervid herds confirmed to be infected with CWD in Canada in 2015
Date confirmed Location Animal type infected January 16 Alberta Elk
First case of chronic wasting disease found in farm elk since 2002
Darcy Henton, Calgary Herald More from Darcy Henton, Calgary Herald
Colette Derworiz, Calgary Herald More from Colette Derworiz, Calgary Herald
Published on: February 9, 2015 | Last Updated: February 9, 2015 11:09 PM MST
An elk with its antlers cut off at a game farm in Alberta.
An elk with its antlers cut off at a game farm in Alberta. larry wong /
Edmonton Journal
An Alberta elk farm is under quarantine after routine testing detected the
first case of chronic wasting disease in domestic elk in more than a
decade.
The fatal nervous system disease that affects elk, moose and deer was
discovered on a farm at an undisclosed location in Alberta early in the year and
subsequent testing in mid-January confirmed it, Alberta Agriculture spokesman
Mike Long said late Monday.
“I can confirm that there is a case in Alberta in farmed elk and that CFIA
(Canadian Food Inspection Agency) is managing the situation,” Long said. “I
believe it is just one animal that tested positive.”
It was the first case of chronic wasting disease in domestic elk since an
outbreak in 2002 resulted in the extermination or “depopulation” of several
herds.
Alberta has more than 200 elk farms that generate more than $10 million in
product sales annually.
Long said the heads of slaughtered farm elk are tested routinely as part of
a disease monitoring process.
“That’s how this sample was detected,” he said.
He couldn’t say why the province didn’t make the discovery public,
deferring questions to the CFIA.
A CFIA spokeswoman said the case would be reported Tuesday in the agency’s
monthly disease report, but she could not say why the incident was not made
public earlier. She had no other information.
Jeffrey English, spokesman for federal Agriculture Minister Gerry Ritz,
said only that tests revealed “a higher per cent of positives than what is
commonly found.”
“Positive cases are found regularly in farmed and wild cervids throughout
Alberta and Saskatchewan,” he said in an email.
Just last October, Agriculture Minister Verlyn Olson boasted there hadn’t
been a case of chronic wasting disease in domestic elk in the province in more
than a decade, despite testing of more than 50,000 animals.
Darrel Rowledge, of the Alliance for Public Wildlife, said he believes the
elk was a two-year-old male from a farm in east central Alberta in the
Lloydminster area.
He is concerned that two levels of government kept the discovery
secret.
“Part of the reason this is so alarming, this would not have come out if it
weren’t for whistleblowers within the government,” said Rowledge.
Just last fall, the province passed legislation to make Alberta one of the
first jurisdictions in North America to proclaim that any elk that stray from a
farm remain the property of the farmers for the rest of their lives. Previously
they were often shot by Wildlife officers as a precaution against the spread of
wasting disease.
Internal government briefing notes obtained by the Herald last spring
warned the move would trigger concerns about “the implications for disease or
genetic contamination, confusion and uncertainty on behalf of hunters who shoot
tagged elk, (and) issues with private elk on private property, including
property damage and compensation.”
But Olson downplayed that concern based on Alberta’s disease-free status
and the relatively few incidents of domestic elk escaping to the wild.
Chronic wasting disease was first detected in a research facility in
Colorado in 1967 and surfaced at a Saskatchewan elk farm in 1996, according to
the CFIA website. Testing is mandatory in Alberta, Saskatchewan, Manitoba and
the Yukon but is voluntary in other jurisdictions.
The disease spreads from animal to animal through saliva and feces. There
is no treatment or vaccine.
The source of the last infection in Alberta in 2002 was never
determined.
dhenton@calgaryherald.com
Canada has had a COVER-UP policy of mad cow disease since about the 17th
case OR 18th case of mad cow disease. AFTER THAT, all FOIA request were ignored
$$$
THIS proves there is indeed an epidemic of mad cow disease in North
America, and it has been covered up for years and years, if not for decades, and
it’s getting worse $$$
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011
and how to hide mad cow disease in Canada Current as of: 2011-01-31
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM
ENCEPHALOPATHY (BSE) IN CANADA
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM
ENCEPHALOPATHY (BSE) IN CANADA
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
Tuesday, May 21, 2013
Canada, USA, Bad feed, mad cows: Why we know three BSE cases had a common
origin and why the SSS policy is in full force $$$
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.
