Texas Parks Wildlife Chronic Wasting Disease CWD Management and Regulations for Hunters 2016 - 2017
Texas Parks Wildlife Chronic Wasting Disease CWD Management and Regulations
for Hunters 2016 – 2017
cwd management and regulations for hunters
Hunters who harvest mule deer, white-tailed deer, or elk within the
Trans-Pecos and Panhandle CWD Zones are REQUIRED to be bring their animals to a
TPWD check station within 24 hours of harvest (see included maps).
» See following pages for locations, operating dates and times, and contact
numbers for each check station.
» Carcass movement restrictions apply in some CWD Zones (page 6). It is
ILLEGAL to take intact deer/elk carcasses outside of CWD Zones in the
Trans-Pecos and Panhandle or bring into Texas from another state, Canadian
provinces, or other areas outside of Texas where CWD is known to exist.
If leaving a CWD Zone immediately after checking animal, please quarter
carcass before coming to check station (see page 7).
» When bringing quartered deer/elk and their associated heads to a check
station, please be sure to remove the head from the carcass 2–3 vertebrae below
the head (see page 7). This will ensure that the appropriate tissues for CWD
testing are not damaged.
» Hunters will receive a CWD check station receipt for compliance, which
has a link to CWD test results posted on the TPWD CWD website. The receipt also
serves as proof-of-sex documentation.
» As an alternative to the TPWD check stations, a list of TPWD-approved
sample collectors will be provided on the TPWD CWD website after Oct 17
(completion of all sample collector trainings).
» Please report any “sick looking” deer/elk while hunting in any CWD Zone
to TPWD.
For more information regarding Chronic Wasting Disease (CWD) management and
regulations visit tpwd.texas.gov/cwd
trans-pecos check stations
SEE MAP
3
CHRONIC WASTING DISEASE SAMPLE RECEIPTScan above for link to CWD test
results.CWD sample number on reverse side.For CWD test results and general
information about CWD, visit:tpwd.texas.gov/cwdPROOF OF SEX Sex: Buck or
AntlerlessSpecies:MD or WTDDate: _____/_____/_____160607 CWD Sampling Cards.indd
16/24/16 2:27 PM
CHECK STATION DATES & HOURS OF OPERATION
Check stations will be open during the entire general mule deer season (Nov
25 to Dec 11) from 9 a.m. to 9 p.m. local time and the following Monday, Dec 12,
from 9 a.m. to 6 p.m. local time.
CHECK STATION LOCATIONS
» VAN HORN: Van Horn Convention Center, 1801 West Broadway Street, Van
Horn, TX. Coordinates (31.037440, -104.852833). Contact number (512)
221-8491.
» EAST US 62/180: Pine Springs TXDOT Rest Area, US 62/180 — Eastbound,
about 7 miles from Texas/New Mexico state line. Coordinates (31.960389,
-104.680334). Contact number (512) 803-6498.
» CORNUDAS: May’s Café on US 62-180 at mile 82.5. Coordinates (31.779729,
-105.471281). Contact number (512) 803-5822.
Hunters who harvest deer/elk in special archery seasons and extended MLDP
seasons should contact TPWD at (512) 221-8491. Please call (512) 221-8491 if you
see any “sick looking” or road killed deer/elk within the Trans-Pecos CWD
Zone.
Hunters who harvest a deer or elk in the Trans-Pecos CWD Zone are REQUIRED
to have their animal sampled for CWD within 24 hours of harvest.
panhandle check stations
SEE MAP
Hunters who harvest a deer or elk in the Panhandle CWD Zone are REQUIRED to
have their animal sampled for CWD within 24 hours of harvest.
CHECK STATION DATES & HOURS OF OPERATION
Open Dates: Nov 5–7, Nov 11–14, Nov 18–Dec 5, Dec 9–12, Dec 16–19, Dec 23,
and Dec 26–Jan 2 from 9 a.m. to 7 p.m. local time.
Please call TPWD at (512) 806-3563 or either check station to have your
animals sampled during dates the check stations are closed.
CHECK STATION LOCATIONS
» DALHART: Rita Blanca Lake Park off of Lake Drive. Check station is across
from People’s Church (1929 Apache Drive). Coordinates (36.038269, -102.506358).
Contact number (512) 803-5972.
» VEGA: Walnut RV Park. Business Loop of I-40, 1403 Vega Blvd. Coordinates
(35.243253, -102.434296). Contact number (512) 803-6158.
Please call either check station for any questions about sampling your
hunter-harvested animals or to report a “sick looking” or road killed deer/elk
within the Panhandle CWD Zone.
medina county area check stations
SEE MAP
Hunters who harvest a deer or elk in the Medina County CWD Zone are
RECOMMENDED to have their animal sampled for CWD within 24 hours of harvest. CWD
sampling of harvested deer/elk and carcass movement restrictions are VOLUNTARY
within the Medina County CWD Zone.
CHECK STATION DATES & HOURS OF OPERATION
Open Dates: Oct 1, 2016 — Jan 15, 2017 from 9 a.m. to 9 p.m. local
time.
Closed Dates: Nov 24, Dec 24 (at 12 p.m.), and Dec 25.
CHECK STATION LOCATIONS
» HONDO: 1701 19th Street, Hondo, TX 78861. Check station is in the parking
lot adjacent to Life Check Drug Store located on Highway 90. Coordinates
(29.346774, -99.148061). Contact number (512) 803-6184.
» TARPLEY: 264 Valentine Road, Tarpley, TX 78883. Check station is located
next to the Tarpley Volunteer Fire Department.
Coordinates (29.657711, -99.279426). Contact number (512) 803-6174.
Please call either check station for any questions about sampling your
hunter-harvested animals or to report a “sick looking” or road killed deer/elk
within the Medina County Voluntary CWD Zone.
hunter precautions
Prions generally concentrate in the brain, spinal cord, eyes, lymph nodes
and spleen, and they are shed in saliva, urine, blood, soft-antler material,
feces, and from decomposition of an infected animal.
Proper disposal of these carcass parts is important to prevent
environmental contamination and spread of this disease to new areas. These
inedible parts should be left at the site of harvest, or disposed of in a
landfill, or buried at least 6 feet deep at the ranch/farm of harvest in any CWD
Zone.
Always use common sense precautions while handling and processing deer and
elk. Never eat meat from a deer/elk that looks sick. Never eat brain, eyeballs,
spinal cord, spleen, or lymph nodes from a deer/elk.
carcass movement restrictions
No deer/elk carcasses or parts of carcasses can enter Texas from a state or
country known to have CWD, and no deer/elk carcasses or parts of carcasses can
be transported out of a CWD Zone in the Trans-Pecos or Panhandle EXCEPT:
» Cut quarters with all brain and spinal cord tissue removed
» Boned meat
» Cut and wrapped meat
» Caped hides with skull not attached
» Skull plate with antlers attached and cleaned of all soft tissue
» Finished taxidermy products
» The skinned or unskinned head of a susceptible species may be transported
to a taxidermist, provided all brain material, soft tissue, spinal column and
any unused portions of the head are disposed of in a landfill in Texas permitted
by TCEQ. The deer head wavier form (see page 7) to transport the intact head may
be obtained from a TPWD CWD check station or the TPWD CWD website.
procedures to bring deer/elk to check stations
» All deer/elk harvested within the Trans-Pecos and Panhandle CWD Zones
must be sampled for CWD.
» Carcass movement restrictions do not apply if the carcass will not be
moved outside of a CWD Zone. However, it is recommended to always properly
dispose of unused carcass parts.
» Hunters leaving a CWD Zone in the Trans-Pecos and Panhandle with their
harvested animal must quarter the deer/elk and remove the head from the carcass
2–3 vertebrae below the head. See illustration.
» Put head in a plastic trash bag and keep cool until arriving at a CWD
check station.
» Heads can be disposed of at the CWD check stations provided the hunter
has a CWD receipt, which serves as a proof-of-sex document.
deer head waiver
Hunters wanting to take an intact skinned or unskinned deer head to a
taxidermist outside of the Trans-Pecos or Panhandle CWD Zones should obtain the
Deer Head Waiver (PWD 1410) at any CWD check station or at the TPWD CWD
website.
The waiver should be completed and kept on your person or with the deer
head until it reaches the taxidermist.
