Early detection of chronic wasting disease prions in urine of pre-symptomatic deer by real-time quaking-induced conversion assay
Short Communication Early detection of chronic wasting disease prions in
urine of pre-symptomatic deer by real-time quaking-induced conversion assay
Volume 7, Issue 3 May/June 2013
Pages 253 – 258
Keywords: RT-QuIC, chronic wasting disease, diagnosis, feces, prion,
surveillance, urine
Authors: Theodore R. John, Hermann M. Schätzl and Sabine Gilch
Theodore R. John Department of Veterinary Sciences; University of Wyoming;
Laramie, WY USA
Hermann M. Schätzl Department of Veterinary Sciences; University of
Wyoming; Laramie, WY USA; Department of Molecular Biology; University of
Wyoming; Laramie, WY USA; Faculty of Veterinary Medicine; Department of
Comparative Biology and Experimental Medicine; University of Calgary; Calgary,
AB Canada
Sabine Gilch Corresponding author: sgilch@ucalgary.ca Department of
Veterinary Sciences; University of Wyoming; Laramie, WY USA; Faculty of
Veterinary Medicine; Department of Ecosystem and Public Health; University of
Calgary; Calgary, AB Canada
Abstract:
Chronic wasting disease (CWD) is a prion disease of captive and
free-ranging deer (Odocoileus spp), elk (Cervus elaphus nelsonii) and moose
(Alces alces shirasi). Unlike in most other prion diseases, in CWD prions are
shed in urine and feces, which most likely contributes to the horizontal
transmission within and between cervid species. To date, CWD ante-mortem
diagnosis is only possible by immunohistochemical detection of protease
resistant prion protein (PrPSc) in tonsil or recto-anal mucosa-associated
lymphoid tissue (RAMALT) biopsies, which requires anesthesia of animals. We
report on detection of CWD prions in urine collected from pre-symptomatic deer
and in fecal extracts by using real time quaking-induced conversion (RT-QuIC).
This assay can be useful for non-invasive pre-symptomatic diagnosis and
surveillance of CWD.
Received: February 7, 2013; Accepted: March 24, 2013; Published Online:
April 10, 2013
snip...
Introduction
Chronic wasting disease (CWD) is to date the most contagious prion disease
and affects captive and free-ranging elk, deer and moose in North America.1,2
The disease is caused by the accumulation of an abnormally folded isoform of the
cellular prion protein PrPC, denominated PrPSc.3,4 CWD is the cervid equivalent
of bovine spongiform encephalopathy (BSE), scrapie in sheep and goat5 or
Creutzfeldt-Jakob disease (CJD) in humans.6 Although transmission studies of CWD
prions to humanized transgenic mice or non-human primates suggest a strong
species barrier,7-9 recent in vitro studies have demonstrated that human PrP can
be converted by CWD prions into PrPSc upon adaptation.10 Therefore, a potential
for zoonotic transmission, as exemplified by BSE,11 cannot be completely
excluded.
A huge body of evidence suggests that CWD can be efficiently transmitted
horizontally within and between cervid species,12 which may be the reason for
geographical spread and increase in case numbers. Horizontal transmission is
explained by the rather unusual peripheral distribution of prions in CWD
affected animals and the high susceptibility to the disease by oral
infection.13,14 Unlike in most other prion diseases, CWD prions can be found in
a wide variety of tissues, such as skeletal and cardiac muscle15,16 or kidney,17
in addition to the lymphoreticular system and blood.18 Furthermore, they are
shed in significant amounts in saliva,18,19 urine19 or feces,20 which enables
oral infection of animals by foraging on contaminated pastures.
In addition, it has been demonstrated that prions can persist in soil21 and
that water in endemic areas can contain CWDassociated PrPSc.22
snip...
We demonstrate that CWD prions are detectable in urine of orally infected
deer prior to the onset of clinical symptoms. Furthermore, we show that fecal
extracts can be used as a seed in RT-QuIC assays. Thereby, we were able to
detect CWD prions in fecal extracts collected at later stages of the disease.
This study provides the first evidence that RT-QuIC can be successfully used for
the preclinical diagnosis of CWD in specimens that are available by non-invasive
methods.
snip...
In summary, we demonstrate that CWD prions can be detected by RT-QuIC in
urine of orally infected white-tailed deer and mule deer at a pre-symptomatic
stage of the disease.
snip...