Current as of: 2015-01-31
Sheep flocks and/or goat herds confirmed to be infected with classical
scrapie in Canada in 2015 Date confirmed Location Animal type infected January 5
Ontario Goat
Wednesday, June 18, 2008
CHRONIC WASTING DISEASE FOUND IN 24 MORE DEER IN ALBERTA
Monday, April 07, 2014
Saskatchewan’s first chronic wasting disease case of the year has been
confirmed 2014
Saturday, October 18, 2014
Chronic wasting disease threatens Canadian agriculture, Alberta MLA says
Tuesday, December 20, 2011
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats)
FarmUpdate DECEMBER 2011The CWD infection rate was nearly 80%, the highest ever
in a North American captive herd. RECOMMENDATION: That the Board approve the
purchase of 80acres of land for $465,000 for the Statewide Wildlife Habitat
Program inPortage County and approve the restrictions on public use of the
site.SUMMARY:
For Immediate Release Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or
Dustin.VandeHoef@IowaAgriculture.gov
TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED
79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today
announced that the test results from the depopulation of a quarantined captive
deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the
herd, tested positive for Chronic Wasting Disease (CWD). The owners of the
quarantined herd have entered into a fence maintenance agreement with the Iowa
Department of Agriculture and Land Stewardship,which requires the owners to
maintain the 8’ foot perimeter fence around the herd premises for five years
after the depopulation was complete and the premises had been cleaned and
disinfected CWD is a progressive, fatal, degenerative neurological disease of
farmed and free-ranging deer, elk, and moose. There is no known treatment or
vaccine for CWD. CWD is not a disease that affects humans.On July 18, 2012, USDA
Animal and Plant Health Inspection Service’s (APHIS)National Veterinary Services
Lab in Ames, IA confirmed that a male whitetail deer harvested from a hunting
preserve in southeast IA was positive for CWD. An investigation revealed that
this animal had just been introduced into the hunting preserve from the
above-referenced captive deer herd in north-central Iowa.The captive deer herd
was immediately quarantined to prevent the spread of CWD. The herd has remained
in quarantine until its depopulation on August 25 to 27, 2014.The Iowa
Department of Agriculture and Land Stewardship participated in a joint operation
to depopulate the infected herd with USDA Veterinary Services, which was the
lead agency, and USDA Wildlife Services.Federal indemnity funding became
available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at
that time, which was before depopulation and testing, at $1,354,250. At that
time a herd plan was developed with the owners and officials from USDA and the
Iowa Department of Agriculture and Land Stewardship.Once the depopulation was
complete and the premises had been cleaned and disinfected, indemnity of
$917,100.00 from the USDA has been or will be paid to the owners as compensation
for the 356 captive deer depopulated.The Iowa Department of Agriculture and Land
Stewardship operates a voluntary CWD program for farms that sell live animals.
Currently 145 Iowa farms participate in the voluntary program. The
above-referenced captive deer facility left the voluntary CWD program prior to
the discovery of the disease as they had stopped selling live animals. All deer
harvested in a hunting preserve must be tested for CWD. -30-
*** see history of this CWD blunder here ;
Tuesday, January 06, 2015
APHIS Provides Additional Information on Chronic Wasting Disease (CWD)
Indemnity Requests January 5, 2015 05:26 PM EST
***please read this***
98 | Veterinary Record | January 24, 2015
EDITORIAL
Scrapie: a particularly persistent pathogen
Cristina Acín
Resistant prions in the environment have been the sword of Damocles for
scrapie control and eradication. Attempts to establish which physical and
chemical agents could be applied to inactivate or moderate scrapie infectivity
were initiated in the 1960s and 1970s,with the first study of this type focusing
on the effect of heat treatment in reducing prion infectivity (Hunter and
Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate
the prion protein are based on the method developed by Kimberlin and
collaborators (1983). This procedure consists of treatment with 20,000 parts per
million free chlorine solution, for a minimum of one hour, of all surfaces that
need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so
on). Despite this, veterinarians and farmers may still ask a range of questions,
such as ‘Is there an official procedure published somewhere?’ and ‘Is there an
international organisation which recommends and defines the exact method of
scrapie decontamination that must be applied?’
From a European perspective, it is difficult to find a treatment that could
be applied, especially in relation to the disinfection of surfaces in lambing
pens of affected flocks. A 999/2001 EU regulation on controlling spongiform
encephalopathies (European Parliament and Council 2001) did not specify a
particular decontamination measure to be used when an outbreak of scrapie is
diagnosed. There is only a brief recommendation in Annex VII concerning the
control and eradication of transmissible spongiform encephalopathies (TSE
s).
Chapter B of the regulation explains the measures that must be applied if
new caprine animals are to be introduced to a holding where a scrapie outbreak
has previously been diagnosed. In that case, the statement indicates that
caprine animals can be introduced ‘provided that a cleaning and disinfection of
all animal housing on the premises has been carried out following
destocking’.