Hunters bringing intact deer heads into Texas from a state or country with
CWD should also have this waiver.
cwd quick facts
» Chronic Wasting Disease (CWD) is a fatal neurological disease in some
deer species such as mule deer, white-tailed deer, elk, red deer, sika, moose,
and reindeer, which is caused by a misfolded protein called a prion.
» Two primary sources of infection for deer are from animal to animal
contact and a contaminated environment by infected animals shedding prions
through body fluids and from decomposition of an infected animal.
» Because eradication is thought to be impossible once CWD becomes
established in a population, it is imperative that a sound CWD management
program be established to reduce the severity of implications resulting from the
disease.
» In order to contain the disease, we must understand the geographic extent
and prevalence of CWD. This is done by collecting samples from hunter-harvested
deer and elk at CWD check stations. Containment strategies include restricting
movements of live deer and elk and certain carcass parts.
» There is no scientific evidence that CWD can infect humans or domestic
livestock.
2016-09-15 CWD voluntary check stations & informational meeting
announced
By Judith Pannebaker BCC Editor
White-tailed deer, one of Bandera’s biggest cash crops – are susceptible
to chronic wasting disease.
With hunting season looming on the horizon in Bandera County, officials are
looking for ways to protect a local cash crop – white-tailed deer. During a
regular meeting on Thursday, Sept. 8, Texas Parks & Wildlife District Leader
Rufus Stephens requested support from the Bandera County Commissioners for a
push to identify deer with chronic wasting disease (CWD).
Accompanied by TPW Biologist Johnny Arrendondo, Stephens asked
commissioners fund utility costs as well as costs associated with a garbage
disposal unit to be located at a voluntary check station at the Tarpley
Volunteer Fire Department during hunting season. The station would check
harvested white-tailed deer for CWD.
According to Stephens, the on-going epidemiological investigation of CWD
has led to the discovery of additional CWD-positive deer in captive breeding
facilities and released deer in high-fenced properties in Medina County. “This
has caused TPWD officials to designate a CWD Surveillance Zone that incorporates
parts of Bandera, Medina and Uvalde counties,” he said.
Through voluntary testing of harvested deer, TPWD officials hope to
determine whether CWD is prevalent in the free-ranging deer inside the
designated surveillance zone.
Judge Richard Evans noted that should the surveillance zone be changed to
one of “containment,” ranchers’ income and property values could be affected.
“You can’t take any part of an animal out of a containment zone – and that
includes heads and antlers,” Evans said. “No one will pay money to hunt in
containment zones.”
Stephens said the check station would be manned from 9 am to 9 pm, seven
days a week, between Oct. 1 and Jan. 15, 2017. “Hunters are asked to bring their
harvested white-tailed deer – or just the head – to the check station where a
wildlife biologist-technician will collect samples for testing. He estimated
that the designated surveillance zone in the portions of the three counties
contained approximately 1,700 deer.
Post-mortem testing to detect the presence of the disease is done on
brainstems and thyroid glands of harvested deer. Additionally, deer killed by
vehicles will also be tested.
Stephens noted that the Tarpley VFD had given permission to utilize their
facilities that included the grounds, electricity and utilities. “However, they
have asked for compensation for utility use,” Stephens told the court.
He also requested that the county fund the rental of a garbage disposal
container to dispose of the deer carcasses and other debris that accumulates
during the operation of the check station. He estimated the total cost during
the hunting season to be approximately $1,000.
Realizing the possible gravity of the CWD situation, commissioners approved
Stephens’ request unanimously.
Last summer, CWD was discovered in deer at a breeding ranch in Medina
County. Earlier, during the 2014-2015 hunting season, a tissue sample collected
from a mule deer harvested in far West Texas tested positive for CWD. This was
the only confirmed case in Texas during that hunting season.
Stephens said in the Hueco Mountains and two other areas, mandatory check
stations are in effect for any harvested deer.
In a related matter, TPWD officials, in conjunction with Medina, Bandera
and Uvalde counties, will host an informational meeting about CWD and the
sampling efforts within portions of those counties for the 2016-2017 hunting
season.
The meeting will take place at 5:30 pm, Thursday, Sept. 15, at the Tarpley
Volunteer Fire Department School House, 264 Valentine Lane, in Tarpley.
Officials will explain how landowners, hunters and interested residents can
help maintain a voluntary surveillance zone in the area.
The informational session will cover:
• a brief explanation about CWD
• how the discovery of CWD in northwestern Medina County might affect
residents of other counties
• The TPWD CWD surveillance plan for this area and how to assist TPWD with
CWD surveillance and sample collection.
The session will also review the following documents for more information
about CWD:
• CWD Fact Sheet
• Deer Handling and Processing Recommendations
• TPWD CWD News Release
CWD is a member of the group of diseases called transmissible spongiform
encephalopathies. Among cervids, CWD is a progressive, fatal disease that
commonly results in altered behavior as a result of microscopic changes made to
the brain of affected animals.
An animal may carry the disease for years without outward indication, but
in the latter stages, signs may include listlessness, lowering of the head,
weight loss, repetitive walking in set patterns and a lack of responsiveness.
To date, no evidence exists that CWD poses a risk to humans or non-cervids.
However, as a precaution, medical personnel with the US Centers for Disease
Control and the World Health Organization recommend not consuming meat from
infected animals.
For more information on this important subject, contact Arredondo in
Bandera County at 830-928-9037 or johnny.arredondo@tpwd.texas.gov.
>>> According to Stephens, the on-going epidemiological
investigation of CWD has led to the discovery of additional CWD-positive deer in
captive breeding facilities and released deer in high-fenced properties in
Medina County.
>>> “This has caused TPWD officials to designate a CWD
Surveillance Zone that incorporates parts of Bandera, Medina and Uvalde
counties,” he said.
>>> He also requested that the county fund the rental of a garbage
disposal container to dispose of the deer carcasses and other debris that
accumulates during the operation of the check station.
CWD TSE PRION HUMAN ZOONOSIS POTENTIAL, has it already happened, and being
masked as sporadic CJD? and what about iatrogenic, or the pass if forward,
friendly fire mode of transmission of cwd to humans, same thing, sporadic cjd ?
*** WDA 2016 NEW YORK ***
We found that CWD adapts to a new host more readily than BSE and that human
PrP was unexpectedly prone to misfolding by CWD prions. In addition, we
investigated the role of specific regions of the bovine, deer and human PrP
protein in resistance to conversion by prions from another species. We have
concluded that the human protein has a region that confers unusual
susceptibility to conversion by CWD prions.
Student Presentations Session 2
The species barriers and public health threat of CWD and BSE prions
Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr.
Edward Hoover1 1Colorado State University
Chronic wasting disease (CWD) is spreading rapidly through cervid
populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease)
arose in the 1980s because cattle were fed recycled animal protein. These and
other prion diseases are caused by abnormal folding of the normal prion protein
(PrP) into a disease causing form (PrPd), which is pathogenic to nervous system
cells and can cause subsequent PrP to misfold. CWD spreads among cervids very
efficiently, but it has not yet infected humans. On the other hand, BSE was
spread only when cattle consumed infected bovine or ovine tissue, but did infect
humans and other species. The objective of this research is to understand the
role of PrP structure in cross-species infection by CWD and BSE. To study the
propensity of each species’ PrP to be induced to misfold by the presence of PrPd
from verious species, we have used an in vitro system that permits detection of
PrPd in real-time. We measured the conversion efficiency of various combinations
of PrPd seeds and PrP substrate combinations. We observed the cross-species
behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found
that CWD adapts to a new host more readily than BSE and that human PrP was
unexpectedly prone to misfolding by CWD prions. In addition, we investigated the
role of specific regions of the bovine, deer and human PrP protein in resistance
to conversion by prions from another species. We have concluded that the human
protein has a region that confers unusual susceptibility to conversion by CWD
prions. CWD is unique among prion diseases in its rapid spread in natural
populations. BSE prions are essentially unaltered upon passage to a new species,
while CWD adapts to the new species. This adaptation has consequences for
surveillance of humans exposed to CWD.
Wildlife Disease Risk Communication Research Contributes to Wildlife Trust
Administration Exploring perceptions about chronic wasting disease risks among
wildlife and agriculture professionals and stakeholders
PRION 2016 TOKYO
Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3,
Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6,
Pierluigi Gambetti1, Qingzhong Kong1,5,6
1Department of Pathology, 3National Prion Disease Pathology Surveillance
Center, 5Department of Neurology, 6National Center for Regenerative Medicine,
Case Western Reserve University, Cleveland, OH 44106, USA.
