Sharpshooters from the Illinois Department of Natural Resources are trying
to monitor the number of deer who are suffering from Chronic Wasting Disease.
A INDR sharpshooter was found last Friday on Henneberry Forest Preserve
property and was escorted back to private land.
DNR Sharpshooter Hunted Deer Illegally on Heneberry Forest Preserve Land on
January 29th
Jim Wyman
Deer with Chronic Wasting Disease
Sharpshooters from the Illinois Department of Natural Resources are trying
to monitor the number of deer who are suffering from Chronic Wasting Disease. A
INDR sharpshooter was found last Friday on Henneberry Forest Preserve property
and was escorted back to private land.
A sharpshooter from the Illinois Department of Natural Resources hunted
deer illegally on Kendall County Forest Preserve land last Friday afternoon.
Kendall County Forest Preserve President Jeff Wehrli told the commissioners
that the DNR hunting occurred at the Hennberry Woods Forest Preserve on Cherry
Road near Oswego.
A DNR sharpshooter was harvesting deer on private property in order to
check for Chronic Wasting Disease, which is a brain disease that affects deer
and is transmittable.
According to Wherli, the sharpshooter had a deer stand on Heneberry Forest
Preserve land.
Kendall County Sheriff's Deputy Mike Mrozek said the call came in to his
department at around 3:00 p.m. Friday. Forest Preserve Commissioner Bob Davidson
told WSPY News that a citizen called him about the hunting.
Forest Preserve Director David Guritz wants to put up signs on the borders
of the Kendall County Forest Preserve land.
Wehrli said the DNR is in Kendall County to monitor Chronic Wasting
Disease.
According to IDNR Wildlife Biologist Joe Rogus, the incidence of Chronic
Wasting Disease should be 1 to 2% of the deer population; however Rogus told the
forest preserve commissioners on January 13th that six out of 19 deer samples
tested positive for CWD in the Oswego zone of Kendall County.
snip...
I was worried about Illinois. what is this about 30% or better cwd positive
from that sample collection. it will be interesting to see the final tally. not
looking good.
strange, I was asking Illinois just last week about samples to date. here
is what they said ;
From:
Sent: Friday, January 29, 2016 11:23 AM
To: Terry S. Singeltary Sr.
Cc: Subject: RE: Illinois Chronic Wasting Disease CWD 2015-2016 testing
update
Mr. Singeltary,
The experts in wildlife here at DNR say that: “Samples are still be tested
at the Galesburg Lab, and status changes daily.
The report to which he refers is our annual report which includes
sharpshooting results, as well.
We just completed the first week of our shooting, which will continue
through the end of March.”
Hope this helps…….
=================
From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net] Sent:
Thursday, January 28, 2016 2:33 PM To:
Subject: Illinois Chronic Wasting Disease CWD 2015-2016 testing
update
Subject: Illinois Chronic Wasting Disease CWD 2015-2016 testing
update
Greetings,
I have not seen the latest Chronic Wasting Disease CWD 2015-2016 testing
figures and what the latest is. the latest thing on the page says ;
Update July 1, 2015:
We now have a total of 538 cases of CWD.
Note: Years are reported by fiscal year: 2015 is the period from July 1,
2014 through June 30, 2015, etc.
is there a link to a more updated cwd testing data, or what are the latest
figures?
kindest regards, terry
=====================end...tss===============
Illinois Chronic Wasting Disease CWD Update January 2016
Chronic Wasting Disease
Page
Content
Update July 1, 2015:
We now have a
total of 538 cases of CWD.
Note: Years
are reported by fiscal year: 2015 is the period from July 1, 2014 through June
30, 2015, etc.
Total
CWD Cases per year:
| Year | Cases |
|---|---|
| 2015 | 71 |
| 2014 | 59 |
| 2013 | 36 |
| 2012 | 36 |
| 2011 | 42 |
| 2010 | 37 |
| 2009 | 30 |
| 2008 | 38 |
| 2007 | 42 |
| 2006 | 51 |
| 2005 | 31 |
| 2004 | 51 |
| 2003 | 14 |
| Total | 538 |
Total
CWD Cases per County:
| County | 2003 | 2004 | 2005 | 2006 | 2007 | 2008 | 2009 | 2010 | 2011 | 2012 | 2013 | 2014 | 2015 | Total |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Boone | 9 | 25 | 13 | 16 | 14 | 11 | 9 | 14 | 7 | 5 | 4 | 5 | 6 | 138 |
| DeKalb | 0 | 4 | 1 | 5 | 6 | 8 | 4 | 3 | 7 | 5 | 7 | 8 | 8 | 66 |
| DuPage | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 1 | 0 | 0 | 1 |
| Grundy | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 2 | 5 | 3 | 3 | 5 | 18 |
| Jo Daviess | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 1 | 0 | 1 | 4 | 7 | 13 |
| Kane | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 4 | 7 | 4 | 5 | 7 | 27 |
| Kankakee | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 1 | 1 |
| Kendall | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 1 | 4 | 6 | 11 |
| Lake | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 1 | 0 | 1 |
| LaSalle | 0 | 0 | 0 | 0 | 1 | 0 | 0 | 0 | 3 | 0 | 1 | 2 | 6 | 13 |
| Livingston | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 2 | 2 |
| McHenry | 2 | 2 | 4 | 4 | 4 | 0 | 4 | 3 | 3 | 3 | 3 | 7 | 6 | 45 |
| Ogle | 0 | 0 | 0 | 2 | 0 | 0 | 1 | 0 | 4 | 2 | 3 | 1 | 2 | 15 |
| Stephenson | 0 | 0 | 0 | 0 | 0 | 1 | 0 | 1 | 1 | 2 | 3 | 4 | 6 | 18 |
| Will | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 2 | 1 | 3 |
| Winnebago | 3 | 20 | 13 | 24 | 17 | 18 | 12 | 16 | 10 | 7 | 5 | 13 | 8 | 166 |
| Total | 14 | 51 | 31 | 51 | 42 | 38 | 30 | 37 | 42 | 36 | 36 | 59 | 71 | 538 |
Locations of CWD-Positive Deer - Updated 7/21/2015
Illinois Loosing Ground to Chronic Wasting Disease CWD
cases mounting with 71 confirmed in 2015 and 538 confirmed cases to date
Chronic Wasting Disease Page Content Update July 1, 2015:
We now have a total of 538 cases of CWD
Note: Years are reported by fiscal year: 2015 is the period
from July 1, 2014 through June 30, 2015, etc.