Issues around cleaning and disinfection are common in prion prevention
recommendations, but relevant authorities, veterinarians and farmers may have
difficulties in finding the specific protocol which applies. The European Food
and Safety Authority (EFSA ) published a detailed report about the efficacy of
certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and
even a formulation of copper or iron metal ions in combination with hydrogen
peroxide, against prions (EFSA 2009). The report was based on scientific
evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006,
Solassol and others 2006) but unfortunately the decontamination measures were
not assessed under outbreak conditions.
The EFSA Panel on Biological Hazards recently published its conclusions on
the scrapie situation in the EU after 10 years of monitoring and control of the
disease in sheep and goats (EFSA 2014), and one of the most interesting findings
was the Icelandic experience regarding the effect of disinfection in scrapie
control. The Icelandic plan consisted of: culling scrapie-affected sheep or the
whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of
stables, sheds, barns and equipment with high pressure washing followed by
cleaning with 500 parts per million of hypochlorite; drying and treatment with
300 ppm of iodophor; and restocking was not permitted for at least two years.
Even when all of these measures were implemented, scrapie recurred on several
farms, indicating that the infectious agent survived for years in the
environment, even as many as 16 years after restocking (Georgsson and others
2006).
In the rest of the countries considered in the EFSA (2014) report,
recommendations for disinfection measures were not specifically defined at the
government level. In the report, the only recommendation that is made for sheep
is repopulation with sheep with scrapie-resistant genotypes. This reduces the
risk of scrapie recurrence but it is difficult to know its effect on the
infection.
Until the EFSA was established (in May 2003), scientific opinions about TSE
s were provided by the Scientific Steering Committee (SSC) of the EC, whose
advice regarding inactivation procedures focused on treating animal waste at
high temperatures (150°C for three hours) and high pressure alkaline hydrolysis
(SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory
Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe
working and the prevention of TSE infection. Annex C of the ACDP report
established that sodium hypochlorite was considered to be effective, but only if
20,000 ppm of available chlorine was present for at least one hour, which has
practical limitations such as the release of chlorine gas, corrosion,
incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its
active chemicals and the stability of dilutions (ACDP 2009).
In an international context, the World Organisation for Animal Health (OIE)
does not recommend a specific disinfection protocol for prion agents in its
Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General
recommendations on disinfection and disinsection (OIE 2014), focuses on
foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on
prion disinfection. Nevertheless, the last update published by the OIE on bovine
spongiform encephalopathy (OIE 2012) indicates that few effective
decontamination techniques are available to inactivate the agent on surfaces,
and recommends the removal of all organic material and the use of sodium
hydroxide, or a sodium hypochlorite solution containing 2 per cent available
chlorine, for more than one hour at 20ºC.
The World Health Organization outlines guidelines for the control of TSE s,
and also emphasises the importance of mechanically cleaning surfaces before
disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO
1999).
Finally, the relevant agencies in both Canada and the USA suggest that the
best treatments for surfaces potentially contaminated with prions are sodium
hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution,
while most commercial household bleaches contain 5.25 per cent sodium
hypochlorite. It is therefore recommended to dilute one part 5.25 per cent
bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency
2013).
So what should we do about disinfection against prions? First, it is
suggested that a single protocol be created by international authorities to
homogenise inactivation procedures and enable their application in all
scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available
chlorine seems to be the procedure used in most countries, as noted in a paper
summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015).
But are we totally sure of its effectiveness as a preventive measure in a
scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease
be needed?
What we can conclude is that, if we want to fight prion diseases, and
specifically classical scrapie, we must focus on the accuracy of diagnosis,
monitoring and surveillance; appropriate animal identification and control of
movements; and, in the end, have homogeneous and suitable protocols to
decontaminate and disinfect lambing barns, sheds and equipment available to
veterinarians and farmers. Finally, further investigations into the resistance
of prion proteins in the diversity of environmental surfaces are required.
References
snip...
98 | Veterinary Record | January 24, 2015
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
Steve A. C. Hawkins, MIBiol, Pathology Department1, Hugh A. Simmons, BVSc
MRCVS, MBA, MA Animal Services Unit1, Kevin C. Gough, BSc, PhD2 and Ben C.
Maddison, BSc, PhD3 + Author Affiliations
1Animal and Plant Health Agency, Woodham Lane, New Haw, Addlestone, Surrey
KT15 3NB, UK 2School of Veterinary Medicine and Science, The University of
Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK 3ADAS
UK, School of Veterinary Medicine and Science, The University of Nottingham,
Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK E-mail for
correspondence: ben.maddison@adas.co.uk Abstract Scrapie of sheep/goats and
chronic wasting disease of deer/elk are contagious prion diseases where
environmental reservoirs are directly implicated in the transmission of disease.