Greetings,
Disturbing to say the least, but it’s not like we have not been telling
them that this is a most dangerous risk factor for further exposure to the TSE
prion disease.
the load factors in the environment here in the USA and Canada from these
many different strains of the TSE prion disease both typical and atypical, must
be great, just from the feces and urine alone, and then you have these 100%
urine deer scents made out of 100% deer urine, and some hunters are splashing it
on like it's cologne, and in the mean time, spreading the CWD TSE prion agent
all over.
what about environment transmission factors with other species such as the
bovine with atypical BSE, atypical scrapie, atypical CWD ? it’s NOT out of the
question folks. see ;
e) Any other cause than from feed or maternal transmission becomes a
potential ‘Third Way’. Possible genuine ‘Third Ways’ are listed and discussed in
detail in the report. Some, though unproven, may increase susceptibility to the
disease. Many are theoretically possible (e.g., environmental contamination
after unauthorised burial of carcasses of non-declared BSE cases) but, if
existent, unlikely to have significantly contributed to the BSE epidemic. They
may, however, initially have been overshadowed by the feed and maternal
transmission routes of transmission and eventually become a factor in the
current trend of the epidemic impeding the rapid total elimination of the
disease.
snip...
III.2. BSE INQUIRY REPORT (INQUIRY 2000) ON HYPOTHESES The BSE Inquiry
(Inquiry, 2000), agreed that MBM was the major vector of BSE in cattle,
including via unintentional cross-contamination of ruminant diets with feed, or
MBM, intended only for monogastric species. They supported the view that
maternal transmission could account for some cases of BSE but were uncertain of
the role environmental contamination and could not absolutely rule out the
transmission of BSE via hormones and veterinary preparations.
snip...
disease in cattle, recycling of infection from infected cattle tissues was
the main way in which further cattle became infected. By contrast, other
considered possible origins (such as from dam to offspring, contamination of
pastures (environmental spread) and/or, through the use of veterinary
preparations) if these occurred, were likely to have made only a small
contribution. Doubt was cast on the statistically calculated figure of 10% for
maternal transmission, as the number of cases in the cohorts approaching five
years of age is now low compared with the number expected. It is noted that
16
Bradley and Wilesmith (1993) reported that in no year between 1988 and 1993
(when the epidemic was at its height) did the actual incidence of BSE in the
offspring of confirmed cases exceed the expected incidence of BSE from the
feed-borne source alone.
As to the Inquiry's hypothesis of several undetected cycles of infection in
the SW of England, the Committee thought although this was plausible but it is
also speculative.
They were very firm that it was not tenable to exclude an unmodified
scrapie agent in sheep being responsible for BSE.
A proposed origin from an African antelope with a natural TSE could not be
substantiated but also could not be completely excluded.
PrP was agreed to play a central and essential role in TSE in general and
BSE in particular. However, the Committee noted that the properties of the
abnormal prion protein were incompletely understood and thus, how the normal
form was converted to the abnormal form and why the properties of the two
protein forms were so different, is also unclear. Whilst the Committee could not
exclude that environmental factors and/or toxic chemicals could be implicated in
the initiation or maintenance of disease, there was no convincing evidence to
support this notion. These factors might however influence susceptibility to
disease or infection.
The Committee pointed to the continuing puzzles of BSE, such as why it
commenced in the UK and did not arise spontaneously and independently in other
parts of the world where similar rendering systems, feeding practices and
scrapie were evident. They sought to explain this observation as follows:
Whilst they agree that no rendering system so far evaluated can guarantee to
eliminate TSE infectivity completely, a tenfold increase in the amount of
infectivity remaining in MBM (compared with that in the pre-BSE era) could be
critical and could have contributed significantly to the epidemic. In the
period 1970 to 1988 feed manufacturers introduced MBM into calf diets in the UK.
This type of feeding was less prevalent in continental Europe (and in Ireland)
and in the USA. However, it is noted that the Horn Review (Horn, 2001) stated
that the incorporation of MBM into concentrate feed of calves in the UK was an
essentially new phenomenon between 1970 and 1988. Even so, before 1970, unless
completely separated feed manufacturing, transportation and storage facilities
were available and used for calf feed, there would still have been an
opportunity to cross-contaminate calf feed with MBM, or with feed for adult
cattle or non-ruminant species that contained MBM. Cross contamination of
ruminant rations is widely regarded as the main reason for cases of BSE born
after feed bans were in place.
Because of the nature of feeding beef calves the incidence of BSE in the
offspring of suckler cows was low compared with that in the offspring of dairy
cows.
Most cattle with BSE became infected when calves (as determined by
modelling).
17
In regard to the origin of the BSE agent the Committee noted as follows:
The UK had the largest sheep and third largest cattle population in the EU and
the highest ratio of sheep to cattle.