4Department of Biological Sciences and Center for Prions and Protein
Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
Chronic wasting disease (CWD) is a widespread and highly transmissible
prion disease in free-ranging and captive cervid species in North America. The
zoonotic potential of CWD prions is a serious public health concern, but the
susceptibility of human CNS and peripheral organs to CWD prions remains largely
unresolved. We reported earlier that peripheral and CNS infections were detected
in transgenic mice expressing human PrP129M or PrP129V. Here we will present an
update on this project, including evidence for strain dependence and influence
of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of
experimental human CWD prions.
PRION 2016 TOKYO
In Conjunction with Asia Pacific Prion Symposium 2016
PRION 2016 Tokyo
Prion 2016
Cervid to human prion transmission
Kong, Qingzhong
Case Western Reserve University, Cleveland, OH, United States
Abstract
Prion disease is transmissible and invariably fatal. Chronic wasting
disease (CWD) is the prion disease affecting deer, elk and moose, and it is a
widespread and expanding epidemic affecting 22 US States and 2 Canadian
provinces so far. CWD poses the most serious zoonotic prion transmission risks
in North America because of huge venison consumption (>6 million deer/elk
hunted and consumed annually in the USA alone), significant prion infectivity in
muscles and other tissues/fluids from CWD-affected cervids, and usually high
levels of individual exposure to CWD resulting from consumption of the affected
animal among often just family and friends. However, we still do not know
whether CWD prions can infect humans in the brain or peripheral tissues or
whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no
essays to reliably detect CWD infection in humans. We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the
brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid
prion strain and influenced by the host (human) prion protein (PrP) primary
sequence;
(3) Reliable essays can be established to detect CWD infection in
humans;and
(4) CWD transmission to humans has already occurred. We will test these
hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in
vitro approaches.
Aim 1 will prove that the classical CWD strain may infect humans in brain
or peripheral lymphoid tissues at low levels by conducting systemic bioassays in
a set of "humanized" Tg mouse lines expressing common human PrP variants using a
number of CWD isolates at varying doses and routes. Experimental "human CWD"
samples will also be generated for Aim 3.
Aim 2 will test the hypothesis that the cervid-to-human prion transmission
barrier is dependent on prion strain and influenced by the host (human) PrP
sequence by examining and comparing the transmission efficiency and phenotypes
of several atypical/unusual CWD isolates/strains as well as a few prion strains
from other species that have adapted to cervid PrP sequence, utilizing the same
panel of humanized Tg mouse lines as in Aim 1.
Aim 3 will establish reliable essays for detection and surveillance of CWD
infection in humans by examining in details the clinical, pathological,
biochemical and in vitro seeding properties of existing and future experimental
"human CWD" samples generated from Aims 1-2 and compare them with those of
common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
Aim 4 will attempt to detect clinical CWD-affected human cases by examining
a significant number of brain samples from prion-affected human subjects in the
USA and Canada who have consumed venison from CWD-endemic areas utilizing the
criteria and essays established in Aim 3. The findings from this proposal will
greatly advance our understandings on the potential and characteristics of
cervid prion transmission in humans, establish reliable essays for CWD zoonosis
and potentially discover the first case(s) of CWD infection in humans.
Public Health Relevance There are significant and increasing human exposure
to cervid prions because chronic wasting disease (CWD, a widespread and highly
infectious prion disease among deer and elk in North America) continues
spreading and consumption of venison remains popular, but our understanding on
cervid-to-human prion transmission is still very limited, raising public health
concerns. This proposal aims to define the zoonotic risks of cervid prions and
set up and apply essays to detect CWD zoonosis using mouse models and in vitro
methods. The findings will greatly expand our knowledge on the potentials and
characteristics of cervid prion transmission in humans, establish reliable
essays for such infections and may discover the first case(s) of CWD infection
in humans.
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL
THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
***********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
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
*** 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.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions
*** 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
*** The data presented here substantiate and expand previous reports on the
existence of different CWD strains.
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.
>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO
CONVERSION OF THE HUMAN PRION PROTEIN<<<
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
Wednesday, January 01, 2014
Molecular Barriers to Zoonotic Transmission of Prions
*** 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.
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.
Yet, it has to be noted that our assessments of PrPTSE levels in skeletal
muscles were based on findings in presumably pre- or subclinically infected
animals. Therefore, the concentration of PrPTSE in skeletal muscles of WTD with
clinically manifest CWD may possibly exceed our estimate which refers to
clinically inconspicuous animals that are more likely to enter the human food
chain. Our tissue blot findings in skeletal muscles from CWD-infected WTD would
be consistent with an anterograde spread of CWD prions via motor nerve fibres to
muscle tissue (figure 4A). Similar neural spreading pathways of muscle infection
were previously found in hamsters orally challenged with scrapie [28] and
suggested by the detection of PrPTSE in muscle fibres and muscle-associated
nerve fascicles of clinically-ill non-human primates challenged with BSE prions
[29]. Whether the absence of detectable PrPTSE in myofibers observed in our
study is a specific feature of CWD in WTD, or was due to a pre- or subclinical
stage of infection in the examined animals, remains to be established. In any
case, our observations support previous findings suggesting the precautionary
prevention of muscle tissue from CWD-infected WTD in the human diet, and
highlight the need to comprehensively elucidate of whether CWD may be
transmissible to humans. While the understanding of TSEs in cervids has made
substantial progress during the past few years, the assessment and management of
risks possibly emanating from prions in skeletal muscles of CWD-infected cervids
requires further research.
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,§ + Author
Affiliations
1 Department of Microbiology, Immunology and Molecular Genetics, University
of Kentucky, Lexington, KY 40536, USA. 2 Sanders Brown Center on Aging,
University of Kentucky, Lexington, KY 40536, USA. 3 Department of Neurology,
University of Kentucky, Lexington, KY 40536, USA. 4 Department of Microbiology,
Immunology and Pathology, Colorado State University, Fort Collins, CO 80523,
USA. 5 Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, CO
80526, USA. ↵§ To whom correspondence should be addressed. E-mail:
gtell2@uky.edu ↵* These authors contributed equally to this work.
↵† Present address: Department of Infectology, Scripps Research Institute,
5353 Parkside Drive, RF-2, Jupiter, FL 33458, USA.
↵‡ Present address: Institute of Neuropathology, University of Zurich,
Schmelzbergstrasse 12, 8091 Zurich, Switzerland.
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.
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin
Because It May Contain Meat Derived From An Elk Confirmed To Have Chronic
Wasting Disease
Contact: Exotic Meats USA 1-800-680-4375
FOR IMMEDIATE RELEASE -- February 9, 2009 -- Exotic Meats USA of San
Antonio, TX is initiating a voluntary recall of Elk Tenderloin because it may
contain meat derived from an elk confirmed to have Chronic Wasting Disease
(CWD). The meat with production dates of December 29, 30 and 31, 2008 was
purchased from Sierra Meat Company in Reno, NV. The infected elk came from Elk
Farm LLC in Pine Island, MN and was among animals slaughtered and processed at
USDA facility Noah’s Ark Processors LLC.
Chronic Wasting Disease (CWD) is a fatal brain and nervous system disease
found in elk and deer. The disease is caused by an abnormally shaped protein
called a prion, which can damage the brain and nerves of animals in the deer
family. Currently, it is believed that the prion responsible for causing CWD in
deer and elk is not capable of infecting humans who eat deer or elk contaminated
with the prion, but the observation of animal-to-human transmission of other
prion-mediated diseases, such as bovine spongiform encephalopathy (BSE), has
raised a theoretical concern regarding the transmission of CWD from deer or elk
to humans. At the present time, FDA believes the risk of becoming ill from
eating CWD-positive elk or deer meat is remote. However, FDA strongly advises
consumers to return the product to the place of purchase, rather than disposing
of it themselves, due to environmental concerns.