In this study, the effectiveness of recommended scrapie farm decontamination
regimens was evaluated by a sheep bioassay using buildings naturally
contaminated with scrapie. Pens within a farm building were treated with either
20,000 parts per million free chorine solution for one hour or were treated with
the same but were followed by painting and full re-galvanisation or replacement
of metalwork within the pen. Scrapie susceptible lambs of the PRNP genotype
VRQ/VRQ were reared within these pens and their scrapie status was monitored by
recto-anal mucosa-associated lymphoid tissue. All animals became infected over
an 18-month period, even in the pen that had been subject to the most stringent
decontamination process. These data suggest that recommended current guidelines
for the decontamination of farm buildings following outbreaks of scrapie do
little to reduce the titre of infectious scrapie material and that environmental
recontamination could also be an issue associated with these premises.
SNIP...
Discussion
Thorough pressure washing of a pen had no effect on the amount of
bioavailable scrapie infectivity (pen B). The routine removal of prions from
surfaces within a laboratory setting is treatment for a minimum of one hour with
20,000 ppm free chlorine, a method originally based on the use of brain
macerates from infected rodents to evaluate the effectiveness of decontamination
(Kimberlin and others 1983). Further studies have also investigated the
effectiveness of hypochlorite disinfection of metal surfaces to simulate the
decontamination of surgical devices within a hospital setting. Such treatments
with hypochlorite solution were able to reduce infectivity by 5.5 logs to lower
than the sensitivity of the bioassay used (Lemmer and others 2004). Analogous
treatment of the pen surfaces did not effectively remove the levels of scrapie
infectivity over that of the control pens, indicating that this method of
decontamination is not effective within a farm setting. This may be due to the
high level of biological matrix that is present upon surfaces within the farm
environment, which may reduce the amount of free chlorine available to
inactivate any infectious prion. Remarkably 1/5 sheep introduced into pen D had
also became scrapie positive within nine months, with all animals in this pen
being RAMALT positive by 18 months of age. Pen D was no further away from the
control pen (pen A) than any of the other pens within this barn. Localised hot
spots of infectivity may be present within scrapie-contaminated environments,
but it is unlikely that pen D area had an amount of scrapie contamination that
was significantly different than the other areas within this building.
Similarly, there were no differences in how the biosecurity of pen D was
maintained, or how this pen was ventilated compared with the other pens. This
observation, perhaps, indicates the slower kinetics of disease uptake within
this pen and is consistent with a more thorough prion removal and
recontamination. These observations may also account for the presence of
inadvertent scrapie cases within other studies, where despite stringent
biosecurity, control animals have become scrapie positive during challenge
studies using barns that also housed scrapie-affected animals (Ryder and others
2009). The bioassay data indicate that the exposure of the sheep to a farm
environment after decontamination efforts thought to be effective in removing
scrapie is sufficient for the animals to become infected with scrapie. The main
exposure routes within this scenario are likely to be via the oral route, during
feeding and drinking, and respiratory and conjunctival routes. It has been
demonstrated that scrapie infectivity can be efficiently transmitted via the
nasal route in sheep (Hamir and others 2008), as is the case for CWD in both
murine models and in white-tailed deer (Denkers and others 2010, 2013).
Recently, it has also been demonstrated that CWD prions presented as dust when
bound to the soil mineral montmorillonite can be infectious via the nasal route
(Nichols and others 2013). When considering pens C and D, the actual source of
the infectious agent in the pens is not known, it is possible that biologically
relevant levels of prion survive on surfaces during the decontamination regimen
(pen C). With the use of galvanising and painting (pen D) covering and sealing
the surface of the pen, it is possible that scrapie material recontaminated the
pens by the movement of infectious prions contained within dusts originating
from other parts of the barn that were not decontaminated or from other areas of
the farm.
Given that scrapie prions are widespread on the surfaces of affected farms
(Maddison and others 2010a), irrespective of the source of the infectious prions
in the pens, this study clearly highlights the difficulties that are faced with
the effective removal of environmentally associated scrapie infectivity. This is
likely to be paralleled in CWD which shows strong similarities to scrapie in
terms of both the dissemination of prions into the environment and the facile
mode of disease transmission. These data further contribute to the understanding
that prion diseases can be highly transmissible between susceptible individuals
not just by direct contact but through highly stable environmental reservoirs
that are refractory to decontamination.