Total CWD Cases per year:
Year Cases 2015 71 2014 59 2013 36 2012 36 2011 42 2010
37 2009 30 2008 38 2007 42 2006 51 2005 31 2004 51 2003 14 Total 538
Monday, August 31, 2015
Illinois Loosing Ground to Chronic Wasting Disease CWD
cases mounting with 71 confirmed in 2015 and 538 confirmed cases to date
see history of CWD in Illinois here
Saturday, February 08, 2014
Illinois CWD confirmed in Will County deer
Chronic Wasting Disease Illinois
Update July 1, 2013:
We now have a total of 408 cases of CWD.
Note: Years are reported by fiscal year: 2013 is the period
from July 1, 2012 through June 30, 2013, etc.
Illinois CWD-Infected Sections - August 15, 2013
Monday, April 08, 2013
Evaluation of a wild white-tailed deer population
management program for controlling chronic wasting disease in Illinois,
2003–2008
Wednesday, January 16, 2013
Illinois DuPage county deer found with Chronic Wasting
Disease CWD
Tuesday, November 13, 2012 ILLINOIS CWD UPDATE NOVEMBER
2012
Thursday, February 10, 2011
CWD ILLINOIS UPDATE FEBRUARY 2011 Locations of CWD-Positive
Deer - Updated 2/07/2011
Thursday, January 28, 2010 CWD ILLINOIS UPDATE 2010
Saturday, March 08, 2008
CWD UPDATE ILLINOIS Stephenson County joins CWD list
game farms help spread cwd, simple fact. it’s been proven.
game farms are not the only risk factor though, however, they are a big part of
the problem, history shows this.
the quarantine of cwd tse prion infected game farms must be
extended to 16 years now.
the CWD LOTTO ENTITLEMENT of captive game farms where the
states pays game farms for CWD MUST BE STOPPED. if the cwd infected farm does
not buy insurance for any and all loss from CWD for them and any party that does
business with them, and or any loss to the state, and or any products there
from, that’s to bad, they should never be allowed to be permitted. in fact, for
any state that does allow game farming, urine mills, sperm mills, antler mills,
velvet mills, big high fence ranch, little low fence farm, in my opinion, it’s
that states responsibility to protect that state, thus, any states that allow
these farms and business there from, it should be mandatory before any permit is
allowed, that game farm must have enough personal insurance that would cover
that farm, any farm that does business with them, and or any products there
from, and the state, before such permit is issued. personally, I am sick and
tired of all the big ag entitlement programs, and that’s all cwd indemnity is.
in fact, the USDA CWD INDEMNITY PROGRAM, should read, THE USDA CWD ENTITLEMENT
PROGRAM.
we cannot, and must not, let the industry regulate itself,
especially with the junk science they try to use.
if they are not going to be science based, they must be
banned.
science has told us for 3 decade or longer, that these are
the things that _might_ work, yet thanks to the industry, and government
catering to industry, regulations there from have failed, because of catering to
the industry, and the cwd tse prion agent has continued to spread during this
time. a fine example is Texas.
I asked someone recently, what sort of hunting legacy do you want to leave
your children, did you want to have where all you have are blind, slobbering,
drooling, stumbling, or maybe even healthy looking subclinical cwd infected
cervid, to go on and expose who knows what (cause cwd is spreading, it has
mutated, and nobody can stop it so far), but is this what we want to leave our
children? the only answer I ever seem to get from anyone in the industry, is
just let cwd take care of itself. well hell, how is that working for us so
far?
this cwd tse prion must be stopped. the vertical and lateral transmission
of this cwd tse prion agent amongst cervids, if cwd jumps species (if it has not
already), and transmits the same ways vertical and lateral in other species, and
the other species are as susceptible from so many different routes and sources,
simply put, we’re screwed. just saying. I am not trying to scare anyone, I am
simply presenting the facts, you must make your own decision or not. we have
ignored these tse prion disease way too long.
HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn
Flats) Farm Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in
a North American captive herd.
RECOMMENDATION: That the Board approve the purchase of 80
acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage
County and approve the restrictions on public use of the site.
SUMMARY:
State pays farmer $298,000 for infected deer herd
Jan. 16, 2016 8:05 p.m.
The State of Wisconsin paid nearly $300,000 to the Eau
Claire County farmer whose deer herd was depopulated after it was found to be
infected with chronic wasting disease.
Rick Vojtik, owner of Fairchild Whitetails in Fairchild,
received an indemnity payment of $298,770 for 228 white-tailed deer killed on
his farm, according to officials with the Department of Agriculture, Trade and
Consumer Protection.
The money was taken from the agency's general program
revenue funded by Wisconsin taxpayers.
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn
Flats) Farm Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in
a North American captive herd.
RECOMMENDATION: That the Board approve the purchase of 80
acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage
County and approve the restrictions on public use of the site.
SUMMARY:
$298,770 + $465,000
THE CWD ENTITLEMENT PROGRAM FOR GAME FARMS MUST BE
STOPPED!
Friday, January 29, 2016
Wisconsin CWD-positive white-tailed deer found on Iowa
County farm January 29, 2016
*** 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).
*** see history of this CWD blunder here ;
On June 5, 2013, DNR conducted a fence inspection, after
gaining approval from surrounding landowners, and confirmed that the fenced had
been cut or removed in at least four separate locations; that the fence had
degraded and was failing to maintain the enclosure around the Quarantined
Premises in at least one area; that at least three gates had been opened;and
that deer tracks were visible in and around one of the open areas in the sand on
both sides of the fence, evidencing movement of deer into the Quarantined
Premises.
The overall incidence of clinical CWD in white-tailed deer
was 82%
Species (cohort) CWD (cases/total) Incidence (%) Age at CWD
death (mo)
”The occurrence of CWD must be viewed against the contest
of the locations in which it occurred. It was an incidental and unwelcome
complication of the respective wildlife research programmes. Despite it’s
subsequent recognition as a new disease of cervids, therefore justifying direct
investigation, no specific research funding was forthcoming. The USDA veiwed it
as a wildlife problem and consequently not their province!” page 26.