Exotic Meats USA purchased 1 case of Elk Tenderloins weighing 16.9 lbs. The
Elk Tenderloin was sold from January 16 – 27, 2009. The Elk Tenderloins was
packaged in individual vacuum packs weighing approximately 3 pounds each. A
total of six packs of the Elk Tenderloins were sold to the public at the Exotic
Meats USA retail store. Consumers who still have the Elk Tenderloins should
return the product to Exotic Meats USA at 1003 NE Loop 410, San Antonio, TX
78209. Customers with concerns or questions about the Voluntary Elk Recall can
call 1-800-680-4375. The safety of our customer has always been and always will
be our number one priority.
Exotic Meats USA requests that for those customers who have products with
the production dates in question, do not consume or sell them and return them to
the point of purchase. Customers should return the product to the vendor. The
vendor should return it to the distributor and the distributor should work with
the state to decide upon how best to dispose. If the consumer is disposing of
the product he/she should consult with the local state EPA office.
#
COLORADO: Farmer's market meat recalled after testing positive for CWD
24.dec.08 9News.com Jeffrey Wolf
Elk meat that was sold at a farmer's market is being recalled because tests
show it was infected with chronic wasting disease. The Boulder County Health
Department and Colorado Department of Public Health and Environment issued the
recall Wednesday after the meat was sold at the Boulder County Fairgrounds on
Dec. 13. Although there isn't any human health risk connected with CWD, the
recalled was issued as a precaution. About 15 elk were bought from a commercial
ranch in Colorado in early December and processed at a licensed plant. All 15
were tested for CWD and one came up positive. The labeling on the product would
have the following information: *Seller: High Wire Ranch *The type of cut:
"chuck roast," "arm roast," "flat iron," "ribeye steak," "New York steak,"
"tenderloin," "sirloin tip roast," "medallions" or "ground meat." *Processor:
Cedaredge Processing *The USDA triangle containing the number "34645" People
with questions about this meat can contact John Pape, epidemiologist at the
Colorado Department of Public Health and Environment at 303-692-2628.
COULD NOT FIND any warning or recalls on these two sites confirming their
recall of CWD infected meat. ...TSS
Wednesday, April 06, 2011
Presence and Seeding Activity of Pathological Prion Protein (PrPTSE) in
Skeletal Muscles of White-Tailed Deer Infected with Chronic Wasting Disease
Prion Infectivity in Fat of Deer with Chronic Wasting Disease
Brent Race,# Kimberly Meade-White,# Richard Race, and Bruce Chesebro* Rocky
Mountain Laboratories, 903 South 4th Street, Hamilton, Montana 59840
Received 2 June 2009/ Accepted 24 June 2009
ABSTRACT Top ABSTRACT TEXT REFERENCES
Chronic wasting disease (CWD) is a neurodegenerative prion disease of
cervids. Some animal prion diseases, such as bovine spongiform encephalopathy,
can infect humans; however, human susceptibility to CWD is unknown. In
ruminants, prion infectivity is found in central nervous system and lymphoid
tissues, with smaller amounts in intestine and muscle. In mice, prion
infectivity was recently detected in fat. Since ruminant fat is consumed by
humans and fed to animals, we determined infectivity titers in fat from two
CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD
infectivity and might be a risk factor for prion infection of other species.
snip...
The highest risk of human contact with CWD might be through exposure to
high-titer CNS tissue through accidental skin cuts or corneal contact at the
time of harvest and butchering. However, the likelihood of a human consuming fat
infected with a low titer of the CWD agent is much higher. It is impossible to
remove all the fat present within muscle tissue, and fat consumption is
inevitable when eating meat. Of additional concern is the fact that meat from an
individual deer harvested by a hunter is typically consumed over multiple meals
by the same group of people. These individuals would thus have multiple
exposures to the CWD agent over time, which might increase the chance for
transfer of infection.
In the Rocky Mountain region of North America, wild deer are subject to
predation by wolves, coyotes, bears, and mountain lions. Although canines such
as wolves and coyotes are not known to be susceptible to prion diseases, felines
definitely are susceptible to BSE (9) and might also be infected by the CWD
agent. Deer infected with the CWD agent are more likely to be killed by
predators such as mountain lions (11). Peripheral tissues, including lymph
nodes, muscle, and fat, which harbor prion infectivity are more accessible for
consumption than CNS tissue, which has the highest level of infectivity late in
disease. Therefore, infectivity in these peripheral tissues may be important in
potential cross-species CWD transmissions in the wild.
The present finding of CWD infectivity in deer fat tissue raises the
possibility that prion infectivity might also be found in fat tissue of other
infected ruminants, such as sheep and cattle, whose fat and muscle tissues are
more widely distributed in both the human and domestic-animal food chains.
Although the infectivity in fat tissues is low compared to that in the CNS,
there may be significant differences among species and between prion strains.
Two fat samples from BSE agent-infected cattle were reported to be negative by
bioassay in nontransgenic RIII mice (3, 6). However, RIII mice are
10,000-fold-less sensitive to BSE agent infection than transgenic mice
expressing bovine PrP (4). It would be prudent to carry out additional
infectivity assays on fat from BSE agent-infected cattle and scrapie
agent-infected sheep using appropriate transgenic mice or homologous species to
determine the risk from these sources.
0C7.04
North American Cervids Harbor Two Distinct CWD Strains
Authors
Angers, R. Seward, T, Napier, D., Browning, S., Miller, M., Balachandran
A., McKenzie, D., Hoover, E., Telling, G. 'University of Kentucky; Colorado
Division of Wildlife, Canadian Food Inspection Agency; University Of Wisconsin;
Colorado State University.
Content
Despite the increasing geographic distribution and host range of CWD,
little is known about the prion strain(s) responsible for distinct outbreaks of
the disease. To address this we inoculated CWD-susceptible Tg(CerPrP)1536+/·
mice with 29 individual prion samples from various geographic locations in North
America. Upon serial passage, intrastudy incubation periods consistently
diverged and clustered into two main groups with means around 210 and 290 days,
with corresponding differences in neuropathology. Prion strain designations were
utilized to distinguish between the two groups: Type I CWD mice succumbed to
disease in the 200 day range and displayed a symmetrical pattern of vacuolation
and PrPSc deposition, whereas Type II CWD mice succumbed to disease near 300
days and displayed a strikingly different pattern characterized by large local
accumulations of florid plaques distributed asymmetrically. Type II CWD bears a
striking resemblance to unstable parental scrapie strains such as 87A which give
rise to stable, short incubation period strains such as ME7 under certain
passage conditions. In agreement, the only groups of CWD-inoculated mice with
unwavering incubation periods were those with Type I CWD. Additionally,
following endpoint titration of a CWD sample, Type I CWD could be recovered only
at the lowest dilution tested (10-1), whereas Type II CWD was detected in mice
inoculated with all dilutions resulting in disease. Although strain properties
are believed to be encoded in the tertiary structure of the infectious prion
protein, we found no biochemical differences between Type I and Type II CWD. Our
data confirm the co·existence of two distinct prion strains in CWD-infected
cervids and suggest that Type II CWD is the parent strain of Type I CWD.
see page 29, and see other CWD studies ;
Sunday, November 23, 2008
PRION October 8th - 10th 2008 Book of Abstracts
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.
Sunday, December 14, 2014
TEXAS 84th Legislature commencing this January, deer breeders are expected
to advocate for bills that will seek to further deregulate their industry
http://chronic-wasting-disease.blogspot.it/2014/12/texas-84th-legislature-commencing-this.html
Saturday, July 09, 2016
Texas Intrastate – within state movement of all Cervid or Trucking Chronic
Wasting Disease CWD TSE Prion Moratorium
Monday, July 18, 2016
Texas Parks Wildlife Dept TPWD HIDING TSE (CWD) in Deer Herds, Farmers
Sampling Own Herds, Rapid Testing, False Negatives, a Recipe for Disaster
Friday, July 01, 2016
*** TEXAS Thirteen new cases of chronic wasting disease (CWD) were
confirmed at a Medina County captive white-tailed deer breeding facility on June
29, 2016***
*** How Did CWD Get Way Down In Medina County, Texas?
DISCUSSION Observations of natural outbreaks of scrapie indicated that the
disease spread from flock to flock by the movement of infected, but apparently
normal, sheep which were incubating the disease.
There was no evidence that the disease spread to adjacent flocks in the
absent of such movements or that vectors or other host species were involved in
the spread of scrapie to sheep or goats; however, these possibilities should be
kept open...