If the proportion of sheep waste material was proportional to the
respective sizes of the sheep and cattle populations, then because there were
estimated to be between 5,000 and 10,000, cases of scrapie p.a. in the UK
(noting there were no corresponding data for other Member States) a high level
of scrapie infectivity could be in MBM (if it was not inactivated). This
infectivity could have included a BSE strain, a fact that cannot yet be ruled
out despite no such strain having been found in individually typed brains of
sheep with scrapie. The Committee recognises that TSE agents mutate and strains
might be selected when transferred over species boundaries. Alternatively (and
speculatively) a new strain could have occurred as a sporadic event (see
sporadic BSE below) or from other animal sources like goats or exotic ungulates.
The committee thus summarise that many of the above events, although not
individually unique to the UK were collectively unique. They raise the
additional point that feeding MBM to calves (apparently much more common in the
UK than elsewhere) as distinct from adults, that the youth of the animal could
be an important susceptibility factor. They recommended this be investigated
experimentally.
snip...
Chronic Wasting Disease CWD, and other TSE prion disease, these TSE prions
know no borders.
these TSE prions know no age restrictions.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around
1112 degrees farenheit.
you cannot cook the TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a
mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the
environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of
protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple
autoclave will not kill this TSE prion agent.
I go from state to state trying to warn of the CWD and other TSE prion
disease in other species, I just made a promise to mom. back then, there was no
information.
so, I submit this to you all in good faith, and hope that you take the time
to read my research of the _sound_, peer review science, not the junk science
that goes with the politics $$$
right or left or teaparty or independent, you cannot escape the TSE prion
disease.
there is a lot of science here to digest, but better digesting this _sound_
science, instead of the junk political science you will hear from the shooting
pen industry.
snip...
see full text of my submission here ;
please see what the U.K. DEFRA recently said ABOUT CWD RISK FACTORS ;
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...
see full text report here ;
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
Research Article
Intranasal Inoculation of White-Tailed Deer (Odocoileus virginianus) with
Lyophilized Chronic Wasting Disease Prion Particulate Complexed to
Montmorillonite Clay
Tracy A. Nichols mail, Terry R. Spraker, Tara D. Rigg, Crystal
Meyerett-Reid, Clare Hoover, Brady Michel, Jifeng Bian, Edward Hoover, Thomas
Gidlewski, Aru Balachandran, Katherine O'Rourke, Glenn C. Telling, Richard
Bowen, [ ... ], Kurt C. VerCauteren equal contributor
Abstract
Chronic wasting disease (CWD), the only known prion disease endemic in
wildlife, is a persistent problem in both wild and captive North American cervid
populations. This disease continues to spread and cases are found in new areas
each year. Indirect transmission can occur via the environment and is thought to
occur by the oral and/or intranasal route. Oral transmission has been
experimentally demonstrated and although intranasal transmission has been
postulated, it has not been tested in a natural host until recently. Prions have
been shown to adsorb strongly to clay particles and upon oral inoculation the
prion/clay combination exhibits increased infectivity in rodent models. Deer and
elk undoubtedly and chronically inhale dust particles routinely while living in
the landscape while foraging and rutting. We therefore hypothesized that dust
represents a viable vehicle for intranasal CWD prion exposure. To test this
hypothesis, CWD-positive brain homogenate was mixed with montmorillonite clay
(Mte), lyophilized, pulverized and inoculated intranasally into white-tailed
deer once a week for 6 weeks. Deer were euthanized at 95, 105, 120 and 175 days
post final inoculation and tissues examined for CWD-associated prion proteins by
immunohistochemistry. Our results demonstrate that CWD can be efficiently
transmitted utilizing Mte particles as a prion carrier and intranasal exposure.
snip...
The results of this study confirm that CWD can be successfully transmitted
IN as a lyophilized prion particulate adsorbed to Mte and that genotype at codon
96 affects the lymphoid distribution of CWD within the body. Additionally, two
novel intranasal tracking methods were employed that provided insight into CWD
translocation within the nasal cavity. The data collected in this study may also
shed light on why there is a higher prevalence of CWD in males, as males
participate in more behaviors that generate dust. We propose chronic, long-term
exposure to CWD prions adsorbed to dust particles to be a natural CWD infection
route in addition to chronic oral and nasal contact exposure.