The presence of these environmentally associated prions in farm buildings
make the control of these diseases a considerable challenge, especially in
animal species such as goats where there is lack of genetic resistance to
scrapie and, therefore, no scope to re-stock farms with animals that are
resistant to scrapie.
Scrapie Sheep Goats Transmissible spongiform encephalopathies (TSE)
Accepted October 12, 2014. Published Online First 31 October 2014
Tuesday, December 16, 2014
Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1,
Affiliations Contributions Corresponding author Journal name: Nature
Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821
Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014
Article tools Citation Reprints Rights & permissions Article metrics
Abstract
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. The serial transmission of different scrapie isolates in
these mice led to the propagation of prions that are phenotypically identical to
those causing sporadic CJD (sCJD) in humans. These results demonstrate that
scrapie prions have a zoonotic potential and raise new questions about the
possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
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
Friday, January 30, 2015
Scrapie: a particularly persistent pathogen
Monday, November 3, 2014
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
PPo3-22:
Detection of Environmentally Associated PrPSc on a Farm with Endemic
Scrapie
Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh
Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of
Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories
Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University
of Nottingham; Sutton Bonington, Loughborough UK
Key words: scrapie, evironmental persistence, sPMCA
Ovine scrapie shows considerable horizontal transmission, yet the routes of
transmission and specifically the role of fomites in transmission remain poorly
defined. Here we present biochemical data demonstrating that on a
scrapie-affected sheep farm, scrapie prion contamination is widespread. It was
anticipated at the outset that if prions contaminate the environment that they
would be there at extremely low levels, as such the most sensitive method
available for the detection of PrPSc, serial Protein Misfolding Cyclic
Amplification (sPMCA), was used in this study. We investigated the distribution
of environmental scrapie prions by applying ovine sPMCA to samples taken from a
range of surfaces that were accessible to animals and could be collected by use
of a wetted foam swab. Prion was amplified by sPMCA from a number of these
environmental swab samples including those taken from metal, plastic and wooden
surfaces, both in the indoor and outdoor environment. At the time of sampling
there had been no sheep contact with these areas for at least 20 days prior to
sampling indicating that prions persist for at least this duration in the
environment. These data implicate inanimate objects as environmental reservoirs
of prion infectivity which are likely to contribute to disease transmission.
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.
*** 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, December 21, 2014
Mucosal immunization with an attenuated Salmonella vaccine partially
protects white-tailed deer from chronic wasting disease
Friday, December 19, 2014
Pan-Provincial Vaccine Enterprise Inc. (PREVENT) Conducting a Chronic
Wasting Disease (CWD) Vaccine Efficacy Trial in Elk
CHRONIC WASTING DISEASE CWD TSE PRION, how much does it pay to find CWD
$$$
CWD, spreading it around...
for the game farm industry, and their constituents, to continue to believe
that they are _NOT_, and or insinuate that they have _NEVER_ been part of the
problem, will only continue to help spread cwd. the game farming industry, from
the shooting pens, to the urine mills, the antler mills, the sperm mills, velvet
mills, shooting pens, to large ranches, are not the only problem, but it is
painfully obvious that they have been part of the problem for decades and
decades, just spreading it around, as with transportation and or exportation and
or importation of cervids from game farming industry, and have been proven to
spread cwd. no one need to look any further than South Korea blunder ;
===========================================
spreading cwd around...
Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of
farmed elk in Saskatchewan in a single epidemic. All of these herds were
depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease
eradication program. Animals, primarily over 12 mo of age, were tested for the
presence CWD prions following euthanasia. Twenty-one of the herds were linked
through movements of live animals with latent CWD from a single infected source
herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily
infected herds.
***The source herd is believed to have become infected via importation of
animals from a game farm in South Dakota where CWD was subsequently diagnosed
(7,4). A wide range in herd prevalence of CWD at the time of herd depopulation
of these herds was observed. Within-herd transmission was observed on some
farms, while the disease remained confined to the introduced animals on other
farms.
spreading cwd around...
Friday, May 13, 2011
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the
Republic of Korea
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the
Republic of Korea
Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim,
Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research
Division, National Veterinary Research and Quarantine Service, Republic of Korea
Chronic wasting disease (CWD) has been recognized as an important prion
disease in native North America deer and Rocky mountain elks. The disease is a
unique member of the transmissible spongiform encephalopathies (TSEs), which
naturally affects only a few species. CWD had been limited to USA and Canada
until 2000.
On 28 December 2000, information from the Canadian government showed that a
total of 95 elk had been exported from farms with CWD to Korea. These consisted
of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72
elk in 1997, which had been held in pre export quarantine at the “source
farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD
surveillance program was initiated by the Ministry of Agriculture and Forestry
(MAF) in 2001.