Tuesday, August 02, 2016
TEXAS TPWD Sets Public Hearings on Deer Movement Rule Proposals in Areas
with CWD Rule Terry S. Singeltary Sr. comment submission
Thursday, August 25, 2016
TPWD Action Disease Detection and Response – Chronic Wasting Disease TPW
Commission Adopts New CWD Zones, Deer Movement Rules August 25, 2016
This map shows the recently imposed Surveillance Zone for CWD in portions
of Bandera, Medina and Uvalde counties.
Monday, September 05, 2016 Pathological features of chronic wasting disease
in reindeer and demonstration of horizontal transmission Major Findings for
Norway
see updated data on the 4 cases of CWD to date in Norway ;
Wednesday, September 7, 2016
An assessment of the long-term persistence of prion infectivity in aquatic
environments
Monday, August 29, 2016
NWHC USGS CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
Friday, September 02, 2016
Chronic Wasting Disease Drives Population Decline of White-Tailed
Deer
Sunday, August 28, 2016
CONFIDENTIAL
Transmissible Spongiform Encephalopathy TSE Prion and how Politics and
Greed by the Industry spread madcow type diseases from species to species and
around the globe
TSE PRIONS AKA MAD COW TYPE DISEASE, LIONS AND TIGERS AND BEARS, OH MY!
Antemortem Detection of Chronic Wasting Disease Prions in Nasal Brush
Collections and Rectal Biopsy Specimens from White-Tailed Deer by Real-Time
Quaking-Induced Conversion
Nicholas J. Haleya*, Chris Siepkera, W. David Walterb, Bruce V. Thomsenc,
Justin J. Greenleed, Aaron D. Lehmkuhlc and Jürgen A. Richta aDepartment of
Diagnostic Medicine and Pathobiology, College of Veterinary Medicine, Kansas
State University, Manhattan, Kansas, USA bU.S. Geological Survey, Pennsylvania
Cooperative Fish and Wildlife Research Unit, Pennsylvania State University,
University Park, Pennsylvania, USA cUSDA, APHIS, VS, STAS, National Veterinary
Service Laboratories, Ames, Iowa, USA dVirus and Prion Research Unit, National
Animal Disease Center, ARS, USDA, Ames, Iowa, USA B. W. Fenwick, Editor + Author
Affiliations
ABSTRACT Chronic wasting disease (CWD), a transmissible spongiform
encephalopathy of cervids, was first documented nearly 50 years ago in Colorado
and Wyoming and has since spread to cervids in 23 states, two Canadian
provinces, and the Republic of Korea. The expansion of this disease makes the
development of sensitive diagnostic assays and antemortem sampling techniques
crucial for the mitigation of its spread; this is especially true in cases of
relocation/reintroduction of farmed or free-ranging deer and elk or surveillance
studies of private or protected herds, where depopulation is contraindicated.
This study sought to evaluate the sensitivity of the real-time quaking-induced
conversion (RT-QuIC) assay by using recto-anal mucosa-associated lymphoid tissue
(RAMALT) biopsy specimens and nasal brush samples collected antemortem from
farmed white-tailed deer (n = 409). Antemortem findings were then compared to
results from ante- and postmortem samples (RAMALT, brainstem, and medial
retropharyngeal lymph nodes) evaluated by using the current gold standard in
vitro assay, immunohistochemistry (IHC) analysis. We hypothesized that the
sensitivity of RT-QuIC would be comparable to IHC analysis in antemortem tissues
and would correlate with both the genotype and the stage of clinical disease.
Our results showed that RAMALT testing by RT-QuIC assay had the highest
sensitivity (69.8%) compared to that of postmortem testing, with a specificity
of >93.9%. These data suggest that RT-QuIC, like IHC analysis, is an
effective assay for detection of PrPCWD in rectal biopsy specimens and other
antemortem samples and, with further research to identify more sensitive
tissues, bodily fluids, or experimental conditions, has potential for
large-scale and rapid automated testing for CWD diagnosis.
FOOTNOTES Received 22 October 2015. Returned for modification 27 November
2015. Accepted 4 February 2016. Accepted manuscript posted online 10 February
2016. Address correspondence to Nicholas J. Haley, nicholas.j.haley@gmail.com.
Citation Haley NJ, Siepker C, Walter WD, Thomsen BV, Greenlee JJ, Lehmkuhl AD,
Richt JA. 2016. Antemortem detection of chronic wasting disease prions in nasal
brush collections and rectal biopsy specimens from white-tailed deer by
real-time quaking-induced conversion. J Clin Microbiol 54:1108–1116.
doi:10.1128/JCM.02699-15.
↵* Present address: Nicholas J. Haley, Department of Microbiology and
Immunology, Midwestern University, Glendale, Arizona, USA.
see also ;
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Title: Antemortem detection of chronic wasting disease prions in nasal
brush collections and rectal biopsies from white-tailed deer by real time
quaking-induced conversion)
Author
item Haley, Nicholas item Siepker, Chris item Walter, W. david item
Thomsen, Bruce item Greenlee, Justin item Lehmkuhl, Aaron item Richt, Jürgen
Submitted to: Journal of Clinical Microbiology Publication Type: Peer
reviewed journal Publication Acceptance Date: 11/27/2015 Publication Date:
2/10/2016 Citation: Haley, N.J., Siepker, C., Walter, W.D., Thomsen, B.V.,
Greenlee, J.J., Lehmkuhl, A.D., Richt, J.A. 2016. Antemortem detection of
chronic wasting disease prions in nasal brush collections and rectal biopsy
specimens from white-tailed deer by real time quaking-induced conversion.
Journal of Clinical Microbiology. 54(4):1108-1116.
Interpretive Summary: Chronic Wasting Disease (CWD), a fatal
neurodegenerative disease that occurs in farmed and wild cervids (deer and elk)
of North America, is a transmissible spongiform encephalopathy (TSE). TSEs are
caused by infectious proteins called prions that are resistant to various
methods of decontamination and environmental degradation. Early diagnosis of CWD
in wild and captive herds would be very helpful to controlling the spread of
CWD, for which there are not yet any preventative or treatment measures
available. The purpose of this study was to test a laboratory method of prion
detection (real-time Quaking Induced Conversion; RT-QuIC) that has the potential
to detect very low levels of infectious prions in samples collected from live
animals against the gold standard diagnostic where abnormal prion in tissues is
stained on a microscope slide. This study reports that RT-QuIC detects more
cases of CWD than standard methods, but also can identify a small number of
animals without CWD as being positive. In the case of CWD, where it is likely
that large numbers of animals within a herd may be positive, misidentifying a
negative as a positive may have less of an impact than in the case of other
prion diseases such as bovine spongiform encephalopathy considering that this
test allows testing much larger numbers of samples with a faster turn around
time than traditional methods. This information could have an impact on
regulatory and wildlife officials developing plans to reduce or eliminate CWD
and cervid farmers that want to ensure that their herd remains CWD-free.
Technical Abstract: Chronic wasting disease (CWD), a transmissible spongiform
encephalopathy of cervids, was first documented nearly fifty years ago in
Colorado and Wyoming and has since spread to cervids in 23 states, 2 Canadian
provinces, and the Republic of Korea. The increasing expansion of this disease
makes the development of sensitive diagnostic assays and antemortem sampling
techniques crucial for the mitigation of spread; this is especially true in
cases of relocation/reintroduction of farmed or free-ranging deer and elk, or
surveillance studies in private or protected herds where depopulation may be
contraindicated. This study sought to evaluate the sensitivity of the real-time
quaking-induced conversion (RT-QuIC) assay in samples collected antemortem.