Citation: Nichols TA, Spraker TR, Rigg TD, Meyerett-Reid C, Hoover C, et
al. (2013) Intranasal Inoculation of White-Tailed Deer (Odocoileus virginianus)
with Lyophilized Chronic Wasting Disease Prion Particulate Complexed to
Montmorillonite Clay. PLoS ONE 8(5): e62455.
doi:10.1371/journal.pone.0062455
Editor: Anthony E. Kincaid, Creighton University, United States of America
Received: November 30, 2012; Accepted: March 21, 2013; Published: May 9,
2013
This is an open-access article, free of all copyright, and may be freely
reproduced, distributed, transmitted, modified, built upon, or otherwise used by
anyone for any lawful purpose. The work is made available under the Creative
Commons CC0 public domain dedication.
Funding: Funding was provided by U.S. Department of Agriculture, Animal and
Plant Health Inspection Service, Veterinary Services (VS). The funders had no
role in study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
Competing interests: The authors have declared that no competing interests
exist.
see full text ;
Thanks again to PLOS et al for full text access to this scientific research
on the CWD TSE prion disease...tss
see more here ;
Wednesday, May 15, 2013
Intranasal Inoculation of White-Tailed Deer (Odocoileus virginianus) with
Lyophilized Chronic Wasting Disease Prion Particulate Complexed to
Montmorillonite Clay
Research Article
Friday, February 08, 2013
*** Behavior of Prions in the Environment: Implications for Prion Biology
Friday, February 25, 2011
Soil clay content underlies prion infection odds Soil clay content
underlies prion infection odds
see full text ;
Saturday, February 04, 2012
Wisconsin 16 MONTH age limit on testing dead deer Game Farm CWD Testing
Protocol Needs To Be Revised
Thursday, June 13, 2013
WISCONSIN DEER FARMING Chronic Wasting Disease CWD DATCP
Tuesday, June 11, 2013
CWD GONE WILD, More cervid escapees from more shooting pens on the loose in
Pennsylvania
Sunday, June 09, 2013
Missouri House forms 13-member Interim Committee on the Cause and Spread of
Chronic Wasting Disease CWD
In August 2010
NEW RULES CAME INTO EFFECT FOR:
1) hunters using natural attractants (e.g., deer urine used for
hunting)
Use of Natural Attractants Prohibited
Ontario Hunters – if you possess and use products that contain, or purport
to contain, any body part of a member of the deer family, you must be aware of
this regulation.
The Amended Regulation
Ontario has passed an amendment to O. Reg 665/98 (Hunting) under the Fish
and Wildlife Conservation Act, 1997. This amendment prohibits possession and use
of products that contain, or purport to contain, body parts of any member of the
deer family including blood, urine, gland oils and other fluids, for the
purposes of hunting. This prohibition applies to body parts and fluids from
hunter-harvested deer or moose and applies to all hunting in Ontario.
One potential pathway for the spread of CWD is from possession and use of
hunting attractants that contain body parts of members of the deer family. These
products contain urine, blood, gland oil or other bodily fluids obtained from
captive/farmed deer, elk or other cervids. This regulation also prohibits
hunters from possessing or using these types of materials (i.e., body fluids and
parts) obtained from wild and farmed cervids for the purposes of hunting in
Ontario. These products may contain infectious material and may be capable of
introducing CWD to Ontario.
Important Information
Hunters in Ontario may still possess and use artificial or plant-based
products that can attract or lure deer and moose but do not contain any body
parts of a member of the deer family. These alternative products are commonly
available from merchants selling hunting equipment as well as through the
Internet.
Why is this Amendment Required?
CWD is not thought to be present in Ontario at this time. However, these
products may contain infectious material and may be capable of introducing CWD
to Ontario. As the source of these products is often of an unknown origin and
from animals of unknown health status, and as CWD continues to be detected in
some captive/farmed deer and elk, these actions must be taken to minimize
risks.
Possession of High Risk Carcass Parts Originating from Outside the Province
Now Prohibited. This applies to all members of the deer family.
Ontario Hunters - if you hunt outside Ontario and bring the carcasses or
parts of any member of the deer family (e.g. white-tailed, mule, black tailed or
other deer and elk, etc.) into Ontario, you need to be aware that the ban on
possessing high risk animal parts now applies to moose and caribou.
The Amended Regulation
Ontario has amended an existing regulation to prohibit the possession in
Ontario of high risk body parts and fluids of members of the deer family
harvested in other jurisdictions to also include moose and caribou.
High risk parts include the head, spinal column, unprocessed antlers or
hide, hoofs, lymph nodes, eyes, spleen, mammary glands, entrails and internal
organs. These animal parts are considered high risk because in sick or infected
animals they contain prions that may transmit CWD.