All elks imported in 1997 were traced back, however elks imported in 1994
were impossible to identify. CWD control measures included stamping out of all
animals in the affected farm, and thorough cleaning and disinfection of the
premises. In addition, nationwide clinical surveillance of Korean native
cervids, and improved measures to ensure reporting of CWD suspect cases were
implemented.
Total of 9 elks were found to be affected. CWD was designated as a
notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.
Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and
2005.
Since February of 2005, when slaughtered elks were found to be positive,
all slaughtered cervid for human consumption at abattoirs were designated as
target of the CWD surveillance program. Currently, CWD laboratory testing is
only conducted by National Reference Laboratory on CWD, which is the Foreign
Animal Disease Division (FADD) of National Veterinary Research and Quarantine
Service (NVRQS).
In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the
human consumption was confirmed as positive. Consequently, all cervid – 54 elks,
41 Sika deer and 5 Albino deer – were culled and one elk was found to be
positive. Epidemiological investigations were conducted by Veterinary
Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary
services.
Epidemiologically related farms were found as 3 farms and all cervid at
these farms were culled and subjected to CWD diagnosis. Three elks and 5
crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.
All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and
confirmed as negative.
Further epidemiological investigations showed that these CWD outbreaks were
linked to the importation of elks from Canada in 1994 based on circumstantial
evidences.
In December 2010, one elk was confirmed as positive at Farm 5.
Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer –
were culled and one Manchurian Sika deer and seven Sika deer were found to be
positive. This is the first report of CWD in these sub-species of deer.
Epidemiological investigations found that the owner of the Farm 2 in CWD
outbreaks in July 2010 had co-owned the Farm 5.
In addition, it was newly revealed that one positive elk was introduced
from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed
(species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as
negative.
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs
of CWD in affected adults are weight loss and behavioural changes that can span
weeks or months (Williams, 2005). In addition, signs might include excessive
salivation, behavioural alterations including a fixed stare and changes in
interaction with other animals in the herd, and an altered stance (Williams,
2005). These signs are indistinguishable from cervids experimentally infected
with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be
introduced into countries with BSE such as GB, for example, infected deer
populations would need to be tested to differentiate if they were infected with
CWD or BSE to minimise the risk of BSE entering the human food-chain via
affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
BSE RUMINANT FEED BAN FOR CERVIDS AND PETS IN THE USA ?
in short, there is none, and never has been.
I am concerned with pets as well.
I strongly, strenuously, urge the FDA et al and scientist (minus the
industry, politicians, and lobbyist there from on all issues), to revisit the
foolish voluntary ban on ruminant feed to cervids, and adopt an immediate
measure to make mandatory the ban of all ruminant feed to all cervids and pets.
... TSS
FDA WARNING LETTER (14-ATL-04) adulterated under Section 402(a)(4) [21
U.S.C. 342(a)(4)] of the Act, protein derived from mammalian tissues to feeds
that may be used for ruminants [21 C.F.R. 589.2000(e)(1)(iii)(B)]
2013
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer
and Elk in Animal Feed; Availability Date: Fri, 16 May 2003 11:47:37 -0500 EMC 1
Terry S. Singeltary Sr. Vol #: 1 http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm
PLEASE SEE FULL TEXT SUBMISSION ;
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan. *** This supports the theory that the importation of BSE
contaminated feedstuff is the source of C-type BSE in Canada. *** It also
suggests a similar cause or source for atypical BSE in these countries. ***
see page 176 of 201 pages...tss
*** Singeltary reply ;
Molecular, Biochemical and Genetic Characteristics of BSE in Canada
*** Singeltary reply ;
ruminant feed ban for cervids in the United States ? 31 Jan 2015 at 20:14
GMT
Susceptibility of European Red Deer (Cervus elaphus elaphus) to Alimentary
Challenge with Bovine Spongiform Encephalopathy
Mark P. Dagleish , * E-mail: mark.dagleish@moredun.ac.uk
Affiliation: Moredun Research Institute, Pentlands Science Park, Bush Loan,
Penicuik, Near Edinburgh EH26 0PZ, United Kingdom
⨯ [ view all ] [ view less ] Susceptibility of European Red Deer (Cervus
elaphus elaphus) to Alimentary Challenge with Bovine Spongiform Encephalopathy
Mark P. Dagleish, Stuart Martin, Philip Steele, Jeanie Finlayson, Samantha L.