Thursday, January 21, 2016
INDIANA With end of long legal challenge last year,
high-fence hunting operations currently unregulated
Tuesday, December 29, 2015
*** TEXAS MONTHLY CHRONIC WASTING DISEASE CWD JANUARY 2016
DEER BREEDERS STILL DON'T GET IT $
Chronic Wasting Unease
*** The emergence of a deadly disease has wildlife
officials and deer breeders eyeing each other suspiciously. ***
game farms help spread cwd, simple fact. it’s been proven.
game farms are not the only risk factor though, however, they are a big part of
the problem, history shows this.
the quarantine of cwd tse prion infected game farms must be
extended to 16 years now.
the CWD LOTTO ENTITLEMENT of captive game farms where the
states pays game farms for CWD MUST BE STOPPED. if the cwd infected farm does
not buy insurance for any and all loss from CWD for them and any party that does
business with them, and or any loss to the state, and or any products there
from, that’s to bad, they should never be allowed to be permitted. in fact, for
any state that does allow game farming, urine mills, sperm mills, antler mills,
velvet mills, big high fence ranch, little low fence farm, in my opinion, it’s
that states responsibility to protect that state, thus, any states that allow
these farms and business there from, it should be mandatory before any permit is
allowed, that game farm must have enough personal insurance that would cover
that farm, any farm that does business with them, and or any products there
from, and the state, before such permit is issued. personally, I am sick and
tired of all the big ag entitlement programs, and that’s all cwd indemnity is.
in fact, the USDA CWD INDEMNITY PROGRAM, should read, THE USDA CWD ENTITLEMENT
PROGRAM.
we cannot, and must not, let the industry regulate itself,
especially with the junk science they try to use.
if they are not going to be science based, they must be
banned.
science has told us for 3 decade or longer, that these are
the things that _might_ work, yet thanks to the industry, and government
catering to industry, regulations there from have failed, because of catering to
the industry, and the cwd tse prion agent has continued to spread during this
time. a fine example is Texas.
Sunday, January 17, 2016
Texas 10,000 deer in Texas tested for deadly disease CWD
TSE, but not tested much in the most logical place, the five-mile radius around
the Medina County captive-deer facility where it was discovered
Friday, January 15, 2016
TEXAS PARKS & WILDLIFE CWD Ante-Mortem Testing
Symposium Texas Disposal Systems Events Pavilion January 12, 2016
Research Project: TRANSMISSION, DIFFERENTIATION, AND
PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
***Title: Transmission of chronic wasting disease to
sentinel reindeer (Rangifer tarandus tarandus)
Authors
item Moore, S - item Kunkle, Robert item Nicholson, Eric
item Richt, Juergen item Hamir, Amirali item Waters, Wade item Greenlee, Justin
Submitted to: American College of Veterinary Pathologists
Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12,
2015 Publication Date: N/A
Technical Abstract:
Chronic wasting disease (CWD) is a naturally-occurring,
fatal neurodegenerative disease of North American cervids. Reindeer (Rangifer
tarandus tarandus) are susceptible to CWD following oral challenge, but CWD has
not been reported in free-ranging caribou (Rangifer tarandus caribou) or farmed
reindeer. Potential contact between CWD-affected cervids and Rangifer species
that are free-ranging or co-housed on farms presents a potential risk of CWD
transmission. The aims of this study were to 1) investigate the transmission of
CWD from white-tailed deer (Odocoileus virginianus; CWD-wtd), mule deer
(Odocoileus hemionus; CWD-md), or elk (Cervus elaphus nelsoni; CWD-elk) to
reindeer via the intracranial route, and 2) to assess for direct and indirect
horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer
fawns were challenged intracranially with CWD-wtd, CWD-md, or CWD-elk. Two years
after challenge of inoculated reindeer, non-inoculated control reindeer were
introduced into the same pen as the CWD-wtd inoculated reindeer (n=4) or into a
pen adjacent to the CWD-md inoculated reindeer (n=2). Reindeer were allowed to
develop clinical disease. At death/euthanasia a complete necropsy examination
was performed, including immunohistochemical testing of tissues for
disease-associated CWD prion protein (PrP-CWD). Intracranially challenged
reindeer developed clinical disease from 21 months post-inoculation (MPI).
PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6 developed
clinical disease during the study period (<57 div="" mpi="">
***We have shown that reindeer are susceptible to CWD from
various cervid sources and can transmit CWD to naive reindeer both directly and
indirectly.
Last Modified: 12/3/2015
***PrP-CWD was detected in 5/6 sentinel reindeer although
only 2/6 developed clinical disease during the study period (<57 div="" mpi="">
***We have shown that reindeer are susceptible to CWD from
various cervid sources and can transmit CWD to naive reindeer both directly and
indirectly.
Tuesday, September 29, 2015
*** Transmission of chronic wasting disease to sentinel
reindeer (Rangifer tarandus tarandus) can transmit CWD to naive reindeer both
directly and indirectly
Research Project: TRANSMISSION, DIFFERENTIATION, AND
PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
CHRONIC WASTING DISEASE CWD TSE PRION AKA MAD COW TYPE
DISEASE
Friday, January 01, 2016
Bayesian Modeling of Prion Disease Dynamics in Mule Deer
Using Population Monitoring and Capture-Recapture Data
Chris Geremia, Michael W. Miller, Jennifer A. Hoeting,
Michael F. Antolin, N. Thompson Hobbs PLOS x Published: October 28, 2015 DOI:
10.1371/journal.pone.0140687
Abstract
Epidemics of chronic wasting disease (CWD) of North
American Cervidae have potential to harm ecosystems and economies. We studied a
migratory population of mule deer (Odocoileus hemionus) affected by CWD for at
least three decades using a Bayesian framework to integrate matrix population
and disease models with long-term monitoring data and detailed process-level
studies. We hypothesized CWD prevalence would be stable or increase between two
observation periods during the late 1990s and after 2010, with higher CWD
prevalence making deer population decline more likely. The weight of evidence
suggested a reduction in the CWD outbreak over time, perhaps in response to
intervening harvest-mediated population reductions. Disease effects on deer
population growth under current conditions were subtle with a 72% chance that
CWD depressed population growth. With CWD, we forecasted a growth rate near one
and largely stable deer population. Disease effects appear to be moderated by
timing of infection, prolonged disease course, and locally variable infection.
Long-term outcomes will depend heavily on whether current conditions hold and
high prevalence remains a localized phenomenon.
Discussion
The protracted time-scale of the CWD outbreak is much
longer than the timespan of our research, which limits our ability to identify
the true explanation of our findings. Nonetheless, our research suggests that,
at least for the foreseeable future (e.g., decades), mule deer populations
sharing the overall survival and infection probabilities estimated from our
analyses may persist but likely will not thrive where CWD becomes established as
an endemic infectious disease.