The regulation applies to all members of the deer family (referred to as
"cervids" and comprising more that 37 species) including all species of deer,
elk, moose and caribou that are harvested outside Ontario and transported back
or possessed in Ontario.
At the time of the initial regulation proposal, moose and caribou were
generally not considered a risk of contracting or transfer of CWD. However,
since that time, wild moose in two U.S. states have tested positive for CWD and
recent scientific evidence indicates that caribou may be susceptible to
infection by CWD. As a result, an amendment under the Fish & Wildlife
Conservation Act, 1997 in now in effect. This amendment expands the definition
of "cervid" in the regulation to include moose and caribou, so that these
species are now also included under the regulation.
Items in the regulation include:
1. It is now illegal in Ontario to possess any part of the antlers, head,
brain, eyes, tonsils, hide, hooves, lymph nodes, spleen, mammary glands,
entrails, internal organs or spinal column of any member of the deer family that
has been killed outside Ontario.
2. The prohibition above (#1) does not apply to finished taxidermy mounts,
tanned skin, canine teeth with no tissue attached.
3. Antlers or antlers with skull cap attached may be legally possessed as
long as there is no tissue or skin attached to them and they are separate from
the remainder of the skull.
4. It is also legal to possess a hide or skin of the head of any member of
the deer family including that part of the hide commonly referred to as the
"cape" only if:
• all other tissue is removed, AND • it is kept in a container from which
nothing can escape, (e.g., cooler taped shut, enclosing the animal in plastic or
a tarp), AND • it is delivered to a tanner or taxidermist within five days of
coming into Ontario.
5. If all or portion of the hide or skin of the head identified above (#4)
is disposed of, it must be done at a waste disposal site authorized under the
Environmental Protection Act such as a municipal landfill.
6. None of these rules (#1 to #5) apply to the prohibited parts (the
antlers, head, brain, eyes, tonsils, hide, hooves, lymph nodes, spleen, mammary
glands, entrails, internal organs or spinal column) of any member of the deer
family if they are transported through Ontario to another jurisdiction in a
container from which nothing can escape, (e.g., cooler taped shut, enclosing the
animal in plastic or a tarp).
7. If you are transporting the antlers, head, brain, eyes, tonsils, hide,
hooves, lymph nodes, spleen, mammary glands, entrails, internal organs or spinal
column of any member of the deer family in a container as described above, it
must be labelled to show the species of cervid, the place where it was acquired
and the name and address of the person who owns the parts in the
container.
8. If you have transported a member of the deer family into Ontario that
was harvested or killed in another jurisdiction, but later find out that it has
tested positive for CWD, you must immediately notify a Ministry of Natural
Resources Office and provide information as requested.
Important Information
Hunters will still be allowed to bring in meat and other parts such as
antlers and hides, if those antlers and hides are properly treated to reduce
risk of CWD transfer (see Items #3 and #4 above).
The regulation applies to all members of the deer family from all states,
provinces or other jurisdictions whether CWD has been detected in that
jurisdiction or not. The regulation does not affect hunters who have harvested
an animal in Ontario. However, persons who wish to export Ontario deer, moose,
elk or caribou should check with applicable jurisdictions should they wish to
possess these Ontario cervids out of province.
Why is this Amendment Required?
CWD is not thought to be present in Ontario at this time. However, it's
possible that by transporting out-of-province infected parts of carcasses into
Ontario, disease-causing prions could be spread into the environment. These
prions may live for years, increasing the risk that Ontario deer, moose, elk or
caribou could become infected with CWD. This regulation will minimize that
risk.
Most North American jurisdictions, whether CWD is present or not, are
taking steps to minimize the spread of CWD. Manitoba and more than 20 states in
the United States have already taken action to address the spread of CWD through
high risk carcass parts.
Transport of Live White-tailed Deer, American Elk, Moose or Woodland
Caribou into Ontario Now Restricted Unless Accompanied by a Provincial
Permit
Transporting live white-tailed deer, American elk, moose, woodland caribou
and their hybrids into Ontario now requires a permit under a new regulation
under the Fish & Wildlife Conservation Act, 1997. This applies to the
transport of live white-tailed deer, American elk, moose and woodland caribou
into Ontario for any purpose, including farming, slaughter, and display in
zoos.
Anyone wishing to transport live white-tailed deer, American elk, moose or
woodland caribou into Ontario is required to meet new conditions to minimize the
risk of spreading Chronic Wasting Disease. MNR now requires written notice
regarding health status and documentation of a premise assessment from the
Ontario Ministry of Agriculture, Food and Rural Affairs (OMAFRA) before issuing
a permit to transport these species into Ontario. Information from OMAFRA on the
permit system.