Eaton, Sílvia Sisó, Paula Stewart, Natalia Fernández-Borges, … Scott Hamilton,
Yvonne Pang PLOS x Published: January 23, 2015 DOI: 10.1371/journal.pone.0116094
Abstract
European red deer (Cervus elaphus elaphus) are susceptible to the agent of
bovine spongiform encephalopathy, one of the transmissible spongiform
encephalopathies, when challenged intracerebrally but their susceptibility to
alimentary challenge, the presumed natural route of transmission, is unknown. To
determine this, eighteen deer were challenged via stomach tube with a large dose
of the bovine spongiform encephalopathy agent and clinical signs, gross and
histological lesions, presence and distribution of abnormal prion protein and
the attack rate recorded. Only a single animal developed clinical disease, and
this was acute with both neurological and respiratory signs, at 1726 days post
challenge although there was significant (27.6%) weight loss in the preceding
141 days. The clinically affected animal had histological lesions of vacuolation
in the neuronal perikaryon and neuropil, typical of transmissible spongiform
encephalopathies. Abnormal prion protein, the diagnostic marker of transmissible
encephalopathies, was primarily restricted to the central and peripheral nervous
systems although a very small amount was present in tingible body macrophages in
the lymphoid patches of the caecum and colon. Serial protein misfolding cyclical
amplification, an in vitro ultra-sensitive diagnostic technique, was positive
for neurological tissue from the single clinically diseased deer. All other
alimentary challenged deer failed to develop clinical disease and were negative
for all other investigations. These findings show that transmission of bovine
spongiform encephalopathy to European red deer via the alimentary route is
possible but the transmission rate is low. Additionally, when deer carcases are
subjected to the same regulations that ruminants in Europe with respect to the
removal of specified offal from the human food chain, the zoonotic risk of
bovine spongiform encephalopathy, the cause of variant Creutzfeldt-Jakob
disease, from consumption of venison is probably very low.
snip...
Discussion This investigation resulted in the first and only known case, to
date, of clinical disease or accumulation of abnormal PrPd in any cervid species
due to oral challenge with BSE. The increase in incubation period compared to
European red deer challenged with BSE intra-cerebrally (1060 days) [33] compared
to oral challenge (1727 days) is approximately 60% and similar to the
differences observed in incubation periods for sheep or goats when challenged
with TSE agents by these two routes [40,41]. The neurological clinical signs
observed could be broadly related to the spongiform encephalopathy and the
accumulation of PrPd in that the restlessness, stereotypic head movements and
pacing may be due to compromise of the nucleus accumbens [42], found in the
striatum, and the laboured breathing due to the lesions in the medulla, where
the respiratory centre is located [43]. Alternatively, the laboured and audible
mouth breathing may have been due to, or contributed to by, compromise of either
of the recurrent laryngeal nerves resulting in some degree of laryngeal
paralysis but we were unable to determine this. Apart from the gradual loss of
body weight, the speed of onset of clinical signs and progression was very rapid
but animal welfare requirements precluded any further longitudinal study of
these. The clinical signs described for this animal are broadly similar to those
reported for clinical BSE in European red deer challenged via the intracerebral
route [33], clinical cases of CWD in deer [44] and clinical cases of BSE in
cattle [45].
snip...see full text ;
ruminant feed ban for cervids in the United States ?
31 Jan 2015 at 20:14 GMT
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan. *** This supports the theory that the importation of BSE
contaminated feedstuff is the source of C-type BSE in Canada. *** It also
suggests a similar cause or source for atypical BSE in these countries. ***
see page 176 of 201 pages...tss
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
*** 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.
when an industry is catering to the public, with products which can risk
human and animal health, in my opinion, you should have NO property rights. you
should not be able to hide behind property rights when you are clearly risking
human and animal health from your product, or the way you handle that product.
if you are going to raise, grow, produce a product for the consumer, you have an
obligation NOT to risk the public domain, public property, and or the wild
animal populations. just my opinion, I still have that right in 2015. ...
CHRONIC WASTING DISEASE CWD TSE PRION, how much does it pay to find CWD
$$$
CWD, spreading it around...
Tuesday, January 06, 2015
APHIS Provides Additional Information on Chronic Wasting Disease (CWD)
Indemnity Requests January 5, 2015 05:26 PM EST
CWD TO HUMANS, AND RISK FACTORS THERE FROM (see latest science)
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
Sunday, June 29, 2014
Chronic wasting disease spreads in West Virginia
Thursday, January 22, 2015
Transmission properties of atypical Creutzfeldt-Jakob disease: a clue to
disease etiology?