‘’Nonetheless, our research suggests that, at least for the
foreseeable future (e.g., decades), mule deer populations sharing the overall
survival and infection probabilities estimated from our analyses may persist but
likely will not thrive where CWD becomes established as an endemic infectious
disease. ‘’
*** Bayesian Modeling of Prion Disease Dynamics in Mule
Deer Using Population Monitoring and Capture-Recapture Data
‘’Mountain lions prey selectively on CWD infected deer [33]
and CWD could result in an abundance of vulnerable prey, thereby enhancing
mountain lion survival and reproduction [20].’’
please see ;
‘’preliminary results suggesting that bobcats (Lynx rufus)
may be susceptible to white-tailed deer (Odocoileus virginianus) chronic wasting
disease agent.’’
references on Feline Spongiform Encephalopathy FSE toward
the bottom, see ;
Assessing Transmissible Spongiform Encephalopathy Species
Barriers with an In Vitro Prion Protein Conversion Assay
Tuesday, December 15, 2015
Chronic Wasting Disease will cause a Wyoming deer herd to
go virtually extinct in 41 years, a five-year study predicts
Study: Chronic Wasting Disease kills 19% of deer herd
annually
*** Infectious agent of sheep scrapie may persist in the
environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
*** Spraker suggested an interesting explanation for the
occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40
years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work
was conducted at this site. When deer were introduced to the pens they occupied
ground that had previously been occupied by sheep.
PL1
Using in vitro prion replication for high sensitive
detection of prions and prionlike proteins and for understanding mechanisms of
transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain
disorders, Department of Neurology, University of Texas Medical School at
Houston.
Prion and prion-like proteins are misfolded protein
aggregates with the ability to selfpropagate to spread disease between cells,
organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o
n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded
form of the prion protein (PrPSc), which propagates by transmitting its
misfolding to the normal prion protein (PrPC). The availability of a procedure
to replicate prions in the laboratory may be important to study the mechanism of
prion and prion-like spreading and to develop high sensitive detection of small
quantities of misfolded proteins in biological fluids, tissues and environmental
samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and
efficient methodology to mimic prion replication in the test tube. PMCA is a
platform technology that may enable amplification of any prion-like misfolded
protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able
to detect the equivalent of one single molecule of infectious PrPSc and
propagate prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of
environmental prion contamination on the horizontal spreading of TSEs. These
experiments have focused on the study of the interaction of prions with plants
and environmentally relevant surfaces. Our results show that plants (both leaves
and roots) bind tightly to prions present in brain extracts and excreta (urine
and feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer
fundamental questions of prion propagation and has broad applications in
research areas including the food industry, blood bank safety and human and
veterinary disease diagnosis.
see ;
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a
reservoir for scrapie transmission
Objects in contact with classical scrapie sheep act as a
reservoir for scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3,
Ben C. Maddison4, Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 2 Pathology Department, Animal and Plant Health
Agency Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal
and Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion
disease of sheep and goats. Prions can persist and remain potentially infectious
in the environment for many years and thus pose a risk of infecting animals
after re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible
disease because it has been reported in naïve, supposedly previously unexposed
sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19,
20). Although the vector for disease transmission is not known, soil is likely
to be an important reservoir for prions (2) where – based on studies in rodents
– prions can adhere to minerals as a biologically active form (21) and remain
infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD)
has re-occurred in mule deer housed in paddocks used by infected deer 2 years
earlier, which was assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie
infection was greater through exposure to contaminated wooden, plastic, and
metal surfaces via water or food troughs, fencing, and hurdles than through
grazing. Drinking from a water trough used by the scrapie flock was sufficient
to cause infection in sheep in a clean building. Exposure to fences and other
objects used for rubbing also led to infection, which supported the hypothesis
that skin may be a vector for disease transmission (9). The risk of these
objects to cause infection was further demonstrated when 87% of 23 sheep
presented with PrPSc in lymphoid tissue after grazing on one of the paddocks,
which contained metal hurdles, a metal lamb creep and a water trough in contact
with the scrapie flock up to 8 weeks earlier, whereas no infection had been
demonstrated previously in sheep grazing on this paddock, when equipped with new
fencing and field furniture. When the contaminated furniture and fencing were
removed, the infection rate dropped significantly to 8% of 12 sheep, with soil
of the paddock as the most likely source of infection caused by shedding of
prions from the scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination
of field furniture sufficient to cause infection was dependent on two factors:
stage of incubation period and time of last use by scrapie-infected sheep.
Drinking from a water trough that had been used by scrapie sheep in the
predominantly pre-clinical phase did not appear to cause infection, whereas
infection was shown in sheep drinking from the water trough used by scrapie
sheep in the later stage of the disease. It is possible that contamination
occurred through shedding of prions in saliva, which may have contaminated the
surface of the water trough and subsequently the water when it was refilled.
Contamination appeared to be sufficient to cause infection only if the trough
was in contact with sheep that included clinical cases. Indeed, there is an
increased risk of bodily fluid infectivity with disease progression in scrapie
(24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light
and heat under natural conditions do not inactivate prions (26), furniture in
contact with the scrapie flock, which was assumed to be sufficiently
contaminated to cause infection, did not act as vector for disease if not used
for 18 months, which suggest that the weathering process alone was sufficient to
inactivate prions.
PrPSc detection by sPMCA is increasingly used as a
surrogate for infectivity measurements by bioassay in sheep or mice. In this
reported study, however, the levels of PrPSc present in the environment were
below the limit of detection of the sPMCA method, yet were still sufficient to
cause infection of in-contact animals. In the present study, the outdoor objects
were removed from the infected flock 8 weeks prior to sampling and were positive
by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also
yielded 2 positive reactions out of 139 in samples from the scrapie-free farm,
the sPMCA assay could not detect PrPSc on any of the objects above the
background of the assay. False positive reactions with sPMCA at a low frequency
associated with de novo formation of infectious prions have been reported (27,
28). This is in contrast to our previous study where we demonstrated that
outdoor objects that had been in contact with the scrapie-infected flock up to
20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis
[4 out of 15 reactions (12)] and was significantly more positive by the assay
compared to analogous samples from the scrapie-free farm. This discrepancy could
be due to the use of a different sPMCA substrate between the studies that may
alter the efficiency of amplification of the environmental PrPSc. In addition,
the present study had a longer timeframe between the objects being in contact
with the infected flock and sampling, which may affect the levels of extractable
PrPSc. Alternatively, there may be potentially patchy contamination of this
furniture with PrPSc, which may have been missed by swabbing. The failure of
sPMCA to detect CWD-associated PrP in saliva from clinically affected deer
despite confirmation of infectivity in saliva-inoculated transgenic mice was
associated with as yet unidentified inhibitors in saliva (29), and it is
possible that the sensitivity of sPMCA is affected by other substances in the
tested material. In addition, sampling of amplifiable PrPSc and subsequent
detection by sPMCA may be more difficult from furniture exposed to weather,
which is supported by the observation that PrPSc was detected by sPMCA more
frequently in indoor than outdoor furniture (12). A recent experimental study
has demonstrated that repeated cycles of drying and wetting of
prion-contaminated soil, equivalent to what is expected under natural weathering
conditions, could reduce PMCA amplification efficiency and extend the incubation
period in hamsters inoculated with soil samples (30). This seems to apply also
to this study even though the reduction in infectivity was more dramatic in the
sPMCA assays than in the sheep model. Sheep were not kept until clinical
end-point, which would have enabled us to compare incubation periods, but the
lack of infection in sheep exposed to furniture that had not been in contact
with scrapie sheep for a longer time period supports the hypothesis that prion
degradation and subsequent loss of infectivity occurs even under natural
conditions.