For information about these new requirements and about the process for
applying for a permit please contact:
•the Animal Health Coordinator with Ontario Ministry of Agriculture, Food
and Rural Affairs (OMAFRA) at (519) 826-7612, or •the Wildlife Health Policy
Advisor with the Ministry of Natural Resources (MNR) at (705) 755-1573.
Why is this Regulation Required?
Chronic Wasting Disease (CWD) is a degenerative, fatal brain disease that
affects certain members of the deer family, including white-tailed deer, elk,
and moose. The disease is believed to be caused by abnormal proteins called
prions. CWD is in the same family of diseases as bovine spongiform
encephalopathy (BSE or Mad Cow Disease).
There is no evidence to date that CWD can be transmitted to humans or to
domestic livestock such as cattle. However, CWD has been detected in wild and/or
captive/farmed deer, elk or moose in 18 U.S. states and two Canadian provinces.
There is a significant risk to wild Ontario deer, elk, caribou and moose if CWD
enters Ontario as the disease is fatal in these species and there is no
cure.
CWD is not believed to be present in the wild in Ontario. One potential
pathway for the spread of CWD is the movement of infected cervids and/or their
hybrids from other jurisdictions that could spread infective prions to other
wild or captive animals in Ontario.
Thursday, June 09, 2011
Detection of CWD prions in salivary, urinary, and intestinal tissues of
deer: potential mechanisms of prion shedding and transmission
Tuesday, September 02, 2008
Detection of infectious prions in urine (Soto et al Available online 13
August 2008.)
2011 AND WE STILL HAVE HUNTERS POURING 100% UNTESTED (potentially CWD
infected) URINE ALL OVER THEMSELVES FOR A KILL. ...TSS
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
now, what about those 'deer scents' of 100% urine', and the prion that is
found in urine, why not just pass the prion with the urine to other
deer...
Mrs. Doe Pee Doe in Estrus Model FDE1 Mrs. Doe Pee's Doe in Estrus is made
from Estrus urine collected at the peak of the rut, blended with Fresh Doe Urine
for an extremely effective buck enticer. Use pre-rut before the does come into
heat. Use during full rut when bucks are most active. Use during post-rut when
bucks are still actively looking for does. 1 oz.
www.gamecalls.net/hunting...lures.html
ELK SCENT/SPRAY BOTTLE
Works anytime of the year *
100 % Cow Elk-in-Heat urine (2oz.) *
Economical - mix with water in spray mist bottle *
Use wind to your advantage
Product Code WP-ESB $9.95
www.elkinc.com/Scent.asp
prions in urine?
DEER & ELK URINE, LURES & SCENT CONTROL DEPARTMENT by MRS.DOE PEE'S
Main Index
The Turkey Pro Sez... "Premium, fresh, top-quality, pure 100% undiluted
deer lures from Mrs. Doe Pee really work. I won't trust anything else when I'm
after big bucks. Sam Collora, owner of the company, proved how well his products
work when he bagged this monster buck in
1996.............snip......end........CWD
snip...end
######## Bovine Spongiform Encephalopathy #########
Thursday, February 17, 2011
Environmental Sources of Scrapie Prions
Saturday, May 14, 2011
Modeling Routes of Chronic Wasting Disease Transmission: Environmental
Prion Persistence Promotes Deer Population Decline and Extinction
Sunday, December 06, 2009
Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer
Long after Oral Exposure to Urine and Feces from CWD+ Deer
Tuesday, June 11, 2013
CWD GONE WILD, More cervid escapees from more shooting pens on the loose in
Pennsylvania
*** 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.
The chances of a person or domestic animal contracting CWD are “extremely
remote,” Richards said. The possibility can’t be ruled out, however. “One could
look at it like a game of chance,” he explained. “The odds (of infection)
increase over time because of repeated exposure. That’s one of the downsides of
having CWD in free-ranging herds: We’ve got this infectious agent out there that
we can never say never to in terms of (infecting) people and domestic
livestock.”