Antemortem findings were then compared to results from ante- and postmortem
samples evaluated using the current gold standard diagnostic assay,
immunohistochemistry (IHC). Recto-anal mucosal associated lymphoid tissue
(RAMALT) biopsies and nasal brush collections from three separate herds of
farmed white-tailed deer (n=409) were evaluated, along with standard postmortem
microscopic analysis of brainstem at the level of the obex and retropharyngeal
lymph nodes. We hypothesized the sensitivity of RT-QuIC would be comparable to
IHC in antemortem tissues, and would correlate with both genotype and stage of
clinical disease. Our results showed that RAMALT testing by RT-QuIC had the
highest sensitivity (69.8%) when compared to postmortem testing. This data
suggests that RT-QuIC, like IHC, is a fairly sensitive assay for detection of
CWD prions in rectal biopsies and other antemortem samples, and with further
investigation has potential for large scale and rapid automated testing for CWD
diagnosis.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Title: Development and characterization of an ex-vivo brain slice culture
model of chronic wasting disease)
Author
item Kondru, Naveen item Greenlee, Justin item West greenlee, Mary item
Manne, Sireesha item Main, Roger item Halbur, Patrick item Kanthasamy, Arthi
item Kanthasamy, Anumantha
Submitted to: Prion Publication Type: Abstract only Publication Acceptance
Date: 3/31/2015 Publication Date: 5/25/2015 Citation: Kondru, N., Greenlee, J.,
Greenlee, H., Manne, S., Kong, Q., Halbur, P., Kanthasamy, A., Kanthasamy, A.
2015. Development and characterization of an ex-vivo brain slice culture model
of chronic wasting disease. Prion 2015. p. S68.
Interpretive Summary: Technical Abstract: Prion diseases have long
incubation times in vivo, therefore, modeling the diseases ex-vivo will advance
the development of rationale-based therapeutic strategies. An organotypic slice
culture assay (POSCA) was recently developed for scrapie prions by inoculating
mouse cerebellar brain slices with RML scrapie. However, efforts to develop a
POSCA model for CWD have been futile due to the species barrier between mouse
and cervids. To overcome this difficulty, we adopted a transgenic cervidized
(Tg12) mouse model and successfully developed an ex-vivo brain slice culture
model for CWD. We prepared 350-µm cerebellar slices from Tg12 mouse pups and
then incubated them with CWD brain homogenate and washed thoroughly. With the
genotypes of the pups blinded, the cultures were grown over 42-48 days before
being tested for CWD infectivity using the recently developed Real-time
quaking-induced conversion (RT-QuIC) assay. Hamster PrP was used as a substrate
for the assay. Slices from Tg12 cervidized pups with PrP+/- genotype tested
positive but slices from the Tg12 PrP -/- genotype did not. Infectivity was
present in 11 out of 11Tg 12 PrP+/-, whereas 0 out of 10 Tg12 PrP -/-. We
successfully cultured POSCA brain slices infected with RML scrapie as confirmed
by RT-QuIC and PK digestion assays. Biochemical studies revealed degenerative
changes and oxidative damage in the prion infected slice cultures. Our results
demonstrate that combining brain slice culture models of prion diseases with the
RT-QuIC assay offers a promising platform for studying the mechanisms of prion
proteinopathies as well as for screening anti-prion therapeutics.
CWD TESTING
Other diagnostic tests and technologies that allow more rapid testing of
larger numbers of samples continue to be developed. A rectal associated mucosal
lymphoid tissue (RAMALT) biopsy (live-animal) test has been developed by
researchers and appears to hold promise for future use in certain CWD monitoring
or management situations in farmed cervids. This technique utilizes the current
IHC testing technologies described above.
*** The RAMALT is not currently approved as an official test for CWD.
Seeded amplification of chronic wasting disease prions in nasal brushings
and recto-anal mucosa associated lymphoid tissues from elk by real time
quaking-induced conversion
Nicholas J. Haley#,a, Chris Siepkera, Laura L. Hoon-Hanksb, Gordon
Mitchellc, W. David Walterd, Matteo Mancae, Ryan J. Monellof, Jenny G. Powersf,
Margaret A. Wildf, Edward A. Hooverb, Byron Caugheye and Jürgen A. Richta +
Author Affiliations
Department of Diagnostic Medicine and Pathobiology, College of Veterinary
Medicine, Kansas State University (KSU), Manhattan, KS, USAa Department of
Microbiology, Immunology and Pathology, College of Veterinary Medicine and
Biomedical Sciences, Colorado State University, Fort Collins, CO, USAb Canadian
Food Inspection Agency, National and OIE Reference Laboratory for Scrapie and
CWD, Ottawa Laboratory Fallowfield, Ottawa, ON, Canadac U.S. Geological Survey,
Pennsylvania Cooperative Fish and Wildlife Research Unit, The Pennsylvania State
University, University Park, PA, USAd TSE/Prion Biochemistry Section, Laboratory
of Persistent Viral Diseases, Rocky Mountain Laboratories (RML), National
Institute of Allergy and Infectious Diseases, Hamilton, MT, USAe National Park
Service, Biological Resources Division, 1201 Oak Ridge Drive, Suite 200, Fort
Collins, Colorado 80525, USAf
ABSTRACT
Chronic wasting disease (CWD), a transmissible spongiform encephalopathy of
cervids, was first documented nearly fifty years ago in Colorado and Wyoming,
and has since been detected across North America and to the Republic of Korea.
The expansion of this disease makes the development of sensitive diagnostic
assays and antemortem sampling techniques crucial for the mitigation of spread;
this is especially true in cases of relocation/reintroduction, or prevalence
studies in large or protected herds where depopulation may be contraindicated.
This study sought to evaluate the sensitivity of the real-time quaking-induced
conversion (RT-QuIC) assay in recto-anal mucosa associated lymphoid tissue
(RAMALT) biopsies and nasal brushings collected antemortem. These findings were
compared to results from ante- and postmortem samples evaluated using
immunohistochemistry (IHC). RAMALT samples were collected from populations of
farmed and free-ranging Rocky Mountain elk (Cervus elaphus nelsoni, n=323), with
nasal brushes collected from a subpopulation of these animals (n=205). We
hypothesized the sensitivity of RT-QuIC would be comparable to IHC in RAMALT,
and would correspond to IHC of postmortem tissues. We found RAMALT sensitivity
(77.3%) to be highly correlative between RT-QuIC and IHC. Sensitivity was lower
when testing nasal brushings (34%), though both RAMALT and nasal brush
sensitivities were dependent on both PRNP genotype and disease progression
determined by obex score. These data suggest that RT-QuIC, like IHC, is a
relatively sensitive assay for detection of CWD prions in RAMALT biopsies, and
with further investigation has potential for large scale and rapid automated
testing for CWD in antemortem samples.
FOOTNOTES
↵#Corresponding author (e-mail: nicholas.j.haley@gmail.com) Copyright ©
2016, American Society for Microbiology. All Rights Reserved. http://jcm.asm.org/content/early/2016/02/11/JCM.02700-15.abstract
Saturday, February 20, 2016
Seeded amplification of chronic wasting disease prions in nasal brushings
and recto-anal mucosa associated lymphoid tissues from elk by real time
quaking-induced conversion
Sunday, February 14, 2016
Antemortem detection of chronic wasting disease prions in nasal brush
collections and rectal biopsies from white-tailed deer by real time
quaking-induced conversion
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Antemortem detection of chronic wasting disease prions in nasal
brush collections and rectal biopsies from white-tailed deer by real time
quaking-induced conversion
Authors
item Haley, Nicholas - item Siepker, Chris - item Walter, W. David - item
Thomsen, Bruce - item Greenlee, Justin item Lehmkuhl, Aaron - item Richt, Jürgen
-
Submitted to: Journal of Clinical Microbiology Publication Type: Peer
Reviewed Journal Publication Acceptance Date: November 27, 2015 Publication
Date: February 10, 2016 Citation: Haley, N.J., Siepker, C., Walter, W.D.,
Thomsen, B.V., Greenlee, J.J., Lehmkuhl, A.D., Richt, J.A. 2016. Antemortem
detection of chronic wasting disease prions in nasal brush collections and
rectal biopsy specimens from white-tailed deer by real time quaking-induced
conversion. Journal of Clinical Microbiology. 54(4):1108-1116.
Interpretive Summary: Chronic Wasting Disease (CWD), a fatal
neurodegenerative disease that occurs in farmed and wild cervids (deer and elk)
of North America, is a transmissible spongiform encephalopathy (TSE). TSEs are
caused by infectious proteins called prions that are resistant to various
methods of decontamination and environmental degradation. Early diagnosis of CWD
in wild and captive herds would be very helpful to controlling the spread of
CWD, for which there are not yet any preventative or treatment measures
available. The purpose of this study was to test a laboratory method of prion
detection (real-time Quaking Induced Conversion; RT-QuIC) that has the potential
to detect very low levels of infectious prions in samples collected from live
animals against the gold standard diagnostic where abnormal prion in tissues is
stained on a microscope slide. This study reports that RT-QuIC detects more
cases of CWD than standard methods, but also can identify a small number of
animals without CWD as being positive. In the case of CWD, where it is likely
that large numbers of animals within a herd may be positive, misidentifying a
negative as a positive may have less of an impact than in the case of other
prion diseases such as bovine spongiform encephalopathy considering that this
test allows testing much larger numbers of samples with a faster turn around
time than traditional methods. This information could have an impact on
regulatory and wildlife officials developing plans to reduce or eliminate CWD
and cervid farmers that want to ensure that their herd remains CWD-free.