In conclusion, the results in the current study indicate
that removal of furniture that had been in contact with scrapie-infected animals
should be recommended, particularly since cleaning and decontamination may not
effectively remove scrapie infectivity (31), even though infectivity declines
considerably if the pasture and the field furniture have not been in contact
with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc
in furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible
spongiform encephalopathy, sheep, field furniture, reservoir, serial protein
misfolding cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as
a reservoir for scrapie transmission ***
Circulation of prions within dust on a scrapie affected
farm
Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A
Hawkins3 and Ben C Maddison2*
Abstract
Prion diseases are fatal neurological disorders that affect
humans and animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of
deer/elk are contagious prion diseases where environmental reservoirs have a
direct link to the transmission of disease. Using protein misfolding cyclic
amplification we demonstrate that scrapie PrPSc can be detected within
circulating dusts that are present on a farm that is naturally contaminated with
sheep scrapie. The presence of infectious scrapie within airborne dusts may
represent a possible route of infection and illustrates the difficulties that
may be associated with the effective decontamination of such scrapie affected
premises.
snip...
Discussion
We present biochemical data illustrating the airborne
movement of scrapie containing material within a contaminated farm environment.
We were able to detect scrapie PrPSc within extracts from dusts collected over a
70 day period, in the absence of any sheep activity. We were also able to detect
scrapie PrPSc within dusts collected within pasture at 30 m but not at 60 m
distance away from the scrapie contaminated buildings, suggesting that the
chance of contamination of pasture by scrapie contaminated dusts decreases with
distance from contaminated farm buildings. PrPSc amplification by sPMCA has been
shown to correlate with infectivity and amplified products have been shown to be
infectious [14,15]. These experiments illustrate the potential for low dose
scrapie infectivity to be present within such samples. We estimate low ng levels
of scrapie positive brain equivalent were deposited per m2 over 70 days, in a
barn previously occupied by sheep affected with scrapie. This movement of dusts
and the accumulation of low levels of scrapie infectivity within this
environment may in part explain previous observations where despite stringent
pen decontamination regimens healthy lambs still became scrapie infected after
apparent exposure from their environment alone [16]. The presence of sPMCA
seeding activity and by inference, infectious prions within dusts, and their
potential for airborne dissemination is highly novel and may have implications
for the spread of scrapie within infected premises. The low level circulation
and accumulation of scrapie prion containing dust material within the farm
environment will likely impede the efficient decontamination of such scrapie
contaminated buildings unless all possible reservoirs of dust are removed.
Scrapie containing dusts could possibly infect animals during feeding and
drinking, and respiratory and conjunctival routes may also be involved. It has
been demonstrated that scrapie can be efficiently transmitted via the nasal
route in sheep [17], as is also the case for CWD in both murine models and in
white tailed deer [18-20].
The sources of dust borne prions are unknown but it seems
reasonable to assume that faecal, urine, skin, parturient material and
saliva-derived prions may contribute to this mobile environmental reservoir of
infectivity. This work highlights a possible transmission route for scrapie
within the farm environment, and this is likely to be paralleled in CWD which
shows strong similarities with scrapie in terms of prion dissemination and
disease transmission. The data indicate that the presence of scrapie prions in
dust is likely to make the control of these diseases a considerable
challenge.
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...
Saturday, January 31, 2015
European red deer (Cervus elaphus elaphus) are susceptible
to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route
I strenuously once again urge the FDA and its industry
constituents, to make it MANDATORY that all ruminant feed be banned to all
ruminants, and this should include all cervids as soon as possible for the
following reasons...
======
In the USA, under the Food and Drug Administrations BSE
Feed Regulation (21 CFR 589.2000) most material (exceptions include milk,
tallow, and gelatin) from deer and elk is prohibited for use in feed for
ruminant animals. With regards to feed for non-ruminant animals, under FDA law,
CWD positive deer may not be used for any animal feed or feed ingredients. For
elk and deer considered at high risk for CWD, the FDA recommends that these
animals do not enter the animal feed system.
***However, this recommendation is guidance and not a
requirement by law.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States?
***
31 Jan 2015 at 20:14 GMT
Research Project: TRANSMISSION, DIFFERENTIATION, AND
PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Scrapie transmits to white-tailed deer by the oral
route and has a molecular profile similar to chronic wasting disease
Authors
item Greenlee, Justin item Moore, S - item Smith, Jodi -
item Kunkle, Robert item West Greenlee, M -
Submitted to: American College of Veterinary Pathologists
Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12,
2015 Publication Date: N/A Technical Abstract: The purpose of this work was to
determine susceptibility of white-tailed deer (WTD) to the agent of sheep
scrapie and to compare the resultant PrPSc to that of the original inoculum and
chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure
(concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All
scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected
in lymphoid tissues at preclinical time points, and deer necropsied after 28
months post-inoculation had clinical signs, spongiform encephalopathy, and
widespread distribution of PrPSc in neural and lymphoid tissues. Western
blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral
cortex had a profile similar to the original scrapie inoculum, whereas WB of
brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile
resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical
scrapie were further passaged to mice expressing cervid prion protein and
intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct
incubation times. Sheep inoculated intranasally with WTD derived scrapie
developed disease, but only after inoculation with the inoculum that had a
scrapie-like profile. The WTD study is ongoing, but deer in both inoculation
groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work
demonstrates that WTD are susceptible to the agent of scrapie, two distinct
molecular profiles of PrPSc are present in the tissues of affected deer, and
inoculum of either profile readily passes to deer.
White-tailed Deer are Susceptible to Scrapie by Natural
Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle;
Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to
better understand the potential host range and origins of prion diseases.
Previous experiments demonstrated that white-tailed deer are susceptible to
sheep-derived scrapie by intracranial inoculation. The purpose of this study was
to determine susceptibility of white-tailed deer to scrapie after a natural
route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and
intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a
sheep clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
PO-039: A comparison of scrapie and chronic wasting disease
in white-tailed deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept.