P35
ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A
WISCONSIN STRAIN OF CWD
Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of
Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2
Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary
Research Institute, 4.Center for Prions and Protein Folding Diseases, 5
Department of Biological Sciences, University of Alberta, Edmonton AB, Canada
T6G 2P5
The identification and characterization of prion strains is increasingly
important for the diagnosis and biological definition of these infectious
pathogens. Although well-established in scrapie and, more recently, in BSE,
comparatively little is known about the possibility of prion strains in chronic
wasting disease (CWD), a disease affecting free ranging and captive cervids,
primarily in North America. We have identified prion protein variants in the
white-tailed deer population and demonstrated that Prnp genotype affects the
susceptibility/disease progression of white-tailed deer to CWD agent. The
existence of cervid prion protein variants raises the likelihood of distinct CWD
strains. Small rodent models are a useful means of identifying prion strains. We
intracerebrally inoculated hamsters with brain homogenates and phosphotungstate
concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD
endemic area) and experimentally infected deer of known Prnp genotypes. These
transmission studies resulted in clinical presentation in primary passage of
concentrated CWD prions. Subclinical infection was established with the other
primary passages based on the detection of PrPCWD in the brains of hamsters and
the successful disease transmission upon second passage. Second and third
passage data, when compared to transmission studies using different CWD inocula
(Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin
white-tailed deer population is different than the strain(s) present in elk,
mule-deer and white-tailed deer from the western United States endemic region.
PPo3-7:
Prion Transmission from Cervids to Humans is Strain-dependent
Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi
Gambetti and Liuting Qing Department of Pathology; Case western Reserve
University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial
Sloan-Kettering Cancer Center; New York, NY USA
Key words: CWD, strain, human transmission
Chronic wasting disease (CWD) is a widespread prion disease in cervids
(deer and elk) in North America where significant human exposure to CWD is
likely and zoonotic transmission of CWD is a concern. Current evidence indicates
a strong barrier for transmission of the classical CWD strain to humans with the
PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD
strains. What remain unknown is whether individuals with the PrP-129VV/MV
genotypes are also resistant to the classical CWD strain and whether humans are
resistant to all natural or adapted cervid prion strains. Here we report that a
human prion strain that had adopted the cervid prion protein (PrP) sequence
through passage in cervidized transgenic mice efficiently infected transgenic
mice expressing human PrP, indicating that the species barrier from cervid to
humans is prion strain-dependent and humans can be vulnerable to novel cervid
prion strains. Preliminary results on CWD transmission in transgenic mice
expressing human PrP-129V will also be discussed.
Acknowledgement Supported by NINDS NS052319 and NIA AG14359.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions
Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A.
Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer's disease and
related Brain disorders; Dept of Neurology; University of Texas Houston Medical
School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular
Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky
Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve
University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago;
Chicago, IL USA
Prion diseases are infectious neurodegenerative disorders affecting humans
and animals that result from the conversion of normal prion protein (PrPC) into
the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of
cervids is a prion disorder of increasing prevalence within the United States
that affects a large population of wild and captive deer and elk. CWD is highly
contagious and its origin, mechanism of transmission and exact prevalence are
currently unclear. The risk of transmission of CWD to humans is unknown.
Defining that risk is of utmost importance, considering that people have been
infected by animal prions, resulting in new fatal diseases. To study the
possibility that human PrPC can be converted into the infectious form by CWD
PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification
(PMCA) technique, which mimic in vitro the process of prion replication. Our
results show that cervid PrPSc can induce the pathological conversion of human
PrPC, but only after the CWD prion strain has been stabilized by successive
passages in vitro or in vivo. Interestingly, this newly generated human PrPSc
exhibits a distinct biochemical pattern that differs from any of the currently
known forms of human PrPSc, indicating that it corresponds to a novel human
prion strain. Our findings suggest that CWD prions have the capability to infect
humans, and that this ability depends on CWD strain adaptation, implying that
the risk for human health progressively increases with the spread of CWD among
cervids.
PPo2-7:
Biochemical and Biophysical Characterization of Different CWD
Isolates
Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin,
Germany
Key words: CWD, strains, FT-IR, AFM
Chronic wasting disease (CWD) is one of three naturally occurring forms of
prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie
in sheep. CWD is contagious and affects captive as well as free ranging cervids.
As long as there is no definite answer of whether CWD can breach the species
barrier to humans precautionary measures especially for the protection of
consumers need to be considered. In principle, different strains of CWD may be
associated with different risks of transmission to humans. Sophisticated strain
differentiation as accomplished for other prion diseases has not yet been
established for CWD. However, several different findings indicate that there
exists more than one strain of CWD agent in cervids. We have analysed a set of
CWD isolates from white-tailed deer and could detect at least two biochemically
different forms of disease-associated prion protein PrPTSE. Limited proteolysis
with different concentrations of proteinase K and/or after exposure of PrPTSE to
different pH-values or concentrations of Guanidinium hydrochloride resulted in
distinct isolate-specific digestion patterns. Our CWD isolates were also
examined in protein misfolding cyclic amplification studies. This showed
different conversion activities for those isolates that had displayed
significantly different sensitivities to limited proteolysis by PK in the
biochemical experiments described above. We further applied Fourier transform
infrared spectroscopy in combination with atomic force microscopy. This
confirmed structural differences in the PrPTSE of at least two disinct CWD
isolates. The data presented here substantiate and expand previous reports on
the existence of different CWD strains.