Technical Abstract: Chronic wasting disease (CWD), a transmissible
spongiform encephalopathy of cervids, was first documented nearly fifty years
ago in Colorado and Wyoming and has since spread to cervids in 23 states, 2
Canadian provinces, and the Republic of Korea. The increasing expansion of this
disease makes the development of sensitive diagnostic assays and antemortem
sampling techniques crucial for the mitigation of spread; this is especially
true in cases of relocation/reintroduction of farmed or free-ranging deer and
elk, or surveillance studies in private or protected herds where depopulation
may be contraindicated. This study sought to evaluate the sensitivity of the
real-time quaking-induced conversion (RT-QuIC) assay in samples collected
antemortem. Antemortem findings were then compared to results from ante- and
postmortem samples evaluated using the current gold standard diagnostic assay,
immunohistochemistry (IHC). Recto-anal mucosal associated lymphoid tissue
(RAMALT) biopsies and nasal brush collections from three separate herds of
farmed white-tailed deer (n=409) were evaluated, along with standard postmortem
microscopic analysis of brainstem at the level of the obex and retropharyngeal
lymph nodes. We hypothesized the sensitivity of RT-QuIC would be comparable to
IHC in antemortem tissues, and would correlate with both genotype and stage of
clinical disease. Our results showed that RAMALT testing by RT-QuIC had the
highest sensitivity (69.8%) when compared to postmortem testing. This data
suggests that RT-QuIC, like IHC, is a fairly sensitive assay for detection of
CWD prions in rectal biopsies and other antemortem samples, and with further
investigation has potential for large scale and rapid automated testing for CWD
diagnosis.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Clinical stage of infection is critical in the antemortem diagnosis
of chronic wasting disease in deer and elk
Authors
item Siepker, Chris - item Haley, Nicholas - item Walter, W. David - item
Hoon-Hanks, Laura - item Monello, Ryan - item Powers, Jenny - item Greenlee,
Justin item Thomsen, Bruce - item Lehmkuhl, Aaron - item Mitchell, Gordon - item
Nichols, Tracy - item Hoover, Edward - item Richt, Juergen -
Submitted to: Prion Publication Type: Abstract Only Publication Acceptance
Date: March 5, 2015 Publication Date: N/A
Technical Abstract: Chronic wasting disease (CWD) is an efficiently
transmitted spongiform encephalopathy of cervids (e.g. deer, elk, and moose),
and is the only known prion disease affecting both free-ranging wildlife and
captive animals. The antemortem detection of CWD and other prion diseases has
proven difficult, due in part to difficulties in identifying an appropriate
peripheral tissue specimen and complications with conventional test sensitivity.
At present, biopsies of the recto-anal mucosal-associated lymphoid tissues
(RAMALT) have shown promising sensitivity and are practical to collect in live
animals. Nasal brush collections have likewise proven both sensitive and
practical for identification of prion infections in humans. In this study, we
evaluated both RAMALT and nasal brush collections by real time quaking-induced
conversion (RT-QuIC), and compared our findings to RAMALT immunohistochemistry
as well as conventional postmortem evaluation of obex and retropharyngeal lymph
node tissues from over 700 captive and free-ranging deer and elk in areas with
endemic CWD. We correlated our results with various clinical findings, including
pathological stage of infection as determined by obex scoring, PrP genotype,
age, and sex. While the sensitivity of RAMALT RT-QuIC analyses exceeded that of
RAMALT IHC (69-80% vs. >44%) and nasal brush collections (15-30%), the
sensitivity of both biopsy and nasal brush analyses were dependent primarily on
clinical stage of disease, although PrP genotype was also an important predictor
of sample positivity. ***Our findings further demonstrate the potential and
limitations of antemortem sample analyses by RT-QuIC in the identification and
management of prion diseases.
*** CHRONIC WASTING DISEASE TESTING PROTOCAL FOR WILD CERVIDAE proposing
the United States Animal Health Association (USAHA) urge the USDA to amend CFR
81.3 ***
Committee Business:
One resolution was proposed by a committee member titled CHRONIC WASTING
DISEASE TESTING PROTOCAL FOR WILD CERVIDAE proposing the United States Animal
Health Association (USAHA) urge the USDA to amend CFR 81.3 (b); proposing wild
cervids captured for interstate movement and release, have two forms of
identification, one of which that is official identification, must be PrP
genotyped for Chronic Wasting Disease resistance, tested for Chronic Wasting
Disease using a rectal biopsy test. The committee discussed and debated the
terms and science related to this resolution proposal including that currently
there is no science indicating there are “genotype resistant” cervids to
acquiring the CWD prion. The term “resistant” is miss-leading. There are only
different cervid genotypes that acquire the infectious prions at different rates
and show clinical signs at variable rates, some at prolonged periods after
acquiring the prion or they are slow to accumulate detectable levels.. Since all
infected animals would be presumed to be capable of shedding the prions into the
environment, genotypes with clinical “resistance” or prolonged indication of
clinical presentation of the disease, may well potentially be considered
prolonged shedders of the prion. Additionally there was discussion put forth by
several committee members concerning the lack of regulatory validation of the
rectal biopsy test. Also, the test can only be used on young animals and there I
significant test sensitivity and specificity variability between cervid species
when using this test. A new motion to the proposed resolution was to table this
resolution, reword the resolution potentially to be a recommendation for USDA to
provide a guidance document to the states for surveillance of CWD on interstate
translocations od wild cervids. It was proposed that this new
resolution/recommendation be discussed during the Farmed Cervid Subcommittee and
forward then to the Captive Wildlfie and Alternative Livestock committee. The
motion was proposed by member Charlie Seale and seconded by member Sean Shaffer
which was passed by committee. The Committee on Wildlife Diseases adjourned at
515 PM.
Tuesday, September 22, 2015
*** Host Determinants of Prion Strain Diversity Independent of Prion
Protein Genotype
Friday, August 28, 2015
*** Chronic Wasting Disease CWD TSE Prion Diagnostics and subclinical
infection
Monday, July 18, 2016
Texas Parks Wildlife Dept TPWD HIDING TSE (CWD) in Deer Herds, Farmers
Sampling Own Herds, Rapid Testing, False Negatives, a Recipe for Disaster
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
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 ;
with CWD TSE Prions, I am not sure there is any absolute yet, other than
what we know with transmission studies, and we know tse prion kill, and tse
prion are bad. science shows to date, that indeed soil, dirt, some better than
others, can act as a carrier. same with objects, farm furniture. take it with
how ever many grains of salt you wish, or not. if load factor plays a role in
the end formula, then everything should be on the table, in my opinion. see
;
***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 ;
Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil
Particles
Author Summary
Transmissible spongiform encephalopathies (TSEs) are a group of incurable
neurological diseases likely caused by a misfolded form of the prion protein.
TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’
disease) in cattle, chronic wasting disease in deer and elk, and
Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are
unique among TSEs because they can be transmitted between animals, and the
disease agents appear to persist in environments previously inhabited by
infected animals. Soil has been hypothesized to act as a reservoir of
infectivity and to bind the infectious agent. In the current study, we orally
dosed experimental animals with a common clay mineral, montmorillonite, or whole
soils laden with infectious prions, and compared the transmissibility to unbound
agent. We found that prions bound to montmorillonite and whole soils remained
orally infectious, and, in most cases, increased the oral transmission of
disease compared to the unbound agent. The results presented in this study
suggest that soil may contribute to environmental spread of TSEs by increasing
the transmissibility of small amounts of infectious agent in the
environment.
tse prion soil
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
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.