Comment from Terry Singeltary Sr.
|
This is a Comment on the Animal and Plant Health
Inspection Service (APHIS) Notice: Agency Information
Collection Activities; Proposals, Submissions, and Approvals: Bovine Spongiform
Encephalopathy; Importation of Animals and Animal
Products
For related information, Open Docket Folder
 Comment
Docket No. APHIS-2014-0107
Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products
Singeltary Submission ;
I believe that there is more risk to the world from Transmissible Spongiform Encephalopathy TSE prion aka mad cow type disease now, coming from the United States and all of North America, than there is risk coming to the USA and North America, from other Countries. I am NOT saying I dont think there is any risk for the BSE type TSE prion coming from other Countries, I am just saying that in 2015, why is the APHIS/USDA/FSIS/FDA still ignoring these present mad cow risk factors in North America like they are not here? North America has more strains of TSE prion disease, in more species (excluding zoo animals in the early BSE days, and excluding the Feline TSE and or Canine TSE, because they dont look, and yes, there has been documented evidence and scientific studies, and DEFRA Hound study, that shows the canine spongiform encephalopathy is very possible, if it has not already happened, just not documented), then any other Country in the world. Mink TME, Deer Elk cervid CWD (multiple strains), cBSE cattle, atypical L-type BSE cattle, atypical H-type BSE cattle, atyical HG type BSE cow (the only cow documented in the world to date with this strain), typical sheep goat Scrapie (multiple strains), and the atypical Nor-98 Scrapie, which has been linked to sporadic CJD, Nor-98 atypical Scrapie has spread from coast to coast. sporadic CJD on the rise, with different strains mounting, victims becoming younger, with the latest nvCJD human mad cow case being documented in Texas again, this case, NOT LINKED TO EUROPEAN TRAVEL CDC. typical BSE can propagate as nvCJD and or sporadic CJD (Collinge et al), and sporadic CJD has now been linked to atypical BSE, Scrapie and atypical Scrapie, and scientist are very concerned with CWD TSE prion in the Cervid populations. in my opinion, the BSE MRR policy, which overtook the BSE GBR risk assessments for each country, and then made BSE confirmed countries legal to trade mad cow disease, which was all brought forth AFTER that fateful day December 23, 2003, when the USA lost its gold card i.e. BSE FREE status, thats the day it all started. once the BSE MRR policy was shoved down every countries throat by USDA inc and the OIE, then the legal trading of Scrapie was validated to be a legal trading commodity, also shoved through by the USDA inc and the OIE, the world then lost 30 years of attempted eradication of the BSE TSE prion disease typical and atypical strains, and the BSE TSE Prion aka mad cow type disease was thus made a legal trading commodity, like it or not. its all about money now folks, trade, to hell with human health with a slow incubating disease, that is 100% fatal once clinical, and forget the fact of exposure, sub-clinical infection, and friendly fire there from i.e. iatrogenic TSE prion disease, the pass it forward mode of the TSE PRION aka mad cow type disease. its all going to be sporadic CJD or sporadic ffi, or sporadic gss, or now the infamous VPSPr. ...problem solved $$$ the USDA/APHIS/FSIS/FDA triple mad cow BSE firewall, well, that was nothing but ink on paper. for this very reason I believe the BSE MRR policy is a total failure, and that this policy should be immediately withdrawn, and set back in place the BSE GBR Risk Assessments, with the BSE GBR risk assessments set up to monitor all TSE PRION disease in all species of animals, and that the BSE GBR risk assessments be made stronger than before. lets start with the recent notice that beef from Ireland will be coming to America. Ireland confirmed around 1655 cases of mad cow disease. with the highest year confirming about 333 cases in 2002, with numbers of BSE confirmed cases dropping from that point on, to a documentation of 1 confirmed case in 2013, to date. a drastic decrease in the feeding of cows to cows i.e. the ruminant mad cow feed ban, and the enforcement of that ban, has drastically reduced the number of BSE cases in Europe, minus a few BABs or BARBs. a far cry from the USDA FDA triple BSE firewall, which was nothing more than ink on paper, where in 2007, in one week recall alone, some 10 MILLION POUNDS OF BANNED POTENTIAL MAD COW FEED WENT OUT INTO COMMERCE IN THE USA. this is 10 years post feed ban. in my honest opinion, due to the blatant cover up of BSE TSE prion aka mad cow disease in the USA, we still have no clue as to the true number of cases of BSE mad cow disease in the USA or North America as a whole. ...just saying. Number of reported cases of bovine spongiform encephalopathy (BSE) in farmed cattle worldwide* (excluding the United Kingdom) Country/Year snip...please see attached pdf file, with references of breaches in the USA triple BSE mad cow firewalls, and recent science on the TSE prion disease. ...TSS Attachments(1)Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission
View
Attachment:
 |
Sunday, January 11, 2015
Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of
Animals and Animal Products Singeltary Submission
TSS
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