2012
Envt.06:
Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates
Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Aru Balachandran,2
Jürgen Richt,3 Vincent Beringue,4 Juan-Maria Torres,5 Paul Brown,1 Bob Hills6
and Jean-Philippe Deslys1
1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Canadian Food
Inspection Agency; Ottawa, ON Canada; 3Kansas State University; Manhattan, KS
USA; 4INRA; Jouy-en-Josas, France; 5INIA; Madrid, Spain; 6Health Canada; Ottawa,
ON Canada
†Presenting author; Email: emmanuel.comoy@cea.fr
The constant increase of chronic wasting disease (CWD) incidence in North
America raises a question about their zoonotic potential. A recent publication
showed their transmissibility to new-world monkeys, but no transmission to
old-world monkeys, which are phylogenetically closer to humans, has so far been
reported. Moreover, several studies have failed to transmit CWD to transgenic
mice overexpressing human PrP. Bovine spongiform encephalopathy (BSE) is the
only animal prion disease for which a zoonotic potential has been proven. We
described the transmission of the atypical BSE-L strain of BSE to cynomolgus
monkeys, suggesting a weak cattle-to-primate species barrier. We observed the
same phenomenon with a cattleadapted strain of TME (Transmissible Mink
Encephalopathy). Since cattle experimentally exposed to CWD strains have also
developed spongiform encephalopathies, we inoculated brain tissue from
CWD-infected cattle to three cynomolgus macaques as well as to transgenic mice
overexpressing bovine or human PrP. Since CWD prion strains are highly
lymphotropic, suggesting an adaptation of these agents after peripheral
exposure, a parallel set of four monkeys was inoculated with CWD-infected cervid
brains using the oral route. Nearly four years post-exposure, monkeys exposed to
CWD-related prion strains remain asymptomatic. In contrast, bovinized and
humanized transgenic mice showed signs of infection, suggesting that CWD-related
prion strains may be capable of crossing the cattle-to-primate species barrier.
Comparisons with transmission results and incubation periods obtained after
exposure to other cattle prion strains (c-BSE, BSE-L, BSE-H and cattle-adapted
TME) will also be presented, in order to evaluate the respective risks of each
strain.
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
Martin L. Daus,1,† Johanna Breyer,2 Katjs Wagenfuehr,1 Wiebke Wemheuer,2
Achim Thomzig,1 Walter Schulz-Schaeffer2 and Michael Beekes1 1Robert Koch
Institut; P24 TSE; Berlin, Germany; 2Department of Neuropathology, Prion and
Dementia Research Unit, University Medical Center Göttingen; Göttingen, Germany
†Presenting author; Email: dausm@rki.de
Chronic wasting disease (CWD) is a contagious, rapidly spreading
transmissible spongiform encephalopathy (TSE) occurring in cervids in North
America. Despite efficient horizontal transmission of CWD among cervids natural
transmission of the disease to other species has not yet been observed. Here, we
report a direct biochemical demonstration of pathological prion protein PrPTSE
and of PrPTSE-associated seeding activity in skeletal muscles of CWD-infected
cervids. The presence of PrPTSE was detected by Western- and postfixed frozen
tissue blotting, while the seeding activity of PrPTSE was revealed by protein
misfolding cyclic amplification (PMCA). The concentration of PrPTSE in skeletal
muscles of CWD-infected WTD was estimated to be approximately 2000- to
10000-fold lower than in brain tissue. Tissue-blot-analyses revealed that PrPTSE
was located in muscle- associated nerve fascicles but not, in detectable
amounts, in myocytes. The presence and seeding activity of PrPTSE in skeletal
muscle from CWD-infected cervids suggests prevention of such tissue in the human
diet as a precautionary measure for food safety, pending on further
clarification of whether CWD may be transmissible to humans.
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other
species
Sunday, November 11, 2012
*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease
November 2012
Friday, December 14, 2012
*** Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans
2005 - December 14, 2012
Saturday, March 09, 2013
Chronic Wasting Disease in Bank Voles: Characterisation of the Shortest
Incubation Time Model for Prion Diseases
TSS
posted by Terry S. Singeltary Sr. at
12:07 PM
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