Agriculture; Agricultural Research Service, National Animal Disease Center;
Ames, IA USA
White-tailed deer are susceptible to the agent of sheep
scrapie by intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from
free-ranging cervids, and the disease is likely to continue to spread
geographically [10]. However, the potential that white-tailed deer may be
susceptible to sheep scrapie by a natural route presents an additional
confounding factor to halting the spread of CWD. This leads to the additional
speculations that
1) infected deer could serve as a reservoir to infect sheep
with scrapie offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to
current endemic areas, but could occur anywhere that sheep with scrapie and
susceptible cervids cohabitate.
This work demonstrates for the first time that white-tailed
deer are susceptible to sheep scrapie by intracerebral inoculation with a high
attack rate and that the disease that results has similarities to CWD. These
experiments will be repeated with a more natural route of inoculation to
determine the likelihood of the potential transmission of sheep scrapie to
white-tailed deer. If scrapie were to occur in white-tailed deer, results of
this study indicate that it would be detected as a TSE, but may be difficult to
differentiate from CWD without in-depth biochemical analysis.
2012
PO-039: A comparison of scrapie and chronic wasting disease
in white-tailed deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept.
Agriculture; Agricultural Research Service, National Animal Disease Center;
Ames, IA USA
snip...
The results of this study suggest that there are many
similarities in the manifestation of CWD and scrapie in WTD after IC inoculation
including early and widespread presence of PrPSc in lymphoid tissues, clinical
signs of depression and weight loss progressing to wasting, and an incubation
time of 21-23 months. Moreover, western blots (WB) done on brain material from
the obex region have a molecular profile similar to CWD and distinct from
tissues of the cerebrum or the scrapie inoculum. However, results of microscopic
and IHC examination indicate that there are differences between the lesions
expected in CWD and those that occur in deer with scrapie: amyloid plaques were
not noted in any sections of brain examined from these deer and the pattern of
immunoreactivity by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were
susceptible to scrapie.
Deer developed clinical signs of wasting and mental
depression and were necropsied from 28 to 33 months PI. Tissues from these deer
were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples
from these deer exhibited two different molecular profiles: samples from obex
resembled CWD whereas those from cerebrum were similar to the original scrapie
inoculum. On further examination by WB using a panel of antibodies, the tissues
from deer with scrapie exhibit properties differing from tissues either from
sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with
scrapie are strongly immunoreactive when probed with mAb P4, however, samples
from WTD with scrapie are only weakly immunoreactive. In contrast, when probed
with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are
weakly immunoreactive and samples from WTD with scrapie are strongly positive.
This work demonstrates that WTD are highly susceptible to sheep scrapie, but on
first passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed
deer were susceptible to scrapie.
White-tailed Deer are Susceptible to Scrapie by Natural
Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle;
Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to
better understand the potential host range and origins of prion diseases.
Previous experiments demonstrated that white-tailed deer are susceptible to
sheep-derived scrapie by intracranial inoculation. The purpose of this study was
to determine susceptibility of white-tailed deer to scrapie after a natural
route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and
intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a
sheep clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
Monday, November 3, 2014
Persistence of ovine scrapie infectivity in a farm
environment following cleaning and decontamination
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.
HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn
Flats) Farm Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in
a North American captive herd.
RECOMMENDATION: That the Board approve the purchase of 80
acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage
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).
*** see history of this CWD blunder here ;
On June 5, 2013, DNR conducted a fence inspection, after
gaining approval from surrounding landowners, and confirmed that the fenced had
been cut or removed in at least four separate locations; that the fence had
degraded and was failing to maintain the enclosure around the Quarantined
Premises in at least one area; that at least three gates had been opened;and
that deer tracks were visible in and around one of the open areas in the sand on
both sides of the fence, evidencing movement of deer into the Quarantined
Premises.
The overall incidence of clinical CWD in white-tailed deer
was 82%
Species (cohort) CWD (cases/total) Incidence (%) Age at CWD
death (mo)
”The occurrence of CWD must be viewed against the contest
of the locations in which it occurred. It was an incidental and unwelcome
complication of the respective wildlife research programmes. Despite it’s
subsequent recognition as a new disease of cervids, therefore justifying direct
investigation, no specific research funding was forthcoming. The USDA veiwed it
as a wildlife problem and consequently not their province!” page 26.
O.05: Transmission of prions to primates after extended
silent incubation periods: Implications for BSE and scrapie risk assessment in
human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie
Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and
Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative
proteinopathies reputed to be transmissible under field conditions since
decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans
evidenced that an animal PD might be zoonotic under appropriate conditions.
Contrarily, in the absence of obvious (epidemiological or experimental) elements
supporting a transmission or genetic predispositions, PD, like the other
proteinopathies, are reputed to occur spontaneously (atpical animal prion
strains, sporadic CJD summing 80% of human prion cases). Non-human primate
models provided the first evidences supporting the transmissibiity of human
prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques
brought major information for BSE risk assessment for human health (Chen, 2014),
according to their phylogenetic proximity to humans and extended lifetime. We
used this model to assess the zoonotic potential of other animal PD from bovine,
ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a
natural classical scrapie isolate to macaque after a 10-year silent incubation
period,
***with features similar to some reported for human cases
of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as
recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and
L-type BSE),
***thus questioning the origin of human sporadic cases. We
will present an updated panorama of our different transmission studies and
discuss the implications of such extended incubation periods on risk assessment
of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
==========================================
***our findings suggest that possible transmission risk of
H-type BSE to sheep and human. Bioassay will be required to determine whether
the PMCA products are infectious to these animals.
==========================================
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO
HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3,
Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western
Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples,
Italy, 3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the
potential to infect human CNS and peripheral lymphoid tissues and that there
might be asymptomatic human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the
potential to infect human CNS and peripheral lymphoid tissues and that there
might be asymptomatic human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and
Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO
USA
Conversely, FSE maintained sufficient BSE characteristics
to more efficiently convert bovine rPrP than feline rPrP. Additionally, human
rPrP was competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein
interactions, the barrier preventing transmission of CWD to humans is less
robust than previously estimated.
================
***This insinuates that, at the level of protein:protein
interactions, the barrier preventing transmission of CWD to humans is less
robust than previously estimated.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update
January 2, 2014
*** chronic wasting disease, there was no absolute barrier
to conversion of the human prion protein.
*** Furthermore, the form of human PrPres produced in this
in vitro assay when seeded with CWD, resembles that found in the most common
human prion disease, namely sCJD of the MM1 subtype.