>>>Particle-associated PrPTSE molecules may migrate from locations
of deposition via transport processes affecting soil particles, including
entrainment in and movement with air and overland flow. <<<
Fate of Prions in Soil: A Review
Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*
Several reports have shown that prions can persist in soil for several
years. Significant interest remains in developing methods that could be applied
to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests
that serine proteases and the microbial consortia in stimulated soils and
compost may partially degrade PrPTSE. Transition metal oxides in soil (viz.
manganese oxide) may also mediate prion inactivation. Overall, the effect of
prion attachment to soil particles on its persistence in the environment is not
well understood, and additional study is needed to determine its implications on
the environmental transmission of scrapie and CWD.
P.161: Prion soil binding may explain efficient horizontal CWD transmission
Conclusion. Silty clay loam exhibits highly efficient prion binding,
inferring a durable environmental reservoir, and an efficient mechanism for
indirect horizontal CWD transmission.
>>>Another alternative would be an absolute prohibition on the
movement of deer within the state for any purpose. While this alternative would
significantly reduce the potential spread of CWD, it would also have the
simultaneous effect of preventing landowners and land managers from implementing
popular management strategies involving the movement of deer, and would deprive
deer breeders of the ability to engage in the business of buying and selling
breeder deer. Therefore, this alternative was rejected because the department
determined that it placed an avoidable burden on the regulated
community.<<<
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 ***
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
>>>Another alternative would be an absolute prohibition on the
movement of deer within the state for any purpose. While this alternative would
significantly reduce the potential spread of CWD, it would also have the
simultaneous effect of preventing landowners and land managers from implementing
popular management strategies involving the movement of deer, and would deprive
deer breeders of the ability to engage in the business of buying and selling
breeder deer. Therefore, this alternative was rejected because the department
determined that it placed an avoidable burden on the regulated
community.<<<
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.
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
Tuesday, July 12, 2016
Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE,
TSE, Prion Zoonosis Science History
see history of NIH may destroy human brain collection
Friday, February 05, 2016
*** Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION
Detections in Farmed Cervids and Wild ***
Sunday, July 17, 2016
*** CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL REPORT UPDATE JULY 17 2016
***
***at present, no cervid PrP allele conferring absolute resistance to prion
infection has been identified.
P-145 Estimating chronic wasting disease resistance in cervids using real
time quaking- induced conversion
Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David
Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2
1 Department of Microbiology and Immunology, Midwestern University, United
States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State
University; 3Prion Research Center; Colorado State University; 4U.S. Geological
Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural
Research Service, United States Department of Agriculture; 6Canadian Food
Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWO
In mammalian species, the susceptibility to prion diseases is affected, in
part, by the sequence of the host's prion protein (PrP). In sheep, a gradation
from scrapie susceptible to resistant has been established both in vivo and in
vitro based on the amino acids present at PrP positions 136, 154, and 171, which
has led to global breeding programs to reduce the prevalence of scrapie in
domestic sheep. In cervids, resistance is commonly characterized as a delayed
progression of chronic wasting disease (CWD); at present, no cervid PrP allele
conferring absolute resistance to prion infection has been identified. To model
the susceptibility of various naturally-occurring and hypothetical cervid PrP
alleles in vitro, we compared the amplification rates and efficiency of various
CWD isolates in recombinant PrPC using real time quaking-induced conversion. We
hypothesized that amplification metrics of these isolates in cervid PrP
substrates would correlate to in vivo susceptibility - allowing susceptibility
prediction for alleles found at 10 frequency in nature, and that there would be
an additive effect of multiple resistant codons in hypothetical alleles. Our
studies demonstrate that in vitro amplification metrics predict in vivo
susceptibility, and that alleles with multiple codons, each influencing
resistance independently, do not necessarily contribute additively to
resistance. Importantly, we found that the white-tailed deer 226K substrate
exhibited the slowest amplification rate among those evaluated, suggesting that
further investigation of this allele and its resistance in vivo are warranted to
determine if absolute resistance to CWD is possible.
***at present, no cervid PrP allele conferring absolute resistance to prion
infection has been identified.
PRION 2016 CONFERENCE TOKYO
Saturday, May 28, 2016
*** Infection and detection of PrPCWD in soil from CWD infected farm in
Korea Prion 2016 Tokyo ***
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
Summary
The previous assessment concentrated on the incursion of disease from North
America through the imports of animal feed or the movement of contaminated
clothing, footwear and equipment. The results suggested that import of pet feed
was a non-negligible risk, but given the unlikely contact of resident deer in GB
with such non-ruminant feed, this was considered overall a negligible to very
low risk. The movement of contaminated clothing, footwear or equipment
(particularly hunting equipment) could pose a very low risk, although the volume
of contaminated soil which would need to be ingested to give rise to an
infection is likely to be higher than would be present. There is a variable
level uncertainty in all these assessments.
The new assessment focuses on an additional potential route of entry: the
importation of natural deer urine lures. The main conclusions from this
assessment are:
In areas of North America where CWD has been reported, given that CWD is
excreted in faeces, saliva, urine and blood, and survives in the environment for
several years there is a medium probability that the deer urine in North America
contains CWD (high uncertainty; depends on the source of deer used for
production).
The risk of a deer in GB being infected per 30 ml bottle of urine
imported from the USA is very low, albeit with high uncertainty. Overall it is
concluded that the risk of at least one infection of deer in the UK with CWD per
year from deer urine lures imported from the USA is medium. This assumes a high
number of 30 ml bottles imported per year from all areas of the USA.
None of the species affected by CWD in North America are present in GB.
For a British species to become infected with CWD following exposure, the dose
and inherent susceptibility of the species will be important. Based on current
scientific evidence Red deer (Cervus elaphus elaphus) are susceptible to CWD,
Fallow deer (Dama dama) are likely to be less susceptible and Roe deer
(Capreolus capreolus) have a gene conferring susceptibility. Therefore, it is
likely that given exposure to an infectious dose of CWD, deer in GB could become
infected with CWD.
Overall, the probability of importing CWD into GB from North America and
causing infection in British deer is uncertain but likely to be negligible to
very low via movement of deer hunters, other tourists and British servicemen and
very low via imported (non-
2
ruminant) animal feed and medium for the use of lures. However, if it was
imported and (a) deer did become infected with CWD, the consequences would be
severe as eradication of the disease is impossible, it is clinically
indistinguishable from BSE infection in deer (Dalgleish et al., 2008) and
populations of wild and farmed deer would be under threat.
The USA has implemented a Herd Certification Programme for farmed and
captive cervids. So far, 29 States are approved for HCP status (APHIS, 2015).
The list includes States such as Colorado, where CWD is present, therefore it is
recommended that any sourcing of such natural urine lures should be not only
from States with an HCP programme, but also from a herd which is registered as
being regularly tested free of CWD.
Animal urine is not considered a commodity which is subject to animal
by-products legislation for imports. Internet sales are common and although a
license would be required, there are no conditions for the safe sourcing of such
products. Deer urine lures are also available in Europe and may be produced from
carcases of hunted deer. The use of deer urine produced from a species not
present in Europe (such as white tailed deer) is questioned for its value with
native GB deer according to the British Deer Society survey.
Background
Thursday, April 07, 2016
What is the risk of chronic wasting disease being introduced into Great
Britain? An updated Qualitative Risk Assessment March 2016
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...
What is the risk of chronic wasting disease being introduced into Great
Britain? A Qualitative Risk Assessment October 2012
Tuesday, September 13, 2016
Prion-Seeding Activity Is widely Distributed in Tissues of Sporadic
Creutzfeldt-Jakob Disease Patients
Wednesday, September 07, 2016
Michigan Launches an investigation into the Detroit Medical Center dirty,
broken and missing surgical instruments, what about the CJD TSE PRION iatrogenic
threat past and present therefrom?
*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes
contaminated during neurosurgery ***
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological
Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a
middle aged woman with progressive dementia were previously implicated in the
accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger
patients. The diagnoses of CJD have been confirmed for all three cases. More
than two years after their last use in humans, after three cleanings and
repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were
implanted in the cortex of a chimpanzee. Eighteen months later the animal became
ill with CJD. This finding serves to re-emphasise the potential danger posed by
reuse of instruments contaminated with the agents of spongiform
encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
Monday, August 22, 2016
CREUTZFELDT JAKOB DISEASE USA 2015 SPORADIC CJD TOTAL FIGURES REACHES
HIGHEST ANNUAL COUNT TO DATE AT 239 CONFIRMED CASES
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
11:33 AM
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