*** These results would seem to suggest that CWD does
indeed have zoonotic potential, at least as judged by the compatibility of CWD
prions and their human PrPC target. Furthermore, extrapolation from this simple
in vitro assay suggests that if zoonotic CWD occurred, it would most likely
effect those of the PRNP codon 129-MM genotype and that the PrPres type would be
similar to that found in the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health
was greatly magnified by the recognition that interspecies transfer of BSE to
humans by beef ingestion resulted in vCJD. While changes in animal feed
constituents and slaughter practices appear to have curtailed vCJD, there is
concern that CWD of free-ranging deer and elk in the U.S. might also cross the
species barrier. Thus, consuming venison could be a source of human prion
disease. Whether BSE and CWD represent interspecies scrapie transfer or are
newly arisen prion diseases is unknown. Therefore, the possibility of
transmission of prion disease through other food animals cannot be ruled out.
There is evidence that vCJD can be transmitted through blood transfusion. There
is likely a pool of unknown size of asymptomatic individuals infected with vCJD,
and there may be asymptomatic individuals infected with the CWD equivalent.
These circumstances represent a potential threat to blood, blood products, and
plasma supplies.
now, let’s see what the authors said about this casual
link, personal communications years ago. see where it is stated NO STRONG
evidence. so, does this mean there IS casual evidence ???? “Our conclusion
stating that we found no strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD
- YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of
which was attached to your email), we did not say CWD in humans will present
like variant CJD. That assumption would be wrong. I encourage you to read the
whole article and call me if you have questions or need more clarification
(phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected
with prion disease from eating venison." Our conclusion stating that we found no
strong evidence of CWD transmission to humans in the article you quoted or in
any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and
Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD -
YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM
......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1:
Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease
Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed
venison were reported to the Surveillance Center***,
snip... full text ;
CJD is so rare in people under age 30, one case in a
billion (leaving out medical mishaps), that four cases under 30 is "very high,"
says Colorado neurologist Bosque. "Then, if you add these other two from
Wisconsin [cases in the newspaper], six cases of CJD in people associated with
venison is very, very high." Only now, with Mary Riley, there are at least
seven, and possibly eight, with Steve, her dining companion. "It's not critical
mass that matters," however, Belay says. "One case would do it for me." The
chance that two people who know each other would both contact CJD, like the two
Wisconsin sportsmen, is so unlikely, experts say, it would happen only once in
140 years.
Given the incubation period for TSEs in humans, it may
require another generation to write the final chapter on CWD in Wisconsin. "Does
chronic wasting disease pass into humans? We'll be able to answer that in 2022,"
says Race. Meanwhile, the state has become part of an immense experiment.
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom,
and scientist telling you to test everything and potential risk factors for
humans ***
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of
Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal
muscle from CWD-infected cervids suggests prevention of such tissue in the human
diet as a precautionary measure for food safety, pending on further
clarification of whether CWD may be transmissible to humans.
Prions in Skeletal Muscles of Deer with Chronic Wasting
Disease Rachel C. Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina
J. Sigurdson4,‡, Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§
snip...
Abstract The emergence of chronic wasting disease (CWD) in
deer and elk in an increasingly wide geographic area, as well as the
interspecies transmission of bovine spongiform encephalopathy to humans in the
form of variant Creutzfeldt Jakob disease, have raised concerns about the
zoonotic potential of CWD. Because meat consumption is the most likely means of
exposure, it is important to determine whether skeletal muscle of diseased
cervids contains prion infectivity. Here bioassays in transgenic mice expressing
cervid prion protein revealed the presence of infectious prions in skeletal
muscles of CWD-infected deer, demonstrating that humans consuming or handling
meat from CWD-infected deer are at risk to prion exposure.
***********CJD REPORT 1994 increased risk for consumption
of veal and venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED
KINGDOM THIRD ANNUAL REPORT AUGUST 1994
Consumption of venison and veal was much less widespread
among both cases and controls. For both of these meats there was evidence of a
trend with increasing frequency of consumption being associated with increasing
risk of CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention
was restricted to pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between
‘’regular’’ veal eating and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a
year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around
this estimate. There is no strong evidence that eating veal less than once per
year is associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD
shows similar pattern, with regular venison eating associated with a 9 FOLD
INCREASE IN RISK OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH
INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating
and CJD is weaker (p = 0.14). When only controls for whom a relative was
interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with
another exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures ceased
to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed
statistical associations between various meats/animal products and INCREASED
RISK OF CJD. When some account was taken of possible confounding, the
association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF
THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were
associated with an increased risk of CJD, including liver consumption which was
associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing
the data from 3 studies in relation to this particular dietary factor, the risk
of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association
Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication
of the third annual report from the CJD Surveillance Unit. I am sorry that you
are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside
body and the Department of Health is committed to publishing their reports as
soon as they become available. In the circumstances it is not the practice to
circulate the report for comment since the findings of the report would not be
amended. In future we can ensure that the British Deer Farmers Association
receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public
fully informed of the results of any research in respect of CJD. This report was
entirely the work of the unit and was produced completely independantly of the
the Department.
The statistical results reqarding the consumption of
venison was put into perspective in the body of the report and was not mentioned
at all in the press release. Media attention regarding this report was low key
but gave a realistic presentation of the statistical findings of the Unit. This
approach to publication was successful in that consumption of venison was
highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or
indeed statistical links between CJD and consumption of venison, would increase,
and quite possibly give damaging credence, to the whole issue. From the low key
media reports of which I am aware it seems unlikely that venison consumption
will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** These results would seem to suggest that CWD does
indeed have zoonotic potential, at least as judged by the compatibility of CWD
prions and their human PrPC target. Furthermore, extrapolation from this simple
in vitro assay suggests that if zoonotic CWD occurred, it would most likely
effect those of the PRNP codon 129-MM genotype and that the PrPres type would be
similar to that found in the most common subtype of sCJD (MM1).***
***This information will have a scientific impact since it
is the first study that demonstrates the transmission of scrapie to a non-human
primate with a close genetic relationship to humans. This information is
especially useful to regulatory officials and those involved with risk
assessment of the potential transmission of animal prion diseases to humans.
***This observation strengthens the questioning of the
harmlessness of scrapie to humans, at a time when protective measures for human
and animal health are being dismantled and reduced as c-BSE is considered
controlled and being eradicated. Our results underscore the importance of
precautionary and protective measures and the necessity for long-term
experimental transmission studies to assess the zoonotic potential of other
animal prion strains.
Thursday, January 15, 2015
INDIANA HB1453 - high fence hunting preserve bill has been
introduced by Rep. Sean Eberhart and he received monetary contribution from
Indiana Deer and Elk Farmers Advocates INC. Indiana Politicians and
contributions from the Game Farm Industry, and whom is taking the bait $$$ will
this buy their vote in support of the cervid game farming industry ??? Indiana
Secretary of State Connie Lawson Summary by: Type Summary Groupings Total Direct
$12,500.00 Total Contributions = $12,500.00 11 matching record(s) found. Export
To: Contributor City, State Type Amount Date Candidate/Committee Name In Kind?
Large? Indiana Deer and Elk Farmers Advocates Inc Shipshewana, IN Direct
$1,000.00 10/25/2012 Bob Heaton for State Representative Committee No Yes View
Indiana Deer and Elk Farmers Advocates Inc Shipshewana, IN Direct $1,000.00
11/01/2012 Steele for Senate Committee No Yes View Indiana Deer and Elk Farmers
Advocates Inc Shipshewana, IN Direct $2,000.00 08/18/2014 Cindy Meyer Ziemke for
State Rep. No No View Indiana Deer and Elk Farmers Advocates Inc. Shipshewana,
IN Direct $500.00 11/26/2012 COMMITTEE TO ELECT BOB CHERRY No No View Indiana
Deer and Elk Farmers Advocates INC. Shipshewana, IN Direct $1,000.00 10/12/2012
Committee to Elect Matt Ubelhor No No View Indiana Deer and Elk Farmers
Advocates Inc. Shipshewana, IN Direct $1,000.00 10/01/2012 Markmessmer.com No No
View Indiana Deer and Elk Farmers Advocates Inc. Shipshewana, IN Direct
$1,000.00 10/25/2012 HERSHMAN FOR SENATE No Yes View Indiana Deer and Elk
Farmers Advocates PAC Shipshewana, IN Direct $2,000.00 09/02/2014 Committee to
Elect Sean Eberhart No No View Indiana Deer and Elk Farmers Advocates, Inc.
Shipshewana, IN Direct $1,000.00 10/15/2012 BILL FRIEND FOR STATE REPRESENTATIVE
COMMITTEE No Yes View Indiana Deer and Elk Farmers Advocates, Inc. Shipshewana,
IN Direct $1,000.00 10/22/2012 Committee to Elect Dan Leonard No Yes View
Indiana Deer and Elk Farmers Advoctes PAC Shipshewana, IN Direct $1,000.00
10/23/2012 Committee to Elect Sean Eberhart No Yes View
http://campaignfinance.in.gov/PublicSite/SearchPages/ContributionSearch.aspx?results=true&LastName=indiana+deer+and+elk+farmers&LastNameSearchType=1&Address=&City=&State=&Zip=&FinanceCategoryID=-32768&ContributionCodeID=-32768&ContributionAmountMinimum=-32768&ContributionAmountMaximum=-32768&ContributionDateBegin=12%3a00%3a00+AM&ContributionDateEnd=12%3a00%3a00+AM&MajorContribution=0&CommitteeCandidateDisplayMode=1&CommitteeName=&CommitteeID=-32768&CommitteeOrgCodeID=-32768&CommitteeNameSearchType=1&CandidateOffice=-32768&CandidateDistrictNumber=&CandidateParty=-32768&Exploratory=&CandidateFirstName=&CandidateLastName=&CandidateLastNameSearchType=&CandidateFirstNameSearchType=
http://campaignfinance.in.gov/PublicSite/SearchPages/ContributionSearch.aspx?results=true&LastName=indiana+deer+and+elk+farmers&LastNameSearchType=1&Address=&City=&State=&Zip=&FinanceCategoryID=-32768&ContributionCodeID=-32768&ContributionAmountMinimum=-32768&ContributionAmountMaximum=-32768&ContributionDateBegin=12%3a00%3a00+AM&ContributionDateEnd=12%3a00%3a00+AM&MajorContribution=0&CommitteeCandidateDisplayMode=1&CommitteeName=&CommitteeID=-32768&CommitteeOrgCodeID=-32768&CommitteeNameSearchType=1&CandidateOffice=-32768&CandidateDistrictNumber=&CandidateParty=-32768&Exploratory=&CandidateFirstName=&CandidateLastName=&CandidateLastNameSearchType=&CandidateFirstNameSearchType=
Total Contributions = $9,500.00 9 matching record(s) found.
Export To: Contributor City, State Type Amount Date Candidate/Committee Name In
Kind? Large? Indiana Deer and Elk Farmers Advocates Inc Shipshewana, IN Direct
$1,000.00 10/25/2012 Bob Heaton for State Representative Committee No Yes View
Indiana Deer and Elk Farmers Advocates Inc Shipshewana, IN Direct $1,000.00
11/01/2012 Steele for Senate Committee No Yes View Indiana Deer and Elk Farmers
Advocates Inc Shipshewana, IN Direct $2,000.00 08/18/2014 Cindy Meyer Ziemke for
State Rep. No No View Indiana Deer and Elk Farmers Advocates Inc. Shipshewana,
IN Direct $500.00 11/26/2012 COMMITTEE TO ELECT BOB CHERRY No No View Indiana
Deer and Elk Farmers Advocates INC. Shipshewana, IN Direct $1,000.00 10/12/2012
Committee to Elect Matt Ubelhor No No View Indiana Deer and Elk Farmers
Advocates Inc. Shipshewana, IN Direct $1,000.00 10/01/2012 Markmessmer.com No No
View Indiana Deer and Elk Farmers Advocates Inc. Shipshewana, IN Direct
$1,000.00 10/25/2012 HERSHMAN FOR SENATE No Yes View Indiana Deer and Elk
Farmers Advocates, Inc. Shipshewana, IN Direct $1,000.00 10/15/2012 BILL FRIEND
FOR STATE REPRESENTATIVE COMMITTEE No Yes View Indiana Deer and Elk Farmers
Advocates, Inc. Shipshewana, IN
Thursday, January 15, 2015
INDIANA HB1453 - high fence hunting preserve bill has been
introduced by Rep. Sean Eberhart and he received monetary contribution from
Indiana Deer and Elk Farmers Advocates INC. Indiana Politicians and
contributions from the Game Farm Industry, and whom is taking the bait $$$ will
this buy their vote in support of the cervid game farming industry ???
Monday, January 11, 2016
*** INDIANA SB109 HIGH FENCE HUNTING LEGISLATION AND RISK
FACTORS FOR CHRONIC WASTING DISEASE CWD TSE PRION
Thursday, January 21, 2016
INDIANA With end of long legal challenge last year,
high-fence hunting operations currently unregulated
Friday, January 29, 2016
Wisconsin CWD-positive white-tailed deer found on Iowa
County farm January 29, 2016
Terry S. Singeltary Sr.
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